TY - JOUR T1 - Influence of age on the secretory rates of the human minor salivary glands and whole saliva. AN - 85257663; pmid-8240083 AB - This investigation comprised two studies of healthy, unmedicated individuals. The first measured the effect of collection time on the volume of secretions of the minor salivary glands at four specified areas of the lower lip of 13 individuals before and after a mild gustatory stimulus. The second (n = 51) monitored the influence of age and gender on the secretory rates of unstimulated labial, buccal and palatal salivary glands. Also, unstimulated and stimulated flow rates of whole saliva were monitored to provide a point of reference. Volumes of minor gland secretions were measured with a Periotron unit. Results of the first study indicated a linear increase in volumes with collection time (15, 30, 45 and 60 s). Flow rates were similar among the four labial sites, approx. 1 microliter/cm2/min, and were not influenced by mild citric acid stimulation. Results of the second study indicated that flow rates differed significantly (p = 0.0001) among the anatomical sites, with similar rates on the right- and left-hand sides. Gender exerted no influence on flow from the minor salivary glands. Similarly, age exerted no influence on flow from the buccal or labial glands. However, the secretory rate for the palatal glands decreased significantly with age (r = -0.44; p < 0.005). As for unstimulated whole saliva, secretory rates were not influenced by age nor gender; rates for stimulated whole saliva increased with age (r = 0.31; p < 0.05). No association was detected between the flow rates of the whole saliva and that of the minor salivary glands. JF - Archives of Oral Biology AU - Shern, R J AU - Fox, P C AU - Li, S H AD - Clinical Investigations and Patient Care Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892. PY - 1993 SP - 755 EP - 761 VL - 38 IS - 9 SN - 0003-9969, 0003-9969 KW - Regression Analysis KW - Age Factors KW - Salivation KW - Sex Factors KW - Human KW - Aging KW - Citric Acid KW - Specimen Handling KW - Aged KW - Secretory Rate KW - Citrates KW - Multivariate Analysis KW - Stimulation, Chemical KW - Salivary Glands, Minor KW - Aged, 80 and over KW - Adult KW - Middle Age KW - Saliva KW - Time Factors KW - Male KW - Female UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85257663?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+Oral+Biology&rft.atitle=Influence+of+age+on+the+secretory+rates+of+the+human+minor+salivary+glands+and+whole+saliva.&rft.au=Shern%2C+R+J%3BFox%2C+P+C%3BLi%2C+S+H&rft.aulast=Shern&rft.aufirst=R&rft.date=1993-09-01&rft.volume=38&rft.issue=9&rft.spage=755&rft.isbn=&rft.btitle=&rft.title=Archives+of+Oral+Biology&rft.issn=00039969&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Sodium- and chloride-dependent transporters in brain, kidney, and gut: lessons from complementary DNA cloning and structure-function studies. AN - 76307857; 7922216 AB - The family of Na(+)- and Cl(-)-dependent, 12 transmembrane domain transporter proteins now includes transporters for neurotransmitter molecules in the brain and for substances important in extraneuronal tissues, including adrenal, kidney, and gut. Transported substrates include monoamine and amino acid neurotransmitters and nonperturbing osmolytes. A common protein topology is predicted and features intracellular N- and C-termini possessing phosphorylation sites and at least one large extramembranous loop with N-linked glycosylation. Using the rat dopamine transporter as a template, molecular modeling of putative transmembrane domains coupled with amino acid sequence conservation analysis indicates amino acid residues potentially involved in substrate and/or ion recognition. Targeting such residues with site-directed mutagenesis will help clarify substrate and ion binding sites and should facilitate rational design of therapeutics to combat depression, locomotor disorders, and substance abuse. JF - Current opinion in nephrology and hypertension AU - Surratt, C K AU - Wang, J B AU - Yuhasz, S AU - Amzel, M AU - Kwon, H M AU - Handler, J S AU - Uhl, G R AD - National Institute on Drug Abuse, National Institutes of Health, Bethesda, Maryland. Y1 - 1993/09// PY - 1993 DA - September 1993 SP - 744 EP - 760 VL - 2 IS - 5 SN - 1062-4821, 1062-4821 KW - Carrier Proteins KW - 0 KW - Chlorides KW - Dopamine Plasma Membrane Transport Proteins KW - Membrane Glycoproteins KW - Membrane Transport Proteins KW - Nerve Tissue Proteins KW - DNA KW - 9007-49-2 KW - Sodium KW - 9NEZ333N27 KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Animals KW - Kidney -- metabolism KW - Models, Molecular KW - Humans KW - Digestive System -- metabolism KW - Dopamine -- metabolism KW - Amino Acid Sequence KW - Brain -- metabolism KW - Structure-Activity Relationship KW - Cloning, Molecular KW - DNA -- genetics KW - Molecular Sequence Data KW - Carrier Proteins -- metabolism KW - Carrier Proteins -- chemistry KW - Carrier Proteins -- genetics KW - Chlorides -- metabolism KW - Sodium -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76307857?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+opinion+in+nephrology+and+hypertension&rft.atitle=Sodium-+and+chloride-dependent+transporters+in+brain%2C+kidney%2C+and+gut%3A+lessons+from+complementary+DNA+cloning+and+structure-function+studies.&rft.au=Surratt%2C+C+K%3BWang%2C+J+B%3BYuhasz%2C+S%3BAmzel%2C+M%3BKwon%2C+H+M%3BHandler%2C+J+S%3BUhl%2C+G+R&rft.aulast=Surratt&rft.aufirst=C&rft.date=1993-09-01&rft.volume=2&rft.issue=5&rft.spage=744&rft.isbn=&rft.btitle=&rft.title=Current+opinion+in+nephrology+and+hypertension&rft.issn=10624821&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-10-28 N1 - Date created - 1994-10-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Role of metallothionein in zinc(II) and chromium(III) mediated tolerance to carbon tetrachloride hepatotoxicity: evidence against a trichloromethyl radical-scavenging mechanism. AN - 76168553; 8292750 AB - The .CCl3 radical generated during the metabolism of CCl4 is readily spin trapped in vivo and in vitro by phenyl N-tert-butylnitrone (PBN) to form the stable PBN/.CCl3 radical adduct, which can then be extracted into organic solvents and detected by ESR spectroscopy. We have used this technique to examine the proposed protective roles of Zn(II), Cr(III), and metallothionein (MT) against carbon tetrachloride toxicity in vivo. Hepatic MT, which is induced by Zn(II), has been proposed to protect against CCl4-induced cellular damage by scavenging the free radical metabolites formed. CCl4-induced hepatotoxicity was significantly suppressed in male Sprague-Dawley rats pretreated with a single dose of 5 mg/kg Zn(II) or Cr(III) according to standard serum assays for liver-specific enzymes, and hepatic MT was elevated after pretreatment with either Zn(II) or Cr(III). In vitro, no difference was detected in either the amount of CCl4-derived free radical metabolites formed or the rate at which they were formed by microsomes from rats pretreated 24 h in advance with 5 mg/kg Zn(II) or Cr(III). Extraction of rat liver with 2:1 chloroform/methanol 1 h after the administration of a 0.8 mL/kg intraperitoneal or intragastric dose of CCl4 also revealed no difference in the amount of trichloromethyl radical spin trapped in vivo following pretreatment with either Zn(II) or Cr(III). These results suggest that pretreatment with either Zn(II) or Cr(III) does not affect CCl4 metabolism nor does the MT significantly scavenge the trichloromethyl free radical metabolite. JF - Chemical research in toxicology AU - Hanna, P M AU - Kadiiska, M B AU - Jordan, S J AU - Mason, R P AD - Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. PY - 1993 SP - 711 EP - 717 VL - 6 IS - 5 SN - 0893-228X, 0893-228X KW - Free Radical Scavengers KW - 0 KW - Chromium KW - 0R0008Q3JB KW - Chloroform KW - 7V31YC746X KW - Metallothionein KW - 9038-94-2 KW - Zinc KW - J41CSQ7QDS KW - Index Medicus KW - Rats KW - Animals KW - Rats, Sprague-Dawley KW - Microsomes, Liver -- metabolism KW - Microsomes, Liver -- enzymology KW - In Vitro Techniques KW - Male KW - Chloroform -- metabolism KW - Chemical and Drug Induced Liver Injury -- prevention & control KW - Zinc -- pharmacology KW - Carbon Tetrachloride Poisoning -- prevention & control KW - Chromium -- pharmacology KW - Metallothionein -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76168553?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+research+in+toxicology&rft.atitle=Role+of+metallothionein+in+zinc%28II%29+and+chromium%28III%29+mediated+tolerance+to+carbon+tetrachloride+hepatotoxicity%3A+evidence+against+a+trichloromethyl+radical-scavenging+mechanism.&rft.au=Hanna%2C+P+M%3BKadiiska%2C+M+B%3BJordan%2C+S+J%3BMason%2C+R+P&rft.aulast=Hanna&rft.aufirst=P&rft.date=1993-09-01&rft.volume=6&rft.issue=5&rft.spage=711&rft.isbn=&rft.btitle=&rft.title=Chemical+research+in+toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-03-01 N1 - Date created - 1994-03-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Cytotoxic effects of vascular smooth muscle cells of the chimeric toxin, heparin binding TGF alpha-Pseudomonas exotoxin. AN - 76163342; 8287449 AB - Smooth muscle cell proliferation appears to be very important in restenosis after angioplasty. A chimeric toxin created by genetically fusing the gene encoding TGF alpha (targets the EGF receptor) to the gene encoding Pseudomonas exotoxin (PE) preferentially kills rapidly proliferating smooth muscle cells. Recently, a heparin binding EGF-like growth factor (HB-EGF) has been identified. The HB domain enhances the mitogenic activity for smooth muscle cells. The purpose of this study was to design a new chimeric toxin, having both heparin binding and EGF receptor binding function, and to determine whether it is more cytotoxic to smooth muscle cells. By recombinant DNA techniques, a new chimeric toxin, HB-TGF alpha-PE4EKDEL, was synthesised. Cytotoxic assays were performed by assessing the capacity to inhibit protein synthesis of rat vascular smooth muscle cells. The toxin preferentially killed rapidly proliferating smooth muscle cells (p < 0.025). The HB domain increased the cytotoxicity of the molecule when compared to the other chimeric toxins tested against smooth muscle cells. The cytotoxic effect of the new molecule was significantly decreased by exogenously added heparin (p < 0.05). The presence of a heparin binding domain increases the smooth muscle cell cytotoxicity of the TGF alpha fusion toxin, perhaps because HB-TGF alpha-PE4EKDEL functions as a molecule with two ligands. It will be important to determine whether the greater smooth muscle cell cytotoxicity that exists in vitro will facilitate the specific targeting and killing of rapidly proliferating cells in vivo. JF - Cardiovascular research AU - Fu, Y M AU - Mesri, E A AU - Yu, Z X AU - Kreitman, R J AU - Pastan, I AU - Epstein, S E AD - National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/09// PY - 1993 DA - September 1993 SP - 1691 EP - 1697 VL - 27 IS - 9 SN - 0008-6363, 0008-6363 KW - Exotoxins KW - 0 KW - Immunotoxins KW - Recombinant Fusion Proteins KW - Transforming Growth Factor alpha KW - transforming growth factor(alpha)-Pseudomonas exotoxin A (35) KW - Heparin KW - 9005-49-6 KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Leucine KW - GMW67QNF9C KW - Index Medicus KW - Rats KW - Animals KW - Rats, Sprague-Dawley KW - Receptor, Epidermal Growth Factor -- metabolism KW - Cells, Cultured KW - Leucine -- metabolism KW - Cell Division -- drug effects KW - Heparin -- metabolism KW - Protein Binding KW - Muscles -- cytology KW - Exotoxins -- pharmacology KW - Muscles -- metabolism KW - Transforming Growth Factor alpha -- pharmacology KW - Recombinant Fusion Proteins -- pharmacology KW - Immunotoxins -- pharmacology KW - Muscles -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76163342?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cardiovascular+research&rft.atitle=Cytotoxic+effects+of+vascular+smooth+muscle+cells+of+the+chimeric+toxin%2C+heparin+binding+TGF+alpha-Pseudomonas+exotoxin.&rft.au=Fu%2C+Y+M%3BMesri%2C+E+A%3BYu%2C+Z+X%3BKreitman%2C+R+J%3BPastan%2C+I%3BEpstein%2C+S+E&rft.aulast=Fu&rft.aufirst=Y&rft.date=1993-09-01&rft.volume=27&rft.issue=9&rft.spage=1691&rft.isbn=&rft.btitle=&rft.title=Cardiovascular+research&rft.issn=00086363&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-02-22 N1 - Date created - 1994-02-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Clinical pharmacological issues in treating psychiatric disorders of patients with mental retardation. AN - 76157819; 8281242 AB - The following practical issues in psychopharmacotherapy of patients with mental retardation (MR) or other developmental disability (DD) are discussed, with some theoretical speculations: Persons with MR/DD have high rates of psychiatric disorders/symptoms, many of which are drug-responsive and not satisfactorily treated with other modalities alone. However, diagnosis is often complicated by concurrent multiple disorders (both psychiatric and medical/surgical), masking or distortion of symptoms, and communication impairments. Comorbidity and associated treatments should be considered in medication choice. Compared to psychiatric patients of normal IQ, patients with MR may be more sensitive to side effects and toxicity as well as responsive to lower doses, possibly related to less neuronal substrate, qualitative brain differences, or developmental stage. Unexpected or disappointing drug responses may also be related to such statistical quirks as "end-of-curve" phenomena. Ripples, ratcheting, and other ecobehavioral considerations influence treatment outcome and drug management. Target symptoms and expected drug benefits should be defined in consultation with caregivers as well as, when possible, the patient. Because drug responses of patients with MR are especially unpredictable, unreliable, sensitive to dose, and fraught with side effects, each medication trial might ideally be approached as a single-subject experiment on a compassionate protocol: quantify the baseline with ratings, behavior counts or other objective measures; start low and titrate slowly; monitor progress with repeated objective measures. JF - Annals of clinical psychiatry : official journal of the American Academy of Clinical Psychiatrists AU - Arnold, L E AD - Child and Adolescent Disorders Research Branch, NIMH, Rockville, Md., 20857. Y1 - 1993/09// PY - 1993 DA - September 1993 SP - 189 EP - 197 VL - 5 IS - 3 SN - 1040-1237, 1040-1237 KW - Psychotropic Drugs KW - 0 KW - Index Medicus KW - Brain -- physiopathology KW - Brain -- abnormalities KW - Psychiatric Status Rating Scales KW - Humans KW - Brain -- drug effects KW - Psychotropic Drugs -- therapeutic use KW - Psychotropic Drugs -- adverse effects KW - Male KW - Female KW - Intellectual Disability -- complications KW - Mental Disorders -- drug therapy KW - Mental Disorders -- metabolism KW - Mental Disorders -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76157819?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+clinical+psychiatry+%3A+official+journal+of+the+American+Academy+of+Clinical+Psychiatrists&rft.atitle=Clinical+pharmacological+issues+in+treating+psychiatric+disorders+of+patients+with+mental+retardation.&rft.au=Arnold%2C+L+E&rft.aulast=Arnold&rft.aufirst=L&rft.date=1993-09-01&rft.volume=5&rft.issue=3&rft.spage=189&rft.isbn=&rft.btitle=&rft.title=Annals+of+clinical+psychiatry+%3A+official+journal+of+the+American+Academy+of+Clinical+Psychiatrists&rft.issn=10401237&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-02-14 N1 - Date created - 1994-02-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - CONF T1 - Fate, transport, and interactions of metals. AN - 76139524; 7903938 JF - Environmental health perspectives AU - Dieter, M P Y1 - 1993/09// PY - 1993 DA - September 1993 SP - 344 EP - 345 VL - 101 IS - 4 KW - Hazardous Waste KW - 0 KW - Metals KW - Index Medicus KW - Risk Factors KW - Humans KW - Environmental Monitoring KW - Metals -- chemistry KW - Metals -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76139524?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=Environmental+health+perspectives&rft.atitle=Fate%2C+transport%2C+and+interactions+of+metals.&rft.au=Dieter%2C+M+P&rft.aulast=Dieter&rft.aufirst=M&rft.date=1993-09-01&rft.volume=101&rft.issue=4&rft.spage=344&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-02-09 N1 - Date created - 1994-02-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Impulse control disorders. AN - 76102220; 7504705 JF - International clinical psychopharmacology AU - Linnoila, M AU - Virkkunen, M AU - George, T AU - Higley, D AD - Laboratory of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD. Y1 - 1993/09// PY - 1993 DA - September 1993 SP - 53 EP - 56 VL - 8 Suppl 1 SN - 0268-1315, 0268-1315 KW - Serotonin KW - 333DO1RDJY KW - Hydroxyindoleacetic Acid KW - 54-16-0 KW - Index Medicus KW - Frontal Lobe -- physiopathology KW - Serotonin -- physiology KW - Alcoholism -- diagnosis KW - Risk Factors KW - Humans KW - Alcoholism -- physiopathology KW - Violence KW - Alcoholism -- psychology KW - Aggression -- physiology KW - Disruptive, Impulse Control, and Conduct Disorders -- diagnosis KW - Disruptive, Impulse Control, and Conduct Disorders -- physiopathology KW - Disruptive, Impulse Control, and Conduct Disorders -- psychology KW - Hydroxyindoleacetic Acid -- cerebrospinal fluid UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76102220?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+clinical+psychopharmacology&rft.atitle=Impulse+control+disorders.&rft.au=Linnoila%2C+M%3BVirkkunen%2C+M%3BGeorge%2C+T%3BHigley%2C+D&rft.aulast=Linnoila&rft.aufirst=M&rft.date=1993-09-01&rft.volume=8+Suppl+1&rft.issue=&rft.spage=53&rft.isbn=&rft.btitle=&rft.title=International+clinical+psychopharmacology&rft.issn=02681315&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-01-11 N1 - Date created - 1994-01-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - A system for testing the development and reversal of anticonvulsant tolerance to benzodiazepines in mice. AN - 76100617; 7902275 AB - Tolerance to the anticonvulsant effects of benzodiazepines limits their use in epilepsy treatment. Animal models producing tolerance have been developed, but they require repetitive injections over several days or use silastic capsules which must be made for each drug and do not provide a constant infusion rate. Alzet 2001 osmotic pumps deliver at a constant rate (1 microliter/h) and dosage can be easily adjusted. Various solvents, PEG 400, propylene glycol, 2% Tween, 50% DMSO, saline, Molecusol, and 0.5% methyl cellulose, were tried and found unsuitable because benzodiazepines were not maintained in solution or proconvulsant activity was seen. Tetraglycol was chosen as it did not demonstrate these shortcomings. Anticonvulsant activity was evaluated by PTZ i.v. tail infusion using forelimb clonus as the endpoint. This study describes a simple method for testing the development of tolerance and its reversal with flumazenil or ZK 93426. At 72 h of pump infusion with diazepam or flunitrazepam, tolerance to anticonvulsant activity was evident. Acute treatment with flumazenil or ZK 93426 reversed this tolerance. When flumazenil or ZK 93426 was given to diazepam tolerant mice, this reversal was complete. In flunitrazepam tolerant mice reversal with flumazenil was partial, but significant. When flumazenil was chronically coinfused with diazepam or flunitrazepam, anticonvulsant activity was antagonized. Similarly, when ZK 93426 was coinfused with diazepam, anticonvulsant activity was antagonized. The method described is suitable for screening putative anticonvulsant drugs for development of tolerance and the reversal of tolerance by other compounds. JF - Epilepsy research AU - Torchin, C D AU - Kapetanovic, I M AU - Kupferberg, H J AD - Preclinical Pharmacology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/09// PY - 1993 DA - September 1993 SP - 27 EP - 35 VL - 16 IS - 1 SN - 0920-1211, 0920-1211 KW - Anti-Anxiety Agents KW - 0 KW - Anticonvulsants KW - Carbolines KW - Solvents KW - Flumazenil KW - 40P7XK9392 KW - Flunitrazepam KW - 620X0222FQ KW - ZK 93426 KW - 89592-45-0 KW - Diazepam KW - Q3JTX2Q7TU KW - Pentylenetetrazole KW - WM5Z385K7T KW - Index Medicus KW - Animals KW - Infusion Pumps, Implantable KW - Diazepam -- pharmacology KW - Mice KW - Infusions, Parenteral KW - Flumazenil -- pharmacology KW - Drug Tolerance KW - Mice, Inbred Strains KW - Pentylenetetrazole -- toxicity KW - Pentylenetetrazole -- administration & dosage KW - Carbolines -- pharmacology KW - Flunitrazepam -- pharmacology KW - Time Factors KW - Male KW - Seizures -- chemically induced KW - Anticonvulsants -- pharmacology KW - Anti-Anxiety Agents -- pharmacology KW - Anti-Anxiety Agents -- administration & dosage KW - Seizures -- physiopathology KW - Seizures -- drug therapy KW - Anticonvulsants -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76100617?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Epilepsy+research&rft.atitle=A+system+for+testing+the+development+and+reversal+of+anticonvulsant+tolerance+to+benzodiazepines+in+mice.&rft.au=Torchin%2C+C+D%3BKapetanovic%2C+I+M%3BKupferberg%2C+H+J&rft.aulast=Torchin&rft.aufirst=C&rft.date=1993-09-01&rft.volume=16&rft.issue=1&rft.spage=27&rft.isbn=&rft.btitle=&rft.title=Epilepsy+research&rft.issn=09201211&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-28 N1 - Date created - 1993-12-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - A measure of tumorigenic potency incorporating dose-response shape. AN - 76095824; 8241378 AB - Many researchers have considered the problem of ranking chemical agents based on their carcinogenic potency. Sawyer et al. (1984, Biometrics 40, 27-40) proposed a carcinogenic potency estimate that incorporates both intercurrent mortality and background tumor rates. Since then, many authors have either generalized the method outlined by Sawyer et al. or developed their own method based on a slightly different adjustment for treatment-related changes in survival. None of these methods, however, has estimated the shape of the dose-response curve and incorporated such an estimate in potency estimation. In this manuscript, a measure of tumorigenic potency is proposed that utilizes the estimated shape of the dose-response relationship, in addition to estimated dose effects, in order to rank chemicals on the basis of carcinogenic risk. Comparison of this new measure to that of Sawyer et al. is done using a large database of animal carcinogenicity experiments from the National Cancer Institute and the National Toxicology Program. JF - Biometrics AU - Meier, K L AU - Bailer, A J AU - Portier, C J AD - Risk Methodology Section, National Institute of Environmental Health Sciences Research Triangle Park, North Carolina 27709. Y1 - 1993/09// PY - 1993 DA - September 1993 SP - 917 EP - 926 VL - 49 IS - 3 SN - 0006-341X, 0006-341X KW - Carcinogens KW - 0 KW - Index Medicus KW - Rats KW - Evaluation Studies as Topic KW - Animals KW - Neoplasms, Experimental -- chemically induced KW - Dose-Response Relationship, Drug KW - Linear Models KW - Models, Statistical KW - Mice KW - Male KW - Female KW - Proportional Hazards Models KW - Carcinogens -- administration & dosage KW - Biometry -- methods KW - Carcinogens -- toxicity KW - Carcinogenicity Tests -- methods KW - Carcinogenicity Tests -- statistics & numerical data UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76095824?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biometrics&rft.atitle=A+measure+of+tumorigenic+potency+incorporating+dose-response+shape.&rft.au=Meier%2C+K+L%3BBailer%2C+A+J%3BPortier%2C+C+J&rft.aulast=Meier&rft.aufirst=K&rft.date=1993-09-01&rft.volume=49&rft.issue=3&rft.spage=917&rft.isbn=&rft.btitle=&rft.title=Biometrics&rft.issn=0006341X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-29 N1 - Date created - 1993-12-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Metabolism and elimination of oxazepam in B6C3F1 and Swiss-Webster mice. AN - 76094830; 7902256 AB - The National Toxicology Program has recently determined oxazepam to be hepatocarcinogenic in mice. To aid in the assessment of the risks associated with human use of this drug, the metabolism and elimination of oxazepam in mice were exhaustively examined in B6C3F1 and Swiss-Webster mice. In this study males were given 25, 250, and 500 mg/kg by gavage, a range that includes doses found to be carcinogenic and noncarcinogenic in the National Toxicology Program bioassay. Metabolism of oxazepam by female mice of both strains was studied following administration of 500 mg/kg. More than 90% of the recovered activity was identified. Few strain differences were detected. Females of both strains metabolize oxazepam to a slightly greater extent than do males. Dose-dependent differences were detected, but they were usually nonlinear over the range examined. The routes of elimination in mice given a single dose of oxazepam were by order of importance: fecal > urinary > expired air. Pretreatment with dosed feed for 14 days (to model autoinduction in bioassay animals) resulted in a significant shift from the fecal to the urinary route of elimination, an approximately 2-fold increase in elimination of oxazepam glucuronide, and a significant decrease in excretion of unchanged oxazepam. Results of this study indicate that following constant exposure to oxazepam, mice metabolize and eliminate oxazepam in a manner more similar to that by humans than that by naive mice. This observation enhances the significance of data obtained in the bioassay and the extrapolation of that data to predict risks to human health. JF - Drug metabolism and disposition: the biological fate of chemicals AU - Griffin, R J AU - Burka, L T AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. PY - 1993 SP - 918 EP - 926 VL - 21 IS - 5 SN - 0090-9556, 0090-9556 KW - Oxazepam KW - 6GOW6DWN2A KW - Index Medicus KW - Animals KW - Sex Characteristics KW - Dose-Response Relationship, Drug KW - Humans KW - Liver -- metabolism KW - Male KW - Female KW - Chromatography, High Pressure Liquid KW - Oxazepam -- pharmacokinetics KW - Oxazepam -- metabolism KW - Mice, Inbred Strains -- metabolism KW - Mice -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76094830?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Drug+metabolism+and+disposition%3A+the+biological+fate+of+chemicals&rft.atitle=Metabolism+and+elimination+of+oxazepam+in+B6C3F1+and+Swiss-Webster+mice.&rft.au=Griffin%2C+R+J%3BBurka%2C+L+T&rft.aulast=Griffin&rft.aufirst=R&rft.date=1993-09-01&rft.volume=21&rft.issue=5&rft.spage=918&rft.isbn=&rft.btitle=&rft.title=Drug+metabolism+and+disposition%3A+the+biological+fate+of+chemicals&rft.issn=00909556&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-28 N1 - Date created - 1993-12-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Hodgkin's disease in adults. Part II. AN - 76046645; 8225893 AB - The development of a secondary cancer is an often fatal and therefore devastating complication of the successful therapy of Hodgkin's disease. The risk of developing a secondary cancer is not the same for all patients, nor is it the same for all treatments. In 1993, treatment decisions are complicated because there are often a number of management approaches that can effectively eradicate Hodgkin's disease. Certain subgroups can be treated safely with more limited therapy. Patients with peripheral IA disease experience excellent survival following involved field radiotherapy alone without staging laparotomy. Early-stage patients with good prognostic factors can be treated with radiotherapy or chemotherapy alone after a discussion of the short and long-term risks of both approaches. If unfavorable prognostic factors are present or if the patient has IIIA disease, we favor chemotherapy alone while others may employ combined modality therapy, a treatment strategy we reserve for patients with massive mediastinal disease. For advanced-stage disease, full-dose combination chemotherapy with a regimen that is familiar to the oncologist should be given. The addition of radiotherapy in this setting has not been shown to be of benefit. Each treatment strategy has to consider the individual patient and their likelihood of developing one of the complications, fatal or otherwise, of treatment. Although secondary complications must be considered in the initial strategy, unfounded fears about toxicity should not detract from delivery of therapy that has the greatest chance of cure while at the same time minimizing the risk to the patient. JF - Investigative radiology AU - Urba, W J AU - Longo, D L AD - Clinical Services Program, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702-1201. Y1 - 1993/09// PY - 1993 DA - September 1993 SP - 848 EP - 859 VL - 28 IS - 9 SN - 0020-9996, 0020-9996 KW - Index Medicus KW - Neoplasms, Second Primary KW - Humans KW - Salvage Therapy KW - Hodgkin Disease -- therapy KW - Hodgkin Disease -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76046645?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Investigative+radiology&rft.atitle=Hodgkin%27s+disease+in+adults.+Part+II.&rft.au=Urba%2C+W+J%3BLongo%2C+D+L&rft.aulast=Urba&rft.aufirst=W&rft.date=1993-09-01&rft.volume=28&rft.issue=9&rft.spage=848&rft.isbn=&rft.btitle=&rft.title=Investigative+radiology&rft.issn=00209996&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-15 N1 - Date created - 1993-12-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Lung cancer, race, and a CYP1A1 genetic polymorphism. AN - 76042791; 8220094 AB - The assessment of human cancer risk using molecular epidemiological techniques involves determining the relative contributions of inherited and acquired genetic predispositions, in the context of environmental exposures. Recently described genetic polymorphisms for CYP1A1, a gene involved in the metabolic activation of polycyclic aromatic hydrocarbons, have been associated with lung cancer risk in a Japanese population. We report herein findings from a United States case-control study of lung cancer (56 cases; 48 controls). The polymerase chain reaction followed by an Msp1 restriction enzyme digestion was used to analyze constitutive DNA but no association between the restriction fragment length polymorphism and lung cancer risk was found (odds ratio, 0.7; 95% confidence interval, = 0.3-1.6). Analysis of genotype by cumulative smoking status did not reveal an elevated risk among lesser or greater smokers. The presence of the CYP1A1 Msp1 site-present allele, which was previously found to be associated with Japanese lung cancer risk, was statistically increased in African compared to Caucasian Americans (odds ratio, 2.9; 95% confidence interval, 1.2-2.7). When stratified by race, however, no association between case status and the polymorphism was observed, but the small number of study subjects within each racial group limited the statistical power. Larger studies are required to evaluate the risk of the CYP1A1 Msp1 polymorphism in African Americans. JF - Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology AU - Shields, P G AU - Caporaso, N E AU - Falk, R T AU - Sugimura, H AU - Trivers, G E AU - Trump, B F AU - Hoover, R N AU - Weston, A AU - Harris, C C AD - Laboratory of Human Carcinogenesis, National Cancer Institute, NIH, Bethesda, Maryland 20892. PY - 1993 SP - 481 EP - 485 VL - 2 IS - 5 SN - 1055-9965, 1055-9965 KW - CYP1A1 KW - DNA, Neoplasm KW - 0 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Homozygote KW - Gene Frequency KW - Humans KW - Asthma -- genetics KW - DNA, Neoplasm -- analysis KW - Smoking -- genetics KW - Lung Diseases, Obstructive -- genetics KW - Neoplasms -- genetics KW - Genotype KW - Polymerase Chain Reaction KW - Blotting, Southern KW - Risk Factors KW - Heterozygote KW - Case-Control Studies KW - DNA, Neoplasm -- genetics KW - African Continental Ancestry Group -- genetics KW - Cytochrome P-450 Enzyme System -- genetics KW - Polymorphism, Genetic -- genetics KW - Lung Neoplasms -- genetics KW - European Continental Ancestry Group -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76042791?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+epidemiology%2C+biomarkers+%26+prevention+%3A+a+publication+of+the+American+Association+for+Cancer+Research%2C+cosponsored+by+the+American+Society+of+Preventive+Oncology&rft.atitle=Lung+cancer%2C+race%2C+and+a+CYP1A1+genetic+polymorphism.&rft.au=Shields%2C+P+G%3BCaporaso%2C+N+E%3BFalk%2C+R+T%3BSugimura%2C+H%3BTrivers%2C+G+E%3BTrump%2C+B+F%3BHoover%2C+R+N%3BWeston%2C+A%3BHarris%2C+C+C&rft.aulast=Shields&rft.aufirst=P&rft.date=1993-09-01&rft.volume=2&rft.issue=5&rft.spage=481&rft.isbn=&rft.btitle=&rft.title=Cancer+epidemiology%2C+biomarkers+%26+prevention+%3A+a+publication+of+the+American+Association+for+Cancer+Research%2C+cosponsored+by+the+American+Society+of+Preventive+Oncology&rft.issn=10559965&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-10 N1 - Date created - 1993-12-10 N1 - Date revised - 2017-01-13 N1 - Gene symbol - CYP1A1 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - A cohort study of smoking, alcohol consumption, and dietary factors for pancreatic cancer (United States). AN - 76039279; 8218880 AB - Risk factors for pancreatic cancer were evaluated in a cohort study of 17,633 White men in the United States who responded to a mailed questionnaire in 1966 and were followed-up through 1986 for mortality. Cigarette smoking and alcohol consumption were found to be important risk factors for pancreatic cancer. Risks increased significantly with number of cigarettes smoked, reaching fourfold for smokers of 25 or more cigarettes per day relative to nonsmokers. Alcohol intake also was related significantly to risk, with consumers of 10 or more drinks per month having three times the risk of nondrinkers, but dose-response trends among drinkers were not smooth. Coffee consumption was unrelated to risk. Dietary analyses revealed a rising rate of pancreatic cancer mortality with increasing consumption of meat after adjustment for other risk factors. Men in the highest quartile of meat intake had about three times the risk of those in the lowest quartile. No consistent association, however, was observed for consumption of fruits, vegetables, or grains. This study confirms cigarette smoking as an important risk factor for pancreatic cancer, and provides evidence that elevated intake of alcohol and meat may increase the risk of this fatal malignancy. JF - Cancer causes & control : CCC AU - Zheng, W AU - McLaughlin, J K AU - Gridley, G AU - Bjelke, E AU - Schuman, L M AU - Silverman, D T AU - Wacholder, S AU - Co-Chien, H T AU - Blot, W J AU - Fraumeni, J F AD - Epidemiology and Biostatistics Program, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/09// PY - 1993 DA - September 1993 SP - 477 EP - 482 VL - 4 IS - 5 SN - 0957-5243, 0957-5243 KW - Coffee KW - 0 KW - Index Medicus KW - Animals KW - Humans KW - Alcoholic Beverages -- statistics & numerical data KW - Tobacco, Smokeless KW - Plants, Toxic KW - Meat KW - Risk Factors KW - European Continental Ancestry Group KW - Fishes KW - Adult KW - Cohort Studies KW - Follow-Up Studies KW - Beer -- statistics & numerical data KW - United States -- epidemiology KW - Male KW - Pancreatic Neoplasms -- mortality KW - Pancreatic Neoplasms -- epidemiology KW - Feeding Behavior KW - Alcohol Drinking -- epidemiology KW - Smoking -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76039279?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+causes+%26+control+%3A+CCC&rft.atitle=A+cohort+study+of+smoking%2C+alcohol+consumption%2C+and+dietary+factors+for+pancreatic+cancer+%28United+States%29.&rft.au=Zheng%2C+W%3BMcLaughlin%2C+J+K%3BGridley%2C+G%3BBjelke%2C+E%3BSchuman%2C+L+M%3BSilverman%2C+D+T%3BWacholder%2C+S%3BCo-Chien%2C+H+T%3BBlot%2C+W+J%3BFraumeni%2C+J+F&rft.aulast=Zheng&rft.aufirst=W&rft.date=1993-09-01&rft.volume=4&rft.issue=5&rft.spage=477&rft.isbn=&rft.btitle=&rft.title=Cancer+causes+%26+control+%3A+CCC&rft.issn=09575243&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-03 N1 - Date created - 1993-12-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Immunocompetence in the long sleep and short sleep mouse lines: baseline versus primed responses. AN - 76038435; 8219412 AB - Two lines of mice which were selectively bred for high (Long Sleep; LS) and low (Short Sleep; SS) reactivities to a sedative dose of ethanol, are also differentiated by agents that act at the GABAA-receptor complex. Since this supramolecular complex may also modulate immune function, measures of immunity have been examined in these lines. In the present study the immune responsiveness before and after an allogeneic priming stimulus was investigated. Lower mitogen-induced T-cell proliferation, mixed leukocyte reaction, and cytotoxic T lymphocyte activity were found in unprimed LS compared to unprimed SS mice. In contrast, the LS line exhibited a marked augmentation of these responses after priming, while the SS mice appeared unresponsive to this challenge. Addition of splenocytes or cell-free splenic cultures from primed mice to cultures from unprimed mice suggested that differences in priming-induced cell-to-cell interactions, rather than the release of a soluble helper factor(s) into the medium, are responsible for the marked augmentation of the secondary response in LS, compared to SS mice. Fewer T-helper and T-suppressor/cytotoxic cells were found in LS compared to SS mice, and this was unaffected by priming. These results extend previous findings demonstrating a higher natural killer cell activity and rate of tumor rejection in LS mice and suggest that these lines may be useful in studying the regulatory role of the GABAA complex in immune function. JF - Brain, behavior, and immunity AU - Fride, E AU - McIntyre, T AU - Skolnick, P AU - Arora, P K AD - Laboratory of Neuroscience, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/09// PY - 1993 DA - September 1993 SP - 231 EP - 242 VL - 7 IS - 3 SN - 0889-1591, 0889-1591 KW - Receptors, GABA KW - 0 KW - Receptors, GABA-A KW - Ethanol KW - 3K9958V90M KW - Index Medicus KW - Lymphocyte Activation -- drug effects KW - Animals KW - Receptors, GABA-A -- physiology KW - Lymphocyte Subsets -- drug effects KW - Cytotoxicity Tests, Immunologic KW - Crosses, Genetic KW - Mice KW - Selection, Genetic KW - Male KW - Immunocompetence -- genetics KW - Sleep -- genetics KW - Immunologic Memory -- drug effects KW - Ethanol -- pharmacology KW - Immunity, Cellular -- drug effects KW - Receptors, GABA -- physiology KW - Mice, Inbred Strains -- physiology KW - Neuroimmunomodulation -- drug effects KW - Immunocompetence -- physiology KW - Mice, Inbred Strains -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76038435?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain%2C+behavior%2C+and+immunity&rft.atitle=Immunocompetence+in+the+long+sleep+and+short+sleep+mouse+lines%3A+baseline+versus+primed+responses.&rft.au=Fride%2C+E%3BMcIntyre%2C+T%3BSkolnick%2C+P%3BArora%2C+P+K&rft.aulast=Fride&rft.aufirst=E&rft.date=1993-09-01&rft.volume=7&rft.issue=3&rft.spage=231&rft.isbn=&rft.btitle=&rft.title=Brain%2C+behavior%2C+and+immunity&rft.issn=08891591&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-10 N1 - Date created - 1993-12-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Glycine stimulates striatal dopamine release in conscious rats. AN - 76037190; 8220914 AB - 1. Glycine is an inhibitory neurotransmitter in the spinal cord and brainstem. The mechanism of this inhibition is via binding of glycine to specific receptors, increasing transmembrane Cl- conductance and hyperpolarizing neurones. Strychnine selectively antagonizes these effects. The role of glycinergic neurones in supraspinal regions is poorly understood. 2. Effects of glycine on release of catecholamines in the striatum were examined by microdialysis in freely-moving rats. Transcription of the genes encoding strychnine-sensitive glycine receptors was assessed in the striatum and substantia nigra, by use of reverse transcription followed by the polymerase chain reaction. 3. Glycine administered via the microdialysis probe dose-dependently increased concentrations of dopamine and its metabolites, dihydroxyphenylacetic acid and homovanillic acid, in the perfusate, indicating increased local release and metabolism of dopamine. Strychnine markedly attenuated these responses. Whereas striatal tissue did not contain mRNA for either the adult or neonatal form of strychnine-sensitive glycine receptor, nigral tissue contained a message for the adult form. 4. The results suggest that dopaminergic cells in the substantia nigra synthesize strychnine-sensitive glycine receptors and transport the receptors to terminals in the striatum. Occupation of the glycine receptors then exerts a net stimulatory effect on striatal dopamine release in vivo. JF - British journal of pharmacology AU - Yadid, G AU - Pacak, K AU - Golomb, E AU - Harvey-White, J D AU - Lieberman, D M AU - Kopin, I J AU - Goldstein, D S AD - Clinical Neuroscience Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/09// PY - 1993 DA - September 1993 SP - 50 EP - 53 VL - 110 IS - 1 SN - 0007-1188, 0007-1188 KW - DNA Primers KW - 0 KW - RNA, Messenger KW - Receptors, Glycine KW - Strychnine KW - H9Y79VD43J KW - Glycine KW - TE7660XO1C KW - Dopamine KW - VTD58H1Z2X KW - Homovanillic Acid KW - X77S6GMS36 KW - Index Medicus KW - Animals KW - Dialysis KW - Receptors, Glycine -- biosynthesis KW - Transcription, Genetic KW - Homovanillic Acid -- metabolism KW - Chromatography, High Pressure Liquid KW - RNA, Messenger -- biosynthesis KW - Substantia Nigra -- metabolism KW - Rats KW - Polymerase Chain Reaction KW - Base Sequence KW - Rats, Sprague-Dawley KW - Molecular Sequence Data KW - Strychnine -- pharmacology KW - Male KW - Receptors, Glycine -- genetics KW - Glycine -- pharmacology KW - Corpus Striatum -- metabolism KW - Dopamine -- metabolism KW - Corpus Striatum -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76037190?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+pharmacology&rft.atitle=Glycine+stimulates+striatal+dopamine+release+in+conscious+rats.&rft.au=Yadid%2C+G%3BPacak%2C+K%3BGolomb%2C+E%3BHarvey-White%2C+J+D%3BLieberman%2C+D+M%3BKopin%2C+I+J%3BGoldstein%2C+D+S&rft.aulast=Yadid&rft.aufirst=G&rft.date=1993-09-01&rft.volume=110&rft.issue=1&rft.spage=50&rft.isbn=&rft.btitle=&rft.title=British+journal+of+pharmacology&rft.issn=00071188&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-14 N1 - Date created - 1993-12-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Brain Res. 1984 Feb 27;294(1):127-32 [6697228] Br J Pharmacol. 1983 Jul;79(3):799-806 [6418249] Anal Biochem. 1987 Apr;162(1):156-9 [2440339] Naunyn Schmiedebergs Arch Pharmacol. 1988 May;337(5):552-5 [2842697] Eur J Pharmacol. 1990 Jan 17;175(3):365-6 [2157604] J Neurochem. 1990 Jun;54(6):2077-81 [2338557] Synapse. 1990;5(3):190-200 [2160740] Neuron. 1990 Dec;5(6):867-73 [2176511] Eur J Pharmacol. 1990 Aug 10;184(2-3):239-50 [2150375] EMBO J. 1991 Sep;10(9):2401-9 [1651228] Br J Pharmacol. 1991 Nov;104(3):760-4 [1797336] Brain Res. 1992 Aug 28;589(1):91-6 [1422825] Eur J Pharmacol. 1992 Oct 20;221(2-3):389-91 [1426016] Exp Brain Res. 1968;6(1):1-18 [5721755] Proc Natl Acad Sci U S A. 1973 Oct;70(10):2832-6 [4200724] Brain Res. 1978 Jan 6;139(1):115-30 [620345] J Neurochem. 1979 May;32(5):1539-45 [438822] Biochem Pharmacol. 1979 Jul 15;28(14):2193-7 [497000] J Neurochem. 1982 Feb;38(2):574-81 [7108557] Nature. 1987 Jul 16-22;328(6127):215-20 [3037383] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The role of agricultural pesticide use in the development of non-Hodgkin's lymphoma in women. AN - 76028162; 8215601 AB - Non-Hodgkin's lymphoma has been found to be associated with agricultural pesticide use in men, but little is known about the risk in women. In a recent population-based, case-control study conducted in eastern Nebraska, no increased risk of non-Hodgkin's lymphoma was found in women who had ever lived or worked on a farm (odds ratio [OR] = 1.0). Neither the use of insecticides (OR = 0.8) nor herbicides (OR = 0.7) on the farm was associated with non-Hodgkin's lymphoma; however, the number of women who mixed or applied pesticides was small, particularly in comparison to men on farms. Small nonsignificant associations were observed among the women who personally handled insecticides (OR = 1.3) or herbicides (OR = 1.2). Women who personally handled organophosphate insecticides had a significant 4.5-fold increased risk of non-Hodgkin's lymphoma. Use of chlorinated hydrocarbon insecticides was associated with an OR of 1.6; however, the use on dairy cattle was associated with a 3-fold increased risk. Pesticide-related risks were greater among women with a family history of cancer, particularly a history of lymphatic or hematopoietic cancer among first-degree relatives. JF - Archives of environmental health AU - Zahm, S H AU - Weisenburger, D D AU - Saal, R C AU - Vaught, J B AU - Babbitt, P A AU - Blair, A AD - Occupational Studies Section, National Cancer Institute, Rockville, Maryland. PY - 1993 SP - 353 EP - 358 VL - 48 IS - 5 SN - 0003-9896, 0003-9896 KW - Agrochemicals KW - 0 KW - Herbicides KW - Insecticides KW - Abridged Index Medicus KW - Index Medicus KW - Odds Ratio KW - Risk Factors KW - Humans KW - Adult KW - Case-Control Studies KW - Aged KW - Middle Aged KW - Female KW - Nebraska -- epidemiology KW - Lymphoma, Non-Hodgkin -- epidemiology KW - Insecticides -- adverse effects KW - Herbicides -- adverse effects KW - Agricultural Workers' Diseases -- epidemiology KW - Agricultural Workers' Diseases -- chemically induced KW - Occupational Exposure -- adverse effects KW - Lymphoma, Non-Hodgkin -- chemically induced KW - Occupational Exposure -- analysis KW - Agrochemicals -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76028162?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+environmental+health&rft.atitle=The+role+of+agricultural+pesticide+use+in+the+development+of+non-Hodgkin%27s+lymphoma+in+women.&rft.au=Zahm%2C+S+H%3BWeisenburger%2C+D+D%3BSaal%2C+R+C%3BVaught%2C+J+B%3BBabbitt%2C+P+A%3BBlair%2C+A&rft.aulast=Zahm&rft.aufirst=S&rft.date=1993-09-01&rft.volume=48&rft.issue=5&rft.spage=353&rft.isbn=&rft.btitle=&rft.title=Archives+of+environmental+health&rft.issn=00039896&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-04 N1 - Date created - 1993-11-04 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 ER - TY - JOUR T1 - Enhanced single-strand conformation polymorphism (SSCP) detection of point mutations utilizing methylmercury hydroxide. AN - 76025578; 8217149 JF - BioTechniques AU - Weghorst, C M AU - Buzard, G S AD - Laboratory of Comparative Carcinogenesis National Cancer Institute, Frederick, MD 21702-1201. Y1 - 1993/09// PY - 1993 DA - September 1993 SP - 396 EP - 8, 400 VL - 15 IS - 3 SN - 0736-6205, 0736-6205 KW - DNA, Single-Stranded KW - 0 KW - Methylmercury Compounds KW - methylmercury hydroxide KW - EZ74BDI0HB KW - Index Medicus KW - Rats KW - Kidney Neoplasms -- genetics KW - Polymerase Chain Reaction KW - Animals KW - Base Sequence KW - Electrophoresis KW - Genes, p53 KW - Molecular Sequence Data KW - Kidney Neoplasms -- chemistry KW - Point Mutation KW - DNA, Single-Stranded -- chemistry KW - Nucleic Acid Conformation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76025578?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BioTechniques&rft.atitle=Enhanced+single-strand+conformation+polymorphism+%28SSCP%29+detection+of+point+mutations+utilizing+methylmercury+hydroxide.&rft.au=Weghorst%2C+C+M%3BBuzard%2C+G+S&rft.aulast=Weghorst&rft.aufirst=C&rft.date=1993-09-01&rft.volume=15&rft.issue=3&rft.spage=396&rft.isbn=&rft.btitle=&rft.title=BioTechniques&rft.issn=07366205&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-26 N1 - Date created - 1993-11-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Low frequency of H-ras activation in naturally occurring hepatocellular tumors of C3H/HeNCr mice. AN - 75999333; 8403222 AB - Previous reports from several laboratories have consistently shown that approximately 30% of spontaneous hepatocellular adenomas and 70-80% of spontaneous hepatocellular carcinomas found in aged B6C3F1 [C57BL/6 (liver tumor resistant) x C3H (liver tumor susceptible)] male mice contain one of three missense point mutations in codon 61 of the H-ras oncogene, CAA-->AAA, CGA or CTA. Irrespective of subline, the C3H mouse, the paternal parent strain of the B6C3F1 hybrid, is more susceptible to spontaneous liver tumorigenesis than the B6C3F1 mouse. However, the role of H-ras in the pathogenesis of hepatocellular tumors in C3H mice is less clear, as widely different frequencies of activation of this gene, but by the same point mutations in codon 61, have been reported by various laboratories. The present study was undertaken to characterize H-ras involvement in hepatocellular tumors of aged C3H/He mice from the NCI-Frederick Cancer Research and Development Center Colony (C3H/HeNCr). Oncogene activation was evaluated in 45 C3H/HeNCr hepatocellular tumors by the NIH 3T3 transfection assays, and point mutations in the H-ras oncogene were detected and characterized in DNA fragments amplified by PCR, using dot blot hybridization analysis with mutation-specific oligonucleotide probes and direct dideoxy sequencing of PCR products. The only transforming gene detected in these tumors by NIH 3T3 transfection was H-ras. Only 17% (1/6) of spontaneous carcinomas and 8% (3/39) of spontaneous adenomas contained transforming H-ras sequences, each with a point mutation in codon 61. In all four cases with H-ras mutations, mutated sequences comprised a minor fraction of total H-ras gene copies in DNA extracted from primary tumors. H-ras mutations thus appear to have arisen relatively late in the pathogenesis of the neoplasms. For comparison, sections of formalin-fixed, paraffin-embedded hepatocellular tumors that occurred in untreated B6C3F1 hybrid mice sired by C3H/HeNCr males were assayed for the same H-ras mutations by PCR and dot blot hybridization. Nine of 13 such tumors (4/6 carcinomas, 5/7 adenomas) were positive. The overall difference in frequency of H-ras codon 61 mutations in hepatocellular tumors in C3H/HeNCr (4/45) versus B6C3F1 (9/13) was highly significant (P = 0.000035, Fisher's exact test). These data indicate that point mutations in H-ras do not generally play a major or an initiating role in spontaneous hepatocarcinogenesis of inbred C3H/HeNCr mice and contrast with the high rate of ras mutations in liver tumors of the B6C3F1 hybrid. JF - Carcinogenesis AU - Enomoto, T AU - Weghorst, C M AU - Ward, J M AU - Anderson, L M AU - Perantoni, A O AU - Rice, J M AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick, MD 21702-1201. Y1 - 1993/09// PY - 1993 DA - September 1993 SP - 1939 EP - 1944 VL - 14 IS - 9 SN - 0143-3334, 0143-3334 KW - H-ras KW - Oligonucleotide Probes KW - 0 KW - Index Medicus KW - Polymerase Chain Reaction KW - Animals KW - 3T3 Cells KW - Base Sequence KW - Transfection KW - Molecular Sequence Data KW - Mice, Inbred C3H KW - Oligonucleotide Probes -- chemistry KW - Mice KW - Male KW - Female KW - Cell Transformation, Neoplastic -- genetics KW - Point Mutation -- genetics KW - Adenoma, Liver Cell -- genetics KW - Genes, ras -- genetics KW - Gene Amplification -- genetics KW - Carcinoma, Hepatocellular -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75999333?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Low+frequency+of+H-ras+activation+in+naturally+occurring+hepatocellular+tumors+of+C3H%2FHeNCr+mice.&rft.au=Enomoto%2C+T%3BWeghorst%2C+C+M%3BWard%2C+J+M%3BAnderson%2C+L+M%3BPerantoni%2C+A+O%3BRice%2C+J+M&rft.aulast=Enomoto&rft.aufirst=T&rft.date=1993-09-01&rft.volume=14&rft.issue=9&rft.spage=1939&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-05 N1 - Date created - 1993-11-05 N1 - Date revised - 2017-01-13 N1 - Gene symbol - H-ras N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Studies on the role of topoisomerases in general, gene- and strand-specific DNA repair. AN - 75983722; 8403208 AB - Using specific inhibitors we have assessed the role of topoisomerases I and II in DNA repair of the overall genome and in both strands of an essential gene, the dihydrofolate reductase (DHFR) gene in chinese hamster ovary (CHO) cells. In these studies we have: (1) used inhibitors of topoisomerases during the repair incubation and (2) studied the DNA repair in cells with altered levels of topoisomerase activity. When cells were allowed to repair after UV irradiation, the gene-specific DNA repair was not affected by either topoisomerase I or topoisomerase II inhibitors alone. However, when topoisomerase I and topoisomerase II inhibitors were added simultaneously the gene- and strand-specific DNA repair were markedly inhibited. In contrast, the overall genome DNA repair was only marginally affected. This suggests that topoisomerases are involved in gene-specific DNA repair and that one type may substitute for the other in the repair process. That concept is further supported by our findings using a mutant cell line with a decreased level of topoisomerase I: gene-specific DNA repair can be inhibited by a topoisomerase II inhibitor alone. By analyzing the steady-state expression of the DHFR gene we find that inhibition of repair in the DHFR gene is not ascribed to an obvious change in the messenger level. Furthermore, using agents other than UV, we observe that the inhibitors have no effect on gene-specific repair of DNA damage introduced by the chemotherapeutic agents cisplatin and nitrogen mustard. JF - Carcinogenesis AU - Stevnsner, T AU - Bohr, V A AD - Laboratory of Molecular Pharmacology, National Cancer Institute, NIH, Bethesda, MD 20892. Y1 - 1993/09// PY - 1993 DA - September 1993 SP - 1841 EP - 1850 VL - 14 IS - 9 SN - 0143-3334, 0143-3334 KW - DHFR KW - Pyrimidine Dimers KW - 0 KW - RNA, Messenger KW - Thiobarbiturates KW - Topoisomerase I Inhibitors KW - Topoisomerase II Inhibitors KW - Mechlorethamine KW - 50D9XSG0VR KW - merbarone KW - 97534-21-9 KW - Tetrahydrofolate Dehydrogenase KW - EC 1.5.1.3 KW - DNA Topoisomerases, Type I KW - EC 5.99.1.2 KW - DNA Topoisomerases, Type II KW - EC 5.99.1.3 KW - Cisplatin KW - Q20Q21Q62J KW - Camptothecin KW - XT3Z54Z28A KW - Index Medicus KW - Animals KW - RNA, Messenger -- metabolism KW - Dose-Response Relationship, Drug KW - CHO Cells -- enzymology KW - CHO Cells -- drug effects KW - Cisplatin -- pharmacology KW - Mechlorethamine -- pharmacology KW - CHO Cells -- radiation effects KW - Cricetinae KW - Pyrimidine Dimers -- genetics KW - DNA Replication -- radiation effects KW - Camptothecin -- pharmacology KW - DNA Topoisomerases, Type I -- physiology KW - Tetrahydrofolate Dehydrogenase -- metabolism KW - DNA Topoisomerases, Type II -- physiology KW - DNA Replication -- drug effects KW - DNA Repair -- drug effects KW - Thiobarbiturates -- pharmacology KW - Tetrahydrofolate Dehydrogenase -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75983722?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Studies+on+the+role+of+topoisomerases+in+general%2C+gene-+and+strand-specific+DNA+repair.&rft.au=Stevnsner%2C+T%3BBohr%2C+V+A&rft.aulast=Stevnsner&rft.aufirst=T&rft.date=1993-09-01&rft.volume=14&rft.issue=9&rft.spage=1841&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-05 N1 - Date created - 1993-11-05 N1 - Date revised - 2017-01-13 N1 - Gene symbol - DHFR N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - A rapid method for cloning mutagenic DNA repair genes: isolation of umu-complementing genes from multidrug resistance plasmids R391, R446b, and R471a. AN - 75943970; 8366028 AB - Genetic and physiological experiments have demonstrated that the products of the umu-like operon are directly required for mutagenic DNA repair in enterobacteria. To date, five such operons have been cloned and studied at the molecular level. Given the apparent wide occurrence of these mutagenic DNA repair genes in enterobacteria, it seems likely that related genes will be identified in other bacterial species and perhaps even in higher organisms. We are interested in identifying such genes. However, standard methods based on either DNA or protein cross-hybridization are laborious and, given the overall homology between previously identified members of this family (41 to 83% at the protein level), would probably have limited success. To facilitate the rapid identification of more diverse umu-like genes, we have constructed two Escherichia coli strains that allow us to identify umu-like genes after phenotypic complementation assays. With these two strains, we have cloned novel umu-like genes from three R plasmids, the IncJ plasmid R391 and two IncL/M plasmids, R446b and R471a. JF - Journal of bacteriology AU - Ho, C AU - Kulaeva, O I AU - Levine, A S AU - Woodgate, R AD - Section on DNA Replication, Repair and Mutagenesis, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/09// PY - 1993 DA - September 1993 SP - 5411 EP - 5419 VL - 175 IS - 17 SN - 0021-9193, 0021-9193 KW - umu KW - DNA, Bacterial KW - 0 KW - Index Medicus KW - Phenotype KW - Ultraviolet Rays KW - DNA, Bacterial -- genetics KW - Restriction Mapping KW - Drug Resistance, Microbial -- genetics KW - Genetic Complementation Test KW - Mutagenesis KW - Cloning, Molecular KW - DNA Repair -- genetics KW - Genes, Bacterial KW - R Factors -- radiation effects KW - Escherichia coli -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75943970?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+bacteriology&rft.atitle=A+rapid+method+for+cloning+mutagenic+DNA+repair+genes%3A+isolation+of+umu-complementing+genes+from+multidrug+resistance+plasmids+R391%2C+R446b%2C+and+R471a.&rft.au=Ho%2C+C%3BKulaeva%2C+O+I%3BLevine%2C+A+S%3BWoodgate%2C+R&rft.aulast=Ho&rft.aufirst=C&rft.date=1993-09-01&rft.volume=175&rft.issue=17&rft.spage=5411&rft.isbn=&rft.btitle=&rft.title=Journal+of+bacteriology&rft.issn=00219193&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-01 N1 - Date created - 1993-10-01 N1 - Date revised - 2017-01-13 N1 - Gene symbol - umu N1 - SuppNotes - Cited By: J Gen Microbiol. 1972 Oct;72(3):543-52 [4564689] J Bacteriol. 1989 May;171(5):2415-23 [2651400] J Gen Microbiol. 1973 Aug;77(2):249-59 [4584057] J Gen Microbiol. 1975 Jan;86(1):88-92 [1089756] Mol Gen Genet. 1977 Nov 14;156(2):121-31 [340898] Mol Gen Genet. 1978 Sep 20;165(1):87-93 [362169] Mutat Res. 1980 Aug;72(1):155-9 [6777687] J Gen Microbiol. 1981 Oct;126(2):305-10 [6279761] Nature. 1982 Nov 18;300(5889):278-81 [6755263] Gene. 1983 Aug;23(2):167-74 [6311684] Gene. 1984 Nov;31(1-3):165-71 [6098521] J Bacteriol. 1985 Apr;162(1):155-61 [2984171] Mol Gen Genet. 1985;199(1):133-40 [3889546] Mutat Res. 1985 Jun-Jul;150(1-2):147-58 [2987687] Proc Natl Acad Sci U S A. 1985 Jun;82(12):4193-7 [3889923] Proc Natl Acad Sci U S A. 1985 Jul;82(13):4331-5 [2989816] Proc Natl Acad Sci U S A. 1985 Jul;82(13):4336-40 [2989817] Mutat Res. 1986 Jul;166(1):29-37 [3014325] Plasmid. 1986 Jul;16(1):30-6 [3016779] Proc Natl Acad Sci U S A. 1987 Oct;84(19):6805-9 [3309946] Proc Natl Acad Sci U S A. 1988 Mar;85(6):1806-10 [3126496] Proc Natl Acad Sci U S A. 1988 Mar;85(6):1811-5 [3279417] Proc Natl Acad Sci U S A. 1988 Mar;85(6):1816-20 [3279418] Mutat Res. 1990 Sep-Nov;236(2-3):301-11 [2169028] Nucleic Acids Res. 1990 Sep 11;18(17):5045-50 [2129552] J Bacteriol. 1991 Feb;173(3):1051-63 [1991707] Crit Rev Biochem Mol Biol. 1990;25(6):415-56 [2292186] Mol Microbiol. 1991 Jan;5(1):149-55 [1707475] J Biol Chem. 1991 Aug 25;266(24):15710-5 [1874728] J Bacteriol. 1991 Sep;173(18):5604-11 [1885540] Mol Gen Genet. 1991 Sep;229(1):81-5 [1910151] Biochimie. 1991 Apr;73(4):479-84 [1911948] Proc Natl Acad Sci U S A. 1991 Oct 15;88(20):9127-31 [1924375] Proc Natl Acad Sci U S A. 1991 Dec 15;88(24):11450-4 [1722334] Mutat Res. 1992 Mar;281(3):221-5 [1371846] J Bacteriol. 1992 May;174(9):2809-15 [1569012] Cell. 1992 May 1;69(3):439-56 [1581960] Cell. 1992 May 1;69(3):457-70 [1581961] Proc Natl Acad Sci U S A. 1992 Sep 1;89(17):8068-72 [1518831] J Bacteriol. 1992 Nov;174(21):6844-51 [1400235] J Bacteriol. 1992 Nov;174(21):6948-55 [1400244] Mol Microbiol. 1992 Aug;6(16):2213-8 [1406263] Science. 1993 Mar 26;259(5103):1892-6 [8456313] Science. 1993 Mar 26;259(5103):1896-9 [8456314] Nucleic Acids Res. 1993 Apr 11;21(7):1577-80 [8479908] Nucleic Acids Res. 1993 Apr 11;21(7):1665 [8479919] Mol Gen Genet. 1972;119(2):93-102 [4565757] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Cross-reactivity of thirteen monoclonal antibodies with ten vaccinia cDNA expressed rat, mouse and human cytochrome P450s. AN - 75942749; 8373431 AB - Twelve monoclonal antibodies (MAbs) to rat cytochrome P450s and one MAb to a scup (fish) P450 have been isolated, characterized, and are currently in common use. Expression of cDNAs for different P450s from a vaccinia vector offers a rapid and simple way toward the production of individual P450s. The thirteen MAbs were examined for their cross-reactivity with ten cDNA expressed human, rat, and mouse P450s. Three MAbs to rat 1A1 and fish 1A1 cross-reacted with cDNA expressed mouse 1A1. One of the latter MAbs, 1-7-1 but none of the others cross-reacted with mouse 1A2. Surprisingly, the fish MAb to 1A1 also cross-reacted with human 2E1. Two MAbs to rat 2B1/2B2 cross-reacted with rat 2A1. An MAb to rat 2C11 cross-reacted with human 2C9. Two MAbs to rat 2E1 cross-reacted with human 2E1. Finally, two MAbs to rat 3A1 cross-reacted strongly with human 3A4. These studies open the door to constructing a library of MAbs with defined binding activity to the P450s of human and other species. JF - Biochemical pharmacology AU - Goldfarb, I AU - Korzekwa, K AU - Krausz, K W AU - Gonzalez, F AU - Gelboin, H V AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/09/01/ PY - 1993 DA - 1993 Sep 01 SP - 787 EP - 790 VL - 46 IS - 5 SN - 0006-2952, 0006-2952 KW - Antibodies, Monoclonal KW - 0 KW - DNA, Viral KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Rats KW - Animals KW - Humans KW - Genetic Vectors KW - Fishes KW - Mice KW - Cross Reactions KW - Vaccinia virus -- genetics KW - Antibodies, Monoclonal -- isolation & purification KW - Cytochrome P-450 Enzyme System -- genetics KW - DNA, Viral -- immunology KW - Cytochrome P-450 Enzyme System -- immunology KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - DNA, Viral -- metabolism KW - Antibodies, Monoclonal -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75942749?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+pharmacology&rft.atitle=Cross-reactivity+of+thirteen+monoclonal+antibodies+with+ten+vaccinia+cDNA+expressed+rat%2C+mouse+and+human+cytochrome+P450s.&rft.au=Goldfarb%2C+I%3BKorzekwa%2C+K%3BKrausz%2C+K+W%3BGonzalez%2C+F%3BGelboin%2C+H+V&rft.aulast=Goldfarb&rft.aufirst=I&rft.date=1993-09-01&rft.volume=46&rft.issue=5&rft.spage=787&rft.isbn=&rft.btitle=&rft.title=Biochemical+pharmacology&rft.issn=00062952&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-14 N1 - Date created - 1993-10-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Methoxyresorufin and benzyloxyresorufin: substrates preferentially metabolized by cytochromes P4501A2 and 2B, respectively, in the rat and mouse. AN - 75940321; 8373445 AB - The cytochrome P450 isozyme specificity for the O-dealkylation of methoxyresorufin (MTR) and benzyloxyresorufin (BZR) in the rat and mouse was investigated. The induction of various alkoxyresorufin O-dealkylation activities was measured in male F344/NCr rats exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin or 3,4,5,3',4',5'-hexachlorobiphenyl. MTR and ethoxyresorufin (ETR) O-dealkylation activities were induced 30- and 80-fold, respectively, in the liver. ETR O-dealkylation activity was induced > 250-fold in the kidney, whereas the metabolism of MTR was induced only 30-fold in this extrahepatic tissue. Phenacetin, a fairly specific CYP1A2 inhibitor, caused concentration-dependent competitive inhibition of MTR O-dealkylation (ki approximately 20 microM at 0.5 microM substrate) in hepatic microsomes from 3,4,5,3',4',5'-hexachlorobiphenyl-treated rats. The corresponding ki for inhibition of ETR O-dealkylation by phenacetin was > or = 333 microM at a 0.5 microM substrate concentration. A monoclonal antibody displaying inhibitory activity against rat CYP1A1 inhibited ETR O-dealkylation activity, whereas it failed to inhibit MTR O-dealkylation activity. In contrast, a monoclonal antibody reactive with both CYP1A1 and CYP1A2 inhibited both O-dealkylation activities to an equal extent. Similar experiments, employing phenacetin or specific monoclonal antibodies, yielded comparable results when performed with mouse microsomes. The maximal induction of MTR O-dealkylation activity in mice was > 100-fold. The P450 isozyme specificity of BZR O-dealkylation was also examined in both rats and mice. Pregnenolone-alpha-carbonitrile, a strong inducer of CYP3A, only weakly induced BZR O-dealkylation activity. In addition, a monoclonal antibody that specifically inhibits CYP2B caused inhibition of BZR metabolism in microsomes from phenobarbital- or dexamethasone-pretreated rats. In B6C3F1 mice exposed to dietary Aroclor 1254, significant induction of hepatic MTR O-dealkylation activity was observed at concentrations lower than those required for the induction of ETR or BZR O-dealkylation. In summary, it would appear that MTR is a relatively specific substrate for CYP1A2 activity in rodents, while BZR appears to be relatively specific for CYP2B. JF - Biochemical pharmacology AU - Nerurkar, P V AU - Park, S S AU - Thomas, P E AU - Nims, R W AU - Lubet, R A AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702. Y1 - 1993/09/01/ PY - 1993 DA - 1993 Sep 01 SP - 933 EP - 943 VL - 46 IS - 5 SN - 0006-2952, 0006-2952 KW - Cytochrome P-450 Enzyme Inhibitors KW - 0 KW - Oxazines KW - Xenobiotics KW - 7-methoxyresorufin KW - 5725-89-3 KW - ethoxyresorufin KW - 5725-91-7 KW - benzyloxyresorufin KW - 87687-02-3 KW - pentoxyresorufin KW - 87687-03-4 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Oxidoreductases KW - EC 1.- KW - Cytochrome P-450 CYP2B1 KW - EC 1.14.14.1 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Enzyme Induction KW - Microsomes -- enzymology KW - Mice KW - Male KW - Oxidoreductases -- metabolism KW - Cytochrome P-450 Enzyme System -- metabolism KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Oxidoreductases -- antagonists & inhibitors KW - Oxazines -- metabolism KW - Oxidoreductases -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75940321?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+pharmacology&rft.atitle=Methoxyresorufin+and+benzyloxyresorufin%3A+substrates+preferentially+metabolized+by+cytochromes+P4501A2+and+2B%2C+respectively%2C+in+the+rat+and+mouse.&rft.au=Nerurkar%2C+P+V%3BPark%2C+S+S%3BThomas%2C+P+E%3BNims%2C+R+W%3BLubet%2C+R+A&rft.aulast=Nerurkar&rft.aufirst=P&rft.date=1993-09-01&rft.volume=46&rft.issue=5&rft.spage=933&rft.isbn=&rft.btitle=&rft.title=Biochemical+pharmacology&rft.issn=00062952&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-14 N1 - Date created - 1993-10-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The medullary dorsal horn. A site of action of morphine in producing facial scratching in monkeys. AN - 75933769; 8363081 AB - Pruritus is a common side effect of epidural and intrathecal morphine administration in humans. This naloxone-reversible pruritus is typically present on the trunk, but is often severe around the eyes and nose, of the patients. The brain stem has been proposed as the site where opioids act to produce this effect. The authors studied the effect of morphine administered into the medullary dorsal horn (MDH), the brain stem homologue of the spinal dorsal horn, on facial-scratching behavior in monkeys. Morphine was unilaterally microinjected into the MDH of rhesus monkeys. Systemic injections of the opioid-receptor antagonist naloxone (0.5 mg/kg intramuscularly) were also made in combination with morphine microinjection. Systemic injections of the antihistamine chlorcyclizine (1.0 and 2.5 mg/kg intramuscularly) were also made to determine if facial scratching was mediated through histamine release. The monkeys were videotaped for 10-15 min before and 1-2 h after opioid microinjection, and the number and location of scratches were counted. A dose-response curve was established for the mu/delta-opioid-receptor agonist morphine (0.5, 1.0, 2.5, and 5.0 micrograms). Specificity of the site of action within the MDH was examined by systematically changing the microinjection site, and examining the area of the face that the monkeys scratched. Morphine produced large dose-dependent increases in facial scratching ipsilateral to the microinjection. Increases in facial scratching were also observed contralateral to the microinjections. These effects were reversed by naloxone. The facial area scratched after microinjection of morphine was directly related to the injection site, with 1-mm changes in the location of the microinjection resulting in pronounced changes in the area of the face that the monkeys scratched. Systemic injection of chlorcyclizine produced only a small, transient attenuation of morphine's effect. Data from this study demonstrate that the MDH is a site where morphine acts to produce facial scratching in monkeys by acting at opioid receptors. It is also likely that the MDH is a site where centrally administered opioids act in producing facial pruritus in humans. The effects of morphine on facial-scratching behavior were only modestly attenuated with chlorcyclizine, indicating a minor involvement of a histamine-dependent mechanism of action. JF - Anesthesiology AU - Thomas, D A AU - Williams, G M AU - Iwata, K AU - Kenshalo, D R AU - Dubner, R AD - Neurobiology and Anesthesiology Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/09// PY - 1993 DA - September 1993 SP - 548 EP - 554 VL - 79 IS - 3 SN - 0003-3022, 0003-3022 KW - Morphine KW - 76I7G6D29C KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Macaca fascicularis KW - Male KW - Facial Dermatoses -- chemically induced KW - Morphine -- adverse effects KW - Spinal Cord -- drug effects KW - Spinal Cord -- physiology KW - Pruritus -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75933769?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Anesthesiology&rft.atitle=The+medullary+dorsal+horn.+A+site+of+action+of+morphine+in+producing+facial+scratching+in+monkeys.&rft.au=Thomas%2C+D+A%3BWilliams%2C+G+M%3BIwata%2C+K%3BKenshalo%2C+D+R%3BDubner%2C+R&rft.aulast=Thomas&rft.aufirst=D&rft.date=1993-09-01&rft.volume=79&rft.issue=3&rft.spage=548&rft.isbn=&rft.btitle=&rft.title=Anesthesiology&rft.issn=00033022&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-30 N1 - Date created - 1993-09-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The paradoxical effect of tumor necrosis factor alpha (TNF-alpha) in endotoxin-induced uveitis. AN - 75924803; 8360023 AB - To investigate the role of TNF-alpha in endotoxin-induced uveitis (EIU) in mice. To neutralize TNF-alpha activity, mice were pretreated with either repeated injections of this cytokine or a single injection of antibody against it. The mice were then injected intraperitoneally with 500 micrograms endotoxin, to induce lethal septic shock, or into the footpad with 200 micrograms to induce EIU. Although both pretreatments conferred protection against the systemic toxic effects of LPS, TNF-resistant mice and mice treated with anti-TNF-alpha antibody demonstrated an exacerbation of EIU when compared to control animals. Unlike its apparent participation in the systemic effect of endotoxin, TNF-alpha is not directly involved in the pathogenesis of EIU and may even protect against the inflammatory processes of this disease. JF - Investigative ophthalmology & visual science AU - Kasner, L AU - Chan, C C AU - Whitcup, S M AU - Gery, I AD - Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/09// PY - 1993 DA - September 1993 SP - 2911 EP - 2917 VL - 34 IS - 10 SN - 0146-0404, 0146-0404 KW - Bacterial Toxins KW - 0 KW - Endotoxins KW - Recombinant Proteins KW - Tumor Necrosis Factor-alpha KW - salmonella toxin KW - Index Medicus KW - Acute Disease KW - Animals KW - Recombinant Proteins -- immunology KW - Mice, Inbred C3H KW - Disease Models, Animal KW - Mice KW - Salmonella typhimurium KW - Female KW - Uveitis, Anterior -- prevention & control KW - Uveitis, Anterior -- immunology KW - Uveitis, Anterior -- pathology KW - Tumor Necrosis Factor-alpha -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75924803?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Investigative+ophthalmology+%26+visual+science&rft.atitle=The+paradoxical+effect+of+tumor+necrosis+factor+alpha+%28TNF-alpha%29+in+endotoxin-induced+uveitis.&rft.au=Kasner%2C+L%3BChan%2C+C+C%3BWhitcup%2C+S+M%3BGery%2C+I&rft.aulast=Kasner&rft.aufirst=L&rft.date=1993-09-01&rft.volume=34&rft.issue=10&rft.spage=2911&rft.isbn=&rft.btitle=&rft.title=Investigative+ophthalmology+%26+visual+science&rft.issn=01460404&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-30 N1 - Date created - 1993-09-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Immunotoxins and recombinant toxins in the treatment of solid carcinomas. AN - 75910097; 8368439 AB - Cancer remains the second most common cause of death in our society, and advanced disease is often refractory to surgical, chemotherapeutic, and radiologic interventions. One novel approach to cancer treatment involves targeting a cytotoxic agent to a cancer cell. Immunotoxins have been developed that contain a potent toxin (either Pseudomonas exotoxin, ricin toxin, or diphtheria toxin) coupled to a targeting moiety that directs the molecule to cells expressing a certain antigen. Chemically coupled immunotoxins have been developed over the past 12 years. These bind to and kill cells expressing many tumor-associated antigens. Initial clinical results were disappointing, but recent results have been more promising. Furthermore, newer immunotoxins have been developed that will soon be in clinical trials. Some of these are recombinant toxins that have been developed using techniques of genetic engineering. Transforming growth factor-alpha, acidic fibroblast growth factor, insulin-like growth factor-1, interleukin-2, interleukin-4, interleukin-6, the binding portions of monoclonal antibodies, and CD4 have been used to direct toxins to cancer cells or cells infected with the human immunodeficiency virus type 1. Efforts are under way to circumvent problems such as immunogenicity that may limit the clinical usefulness of immunotoxins. JF - American journal of surgery AU - Theuer, C P AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/09// PY - 1993 DA - September 1993 SP - 284 EP - 288 VL - 166 IS - 3 SN - 0002-9610, 0002-9610 KW - Antibodies, Monoclonal KW - 0 KW - Bacterial Toxins KW - Exotoxins KW - Immunotoxins KW - Recombinant Proteins KW - Transforming Growth Factor alpha KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Transforming Growth Factor alpha -- therapeutic use KW - Humans KW - Forecasting KW - Exotoxins -- therapeutic use KW - Antibodies, Monoclonal -- therapeutic use KW - Recombinant Proteins -- metabolism KW - Bacterial Toxins -- therapeutic use KW - Immunotoxins -- therapeutic use KW - Immunotoxins -- metabolism KW - Neoplasms -- therapy KW - Recombinant Proteins -- therapeutic use KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75910097?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+surgery&rft.atitle=Immunotoxins+and+recombinant+toxins+in+the+treatment+of+solid+carcinomas.&rft.au=Theuer%2C+C+P%3BPastan%2C+I&rft.aulast=Theuer&rft.aufirst=C&rft.date=1993-09-01&rft.volume=166&rft.issue=3&rft.spage=284&rft.isbn=&rft.btitle=&rft.title=American+journal+of+surgery&rft.issn=00029610&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-04 N1 - Date created - 1993-10-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Phase I study of high-dose piroxantrone with granulocyte colony-stimulating factor. AN - 75904489; 7689093 AB - We performed a phase I trial of piroxantrone with and without granulocyte colony-stimulating factor (G-CSF) to determine whether the use of this cytokine would enable us to increase the dose-intensity of piroxantrone. Thirty-eight patients received 121 courses of piroxantrone administered once every 21 days. Initial patient cohorts received piroxantrone alone starting at 150 mg/m2 and the dose was escalated in subsequent patients until dose-limiting toxicity (DLT) was reached. Patient cohorts then received escalating doses of piroxantrone starting at 185 mg/m2 administered with G-CSF beginning day 2. Dose-limiting neutropenia occurred in three of six patients treated with 185 mg/m2 piroxantrone; the maximum-tolerated dose (MTD) of piroxantrone alone was 150 mg/m2. Three of six patients treated with piroxantrone and G-CSF exhibited dose-limiting thrombocytopenia at 445 mg/m2; the MTD of piroxantrone with G-CSF was thus 355 mg/m2. Seven patients developed symptomatic congestive heart failure (CHF) at cumulative piroxantrone doses ranging from 855 to 2,475 mg/m2 and two have died of cardiotoxicity. Of these patients, six of seven had previously received doxorubicin. Other nonhematologic toxicity was mild. The use of G-CSF results in a more than twofold increase in the MTD of piroxantrone. However, symptomatic cardiotoxicity is prominent, especially in patients who have received prior treatment with anthracyclines. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Savarese, D M AU - Denicoff, A M AU - Berg, S L AU - Hillig, M AU - Baker, S P AU - O'Shaughnessy, J A AU - Chow, C AU - Otterson, G A AU - Balis, F M AU - Poplack, D G AD - Medicine Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/09// PY - 1993 DA - September 1993 SP - 1795 EP - 1803 VL - 11 IS - 9 SN - 0732-183X, 0732-183X KW - Anthraquinones KW - 0 KW - Antineoplastic Agents KW - Pyrazoles KW - Granulocyte Colony-Stimulating Factor KW - 143011-72-7 KW - piroxantrone KW - YL4TY9WH22 KW - Index Medicus KW - Drug Administration Schedule KW - Bone Marrow Diseases -- prevention & control KW - Bone Marrow Diseases -- chemically induced KW - Logistic Models KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Male KW - Female KW - Multivariate Analysis KW - Pyrazoles -- administration & dosage KW - Neoplasms -- drug therapy KW - Anthraquinones -- adverse effects KW - Granulocyte Colony-Stimulating Factor -- therapeutic use KW - Antineoplastic Agents -- administration & dosage KW - Anthraquinones -- administration & dosage KW - Pyrazoles -- adverse effects KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75904489?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=Phase+I+study+of+high-dose+piroxantrone+with+granulocyte+colony-stimulating+factor.&rft.au=Savarese%2C+D+M%3BDenicoff%2C+A+M%3BBerg%2C+S+L%3BHillig%2C+M%3BBaker%2C+S+P%3BO%27Shaughnessy%2C+J+A%3BChow%2C+C%3BOtterson%2C+G+A%3BBalis%2C+F+M%3BPoplack%2C+D+G&rft.aulast=Savarese&rft.aufirst=D&rft.date=1993-09-01&rft.volume=11&rft.issue=9&rft.spage=1795&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=0732183X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-23 N1 - Date created - 1993-09-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Functional studies of a germ-line polymorphism at codon 47 within the p53 gene. AN - 75895359; 8352280 AB - A rare germ-line polymorphism in codon 47 of the p53 gene replaces the wild-type proline (CCG) with a serine (TCG). Restriction analysis of 101 human samples revealed the frequency of the rare allele to be 0% (n = 69) in Caucasians and 4.7% (3/64, n = 32) among African-Americans. To investigate the consequence of this amino acid substitution, a cDNA construct (p53 mut47ser) containing the mutation was introduced into a lung adenocarcinoma cell line (Calu-6) that does not express p53. A growth suppression similar to that obtained after introduction of a wild-type p53 cDNA construct was observed, in contrast to the result obtained by introduction of p53 mut143ala. Furthermore, expression of neither p53 mut47ser nor wild-type p53 was tolerated by growing cells. In transient expression assays, both mut47ser and wild-type p53 activated the expression of a reporter gene linked to a p53 binding sequence (PG13-CAT) and inhibited the expression of the luciferase gene under the control of the Rous sarcoma virus promoter (RSVluc). In the same assay, mut143ala did not activate the expression of PG13-CAT and produced only a slight inhibitory effect on RSVluc. These findings indicate that the p53 variant with a serine at codon 47 should be considered as a rare germ-line polymorphism that does not alter the growth-suppression activity of p53. JF - American journal of human genetics AU - Felley-Bosco, E AU - Weston, A AU - Cawley, H M AU - Bennett, W P AU - Harris, C C AD - Laboratory of Human Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/09// PY - 1993 DA - September 1993 SP - 752 EP - 759 VL - 53 IS - 3 SN - 0002-9297, 0002-9297 KW - Tumor Suppressor Protein p53 KW - 0 KW - Serine KW - 452VLY9402 KW - Proline KW - 9DLQ4CIU6V KW - Index Medicus KW - United States KW - Gene Frequency KW - Humans KW - European Continental Ancestry Group -- genetics KW - Structure-Activity Relationship KW - Serine -- genetics KW - Cloning, Molecular KW - Mutagenesis, Site-Directed KW - Proline -- genetics KW - Polymerase Chain Reaction KW - Alleles KW - Base Sequence KW - Tumor Cells, Cultured KW - African Continental Ancestry Group -- genetics KW - Transfection KW - Molecular Sequence Data KW - Immunohistochemistry KW - Tumor Suppressor Protein p53 -- physiology KW - Polymorphism, Genetic KW - Genes, p53 -- genetics KW - Point Mutation KW - Tumor Suppressor Protein p53 -- chemistry KW - Tumor Suppressor Protein p53 -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75895359?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+human+genetics&rft.atitle=Functional+studies+of+a+germ-line+polymorphism+at+codon+47+within+the+p53+gene.&rft.au=Felley-Bosco%2C+E%3BWeston%2C+A%3BCawley%2C+H+M%3BBennett%2C+W+P%3BHarris%2C+C+C&rft.aulast=Felley-Bosco&rft.aufirst=E&rft.date=1993-09-01&rft.volume=53&rft.issue=3&rft.spage=752&rft.isbn=&rft.btitle=&rft.title=American+journal+of+human+genetics&rft.issn=00029297&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-16 N1 - Date created - 1993-09-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1992 Jul 15;89(14):6413-7 [1631137] Cancer Epidemiol Biomarkers Prev. 1992 Sep-Oct;1(6):481-3 [1302561] Science. 1993 Jan 1;259(5091):84-7 [8418500] Nature. 1984 Dec 13-19;312(5995):646-9 [6095116] Nature. 1984 Dec 13-19;312(5995):649-51 [6390217] Nature. 1984 Dec 13-19;312(5995):651-4 [6095117] EMBO J. 1985 May;4(5):1251-5 [4006916] Mol Cell Biol. 1986 Dec;6(12):4650-6 [3025664] Mol Cell Biol. 1987 Feb;7(2):725-37 [3821727] Mol Cell Biol. 1987 Feb;7(2):961-3 [3547088] Anal Biochem. 1987 Apr;162(1):156-9 [2440339] Mol Cell Biol. 1988 Feb;8(2):531-9 [2832726] EMBO J. 1990 May;9(5):1595-602 [1691710] Science. 1990 Aug 24;249(4971):912-5 [2144057] Nucleic Acids Res. 1990 Aug 25;18(16):4963 [1697680] Oncogene. 1990 Sep;5(9):1409-10 [1977117] Science. 1990 Nov 30;250(4985):1233-8 [1978757] Mol Cell Biol. 1991 Jan;11(1):1-11 [1986214] Science. 1991 Jun 21;252(5013):1708-11 [2047879] Cancer Res. 1991 Aug 1;51(15):4090-6 [1855224] Proc Natl Acad Sci U S A. 1991 Sep 1;88(17):7605-9 [1652755] Oncogene. 1991 Sep;6(9):1691-2 [1923533] Am J Pathol. 1991 Oct;139(4):839-45 [1656762] Proc Natl Acad Sci U S A. 1991 Nov 15;88(22):9979-83 [1946467] Proc Natl Acad Sci U S A. 1992 Apr 1;89(7):2759-63 [1557382] Cancer Res. 1992 Apr 15;52(8):2340-3 [1559236] N Engl J Med. 1992 May 14;326(20):1301-8 [1565143] N Engl J Med. 1992 May 14;326(20):1309-15 [1565144] J Virol. 1992 Aug;66(8):4757-62 [1352831] Cancer Res. 1992 Dec 15;52(24):6976-8 [1458490] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Phase II study of fluorouracil, leucovorin, and interferon alfa-2a in metastatic colorectal carcinoma. AN - 75884729; 8355041 AB - To test the activity of a regimen of interferon alfa-2a (IFN alpha-2a) 5 x 10(6) U/m2 subcutaneously (SC) days 1 through 7 combined with leucovorin 500 mg/m2/d intravenously (IV) over 30 minutes and fluorouracil (5-FU) 370 mg/m2/d through IV push 1 hour after leucovorin days 2 through 6 in a phase II study. Forty-six patients with a good performance status (PS) with measurable colorectal cancer and no prior therapy for metastatic disease were entered. Cycles were repeated at 3-week intervals if toxicity had resolved. The 5-FU dose was increased by 15% if toxicity was mild, and decreased by 15% for grade 3 to 4 nonhematologic or grade 4 hematologic toxicity. Three complete responses (CRs) and 21 partial responses (PRs) were seen among 44 assessable patients (54%; 95% confidence interval, 39% to 70%). A moderately strong association was noted between PS and response: PS O (n = 26), two CRs and 15 PRs (65%); PS 1 (n = 13), one CR and six PRs (54%); PS 2 (n = 5), zero CRs and zero PRs (0%; two-tailed P = .026). With a median follow-up duration of 18.8 months, the median time to treatment failure (TTF) and survival were 7.8 months and 16.3 months, respectively. Doses were escalated to 425 mg/m2/d 5-FU in 10 patients, but only four tolerated the higher dose. When expressed as the most severe degree of toxicity experienced by each patient across all cycles, grade 3 to 4 toxicity of the following types was observed; mucositis, 37%; diarrhea, 40%; rash, 7%; fatigue, 14%; granulocytopenia, 13%. Dose-limiting toxicity at 370 mg/m2/d 5-FU eventually occurred in 28 patients (61%). Twelve patients (26%) required an IFN alpha-2a dose reduction for constitutional toxicity. This regimen has promising activity in advanced colorectal cancer, particularly in patients with an Eastern Cooperative Oncology Group (ECOG) PS of 0 to 1. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Grem, J L AU - Jordan, E AU - Robson, M E AU - Binder, R A AU - Hamilton, J M AU - Steinberg, S M AU - Arbuck, S G AU - Beveridge, R A AU - Kales, A N AU - Miller, J A AD - Clinical Oncology Program, National Cancer Institute, Bethesda, MD. Y1 - 1993/09// PY - 1993 DA - September 1993 SP - 1737 EP - 1745 VL - 11 IS - 9 SN - 0732-183X, 0732-183X KW - Interferon-alpha KW - 0 KW - Recombinant Proteins KW - interferon alfa-2a KW - 47RRR83SK7 KW - Leucovorin KW - Q573I9DVLP KW - Fluorouracil KW - U3P01618RT KW - Index Medicus KW - Fluorouracil -- administration & dosage KW - Drug Administration Schedule KW - Interferon-alpha -- administration & dosage KW - Leucovorin -- administration & dosage KW - Humans KW - Adult KW - Neoplasm Metastasis KW - Aged KW - Middle Aged KW - Male KW - Female KW - Survival Analysis KW - Colorectal Neoplasms -- pathology KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Colorectal Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75884729?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=Phase+II+study+of+fluorouracil%2C+leucovorin%2C+and+interferon+alfa-2a+in+metastatic+colorectal+carcinoma.&rft.au=Grem%2C+J+L%3BJordan%2C+E%3BRobson%2C+M+E%3BBinder%2C+R+A%3BHamilton%2C+J+M%3BSteinberg%2C+S+M%3BArbuck%2C+S+G%3BBeveridge%2C+R+A%3BKales%2C+A+N%3BMiller%2C+J+A&rft.aulast=Grem&rft.aufirst=J&rft.date=1993-09-01&rft.volume=11&rft.issue=9&rft.spage=1737&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=0732183X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-23 N1 - Date created - 1993-09-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Risk for sustained amenorrhea in patients with systemic lupus erythematosus receiving intermittent pulse cyclophosphamide therapy. AN - 75859497; 8338289 AB - To determine the risk for secondary amenorrhea after pulse cyclophosphamide therapy in premenopausal women with systemic lupus erythematosus. Controlled, retrospective clinical study. Government referral-based research hospital. Thirty-nine women younger than 40 years treated with pulse cyclophosphamide therapy for active lupus nephritis or neuropsychiatric lupus. Sixteen women who received pulses of intravenous methylprednisolone were controls. Sixteen patients received pulse cyclophosphamide (0.5 to 1.0 g/m2 body surface area) monthly for a total of 7 doses (short-CY), and 23 patients received 15 or more doses (long-CY). Control patients were treated with monthly pulses of methylprednisolone (1.0 g/m2) for a total of nine doses. Rates of amenorrhea were evaluated according to duration of treatment (number of doses) and age at the initiation of pulse therapy. Two of 16 patients (12%) in the Short-CY group and 9 of 23 (39%) in the long-CY group developed sustained amenorrhea (P = 0.07). Rates of sustained amenorrhea (short- and long-CY) according to age at the start of pulse therapy were: or = 31 years, 5/8 (62%) (P = 0.04). The increased risk for sustained amenorrhea in patients treated with long-CY was most evident in patients older than 25 years (short-CY [2/12] compared with long-CY [7/11]; P = 0.03). Three other patients with short-CY had reversal of amenorrhea fewer than 12 months after cessation of therapy. Amenorrhea was not observed in any of the 16 control patients. Intermittent pulse cyclophosphamide therapy in patients with systemic lupus erythematosus is associated with sustained amenorrhea, which is related to both age and number of doses of cyclophosphamide. JF - Annals of internal medicine AU - Boumpas, D T AU - Austin, H A AU - Vaughan, E M AU - Yarboro, C H AU - Klippel, J H AU - Balow, J E AD - National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland. Y1 - 1993/09/01/ PY - 1993 DA - 1993 Sep 01 SP - 366 EP - 369 VL - 119 IS - 5 SN - 0003-4819, 0003-4819 KW - Cyclophosphamide KW - 8N3DW7272P KW - Abridged Index Medicus KW - Index Medicus KW - Drug Administration Schedule KW - Age Factors KW - Lupus Nephritis -- drug therapy KW - Risk Factors KW - Humans KW - Ovary -- drug effects KW - Adult KW - Retrospective Studies KW - Female KW - Fertility -- drug effects KW - Cyclophosphamide -- administration & dosage KW - Lupus Erythematosus, Systemic -- drug therapy KW - Amenorrhea -- chemically induced KW - Cyclophosphamide -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75859497?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+internal+medicine&rft.atitle=Risk+for+sustained+amenorrhea+in+patients+with+systemic+lupus+erythematosus+receiving+intermittent+pulse+cyclophosphamide+therapy.&rft.au=Boumpas%2C+D+T%3BAustin%2C+H+A%3BVaughan%2C+E+M%3BYarboro%2C+C+H%3BKlippel%2C+J+H%3BBalow%2C+J+E&rft.aulast=Boumpas&rft.aufirst=D&rft.date=1993-09-01&rft.volume=119&rft.issue=5&rft.spage=366&rft.isbn=&rft.btitle=&rft.title=Annals+of+internal+medicine&rft.issn=00034819&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-26 N1 - Date created - 1993-08-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Inhibition of DNA repair and sensitization of cisplatin in human ovarian carcinoma cells by interleukin-1 alpha. AN - 75897029; 8363610 AB - Interleukin-1 alpha induced an increase in both the cellular accumulation of cis-diamminedichloroplatinum (II) (cisplatin) and DNA platination and significantly reduced the removal of platinum from DNA of human ovarian (NIH: OVCAR-3) carcinoma cells in culture. The combinations of IL-1 alpha and cisplatin were highly synergistic against these ovarian carcinoma cells and maximum levels of sensitization (15-20-fold) were observed during simultaneous exposure of cisplatin and IL-1 alpha. IL-1 alpha specific receptor antagonist decreased this synergy. These results strongly indicate that IL-1 alpha inhibits DNA repair, and this inhibition of DNA repair may explain, in part, a strong synergistic interaction between IL-1 alpha and cisplatin in NIH: OVCAR-3 cells. JF - Biochemical and biophysical research communications AU - Benchekroun, M N AU - Parker, R AU - Reed, E AU - Sinha, B K AD - Biochemical and Molecular Pharmacology Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/08/31/ PY - 1993 DA - 1993 Aug 31 SP - 294 EP - 300 VL - 195 IS - 1 SN - 0006-291X, 0006-291X KW - Interleukin-1 KW - 0 KW - Receptors, Interleukin-1 KW - Recombinant Proteins KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Recombinant Proteins -- toxicity KW - Ovarian Neoplasms KW - Tumor Cells, Cultured KW - Cell Survival -- drug effects KW - Dose-Response Relationship, Drug KW - Kinetics KW - Humans KW - Receptors, Interleukin-1 -- antagonists & inhibitors KW - Drug Synergism KW - Female KW - Cell Line KW - Cisplatin -- toxicity KW - Interleukin-1 -- toxicity KW - Cisplatin -- metabolism KW - DNA Repair -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75897029?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+and+biophysical+research+communications&rft.atitle=Inhibition+of+DNA+repair+and+sensitization+of+cisplatin+in+human+ovarian+carcinoma+cells+by+interleukin-1+alpha.&rft.au=Benchekroun%2C+M+N%3BParker%2C+R%3BReed%2C+E%3BSinha%2C+B+K&rft.aulast=Benchekroun&rft.aufirst=M&rft.date=1993-08-31&rft.volume=195&rft.issue=1&rft.spage=294&rft.isbn=&rft.btitle=&rft.title=Biochemical+and+biophysical+research+communications&rft.issn=0006291X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-28 N1 - Date created - 1993-09-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Requirement of phenylalanine 343 for the preferential delta 4-lyase versus delta 5-lyase activity of rat CYP17. AN - 75889081; 8349703 AB - Site-directed mutagenesis of a domain (amino acids 343-348) within the conserved region of rat CYP17 was performed to investigate species-specific differences between rat and human/bovine delta 4-versus delta 5-lyase activity. This domain displays substantial deviations between the rat and human/bovine/pig sequences and includes Arg346, which is known to be essential for delta 4-lyase (Kitamura, M., Buczko, E., and Dufau, M. L. (1991) Mol. Endocrinol. 5, 1373-1380) and delta 5-lyase activities. Analysis of the delta 4-lyase activity of mutant rat CYP17 cDNA expressed in nonsteroidogenic COS-1 cells revealed that substitution of Phe at position 343 in the rat with Ile of the human/bovine sequence resulted in a reduction in delta 4-lyase activity to levels in the range of the delta 5-supported reaction. This Phe343-->Ile mutant CYP17 did not exhibit changes either in delta 5-supported lyase activity or in delta 4- and delta 5-hydroxylase activities. Substitution of Asn344, Ser347, and His348 in rat CYP17 with the corresponding bovine amino acids Ser, Asn, and Arg did not enhance this effect. Thus, the reduced activity of the bovine CYP17 delta 4-lyase reaction can be mimicked in part in the rat polypeptide by the substitution of Phe343 with the bovine counterpart, Ile. Unlike the bovine CYP17-catalyzed reaction, the rat Phe343-->Ile mutant exhibited a low level lyase activity (kcat) that did not discriminate between delta 4- and delta 5-substrates. These results suggest that the presence of Phe343 enhances the delta 4-supported lyase activity possibly through stabilization of a delta 4-specific interaction. JF - The Journal of biological chemistry AU - Koh, Y AU - Buczko, E AU - Dufau, M L AD - Section on Molecular Endocrinology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/08/25/ PY - 1993 DA - 1993 Aug 25 SP - 18267 EP - 18271 VL - 268 IS - 24 SN - 0021-9258, 0021-9258 KW - CYP17 KW - Recombinant Proteins KW - 0 KW - Phenylalanine KW - 47E5O17Y3R KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Steroid 17-alpha-Hydroxylase KW - EC 1.14.14.19 KW - Aldehyde-Lyases KW - EC 4.1.2.- KW - Index Medicus KW - Animals KW - Recombinant Proteins -- biosynthesis KW - Models, Molecular KW - Humans KW - Amino Acid Sequence KW - Microsomes -- enzymology KW - Binding Sites KW - Cloning, Molecular KW - Rats KW - Mutagenesis, Site-Directed KW - Recombinant Proteins -- isolation & purification KW - Blotting, Western KW - Cattle KW - Transfection KW - Recombinant Proteins -- metabolism KW - Kinetics KW - Molecular Sequence Data KW - Substrate Specificity KW - Sequence Homology, Amino Acid KW - Cell Line KW - Protein Conformation KW - Steroid 17-alpha-Hydroxylase -- metabolism KW - Aldehyde-Lyases -- metabolism KW - Steroid 17-alpha-Hydroxylase -- isolation & purification KW - Cytochrome P-450 Enzyme System -- metabolism KW - Steroid 17-alpha-Hydroxylase -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75889081?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Requirement+of+phenylalanine+343+for+the+preferential+delta+4-lyase+versus+delta+5-lyase+activity+of+rat+CYP17.&rft.au=Koh%2C+Y%3BBuczko%2C+E%3BDufau%2C+M+L&rft.aulast=Koh&rft.aufirst=Y&rft.date=1993-08-25&rft.volume=268&rft.issue=24&rft.spage=18267&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-16 N1 - Date created - 1993-09-16 N1 - Date revised - 2017-01-13 N1 - Gene symbol - CYP17 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Cloning and site-directed mutagenesis of human ADP-ribosylarginine hydrolase. AN - 75889061; 8349667 AB - Mono-ADP-ribosylation of arginine is a reversible modification of proteins with NAD:arginine ADP-ribosyltransferases and ADP-ribosylarginine hydrolases catalyzing the opposing reactions in the cycle. ADP-ribosylarginine hydrolases differ in their dithiothreitol (DTT) requirements. Rat and mouse hydrolases require DTT for maximal activity, but calf, guinea pig, and human hydrolases are DTT-independent. To define the molecular basis for these differences, brain ADP-ribosylarginine hydrolases were cloned. Deduced amino acid sequences of mouse and rat hydrolases were 94% identical with 5 conserved cysteines. The human hydrolase sequence was 83% identical to that of rat but contained only 4 cysteines with cysteine 108 in rat corresponding to serine 103 in human. To investigate the role of rat cysteine 108, human and rat wild-type hydrolases and mutants, in which serine 103 in human was replaced by cysteine (S103C) and cysteine 108 in rat was replaced by serine (C108S), were expressed in Escherichia coli. Affinity-purified anti-rat brain hydrolase antibodies reacted with recombinant wild-type rat hydrolase, but only weakly with the C108S mutant. They did not react with human wild-type or the S103C mutant. Human hydrolase and rat C108S were DTT-independent; human S103C was, however, DTT-dependent. These data clearly show that cysteine 108 in rat hydrolase plays a critical role in DTT dependence and may be important in immunoreactivity. JF - The Journal of biological chemistry AU - Takada, T AU - Iida, K AU - Moss, J AD - Laboratory of Cellular Metabolism, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/08/25/ PY - 1993 DA - 1993 Aug 25 SP - 17837 EP - 17843 VL - 268 IS - 24 SN - 0021-9258, 0021-9258 KW - Oligodeoxyribonucleotides KW - 0 KW - Recombinant Proteins KW - DNA KW - 9007-49-2 KW - Hydrolases KW - EC 3.- KW - Glycoside Hydrolases KW - EC 3.2.1.- KW - N-Glycosyl Hydrolases KW - EC 3.2.2.- KW - ADP-ribosylarginine hydrolase KW - EC 3.2.2.19 KW - Dithiothreitol KW - T8ID5YZU6Y KW - Index Medicus KW - Animals KW - Recombinant Proteins -- biosynthesis KW - Guinea Pigs KW - Humans KW - Mice KW - Amino Acid Sequence KW - Cloning, Molecular KW - Rats KW - Recombinant Proteins -- isolation & purification KW - DNA -- isolation & purification KW - Base Sequence KW - Cattle KW - Chromatography, Gel KW - Recombinant Proteins -- metabolism KW - Kinetics KW - DNA -- genetics KW - Dithiothreitol -- pharmacology KW - Molecular Sequence Data KW - Sequence Homology, Amino Acid KW - Mutagenesis, Site-Directed KW - Hydrolases -- metabolism KW - Hydrolases -- isolation & purification KW - Hydrolases -- genetics KW - Lung -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75889061?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Cloning+and+site-directed+mutagenesis+of+human+ADP-ribosylarginine+hydrolase.&rft.au=Takada%2C+T%3BIida%2C+K%3BMoss%2C+J&rft.aulast=Takada&rft.aufirst=T&rft.date=1993-08-25&rft.volume=268&rft.issue=24&rft.spage=17837&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-16 N1 - Date created - 1993-09-16 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - L13290; GENBANK; L13291 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Sulfhydryl reagents and cAMP-dependent kinase increase the sensitivity of the inositol 1,4,5-trisphosphate receptor in hepatocytes. AN - 75888818; 8394353 AB - Sulfhydryl reagents such as tert-butyl hydroperoxide (TBHP) have been shown to increase cytosolic Ca2+ concentration ([Ca2+]i) in rat hepatocytes in a way that resembles responses to Ca(2+)-mobilizing hormones (Saikada, I., Thomas, A. P., and Farber, J. L. (1991) J. Biol. Chem. 266, 717-722; Rooney, T. A., Renard, D. C., Sass, E. J., and Thomas, A. P. (1991) J. Biol. Chem. 266, 12272-12282) and to increase the amount of Ca2+ released by inositol 1,4,5-trisphosphate ((1,4,5)IP3) from permeable rat liver cells (Rooney et al., 1991, op. cit.; Missiaen, L., Taylor, C. W., and Berridge, M. J. (1991) Nature 352, 241-244; Renard, D. C., Seitz, M. B., and Thomas, A. P. (1992) Biochem. J. 284, 507-512). The effects of sulfhydryl reagents were studied in fura-2-injected rat and guinea pig hepatocytes and compared with the actions of cAMP (Burgess, G. M., Bird, G. St. J., Obie, J. F., and Putney, J. W., Jr. (1991) J. Biol. Chem. 261, 4772-4781). In rat liver cells, the increases in [Ca2+]i induced by TBHP and thimerosal were prevented by microinjection of the cells with the (1,4,5)IP3 receptor antagonist heparin. In guinea pig hepatocytes, TBHP was not able to increase [Ca2+]i unless the cells were pretreated with angiotensin II to raise endogenous levels of (1,4,5)IP3 or were first injected with a sub-threshold concentration of inositol 2,4,5-trisphosphate ((2,4,5)IP3). The responses to TBHP in (2,4,5)IP3-injected guinea pig cells were also blocked by heparin. In many respects, the actions of TBHP appeared to be similar to those of cAMP, which has previously been shown to increase sensitivity to (1,4,5)IP3 in intact guinea pig hepatocytes (Burgess et al., 1991, op. cit.). TBHP also mimicked the effect of cAMP-dependent kinase (PKA) in permeabilized guinea pig hepatocytes by increasing the amount of Ca2+ released by (1,4,5)IP3. The responses to TBHP and cAMP in (2,4,5)IP3-injected guinea pig hepatocytes differed, however, in that the increase in [Ca2+]i evoked by elevating intracellular cAMP was greatly reduced by Wiptide, an inhibitor of PKA, while Wiptide had no effect on the Ca2+ transients induced by TBHP. This provides evidence that the sensitizing effect of TBHP is not mediated by PKA and is more likely to be a direct effect on the inositol trisphosphate receptor. It is possible, however, that the sulfhydryl reagents and PKA act on a common regulatory site on the receptor protein. JF - The Journal of biological chemistry AU - Bird, G S AU - Burgess, G M AU - Putney, J W AD - Calcium Regulation Section, National Institute of Environmental Health Sciences, Research Traingle Park, North Carolina 27709. Y1 - 1993/08/25/ PY - 1993 DA - 1993 Aug 25 SP - 17917 EP - 17923 VL - 268 IS - 24 SN - 0021-9258, 0021-9258 KW - Calcium Channels KW - 0 KW - Inositol 1,4,5-Trisphosphate Receptors KW - Inositol Phosphates KW - Oxidants KW - Peroxides KW - Receptors, Cell Surface KW - Receptors, Cytoplasmic and Nuclear KW - Sulfhydryl Reagents KW - Bucladesine KW - 63X7MBT2LQ KW - Inositol 1,4,5-Trisphosphate KW - 85166-31-0 KW - Heparin KW - 9005-49-6 KW - inositol 2,4,5-trisphosphate KW - 91840-07-2 KW - tert-Butylhydroperoxide KW - 955VYL842B KW - Protein Kinases KW - EC 2.7.- KW - Isoproterenol KW - L628TT009W KW - Calcium KW - SY7Q814VUP KW - Fura-2 KW - TSN3DL106G KW - Index Medicus KW - Rats KW - Animals KW - Oxidants -- pharmacology KW - Guinea Pigs KW - Cells, Cultured KW - Kinetics KW - Heparin -- pharmacology KW - Cell Membrane Permeability KW - Bucladesine -- pharmacology KW - Isoproterenol -- pharmacology KW - Inositol Phosphates -- pharmacology KW - Peroxides -- pharmacology KW - Liver -- metabolism KW - Inositol 1,4,5-Trisphosphate -- metabolism KW - Inositol 1,4,5-Trisphosphate -- pharmacology KW - Calcium -- metabolism KW - Protein Kinases -- pharmacology KW - Receptors, Cell Surface -- metabolism KW - Protein Kinases -- metabolism KW - Liver -- drug effects KW - Sulfhydryl Reagents -- pharmacology KW - Receptors, Cell Surface -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75888818?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Sulfhydryl+reagents+and+cAMP-dependent+kinase+increase+the+sensitivity+of+the+inositol+1%2C4%2C5-trisphosphate+receptor+in+hepatocytes.&rft.au=Bird%2C+G+S%3BBurgess%2C+G+M%3BPutney%2C+J+W&rft.aulast=Bird&rft.aufirst=G&rft.date=1993-08-25&rft.volume=268&rft.issue=24&rft.spage=17917&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-16 N1 - Date created - 1993-09-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - L-deprenyl confers specific protection against MPTP-induced Parkinson's disease-like movement disorder in the goldfish. AN - 76093145; 8243537 AB - Administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the goldfish causes a reversible, Parkinson's disease-like syndrome which includes loss of noradrenaline and dopamine from the brain, accumulation of the toxic metabolite 1-methyl-4-phenylpyridinium species (MPP+), and substantial reduction in movement. L-Deprenyl, a selective monoamine oxidase-B inhibitor, protects the goldfish from loss of movement, but clorgyline, a selective monoamine oxidase-A inhibitor, has no such protective action. L-Deprenyl and clorgyline primarily inhibit goldfish brain monoamine oxidase-B and monoamine oxidase-A, respectively. The mechanism by which MPTP causes reduced movement in goldfish is to cause an increase in resting time. Otherwise normal average velocity occurred during periods of movement. L-Deprenyl protection results in entirely 'normal' levels of resting time and average velocity during times of movement. Equivalent observations regarding l-deprenyl and clorgyline have been made in primate models of MPTP toxicity, and l-deprenyl is used for treatment of Parkinson's disease in humans. Therefore it is suggested that the evolutionarily equivalent subcortical circuitry and neural density of the goldfish brain may provide a useful model upon which to search for drugs relevant to human Parkinson's disease. JF - European journal of pharmacology AU - Adeyemo, O M AU - Youdim, M B AU - Markey, S P AU - Markey, C J AU - Pollard, H B AD - Laboratory of Cell Biology and Genetics, N.I.D.D.K., National Institute of Health, Bethesda, MD 20892. Y1 - 1993/08/24/ PY - 1993 DA - 1993 Aug 24 SP - 185 EP - 193 VL - 240 IS - 2-3 SN - 0014-2999, 0014-2999 KW - Selegiline KW - 2K1V7GP655 KW - Monoamine Oxidase KW - EC 1.4.3.4 KW - Clorgyline KW - LYJ16FZU9Q KW - Dopamine KW - VTD58H1Z2X KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Brain -- enzymology KW - Animals KW - Norepinephrine -- metabolism KW - Brain -- drug effects KW - Dopamine -- metabolism KW - Monoamine Oxidase -- metabolism KW - Parkinson Disease, Secondary -- chemically induced KW - Selegiline -- pharmacology KW - MPTP Poisoning KW - Goldfish KW - Disease Models, Animal KW - Motor Activity -- drug effects KW - Clorgyline -- pharmacology KW - Parkinson Disease, Secondary -- prevention & control KW - Parkinson Disease, Secondary -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76093145?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+pharmacology&rft.atitle=L-deprenyl+confers+specific+protection+against+MPTP-induced+Parkinson%27s+disease-like+movement+disorder+in+the+goldfish.&rft.au=Adeyemo%2C+O+M%3BYoudim%2C+M+B%3BMarkey%2C+S+P%3BMarkey%2C+C+J%3BPollard%2C+H+B&rft.aulast=Adeyemo&rft.aufirst=O&rft.date=1993-08-24&rft.volume=240&rft.issue=2-3&rft.spage=185&rft.isbn=&rft.btitle=&rft.title=European+journal+of+pharmacology&rft.issn=00142999&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-01-03 N1 - Date created - 1994-01-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The G protein alpha s subunit incorporates [3H]palmitic acid and mutation of cysteine-3 prevents this modification. AN - 75879862; 8347607 AB - We investigated whether alpha s could be acylated by palmitate by transfecting COS cells with the cDNA for the wild-type, long form of alpha s and metabolically labeling with [3H]palmitate or [35S]methionine. Cells were separated into particulate and soluble fractions and immunoprecipitated with a specific peptide antibody. [3H]Palmitate was incorporated into both endogenous and transfected alpha s. Inhibition of protein synthesis with cycloheximide did not block the radiolabeling of alpha s with [3H]palmitate. Hydroxylamine treatment caused a release of the tritium radiolabel, demonstrating that the incorporation was through a thioester bond. The tritium radiolabel was base-labile and comigrated with [3H]palmitate on thin-layer chromatography. The third residue of the wild-type alpha s was mutated from a cysteine to an alanine by site-directed mutagenesis. This mutant was expressed in COS cells and localized to the particulate fraction as determined by immunoprecipitation of the [35S]methionine-labeled cells. The cysteine-3 mutant did not undergo radiolabeling with [3H]palmitate, indicating that this residue is crucial for the modification. JF - Biochemistry AU - Degtyarev, M Y AU - Spiegel, A M AU - Jones, T L AD - Molecular Pathophysiology Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/08/17/ PY - 1993 DA - 1993 Aug 17 SP - 8057 EP - 8061 VL - 32 IS - 32 SN - 0006-2960, 0006-2960 KW - Palmitic Acids KW - 0 KW - Tritium KW - 10028-17-8 KW - Palmitic Acid KW - 2V16EO95H1 KW - Cycloheximide KW - 98600C0908 KW - Methionine KW - AE28F7PNPL KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Cysteine KW - K848JZ4886 KW - Index Medicus KW - Animals KW - Immunoblotting KW - Gene Expression KW - Methionine -- metabolism KW - Rats KW - Base Sequence KW - Transfection KW - Cycloheximide -- pharmacology KW - Molecular Sequence Data KW - Immunosorbent Techniques KW - Cell Line KW - Mutagenesis, Site-Directed KW - Palmitic Acids -- metabolism KW - GTP-Binding Proteins -- metabolism KW - Cysteine -- genetics KW - GTP-Binding Proteins -- chemistry KW - GTP-Binding Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75879862?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemistry&rft.atitle=The+G+protein+alpha+s+subunit+incorporates+%5B3H%5Dpalmitic+acid+and+mutation+of+cysteine-3+prevents+this+modification.&rft.au=Degtyarev%2C+M+Y%3BSpiegel%2C+A+M%3BJones%2C+T+L&rft.aulast=Degtyarev&rft.aufirst=M&rft.date=1993-08-17&rft.volume=32&rft.issue=32&rft.spage=8057&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-16 N1 - Date created - 1993-09-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Phencyclidine, a psychotomimetic agent and drug of abuse, is a suicide inhibitor of brain nitric oxide synthase. AN - 75899672; 7688965 AB - Phencyclidine, 1-(1-phenylcyclohexyl)piperidine, was shown in this study to be an effective irreversible inhibitor of brain nitric oxide synthase, the enzyme responsible for the conversion of L-arginine to nitric oxide. The inactivation of nitric oxide synthase was time- and concentration-dependent and required reduced nicotinamide adenine dinucleotide phosphate, a necessary cofactor for nitric oxide synthesis. These results indicate that phencyclidine is metabolized by nitric oxide synthase to reactive intermediates that irreversibly inactivate the enzyme. The inactivation of nitric oxide synthase by xenobiotics, such as phencyclidine, may be pharmacologically and toxicologically important due to the role of nitric oxide in a variety of physiological processes. JF - Biochemical and biophysical research communications AU - Osawa, Y AU - Davila, J C AD - Laboratory of Chemical Pharmacology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/08/16/ PY - 1993 DA - 1993 Aug 16 SP - 1435 EP - 1439 VL - 194 IS - 3 SN - 0006-291X, 0006-291X KW - Nitric Oxide Synthase KW - EC 1.14.13.39 KW - Amino Acid Oxidoreductases KW - EC 1.4.- KW - Phencyclidine KW - J1DOI7UV76 KW - Index Medicus KW - Rats KW - Animals KW - Dose-Response Relationship, Drug KW - Cytosol -- enzymology KW - Rats, Wistar KW - Brain -- enzymology KW - Amino Acid Oxidoreductases -- antagonists & inhibitors KW - Phencyclidine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75899672?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+and+biophysical+research+communications&rft.atitle=Phencyclidine%2C+a+psychotomimetic+agent+and+drug+of+abuse%2C+is+a+suicide+inhibitor+of+brain+nitric+oxide+synthase.&rft.au=Osawa%2C+Y%3BDavila%2C+J+C&rft.aulast=Osawa&rft.aufirst=Y&rft.date=1993-08-16&rft.volume=194&rft.issue=3&rft.spage=1435&rft.isbn=&rft.btitle=&rft.title=Biochemical+and+biophysical+research+communications&rft.issn=0006291X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-15 N1 - Date created - 1993-09-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Dopamine transporter gene polymorphisms are not associated with polysubstance abuse. AN - 75973232; 8399824 JF - Biological psychiatry AU - Persico, A M AU - Vandenbergh, D J AU - Smith, S S AU - Uhl, G R AD - Molecular Neurobiology Branch, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1993/08/15/ PY - 1993 DA - 1993 Aug 15 SP - 265 EP - 267 VL - 34 IS - 4 SN - 0006-3223, 0006-3223 KW - Biomarkers KW - 0 KW - DNA KW - 9007-49-2 KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Dopamine -- genetics KW - Psychiatric Status Rating Scales KW - Polymorphism, Genetic -- genetics KW - Humans KW - DNA -- genetics KW - Gene Expression KW - Biological Transport KW - Dopamine -- metabolism KW - DNA -- physiology KW - Male KW - Female KW - Substance-Related Disorders -- diagnosis KW - Substance-Related Disorders -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75973232?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biological+psychiatry&rft.atitle=Dopamine+transporter+gene+polymorphisms+are+not+associated+with+polysubstance+abuse.&rft.au=Persico%2C+A+M%3BVandenbergh%2C+D+J%3BSmith%2C+S+S%3BUhl%2C+G+R&rft.aulast=Persico&rft.aufirst=A&rft.date=1993-08-15&rft.volume=34&rft.issue=4&rft.spage=265&rft.isbn=&rft.btitle=&rft.title=Biological+psychiatry&rft.issn=00063223&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-17 N1 - Date created - 1993-11-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Replication of UV-irradiated DNA in human cell extracts: evidence for mutagenic bypass of pyrimidine dimers. AN - 75912776; 8356079 AB - We have examined the efficiency and fidelity of simian virus 40-origin-dependent replication of UV-irradiated double-stranded DNA in extracts of human cells. Using as a mutational target the alpha-complementation domain of the Escherichia coli lacZ gene in bacteriophage M13mp2 DNA, replication of undamaged DNA in HeLa cell extracts was highly accurate, whereas replication of DNA irradiated with UV light (280-320 nm) was both less efficient and less accurate. Replication was inhibited by irradiation in a dose-dependent manner. Nonetheless, covalently closed, monomer-length circular products were generated that were resistant to digestion by Dpn I, showing that they resulted from semiconservative replication. These products were incised by T4 endonuclease V, whereas the undamaged replication products were not, suggesting that pyrimidine dimers were bypassed during replication. When replicated, UV-irradiated DNA was used to transfect an E. coli alpha-complementation host strain to score mutant M13mp2 plaques, the mutant plaque frequency was substantially higher than that obtained with either unirradiated, replicated DNA, or unreplicated, UV-irradiated DNA. Both the increased mutagenicity and the inhibition of replication associated with UV irradiation were reversed by treatment of the irradiated DNA with photolyase before replication. Sequence analysis of mutants resulting from replication of UV-irradiated DNA demonstrated that most mutants contained C-->T transition errors at dipyrimidine sites. A few mutants contained 1-nt frameshift errors or tandem double CC-->TT substitutions. The data are consistent with the interpretation that pyrimidine dimers are bypassed during replication by the multiprotein replication apparatus in human cell extracts and that this bypass is mutagenic primarily via misincorporation of dAMP opposite a cytosine (or uracil) in the dimer. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Thomas, D C AU - Kunkel, T A AD - Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/08/15/ PY - 1993 DA - 1993 Aug 15 SP - 7744 EP - 7748 VL - 90 IS - 16 SN - 0027-8424, 0027-8424 KW - Deoxycytosine Nucleotides KW - 0 KW - Pyrimidine Dimers KW - 2'-deoxycytidine 5'-triphosphate KW - 2056-98-6 KW - DNA KW - 9007-49-2 KW - Deoxyribodipyrimidine Photo-Lyase KW - EC 4.1.99.3 KW - Index Medicus KW - Deoxycytosine Nucleotides -- metabolism KW - Deoxyribodipyrimidine Photo-Lyase -- metabolism KW - HeLa Cells KW - Electrophoresis, Polyacrylamide Gel KW - Humans KW - Restriction Mapping KW - Electrophoresis, Agar Gel KW - Escherichia coli -- genetics KW - Escherichia coli -- enzymology KW - Dose-Response Relationship, Radiation KW - DNA -- isolation & purification KW - Ultraviolet Rays KW - DNA Replication -- radiation effects KW - Pyrimidine Dimers -- metabolism KW - DNA -- radiation effects KW - DNA -- biosynthesis KW - Mutagenesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75912776?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Replication+of+UV-irradiated+DNA+in+human+cell+extracts%3A+evidence+for+mutagenic+bypass+of+pyrimidine+dimers.&rft.au=Thomas%2C+D+C%3BKunkel%2C+T+A&rft.aulast=Thomas&rft.aufirst=D&rft.date=1993-08-15&rft.volume=90&rft.issue=16&rft.spage=7744&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-23 N1 - Date created - 1993-09-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Genetics. 1974 Sep;78(1):139-48 [4442699] Mol Cell Biol. 1993 Jan;13(1):533-42 [8417349] Photochem Photobiol. 1978 Mar;27(3):297-307 [733927] J Mol Biol. 1980 Apr;138(2):299-319 [6251226] Proc Natl Acad Sci U S A. 1983 Mar;80(6):1541-5 [6340105] J Mol Biol. 1984 Mar 5;173(3):293-305 [6230459] J Mol Biol. 1984 Dec 5;180(2):217-37 [6439876] J Biol Chem. 1985 May 10;260(9):5787-96 [3988773] J Mol Biol. 1985 Mar 5;182(1):65-8 [2987509] Mol Cell Biol. 1985 Jun;5(6):1238-46 [2993858] Proc Natl Acad Sci U S A. 1986 Jul;83(13):4599-603 [2941756] J Biol Chem. 1986 Nov 5;261(31):14496-505 [3533921] Proc Natl Acad Sci U S A. 1986 Nov;83(21):8273-7 [3464953] Mol Cell Biol. 1986 Jan;6(1):277-85 [3537686] Mol Cell Biol. 1986 Oct;6(10):3349-56 [3540589] Mol Cell Biol. 1986 Oct;6(10):3443-50 [3025594] Proc Natl Acad Sci U S A. 1987 Dec;84(24):9103-7 [3480533] J Mol Biol. 1987 Nov 20;198(2):187-202 [2828636] J Biol Chem. 1988 Mar 25;263(9):4450-9 [2831231] Proc Natl Acad Sci U S A. 1988 Oct;85(19):7064-8 [3174620] Annu Rev Biochem. 1988;57:29-67 [3052275] Proc Natl Acad Sci U S A. 1988 Nov;85(21):8141-5 [3054882] J Biol Chem. 1988 Dec 5;263(34):17889-92 [2848017] Carcinogenesis. 1989 Jan;10(1):1-11 [2642748] Proc Natl Acad Sci U S A. 1990 Nov;87(22):9005-9 [2247476] Mol Cell Biol. 1991 Apr;11(4):1927-34 [2005888] Proc Natl Acad Sci U S A. 1991 Apr 15;88(8):3465-9 [1901658] J Mol Biol. 1991 Apr 20;218(4):667-73 [1902520] Nucleic Acids Res. 1991 May 11;19(9):2411-5 [1674998] J Biol Chem. 1991 Jun 25;266(18):11766-73 [2050676] Mol Carcinog. 1991;4(3):196-202 [2064725] Proc Natl Acad Sci U S A. 1991 Sep 1;88(17):7810-4 [1652764] Proc Natl Acad Sci U S A. 1991 Nov 1;88(21):9685-9 [1946387] Proc Natl Acad Sci U S A. 1991 Nov 15;88(22):10124-8 [1946433] Biochemistry. 1991 Dec 24;30(51):11751-9 [1751492] Proc Natl Acad Sci U S A. 1992 Feb 15;89(4):1159-63 [1741372] Biochemistry. 1992 Apr 14;31(14):3671-81 [1567822] Proc Natl Acad Sci U S A. 1974 Sep;71(9):3363-6 [4530308] Mol Gen Genet. 1988 Nov;214(3):396-404 [3063945] Mol Cell Biol. 1988 Dec;8(12):5425-31 [3072480] Biochemistry. 1989 Jan 24;28(2):775-9 [2713344] Mol Cell Biol. 1989 Mar;9(3):1277-83 [2725498] Mutat Res. 1989 Sep;218(2):49-65 [2671706] J Biol Chem. 1989 Oct 25;264(30):18005-10 [2808361] Proc Natl Acad Sci U S A. 1989 Nov;86(22):8922-6 [2813430] Annu Rev Cell Biol. 1989;5:197-245 [2557059] Biochemistry. 1990 Feb 13;29(6):1624-32 [2185842] J Biol Chem. 1990 Oct 25;265(30):18043-6 [1976634] Mutat Res. 1992 Aug;274(2):135-45 [1378205] Biochemistry. 1992 Jul 28;31(29):6794-800 [1637815] Exp Cell Res. 1992 Aug;201(2):462-9 [1322318] Nucleic Acids Res. 1992 Oct 25;20(20):5403-6 [1359505] Proc Natl Acad Sci U S A. 1992 Nov 15;89(22):11036-40 [1438310] J Mol Biol. 1977 Dec 15;117(3):525-67 [609095] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Ly-GDI, a GDP-dissociation inhibitor of the RhoA GTP-binding protein, is expressed preferentially in lymphocytes. AN - 75904756; 8356058 AB - The Ras-related small GTP-binding proteins are involved in diverse cellular events, including cell signaling, proliferation, cytoskeletal organization, and secretion. The interconversion of the active, GTP-bound form of the protein to the inactive, GDP-bound form is influenced by two types of regulatory proteins, those that alter the intrinsic GTPase activity of the GTP-binding protein and those that affect the rate of GDP/GTP exchange. By utilizing a subtractive hybridization approach, we have isolated a human gene encoding Ly-GDI, a protein that has striking homology to the product of a previously cloned gene, Rho-GDI, which inhibits GDP/GTP exchange on the Rho family of GTPases. In contrast to Rho-GDI, which is ubiquitously expressed, Ly-GDI is expressed only in hematopoietic tissues and predominantly in B- and T-lymphocyte cell lines. The full-length Ly-GDI cDNA encodes a 27-kDa protein which binds to RhoA and inhibits GDP dissociation from RhoA. Stimulation of T lymphocytes with phorbol ester leads to phosphorylation of Ly-GDI, suggesting an involvement of Ly-GDI in lymphocyte activation pathways. Cell type-specific regulators of the Ras-like GTP-binding proteins may provide one mechanism by which different cell types respond uniquely to signals transduced through the same cell surface receptor or may provide a way by which the GTP-binding proteins can be uniquely engaged by tissue-restricted receptors. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Scherle, P AU - Behrens, T AU - Staudt, L M AD - Metabolism Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/08/15/ PY - 1993 DA - 1993 Aug 15 SP - 7568 EP - 7572 VL - 90 IS - 16 SN - 0027-8424, 0027-8424 KW - ARHGDIB protein, human KW - 0 KW - Guanine Nucleotide Dissociation Inhibitors KW - Phosphates KW - Proteins KW - Tumor Suppressor Proteins KW - rho Guanine Nucleotide Dissociation Inhibitor beta KW - rho-Specific Guanine Nucleotide Dissociation Inhibitors KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - rhoA GTP-Binding Protein KW - EC 3.6.5.2 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Humans KW - Amino Acid Sequence KW - Plasmids KW - Proteins -- genetics KW - Cloning, Molecular KW - Lymphocyte Activation KW - Phosphates -- metabolism KW - Tumor Cells, Cultured KW - Kinetics KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Sequence Homology, Amino Acid KW - Cell Line KW - Gene Library KW - Protein Biosynthesis KW - B-Lymphocytes -- drug effects KW - GTP-Binding Proteins -- antagonists & inhibitors KW - B-Lymphocytes -- immunology KW - T-Lymphocytes -- drug effects KW - B-Lymphocytes -- metabolism KW - T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75904756?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Ly-GDI%2C+a+GDP-dissociation+inhibitor+of+the+RhoA+GTP-binding+protein%2C+is+expressed+preferentially+in+lymphocytes.&rft.au=Scherle%2C+P%3BBehrens%2C+T%3BStaudt%2C+L+M&rft.aulast=Scherle&rft.aufirst=P&rft.date=1993-08-15&rft.volume=90&rft.issue=16&rft.spage=7568&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-23 N1 - Date created - 1993-09-23 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - L20688; GENBANK N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1990 Aug;87(15):5998-6002 [2116014] Proc Natl Acad Sci U S A. 1993 Feb 15;90(4):1479-83 [8434008] Cell. 1984 Jul;37(3):767-78 [6204768] Cell. 1986 Nov 7;47(3):401-12 [3094963] Nucleic Acids Res. 1987 Feb 25;15(4):1869 [3822842] Science. 1987 Oct 23;238(4826):542-5 [2821624] Oncogene. 1988 Aug;3(2):201-4 [3045729] Gene. 1988 Jul 15;67(1):31-40 [3047011] EMBO J. 1988 Aug;7(8):2465-73 [3056717] Science. 1989 Jan 20;243(4889):355-61 [2783497] J Biol Chem. 1989 Jul 25;264(21):12394-401 [2501306] Mol Cell Biol. 1989 May;9(5):2058-66 [2501657] J Biol Chem. 1989 Oct 5;264(28):16378-82 [2674130] Cell. 1990 Feb 9;60(3):375-86 [2302733] Science. 1990 Apr 6;248(4951):67-9 [2181667] Nucleic Acids Res. 1990 Mar 25;18(6):1587-93 [2326198] J Biol Chem. 1990 Jun 5;265(16):9373-80 [2111820] Mol Cell Biol. 1990 Aug;10(8):4116-22 [2115118] Science. 1990 Aug 10;249(4969):635-40 [2116664] Nature. 1990 Aug 23;346(6286):719-23 [2201921] Oncogene. 1990 Sep;5(9):1321-8 [2120668] Nature. 1990 Nov 8;348(6297):125-32 [2122258] Proc Natl Acad Sci U S A. 1990 Oct;87(20):8008-12 [2172971] Oncogene. 1991 Jan;6(1):119-24 [1899476] Oncogene. 1991 Apr;6(4):515-22 [1903193] Anal Biochem. 1991 Feb 1;192(2):262-7 [1852137] Cell. 1991 Jun 14;65(6):1033-42 [1904317] Biochem J. 1991 Jun 15;276 ( Pt 3):833-6 [1905930] J Immunol. 1991 Aug 15;147(4):1139-46 [1907989] Nature. 1991 Oct 17;353(6345):668-70 [1922386] Biochem Biophys Res Commun. 1992 Jan 31;182(2):921-30 [1734890] J Cell Biol. 1992 Mar;116(5):1211-20 [1346786] J Biol Chem. 1992 Mar 5;267(7):4289-91 [1537820] Am J Physiol. 1992 Apr;262(4 Pt 1):C916-26 [1566818] Cell. 1992 May 1;69(3):539-49 [1581965] Cell. 1992 Jul 24;70(2):351-64 [1638635] Nature. 1992 Jul 23;358(6384):351-4 [1379346] Cell. 1992 Aug 7;70(3):389-99 [1643657] Cell. 1992 Aug 7;70(3):401-10 [1643658] Nature. 1992 Sep 10;359(6391):153-4 [1522900] J Immunol. 1992 Oct 1;149(7):2271-80 [1388187] EMBO J. 1992 Dec;11(12):4549-56 [1425589] Science. 1992 Oct 30;258(5083):812-5 [1439791] Nature. 1983 Mar 3;302(5903):33-7 [6298635] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The N-terminal region of the 37-kDa translocated fragment of Pseudomonas exotoxin A aborts translocation by promoting its own export after microsomal membrane insertion. AN - 75902668; 8356083 AB - The 37-kDa C-terminal fragment of Pseudomonas exotoxin A (PE; termed PE37 and composed of aa 280-613 of PE) translocates to the cell cytosol to cause cell death. PE37 requires a C-terminal endoplasmic reticulum retention sequence to be cytotoxic, indicating that the toxin may translocate to the cytosol from the endoplasmic reticulum. We show here that the N-terminal region of nascent PE37 can be inserted into the membrane of canine pancreatic microsomes by the preprocecropin signal sequence but then is exported or released from microsomes. The 34 N-terminal amino acids of the toxin fragment are sufficient to arrest translocation and prevent the microsomal accumulation of nascent chains that otherwise are sequestered into microsomes. These data support a role for the N-terminal region of PE37 in the translocation of the toxin from the endoplasmic reticulum to the cytosol in mammalian cells. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Theuer, C P AU - Buchner, J AU - FitzGerald, D AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/08/15/ PY - 1993 DA - 1993 Aug 15 SP - 7774 EP - 7778 VL - 90 IS - 16 SN - 0027-8424, 0027-8424 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - Oligopeptides KW - Peptide Fragments KW - RNA, Messenger KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - Endoplasmic Reticulum -- metabolism KW - Peptide Fragments -- metabolism KW - Protein Biosynthesis KW - Animals KW - Cytosol -- metabolism KW - Peptide Fragments -- toxicity KW - Amino Acid Sequence KW - Cell Death -- drug effects KW - Plasmids KW - Mutagenesis, Site-Directed KW - RNA, Messenger -- metabolism KW - Pancreas -- metabolism KW - Restriction Mapping KW - Polymerase Chain Reaction -- methods KW - Dogs KW - Molecular Sequence Data KW - Templates, Genetic KW - Pseudomonas aeruginosa -- metabolism KW - Exotoxins -- genetics KW - Microsomes -- metabolism KW - Exotoxins -- metabolism KW - Oligopeptides -- metabolism KW - Exotoxins -- toxicity KW - Oligopeptides -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75902668?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=The+N-terminal+region+of+the+37-kDa+translocated+fragment+of+Pseudomonas+exotoxin+A+aborts+translocation+by+promoting+its+own+export+after+microsomal+membrane+insertion.&rft.au=Theuer%2C+C+P%3BBuchner%2C+J%3BFitzGerald%2C+D%3BPastan%2C+I&rft.aulast=Theuer&rft.aufirst=C&rft.date=1993-08-15&rft.volume=90&rft.issue=16&rft.spage=7774&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-23 N1 - Date created - 1993-09-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: FEBS Lett. 1991 Jul 22;285(2):182-8 [1855588] Science. 1991 May 24;252(5009):1171-3 [1851576] Science. 1991 Nov 22;254(5035):1173-7 [1683495] Annu Rev Biochem. 1992;61:331-54 [1497314] J Biol Chem. 1992 Aug 25;267(24):16872-7 [1512230] Science. 1992 Nov 6;258(5084):931-6 [1332192] J Biol Chem. 1992 Dec 5;267(34):24328-32 [1447183] J Biol Chem. 1992 Dec 15;267(35):25396-401 [1460035] J Urol. 1993 Jun;149(6):1626-32 [8501821] Nature. 1970 Aug 15;227(5259):680-5 [5432063] Proc Natl Acad Sci U S A. 1975 Jun;72(6):2284-8 [166383] J Cell Biol. 1975 Dec;67(3):835-51 [811671] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5598-602 [271987] Proc Natl Acad Sci U S A. 1979 Apr;76(4):1795-9 [109833] J Biol Chem. 1979 Sep 25;254(18):9237-46 [479192] J Biol Chem. 1980 Apr 25;255(8):3600-4 [7364760] J Biol Chem. 1982 Jun 25;257(12):6796-801 [7085604] J Cell Biol. 1982 Nov;95(2 Pt 1):463-9 [6292235] J Cell Biol. 1982 Nov;95(2 Pt 1):470-7 [6292236] J Biol Chem. 1983 Aug 10;258(15):9488-95 [6348046] Methods Enzymol. 1983;96:94-111 [6656656] J Biol Chem. 1984 Sep 10;259(17):10700-4 [6206060] Proc Natl Acad Sci U S A. 1986 Feb;83(3):581-5 [3511473] Proc Natl Acad Sci U S A. 1986 Mar;83(5):1320-4 [3006045] J Cell Biol. 1986 Dec;103(6 Pt 1):2253-61 [3097028] Cell. 1987 Jan 16;48(1):129-36 [3098436] J Cell Biol. 1988 Apr;106(4):1093-104 [3283145] Infect Immun. 1988 Dec;56(12):3095-8 [2460407] J Biol Chem. 1988 Nov 15;263(32):17063-70 [3053702] J Biol Chem. 1989 Aug 25;264(24):14256-61 [2503515] Proc Natl Acad Sci U S A. 1990 Jan;87(1):308-12 [2104981] J Biol Chem. 1990 Nov 25;265(33):20678-85 [2122978] Cell. 1991 May 3;65(3):371-80 [1902142] J Biol Chem. 1991 Sep 15;266(26):17376-81 [1910044] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The N-terminal coiled-coil domain of beta is essential for gamma association: a model for G-protein beta gamma subunit interaction. AN - 75902559; 8356073 AB - We have identified the N terminus of the beta subunit as an essential domain for G-protein beta gamma assembly. A C-terminal fragment, beta 1-(130-340), fails to bind gamma unless coexpressed with the complementary N-terminal fragment, beta 1-(1-129). Deletion of the N-terminal 33 residues of beta 1, a region identified by computer algorithm to favor coiled-coil formation, abolishes gamma 2 association. On the basis of these findings, we propose a coiled-coil model of beta gamma interaction and refine this by computer-assisted molecular modeling. The model is tested by further mutagenesis: reversing the charge of residues in beta 1 that are hypothesized to be involved in interhelical salt bridges precludes gamma association. Insertions in the coiled-coil region, which disrupt the proposed hydrophobic interface, prevent gamma association. This structural basis for beta gamma dimerization provides a starting point for the design of beta and gamma mutants that can be used to map regions in beta gamma critical for interactions with the alpha subunit, receptors, and effectors. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Garritsen, A AU - van Galen, P J AU - Simonds, W F AD - Molecular Pathophysiology Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/08/15/ PY - 1993 DA - 1993 Aug 15 SP - 7706 EP - 7710 VL - 90 IS - 16 SN - 0027-8424, 0027-8424 KW - DNA-Binding Proteins KW - 0 KW - Fungal Proteins KW - Macromolecular Substances KW - Peptide Fragments KW - Saccharomyces cerevisiae Proteins KW - Arginine KW - 94ZLA3W45F KW - Protein Kinases KW - EC 2.7.- KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Index Medicus KW - Animals KW - Electrophoresis, Polyacrylamide Gel KW - Models, Molecular KW - Algorithms KW - Peptide Fragments -- isolation & purification KW - Amino Acid Sequence KW - Fungal Proteins -- chemistry KW - Mutagenesis, Site-Directed KW - Protein Kinases -- metabolism KW - Fungal Proteins -- metabolism KW - Transfection KW - Cell Line KW - Sequence Deletion KW - Protein Kinases -- chemistry KW - Protein Structure, Secondary KW - GTP-Binding Proteins -- metabolism KW - GTP-Binding Proteins -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75902559?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=The+N-terminal+coiled-coil+domain+of+beta+is+essential+for+gamma+association%3A+a+model+for+G-protein+beta+gamma+subunit+interaction.&rft.au=Garritsen%2C+A%3Bvan+Galen%2C+P+J%3BSimonds%2C+W+F&rft.aulast=Garritsen&rft.aufirst=A&rft.date=1993-08-15&rft.volume=90&rft.issue=16&rft.spage=7706&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-23 N1 - Date created - 1993-09-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 1992 Jul 15;267(20):13807-10 [1629181] Mol Biol Cell. 1992 Jan;3(1):49-61 [1550955] Curr Opin Genet Dev. 1992 Apr;2(2):205-10 [1638114] J Gen Physiol. 1992 Jun;99(6):961-83 [1640222] Nature. 1992 Jul 30;358(6385):424-6 [1322501] Science. 1992 Aug 28;257(5074):1264-7 [1325672] Cell. 1992 Sep 18;70(6):869-72 [1525824] Endocr Rev. 1992 Aug;13(3):536-65 [1425488] J Biol Chem. 1992 Nov 15;267(32):23409-17 [1429682] FEBS Lett. 1992 Dec 14;314(2):105-8 [1459238] EMBO J. 1992 Dec;11(13):4805-13 [1464310] Nature. 1992 Dec 17;360(6405):684-6 [1465133] Science. 1993 Feb 5;259(5096):832-4 [8094261] Cell. 1993 May 21;73(4):631-41 [8388779] J Biol Chem. 1951 Nov;193(1):265-75 [14907713] Nature. 1970 Aug 15;227(5259):680-5 [5432063] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] J Biol Chem. 1983 Sep 10;258(17):10503-10 [6136510] Nucleic Acids Res. 1984 Jan 11;12(1 Pt 1):387-95 [6546423] Proc Natl Acad Sci U S A. 1984 Nov;81(22):6948-52 [6438626] Proc Natl Acad Sci U S A. 1986 Apr;83(7):2162-6 [3083416] Anal Biochem. 1986 Aug 15;157(1):144-53 [3532863] Proc Natl Acad Sci U S A. 1987 Jun;84(11):3623-7 [3108876] J Biol Chem. 1987 Oct 25;262(30):14683-8 [3117789] Methods Enzymol. 1987;155:335-50 [3431465] Cell. 1989 Feb 10;56(3):467-77 [2536595] Proteins. 1990;7(1):1-15 [2184436] J Biol Chem. 1990 Aug 5;265(22):12995-9 [2115886] J Biol Chem. 1991 Mar 5;266(7):4538-44 [1900295] J Biol Chem. 1991 Mar 25;266(9):5363-6 [1706334] Science. 1991 May 24;252(5009):1162-4 [2031185] Science. 1991 Oct 25;254(5031):539-44 [1948029] Cell. 1992 Feb 21;68(4):699-708 [1739975] Biochemistry. 1992 Mar 24;31(11):2905-11 [1550816] Proc Natl Acad Sci U S A. 1992 Jul 1;89(13):6220-4 [1631113] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - A recombinant immunotoxin containing a disulfide-stabilized Fv fragment. AN - 75895989; 8356052 AB - B3(dsFv)-PE38KDEL is a recombinant immunotoxin composed of the Fv region of monoclonal antibody B3 connected to a truncated form of Pseudomonas exotoxin (PE38KDEL), in which the unstable Fv heterodimer (composed of heavy- and light-chain variable regions) is held together and stabilized by a disulfide bond [termed disulfide-stabilized Fv (dsFV)]. A computer modeled structure of the B3(Fv), made by mutating and energy minimizing the amino acid sequence and structure of McPC603, enabled us to identify positions in conserved framework regions that "hypothetically" could be used for disulfide stabilization without changing the structure or affecting antigen binding. This prediction was evaluated experimentally by constructing a disulfide-linked two-chain dsFv-immunotoxin that was produced in Escherichia coli. The activity and specificity of this immunotoxin was indistinguishable from its single-chain Fv (scFv) counterpart, indicating that, as in B3(scFv), the structure of the binding region is retained in B3(dsFv). Because we introduced the stabilizing disulfide bond in between two framework residues in a position that is conserved in most Fv molecules, this method of linkage between the heavy- and light-chain variable regions should be generally applicable to construct immunotoxins and dsFv molecules using other antibodies. Furthermore, the finding that B3(dsFv) was much more stable at 37 degrees C in human plasma than B3(scFv) indicates that dsFvs are possibly more versatile for therapeutic application than scFvs. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Brinkmann, U AU - Reiter, Y AU - Jung, S H AU - Lee, B AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/08/15/ PY - 1993 DA - 1993 Aug 15 SP - 7538 EP - 7542 VL - 90 IS - 16 SN - 0027-8424, 0027-8424 KW - Antibodies, Monoclonal KW - 0 KW - Bacterial Toxins KW - Disulfides KW - Exotoxins KW - Immunotoxins KW - Macromolecular Substances KW - Oligodeoxyribonucleotides KW - Recombinant Proteins KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - Drug Stability KW - Computer Simulation KW - Recombinant Proteins -- biosynthesis KW - Humans KW - Cloning, Molecular KW - Recombinant Proteins -- toxicity KW - Mutagenesis, Site-Directed KW - Base Sequence KW - Disulfides -- analysis KW - Tumor Cells, Cultured KW - Cell Survival -- drug effects KW - Restriction Mapping KW - Molecular Sequence Data KW - Recombinant Proteins -- chemistry KW - Pseudomonas aeruginosa KW - Cell Line KW - Antibodies, Monoclonal -- biosynthesis KW - Immunotoxins -- toxicity KW - Immunotoxins -- biosynthesis KW - Exotoxins -- chemistry KW - Antibodies, Monoclonal -- chemistry KW - Immunotoxins -- chemistry KW - Antibodies, Monoclonal -- toxicity KW - Exotoxins -- biosynthesis KW - Exotoxins -- toxicity KW - Protein Conformation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75895989?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=A+recombinant+immunotoxin+containing+a+disulfide-stabilized+Fv+fragment.&rft.au=Brinkmann%2C+U%3BReiter%2C+Y%3BJung%2C+S+H%3BLee%2C+B%3BPastan%2C+I&rft.aulast=Brinkmann&rft.aufirst=U&rft.date=1993-08-15&rft.volume=90&rft.issue=16&rft.spage=7538&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-23 N1 - Date created - 1993-09-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1985 Jan;82(2):488-92 [3881765] J Immunol. 1993 Apr 1;150(7):2774-82 [8454854] Cell. 1987 Jan 16;48(1):129-36 [3098436] Proc Natl Acad Sci U S A. 1988 Aug;85(16):5879-83 [3045807] Science. 1988 Oct 21;242(4877):423-6 [3140379] Nature. 1989 Jun 1;339(6223):394-7 [2498664] Proc Natl Acad Sci U S A. 1990 Feb;87(3):1066-70 [2105495] Biochemistry. 1990 Feb 13;29(6):1362-7 [2110478] Proc Natl Acad Sci U S A. 1991 Apr 15;88(8):3358-62 [2014255] Cancer Res. 1991 Jul 15;51(14):3781-7 [1648444] Proc Natl Acad Sci U S A. 1991 Oct 1;88(19):8616-20 [1924323] Biochemistry. 1991 Oct 22;30(42):10117-25 [1931943] Cancer Res. 1991 Dec 1;51(23 Pt 1):6363-71 [1933899] Proc Natl Acad Sci U S A. 1991 Nov 15;88(22):10134-7 [1719545] Science. 1991 Nov 22;254(5035):1173-7 [1683495] Cancer Res. 1992 Jun 15;52(12):3402-8 [1596900] Proc Natl Acad Sci U S A. 1992 Jul 1;89(13):5867-71 [1352878] Anal Biochem. 1992 Sep;205(2):263-70 [1332541] Biotechniques. 1993 Feb;14(2):256-65 [8431292] J Mol Biol. 1986 Aug 20;190(4):593-604 [3097327] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Characterization of two allelic variants of a human pregnancy-specific glycoprotein gene. AN - 75879194; 8349632 AB - The pregnancy-specific glycoproteins (PSGs) of the human placenta are a group of proteins that together with the carcinoembryonic antigens comprise a subfamily within the immunoglobulin superfamily. To study the control of PSG expression, we isolated and characterized PSG genes and identified cis-acting DNA elements in the 5'-flanking gene regions essential for PSG expression. Two overlapping PSG cosmid clones, which contain two allelic variants of a PSG gene (PSG12 and PSG12 psi), were isolated from an unamplified library made from a single individual. Cosmid 1 contains exons 1 (5'/L) and 2 (L/N) of the PSG12 gene located downstream of a previously identified PSG1-I gene. Cosmid 6 contains a portion of the PSG1-I gene lacking exons 1 and 2 upstream of a complete PSG12 psi transcription unit. Sequence comparison indicates that exons 5'/L and L/N in PSG12 and PSG12 psi are 99% identical, except that the L/N exon in the PSG12 psi gene contains a stop codon. Both PSG12 and PSG12 psi transcripts were detected in the human placenta, indicating that both genes are actively transcribed. However, the PSG12 psi gene may represent an allelic pseudogene variant of the PSG12 gene, because all identified PSGs contain a functional N-domain. Primer extension analysis showed that the PSG12 gene starts at a cluster of sites located at -106 to -104 base pairs with respect to the translation start site. In transient transfection assays using a chloramphenicol acetyltransferase reporter gene, we demonstrated that the -835 to -34 DNA region upstream of the translation start site of PSG12 or PSG12 psi contained both positive and negative elements that control PSG expression. Deletion analysis showed that nucleotides -172 to -34 in the PSG12 gene could function as a promoter. Gel retardation analysis showed that protein factors in human placental cell extract formed four complexes (I, II, IIa, and III) with the PSG12(-172/-34) DNA. Site-directed mutagenesis that prevents protein factor binding to the PSG12 promoter resulted in a marked reduction in transcription activation, locating the core enhancers at nucleotides -148 to -141 and -60 to -55. Mutagenesis studies also showed that the ACAGC repeats at nucleotides -84 to -68 in the PSG12 5'-flanking are essential for expression of the PSG12 gene in human placental cells. JF - The Journal of biological chemistry AU - Lei, K J AU - Wang, C AU - Chamberlin, M E AU - Liu, J L AU - Pan, C J AU - Chou, J Y AD - Human Genetics Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/08/15/ PY - 1993 DA - 1993 Aug 15 SP - 17528 EP - 17538 VL - 268 IS - 23 SN - 0021-9258, 0021-9258 KW - Glycoproteins KW - 0 KW - Pregnancy Proteins KW - Pregnancy-Specific beta 1-Glycoproteins KW - RNA Caps KW - pregnancy-specific beta-1-glycoprotein 12 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Pseudogenes KW - Sequence Homology, Nucleic Acid KW - Humans KW - Transcription, Genetic KW - Amino Acid Sequence KW - Alleles KW - Base Sequence KW - Promoter Regions, Genetic KW - Restriction Mapping KW - Molecular Sequence Data KW - Placenta -- metabolism KW - Genetic Variation KW - Glycoproteins -- biosynthesis KW - Pregnancy Proteins -- genetics KW - Glycoproteins -- genetics KW - Pregnancy Proteins -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75879194?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Characterization+of+two+allelic+variants+of+a+human+pregnancy-specific+glycoprotein+gene.&rft.au=Lei%2C+K+J%3BWang%2C+C%3BChamberlin%2C+M+E%3BLiu%2C+J+L%3BPan%2C+C+J%3BChou%2C+J+Y&rft.aulast=Lei&rft.aufirst=K&rft.date=1993-08-15&rft.volume=268&rft.issue=23&rft.spage=17528&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-15 N1 - Date created - 1993-09-15 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - L14723; GENBANK; L14724; L14725; L14726; L14727; L14728; M62717; L14729 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Orientation of cholera toxin bound to target cells. AN - 75876647; 8349592 AB - Cholera toxin (CT) consists of a pentameric B subunit that binds to specific cell surface receptors identified as ganglioside GM1 and an A subunit that activates adenylylcyclase. The A subunit consists of A1 and A2 peptides linked by a disulfide bond; A2 acts to connect A to B, whereas A1 is an ADP-ribosyltransferase that modifies the alpha subunit of the stimulatory G protein (Gs). How the toxin is oriented when it binds to the cell surface and the related issue of the mechanism by which A1 gains access to Gs alpha are not known. In the present study, we used subunit-specific antibodies and their corresponding Fab fragments to assess their affects on holotoxin binding to target cells and their immunoreactivity to cell-bound toxin. Our results suggest that CT binds with A1 facing away from the membrane. Our hypothesis is further supported by the ability to assemble active CT on the cell surface of cultured human intestinal and neurotumor cells by the sequential addition of purified B and A subunits. We also observed that when cells containing bound CT were incubated at 37 degrees C, both subunits rapidly became inaccessible to their respective antibodies. We propose that the holotoxin binds with its A subunit facing away from the membrane and must enter the cell in order for A1 to be released, gain access to Gs alpha, and activate adenylylcyclase. JF - The Journal of biological chemistry AU - Orlandi, P A AU - Fishman, P H AD - Membrane Biochemistry Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/08/15/ PY - 1993 DA - 1993 Aug 15 SP - 17038 EP - 17044 VL - 268 IS - 23 SN - 0021-9258, 0021-9258 KW - Immune Sera KW - 0 KW - Immunoglobulin Fab Fragments KW - Cholera Toxin KW - 9012-63-9 KW - Index Medicus KW - Tumor Cells, Cultured KW - Kinetics KW - Humans KW - Temperature KW - Immune Sera -- immunology KW - Immunoglobulin Fab Fragments -- immunology KW - Cell Membrane -- metabolism KW - Cell Line KW - Protein Conformation KW - Cholera Toxin -- immunology KW - Cholera Toxin -- chemistry KW - Cholera Toxin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75876647?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Orientation+of+cholera+toxin+bound+to+target+cells.&rft.au=Orlandi%2C+P+A%3BFishman%2C+P+H&rft.aulast=Orlandi&rft.aufirst=P&rft.date=1993-08-15&rft.volume=268&rft.issue=23&rft.spage=17038&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-15 N1 - Date created - 1993-09-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Identification of the major phosphorylation sites of the Raf-1 kinase. AN - 75874564; 8349614 AB - Treatment of cells with various growth factors and mitogens results in the rapid hyperphosphorylation and activation of the Raf-1 kinase. To determine if phosphorylation events affect Raf-1 activity, we have initiated experiments to identify the phosphorylation sites of Raf-1. In this report, we find that Ser43, Ser259, and Ser621 are the major sites of Raf-1 which are phosphorylated in mammalian cells and in Sf9 insect cells infected with a recombinant baculovirus encoding human Raf-1. Mutant Raf-1 proteins lacking kinase activity are also phosphorylated on these sites in vivo, indicating that these phosphorylation events are not a consequence of autophosphorylation. Furthermore, we find that Thr268 is the predominant Raf-1 residue phosphorylated in in vitro autokinase assays. In addition, we have examined the biochemical activity of baculovirus-expressed Raf-1 proteins containing mutations at these phosphorylation sites. In in vitro protein kinase assays Ser259 mutant proteins were 2-fold more active than wild-type Raf-1 and Ser621 mutant proteins were inactive as kinases. Analysis of the residues surrounding Ser259 and Ser621 indicates that RSXSXP may be a consensus sequence for the kinase responsible for phosphorylation of Raf-1 at these sites. Interestingly, these RSXSXP sequences are completely conserved throughout evolution in all Raf family members. JF - The Journal of biological chemistry AU - Morrison, D K AU - Heidecker, G AU - Rapp, U R AU - Copeland, T D AD - ABL-Basic Research Program, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland 21702. Y1 - 1993/08/15/ PY - 1993 DA - 1993 Aug 15 SP - 17309 EP - 17316 VL - 268 IS - 23 SN - 0021-9258, 0021-9258 KW - Proto-Oncogene Proteins KW - 0 KW - Serine KW - 452VLY9402 KW - Protein-Serine-Threonine Kinases KW - EC 2.7.11.1 KW - Proto-Oncogene Proteins c-raf KW - Index Medicus KW - 3T3 Cells KW - Animals KW - Humans KW - Amino Acid Sequence KW - Mice KW - Moths KW - Serine -- metabolism KW - Chromatography, High Pressure Liquid KW - Cloning, Molecular KW - Rats KW - Mutagenesis, Site-Directed KW - Baculoviridae KW - Phosphorylation KW - Electrophoresis, Gel, Two-Dimensional KW - Molecular Sequence Data KW - Cell Line KW - Protein-Serine-Threonine Kinases -- metabolism KW - Proto-Oncogene Proteins -- metabolism KW - Protein-Serine-Threonine Kinases -- genetics KW - Proto-Oncogene Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75874564?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Identification+of+the+major+phosphorylation+sites+of+the+Raf-1+kinase.&rft.au=Morrison%2C+D+K%3BHeidecker%2C+G%3BRapp%2C+U+R%3BCopeland%2C+T+D&rft.aulast=Morrison&rft.aufirst=D&rft.date=1993-08-15&rft.volume=268&rft.issue=23&rft.spage=17309&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-15 N1 - Date created - 1993-09-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - 'Cold SSCP': a simple, rapid and non-radioactive method for optimized single-strand conformation polymorphism analyses. AN - 75930426; 8367279 AB - A rapid (< 2.5 hrs) method for single-strand conformation polymorphism (SSCP) analysis of PCR products that allows the use of ethidium bromide staining is described. PCR products ranging in size from 117 to 256 bp were evaluated for point mutations and polymorphisms by 'cold SSCP' in commercially available pre-cast polyacrylamide mini-gels. Several electrophoretic parameters (running temperature, buffers, denaturants, DNA concentration, and gel polyacrylamide concentration) were found to influence the degree of strand separation and appeared to be PCR fragment specific. Use of the 'cold' SSCP technique and the mini-gel format allowed us to readily optimize the electrophoretic conditions for each PCR fragment. This greatly increased our ability to detect polymorphisms compared to conventional, radioisotope-labeled 'hot' SSCP, typically run under two standard temperature conditions. Excellent results have been obtained in resolving mutant PCR fragments from human p53 exons 5 through 8, human HLA-DQA, human K-ras exons 1 and 2, and rat K-ras exon 3. Polymorphisms could be detected when mutant DNA comprised as little as 3% of the total gene copies in a PCR mixture. Compared to standard 'hot' SSCP, this novel non-isotopic method has additional advantages of dramatically increased speed, precise temperature control, reproducibility, and easily and inexpensively obtainable reagents and equipment. This new method also lacks the safety and hazardous waste management concerns associated with radioactive methods. JF - Nucleic acids research AU - Hongyo, T AU - Buzard, G S AU - Calvert, R J AU - Weghorst, C M AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick, MD. Y1 - 1993/08/11/ PY - 1993 DA - 1993 Aug 11 SP - 3637 EP - 3642 VL - 21 IS - 16 SN - 0305-1048, 0305-1048 KW - Buffers KW - 0 KW - DNA, Single-Stranded KW - Index Medicus KW - Rats KW - Genes, ras KW - Animals KW - Nucleic Acid Denaturation KW - Genes, p53 KW - Electrophoresis, Polyacrylamide Gel KW - Humans KW - Temperature KW - Indicator Dilution Techniques KW - Nucleic Acid Conformation KW - Cell Line KW - Polymorphism, Genetic KW - DNA, Single-Stranded -- analysis KW - Polymerase Chain Reaction -- methods KW - DNA, Single-Stranded -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75930426?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+acids+research&rft.atitle=%27Cold+SSCP%27%3A+a+simple%2C+rapid+and+non-radioactive+method+for+optimized+single-strand+conformation+polymorphism+analyses.&rft.au=Hongyo%2C+T%3BBuzard%2C+G+S%3BCalvert%2C+R+J%3BWeghorst%2C+C+M&rft.aulast=Hongyo&rft.aufirst=T&rft.date=1993-08-11&rft.volume=21&rft.issue=16&rft.spage=3637&rft.isbn=&rft.btitle=&rft.title=Nucleic+acids+research&rft.issn=03051048&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-01 N1 - Date created - 1993-10-01 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Genomics. 1989 Nov;5(4):874-9 [2687159] Hum Mutat. 1992;1(2):91-6 [1301206] Nucleic Acids Res. 1991 May 11;19(9):2500 [2041788] Nucleic Acids Res. 1991 Jun 11;19(11):3154 [2057373] Nature. 1991 Jul 4;352(6330):77-9 [2062380] Biochem Biophys Res Commun. 1991 Oct 15;180(1):380-5 [1656975] Nucleic Acids Res. 1992 Jan 11;20(1):145 [1738597] Nature. 1992 Feb 6;355(6360):548-51 [1346925] Nucleic Acids Res. 1992 Feb 25;20(4):871-8 [1371869] Trends Genet. 1992 Feb;8(2):49 [1373540] Biochem Biophys Res Commun. 1992 Apr 15;184(1):73-9 [1373618] Mol Cell Probes. 1992 Oct;6(5):357-9 [1282203] Hum Genet. 1992 Nov;90(3):303-4 [1283151] PCR Methods Appl. 1992 Aug;2(1):10-3 [1490170] Lab Invest. 1993 Mar;68(3):361-6 [8450652] Cell. 1993 Mar 26;72(6):971-83 [8458085] Hum Genet. 1993 Mar;91(2):151-6 [8385067] Hum Genet. 1993 Mar;91(2):163-8 [8462975] Nucleic Acids Res. 1991 Jan 25;19(2):405-6 [2014179] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Cloning, sequencing, and mutation of thiol-specific antioxidant gene of Saccharomyces cerevisiae. AN - 75892723; 8344960 AB - We have previously shown that the yeast Saccharomyces cerevisiae contains an antioxidant enzyme that can provide protection against a thiol-containing oxidation system but not against an oxidation system without thiol. This 25-kDa enzyme was thus named thiol-specific antioxidant (TSA). We have now isolated and sequenced a yeast genomic DNA fragment that encodes TSA. Comparison of the predicted amino acid sequence of TSA with those of conventional antioxidant enzymes, including catalases, peroxidases, and superoxide dismutases, revealed no sequence homology. The 195-amino acid TSA sequence contains 2 cysteine residues. Southern blot analysis of petite yeast DNA, studies with protein synthesis inhibitors, and protein immunoblot analyses of cytosolic and mitochondrial proteins suggest that TSA is a cytosolic protein encoded by nuclear DNA (chromosome XIII). The yeast TSA gene was selectively disrupted by homologous recombination. The haploid tsa mutant was viable under air, suggesting that TSA is not essential for cell viability. The growth rates of the tsa mutant and wild-type strains were identical under anaerobic conditions. However, under aerobic conditions, especially in the presence of methyl viologen or a peroxide (t-butyl hydroperoxide or H2O2), the growth rate of the mutant was significantly less than that of wild-type cells. This result suggests that TSA is a physiologically important antioxidant. JF - The Journal of biological chemistry AU - Chae, H Z AU - Kim, I H AU - Kim, K AU - Rhee, S G AD - Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/08/05/ PY - 1993 DA - 1993 Aug 05 SP - 16815 EP - 16821 VL - 268 IS - 22 SN - 0021-9258, 0021-9258 KW - TSA KW - Antioxidants KW - 0 KW - DNA, Fungal KW - Fungal Proteins KW - Chloramphenicol KW - 66974FR9Q1 KW - Peroxidases KW - EC 1.11.1.- KW - Peroxiredoxins KW - EC 1.11.1.15 KW - Index Medicus KW - Immunoblotting KW - Base Sequence KW - Blotting, Northern KW - Blotting, Southern KW - Kinetics KW - Restriction Mapping KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Mutagenesis KW - Cloning, Molecular KW - Saccharomyces cerevisiae -- genetics KW - Genes, Fungal KW - Saccharomyces cerevisiae -- growth & development KW - Saccharomyces cerevisiae -- enzymology KW - Fungal Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75892723?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Cloning%2C+sequencing%2C+and+mutation+of+thiol-specific+antioxidant+gene+of+Saccharomyces+cerevisiae.&rft.au=Chae%2C+H+Z%3BKim%2C+I+H%3BKim%2C+K%3BRhee%2C+S+G&rft.aulast=Chae&rft.aufirst=H&rft.date=1993-08-05&rft.volume=268&rft.issue=22&rft.spage=16815&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-07 N1 - Date created - 1993-09-07 N1 - Date revised - 2017-01-13 N1 - Gene symbol - TSA N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Specific glycosylation site mutations of the insulin receptor alpha subunit impair intracellular transport. AN - 75907069; 8347587 AB - The insulin receptor is a transmembrane protein found on multiple cell types. This receptor is synthesized as a 190-kDa proreceptor which is cleaved to produce mature alpha and beta subunits. The proreceptor contains 18 potential sites for N-linked glycosylation: 14 on the alpha subunit and 4 on the beta subunit. The codons for asparagine in the first four sites at the amino terminus of the alpha subunit were mutated to code for glutamine. This mutant receptor cDNA was stably transfected into NIH 3T3 cells. The insulin receptor produced in these cells remained in the proreceptor form; no mature alpha and beta subunits were produced. The proreceptor was slightly smaller on SDS-PAGE gels than the wild-type proreceptor and contained four less oligosaccharide chains by tryptic peptide mapping. The carbohydrate chains on the mutant proreceptor remained endoglycosidase H sensitive. However, in the presence of brefeldin A, these oligosaccharide chains could be processed to endoglycosidase H resistant chains. By immunofluorescence, the mutant proreceptor was shown to be localized to the endoplasmic reticulum. No insulin receptors could be found on the cell-surface either with cell surface labeling with biotin or with 125I-insulin binding. Thus, glycosylation of the first four N-linked glycosylation sites of the insulin receptor is necessary for the proper processing and intracellular transport of the receptor. This is in contrast to glycosylation at the four sites on the beta subunit which appear not to be important for processing but necessary for signal transduction. Therefore, N-linked glycosylation of the insulin receptor at specific sites has multiple distinctive roles. JF - Biochemistry AU - Collier, E AU - Carpentier, J L AU - Beitz, L AU - Carol, H AU - Taylor, S I AU - Gorden, P AD - Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/08/03/ PY - 1993 DA - 1993 Aug 03 SP - 7818 EP - 7823 VL - 32 IS - 30 SN - 0006-2960, 0006-2960 KW - Insulin KW - 0 KW - Glutamine KW - 0RH81L854J KW - Asparagine KW - 7006-34-0 KW - DNA KW - 9007-49-2 KW - Receptor, Insulin KW - EC 2.7.10.1 KW - Index Medicus KW - 3T3 Cells KW - Animals KW - Peptide Mapping KW - Electrophoresis, Polyacrylamide Gel KW - Glutamine -- metabolism KW - Humans KW - Asparagine -- metabolism KW - Biological Transport KW - Insulin -- metabolism KW - Mice KW - Glycosylation KW - Mutagenesis, Site-Directed KW - Transfection KW - Fluorescent Antibody Technique KW - Receptor, Insulin -- genetics KW - Receptor, Insulin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75907069?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemistry&rft.atitle=Specific+glycosylation+site+mutations+of+the+insulin+receptor+alpha+subunit+impair+intracellular+transport.&rft.au=Collier%2C+E%3BCarpentier%2C+J+L%3BBeitz%2C+L%3BCarol%2C+H%3BTaylor%2C+S+I%3BGorden%2C+P&rft.aulast=Collier&rft.aufirst=E&rft.date=1993-08-03&rft.volume=32&rft.issue=30&rft.spage=7818&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-10 N1 - Date created - 1993-09-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Nephrotoxicity and hydration management for cisplatin, carboplatin, and ormaplatin. AN - 85256329; pmid-8375728 AB - Renal toxicity is a prominent component of the toxicity profile of platinum-based chemotherapy. Kidney damage, once dose limiting for cisplatin, occurs in some patients who receive carboplatin and may occur with the third-generation platinum analog ormaplatin. Herein, we review what is known about the pathophysiology of therapy-induced renal toxicity for each of these agents and what is known about appropriate maneuvers to circumvent this toxicity. For cisplatin, hydration is always indicated and mannitol may be useful in selected settings. Furosemide is probably not generally useful. For carboplatin, hydration is important for patients with impaired renal function and for patients receiving high doses of drug (> or = 800 mg/m2). For ormplatin, renal toxicity appears not be prominent when hydration is administered in a fashion similar to cisplatin hydration. Detailed suggestions regarding the protection of kidney function when using these compounds are presented. JF - Gynecologic Oncology AU - Cornelison, T L AU - Reed, E AD - Medicine Branch, National Cancer Institute, Bethesda, Maryland 20892. PY - 1993 SP - 147 EP - 158 VL - 50 IS - 2 SN - 0090-8258, 0090-8258 KW - Cisplatin KW - Antineoplastic Agents KW - Mannitol KW - Human KW - Animal KW - Kidney KW - Organoplatinum Compounds KW - Saline Solution, Hypertonic KW - Carboplatin KW - Furosemide KW - Fluid Therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85256329?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gynecologic+Oncology&rft.atitle=Nephrotoxicity+and+hydration+management+for+cisplatin%2C+carboplatin%2C+and+ormaplatin.&rft.au=Cornelison%2C+T+L%3BReed%2C+E&rft.aulast=Cornelison&rft.aufirst=T&rft.date=1993-08-01&rft.volume=50&rft.issue=2&rft.spage=147&rft.isbn=&rft.btitle=&rft.title=Gynecologic+Oncology&rft.issn=00908258&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Memory in patients with cerebellar degeneration. AN - 85162918; pmid-8351008 AB - Eleven patients with relatively selective cerebellar degeneration and 11 normal control subjects underwent a comprehensive neurologic and neuropsychological examination. The neuropsychological tests assessed general intellectual ability, different aspects of memory (effortful, automatic, and implicit memory processes), speed of information processing, and verbal fluency (using both category and letter fluency tasks). The results indicated that cerebellar patients were significantly impaired only on tasks requiring the use of executive functions, such as the initiation/perseveration subtest of the Mattis Dementia Rating Scale or the fluency tests, and on memory measures requiring greater processing effort. They performed normally on automatic and implicit measures of memory. Performance on the effortful memory and executive measures was not associated with neurologic variables or mood state. After controlling for the initiation/perseveration deficit, the effortful memory scores of the cerebellar patients were no longer different from those of controls. The present study suggests that memory in patients with relatively pure cerebellar dysfunction is only partially compromised and that the impairment is secondary to a deficit in executive functions. JF - Neurology AU - Appollonio, I M AU - Grafman, J AU - Schwartz, V AU - Massaquoi, S AU - Hallett, M AD - Cognitive Neuroscience Section, NINDS, NIH, Bethesda, MD 20892. PY - 1993 SP - 1536 EP - 1544 VL - 43 IS - 8 SN - 0028-3878, 0028-3878 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85162918?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurology&rft.atitle=Memory+in+patients+with+cerebellar+degeneration.&rft.au=Appollonio%2C+I+M%3BGrafman%2C+J%3BSchwartz%2C+V%3BMassaquoi%2C+S%3BHallett%2C+M&rft.aulast=Appollonio&rft.aufirst=I&rft.date=1993-08-01&rft.volume=43&rft.issue=8&rft.spage=1536&rft.isbn=&rft.btitle=&rft.title=Neurology&rft.issn=00283878&rft_id=info:doi/ LA - English DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Conformationally constrained analogues of diacylglycerol (DAG)--II. Differential interaction of delta-lactones and gamma-lactones with protein kinase C (PK-C). AN - 76306851; 8081841 AB - Starting with L- or D-tri-O-acetylglucal, the corresponding L- and D-isomers of 4-O-tetradecanoyl-2,3-dideoxyglucono-1,5-lactone (2a and 2b) were synthesized as rigid diacylglycerol (DAG) analogues. Consistent with results obtained previously with the equivalent L- and D-1,4-lactones (1a and 1b), the L-isomer (2a) was more potent in activating protein kinase C (PK-C) and inhibiting the binding of [3H]phorbol-12,13-dibutyrate to the enzyme's regulatory domain. In these experiments the difference in potency observed between the optical antipodes of the gluconolactones (2a and 2b) was greatly increased relative to the corresponding ribonolactones (1a and 1b). These results indicate that PK-C is more able to discriminate between optical antipodes, in favor of the L-isomer, as the lactone ring increases from five to six. JF - Bioorganic & medicinal chemistry AU - Lee, J AU - Marquez, V E AU - Blumberg, P M AU - Krausz, K W AU - Kazanietz, M G AD - Laboratory of Medicinal Chemistry, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 119 EP - 123 VL - 1 IS - 2 SN - 0968-0896, 0968-0896 KW - Diglycerides KW - 0 KW - Myristates KW - Pyrones KW - 4-O-tetradecanoyl-2,3-dideoxyglucono-1,5-lactone KW - 153764-21-7 KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Index Medicus KW - Stereoisomerism KW - Phosphorylation KW - Enzyme Activation KW - Kinetics KW - Chromatography, Thin Layer KW - Magnetic Resonance Spectroscopy KW - Binding Sites KW - Pyrones -- pharmacology KW - Protein Kinase C -- metabolism KW - Diglycerides -- chemistry KW - Myristates -- chemistry KW - Diglycerides -- pharmacology KW - Myristates -- metabolism KW - Phorbol 12,13-Dibutyrate -- metabolism KW - Myristates -- pharmacology KW - Pyrones -- chemistry KW - Pyrones -- metabolism KW - Diglycerides -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76306851?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bioorganic+%26+medicinal+chemistry&rft.atitle=Conformationally+constrained+analogues+of+diacylglycerol+%28DAG%29--II.+Differential+interaction+of+delta-lactones+and+gamma-lactones+with+protein+kinase+C+%28PK-C%29.&rft.au=Lee%2C+J%3BMarquez%2C+V+E%3BBlumberg%2C+P+M%3BKrausz%2C+K+W%3BKazanietz%2C+M+G&rft.aulast=Lee&rft.aufirst=J&rft.date=1993-08-01&rft.volume=1&rft.issue=2&rft.spage=119&rft.isbn=&rft.btitle=&rft.title=Bioorganic+%26+medicinal+chemistry&rft.issn=09680896&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-10-13 N1 - Date created - 1994-10-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Seizures associated with antidepressants: a review. AN - 76115870; 8253696 AB - Seizures are uncommon, but serious, adverse effects of antidepressant drugs. A better understanding of drug-related seizure risk, its predictors, and its neurophysiologic basis might help clinicians avoid this adverse event. A better understanding of the factors involved in the determination of seizure risk would be helpful for interpretation of seizure rates reported. The authors review case reports, series of cases, and information from clinical trials of antidepressants to determine antidepressant-related seizure risk. Predisposing factors are identified. Effects of dose, blood levels, and duration of treatment on seizure risk are examined. Electrophysiologic and in vitro models of drug-related seizure induction are discussed. A significant proportion of drug-related seizures occurs in individuals with an identifiable predisposition, such as previous seizures, sedative or alcohol withdrawal, and multiple concomitant medications. Seizure risk for most antidepressants increases with dose (or blood level), and comparisons between drugs should consider seizure rates at the effective dose (or blood level) for each drug. For imipramine, the most frequently studied tricyclic, the literature indicates a seizure rate between 0.3% and 0.6% at effective doses. In unselected patients and at higher doses, these rates may be higher. Fluoxetine, sertraline, fluvoxamine, trazodone, nomifensine, and the monoamine oxidase inhibitors have a lower seizure risk. Estimates for recently marketed antidepressants with intermediate seizure risk are complicated by the fact that effective doses and blood levels are not well established. Assessment of seizure risk in individuals involves consideration of predisposing factors, the antidepressant selected, and the bioavailability of the drug. Future studies of seizure risk would benefit from the use of specified criteria for determination of probable seizure events, a priori definition of predisposing exclusions, samples sufficiently large to provide adequate power, blood level monitoring, and inclusion of duration of drug treatment in the calculation of risk. JF - The Journal of clinical psychiatry AU - Rosenstein, D L AU - Nelson, J C AU - Jacobs, S C AD - National Institute of Mental Health, Bethesda, Md. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 289 EP - 299 VL - 54 IS - 8 SN - 0160-6689, 0160-6689 KW - Antidepressive Agents KW - 0 KW - Imipramine KW - OGG85SX4E4 KW - Index Medicus KW - Causality KW - Imipramine -- adverse effects KW - Epilepsy -- chemically induced KW - Imipramine -- blood KW - Imipramine -- pharmacokinetics KW - Dose-Response Relationship, Drug KW - Risk Factors KW - Humans KW - Incidence KW - Depressive Disorder -- drug therapy KW - Epilepsy -- epidemiology KW - Biological Availability KW - Seizures -- chemically induced KW - Antidepressive Agents -- pharmacokinetics KW - Antidepressive Agents -- blood KW - Seizures -- epidemiology KW - Antidepressive Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76115870?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+clinical+psychiatry&rft.atitle=Seizures+associated+with+antidepressants%3A+a+review.&rft.au=Rosenstein%2C+D+L%3BNelson%2C+J+C%3BJacobs%2C+S+C&rft.aulast=Rosenstein&rft.aufirst=D&rft.date=1993-08-01&rft.volume=54&rft.issue=8&rft.spage=289&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+clinical+psychiatry&rft.issn=01606689&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-01-07 N1 - Date created - 1994-01-07 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: J Clin Psychiatry. 1994 Jun;55(6):267 [8071288] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Molecular basis of muscarinic acetylcholine receptor function. AN - 76085232; 8249149 AB - Muscarinic acetylcholine receptors play important roles in numerous physiological functions including higher cognitive processes such as memory and learning. Consistent with the well-documented pharmacological heterogeneity of muscarinic receptors, molecular cloning studies have revealed the existence of five distinct muscarinic receptor proteins (M1-M5). Structure-function relationship studies of the cloned receptors have been greatly aided by the high degree of structural homology that muscarinic receptors share with other G protein-coupled receptors. In this review, Jürgen Wess discusses recent mutagenesis studies that have considerably advanced our knowledge of the molecular details underlying muscarinic receptor function. JF - Trends in pharmacological sciences AU - Wess, J AD - National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Laboratory of Bio-organic Chemistry, Bethesda, MD 20892. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 308 EP - 313 VL - 14 IS - 8 SN - 0165-6147, 0165-6147 KW - Receptors, Muscarinic KW - 0 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Index Medicus KW - Animals KW - GTP-Binding Proteins -- metabolism KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Protein Binding KW - Structure-Activity Relationship KW - Protein Conformation KW - Receptors, Muscarinic -- drug effects KW - Receptors, Muscarinic -- chemistry KW - Receptors, Muscarinic -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76085232?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Trends+in+pharmacological+sciences&rft.atitle=Molecular+basis+of+muscarinic+acetylcholine+receptor+function.&rft.au=Wess%2C+J&rft.aulast=Wess&rft.aufirst=J&rft.date=1993-08-01&rft.volume=14&rft.issue=8&rft.spage=308&rft.isbn=&rft.btitle=&rft.title=Trends+in+pharmacological+sciences&rft.issn=01656147&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-30 N1 - Date created - 1993-12-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Billion-fold difference in the toxic potencies of two excitatory plant amino acids, L-BOAA and L-BMAA: biochemical and morphological studies using mouse brain slices. AN - 76067496; 7901822 AB - Plant amino acids beta-N-oxalylamino-L-alanine (L-BOAA, present in Lathyrus sativus) and beta-N-methylamino-L-alanine (L-BMAA, present in Cycas circinalis) have been implicated in the pathogenesis of human neurological disorders lathyrism and amyotrophic lateral sclerosis-Parkinson's dementia complex of Guam (ALS-PD), respectively. In view of the conflicting reports that have emerged on the role of L-BMAA in ALS-PD, we reinvestigated the comparative toxicity of L-BMAA and L-BOAA. We report here the potent toxicity of L-BOAA as examined in an in vitro model consisting of sagittal slices of mouse brain. Incubation of sagittal slices of mouse brain with L-BOAA (1 pM) resulted in significant leakage of lactate dehydrogenase (LDH) and potassium from the slices into the medium. Under similar conditions, L-BMAA-induced LDH leakage from the slices into the medium was observed only at very high concentration of the toxin, namely 1 mM. N-Methyl-D-aspartate (NMDA) receptor antagonists ameliorated the toxic effects of L-BMAA, while non-NMDA receptor antagonists (quinoxalinediones) protected against the toxicity of L-BOAA. Incubation of slices with L-BOAA for 1 h resulted in extensive vacuolation and degeneration of neurons in the thalamus and brain stem, and to a lesser extent in the hippocampus and cerebellar nuclei. The large sized neurons appeared to be affected to a greater extent than the smaller ones. The neurons in other areas of the brain also revealed variable degree of degeneration with swelling of axons and dendrites.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Neuroscience research AU - Pai, K S AU - Shankar, S K AU - Ravindranath, V AD - Department of Neurochemistry, National Institute of Mental Health and Neuro Sciences, Bangalore, India. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 241 EP - 248 VL - 17 IS - 3 SN - 0168-0102, 0168-0102 KW - Amino Acids, Diamino KW - 0 KW - Excitatory Amino Acid Antagonists KW - Neurotoxins KW - Quinoxalines KW - beta-N-methylamino-L-alanine KW - 108SA6URTV KW - 2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline KW - 118876-58-7 KW - beta-Alanine KW - 11P2JDE17B KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - 6-Cyano-7-nitroquinoxaline-2,3-dione KW - 6OTE87SCCW KW - oxalyldiaminopropionic acid KW - 7554-90-7 KW - L-Lactate Dehydrogenase KW - EC 1.1.1.27 KW - Potassium KW - RWP5GA015D KW - Index Medicus KW - Animals KW - Paraffin Embedding KW - In Vitro Techniques KW - Mice KW - Histocytochemistry KW - Quinoxalines -- pharmacology KW - Potassium -- metabolism KW - L-Lactate Dehydrogenase -- metabolism KW - Dizocilpine Maleate -- pharmacology KW - Plants -- chemistry KW - Brain -- enzymology KW - beta-Alanine -- analogs & derivatives KW - Brain Chemistry -- drug effects KW - Brain -- drug effects KW - Brain -- anatomy & histology KW - Amino Acids, Diamino -- toxicity KW - beta-Alanine -- toxicity KW - Neurotoxins -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76067496?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroscience+research&rft.atitle=Billion-fold+difference+in+the+toxic+potencies+of+two+excitatory+plant+amino+acids%2C+L-BOAA+and+L-BMAA%3A+biochemical+and+morphological+studies+using+mouse+brain+slices.&rft.au=Pai%2C+K+S%3BShankar%2C+S+K%3BRavindranath%2C+V&rft.aulast=Pai&rft.aufirst=K&rft.date=1993-08-01&rft.volume=17&rft.issue=3&rft.spage=241&rft.isbn=&rft.btitle=&rft.title=Neuroscience+research&rft.issn=01680102&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-13 N1 - Date created - 1993-12-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Inducible accessory function of a macrophage cell line. AN - 76053008; 7901265 AB - Costimulatory molecules in addition to occupancy of the T-cell antigen receptor, are required to induce T-cell proliferation. Previous work suggested that membrane molecules responsible for costimulatory activity were not constitutively expressed on the antigen presenting cell (APC) surface. In the present study, we have identified a cloned macrophage cell line (FLJ2) with inducible APC function. The unactivated FLJ2 line could not induce T-cell proliferation. FLJ2 could present alloantigen, and stimulate proliferation of either a T-cell clone or normal resting T cells following activation with IFN gamma or unexpectedly with lipopolysaccharide (LPS)-Activated FLJ2 cells could be fixed and APC function was preserved. The relevant inducible molecules required for APC function appeared distinct from Ia and IL1. The expression of ICAM-1 and LFA-1 was increased during activation and anti-LFA-1 antibody blocked APC function. This suggests that one important feature of the activation process may be improvement of cellular adhesion. JF - Immunopharmacology and immunotoxicology AU - Aiello, F B AU - Gusella, L AU - Longo, D L AU - Birchenall-Roberts, M AU - Takacs, L AU - Takei, F AU - Ruscetti, F AU - Musiani, P AU - Durum, S K AD - Biological Carcinogenesis and Development Program, Program Resources Inc./DynCorp, NCI-Frederick Cancer Research and Development Center, MD. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 327 EP - 353 VL - 15 IS - 4 SN - 0892-3973, 0892-3973 KW - Cell Adhesion Molecules KW - 0 KW - Histocompatibility Antigens Class II KW - Interleukin-1 KW - Lipopolysaccharides KW - Lymphocyte Function-Associated Antigen-1 KW - Recombinant Proteins KW - Intercellular Adhesion Molecule-1 KW - 126547-89-5 KW - Interferon-gamma KW - 82115-62-6 KW - Index Medicus KW - Animals KW - Interleukin-1 -- biosynthesis KW - Lymphocyte Function-Associated Antigen-1 -- metabolism KW - Lipopolysaccharides -- pharmacology KW - Interferon-gamma -- pharmacology KW - Mice KW - Mice, Inbred BALB C KW - Lymphocyte Activation KW - Mice, Inbred C57BL KW - Mice, Inbred C3H KW - Cell Adhesion Molecules -- metabolism KW - T-Lymphocytes -- immunology KW - Cell Line KW - Female KW - Macrophages -- immunology KW - Antigen-Presenting Cells -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76053008?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Immunopharmacology+and+immunotoxicology&rft.atitle=Inducible+accessory+function+of+a+macrophage+cell+line.&rft.au=Aiello%2C+F+B%3BGusella%2C+L%3BLongo%2C+D+L%3BBirchenall-Roberts%2C+M%3BTakacs%2C+L%3BTakei%2C+F%3BRuscetti%2C+F%3BMusiani%2C+P%3BDurum%2C+S+K&rft.aulast=Aiello&rft.aufirst=F&rft.date=1993-08-01&rft.volume=15&rft.issue=4&rft.spage=327&rft.isbn=&rft.btitle=&rft.title=Immunopharmacology+and+immunotoxicology&rft.issn=08923973&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-03 N1 - Date created - 1993-12-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Substitutions of different regions of the third cytoplasmic loop of the thyrotropin (TSH) receptor have selective effects on constitutive, TSH-, and TSH receptor autoantibody-stimulated phosphoinositide and 3',5'-cyclic adenosine monophosphate signal generation. AN - 76050454; 7901757 AB - TSH and immunoglobulin G (IgG) preparations from patients with Graves' disease increase inositol phosphate as well as cAMP formation in Cos-7 cells transfected with rat TSH receptor (TSHR) cDNA. In a previous report, we mutated alanine 623 of the third cytoplasmic loop (residues 605-625) of the TSHR and showed it was critical for TSH and Graves' IgG initiation of phosphatidylinositol bisphosphate (PIP2) but not cAMP signaling. In this report, we substituted residues in the third loop of the TSHR with sequences from the N- and C-termini of the third loop of the alpha 1- and beta 2-adrenergic receptors (ARs), which computer analysis has identified as homologous to those in the TSHR. Alanine 623 is conserved in most ARs as well as in glycoprotein hormone receptors; there is, therefore, no change in alanine 623. After transfection of the mutant TSHR cDNAs into Cos-7 cells, we show that the mutant proteins are normally synthesized, processed, and incorporated into the membrane bilayer by Western blotting with a specific receptor antibody. We also show that the dissociation constant for TSH binding in all mutants is the same or lower than wild type TSHR. We then evaluated the ability of TSH or Graves' IgG to increase PIP2 and cAMP signals in each transfectant. Mutants A622 and B621 replace, respectively, residues 622-625 and 621-625 of the TSHR with alpha 1- and beta 2-AR residues from the C-terminus of the third cytoplasmic loop; mutants A607 and B605 replace, respectively, TSHR residues 607-609 and 605-609 with N-terminus residues from alpha 1- and beta 2-AR. All four mutants, like the alanine 623 mutant, result in transfected cells which lose TSH and Graves' IgG initiation of PIP2 but not cAMP signalling. Like the alanine 623 mutation to glutamic acid, the A607, B605, A622, and B621 mutants also result in decreased basal cAMP, but not inositol phosphate levels, relative to wild type receptor. In contrast to these results, mutants A610, B610, A617, and B617, which replace residues 610-613 or 617-620 of the TSHR with corresponding residues of the alpha 1- and beta 2-AR, retain TSH and Graves' IgG responsiveness in both inositol phosphate and cAMP assays. Mutation of residues 610-613, in fact, potentiates TSH-increased inositol phosphate production, despite having no effect on TSH-increased cAMP production.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Molecular endocrinology (Baltimore, Md.) AU - Kosugi, S AU - Okajima, F AU - Ban, T AU - Hidaka, A AU - Shenker, A AU - Kohn, L D AD - Cell Regulation Section, National Institute of Diabetes and Digestive and Kidney Diseases Bethesda, Maryland 20892. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 1009 EP - 1020 VL - 7 IS - 8 SN - 0888-8809, 0888-8809 KW - Autoantibodies KW - 0 KW - Immunoglobulin G KW - Immunoglobulins, Thyroid-Stimulating KW - Phosphatidylinositol 4,5-Diphosphate KW - Phosphatidylinositol Phosphates KW - Receptors, Adrenergic KW - Receptors, Thyrotropin KW - Recombinant Fusion Proteins KW - Thyrotropin KW - 9002-71-5 KW - Cyclic AMP KW - E0399OZS9N KW - Index Medicus KW - Animals KW - Models, Molecular KW - Humans KW - Immunoglobulin G -- pharmacology KW - Receptors, Adrenergic -- genetics KW - Amino Acid Sequence KW - Fibroblasts KW - Recombinant Fusion Proteins -- metabolism KW - Mutagenesis, Site-Directed KW - Transfection KW - Cercopithecus aethiops KW - Molecular Sequence Data KW - Graves Disease -- immunology KW - Cell Line KW - Receptors, Thyrotropin -- chemistry KW - Thyrotropin -- pharmacology KW - Receptors, Thyrotropin -- physiology KW - Receptors, Thyrotropin -- immunology KW - Autoantibodies -- pharmacology KW - Phosphatidylinositol Phosphates -- physiology KW - Cyclic AMP -- physiology KW - Protein Structure, Tertiary KW - Signal Transduction KW - Receptors, Thyrotropin -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76050454?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.atitle=Substitutions+of+different+regions+of+the+third+cytoplasmic+loop+of+the+thyrotropin+%28TSH%29+receptor+have+selective+effects+on+constitutive%2C+TSH-%2C+and+TSH+receptor+autoantibody-stimulated+phosphoinositide+and+3%27%2C5%27-cyclic+adenosine+monophosphate+signal+generation.&rft.au=Kosugi%2C+S%3BOkajima%2C+F%3BBan%2C+T%3BHidaka%2C+A%3BShenker%2C+A%3BKohn%2C+L+D&rft.aulast=Kosugi&rft.aufirst=S&rft.date=1993-08-01&rft.volume=7&rft.issue=8&rft.spage=1009&rft.isbn=&rft.btitle=&rft.title=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.issn=08888809&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-16 N1 - Date created - 1993-12-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Large granular lymphocytosis in a patient infected with HTLV-II. AN - 76020675; 8217341 AB - HTLV-II has been associated with a variety of lymphoproliferative disorders, including atypical hairy cell leukemia, chronic T cell leukemia, T prolymphocytic leukemia, and large granular lymphocytic leukemia. However, a direct or indirect role for HTLV-II in these disorders is not yet firmly established. We studied a patient diagnosed as having leukemia of the large granular lymphocyte (LGL) type who was HTLV-II seropositive, to determine if the expanded cell population was infected. Two populations of CD3-CD16+ LGL were identified; one was CD8+, the other CD8-. Populations of cells with these surface markers as well as normal CD3+CD4+ and CD3+CD8+ cells were separated by flow cytometric methods, DNA extracted, and gene regions of HTLV-II pol and tax amplified, using the polymerase chain reaction, and probed after Southern blotting. HTLV-II was detected in the CD3+CD8+ population, and not in the CD3-CD16+ large granular lymphocyte population. This finding indicates that the role of HTLV-II, if any, in LGL proliferation is indirect. JF - AIDS research and human retroviruses AU - Martin, M P AU - Biggar, R J AU - Hamlin-Green, G AU - Staal, S AU - Mann, D AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 715 EP - 719 VL - 9 IS - 8 SN - 0889-2229, 0889-2229 KW - pol KW - tax KW - Antigens, CD KW - 0 KW - DNA, Viral KW - Index Medicus KW - AIDS/HIV KW - Genes, pX KW - Antigens, CD -- analysis KW - Human T-lymphotropic virus 2 -- genetics KW - DNA, Viral -- analysis KW - Humans KW - Middle Aged KW - Flow Cytometry KW - Immunophenotyping KW - Male KW - Genes, pol KW - Leukemia, Lymphoid -- complications KW - HTLV-II Infections -- complications KW - Lymphocytosis -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76020675?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS+research+and+human+retroviruses&rft.atitle=Large+granular+lymphocytosis+in+a+patient+infected+with+HTLV-II.&rft.au=Martin%2C+M+P%3BBiggar%2C+R+J%3BHamlin-Green%2C+G%3BStaal%2C+S%3BMann%2C+D&rft.aulast=Martin&rft.aufirst=M&rft.date=1993-08-01&rft.volume=9&rft.issue=8&rft.spage=715&rft.isbn=&rft.btitle=&rft.title=AIDS+research+and+human+retroviruses&rft.issn=08892229&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-08 N1 - Date created - 1993-12-08 N1 - Date revised - 2017-01-13 N1 - Gene symbol - pol; tax N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Detection of DNA damage-recognition proteins using the band-shift assay and southwestern hybridization. AN - 76001949; 8404810 AB - We describe electrophoresis and biochemical conditions that allow detection of damaged DNA-binding proteins in cell extracts. In addition, we present an overview of the damage-recognition DNA-binding proteins from eukaryotic cells and discuss their hypothetical role in DNA repair. JF - Electrophoresis AU - Protić, M AU - Levine, A S AD - Section on DNA Replication, Repair and Mutagenesis, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 682 EP - 692 VL - 14 IS - 8 SN - 0173-0835, 0173-0835 KW - DNA-Binding Proteins KW - 0 KW - Transcription Factors KW - Index Medicus KW - Base Sequence KW - Nucleic Acid Hybridization -- methods KW - Molecular Sequence Data KW - Transcription Factors -- analysis KW - Binding Sites KW - DNA-Binding Proteins -- analysis KW - Blotting, Western KW - DNA Repair KW - DNA Damage KW - Blotting, Southern UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76001949?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Electrophoresis&rft.atitle=Detection+of+DNA+damage-recognition+proteins+using+the+band-shift+assay+and+southwestern+hybridization.&rft.au=Proti%C4%87%2C+M%3BLevine%2C+A+S&rft.aulast=Proti%C4%87&rft.aufirst=M&rft.date=1993-08-01&rft.volume=14&rft.issue=8&rft.spage=682&rft.isbn=&rft.btitle=&rft.title=Electrophoresis&rft.issn=01730835&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-19 N1 - Date created - 1993-11-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Comparative carcinogenicity of 5,5-diphenylhydantoin with or without perinatal exposure in rats and mice. AN - 76000669; 8405780 AB - Chronic toxicity and carcinogenicity studies of 5,5-diphenylhydantoin (DPH), were conducted in F344/N rats and B6C3F1 mice of each sex. The major objective of the study was to determine if incorporating exposure to DPH during the perinatal period, in addition to conventional exposure of animals for 2 years, enhances the sensitivity of the bioassay to identify the carcinogenic potential of chemical. The studies were designed to determine the toxic and carcinogenic effects of dietary DPH in rats and mice receiving; (1) the perinatal administration including exposure of maternal animals prior to breeding, through gestation, lactation, weaning, and continued dietary exposure of offspring to the age of 8 weeks followed by control diet for 2 years, (2) exposure for 2 years beginning at the age of 8 weeks, and (3) of combined perinatal/adult exposure to DPH (perinatal exposure to 8 weeks of age followed by the adult exposure for 2 years). During the perinatal period, rats were exposed to DPH at dose levels ranging from 63 to 630 ppm and adult exposure concentrations ranged from 240 to 2400 ppm in diet. In the mice, the perinatal exposure ranged from 21 to 210 ppm in both males and females. In the adult exposure portion of the mouse studies, the dietary levels ranged from 30 to 300 ppm in males and 60 to 600 ppm in females. A total of eight dose groups (including controls) were used with 60 animals in each group. The only effect of perinatal exposure alone on tumor rate was a marginal increase in the incidence of hepatocellular neoplasms in female mice. The adult exposure to DPH significantly increased the incidence of hepatocellular neoplasms in female mice. There were also marginal increases in the incidence of liver tumors in male rats exposed to high DPH dietary concentrations during the adult-only regimen. Combined perinatal and adult dietary exposure to 5,5-diphenylhydantoin confirmed the findings for the increased incidences of hepatocellular neoplasms in male rats and female mice, although combined exposure did not enhance these effects. However, in male mice, perinatal and adult exposure resulted in an increase in the incidence of hepatocellular neoplasms that was not seen when dietary exposure was limited to the adult period only. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Chhabra, R S AU - Bucher, J R AU - Haseman, J K AU - Elwell, M R AU - Kurtz, P J AU - Carlton, B D AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 174 EP - 186 VL - 21 IS - 2 SN - 0272-0590, 0272-0590 KW - Carcinogens KW - 0 KW - Phenytoin KW - 6158TKW0C5 KW - Index Medicus KW - Rats KW - Litter Size -- drug effects KW - Animals KW - Rats, Inbred F344 KW - Body Weight -- drug effects KW - Mice, Inbred C57BL KW - Liver Neoplasms, Experimental -- chemically induced KW - Mice KW - Adenoma, Liver Cell -- chemically induced KW - Male KW - Female KW - Carcinoma, Hepatocellular -- chemically induced KW - Pregnancy KW - Fetal Death KW - Phenytoin -- toxicity KW - Carcinogens -- toxicity KW - Prenatal Exposure Delayed Effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76000669?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.atitle=Comparative+carcinogenicity+of+5%2C5-diphenylhydantoin+with+or+without+perinatal+exposure+in+rats+and+mice.&rft.au=Chhabra%2C+R+S%3BBucher%2C+J+R%3BHaseman%2C+J+K%3BElwell%2C+M+R%3BKurtz%2C+P+J%3BCarlton%2C+B+D&rft.aulast=Chhabra&rft.aufirst=R&rft.date=1993-08-01&rft.volume=21&rft.issue=2&rft.spage=174&rft.isbn=&rft.btitle=&rft.title=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.issn=02720590&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-02 N1 - Date created - 1993-11-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Fundam Appl Toxicol 1994 Jan;22(1):159 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Gender-related behavior in women exposed prenatally to diethylstilbestrol. AN - 75994446; 8404755 AB - Accumulating evidence in experimental animals over the past three decades suggests that mammalian brain development and differentiation of the central nervous system are influenced by perinatal exposure to sex hormones. Hence, changes in human behavioral patterns may be associated with prenatal exposure to estrogenic substances such as diethylstilbestrol (DES). This paper reviews relevant studies from a series of laboratories and finds that no clear-cut differences can be demonstrated to date between unexposed and DES-exposed women in gender-related behavior, although the physical and psychological impact of the problems associated with exposure to DES are well documented. If both prenatal and postnatal influences such as social, economic, and environmental factors are taken into consideration, individual variation is more apparent than differences in gender-related behavior between unexposed and DES-exposed women. In summary, gender-related behavior is determined by a complex array of interacting factors, and prenatal influences are only one of many developmental events. More studies are needed using larger populations with carefully controlled selection criteria to suggest a direct role of prenatal DES exposure on subsequent gender-related behavior. JF - Environmental health perspectives AU - Newbold, R R AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 208 EP - 213 VL - 101 IS - 3 SN - 0091-6765, 0091-6765 KW - Diethylstilbestrol KW - 731DCA35BT KW - Index Medicus KW - Humans KW - Adult KW - Child KW - Adolescent KW - Male KW - Female KW - Prenatal Exposure Delayed Effects KW - Pregnancy KW - Diethylstilbestrol -- adverse effects KW - Sex Characteristics KW - Sexual Behavior -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75994446?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Gender-related+behavior+in+women+exposed+prenatally+to+diethylstilbestrol.&rft.au=Newbold%2C+R+R&rft.aulast=Newbold&rft.aufirst=R&rft.date=1993-08-01&rft.volume=101&rft.issue=3&rft.spage=208&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-18 N1 - Date created - 1993-11-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Comp Neurol. 1990 Dec 22;302(4):697-706 [1707064] J Neurosci. 1991 Apr;11(4):933-42 [2010816] Cancer Res. 1980 Nov;40(11):3988-99 [7193511] N Engl J Med. 1980 Mar 13;302(11):609-13 [7351908] Endocrinology. 1978 Aug;103(2):501-12 [744098] Fertil Steril. 1979 Feb;31(2):142-6 [761676] Pediatrics. 1978 Dec;62(6 Pt 2):1166-70 [724354] Nature. 1977 Apr 7;266(5602):561-2 [859624] Am J Obstet Gynecol. 1977 May 1;128(1):51-9 [851159] Psychoneuroendocrinology. 1980 Dec;5(4):269-85 [7208750] J Comp Neurol. 1991 Oct 1;312(1):97-104 [1744245] Horm Behav. 1981 Dec;15(4):325-76 [7035327] J Pharmacol Exp Ther. 1982 Apr;221(1):173-82 [7062281] Am J Obstet Gynecol. 1982 Apr 1;142(7):905-21 [6121486] Cancer Res. 1982 May;42(5):2003-11 [7066910] J Steroid Biochem. 1981 Dec;15:497-500 [6803070] Obstet Gynecol. 1982 Jun;59(6 Suppl):68S-72S [7088431] Fertil Steril. 1982 Sep;38(3):364-71 [7117561] Psychol Bull. 1982 Jul;92(1):56-80 [7134329] Biol Reprod. 1983 Apr;28(3):735-44 [6850046] Teratology. 1983 Jun;27(3):417-26 [6879463] J Reprod Med. 1983 Dec;28(12):851-6 [6663585] Biol Reprod. 1984 Mar;30(2):471-8 [6704476] Am J Obstet Gynecol. 1984 Apr 1;148(7):973-84 [6711635] Am J Obstet Gynecol. 1977 May 1;128(1):43-50 [851158] Obstet Gynecol. 1977 Jan;49(1):1-8 [318736] Med Clin North Am. 1974 Jul;58(4):793-810 [4276416] Arch Gen Psychiatry. 1973 Apr;28(4):554-61 [4734959] N Engl J Med. 1972 Dec 21;287(25):1259-64 [4636892] N Engl J Med. 1971 Apr 15;284(15):878-81 [5549830] Neuroendocrinology. 1971;7(3):146-55 [5101953] J Am Acad Child Adolesc Psychiatry. 1991 Jan;30(1):29-37 [2005061] Horm Behav. 1989 Dec;23(4):526-41 [2606466] J Neurosci. 1989 Feb;9(2):497-506 [2918374] Brain Res. 1988 Jul 26;456(2):271-4 [3208082] Horm Behav. 1987 Sep;21(3):402-17 [3666690] Psychosom Med. 1987 Mar-Apr;49(2):183-96 [3575605] Teratog Carcinog Mutagen. 1985;5(6):473-80 [2874632] Psychosom Med. 1985 Nov-Dec;47(6):497-511 [4070521] Horm Behav. 1985 Sep;19(3):331-47 [4054856] Nebr Symp Motiv. 1984;32:37-57 [6398858] Arch Sex Behav. 1985 Feb;14(1):57-77 [3977584] Arch Sex Behav. 1984 Oct;13(5):457-77 [6240240] Science. 1981 Mar 20;211(4488):1294-302 [6163211] Horm Behav. 1984 Sep;18(3):359-66 [6489946] Fundam Appl Toxicol. 1984 Oct;4(5):686-91 [6510599] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Leucovorin modulation of fluorouracil. AN - 75982338; 8398636 AB - Fluorouracil remains the single most active chemotherapy agent in colorectal cancer. One of its principal mechanisms of action is inhibition of the enzyme thymidylate synthase (TS), a central enzymatic step in de novo pyrimidine synthesis. Leucovorin, which is metabolized intracellularly to polyglutamated 5,10-methylenetetrahydrofolate, modulates the cellular cytotoxicity of fluorouracil by increasing TS inhibition in vitro and in vivo. Leucovorin modulation of fluorouracil has been studied in preclinical systems and in a large number of clinical trials using various doses and schedules of both drugs. The collective data support the use of continuous infusion or repetitive low-dose schedules of leucovorin. Furthermore, these schedules appear to be less dependent on the leucovorin dose to achieve maximal clinical efficacy than does intermittent single bolus therapy. These schedules appear to be the most effective in the generation of the higher polyglutamates of 5,10-methylenetetrahydrofolate, the most efficient intracellular folate metabolite for ternary complex formation and TS inhibition. JF - Oncology (Williston Park, N.Y.) AU - Grogan, L AU - Sotos, G A AU - Allegra, C J AD - NCI-Navy Medical Oncology Branch, National Cancer Institute, Bethesda, Maryland. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 63 EP - 72; discussion 75-6 VL - 7 IS - 8 SN - 0890-9091, 0890-9091 KW - Leucovorin KW - Q573I9DVLP KW - Fluorouracil KW - U3P01618RT KW - Index Medicus KW - Neoplasms -- drug therapy KW - Humans KW - Drug Synergism KW - Fluorouracil -- administration & dosage KW - Leucovorin -- administration & dosage KW - Fluorouracil -- pharmacology KW - Leucovorin -- pharmacology KW - Fluorouracil -- pharmacokinetics KW - Leucovorin -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75982338?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncology+%28Williston+Park%2C+N.Y.%29&rft.atitle=Leucovorin+modulation+of+fluorouracil.&rft.au=Grogan%2C+L%3BSotos%2C+G+A%3BAllegra%2C+C+J&rft.aulast=Grogan&rft.aufirst=L&rft.date=1993-08-01&rft.volume=7&rft.issue=8&rft.spage=63&rft.isbn=&rft.btitle=&rft.title=Oncology+%28Williston+Park%2C+N.Y.%29&rft.issn=08909091&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-08 N1 - Date created - 1993-11-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Chemotherapy agents: Part I. AN - 75981707; 8402608 JF - Cancer nursing AU - Levy, W AU - Meadows, B S AU - Quint-Kasner, S AU - Carroll, R AU - Gorrell, C R AD - Clinical Center Nursing Department, National Institutes of Health, Bethesda, Maryland. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 321 EP - 325 VL - 16 IS - 4 SN - 0162-220X, 0162-220X KW - Alkylating Agents KW - 0 KW - Antibiotics, Antineoplastic KW - Antimetabolites, Antineoplastic KW - Antineoplastic Agents KW - Index Medicus KW - Nursing KW - Alkylating Agents -- therapeutic use KW - Antibiotics, Antineoplastic -- pharmacology KW - Humans KW - Education, Nursing, Continuing KW - Alkylating Agents -- pharmacology KW - Antimetabolites, Antineoplastic -- therapeutic use KW - Antimetabolites, Antineoplastic -- pharmacology KW - Antibiotics, Antineoplastic -- therapeutic use KW - Antineoplastic Agents -- administration & dosage KW - Programmed Instruction as Topic KW - Antineoplastic Agents -- therapeutic use KW - Oncology Nursing -- education UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75981707?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+nursing&rft.atitle=Chemotherapy+agents%3A+Part+I.&rft.au=Levy%2C+W%3BMeadows%2C+B+S%3BQuint-Kasner%2C+S%3BCarroll%2C+R%3BGorrell%2C+C+R&rft.aulast=Levy&rft.aufirst=W&rft.date=1993-08-01&rft.volume=16&rft.issue=4&rft.spage=321&rft.isbn=&rft.btitle=&rft.title=Cancer+nursing&rft.issn=0162220X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-15 N1 - Date created - 1993-11-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Prospects for prevention of neural tube defects by vitamin supplementation. AN - 75980783; 8400468 AB - Recent studies have resolved the debate over the role of vitamins in preventing neural tube defects. The British Medical Research Council trial demonstrated that 4 mg of folate daily, but not other vitamins, prevented 72% of recurrences. The Hungarian trial prevented neural tube defects in women who had not previously had affected children by giving multivitamins containing 0.8 mg of folate. The US Public Health Service currently recommends that women at risk for becoming pregnant take 0.4 mg of folate daily. Unfortunately, most pregnancies are unplanned, and women not planning to become pregnant may not follow this recommendation. Therefore, the US Food and Drug Administration is exploring methods of food fortification. Because large doses of folate have been reported to ameliorate B12 deficiency anemia while allowing neurologic damage to progress, and to cause electroencephalogram abnormalities in epileptics, it is important to plan fortification carefully and to monitor both toxicity and benefits. JF - Current opinion in neurology and neurosurgery AU - Mills, J L AU - Simpson, J L AD - National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 554 EP - 558 VL - 6 IS - 4 SN - 0951-7383, 0951-7383 KW - Vitamins KW - 0 KW - Folic Acid KW - 935E97BOY8 KW - Ascorbic Acid KW - PQ6CK8PD0R KW - Index Medicus KW - Ascorbic Acid -- administration & dosage KW - Vitamin B 12 Deficiency -- prevention & control KW - Dose-Response Relationship, Drug KW - Humans KW - Food, Fortified KW - Infant, Newborn KW - Ascorbic Acid -- adverse effects KW - Folic Acid -- adverse effects KW - Female KW - Pregnancy KW - Folic Acid -- administration & dosage KW - Vitamins -- adverse effects KW - Vitamins -- administration & dosage KW - Neural Tube Defects -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75980783?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+opinion+in+neurology+and+neurosurgery&rft.atitle=Prospects+for+prevention+of+neural+tube+defects+by+vitamin+supplementation.&rft.au=Mills%2C+J+L%3BSimpson%2C+J+L&rft.aulast=Mills&rft.aufirst=J&rft.date=1993-08-01&rft.volume=6&rft.issue=4&rft.spage=554&rft.isbn=&rft.btitle=&rft.title=Current+opinion+in+neurology+and+neurosurgery&rft.issn=09517383&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-05 N1 - Date created - 1993-11-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Postpubertal emergence of hyperresponsiveness to stress and to amphetamine after neonatal excitotoxic hippocampal damage: a potential animal model of schizophrenia. AN - 75964830; 8397725 AB - The constellation of major phenomena associated with schizophrenia (e.g., postpubertal onset, congenital hippocampal area damage, cortical functional deficits, limbic dopamine (DA) dysregulation, and vulnerability to stress) have been difficult to explain with a unitary animal model. Although it has been shown that rats develop increased mesolimbic DA transmission and reduced cortical DA turnover following adult excitotoxic lesions of the ventral hippocampus (VH), the implications of early developmental VH lesions are not known. To determine the developmental sequelae of such changes, we produced ibotenic acid lesions of the ventral hippocampal formation in rats on the 7th day after birth (PD7). Motor activity in a novel environment, after saline injection and after d-amphetamine administration were similar in control and lesioned rats at PD35. However, in early adulthood, at PD56, animals with the hippocampal lesion were hyperactive in each of these conditions. The emergence of the hyperactivity at PD56 could be prevented by pretreatment with haloperidol. Moreover, rats lesioned as neonates, in contrast to a similar lesion induced in adult animals, were also hyperresponsive to stress evaluated with a swim test. This latter effect is analogous to that seen after adult lesions of the medial prefrontal cortex, rather than after adult lesions of VH, suggesting that the neonatal VH lesion may affect functional development of the medial prefrontal cortex. These results demonstrate that in rats with neonatally induced excitotoxic VH lesions, behavioral indices consistent with increased mesolimbic DA responsivity to stressful and to pharmacologic stimuli emerge only in early adulthood. Homologous mechanisms may underlie certain aspects of the pathophysiology of schizophrenia. JF - Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology AU - Lipska, B K AU - Jaskiw, G E AU - Weinberger, D R AD - Clinical Brain Disorders Branch, National Institute of Mental Health, Washington, DC 20032. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 67 EP - 75 VL - 9 IS - 1 SN - 0893-133X, 0893-133X KW - Ibotenic Acid KW - 2552-55-8 KW - Haloperidol KW - J6292F8L3D KW - Dextroamphetamine KW - TZ47U051FI KW - Index Medicus KW - Rats KW - Animals KW - Swimming KW - Rats, Sprague-Dawley KW - Haloperidol -- pharmacology KW - Disease Models, Animal KW - Motor Activity -- drug effects KW - Ibotenic Acid -- toxicity KW - Female KW - Pregnancy KW - Hippocampus -- physiology KW - Animals, Newborn -- psychology KW - Hippocampus -- pathology KW - Schizophrenia -- physiopathology KW - Stress, Psychological -- psychology KW - Hippocampus -- drug effects KW - Dextroamphetamine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75964830?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuropsychopharmacology+%3A+official+publication+of+the+American+College+of+Neuropsychopharmacology&rft.atitle=Postpubertal+emergence+of+hyperresponsiveness+to+stress+and+to+amphetamine+after+neonatal+excitotoxic+hippocampal+damage%3A+a+potential+animal+model+of+schizophrenia.&rft.au=Lipska%2C+B+K%3BJaskiw%2C+G+E%3BWeinberger%2C+D+R&rft.aulast=Lipska&rft.aufirst=B&rft.date=1993-08-01&rft.volume=9&rft.issue=1&rft.spage=67&rft.isbn=&rft.btitle=&rft.title=Neuropsychopharmacology+%3A+official+publication+of+the+American+College+of+Neuropsychopharmacology&rft.issn=0893133X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-08 N1 - Date created - 1993-11-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Directionality of fission yeast mating-type interconversion is controlled by the location of the donor loci. AN - 75956078; 8375648 AB - Cells of homothallic strains of Schizosaccharomyces pombe efficiently switch between two mating types called P and M. The phenotypic switches are due to conversion of the expressed mating-type locus (mat1) by two closely linked silent loci, mat2-P and mat3-M, that contain unexpressed information for the P and M mating types, respectively. In this process, switching-competent cells switch to the opposite mating type in 72-90% of the cell divisions. Hence, mat2-P is a preferred donor of information to mat1 in M cells, whereas mat3-M is a preferred donor in P cells. We investigated the reason for the donor preference by constructing a strain in which the genetic contents of the donor loci were swapped. We found that switching to the opposite mating type was very inefficient in that strain. This shows that the location of the silent cassettes in the chromosome, rather than their content, is the deciding factor for recognition of the donor for each cell type. We propose a model in which switching is achieved by regulating accessibility of the donor loci, perhaps by changing the chromatin structure in the mating-type region, thus promoting an intrachromosomal folding of mat2 or mat3 onto mat1 in a cell type-specific fashion. We also present evidence for the involvement of the Swi6 and Swi6-mod trans-acting factors in the donor-choice mechanism. We suggest that these factors participate in forming the proposed folded structure. JF - Genetics AU - Thon, G AU - Klar, A J AD - NCI-Frederick Cancer Research and Development Center, ABL-Basic Research Program, Maryland 21702-1201. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 1045 EP - 1054 VL - 134 IS - 4 SN - 0016-6731, 0016-6731 KW - DNA, Fungal KW - 0 KW - Fungal Proteins KW - SWI6 protein, S cerevisiae KW - Saccharomyces cerevisiae Proteins KW - Trans-Activators KW - Transcription Factors KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Trans-Activators -- metabolism KW - Fungal Proteins -- metabolism KW - Base Sequence KW - Genes, Switch KW - Transcription Factors -- metabolism KW - Restriction Mapping KW - Recombination, Genetic KW - Schizosaccharomyces -- genetics KW - Gene Conversion KW - Genes, Fungal KW - Genes, Mating Type, Fungal UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75956078?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Genetics&rft.atitle=Directionality+of+fission+yeast+mating-type+interconversion+is+controlled+by+the+location+of+the+donor+loci.&rft.au=Thon%2C+G%3BKlar%2C+A+J&rft.aulast=Thon&rft.aufirst=G&rft.date=1993-08-01&rft.volume=134&rft.issue=4&rft.spage=1045&rft.isbn=&rft.btitle=&rft.title=Genetics&rft.issn=00166731&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-18 N1 - Date created - 1993-10-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Mol Gen Genet. 1968;102(4):301-6 [5743433] Mol Gen Genet. 1979 Feb 26;170(2):145-8 [285317] J Bacteriol. 1983 Jan;153(1):163-8 [6336730] EMBO J. 1984 Mar;3(3):603-10 [6325178] Proc Natl Acad Sci U S A. 1984 Jun;81(11):3481-5 [6587363] Mol Cell Biol. 1986 Jan;6(1):80-9 [3023839] EMBO J. 1988 May;7(5):1537-47 [2900761] EMBO J. 1989 Jan;8(1):269-76 [2714252] EMBO J. 1990 May;9(5):1407-15 [2328720] Methods Enzymol. 1991;194:795-823 [2005825] EMBO J. 1991 Oct;10(10):3025-32 [1915277] Genetics. 1991 Dec;129(4):1033-42 [1783290] Curr Genet. 1991 Nov;20(5):379-83 [1807828] Mol Gen Genet. 1992 Jun;233(3):436-42 [1620099] Genetics. 1992 Jun;131(2):287-96 [1644273] Genetics. 1992 Dec;132(4):929-42 [1459444] Nature. 1993 Jan 21;361(6409):271-3 [8423854] Cold Spring Harb Symp Quant Biol. 1958;23:161-70 [13635553] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Mutants of Escherichia coli with increased fidelity of DNA replication. AN - 75953992; 8375645 AB - To improve our understanding of the role of DNA replication fidelity in mutagenesis, we undertook a search for Escherichia coli antimutator strains with increased fidelity of DNA replication. The region between 4 and 5 min of the E. coli chromosome was mutagenized using localized mutagenesis mediated by bacteriophage P1. This region contains the dnaE and dnaQ genes, which encode, respectively, the DNA polymerase (alpha subunit) and 3' exonucleolytic proofreading activity (epsilon subunit) of DNA polymerase III holoenzyme, the enzyme primarily responsible for replicating the bacterial chromosome. The mutated bacteria were screened for antimutator phenotype in a strain defective in DNA mismatch repair (mutL), using a papillation assay based on the reversion of the galK2 mutation. In a mutL strain, mutations result primarily from DNA replication errors. Among 10,000 colonies, seven mutants were obtained whose level of papillation was reduced 5-30-fold. These mutants also displayed decreased mutation frequencies for rifampicin or nalidixic acid resistance as well as for other markers. Mapping by P1 transduction and complementation showed each to reside in dnaE. These observations support the idea that the mutants represent antimutators which replicate their DNA with increased fidelity. Mutation rates were reduced in both mutL and mutT backgrounds, but mutagenesis by ultraviolet light was not significantly affected, suggesting that the antimutator effect may be largely restricted to normal DNA replication. JF - Genetics AU - Fijalkowska, I J AU - Dunn, R L AU - Schaaper, R M AD - Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 1023 EP - 1030 VL - 134 IS - 4 SN - 0016-6731, 0016-6731 KW - dnaE KW - dnaQ KW - Bacterial Proteins KW - 0 KW - DNA, Bacterial KW - Escherichia coli Proteins KW - DNA Polymerase III KW - EC 2.7.7.- KW - DNA polymerase III, alpha subunit KW - Phosphoric Monoester Hydrolases KW - EC 3.1.3.2 KW - Pyrophosphatases KW - EC 3.6.1.- KW - mutT protein, E coli KW - Index Medicus KW - Bacterial Proteins -- genetics KW - SOS Response (Genetics) KW - Genetic Complementation Test KW - DNA Polymerase III -- genetics KW - DNA Polymerase III -- metabolism KW - Chromosome Mapping KW - Mutagenesis KW - DNA, Bacterial -- genetics KW - DNA, Bacterial -- biosynthesis KW - Escherichia coli -- genetics KW - Escherichia coli -- enzymology KW - Mutation KW - DNA Replication UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75953992?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Genetics&rft.atitle=Mutants+of+Escherichia+coli+with+increased+fidelity+of+DNA+replication.&rft.au=Fijalkowska%2C+I+J%3BDunn%2C+R+L%3BSchaaper%2C+R+M&rft.aulast=Fijalkowska&rft.aufirst=I&rft.date=1993-08-01&rft.volume=134&rft.issue=4&rft.spage=1023&rft.isbn=&rft.btitle=&rft.title=Genetics&rft.issn=00166731&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-18 N1 - Date created - 1993-10-18 N1 - Date revised - 2017-01-13 N1 - Gene symbol - dnaE; dnaQ N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1966 Feb;55(2):274-81 [5328724] Cold Spring Harb Symp Quant Biol. 1968;33:339-44 [5254574] Proc Natl Acad Sci U S A. 1970 Jul;66(3):823-9 [5269245] Mol Gen Genet. 1971;113(3):273-84 [4946856] Mol Gen Genet. 1975 Aug 5;139(1):9-18 [1101031] Mol Gen Genet. 1977 May 20;153(1):87-97 [329107] J Bacteriol. 1978 Mar;133(3):1197-202 [346561] Mutat Res. 1978 Oct;52(1):11-24 [366396] Genetics. 1980 Dec;96(4):819-39 [7021317] Mol Gen Genet. 1982;185(1):43-50 [6211591] J Bacteriol. 1983 Mar;153(3):1361-7 [6337996] J Mol Biol. 1983 Jul 15;167(4):757-71 [6224021] Proc Natl Acad Sci U S A. 1987 Sep;84(17):6220-4 [3306672] Annu Rev Biochem. 1988;57:519-50 [3052282] Proc Natl Acad Sci U S A. 1988 Nov;85(21):8126-30 [3054881] J Bacteriol. 1989 Oct;171(10):5572-80 [2551891] Microbiol Rev. 1990 Jun;54(2):130-97 [2194094] J Bacteriol. 1991 Jan;173(1):334-44 [1987124] J Biol Chem. 1991 Mar 15;266(8):5055-61 [2002048] J Biol Chem. 1991 Oct 15;266(29):19127-30 [1918028] Genetics. 1991 Oct;129(2):317-26 [1660424] Nature. 1992 Jan 16;355(6357):273-5 [1309939] Annu Rev Genet. 1991;25:229-53 [1812808] Genetics. 1993 Aug;134(4):1031-8 [8375646] Genetics. 1993 Aug;134(4):1039-44 [8375647] J Gen Microbiol. 1954 Dec;11(3):364-79 [13221757] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Stopping a clinical trial very early because of toxicity: summarizing the evidence. AN - 75932560; 7689943 AB - When a trial is stopped early because of a specific toxicity, it may be important to summarize the statistical evidence for stopping. Such a summary needs to take into account the sequential nature of the stopping rule. We address some practical issues involved in analyzing such toxicity data coming from a trial that was stopped after the fourth patient was evaluated. JF - Controlled clinical trials AU - Korn, E L AU - Yu, K F AU - Miller, L L AD - Biometric Research Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 286 EP - 295 VL - 14 IS - 4 SN - 0197-2456, 0197-2456 KW - Granulocyte Colony-Stimulating Factor KW - 143011-72-7 KW - Index Medicus KW - Humans KW - Granulocyte Colony-Stimulating Factor -- adverse effects KW - Bayes Theorem KW - Confidence Intervals KW - Leukopenia -- etiology KW - Drug-Related Side Effects and Adverse Reactions KW - Clinical Trials as Topic -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75932560?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Controlled+clinical+trials&rft.atitle=Stopping+a+clinical+trial+very+early+because+of+toxicity%3A+summarizing+the+evidence.&rft.au=Korn%2C+E+L%3BYu%2C+K+F%3BMiller%2C+L+L&rft.aulast=Korn&rft.aufirst=E&rft.date=1993-08-01&rft.volume=14&rft.issue=4&rft.spage=286&rft.isbn=&rft.btitle=&rft.title=Controlled+clinical+trials&rft.issn=01972456&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-06 N1 - Date created - 1993-10-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Control Clin Trials. 1995 Apr;16(2):131-2 [7789136] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Parkinson's disease: past, present, and future. AN - 75932400; 8397719 AB - The development of understanding of the pathophysiology and modes of treatment of Parkinson's disease represents one of the triumphs of modern medicine, encompassing astute clinical observation, utilization of basic research findings regarding dopamine to develop the first rational treatment of a degenerative disorder of the central nervous system, and remains at the frontiers of neurologic science. After characterization of the clinical and pathologic features of Parkinson's disease, rational treatment awaited the discovery of the deficit in basal ganglia dopamine. On the basis of this observation and the known biosynthetic pathways for dopamine formation, levodopa was introduced. Use of metabolic inhibitors to prolong and potentiate the effects and avoid the deleterious side effects of levodopa enhanced the efficacy of this neurotransmitter replacement strategy. The discovery and characterization of dopamine receptor subtypes and the availability of selective dopamine agonists provided additional therapeutic approaches, but failed to address the underlying cause of the degenerative process. The discovery and disclosure of the mechanisms of toxicity of the relatively selective nigrostriatal neurotoxin, 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP), triggered a resurgence of interest in etiological factors which might contribute to the development of parkinsonism and together with the report that inhibition of monoamine oxidase B with deprenyl not only potentiated the effects of levodopa, but appeared to prolong the life of parkinsonian patients, resulted in a large-scale trial of drugs that might arrest the degenerative process. Furthermore, the MPTP primate model of Parkinson's disease has encouraged development of fetal mesencephalic and other tissue implant approaches to reversal of parkinsonism. Although much of this is still in the experimental stages, hopes are high that new and more effective therapies will be developed and that similar techniques might be applicable to a wide variety of neuropsychiatric disorders. JF - Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology AU - Kopin, I J AD - Intramural Research, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 1 EP - 12 VL - 9 IS - 1 SN - 0893-133X, 0893-133X KW - Index Medicus KW - History of medicine KW - Animals KW - History, 20th Century KW - Humans KW - Parkinson Disease -- physiopathology KW - Parkinson Disease -- history UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75932400?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuropsychopharmacology+%3A+official+publication+of+the+American+College+of+Neuropsychopharmacology&rft.atitle=Parkinson%27s+disease%3A+past%2C+present%2C+and+future.&rft.au=Kopin%2C+I+J&rft.aulast=Kopin&rft.aufirst=I&rft.date=1993-08-01&rft.volume=9&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Neuropsychopharmacology+%3A+official+publication+of+the+American+College+of+Neuropsychopharmacology&rft.issn=0893133X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-08 N1 - Date created - 1993-11-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Identification of P-glycoprotein/multidrug resistance genes from model organisms. AN - 75928050; 8361216 AB - Using degenerate oligonucleotides from conserved portions of the ATP-binding domain of the active transporter genes, several new members of this gene superfamily have been cloned from Drosophila, Saccharomyces cerevisiae, and E. coli DNA. The Drosophila and E. coli genes contain two sets of transmembrane domains and two ATP-binding domains, whereas the yeast gene contains single transmembrane and ATP-binding domains. All three genes show a high degree of similarity to the mammalian P-glycoprotein/multidrug resistance (MDR) genes. The E. coli sequence is the only known transporter gene containing both ATP and transmembrane domains in a single open reading frame. While the function of these sequences has not been determined, they may prove to be useful for developing a model to study the function of P-glycoproteins. JF - Leukemia AU - Allikmets, R AU - Gerrard, B AU - Stewart, C AU - White, M AU - Dean, M AD - Laboratory of Viral Carcinogenesis, Program Resources Inc./DynCorp, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - S13 EP - S17 VL - 7 Suppl 2 SN - 0887-6924, 0887-6924 KW - MDR KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Index Medicus KW - Polymerase Chain Reaction KW - Animals KW - Base Sequence KW - Sequence Alignment KW - Chromosome Banding KW - Adenosine Triphosphate -- metabolism KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Adenosine Triphosphate -- genetics KW - Saccharomyces cerevisiae -- genetics KW - Drug Resistance -- genetics KW - Conserved Sequence -- genetics KW - Drosophila melanogaster -- genetics KW - Escherichia coli -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75928050?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Leukemia&rft.atitle=Identification+of+P-glycoprotein%2Fmultidrug+resistance+genes+from+model+organisms.&rft.au=Allikmets%2C+R%3BGerrard%2C+B%3BStewart%2C+C%3BWhite%2C+M%3BDean%2C+M&rft.aulast=Allikmets&rft.aufirst=R&rft.date=1993-08-01&rft.volume=7+Suppl+2&rft.issue=&rft.spage=S13&rft.isbn=&rft.btitle=&rft.title=Leukemia&rft.issn=08876924&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-30 N1 - Date created - 1993-09-30 N1 - Date revised - 2017-01-13 N1 - Gene symbol - MDR N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - 1992 Stohlman Memorial Lecture: targeting the IL-2 receptor. AN - 75921560; 8361223 AB - Patients with human T-cell lymphotropic virus I (HTLV-I)-associated leukemia/lymphoma were treated with different forms of IL-2 receptor (IL-2R)-directed therapy that exploit the difference in IL-2R expression between normal and malignant cells. Using unmodified anti-Tac monoclonal antibody, one-third of the patients with adult T-cell leukemia (ATL) treated have undergone a remission, in two cases complete. There was little toxicity observed; however, unmodified monoclonal antibodies are limited by their immunogenicity and their poor effector functions. To address these issues, "humanized" anti-Tac was produced that contains the complementarity-determining regions from the mouse with the remainder of the molecule derived from human IgG1 kappa. This antibody is dramatically less immunogenic than the murine version, has improved pharmacokinetics, and, in contrast to the parent antibody, manifests antibody-dependent cellular cytotoxicity (ADCC). To enhance its effector function, anti-Tac was armed with toxins and alpha- and beta-emitting radionuclides. In a clinical trial of 90Y-anti-Tac in ATL patients, at the doses used (5, 10, and 15 mCi 90Y-anti-Tac per patient), 10 of the 15 patients with ATL treated to date underwent sustained partial or complete remission. Thus, the clinical application of IL-2R-directed therapy represents a new perspective for the prevention of allograft rejection and for the treatment of graft-versus-host disease, select autoimmune disorders, and leukemia/lymphoma. JF - Leukemia AU - Waldmann, T A AD - Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - S151 EP - S156 VL - 7 Suppl 2 SN - 0887-6924, 0887-6924 KW - Antibodies, Monoclonal KW - 0 KW - Immunotoxins KW - Receptors, Interleukin-2 KW - Index Medicus KW - AIDS/HIV KW - Humans KW - Immunotoxins -- therapeutic use KW - Lymphocyte Activation KW - Receptors, Interleukin-2 -- metabolism KW - Leukemia-Lymphoma, Adult T-Cell -- therapy KW - Leukemia-Lymphoma, Adult T-Cell -- radiotherapy KW - Receptors, Interleukin-2 -- immunology KW - Immunotherapy -- methods KW - Antibodies, Monoclonal -- therapeutic use KW - Antibodies, Monoclonal -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75921560?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Leukemia&rft.atitle=1992+Stohlman+Memorial+Lecture%3A+targeting+the+IL-2+receptor.&rft.au=Waldmann%2C+T+A&rft.aulast=Waldmann&rft.aufirst=T&rft.date=1993-08-01&rft.volume=7+Suppl+2&rft.issue=&rft.spage=S151&rft.isbn=&rft.btitle=&rft.title=Leukemia&rft.issn=08876924&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-30 N1 - Date created - 1993-09-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - A decomposition product of a contaminant implicated in L-tryptophan eosinophilia myalgia syndrome affects spinal cord neuronal cell death and survival through stereospecific, maturation and partly interleukin-1-dependent mechanisms. AN - 75916798; 8355179 AB - The L-tryptophan eosinophilia myalgia syndrome (L-TRP-EMS), an inflammatory syndrome characterized by eosinophilia, myalgias, perimyositis, fasciitis and neuropathies, occurred in epidemic proportions in the United States in the summer and fall of 1989. The neuropathic clinical features in L-TRP EMS are complex and mixed. In the present study, one of the impurities most highly associated with development of L-TRP EMS, 1,1'-ethylidenebis[L-tryptophan] (EBT), and two of its diastereoisomeric breakdown products, were compared for evidence of neurotoxicity in vitro. In 1-month-old spinal cord cultures derived from fetal mice, synthetic (-)-(1S,3S)-1-methyl-1,2,3,4-tetrahydro-beta-carboline-3-carboxylic acid (1S-beta-C) produced a 30 to 35% loss in numbers of neurons. Toxicity was not apparent after treatment with the R-isomer of the same compound or with the parent compound, EBT. Cotreatment of cultures with 1S-beta-C and neutralizing antiserum to interleukin-1 alpha (IL-1 alpha), or with 1S-beta-C and neutralizing antiserum against the murine IL-1 receptor, prevented neuronal cell death associated with 1S-beta-C. Recombinant IL-1 alpha also produced neuronal killing that was not additive to that observed with the 1S-beta-C treatment. In contrast, in immature spinal cord neuronal cultures, the 1S-beta-C, but not the 1R-beta-C or EBT, prevented the 30% cell death which normally occurs in these cultures. Neither neutralizing anti-IL-1 antibody, nor anti-IL-1 receptor antibody blocked the neuronal survival effect, suggesting that 1S-beta-C induces neuronal survival through a receptor-mediated mechanism independent of IL-1.(ABSTRACT TRUNCATED AT 250 WORDS) JF - The Journal of pharmacology and experimental therapeutics AU - Brenneman, D E AU - Page, S W AU - Schultzberg, M AU - Thomas, F S AU - Zelazowski, P AU - Burnet, P AU - Avidor, R AU - Sternberg, E M AD - Section on Developmental and Molecular Pharmacology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 1029 EP - 1035 VL - 266 IS - 2 SN - 0022-3565, 0022-3565 KW - Carbolines KW - 0 KW - Interleukin-1 KW - Receptors, Interleukin-1 KW - Recombinant Proteins KW - 1,1'-ethylidene bis(tryptophan) KW - 132685-02-0 KW - 1-methyl-1,2,3,4-tetrahydro-beta-carboline-3-carboxylic acid KW - 5470-37-1 KW - Tryptophan KW - 8DUH1N11BX KW - Index Medicus KW - Animals KW - Stereoisomerism KW - Recombinant Proteins -- pharmacology KW - Cell Survival -- drug effects KW - Cells, Cultured KW - Mice KW - Receptors, Interleukin-1 -- physiology KW - Cell Death -- drug effects KW - Female KW - Pregnancy KW - Interleukin-1 -- physiology KW - Tryptophan -- analogs & derivatives KW - Tryptophan -- toxicity KW - Drug Contamination KW - Spinal Cord -- drug effects KW - Eosinophilia-Myalgia Syndrome -- etiology KW - Carbolines -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75916798?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.atitle=A+decomposition+product+of+a+contaminant+implicated+in+L-tryptophan+eosinophilia+myalgia+syndrome+affects+spinal+cord+neuronal+cell+death+and+survival+through+stereospecific%2C+maturation+and+partly+interleukin-1-dependent+mechanisms.&rft.au=Brenneman%2C+D+E%3BPage%2C+S+W%3BSchultzberg%2C+M%3BThomas%2C+F+S%3BZelazowski%2C+P%3BBurnet%2C+P%3BAvidor%2C+R%3BSternberg%2C+E+M&rft.aulast=Brenneman&rft.aufirst=D&rft.date=1993-08-01&rft.volume=266&rft.issue=2&rft.spage=1029&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.issn=00223565&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-17 N1 - Date created - 1993-09-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Genotype/phenotype discordance for human arylamine N-acetyltransferase (NAT2) reveals a new slow-acetylator allele common in African-Americans. AN - 75914060; 8102597 AB - Carcinogenic arylamines are acetylated by the hepatic N-acetyltransferase. This enzyme is polymorphic in humans and in some epidemiological studies, the slow-acetylator phenotype has been associated with higher risk of bladder cancer and lower risk of colorectal cancer. The presence of two germline copies of any of several mutant alleles of the NAT2 gene produces a slow-acetylation phenotype. We used a PCR-RFLP technique to identify three known slow-acetylator alleles (M1, M2 and M3). Comparison of results from PCR-RFLP genotyping with caffeine metabolism phenotyping in 42 individuals suggested that an additional slow-acetylator allele was present in our sampled population. We sequenced the NAT2 gene for several discordant slow-acetylator individuals and found a G > A base-change in codon 64 that caused a Arg > Glu amino acid substitution. This sequence change, termed the 'M4' allele, was found in all of the discordant individuals in our population and apparently causes a slow-acetylation phenotype. In addition, we have determined that NAT2 allele frequencies in 372 Caucasian-Americans (WT = 0.25, M1 = 0.45, M2 = 0.28, M3 = 0.02, and M4 = 0.00) and in 128 African-Americans (WT = 0.36, M1 = 0.30, M2 = 0.22, M3 = 0.02 and M4 = 0.09) are significantly different (P < 0.0001). The M4 allele was not found in 372 unrelated Caucasians and appears to be of African origin. JF - Carcinogenesis AU - Bell, D A AU - Taylor, J A AU - Butler, M A AU - Stephens, E A AU - Wiest, J AU - Brubaker, L H AU - Kadlubar, F F AU - Lucier, G W AD - Laboratory of Biochemical Risk Analysis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 1689 EP - 1692 VL - 14 IS - 8 SN - 0143-3334, 0143-3334 KW - NAT2 KW - Xanthines KW - 0 KW - Caffeine KW - 3G6A5W338E KW - Uracil KW - 56HH86ZVCT KW - 1-methylxanthine KW - 7EE8WCA32U KW - 5-acetylamino-6-formylamino-3-methyluracil KW - 85438-96-6 KW - Arylamine N-Acetyltransferase KW - EC 2.3.1.5 KW - Index Medicus KW - United States KW - Caffeine -- metabolism KW - Uracil -- analogs & derivatives KW - Humans KW - Amino Acid Sequence KW - Xanthines -- urine KW - Caffeine -- urine KW - Genotype KW - Phenotype KW - Acetylation KW - Polymerase Chain Reaction KW - Base Sequence KW - Polymorphism, Restriction Fragment Length KW - Molecular Sequence Data KW - Sequence Homology, Amino Acid KW - Uracil -- urine KW - Alleles KW - African Continental Ancestry Group -- genetics KW - Arylamine N-Acetyltransferase -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75914060?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Genotype%2Fphenotype+discordance+for+human+arylamine+N-acetyltransferase+%28NAT2%29+reveals+a+new+slow-acetylator+allele+common+in+African-Americans.&rft.au=Bell%2C+D+A%3BTaylor%2C+J+A%3BButler%2C+M+A%3BStephens%2C+E+A%3BWiest%2C+J%3BBrubaker%2C+L+H%3BKadlubar%2C+F+F%3BLucier%2C+G+W&rft.aulast=Bell&rft.aufirst=D&rft.date=1993-08-01&rft.volume=14&rft.issue=8&rft.spage=1689&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-21 N1 - Date created - 1993-09-21 N1 - Date revised - 2017-01-13 N1 - Gene symbol - NAT2 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Prolactin induces maturation of glucose sensing mechanisms in cultured neonatal rat islets. AN - 75911525; 8344197 AB - The effects of PRL treatment on insulin content and secretion, and 86Rb and 45Ca fluxes from neonatal rat islets maintained in culture for 7-9 days were studied. PRL treatment enhanced islet insulin content by 40% and enhanced early insulin secretion evoked by 16.7 mM glucose. Insulin release stimulated by oxotremorine-M, a muscarinic agonist, in the presence of glucose (8.3 or 16.7 mM) was unchanged by PRL treatment. However, PRL treatment potentiated phorbol 12,13-dibutyrate-stimulated insulin secretion in the presence of the above glucose concentrations. PRL treatment potentiated the reduction in 86Rb efflux induced by glucose or tolbutamide and enhanced the increase in 86Rb efflux evoked by diazoxide. PRL treatment slightly potentiated the increment in 45Ca uptake induced by high concentrations of K+, but failed to affect the increment evoked by 16.7 mM glucose. Since glucose-induced 45Ca uptake was not affected by PRL, we suggest that the enhancement in first phase insulin secretion evoked by glucose in the PRL-treated islets occurs at a step in the secretory process that may involve protein kinase-C. These data further support observations that PRL treatment increases islet sensitivity to glucose. JF - Endocrinology AU - Boschero, A C AU - Crepaldi, S C AU - Carneiro, E M AU - Delattre, E AU - Atwater, I AD - Laboratory of Cell Biology and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 515 EP - 520 VL - 133 IS - 2 SN - 0013-7227, 0013-7227 KW - Calcium Radioisotopes KW - 0 KW - Insulin KW - Rubidium Radioisotopes KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Oxotremorine KW - 5RY0UWH1JL KW - oxotremorine M KW - 63939-65-1 KW - Prolactin KW - 9002-62-4 KW - Tolbutamide KW - 982XCM1FOI KW - Glucose KW - IY9XDZ35W2 KW - Potassium KW - RWP5GA015D KW - Abridged Index Medicus KW - Index Medicus KW - Rats KW - Calcium Radioisotopes -- metabolism KW - Animals KW - Oxotremorine -- pharmacology KW - Cells, Cultured KW - Tolbutamide -- pharmacology KW - Rubidium Radioisotopes -- metabolism KW - Potassium -- pharmacology KW - Insulin -- secretion KW - Oxotremorine -- analogs & derivatives KW - Drug Synergism KW - Phorbol 12,13-Dibutyrate -- pharmacology KW - Animals, Newborn KW - Islets of Langerhans -- growth & development KW - Glucose -- pharmacology KW - Islets of Langerhans -- drug effects KW - Prolactin -- pharmacology KW - Islets of Langerhans -- secretion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75911525?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Endocrinology&rft.atitle=Prolactin+induces+maturation+of+glucose+sensing+mechanisms+in+cultured+neonatal+rat+islets.&rft.au=Boschero%2C+A+C%3BCrepaldi%2C+S+C%3BCarneiro%2C+E+M%3BDelattre%2C+E%3BAtwater%2C+I&rft.aulast=Boschero&rft.aufirst=A&rft.date=1993-08-01&rft.volume=133&rft.issue=2&rft.spage=515&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=00137227&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-03 N1 - Date created - 1993-09-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Repair of ribosomal RNA genes in hamster cells after UV irradiation, or treatment with cisplatin or alkylating agents. AN - 75910243; 8353843 AB - We have measured the DNA damage formation and repair in the ribosomal and the dihydrofolate reductase (DHFR) genes after treatment of hamster cells with different types of DNA damaging agents. In mammalian cells, the ribosomal DNA (rDNA) is transcribed by RNA polymerase I, whereas the DHFR is transcribed by RNA polymerase II, whereas the DHFR is transcribed by RNA polymerase II. Cells were treated with agents that induce different types of lesions, and that are known to be repaired via different pathways. We used UV (254 nm) irradiation, treatment with cisplatin and treatment with the alkylating agents nitrogen mustard (HN2) and methyl methanesulphonate (MMS). UV induced pyrimidine dimers were detected with the enzyme T4 endonuclease V, which creates nicks at the dimer sites; the breaks are then resolved and identified by denaturing electrophoresis and Southern blot. Intrastrand adducts formed by the alkylating agents HN2 and MMS were quantitated by generating strand breaks at abasic sites after neutral depurination. Interstrand crosslinks (ICL) formed by HN2 and cisplatin were detected by a denaturation-reannealing reaction before neutral agarose gel-electrophoresis. We find that the repair of the pyrimidine dimers is significantly less efficient in the RNA polymerase I transcribed rDNA genes than in RNA polymerase II transcribed DHFR gene at 8 and 24 h after irradiation. ICL and intrastrand adducts induced by HN2 are also removed more slowly from the rDNA than from the DHFR gene. In contrast, MMS induced intrastrand adducts and cisplatin induced ICL are repaired equally efficiently in the RNA polymerase I and RNA polymerase II transcribed genes. We conclude that for some types of DNA damage, there is less repair in the ribosomal genes than in the DHFR; but for other DNA lesions there is no difference. The difference in repair efficiency between the rDNA and the DHFR genes may reflect the different RNA polymerase involved in their transcription. It may, however, alternatively, reflect the different nuclear localization of these genes. JF - Carcinogenesis AU - Stevnsner, T AU - May, A AU - Petersen, L N AU - Larminat, F AU - Pirsel, M AU - Bohr, V A AD - Laboratory of Molecular Pharmacology, National Cancer Institute, NIH, Bethesda, MD 20892. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 1591 EP - 1596 VL - 14 IS - 8 SN - 0143-3334, 0143-3334 KW - DHFR KW - rRNA KW - Alkylating Agents KW - 0 KW - DNA, Ribosomal KW - Pyrimidine Dimers KW - RNA, Ribosomal KW - Mechlorethamine KW - 50D9XSG0VR KW - Guanine KW - 5Z93L87A1R KW - Methyl Methanesulfonate KW - AT5C31J09G KW - Tetrahydrofolate Dehydrogenase KW - EC 1.5.1.3 KW - RNA Polymerase II KW - EC 2.7.7.- KW - RNA Polymerase I KW - EC 2.7.7.6 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Animals KW - DNA Damage KW - Pyrimidine Dimers -- metabolism KW - CHO Cells -- drug effects KW - Transcription, Genetic -- genetics KW - RNA Polymerase I -- genetics KW - Guanine -- metabolism KW - Mechlorethamine -- toxicity KW - RNA Polymerase II -- genetics KW - CHO Cells -- physiology KW - CHO Cells -- radiation effects KW - DNA, Ribosomal -- genetics KW - Tetrahydrofolate Dehydrogenase -- genetics KW - Cricetinae KW - DNA Repair -- genetics KW - Cisplatin -- toxicity KW - Genes -- drug effects KW - Ultraviolet Rays -- adverse effects KW - RNA, Ribosomal -- genetics KW - RNA, Ribosomal -- radiation effects KW - Alkylating Agents -- toxicity KW - Genes -- radiation effects KW - Genes -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75910243?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Repair+of+ribosomal+RNA+genes+in+hamster+cells+after+UV+irradiation%2C+or+treatment+with+cisplatin+or+alkylating+agents.&rft.au=Stevnsner%2C+T%3BMay%2C+A%3BPetersen%2C+L+N%3BLarminat%2C+F%3BPirsel%2C+M%3BBohr%2C+V+A&rft.aulast=Stevnsner&rft.aufirst=T&rft.date=1993-08-01&rft.volume=14&rft.issue=8&rft.spage=1591&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-21 N1 - Date created - 1993-09-21 N1 - Date revised - 2017-01-13 N1 - Gene symbol - DHFR; rRNA N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Tityustoxin-K alpha, a structurally novel and highly potent K+ channel peptide toxin, interacts with the alpha-dendrotoxin binding site on the cloned Kv1.2 K+ channel. AN - 75907059; 8355670 AB - The interaction between two nonhomologous K+ channel toxins, Tityus serrulatus (scorpion) toxin tityustoxin-K alpha (TsTX-K alpha) and Dendroaspis angusticeps (snake) toxin dendrotoxin (alpha-DTX), was investigated on K+ currents in B82 fibroblast cells transformed to express the Kv1.2 K+ channel. As demonstrated previously, alpha-DTX was a potent blocker of the K+ current (Kd, 2.8 nM). Recombinant TsTX-K alpha produced a similar block of the current but was 1 order of magnitude more potent (Kd, 0.21 nM). TsTX-K alpha did not affect the kinetic properties of the current or its voltage dependence of activation. Experiments with excised and cell-attached patch recordings demonstrated that TsTX-K alpha blocks the K+ channel by binding to an extracellular site. In the presence of TsTX-K alpha the blocking potency of alpha-DTX was reduced, whereas the potency of 4-aminopyridine, which also blocks the channel, was unaffected. alpha-DTX caused a rightward shift in the scaled concentration-response curve for TsTX-K alpha, the magnitude of which was reasonably well predicted by a model in which there is a competitive interaction between the two peptide toxins. We conclude that TsTX-K alpha and alpha-DTX block the Kv1.2 K+ channel by binding to the same or closely related sites. JF - Molecular pharmacology AU - Werkman, T R AU - Gustafson, T A AU - Rogowski, R S AU - Blaustein, M P AU - Rogawski, M A AD - Neuronal Excitability Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 430 EP - 436 VL - 44 IS - 2 SN - 0026-895X, 0026-895X KW - Elapid Venoms KW - 0 KW - Neurotoxins KW - Potassium Channels KW - Recombinant Proteins KW - Scorpion Venoms KW - tityustoxin KW - 39465-37-7 KW - dendrotoxin KW - 74811-93-1 KW - Index Medicus KW - Animals KW - Base Sequence KW - Recombinant Proteins -- pharmacology KW - Recombinant Proteins -- metabolism KW - Dose-Response Relationship, Drug KW - Binding, Competitive KW - Molecular Sequence Data KW - Electrophysiology KW - Cell Line KW - Binding Sites KW - Elapid Venoms -- pharmacology KW - Scorpion Venoms -- pharmacology KW - Neurotoxins -- metabolism KW - Scorpion Venoms -- metabolism KW - Neurotoxins -- pharmacology KW - Potassium Channels -- drug effects KW - Elapid Venoms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75907059?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+pharmacology&rft.atitle=Tityustoxin-K+alpha%2C+a+structurally+novel+and+highly+potent+K%2B+channel+peptide+toxin%2C+interacts+with+the+alpha-dendrotoxin+binding+site+on+the+cloned+Kv1.2+K%2B+channel.&rft.au=Werkman%2C+T+R%3BGustafson%2C+T+A%3BRogowski%2C+R+S%3BBlaustein%2C+M+P%3BRogawski%2C+M+A&rft.aulast=Werkman&rft.aufirst=T&rft.date=1993-08-01&rft.volume=44&rft.issue=2&rft.spage=430&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmacology&rft.issn=0026895X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-23 N1 - Date created - 1993-09-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Characterization of ligand and substrate specificity for the calcium-dependent and calcium-independent protein kinase C isozymes. AN - 75906670; 8355667 AB - Analysis of [3H]phorbol-12,13-dibutyrate (PDBu) binding was performed with protein kinase C (PKC)-alpha, -beta 1, -gamma, -delta, -epsilon, -eta, and -zeta produced in Sf9 insect cells using the baculovirus expression system. With the exception of PKC-zeta, all of the PKC isozymes bound [3H]PDBu with high affinity (Kd < 1 nM), either in the presence or in the absence of calcium. Scatchard analysis using 100% phosphatidylserine vesicles revealed slightly lower affinity for the calcium-independent isozymes (PKC-delta, -epsilon, and -eta) than for the calcium-dependent isozymes (PKC-alpha, -beta, and -gamma). Competition for [3H]PDBu binding by different classes of PKC activators showed that 12-deoxyphorbol esters, mezerein, and octahydromezerein likewise possessed lower affinity for the calcium-independent isozymes. The mezerein analog thymeleatoxin was the most marked example, being almost 20-fold less potent for binding to PKC-epsilon and -eta than to PKC-beta 1. In contrast, the indole alkaloids (-)-indolactam V and (-)-octylindolactam V and the postulated endogenous activator 1,2-diacylglycerol bound with similar affinities to all of the PKC isoforms, suggesting that different residues/configurations in the binding sites of the different PKC isozymes might be involved in interaction with the pharmacophore of the activators. The seven PKC isozymes also showed clearly different substrate specificities with exogenous peptide and protein substrates. The heterogeneous behavior of the different members of the PKC family with ligands and substrates may contribute to the heterogeneity of PKC-mediated pathways at the cellular level. JF - Molecular pharmacology AU - Kazanietz, M G AU - Areces, L B AU - Bahador, A AU - Mischak, H AU - Goodnight, J AU - Mushinski, J F AU - Blumberg, P M AD - Molecular Mechanisms of Tumor Promotion Section, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 298 EP - 307 VL - 44 IS - 2 SN - 0026-895X, 0026-895X KW - Isoenzymes KW - 0 KW - Recombinant Proteins KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Baculoviridae -- genetics KW - Animals KW - Base Sequence KW - Recombinant Proteins -- metabolism KW - Enzyme Activation KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Substrate Specificity KW - Recombinant Proteins -- chemistry KW - Moths KW - Cell Line KW - Structure-Activity Relationship KW - Protein Kinase C -- metabolism KW - Calcium -- metabolism KW - Phorbol 12,13-Dibutyrate -- metabolism KW - Protein Kinase C -- chemistry KW - Isoenzymes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75906670?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+pharmacology&rft.atitle=Characterization+of+ligand+and+substrate+specificity+for+the+calcium-dependent+and+calcium-independent+protein+kinase+C+isozymes.&rft.au=Kazanietz%2C+M+G%3BAreces%2C+L+B%3BBahador%2C+A%3BMischak%2C+H%3BGoodnight%2C+J%3BMushinski%2C+J+F%3BBlumberg%2C+P+M&rft.aulast=Kazanietz&rft.aufirst=M&rft.date=1993-08-01&rft.volume=44&rft.issue=2&rft.spage=298&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmacology&rft.issn=0026895X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-23 N1 - Date created - 1993-09-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Generation of varicella-zoster virus (VZV) and viral mutants from cosmid DNAs: VZV thymidylate synthetase is not essential for replication in vitro. AN - 75906322; 8394020 AB - Four overlapping cosmid clones were constructed that contain the complete genome of the attenuated Oka strain of VZV. Transfection of human melanoma cells with the four cosmids resulted in production of infectious VZV. A double-stranded oligonucleotide, encoding a stop codon in all three open reading frames, was inserted into one of the cosmids at the 5' end of the viral thymidylate synthetase gene. Transfection of melanoma cells with the mutant cosmid, along with the other three cosmids, resulted in VZV that does not express the viral thymidylate synthetase protein. The mutant virus grew at a rate similar to that of the parental Oka strain virus. Production of recombinant VZV using cosmid DNAs will be useful for studying the function of viral genes in VZV replication and establishment of latency. Furthermore, manipulation of the Oka strain of VZV might allow one to produce a vaccine virus that does not establish latency in the central nervous system or a virus that encodes foreign antigens for use as a polyvalent live virus vaccine. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Cohen, J I AU - Seidel, K E AD - Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/08/01/ PY - 1993 DA - 1993 Aug 01 SP - 7376 EP - 7380 VL - 90 IS - 15 SN - 0027-8424, 0027-8424 KW - DNA, Viral KW - 0 KW - Oligodeoxyribonucleotides KW - Viral Structural Proteins KW - Thymidylate Synthase KW - EC 2.1.1.45 KW - Acyclovir KW - X4HES1O11F KW - Index Medicus KW - Humans KW - Cosmids KW - Cloning, Molecular KW - Structure-Activity Relationship KW - Mutagenesis, Site-Directed KW - Base Sequence KW - Acyclovir -- pharmacology KW - Tumor Cells, Cultured KW - Transfection KW - Oligodeoxyribonucleotides -- chemistry KW - In Vitro Techniques KW - Molecular Sequence Data KW - Genes, Viral KW - Viral Structural Proteins -- genetics KW - DNA, Viral -- genetics KW - Virus Replication KW - Thymidylate Synthase -- genetics KW - Herpesvirus 3, Human -- growth & development KW - Herpesvirus 3, Human -- genetics KW - Herpesvirus 3, Human -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75906322?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Generation+of+varicella-zoster+virus+%28VZV%29+and+viral+mutants+from+cosmid+DNAs%3A+VZV+thymidylate+synthetase+is+not+essential+for+replication+in+vitro.&rft.au=Cohen%2C+J+I%3BSeidel%2C+K+E&rft.aulast=Cohen&rft.aufirst=J&rft.date=1993-08-01&rft.volume=90&rft.issue=15&rft.spage=7376&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-07 N1 - Date created - 1993-09-07 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Virol. 1992 Sep;66(9):5298-304 [1323696] Proc Natl Acad Sci U S A. 1986 Jun;83(11):3604-8 [3012520] J Gen Virol. 1986 Sep;67 ( Pt 9):1759-816 [3018124] J Gen Virol. 1987 May;68 ( Pt 5):1449-55 [3033144] Proc Natl Acad Sci U S A. 1987 Jun;84(11):3896-900 [3035557] Nucleic Acids Res. 1988 Mar 25;16(6):2601-12 [2834694] J Virol. 1988 Jun;62(6):2191-5 [2835520] J Virol. 1988 Sep;62(9):3530-5 [3404583] Proc Natl Acad Sci U S A. 1989 Feb;86(3):1051-5 [2536930] J Virol. 1989 May;63(5):2392-5 [2539528] J Virol. 1990 Oct;64(10):4691-6 [2168958] J Gen Virol. 1991 Mar;72 ( Pt 3):475-86 [1848588] J Virol. 1991 May;65(5):2761-5 [1850051] J Gen Virol. 1991 Jun;72 ( Pt 6):1393-9 [1646279] N Engl J Med. 1991 Nov 28;325(22):1545-50 [1658650] J Virol. 1992 Jan;66(1):359-66 [1309252] J Infect Dis. 1992 Aug;166 Suppl 1:S63-8 [1320652] Biken J. 1975 Mar;18(1):25-33 [167707] Infect Immun. 1978 Jan;19(1):199-203 [203532] J Virol. 1981 Nov;40(2):516-25 [6275100] J Virol. 1983 Nov;48(2):377-83 [6312095] J Virol. 1984 Mar;49(3):938-46 [6321774] J Virol. 1992 Dec;66(12):7303-8 [1366099] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Depression of catalase gene expression after immortalization and transformation of mouse liver cells. AN - 75905676; 8353835 AB - To understand the molecular basis of the remarkable decrease of catalase activity after immortalization and malignant transformation of mouse liver cells, expression of the catalase gene was studied in in vivo mouse liver cells and nontransformed normal mouse liver cell line as well as liver cell lines transformed by N-methyl-N-nitro-N-nitrosoguanidine, SV40 virus or by conventional subcultivation. In vivo liver cells had much greater levels of catalase mRNA and immunoreactive protein than in vitro cell lines, which correlates with elevated enzyme activity. Among the cell lines, normal cells had in general higher mRNA levels and more catalase protein than that of the transformed cell lines, also correlating with enzyme activity. The down regulation of catalase gene expression seen in transformed lines may occur transcriptionally rather than posttranscriptionally as demonstrated by cycloheximide and/or actinomycin D treatment. The striking difference in catalase gene expression seen between liver tissue and liver cell lines was unlikely due to gross structural alterations in the catalase gene, but might be explained by a remarkable difference in methylation status of the catalase gene, as demonstrated by Southern blot analysis following HpaII digestion. Our results suggested that during cellular immortalization and malignant transformation, a change in the oxidant stress ultimately led to a cellular response that, in turn, led to down regulation of the catalase gene. JF - Carcinogenesis AU - Sun, Y AU - Colburn, N H AU - Oberley, L W AD - Cell Biology Section, National Cancer Institute, Frederick Cancer Research and Development Center, MD. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 1505 EP - 1510 VL - 14 IS - 8 SN - 0143-3334, 0143-3334 KW - Neoplasm Proteins KW - 0 KW - Catalase KW - EC 1.11.1.6 KW - Index Medicus KW - Animals KW - Down-Regulation -- physiology KW - Neoplasm Proteins -- immunology KW - Neoplasm Proteins -- genetics KW - Transcription, Genetic -- genetics KW - Mice, Nude KW - Mice KW - Cell Line, Transformed KW - Mice, Inbred BALB C KW - Neoplasm Proteins -- metabolism KW - Methylation KW - Cell Line KW - Catalase -- metabolism KW - Liver -- enzymology KW - Liver -- cytology KW - Gene Expression Regulation, Enzymologic -- genetics KW - Cell Transformation, Neoplastic -- metabolism KW - Catalase -- genetics KW - Liver -- physiology KW - Cell Transformation, Neoplastic -- genetics KW - Gene Expression Regulation, Neoplastic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75905676?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Depression+of+catalase+gene+expression+after+immortalization+and+transformation+of+mouse+liver+cells.&rft.au=Sun%2C+Y%3BColburn%2C+N+H%3BOberley%2C+L+W&rft.aulast=Sun&rft.aufirst=Y&rft.date=1993-08-01&rft.volume=14&rft.issue=8&rft.spage=1505&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-21 N1 - Date created - 1993-09-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Effects of the selective sigma receptor ligand, 6-[6-(4-hydroxypiperidinyl)hexyloxy]-3-methylflavone (NPC 16377), on behavioral and toxic effects of cocaine. AN - 75905634; 8355185 AB - Certain sigma receptor ligands have been shown to block locomotor stimulation produced by cocaine at doses that do not have significant behavioral activity when given alone. Using a potent and selective ligand of sigma binding sites, 6-[6-(4-hydroxypiperidinyl)hexyloxy]-3-methylflavone (NPC 16377), we further investigated the influence of sigma ligands on additional behavioral and toxic effects of cocaine in mice. A behaviorally inactive dose of NPC 16377 shifted the dose-effect function for the locomotor stimulant effects of cocaine to the right by a factor of 2.5. A higher dose of NPC 16377 produced an insurmountable blockade of this stimulant effect of cocaine. Prior exposure to cocaine enhances the locomotor stimulant effects of cocaine (sensitization). NPC 16377 prevented the development of cocaine sensitization without producing behavioral effects of its own. However, NPC 16377 was unable to block the expression of sensitization in mice previously exposed to cocaine. NPC 16377 also did not consistently alter the discriminative stimulus effects of cocaine or methamphetamine in rats discriminating either 3 or 10 mg/kg of cocaine, or 1 mg/kg of methamphetamine from saline. The potential phencyclidine-like behavioral effects of NPC 16377 were also evaluated. Unlike the NMDA channel ligand, dizocilpine, NPC 16377 did not increase responding under a fixed-interval schedule of food presentation in rats nor did it substitute for the discriminative stimulus effects of either 1.5 mg/kg of phencyclidine or 0.2 mg/kg of dizocilpine in rats discriminating these drugs from saline. NPC 16377 displayed limited but significant anticonvulsant activity against diazepam-sensitive cocaine convulsions. The lethal effects of higher doses of cocaine were neither significantly blocked nor enhanced in rats or mice with NPC 16377. These findings extend earlier observations on the cocaine-blocking effects of sigma ligands to a novel structure with exceptional selectivity for sigma sites. These data indicate that some sigma ligands may be capable of altering certain behavioral and toxic actions of cocaine without notable behavioral side effects as evidenced in preclinical tests. As such, these compounds may ultimately be useful in the treatment of cocaine abuse. JF - The Journal of pharmacology and experimental therapeutics AU - Witkin, J M AU - Terry, P AU - Menkel, M AU - Hickey, P AU - Pontecorvo, M AU - Ferkany, J AU - Katz, J L AD - Psychobiology Section, National Institute on Drug Abuse, Baltimore, Maryland. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 473 EP - 482 VL - 266 IS - 2 SN - 0022-3565, 0022-3565 KW - Flavonoids KW - 0 KW - Piperidines KW - Receptors, sigma KW - 6-(6-(4-hydroxypiperidinyl)hexyloxy)-3-methylflavone hydrochloride KW - 139652-86-1 KW - Methamphetamine KW - 44RAL3456C KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Seizures -- chemically induced KW - Rats KW - Discrimination Learning -- drug effects KW - Animals KW - Rats, Sprague-Dawley KW - Methamphetamine -- pharmacology KW - Mice KW - Male KW - Conditioning (Psychology) -- drug effects KW - Piperidines -- pharmacology KW - Receptors, sigma -- drug effects KW - Cocaine -- toxicity KW - Motor Activity -- drug effects KW - Flavonoids -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75905634?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.atitle=Effects+of+the+selective+sigma+receptor+ligand%2C+6-%5B6-%284-hydroxypiperidinyl%29hexyloxy%5D-3-methylflavone+%28NPC+16377%29%2C+on+behavioral+and+toxic+effects+of+cocaine.&rft.au=Witkin%2C+J+M%3BTerry%2C+P%3BMenkel%2C+M%3BHickey%2C+P%3BPontecorvo%2C+M%3BFerkany%2C+J%3BKatz%2C+J+L&rft.aulast=Witkin&rft.aufirst=J&rft.date=1993-08-01&rft.volume=266&rft.issue=2&rft.spage=473&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.issn=00223565&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-17 N1 - Date created - 1993-09-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Frequent cocaine users and their use of treatment. AN - 75903735; 8342725 AB - Despite decreases in the number of cocaine users since 1985, the consequences of cocaine use continue to rise. This paper provides descriptive data on frequent cocaine users that will help to explain these diverging trends and enable treatment planners to better predict the types of cocaine users who are likely to seek treatment. Data from the National Household Survey on Drug Abuse were used to study the characteristics of frequent cocaine users since 1985. The 1991 data were used to compare frequent users with infrequent users and nonusers. Since 1985, frequent cocaine users have become older. In 1991, they were likely to be unemployed (32.4%), unmarried (82.3%), and without health insurance (39.4%). Most were cigarette smokers (86.8%) and marijuana users (88.4%), and 32.0% reported getting drunk weekly. Criminal behavior was more likely among frequent cocaine users than among frequent cocaine users than among infrequent users and nonusers. Almost a third (30.0%) reported drug abuse treatment experience in the past year. Despite the recent decreases in overall prevalence of cocaine use, the need for treatment of cocaine abusers will continue. Treatment must address multiple problems that occur in conjunction with cocaine abuse. JF - American journal of public health AU - Gfroerer, J C AU - Brodsky, M D AD - National Institute on Drug Abuse, Rockville, Md. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 1149 EP - 1154 VL - 83 IS - 8 SN - 0090-0036, 0090-0036 KW - Cocaine KW - I5Y540LHVR KW - Abridged Index Medicus KW - Index Medicus KW - Socioeconomic Factors KW - Crime KW - Humans KW - Health Status KW - Health Services -- utilization KW - Adult KW - Child KW - Adolescent KW - United States -- epidemiology KW - Male KW - Female KW - Substance-Related Disorders -- rehabilitation KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75903735?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+public+health&rft.atitle=Frequent+cocaine+users+and+their+use+of+treatment.&rft.au=Gfroerer%2C+J+C%3BBrodsky%2C+M+D&rft.aulast=Gfroerer&rft.aufirst=J&rft.date=1993-08-01&rft.volume=83&rft.issue=8&rft.spage=1149&rft.isbn=&rft.btitle=&rft.title=American+journal+of+public+health&rft.issn=00900036&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-02 N1 - Date created - 1993-09-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Int J Addict. 1990-1991;25(3A):377-409 [2289843] Br J Addict. 1992 Sep;87(9):1345-51 [1392556] Int J Addict. 1992;27(7):817-47 [1618584] JAMA. 1991 Oct 23-30;266(16):2272-3 [1920728] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Evolving risk factors for infectious complications of cancer therapy. AN - 75901292; 8354656 AB - Advances in the supportive care of cancer patients have led to improved long-term outcomes. Infection, however, remains the most significant complication of cancer therapy. The author reviews the impact of new cancer therapies on the risk factors for infectious complications and the impact of therapy on the alterations in host defense. The relative importance of therapy-induced changes are contrasted with immunologic abnormalities associated with specific cancers. In addition, the author contrasts these changes with the infectious complications of human immunodeficiency virus infection, highlighting common themes in immunocompromised patients. JF - Hematology/oncology clinics of North America AU - Chanock, S AD - Pediatric Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 771 EP - 793 VL - 7 IS - 4 SN - 0889-8588, 0889-8588 KW - Anti-Bacterial Agents KW - 0 KW - Antineoplastic Agents KW - Cytokines KW - Index Medicus KW - AIDS/HIV KW - Streptococcal Infections -- etiology KW - Anti-Bacterial Agents -- therapeutic use KW - Acquired Immunodeficiency Syndrome -- complications KW - Cytokines -- therapeutic use KW - Risk Factors KW - Humans KW - Drug Resistance, Microbial KW - Pneumonia, Pneumocystis -- etiology KW - Neutropenia -- chemically induced KW - Infection Control KW - Cross Infection -- prevention & control KW - Antineoplastic Agents -- adverse effects KW - Infection -- etiology KW - Neoplasms -- complications KW - Immunocompromised Host KW - Neoplasms -- etiology KW - Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75901292?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hematology%2Foncology+clinics+of+North+America&rft.atitle=Evolving+risk+factors+for+infectious+complications+of+cancer+therapy.&rft.au=Chanock%2C+S&rft.aulast=Chanock&rft.aufirst=S&rft.date=1993-08-01&rft.volume=7&rft.issue=4&rft.spage=771&rft.isbn=&rft.btitle=&rft.title=Hematology%2Foncology+clinics+of+North+America&rft.issn=08898588&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-21 N1 - Date created - 1993-09-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Ultraviolet-induced mutations in Cockayne syndrome cells are primarily caused by cyclobutane dimer photoproducts while repair of other photoproducts is normal. AN - 75900615; 8346243 AB - We compared the contribution to mutagenesis in Cockayne syndrome (CS) cells of the major class of UV photoproducts, the cyclobutane pyrimidine dimer, to that of other DNA photoproducts by using the mutagenesis shuttle vector pZ189. Lymphoblastoid cell lines from the DNA repair-deficient disorders CS and xeroderma pigmentosum (XP) and a normal line were transfected with UV-treated pZ189. Cyclobutane dimers were selectively removed before transfection by photoreactivation (PR), leaving nondimer photoproducts intact. After UV exposure and replication in CS and XP cells, plasmid survival was abnormally reduced and mutation frequency was abnormally elevated. After PR, plasmid survival increased and mutation frequency in CS cells decreased to normal levels but remained abnormal in XP cells. Sequence analysis of > 200 mutant plasmids showed that with CS cells a major mutational hot spot was caused by unrepaired cyclobutane dimers. These data indicate that with both CS and XP cyclobutane dimers are major photoproducts generating reduced plasmid survival and increased mutation frequency. However, unlike XP, CS cells are proficient in repair of nondimer photoproducts. Since XP but not CS patients have a high frequency of UV-induced skin cancers, our data suggest that prevention of UV-induce skin cancers is associated with proficient repair of nondimer photoproducts. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Parris, C N AU - Kraemer, K H AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/08/01/ PY - 1993 DA - 1993 Aug 01 SP - 7260 EP - 7264 VL - 90 IS - 15 SN - 0027-8424, 0027-8424 KW - supF KW - Pyrimidine Dimers KW - 0 KW - Index Medicus KW - Ultraviolet Rays KW - Genes, Bacterial KW - Base Sequence KW - Cells, Cultured KW - Humans KW - In Vitro Techniques KW - Molecular Sequence Data KW - Xeroderma Pigmentosum -- genetics KW - Plasmids KW - DNA Repair KW - Cockayne Syndrome -- genetics KW - Mutagenesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75900615?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Generation+of+varicella-zoster+virus+%28VZV%29+and+viral+mutants+from+cosmid+DNAs%3A+VZV+thymidylate+synthetase+is+not+essential+for+replication+in+vitro.&rft.au=Cohen%2C+J+I%3BSeidel%2C+K+E&rft.aulast=Cohen&rft.aufirst=J&rft.date=1993-08-01&rft.volume=90&rft.issue=15&rft.spage=7376&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-07 N1 - Date created - 1993-09-07 N1 - Date revised - 2017-01-13 N1 - Gene symbol - supF N1 - SuppNotes - Cited By: Am J Med Genet. 1992 Jan 1;42(1):68-84 [1308368] Biochemistry. 1993 Jan 19;32(2):472-81 [8422356] J Invest Dermatol. 1978 May;70(5):237-9 [641373] Arch Neurol. 1978 Jun;35(6):337-45 [655905] Am J Hum Genet. 1978 Nov;30(6):590-601 [747187] Cancer Res. 1979 Oct;39(10):4237-41 [157803] Mutat Res. 1980 Jan;69(1):107-12 [7360141] Science. 1980 Sep 19;209(4463):1392-6 [6251547] Cancer Res. 1982 Apr;42(4):1473-8 [6174225] Mutat Res. 1982 Dec;106(2):347-56 [6185841] Mutat Res. 1984 Feb;131(2):61-70 [6700618] J Invest Dermatol. 1984 May;82(5):480-4 [6096450] J Biol Chem. 1985 Sep 25;260(21):11438-41 [3900062] Gene. 1985;38(1-3):233-7 [2998945] Cancer Res. 1986 Feb;46(2):1005-9 [3940625] Photochem Photobiol. 1986 May;43(5):509-13 [3526363] Proc Natl Acad Sci U S A. 1986 Sep;83(18):6945-9 [3529093] Proc Natl Acad Sci U S A. 1986 Nov;83(21):8273-7 [3464953] Carcinogenesis. 1987 Jan;8(1):53-7 [3802395] Arch Dermatol. 1987 Feb;123(2):241-50 [3545087] Proc Natl Acad Sci U S A. 1987 Jun;84(11):3782-6 [3473483] Mutat Res. 1989 Mar-May;220(2-3):55-60 [2538741] Mutat Res. 1989 Mar-May;220(2-3):61-72 [2494447] Birth Defects Orig Artic Ser. 1989;25(2):61-82 [2655741] Photodermatol. 1989 Feb;6(1):1-15 [2660122] Photochem Photobiol. 1989 Jun;49(6):805-19 [2672059] J Mol Biol. 1990 Apr 5;212(3):433-6 [2182882] Proc Natl Acad Sci U S A. 1990 Jun;87(12):4707-11 [2352945] Mutat Res. 1991 Jan;254(1):97-105 [1986277] Mutat Res. 1991 Mar;254(2):119-23 [1848350] Br J Dermatol. 1991 May;124(5):453-60 [2039722] Mutat Res. 1991 Nov;255(3):281-91 [1719400] Exp Cell Res. 1992 Aug;201(2):462-9 [1322318] Cancer Res. 1977 Mar;37(3):904-10 [837385] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Mutations in the alpha subunit of eukaryotic translation initiation factor 2 (eIF-2 alpha) that overcome the inhibitory effect of eIF-2 alpha phosphorylation on translation initiation. AN - 75900558; 8102207 AB - Phosphorylation of eIF-2 alpha in Saccharomyces cerevisiae by the protein kinase GCN2 leads to inhibition of general translation initiation and a specific increase in translation of GCN4 mRNA. We isolated mutations in the eIF-2 alpha structural gene that do not affect the growth rate of wild-type yeast but which suppress the toxic effects of eIF-2 alpha hyperphosphorylation catalyzed by mutationally activated forms of GCN2. These eIF-2 alpha mutations also impair translational derepression of GCN4 in strains expressing wild-type GCN2 protein. All four mutations alter single amino acids within 40 residues of the phosphorylation site in eIF-2 alpha; however, three alleles do not decrease the level of eIF-2 alpha phosphorylation. We propose that these mutations alter the interaction between eIF-2 and its recycling factor eukaryotic translation initiation factor 2B (eIF-2B) in a way that diminishes the inhibitory effect of phosphorylated eIF-2 on the essential function of eIF-2B in translation initiation. These mutations may identify a region in eIF-2 alpha that participates directly in a physical interaction with the GCN3 subunit of eIF-2B. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Vazquez de Aldana, C R AU - Dever, T E AU - Hinnebusch, A G AD - Section on Molecular Genetics of Lower Eukaryotes, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/08/01/ PY - 1993 DA - 1993 Aug 01 SP - 7215 EP - 7219 VL - 90 IS - 15 SN - 0027-8424, 0027-8424 KW - Eukaryotic Initiation Factor-2 KW - 0 KW - Guanine Nucleotide Exchange Factors KW - Oligodeoxyribonucleotides KW - Proteins KW - Protein-Serine-Threonine Kinases KW - EC 2.7.11.1 KW - eIF-2 Kinase KW - Index Medicus KW - Gene Expression Regulation, Fungal KW - Base Sequence KW - Protein-Serine-Threonine Kinases -- metabolism KW - Phosphorylation KW - Oligodeoxyribonucleotides -- chemistry KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Proteins -- metabolism KW - Genes, Suppressor KW - Structure-Activity Relationship KW - Saccharomyces cerevisiae -- genetics KW - Peptide Chain Initiation, Translational KW - Eukaryotic Initiation Factor-2 -- metabolism KW - Eukaryotic Initiation Factor-2 -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75900558?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Mutations+in+the+alpha+subunit+of+eukaryotic+translation+initiation+factor+2+%28eIF-2+alpha%29+that+overcome+the+inhibitory+effect+of+eIF-2+alpha+phosphorylation+on+translation+initiation.&rft.au=Vazquez+de+Aldana%2C+C+R%3BDever%2C+T+E%3BHinnebusch%2C+A+G&rft.aulast=Vazquez+de+Aldana&rft.aufirst=C&rft.date=1993-08-01&rft.volume=90&rft.issue=15&rft.spage=7215&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-07 N1 - Date created - 1993-09-07 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Proc Natl Acad Sci U S A. 1993 Jun 1;90(11):5350-4 [8506384] Mol Cell Biol. 1984 Jul;4(7):1326-33 [6095062] J Biol Chem. 1987 Jan 25;262(3):1206-12 [2948954] Methods Enzymol. 1987;154:164-75 [3323810] Microbiol Rev. 1988 Jun;52(2):248-73 [3045517] Proc Natl Acad Sci U S A. 1989 Apr;86(8):2784-8 [2649894] Genetics. 1989 May;122(1):19-27 [2659436] Mol Cell Biol. 1990 Jun;10(6):2820-31 [2188100] Genetics. 1990 Nov;126(3):549-62 [2249755] Mol Cell Biol. 1991 Jan;11(1):486-96 [1986242] Methods Enzymol. 1991;194:195-230 [2005788] Mol Cell Biol. 1991 Jun;11(6):3203-16 [2038326] Mol Cell Biol. 1991 Jun;11(6):3217-28 [2038327] Annu Rev Biochem. 1991;60:717-55 [1883206] Cell. 1992 Feb 7;68(3):585-96 [1739968] EMBO J. 1992 Apr;11(4):1553-62 [1348691] Mol Cell Biol. 1992 Dec;12(12):5801-15 [1448107] Mol Cell Biol. 1993 Mar;13(3):1920-32 [8441423] Proc Natl Acad Sci U S A. 1993 May 15;90(10):4616-20 [8099443] J Bacteriol. 1983 Jan;153(1):163-8 [6336730] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Expression of transduced tropomyosin 1 cDNA suppresses neoplastic growth of cells transformed by the ras oncogene. AN - 75899265; 8346214 AB - Synthesis of certain members of the tropomyosin family of microfilament-associated proteins is suppressed in fibroblasts neoplastically transformed by a number of retroviral oncogenes, by transforming growth factor alpha, and by chemical mutagens. To test whether tropomyosin suppression is a required event in neoplastic transformation, expression of one of two suppressed tropomyosins in NIH 3T3 mouse cells transformed by the ras oncogene was restored by retrovirally mediated cDNA transfer. Cells expressing the inserted cDNA showed partial restoration of microfilament bundle formation (which is typically deranged in transformed cells) together with increased cytoplasmic spreading. More importantly, they lost anchorage-independent growth capability, and the onset of tumor growth in athymic mice was delayed. When tumors arose they no longer expressed the inserted cDNA. These observations support the conclusion that tropomyosin suppression is a necessary event for the expression of components of the transformed phenotype, particularly with respect to anchorage-independent growth and tumorigenesis, which correlate closely with neoplastic potential. This potentially reversible requirement may link different initial events produced by a variety of oncogenic modalities to a common pathway leading to neoplastic growth. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Prasad, G L AU - Fuldner, R A AU - Cooper, H L AD - Cell and Molecular Physiology Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/08/01/ PY - 1993 DA - 1993 Aug 01 SP - 7039 EP - 7043 VL - 90 IS - 15 SN - 0027-8424, 0027-8424 KW - TM1 KW - RNA, Messenger KW - 0 KW - Tropomyosin KW - Index Medicus KW - Animals KW - 3T3 Cells KW - Transfection KW - Neoplasms, Experimental -- genetics KW - In Vitro Techniques KW - Gene Expression KW - Mice, Nude KW - Mice KW - RNA, Messenger -- genetics KW - Cell Division KW - Cell Adhesion KW - Genes, ras KW - Tropomyosin -- metabolism KW - Tropomyosin -- genetics KW - Cell Transformation, Neoplastic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75899265?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Expression+of+transduced+tropomyosin+1+cDNA+suppresses+neoplastic+growth+of+cells+transformed+by+the+ras+oncogene.&rft.au=Prasad%2C+G+L%3BFuldner%2C+R+A%3BCooper%2C+H+L&rft.aulast=Prasad&rft.aufirst=G&rft.date=1993-08-01&rft.volume=90&rft.issue=15&rft.spage=7039&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-07 N1 - Date created - 1993-09-07 N1 - Date revised - 2017-01-13 N1 - Gene symbol - TM1 N1 - SuppNotes - Cited By: Crit Rev Oncog. 1991;2(2):125-60 [1854833] Cancer Res. 1991 Jul 15;51(14):3657-62 [1712245] Biochem Biophys Res Commun. 1991 Jun 28;177(3):1068-75 [2059197] Bioessays. 1991 Sep;13(9):429-37 [1796905] Oncogene. 1992 Mar;7(3):553-61 [1549369] Oncogene. 1992 Apr;7(4):769-73 [1565472] Proc Natl Acad Sci U S A. 1992 May 1;89(9):3952-6 [1570319] J Cell Biol. 1992 Oct;119(2):427-38 [1400584] Proc Natl Acad Sci U S A. 1993 Jan 15;90(2):383-7 [8380636] Cancer Lett. 1993 Feb;68(2-3):95-104 [8443798] J Mol Biol. 1972 Jul 21;68(2):383-7 [5069793] Proc Natl Acad Sci U S A. 1975 Mar;72(3):994-8 [165499] J Cell Biol. 1979 Jul;82(1):1-16 [383723] Proc Natl Acad Sci U S A. 1981 Sep;78(9):5633-7 [6272310] Biochim Biophys Acta. 1982 Apr 29;720(2):154-62 [6282338] Cancer Res. 1982 Dec;42(12):5183-90 [7139623] Cell. 1982 Jul;29(3):791-7 [6817926] Proc Natl Acad Sci U S A. 1983 Sep;80(18):5602-6 [6604274] J Biol Chem. 1983 Nov 25;258(22):13954-64 [6315714] Cell. 1983 May;33(1):153-9 [6678608] CRC Crit Rev Biochem. 1984;16(3):235-305 [6383715] Gene. 1984 Oct;30(1-3):211-7 [6096215] Mol Cell Biol. 1985 May;5(5):972-83 [4000123] Cancer Invest. 1986;4(1):43-60 [3006881] Mol Cell Biol. 1986 Jul;6(7):2721-6 [3785208] Mol Cell Biol. 1986 Nov;6(11):3582-95 [2432392] Annu Rev Cell Biol. 1985;1:353-402 [3030380] Cancer Res. 1987 Aug 15;47(16):4493-500 [3496963] Oncogene Res. 1988;3(1):51-65 [3060798] Prog Clin Biol Res. 1989;288:25-34 [2541449] Anticancer Res. 1989 Sep-Oct;9(5):1367-76 [2556070] Cancer Res. 1990 Apr 1;50(7):2105-12 [2317800] Anticancer Res. 1990 Jan-Feb;10(1):1-22 [2185684] Curr Opin Cell Biol. 1990 Apr;2(2):241-5 [2163659] J Cell Biol. 1990 Jul;111(1):95-102 [2164032] Cancer Treat Res. 1989;47:177-95 [2576997] Acta Physiol Scand Suppl. 1990;592:93-133 [2267948] Cell. 1991 Jan 25;64(2):235-48 [1988146] Cell. 1991 Jan 25;64(2):249-70 [1988147] J Biol Chem. 1991 Mar 25;266(9):5891-7 [2005125] Biochemistry. 1991 Jun 11;30(23):5682-8 [2043610] Curr Opin Biotechnol. 1991 Oct;2(5):708-12 [1367722] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Interleukin 1 induction of the c-jun promoter. AN - 75891268; 8346217 AB - Interleukin 1 (IL-1) induces pleiotropic effects in many cell types during inflammation and immunity. We have recently shown how the IL-1 signal is transmitted to the nucleus: In T cells and in pituitary cells, IL-1 induced genes via activation of the nuclear factor AP-1. We now demonstrate how IL-1 activates the AP-1 factor in liver cells, which are a major target for IL-1 during the acute phase response in vivo. IL-1 induced gene transcription of both AP-1 components, c-jun and c-fos. IL-1 also increased the stability of c-jun mRNA. We define two enhancer sites in the jun promoter that are required for induction by IL-1. Although the binding sites share some similarity with the AP-1 binding site, the nuclear factors binding the jun motifs are not composed of Jun or Fos proteins. Thus these data identify two binding proteins that serve as one of the first nuclear targets for IL-1 signal transduction. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Muegge, K AU - Vila, M AU - Gusella, G L AU - Musso, T AU - Herrlich, P AU - Stein, B AU - Durum, S K AD - Biological Carcinogenesis and Development Program, Program Resources Inc./Dyncorp, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702-1201. Y1 - 1993/08/01/ PY - 1993 DA - 1993 Aug 01 SP - 7054 EP - 7058 VL - 90 IS - 15 SN - 0027-8424, 0027-8424 KW - c-jun KW - jun1 KW - jun2 KW - DNA-Binding Proteins KW - 0 KW - Interleukin-1 KW - Nuclear Proteins KW - Oligodeoxyribonucleotides KW - Proto-Oncogene Proteins c-jun KW - RNA, Messenger KW - Index Medicus KW - Protein Biosynthesis KW - Base Sequence KW - Tumor Cells, Cultured KW - RNA, Messenger -- metabolism KW - Oligodeoxyribonucleotides -- chemistry KW - Humans KW - In Vitro Techniques KW - Molecular Sequence Data KW - Transcription, Genetic KW - Proto-Oncogene Proteins c-jun -- metabolism KW - Nuclear Proteins -- metabolism KW - DNA-Binding Proteins -- metabolism KW - Interleukin-1 -- physiology KW - Promoter Regions, Genetic KW - Gene Expression Regulation KW - Liver -- physiology KW - Genes, jun UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75891268?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Interleukin+1+induction+of+the+c-jun+promoter.&rft.au=Muegge%2C+K%3BVila%2C+M%3BGusella%2C+G+L%3BMusso%2C+T%3BHerrlich%2C+P%3BStein%2C+B%3BDurum%2C+S+K&rft.aulast=Muegge&rft.aufirst=K&rft.date=1993-08-01&rft.volume=90&rft.issue=15&rft.spage=7054&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-07 N1 - Date created - 1993-09-07 N1 - Date revised - 2017-01-13 N1 - Gene symbol - c-jun; jun1; jun2 N1 - SuppNotes - Cited By: Mol Cell Biol. 1987 Jun;7(6):2256-66 [3037355] Mol Cell Biol. 1992 Oct;12(10):4472-7 [1406636] Science. 1988 Jul 29;241(4865):585-9 [2969618] Cell. 1988 Nov 4;55(3):395-7 [3141060] Cell. 1988 Dec 2;55(5):875-85 [3142689] Anal Biochem. 1988 Oct;174(1):209-14 [3218734] Nature. 1989 Feb 16;337(6208):661-3 [2537468] Mol Cell Biol. 1989 Mar;9(3):959-64 [2542770] Science. 1989 Oct 13;246(4927):249-51 [2799385] Cell. 1989 Dec 22;59(6):979-86 [2513128] EMBO J. 1990 Jun;9(6):1897-906 [2112087] Eur J Biochem. 1990 Aug 28;192(1):75-9 [2169419] Mol Cell Biol. 1990 Nov;10(11):5857-64 [2172787] Proc Natl Acad Sci U S A. 1990 Oct;87(20):7871-4 [1978316] New Biol. 1989 Dec;1(3):239-46 [2487289] Mol Endocrinol. 1990 Jul;4(7):973-80 [2178224] New Biol. 1990 Feb;2(2):143-50 [2150599] Mol Cell Biol. 1991 May;11(5):2804-11 [1901948] J Biol Chem. 1991 May 25;266(15):9363-6 [1851743] Nature. 1991 Oct 17;353(6345):670-4 [1922387] J Biol Chem. 1991 Nov 25;266(33):22661-70 [1658005] Biochemistry. 1979 Nov 27;18(24):5294-9 [518835] Nucleic Acids Res. 1992 Feb 25;20(4):897-902 [1542579] Photochem Photobiol. 1992 Mar;55(3):409-15 [1561239] Annu Rev Biochem. 1992;61:1053-95 [1497306] Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] Nature. 1984 Oct 4-10;311(5985):433-8 [6090941] FEBS Lett. 1985 Oct 21;191(1):7-12 [2996929] Mol Cell Biol. 1985 Oct;5(10):2866-9 [3879767] Cell. 1987 Jun 19;49(6):729-39 [3034432] Cell. 1987 Jun 19;49(6):741-52 [3034433] DNA. 1988 Jan-Feb;7(1):47-55 [3349904] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Chromatin disruption in the promoter of human immunodeficiency virus type 1 during transcriptional activation. AN - 75889653; 8344262 AB - Chromatin organization of eukaryotic promoters is increasingly recognized as an important factor in the regulation of transcription in vivo. To determine the role of chromatin in HIV-1 expression, we have examined the nucleosome organization of the promoter of HIV-1 under low and high transcription rates. Independently of the cell line examined, nucleosomes are precisely positioned in the viral 5' long terminal repeat (5' LTR) and define two large nucleosome-free regions encompassing nt 200-450 and 610-720. A nucleosome positioned between these two regions, immediately after the transcription initiation site (nuc-1), is disrupted following TPA or TNF-alpha treatment. The disruption of nuc-1 from DNA is independent of DNA replication since it is completed in 20 min and independent of transcription as it is alpha-amanitin insensitive. A model is proposed in which nuc-1 plays an organizing role in the HIV-1 promoter to bring in close proximity factors bound to DNA in the two nucleosome-free regions, upstream and downstream of the site of transcription initiation. These results define chromatin as an integral component of the HIV-1 transcriptional regulatory machinery and identify a chromatin transition associated with activation of viral gene expression. JF - The EMBO journal AU - Verdin, E AU - Paras, P AU - Van Lint, C AD - Laboratory of Viral and Molecular Pathogenesis, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD 20892. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 3249 EP - 3259 VL - 12 IS - 8 SN - 0261-4189, 0261-4189 KW - Alkylating Agents KW - 0 KW - Amanitins KW - Chromatin KW - DNA, Viral KW - Nucleosomes KW - Sulfuric Acid Esters KW - Deoxyribonuclease I KW - EC 3.1.21.1 KW - Micrococcal Nuclease KW - EC 3.1.31.1 KW - dimethyl sulfate KW - JW5CW40Z50 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - AIDS/HIV KW - Alkylating Agents -- pharmacology KW - HIV Long Terminal Repeat -- genetics KW - Nucleosomes -- metabolism KW - Sulfuric Acid Esters -- pharmacology KW - Deoxyribonuclease I -- pharmacology KW - Base Sequence KW - Amanitins -- pharmacology KW - Restriction Mapping KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Micrococcal Nuclease -- pharmacology KW - Cell Line KW - DNA Replication KW - HIV-1 -- genetics KW - Promoter Regions, Genetic KW - Transcriptional Activation -- physiology KW - Chromatin -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75889653?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+EMBO+journal&rft.atitle=Chromatin+disruption+in+the+promoter+of+human+immunodeficiency+virus+type+1+during+transcriptional+activation.&rft.au=Verdin%2C+E%3BParas%2C+P%3BVan+Lint%2C+C&rft.aulast=Verdin&rft.aufirst=E&rft.date=1993-08-01&rft.volume=12&rft.issue=8&rft.spage=3249&rft.isbn=&rft.btitle=&rft.title=The+EMBO+journal&rft.issn=02614189&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-08 N1 - Date created - 1993-09-08 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Virol. 1991 Sep;65(9):4645-53 [1678437] Annu Rev Biochem. 1991;60:577-630 [1883204] J Virol. 1991 Dec;65(12):6790-9 [1942252] Science. 1991 Nov 8;254(5033):815-20 [1658933] Cell. 1991 Nov 29;67(5):833-6 [1959130] Nature. 1992 Jan 16;355(6357):219-24 [1731219] EMBO J. 1991 Mar;10(3):607-15 [2001676] Trends Genet. 1991 Jan;7(1):9-14 [2003337] New Biol. 1990 Jan;2(1):20-31 [2078551] Genes Dev. 1991 Apr;5(4):683-96 [2010092] New Biol. 1989 Nov;1(2):127-35 [2562218] Cell. 1991 Apr 19;65(2):241-8 [2015625] J Virol. 1992 Mar;66(3):1809-13 [1738210] Nucleic Acids Res. 1992 Jan 25;20(2):273-8 [1311071] Proc Natl Acad Sci U S A. 1992 Feb 15;89(4):1229-33 [1741376] J Virol. 1992 Jul;66(7):4488-96 [1602555] AIDS. 1992 Apr;6(4):347-63 [1616633] Curr Opin Genet Dev. 1992 Apr;2(2):293-8 [1638124] Cell. 1992 Oct 2;71(1):11-22 [1394427] Cell. 1992 Nov 27;71(5):853-64 [1423633] Trends Genet. 1992 Nov;8(11):365-8 [1440870] Science. 1992 Dec 11;258(5089):1780-4 [1465613] Cell. 1993 Jan 15;72(1):73-84 [8422685] EMBO J. 1993 Feb;12(2):423-33 [8440235] EMBO J. 1987 Aug;6(8):2321-8 [2822386] Science. 1987 Nov 6;238(4828):800-2 [3313729] Nature. 1987 Dec 3-9;330(6147):489-93 [2825027] EMBO J. 1987 Dec 1;6(12):3761-70 [3428273] EMBO J. 1988 Jul;7(7):2221-8 [3046934] Annu Rev Biochem. 1988;57:159-97 [3052270] Genes Dev. 1988 Sep;2(9):1101-14 [2847959] J Biol Chem. 1988 Dec 25;263(36):19259-62 [3198625] Cell. 1988 Dec 23;55(6):1137-45 [2849508] J Immunol. 1989 Jan 15;142(2):431-8 [2463307] Proc Natl Acad Sci U S A. 1989 Apr;86(7):2336-40 [2494664] Nature. 1989 May 4;339(6219):70-3 [2654643] J Virol. 1989 Aug;63(8):3213-9 [2545899] Cell. 1989 Jul 14;58(1):27-36 [2502314] Methods Enzymol. 1989;170:269-89 [2770542] EMBO J. 1989 Aug;8(8):2343-51 [2792088] J Virol. 1989 Nov;63(11):4919-24 [2795721] Science. 1989 Nov 10;246(4931):780-6 [2814500] Genes Dev. 1989 Nov;3(11):1814-22 [2558048] Nature. 1990 Jan 25;343(6256):387-9 [2405281] Bioessays. 1992 Sep;14(9):597-603 [1365915] J Mol Biol. 1984 Jul 15;176(4):535-57 [6086935] Cell. 1984 Aug;38(1):29-38 [6088072] Cell. 1985 Jul;41(3):813-23 [2988790] J Biol Chem. 1985 Dec 5;260(28):15318-24 [2415517] Science. 1986 May 9;232(4751):755-9 [3008338] J Exp Med. 1986 Jul 1;164(1):280-90 [3014036] Mol Cell Biol. 1986 Mar;6(3):779-91 [3022129] EMBO J. 1986 Oct;5(10):2689-96 [3536481] Cell. 1987 Apr 24;49(2):203-10 [3568125] J Mol Biol. 1987 May 5;195(1):143-73 [3656408] Cell. 1990 Mar 9;60(5):719-31 [2155706] J Biol Chem. 1990 Apr 5;265(10):5736-46 [2180934] J Mol Biol. 1990 Apr 5;212(3):481-93 [2325130] Immunol Today. 1990 May;11(5):176-80 [2186752] Nucleic Acids Res. 1990 May 11;18(9):2739-47 [2339060] Annu Rev Immunol. 1990;8:453-75 [2188670] Cell. 1990 Jun 29;61(7):1271-6 [2364429] EMBO J. 1990 Aug;9(8):2523-8 [2196175] Proc Natl Acad Sci U S A. 1990 Oct;87(19):7405-9 [2170977] Cell. 1990 Nov 16;63(4):655-7 [2225069] Genes Dev. 1990 Dec;4(12A):2061-74 [2269426] Genes Dev. 1990 Dec;4(12B):2397-408 [2149119] New Biol. 1990 Aug;2(8):712-8 [2282368] Proc Natl Acad Sci U S A. 1991 May 1;88(9):4045-9 [2023953] Genes Dev. 1991 May;5(5):820-6 [1851121] Genes Dev. 1991 Jun;5(6):1102-13 [2044957] Proc Natl Acad Sci U S A. 1991 Jul 1;88(13):5670-4 [2062845] Genes Dev. 1991 Jul;5(7):1285-98 [2065977] J Virol. 1991 Aug;65(8):4350-8 [2072454] EMBO J. 1991 Sep;10(9):2569-76 [1678348] Erratum In: EMBO J 1993 Dec;12(12):4900 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Lack of effect of carcinogen treatment on development of tumors arising spontaneously in Fischer 344 rats. AN - 75888819; 8345536 AB - The incidence of a set of neoplasms arising "spontaneously" in Fischer 344 (F344) rats was determined in control and carcinogen-treated animals. Data were obtained from approximately 9000 rats (4000 males and 5000 females) used to study the carcinogenicity of a variety of alkylating compounds, including N-nitroso compounds, azoxyalkanes, and triazenes. In these experiments treated rats and controls were allowed to die naturally and were necropsied, and the tissues were examined histopathologically. The spontaneous neoplasms of interest were mononuclear cell leukemia and neoplasms of the anterior pituitary, adrenal medulla, pancreas, thyroid gland, mammary gland, and testis. These tumors were generally absent from control animals that (rarely) died before 70 wk of age. Although many carcinogen-treated rats died early with treatment-related tumors, a substantial number (1700 males and 2300 females) survived as long as controls. The incidence of spontaneous neoplasms was determined among controls and chemically treated rats at 10-wk intervals from 0 to 140 wk. The incidence of spontaneous tumors was not higher and was frequently statistically lower among treated rats than the corresponding incidence in controls, with the exception of leukemia in female rats. The same result was obtained with the subset of carcinogens not requiring metabolic activation (mostly alkylnitrosoureas). These data indicate that in this rat tumor model system, the alkylating carcinogens, while capable collectively of tumor induction at more than 20 sites, did not accelerate the development of any of the six spontaneously arising solid tumors. This suggests that these spontaneous tumors might arise by a mechanism that is unresponsive to the actions of the alkylating carcinogens. JF - Journal of toxicology and environmental health AU - Lijinsky, W AU - Riggs, C W AU - Walters, P T AD - ABL-Basic Research Program, NCI Frederick Cancer Research and Development Center, Maryland. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 527 EP - 538 VL - 39 IS - 4 SN - 0098-4108, 0098-4108 KW - Carcinogens KW - 0 KW - Nitroso Compounds KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Databases, Factual KW - Nitroso Compounds -- toxicity KW - Male KW - Female KW - Neoplasms, Experimental -- chemically induced KW - Carcinogens -- toxicity KW - Neoplasms, Experimental -- mortality KW - Neoplasms, Experimental -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75888819?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+toxicology+and+environmental+health&rft.atitle=Lack+of+effect+of+carcinogen+treatment+on+development+of+tumors+arising+spontaneously+in+Fischer+344+rats.&rft.au=Lijinsky%2C+W%3BRiggs%2C+C+W%3BWalters%2C+P+T&rft.aulast=Lijinsky&rft.aufirst=W&rft.date=1993-08-01&rft.volume=39&rft.issue=4&rft.spage=527&rft.isbn=&rft.btitle=&rft.title=Journal+of+toxicology+and+environmental+health&rft.issn=00984108&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-08 N1 - Date created - 1993-09-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Hippocampal neurons exhibit cyclothiazide-sensitive rapidly desensitizing responses to kainate. AN - 75879524; 7688040 AB - In whole-cell recordings from mammalian CNS neurons, AMPA-preferring glutamate receptors exhibit strong desensitization in response to AMPA, glutamate, and quisqualate, but not to kainate or domoate. Such desensitization is reduced by lectins, by the nootropic drug aniracetam, and by diazoxide. None of these compounds strongly modulate responses to kainate and domoate, consistent with the apparent lack of desensitization to these agonists. We now report experiments on hippocampal neurons in which responses to kainate were strongly potentiated by cyclothiazide, a benzothiadiazine diuretic and antihypertensive drug structurally related to diazoxide. Cyclothiazide increased the maximum response to a saturating concentration of kainate by approximately 300% and produced a shift to the left in the kainate dose-response curve. Because cyclothiazide was considerably more effective than aniracetam in reducing desensitization evoked by glutamate, we tested the possibility that potentiation of responses to kainate was due to block of a previously undetected component of desensitization in the response to kainate itself. In outside-out patches responses to rapid perfusion of 3 mM kainate showed 34% desensitization, the onset of which developed with a time constant of 2.2 msec. Desensitization of responses to kainate was abolished by 100 microM cyclothiazide, as was the much stronger desensitization evoked by glutamate and AMPA. Cyclothiazide also slowed the rate of deactivation of responses to kainate recorded after return to agonist-free solution. Current-voltage plots for control responses to kainate exhibited outward rectification that was associated with a reduction in the amount of desensitization on depolarization. Both effects were absent in the presence of cyclothiazide, suggesting that rectification of responses to kainate was due to the voltage dependence of desensitization. The complete block of desensitization produced by cyclothiazide provides a powerful new tool for analysis of allosteric regulatory mechanisms at AMPA-preferring glutamate receptors. JF - The Journal of neuroscience : the official journal of the Society for Neuroscience AU - Patneau, D K AU - Vyklicky, L AU - Mayer, M L AD - Laboratory of Cellular and Molecular Neurophysiology, NICHD, NIH, Bethesda, Maryland 20892. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 3496 EP - 3509 VL - 13 IS - 8 SN - 0270-6474, 0270-6474 KW - Benzothiadiazines KW - 0 KW - Glutamates KW - Ibotenic Acid KW - 2552-55-8 KW - Glutamic Acid KW - 3KX376GY7L KW - alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid KW - 77521-29-0 KW - Quisqualic Acid KW - 8OC22C1B99 KW - cyclothiazide KW - P71U09G5BW KW - Kainic Acid KW - SIV03811UC KW - Index Medicus KW - Animals KW - Dose-Response Relationship, Drug KW - Electrophysiology KW - Ibotenic Acid -- pharmacology KW - Rats KW - Quisqualic Acid -- pharmacology KW - Animals, Newborn KW - Drug Tolerance KW - Rats, Sprague-Dawley KW - Cells, Cultured KW - Evoked Potentials KW - Glutamates -- pharmacology KW - Ibotenic Acid -- analogs & derivatives KW - Kinetics KW - Drug Synergism KW - Kainic Acid -- pharmacology KW - Hippocampus -- physiology KW - Benzothiadiazines -- pharmacology KW - Neurons -- drug effects KW - Hippocampus -- cytology KW - Neurons -- physiology KW - Hippocampus -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75879524?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+neuroscience+%3A+the+official+journal+of+the+Society+for+Neuroscience&rft.atitle=Hippocampal+neurons+exhibit+cyclothiazide-sensitive+rapidly+desensitizing+responses+to+kainate.&rft.au=Patneau%2C+D+K%3BVyklicky%2C+L%3BMayer%2C+M+L&rft.aulast=Patneau&rft.aufirst=D&rft.date=1993-08-01&rft.volume=13&rft.issue=8&rft.spage=3496&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+neuroscience+%3A+the+official+journal+of+the+Society+for+Neuroscience&rft.issn=02706474&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-02 N1 - Date created - 1993-09-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - ENU-induced mutagenesis at a single A: T base pair in transgenic mice containing phi X174. AN - 75879106; 7688099 AB - Transgenic mice containing the bacteriophage phi X174 am3 as a chromosomally integrated and recoverable marker for in vivo mutation have been produced to measure spontaneous and induced substitutions at an A:T base pair among single copies. phi X174 was chosen for its small size (5 kb), unique sequence, and the opportunity to take advantage of previously reported in vitro data on mutation and repair; the am3 site provides sequence specificity in a reversion assay for mutation of an A:T base pair. Inbred C57Bl/6 mice have been made homozygous for approximately 100 copies of the the phage sequence without any apparent detrimental effects on the homozygous individuals. Recoveries of phage from mouse tissues are in the range of 1-5 x 10(7) PFU per micrograms mouse DNA; both recovery and mutation are independent of endogenous CpG methylation. Background mutation frequencies are 2-4 x 10(-7) among phage recovered from liver, brain, spleen, and kidney. Adult mice were treated with 200 mg/kg N-ethyl-N-nitrosourea, and phage were recovered at 2 and 14 days after treatment. At 2 days after treatment we observed a slight increase only among phage isolated from the brain of one mouse out of four. At 14 days after ENU treatment, there were significant increases in mutation frequencies among phage recovered from the liver (6 x) and spleen (10 x). These results demonstrate (1) response of a single A:T base pair to alkylation-induced mutation in a nonexpressed gene, (2) the role of cell proliferation in somatic mutagenesis, and (3) provide a model for a transgenic approach for study of site-specific mutagenesis in vivo in higher eukaryotes. JF - Mutation research AU - Burkhart, J G AU - Burkhart, B A AU - Sampson, K S AU - Malling, H V AD - Laboratory of Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 69 EP - 81 VL - 292 IS - 1 SN - 0027-5107, 0027-5107 KW - Dinucleoside Phosphates KW - 0 KW - Mutagens KW - cytidylyl-3'-5'-guanosine KW - 2382-65-2 KW - DNA KW - 9007-49-2 KW - Adenine KW - JAC85A2161 KW - Ethylnitrosourea KW - P8M1T4190R KW - Thymine KW - QR26YLT7LT KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Animals KW - Base Sequence KW - Homozygote KW - Molecular Sequence Data KW - Mice, Inbred C57BL KW - Mice KW - Dinucleoside Phosphates -- metabolism KW - Mice, Transgenic KW - Methylation KW - Male KW - Female KW - Bacteriophage phi X 174 -- isolation & purification KW - Mutagenicity Tests KW - Ethylnitrosourea -- toxicity KW - Mutagens -- toxicity KW - Bacteriophage phi X 174 -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75879106?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutation+research&rft.atitle=ENU-induced+mutagenesis+at+a+single+A%3A+T+base+pair+in+transgenic+mice+containing+phi+X174.&rft.au=Burkhart%2C+J+G%3BBurkhart%2C+B+A%3BSampson%2C+K+S%3BMalling%2C+H+V&rft.aulast=Burkhart&rft.aufirst=J&rft.date=1993-08-01&rft.volume=292&rft.issue=1&rft.spage=69&rft.isbn=&rft.btitle=&rft.title=Mutation+research&rft.issn=00275107&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-30 N1 - Date created - 1993-08-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Current dosage and schedule issues in the development of paclitaxel (Taxol). AN - 75864441; 8102016 AB - Basic questions regarding optimal dose and schedule of anticancer drug administration frequently persist long after regulatory approval and commercial availability of a drug. For paclitaxel (TAXOL), these questions were considered early in drug development. This paper reviews the available preclinical studies that assessed different drug concentrations and durations of drug exposure. The current status of clinical trials designed to help resolve these issues is also reviewed. JF - Seminars in oncology AU - Arbuck, S G AU - Canetta, R AU - Onetto, N AU - Christian, M C AD - Developmental Chemotherapy Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 31 EP - 39 VL - 20 IS - 4 Suppl 3 SN - 0093-7754, 0093-7754 KW - Paclitaxel KW - P88XT4IS4D KW - Index Medicus KW - Animals KW - Bone Marrow Diseases -- chemically induced KW - Dose-Response Relationship, Drug KW - Humans KW - Clinical Trials as Topic KW - Mice KW - Microtubules -- drug effects KW - Peripheral Nervous System Diseases -- chemically induced KW - Rats KW - Drug Evaluation KW - Drug Hypersensitivity -- etiology KW - Dogs KW - Time Factors KW - Drug Evaluation, Preclinical KW - Paclitaxel -- administration & dosage KW - Neoplasms -- drug therapy KW - Paclitaxel -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75864441?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Seminars+in+oncology&rft.atitle=Current+dosage+and+schedule+issues+in+the+development+of+paclitaxel+%28Taxol%29.&rft.au=Arbuck%2C+S+G%3BCanetta%2C+R%3BOnetto%2C+N%3BChristian%2C+M+C&rft.aulast=Arbuck&rft.aufirst=S&rft.date=1993-08-01&rft.volume=20&rft.issue=4+Suppl+3&rft.spage=31&rft.isbn=&rft.btitle=&rft.title=Seminars+in+oncology&rft.issn=00937754&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-27 N1 - Date created - 1993-08-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Suppression of arthritis by an inhibitor of nitric oxide synthase. AN - 75862262; 7688035 AB - Nitric oxide (NO), a toxic radical gas produced during the metabolism of L-arginine by NO synthase (NOS), has been implicated as a mediator of immune and inflammatory responses. A single injection of streptococcal cell wall fragments (SCW) induces the accumulation of inflammatory cells within the synovial tissue and a cell-mediated immune response that leads destructive lesions. We show here that NO production is elevated in the inflamed joints of SCW-treated rats. Administration of NG-monomethyl-L-arginine, an inhibitor of NOS, profoundly reduced the synovial inflammation and tissue damage as measured by an articular index and reflected in the histopathology. These studies implicate the NO pathway in the pathogenesis of an inflammatory arthritis and demonstrate the ability of a NOS inhibitor to modulate the disease. JF - The Journal of experimental medicine AU - McCartney-Francis, N AU - Allen, J B AU - Mizel, D E AU - Albina, J E AU - Xie, Q W AU - Nathan, C F AU - Wahl, S M AD - Laboratory of Immunology, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/08/01/ PY - 1993 DA - 1993 Aug 01 SP - 749 EP - 754 VL - 178 IS - 2 SN - 0022-1007, 0022-1007 KW - omega-N-Methylarginine KW - 27JT06E6GR KW - Nitric Oxide KW - 31C4KY9ESH KW - Arginine KW - 94ZLA3W45F KW - Nitric Oxide Synthase KW - EC 1.14.13.39 KW - Amino Acid Oxidoreductases KW - EC 1.4.- KW - Index Medicus KW - Streptococcus KW - Rats KW - Acute Disease KW - Animals KW - Rats, Sprague-Dawley KW - Culture Techniques KW - Cell Wall KW - Nitric Oxide -- metabolism KW - Synovial Membrane -- metabolism KW - Female KW - Synovial Membrane -- pathology KW - Arginine -- therapeutic use KW - Arthritis -- etiology KW - Amino Acid Oxidoreductases -- antagonists & inhibitors KW - Arthritis -- drug therapy KW - Arginine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75862262?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+experimental+medicine&rft.atitle=Suppression+of+arthritis+by+an+inhibitor+of+nitric+oxide+synthase.&rft.au=McCartney-Francis%2C+N%3BAllen%2C+J+B%3BMizel%2C+D+E%3BAlbina%2C+J+E%3BXie%2C+Q+W%3BNathan%2C+C+F%3BWahl%2C+S+M&rft.aulast=McCartney-Francis&rft.aufirst=N&rft.date=1993-08-01&rft.volume=178&rft.issue=2&rft.spage=749&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+experimental+medicine&rft.issn=00221007&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-30 N1 - Date created - 1993-08-30 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Science. 1987 Jan 23;235(4787):473-6 [2432665] Proc Natl Acad Sci U S A. 1993 Apr 1;90(7):3024-7 [7681993] Am J Physiol. 1988 Apr;254(4 Pt 1):E459-67 [3354662] J Immunol. 1988 Oct 1;141(7):2407-12 [3139757] Proc Natl Acad Sci U S A. 1990 May;87(9):3629-32 [2333306] J Immunol. 1990 Oct 1;145(7):2220-6 [2144548] Rheum Dis Clin North Am. 1990 Aug;16(3):513-37 [2217956] J Immunol. 1991 Feb 15;146(4):1294-302 [1991968] J Immunol. 1991 Apr 15;146(8):2719-23 [1707918] J Immunol. 1991 Jul 1;147(1):144-8 [1904899] Proc Natl Acad Sci U S A. 1991 Jun 1;88(11):4651-5 [1675786] Pharmacol Rev. 1991 Jun;43(2):109-42 [1852778] Biochem Biophys Res Commun. 1991 Aug 15;178(3):913-20 [1831356] J Immunol. 1991 Oct 15;147(8):2559-64 [1655894] J Immunol. 1991 Dec 1;147(11):3915-20 [1658153] Agents Actions Suppl. 1991;35:29-34 [1781421] Biochem J. 1992 Feb 1;281 ( Pt 3):627-30 [1371384] Proc Natl Acad Sci U S A. 1992 Mar 15;89(6):2051-5 [1372433] Science. 1992 Apr 10;256(5054):225-8 [1373522] J Exp Med. 1992 Jul 1;176(1):303-7 [1319459] J Clin Invest. 1992 Aug;90(2):679-83 [1379617] FASEB J. 1992 Sep;6(12):3051-64 [1381691] Inflammation. 1992 Aug;16(4):295-305 [1526662] J Biol Chem. 1992 Dec 5;267(34):24173-6 [1280257] Ann Rheum Dis. 1992 Nov;51(11):1219-22 [1466599] Anal Biochem. 1987 Apr;162(1):156-9 [2440339] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Synergistic increase of phorbol ester-induced c-fos mRNA expression by retinoic acid through stabilization of the c-fos message. AN - 75859347; 8336949 AB - Retinoic acid (RA) has been shown to be able to antagonize or synergize with phorbol 12-myristate 13-acetate (PMA). In contrast to its antagonistic effects on PMA-dependent gene expression, no molecular target or mechanism of synergism has been characterized yet. We now report, that RA synergistically enhances the induction of c-fos, but not c-jun mRNA by PMA in cells whose growth was stimulated by RA alone. The responding cells were hybrids of tumor cell lines whose growth and PMA-dependent c-fos mRNA expression remained unaffected by RA. The increase in PMA-dependent c-fos expression required pretreatment of cells with RA for at least 2-4 h and was achieved at doses as low as 10(-10) M. Nuclear run-on experiments and transient transfection assays using a chimeric reporter gene construct with sequences from the c-fos promoter indicated that RA did not affect PMA-dependent c-fos transcription. Instead, RA stabilized the c-fos message after induction by PMA as assessed by measuring the half-life of c-fos mRNA in actinomycin D-treated cells. This post-transcriptional regulation provides a mechanism whereby RA can synergistically enhance gene expression by PMA. JF - Oncogene AU - Busam, K J AU - Geiser, A G AU - Roberts, A B AU - Sporn, M B AD - Laboratory of Chemoprevention, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 2267 EP - 2273 VL - 8 IS - 8 SN - 0950-9232, 0950-9232 KW - c-fos KW - RNA, Messenger KW - 0 KW - Tretinoin KW - 5688UTC01R KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Tumor Cells, Cultured KW - Dose-Response Relationship, Drug KW - Humans KW - Transcription, Genetic KW - Drug Synergism KW - Genes, jun KW - Tretinoin -- pharmacology KW - RNA, Messenger -- analysis KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Genes, fos KW - Gene Expression Regulation -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75859347?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncogene&rft.atitle=Synergistic+increase+of+phorbol+ester-induced+c-fos+mRNA+expression+by+retinoic+acid+through+stabilization+of+the+c-fos+message.&rft.au=Busam%2C+K+J%3BGeiser%2C+A+G%3BRoberts%2C+A+B%3BSporn%2C+M+B&rft.aulast=Busam&rft.aufirst=K&rft.date=1993-08-01&rft.volume=8&rft.issue=8&rft.spage=2267&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=09509232&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-25 N1 - Date created - 1993-08-25 N1 - Date revised - 2017-01-13 N1 - Gene symbol - c-fos N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Polycyclic aromatic hydrocarbon-DNA adducts in human lung and cancer susceptibility genes. AN - 75858591; 8339251 AB - Molecular dosimetry for polycyclic aromatic hydrocarbon-DNA adducts, genetic predisposition to cancer, and their interrelationships are under study in numerous laboratories. This report describes a modified 32P-postlabeling assay for the detection of polycyclic aromatic hydrocarbon-DNA adducts that uses immunoaffinity chromatography to enhance chemical specificity and quantitative reliability. The assay incorporates internal standards to determine direct molar ratios of adducts to unmodified nucleotides and to assess T4 polynucleotide kinase labeling efficiency. High performance liquid chromatography is used to assure adequacy of DNA enzymatic digestion. The assay was validated using radiolabeled benzo(a)pyrene-diol-epoxide modified DNA (r = 0.76, P < 0.05) thereby assessing all variables from enzymatic digestion to detection. Thirty-eight human lung samples were examined and adducts were detected in seven. A subset of samples also was examined for benzo(a)pyrene-diol-epoxide-DNA adducts by immunoaffinity chromatography, high performance liquid chromatography, and synchronous fluorescence spectroscopy. A high correlation between the two assays was found (P = 0.006). The lung samples were then analyzed by the polymerase chain reaction for the presence of mutations in the cytochrome P-450 (CYP) 1A1 and glutathione S-transferase mu (GST mu) genes. A positive association was identified for adduct levels and GST mu null genotypes (P = 0.038). No correlation was found between polycyclic aromatic hydrocarbon-adduct levels and CYP1A1 exon 7 mutations. Age, race, and serum cotinine were not related to adduct levels. Multivariate analysis indicated that only the GST mu genotype was associated with polycyclic aromatic hydrocarbon-DNA adduct levels. This work demonstrates that the 32P-postlabeling assay can be modified for chemically specific adduct detection and that it can be used in the assessment of potentially important genetic factors for cancer risk. The absence of a functional GST mu gene in humans is likely one such factor. JF - Cancer research AU - Shields, P G AU - Bowman, E D AU - Harrington, A M AU - Doan, V T AU - Weston, A AD - Laboratory of Human Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1993/08/01/ PY - 1993 DA - 1993 Aug 01 SP - 3486 EP - 3492 VL - 53 IS - 15 SN - 0008-5472, 0008-5472 KW - CYPA1 KW - GST&mgr; KW - DNA Adducts KW - 0 KW - Polycyclic Compounds KW - benzo(a)pyrene-7,8-dihydrodiol-9,10-epoxide-DNA KW - 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide KW - 55097-80-8 KW - 7,8-dihydroxy-9,10-epoxide-7,8,9,10-tetrahydrobenzo(a)pyrene-10-deoxyguanosine KW - 62698-04-8 KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Glutathione Transferase KW - EC 2.5.1.18 KW - Deoxyguanosine KW - G9481N71RO KW - Index Medicus KW - Genotype KW - Base Sequence KW - Disease Susceptibility KW - Polymorphism, Genetic KW - Humans KW - Molecular Sequence Data KW - Deoxyguanosine -- analysis KW - Mutation KW - Deoxyguanosine -- analogs & derivatives KW - 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide -- analogs & derivatives KW - 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide -- analysis KW - Cytochrome P-450 Enzyme System -- genetics KW - DNA -- metabolism KW - Lung -- chemistry KW - DNA -- analysis KW - Glutathione Transferase -- genetics KW - Polycyclic Compounds -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75858591?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Polycyclic+aromatic+hydrocarbon-DNA+adducts+in+human+lung+and+cancer+susceptibility+genes.&rft.au=Shields%2C+P+G%3BBowman%2C+E+D%3BHarrington%2C+A+M%3BDoan%2C+V+T%3BWeston%2C+A&rft.aulast=Shields&rft.aufirst=P&rft.date=1993-08-01&rft.volume=53&rft.issue=15&rft.spage=3486&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-02 N1 - Date created - 1993-09-02 N1 - Date revised - 2017-01-13 N1 - Gene symbol - CYPA1; GST&mgr; N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Chimeric tick-borne encephalitis and dengue type 4 viruses: effects of mutations on neurovirulence in mice. AN - 75858358; 8331735 AB - Two new chimeric flaviviruses were constructed from full-length cDNAs that contained tick-borne encephalitis virus (TBEV) CME or ME structural protein genes and the remaining genes derived from dengue type 4 virus (DEN4). Studies involving mice inoculated intracerebrally with the ME chimeric virus indicated that it retained the neurovirulence of its TBEV parent from which its pre-M and E genes were derived. However, unlike parental TBEV, the chimeric virus did not produce encephalitis when mice were inoculated peripherally, indicating a loss of neuroinvasiveness. In the present study, the ME chimeric virus (vME) was subjected to mutational analysis in an attempt to reduce or ablate neurovirulence measured by direct inoculation of virus into the brain. We identified three distinct mutations that were each associated independently with a significant reduction of mouse neurovirulence of vME. These mutations ablated (i) the TBEV pre-M cleavage site, (ii) the TBEV E glycosylation site, or (iii) the first DEN4 NS1 glycosylation site. In contrast, ablation of the second DEN4 NS1 glycosylation site or the TBE pre-M glycosylation site or amino acid substitution at two positions in the TBEV E protein increased neurovirulence. The only conserved feature of the three attenuated mutants was restriction of virus yield in both simian and mosquito cells. Following parenteral inoculation, these attenuated mutants induced complete resistance in mice to fatal encephalitis caused by the highly neurovirulent vME. JF - Journal of virology AU - Pletnev, A G AU - Bray, M AU - Lai, C J AD - Molecular Viral Biology Section, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 4956 EP - 4963 VL - 67 IS - 8 SN - 0022-538X, 0022-538X KW - Oligodeoxyribonucleotides KW - 0 KW - Viral Proteins KW - Methionine KW - AE28F7PNPL KW - Index Medicus KW - Viral Proteins -- genetics KW - Animals KW - Viral Plaque Assay KW - Methionine -- metabolism KW - Viral Proteins -- biosynthesis KW - Amino Acid Sequence KW - Mice KW - Glycosylation KW - Plasmids KW - Mice, Inbred BALB C KW - Base Sequence KW - Chimera KW - Transfection KW - Cells, Cultured KW - Kinetics KW - Restriction Mapping KW - Molecular Sequence Data KW - Cell Line KW - Encephalitis Viruses, Tick-Borne -- pathogenicity KW - Dengue -- physiopathology KW - Brain -- microbiology KW - Dengue Virus -- genetics KW - Mutagenesis, Site-Directed KW - Encephalitis Viruses, Tick-Borne -- genetics KW - Dengue Virus -- growth & development KW - Virulence -- genetics KW - Brain -- pathology KW - Encephalitis Viruses, Tick-Borne -- growth & development KW - Point Mutation KW - Dengue Virus -- pathogenicity KW - Encephalitis, Tick-Borne -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75858358?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Chimeric+tick-borne+encephalitis+and+dengue+type+4+viruses%3A+effects+of+mutations+on+neurovirulence+in+mice.&rft.au=Pletnev%2C+A+G%3BBray%2C+M%3BLai%2C+C+J&rft.aulast=Pletnev&rft.aufirst=A&rft.date=1993-08-01&rft.volume=67&rft.issue=8&rft.spage=4956&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-16 N1 - Date created - 1993-08-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1987 Apr;84(7):2019-23 [3470774] Virology. 1992 Dec;191(2):921-31 [1280384] Virology. 1987 Aug;159(2):237-43 [2441520] Virology. 1988 Sep;166(1):197-205 [3413985] Virology. 1989 Mar;169(1):90-9 [2466373] J Virol. 1989 Jun;63(6):2853-6 [2724416] Virology. 1990 Jan;174(1):250-63 [2136778] Virology. 1990 Feb;174(2):450-8 [2154882] Virology. 1990 Aug;177(2):541-52 [2371768] J Virol. 1990 Sep;64(9):4356-63 [2143542] Virology. 1991 Jan;180(1):411-5 [1845834] J Gen Virol. 1991 Jun;72 ( Pt 6):1323-9 [1710648] Proc Natl Acad Sci U S A. 1991 Jun 15;88(12):5139-43 [2052593] Virus Genes. 1991 Apr;5(2):95-109 [1829286] Nature. 1970 Aug 15;227(5259):680-5 [5432063] Virology. 1979 May;95(1):197-207 [442540] FEBS Lett. 1986 May 12;200(2):317-21 [3709796] Virology. 1986 Nov;155(1):77-88 [3022479] Bioorg Khim. 1991 Mar;17(3):334-42 [1712201] Proc Natl Acad Sci U S A. 1991 Nov 15;88(22):10342-6 [1682924] Virology. 1991 Dec;185(2):891-5 [1720591] Virology. 1992 Apr;187(2):573-90 [1312269] Virology. 1992 Sep;190(1):515-21 [1326816] Proc Natl Acad Sci U S A. 1992 Nov 1;89(21):10532-6 [1438242] Virology. 1987 Aug;159(2):217-28 [3039728] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - EPOCH chemotherapy: toxicity and efficacy in relapsed and refractory non-Hodgkin's lymphoma. AN - 75856389; 7687667 AB - Based on in vitro evidence that tumor cells are less resistant to prolonged exposure to low concentrations of the natural product class, compared with brief higher concentration exposure, we developed a chemotherapy regimen (etoposide, vincristine, doxorubicin, cyclophosphamide, and prednisone [EPOCH]) in which the natural products are administered as a continuous infusion. This is a phase II study of etoposide, vincristine, and doxorubicin, administered as a 96-hour continuous infusion, with intravenous (IV) bolus cyclophosphamide and oral prednisone (EPOCH) in 74 consecutive patients who relapsed from or failed to respond to most of the same drugs administered on a bolus schedule. Patients with aggressive lymphomas who achieved a good response after EPOCH were eligible to undergo bone marrow transplantation. Patients with intermediate- or high-grade lymphoma comprised 76% of this series and 77% had stage IV disease. Seventy-one percent had previously received all of the drugs contained in the EPOCH regimen and 92% had received at least four of the drugs. Seventy patients were assessable for response, of whom 19 (27%) achieved a complete remission (CR) and 42 (60%) a partial remission (PR). Among 21 patients who had no response to prior chemotherapy, 15 (71%) responded, but only one achieved a CR. Patients who relapsed from an initial CR had a 100% response rate, with 76% CRs. With a median potential follow-up duration of 19 months, there was a 28% probability of being event-free at 1 year. Toxicity was primarily hematologic with neutropenia during 51% of cycles, but only a 17% incidence of febrile neutropenia. Gastrointestinal, neurologic, and cardiac toxicity were minimal. EPOCH chemotherapy was well tolerated and highly effective in patients who were resistant to or relapsed from the same drugs administered on a bolus schedule, suggesting that continuous infusion of the natural drug component of this regimen is capable of partially reversing drug resistance and reducing toxicity. Dose-intensity (DI) was > or = that achieved in primary treatment regimens for aggressive lymphomas. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Wilson, W H AU - Bryant, G AU - Bates, S AU - Fojo, A AU - Wittes, R E AU - Steinberg, S M AU - Kohler, D R AU - Jaffe, E S AU - Herdt, J AU - Cheson, B D AD - Medicine Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 1573 EP - 1582 VL - 11 IS - 8 SN - 0732-183X, 0732-183X KW - Granulocyte Colony-Stimulating Factor KW - 143011-72-7 KW - Vincristine KW - 5J49Q6B70F KW - Etoposide KW - 6PLQ3CP4P3 KW - Doxorubicin KW - 80168379AG KW - Cyclophosphamide KW - 8N3DW7272P KW - Prednisone KW - VB0R961HZT KW - Index Medicus KW - Cyclophosphamide -- administration & dosage KW - Drug Administration Schedule KW - Granulocyte Colony-Stimulating Factor -- therapeutic use KW - Infusions, Intravenous KW - Humans KW - Vincristine -- administration & dosage KW - Neutropenia -- chemically induced KW - Aged KW - Drug Resistance KW - Doxorubicin -- administration & dosage KW - Recurrence KW - Etoposide -- administration & dosage KW - Adult KW - Treatment Outcome KW - Middle Aged KW - Neutropenia -- drug therapy KW - Prednisone -- administration & dosage KW - Female KW - Male KW - Survival Analysis KW - Lymphoma, Non-Hodgkin -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75856389?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=EPOCH+chemotherapy%3A+toxicity+and+efficacy+in+relapsed+and+refractory+non-Hodgkin%27s+lymphoma.&rft.au=Wilson%2C+W+H%3BBryant%2C+G%3BBates%2C+S%3BFojo%2C+A%3BWittes%2C+R+E%3BSteinberg%2C+S+M%3BKohler%2C+D+R%3BJaffe%2C+E+S%3BHerdt%2C+J%3BCheson%2C+B+D&rft.aulast=Wilson&rft.aufirst=W&rft.date=1993-08-01&rft.volume=11&rft.issue=8&rft.spage=1573&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=0732183X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-26 N1 - Date created - 1993-08-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Requirement for Raf and MAP kinase function during the meiotic maturation of Xenopus oocytes. AN - 75854196; 8335690 AB - The role of Raf and MAPK (mitogen-activated protein kinase) during the maturation of Xenopus oocytes was investigated. Treatment of oocytes with progesterone resulted in a shift in the electrophoretic mobility of Raf at the onset of germinal vesicle breakdown (GVBD), which was coincident with the activation of MAPK. Expression of a kinase-defective mutant of the human Raf-1 protein (KD-RAF) inhibited progesterone-mediated MAPK activation. MAPK activation was also inhibited by KD-Raf in oocytes expressing signal transducers of the receptor tyrosine kinase (RTK) pathway, including an activated tyrosine kinase (Tpr-Met), a receptor tyrosine kinase (EGFr), and Ha-RasV12. KD-RAF completely inhibited GVBD induced by the RTK pathway. In contrast, KD-RAF did not inhibit GVBD and the progression to Meiosis II in progesterone-treated oocytes. Injection of Mos-specific antisense oligodeoxyribonucleotides inhibited MAPK activation in response to progesterone and Tpr-Met, but failed to inhibit these events in oocytes expressing an oncogenic deletion mutant of Raf-1 (delta N'Raf). Injection of antisense oligodeoxyribonucleotides to Mos also reduced the progesterone- and Tpr-Met-induced electrophoretic mobility shift of Xenopus Raf. These results demonstrate that RTKs and progesterone participate in distinct yet overlapping signaling pathways resulting in the activation of maturation or M-phase promoting factor (MPF). Maturation induced by the RTK pathway requires activation of Raf and MAPK, while progesterone-induced maturation does not. Furthermore, the activation of MAPK in oocytes appears to require the expression of Mos. JF - The Journal of cell biology AU - Fabian, J R AU - Morrison, D K AU - Daar, I O AD - Molecular Mechanisms of Carcinogenesis Laboratory, NCI-Frederick Cancer Research and Development Center, Maryland 21702. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 645 EP - 652 VL - 122 IS - 3 SN - 0021-9525, 0021-9525 KW - Oligodeoxyribonucleotides KW - 0 KW - Proto-Oncogene Proteins KW - Progesterone KW - 4G7DS2Q64Y KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Protein-Serine-Threonine Kinases KW - EC 2.7.11.1 KW - Proto-Oncogene Proteins c-mos KW - Proto-Oncogene Proteins c-raf KW - Mitogen-Activated Protein Kinase 1 KW - EC 2.7.11.24 KW - Index Medicus KW - Xenopus laevis KW - Animals KW - Base Sequence KW - Enzyme Activation KW - Progesterone -- pharmacology KW - Molecular Sequence Data KW - Signal Transduction KW - Female KW - Proto-Oncogene Proteins c-mos -- biosynthesis KW - Protein-Serine-Threonine Kinases -- metabolism KW - Meiosis -- drug effects KW - Proto-Oncogene Proteins -- metabolism KW - Oocytes -- drug effects KW - Oocytes -- physiology KW - Protein-Tyrosine Kinases -- metabolism KW - Proto-Oncogene Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75854196?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Trends+in+pharmacological+sciences&rft.atitle=Molecular+basis+of+muscarinic+acetylcholine+receptor+function.&rft.au=Wess%2C+J&rft.aulast=Wess&rft.aufirst=J&rft.date=1993-08-01&rft.volume=14&rft.issue=8&rft.spage=308&rft.isbn=&rft.btitle=&rft.title=Trends+in+pharmacological+sciences&rft.issn=01656147&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-24 N1 - Date created - 1993-08-24 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Cell Biol. 1991 Jul;114(2):329-35 [1830055] EMBO J. 1991 Sep;10(9):2661-8 [1714387] J Biol Chem. 1991 Aug 15;266(23):14964-9 [1869534] Nature. 1991 Sep 12;353(6340):170-3 [1716348] Nature. 1991 Oct 17;353(6345):670-4 [1922387] Mol Cell Biol. 1991 Dec;11(12):5985-91 [1719375] Biol Cell. 1991;72(1-2):39-45 [1721855] Cancer Cells. 1991 Nov;3(11):445-9 [1662059] J Biol Chem. 1992 Mar 5;267(7):4408-15 [1311309] Nature. 1992 Feb 13;355(6361):649-52 [1531698] Science. 1992 Sep 4;257(5075):1404-7 [1326789] Cell. 1992 Oct 16;71(2):335-42 [1330321] J Biol Chem. 1992 Dec 5;267(34):24796-804 [1332967] Nature. 1992 Dec 10;360(6404):534-5 [1334231] Nature. 1992 Dec 10;360(6404):600-3 [1461284] Mol Cell Biol. 1993 Feb;13(2):1163-72 [8423783] Science. 1993 Jan 22;259(5094):525-8 [7678707] Cell. 1993 Feb 12;72(3):407-14 [8381718] EMBO J. 1993 Feb;12(2):787-94 [8440264] Mol Cell Biol. 1993 Apr;13(4):2546-53 [8384311] EMBO J. 1988 Mar;7(3):775-81 [3135183] Nature. 1988 Oct 6;335(6190):519-25 [2971141] Dev Biol. 1988 Nov;130(1):28-36 [3181631] Proc Natl Acad Sci U S A. 1988 Dec;85(23):8855-9 [3057494] J Biol Chem. 1989 Jan 15;264(2):856-61 [2463250] Mol Cell Biol. 1989 Feb;9(2):639-47 [2710120] Cell. 1989 Aug 25;58(4):649-57 [2475255] Proc Natl Acad Sci U S A. 1989 Sep;86(18):6940-3 [2550926] Nature. 1989 Nov 30;342(6249):512-8 [2531292] J Biol Chem. 1990 Feb 15;265(5):2713-9 [2154457] J Biol Chem. 1990 Mar 15;265(8):4730-5 [2155237] Exp Cell Res. 1975 Mar 15;91(2):381-8 [165088] Science. 1979 Sep 28;205(4413):1397-9 [472755] Int Rev Cytol. 1979;57:185-282 [385540] Dev Biol. 1981 Jul 30;85(2):309-16 [6266902] Proc Natl Acad Sci U S A. 1983 Jul;80(14):4218-22 [6308607] Nucleic Acids Res. 1984 Sep 25;12(18):7057-70 [6207484] Virology. 1985 Oct 15;146(1):78-89 [2994296] Cell. 1985 Dec;43(3 Pt 2):615-21 [2416466] Cell. 1986 Jun 20;45(6):895-904 [2423252] Mol Cell Biol. 1987 Mar;7(3):1171-9 [3561413] Mol Cell Biol. 1987 Mar;7(3):1285-8 [3550436] Science. 1987 May 15;236(4803):840-3 [3554510] J Biol Chem. 1988 Apr 15;263(11):5396-401 [3258598] Cell. 1988 Apr 22;53(2):185-95 [2834064] J Cell Biol. 1990 Mar;110(3):731-42 [1689732] Mol Cell Biol. 1990 Jun;10(6):2503-12 [2188091] J Biol Chem. 1990 Jul 15;265(20):11487-94 [2142153] J Biol Chem. 1990 Jul 15;265(20):11495-501 [2142154] Science. 1990 Jul 6;249(4964):64-7 [2164259] J Biol Chem. 1990 Sep 15;265(26):15471-80 [2394735] FEBS Lett. 1990 Oct 1;271(1-2):119-22 [2171996] Eur J Biochem. 1990 Nov 13;193(3):661-9 [2174361] Nature. 1991 Jan 17;349(6306):251-4 [1702878] Cell. 1991 Feb 8;64(3):479-82 [1846778] Nature. 1991 Jan 31;349(6308):426-8 [1992343] J Biol Chem. 1991 Mar 5;266(7):4220-7 [1705548] Mol Cell Biol. 1991 Apr;11(4):1965-71 [2005892] Biochem Cell Biol. 1990 Dec;68(12):1297-330 [2085430] Mol Cell Biol. 1991 May;11(5):2517-28 [1708093] Adv Cancer Res. 1992;58:53-73 [1312290] Cell. 1992 Mar 20;68(6):1041-50 [1312393] EMBO J. 1992 Mar;11(3):973-82 [1312468] Science. 1992 Jan 10;255(5041):212-5 [1313186] Proc Natl Acad Sci U S A. 1992 Apr 1;89(7):2922-6 [1372995] Genes Dev. 1992 Apr;6(4):545-56 [1313769] Nature. 1992 Jul 30;358(6385):417-21 [1322500] Trends Biochem Sci. 1992 Jun;17(6):233-8 [1323888] Cell Growth Differ. 1992 Feb;3(2):135-42 [1504018] Mol Cell Biol. 1992 Sep;12(9):3776-83 [1508183] Cancer Cells. 1990 Dec;2(12):377-82 [2150916] Science. 1991 Apr 26;252(5005):558-61 [1850550] Cell. 1991 May 17;65(4):663-75 [2032290] Proc Natl Acad Sci U S A. 1991 Jul 1;88(13):5794-8 [1648231] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Analysis of the functional and host range-determining regions of the murine ectropic and amphotropic retrovirus envelope proteins. AN - 75854106; 8331726 AB - A series of Moloney murine leukemia virus (Mo-MuLV) envelope gene constructs were analyzed for biological activity. Three classes of recombinant envelopes were examined: insertions, deletions, and chimeras. Insertion (4 to 5 amino acids) and deletion (31 to 62 amino acids) mutants spanned most of the SU (gp70)-coding region and were all biologically inactive. Radioimmunoprecipitation demonstrated that the mutant envelope proteins were incorrectly processed. The Pr80env envelope precursor proteins failed to obtain the proper posttranslational modifications and were not cleaved into SU (gp70) and TM (p15E), suggesting that disruption of Pr80env structure prevents intracellular transport and processing. To analyze the functional domains of the SU portion of the Env protein, we assembled several chimeric constructs. In these constructs, portions of the ecotropic Mo-MuLV envelope gene were replaced with corresponding sequences from the 4070A amphotropic MuLV envelope. Using a retroviral vector pseudotyping assay, 5 of 12 chimeric envelope proteins were shown to be biologically active. Host range was determined by retroviral vector transduction of the appropriate cell, by viral interference studies, and by the productive infection of Chinese hamster ovary cells expressing the murine ecotropic receptor. These results permit assignment of the amino acids responsible for host range determination. Ecotropic host range is determined by the first 88 amino acids of the Mo-MuLV SU, while the amphotropic host range-determining region spans the first 157 amino acids of the 4070A SU. JF - Journal of virology AU - Morgan, R A AU - Nussbaum, O AU - Muenchau, D D AU - Shu, L AU - Couture, L AU - Anderson, W F AD - Molecular Hematology Branch, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 4712 EP - 4721 VL - 67 IS - 8 SN - 0022-538X, 0022-538X KW - env KW - Gene Products, env KW - 0 KW - Recombinant Fusion Proteins KW - Recombinant Proteins KW - beta-Galactosidase KW - EC 3.2.1.23 KW - Index Medicus KW - AIDS/HIV KW - 3T3 Cells KW - Animals KW - Recombinant Fusion Proteins -- isolation & purification KW - Amino Acid Sequence KW - Mice KW - Cloning, Molecular KW - Recombinant Fusion Proteins -- metabolism KW - Recombinant Proteins -- isolation & purification KW - beta-Galactosidase -- metabolism KW - Transfection KW - Recombinant Proteins -- metabolism KW - Restriction Mapping KW - Molecular Sequence Data KW - beta-Galactosidase -- genetics KW - Cell Line KW - Mutagenesis, Insertional KW - Sequence Deletion KW - Gene Products, env -- metabolism KW - Gene Products, env -- isolation & purification KW - Defective Viruses -- genetics KW - Genes, env KW - Defective Viruses -- metabolism KW - Moloney murine leukemia virus -- genetics KW - Gene Products, env -- genetics KW - Moloney murine leukemia virus -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75854106?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Analysis+of+the+functional+and+host+range-determining+regions+of+the+murine+ectropic+and+amphotropic+retrovirus+envelope+proteins.&rft.au=Morgan%2C+R+A%3BNussbaum%2C+O%3BMuenchau%2C+D+D%3BShu%2C+L%3BCouture%2C+L%3BAnderson%2C+W+F&rft.aulast=Morgan&rft.aufirst=R&rft.date=1993-08-01&rft.volume=67&rft.issue=8&rft.spage=4712&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-16 N1 - Date created - 1993-08-16 N1 - Date revised - 2017-01-13 N1 - Gene symbol - env N1 - SuppNotes - Cited By: EMBO J. 1986 Dec 1;5(12):3133-42 [3102226] J Virol. 1986 May;58(2):359-66 [3009853] J Virol. 1987 Sep;61(9):2659-69 [3039159] Methods Enzymol. 1987;152:684-704 [3657593] J Virol. 1988 Jan;62(1):168-75 [2824845] J Virol. 1988 Mar;62(3):1016-21 [2828650] J Virol. 1988 Apr;62(4):1120-4 [2831375] Proc Natl Acad Sci U S A. 1988 Nov;85(22):8688-92 [2847170] J Virol. 1989 Feb;63(2):647-58 [2911118] Cell. 1989 May 19;57(4):659-66 [2541919] J Virol. 1989 Sep;63(9):3561-8 [2547985] Ann N Y Acad Sci. 1989;567:39-49 [2552892] J Virol. 1990 Feb;64(2):757-66 [2153240] J Virol. 1991 Aug;65(8):4026-32 [2072445] Virology. 1991 Aug;183(2):545-54 [1853560] Nature. 1991 Aug 22;352(6337):725-8 [1652100] Virology. 1992 Jan;186(1):161-6 [1309273] J Virol. 1992 Mar;66(3):1468-75 [1310758] J Virol. 1992 Apr;66(4):2281-7 [1312632] J Virol. 1992 Aug;66(8):4632-8 [1321266] J Natl Cancer Inst. 1960 Apr;24:933-51 [14423465] Proc Natl Acad Sci U S A. 1969 Jul;63(3):753-8 [4186808] Nature. 1970 Aug 15;227(5259):680-5 [5432063] Cell. 1975 Jan;4(1):31-6 [803875] Virology. 1977 Feb;76(2):539-53 [190766] J Virol. 1977 Sep;23(3):787-98 [894795] J Virol. 1978 Jun;26(3):750-61 [78989] J Virol. 1979 Feb;29(2):735-43 [430608] J Virol. 1979 Apr;30(1):157-65 [225513] J Virol. 1979 Jun;30(3):720-8 [225541] Proc Natl Acad Sci U S A. 1980 Nov;77(11):6420-4 [6935656] Nature. 1981 Oct 15-21;293(5833):543-8 [6169994] J Virol. 1982 May;42(2):519-29 [6283170] J Virol. 1982 Oct;44(1):19-31 [7143566] Virology. 1983 Mar;125(2):513-8 [6836918] J Virol. 1983 Jun;46(3):1056-60 [6190011] J Virol. 1983 Jun;46(3):718-25 [6574260] J Virol. 1984 Jan;49(1):214-22 [6197537] J Virol. 1984 Feb;49(2):452-8 [6198530] J Virol. 1984 Jun;50(3):864-71 [6328017] J Virol. 1985 Jan;53(1):32-9 [2981357] Cell. 1986 May 9;45(3):365-74 [3009025] J Virol. 1987 May;61(5):1639-46 [3502707] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - A phase II study of continuous infusion 5-fluorouracil and leucovorin with weekly cisplatin in metastatic colorectal carcinoma. AN - 75852480; 8334622 AB - Prolonged infusional 5-fluorouracil (5-FU) and bolus 5-FU modulated by leucovorin are associated with higher response rates than bolus 5-FU alone. Cisplatin enhances 5-FU cytotoxicity in some preclinical models. The authors tested the feasibility of combining concurrent infusional leucovorin (500 mg/m2/d) with protracted infusional 5-FU (200 mg/m2/d) and weekly bolus cisplatin (20 mg/m2) in 22 patients with metastatic colorectal cancer. Four partial responses (PR) were noticed among 21 evaluable patients (19%). The median time to treatment failure and median survival were 6 months and 11 months, respectively. All but two patients required 5-FU dose reduction after a median of 2 weeks because of mucositis. However, severe mucositis and diarrhea occurred in only 18% and 5% of the patients, respectively. Palmar-plantar erythrodysesthesia of mild to moderate severity occurred in 55% of patients. Megaloblastic changes were evident in the peripheral blood during therapy, and may reflect prolonged DNA-directed toxicity of 5-FU. The median tolerated dose level of 5-FU was 113 mg/m2/d (range, 64-150 mg/m2/d). Mean steady-state plasma concentrations (Cpss) of 5-FU appeared to increase linearly from 0.19 microM to 0.39 microM over the dose range 64 to 200 mg/m2/d. Patients with grade 2 gastrointestinal toxicity had significantly higher 5-FU Cpss than patients with grade 0 or 1 toxicity. The early onset of toxicity with this regimen of protracted infusional 5-FU/high-dose leucovorin and weekly cisplatin required marked attenuation of the 5-FU dose intensity, and the results were no better than that expected with infusional 5-FU alone. JF - Cancer AU - Grem, J L AU - McAtee, N AU - Balis, F AU - Murphy, R AU - Venzon, D AU - Kramer, B AU - Goldspiel, B AU - Begley, M AU - Allegra, C J AD - National Cancer Institute-Navy Medical Oncology Branch, National Naval Medical Center, Bethesda, Maryland 20889. Y1 - 1993/08/01/ PY - 1993 DA - 1993 Aug 01 SP - 663 EP - 668 VL - 72 IS - 3 SN - 0008-543X, 0008-543X KW - Cisplatin KW - Q20Q21Q62J KW - Leucovorin KW - Q573I9DVLP KW - Fluorouracil KW - U3P01618RT KW - Abridged Index Medicus KW - Index Medicus KW - Treatment Failure KW - Infusions, Intravenous KW - Dose-Response Relationship, Drug KW - Humans KW - Leucovorin -- administration & dosage KW - Leucovorin -- adverse effects KW - Aged KW - Cisplatin -- administration & dosage KW - Fluorouracil -- administration & dosage KW - Fluorouracil -- adverse effects KW - Adult KW - Neoplasm Metastasis KW - Middle Aged KW - Cisplatin -- adverse effects KW - Fluorouracil -- pharmacokinetics KW - Male KW - Female KW - Survival Analysis KW - Rectal Neoplasms -- mortality KW - Rectal Neoplasms -- drug therapy KW - Colonic Neoplasms -- mortality KW - Colonic Neoplasms -- drug therapy KW - Rectal Neoplasms -- pathology KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Colonic Neoplasms -- pathology KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75852480?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=A+phase+II+study+of+continuous+infusion+5-fluorouracil+and+leucovorin+with+weekly+cisplatin+in+metastatic+colorectal+carcinoma.&rft.au=Grem%2C+J+L%3BMcAtee%2C+N%3BBalis%2C+F%3BMurphy%2C+R%3BVenzon%2C+D%3BKramer%2C+B%3BGoldspiel%2C+B%3BBegley%2C+M%3BAllegra%2C+C+J&rft.aulast=Grem&rft.aufirst=J&rft.date=1993-08-01&rft.volume=72&rft.issue=3&rft.spage=663&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-24 N1 - Date created - 1993-08-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Mechanism of developmental regulation of alpha pi, the chicken embryonic alpha-globin gene. AN - 75852019; 8336706 AB - The chicken alpha pi-globin gene is expressed during development only in the primitive erythrocyte lineage and not in the definitive lineage. We show that stage-specific expression is maintained when plasmids containing the alpha pi promoter are transfected into primitive and definitive lineage primary erythroid cells and that the information contained in the promoter is sufficient to confer this specificity. Detailed analysis of binding sites in the promoter for trans-acting factors, together with studies of the effects of mutagenesis on expression, reveals that the factors critical to stage-specific expression are all present in both primitive and definitive lineages, but at various concentrations. We identify three proteins, an NF1 family member, a Y-box factor, and an Sp1-like factor, which interact to stimulate or inhibit transcription. We propose that the concentration-dependent action of these factors, together with the general erythroid factor GATA-1, is responsible for the stage-specific expression of the alpha pi-globin gene. JF - Molecular and cellular biology AU - Knezetic, J A AU - Felsenfeld, G AD - Laboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 4632 EP - 4639 VL - 13 IS - 8 SN - 0270-7306, 0270-7306 KW - DNA-Binding Proteins KW - 0 KW - Nuclear Proteins KW - RNA, Messenger KW - Globins KW - 9004-22-2 KW - Index Medicus KW - Animals KW - Chick Embryo KW - DNA Mutational Analysis KW - RNA, Messenger -- genetics KW - Cloning, Molecular KW - Promoter Regions, Genetic KW - Base Sequence KW - Genes KW - Transfection KW - Cells, Cultured KW - Enhancer Elements, Genetic KW - In Vitro Techniques KW - Molecular Sequence Data KW - Nuclear Proteins -- metabolism KW - Sequence Deletion KW - DNA-Binding Proteins -- metabolism KW - Globins -- genetics KW - Gene Expression Regulation KW - Chickens -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75852019?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+cellular+biology&rft.atitle=Mechanism+of+developmental+regulation+of+alpha+pi%2C+the+chicken+embryonic+alpha-globin+gene.&rft.au=Knezetic%2C+J+A%3BFelsenfeld%2C+G&rft.aulast=Knezetic&rft.aufirst=J&rft.date=1993-08-01&rft.volume=13&rft.issue=8&rft.spage=4632&rft.isbn=&rft.btitle=&rft.title=Molecular+and+cellular+biology&rft.issn=02707306&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-24 N1 - Date created - 1993-08-24 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Philos Trans R Soc Lond B Biol Sci. 1973 Oct 25;266(877):225-305 [4147843] Development. 1992 Aug;115(4):1149-64 [1451662] Cell. 1981 May;24(2):333-44 [7237551] Proc Natl Acad Sci U S A. 1986 Jun;83(12):4312-6 [3459175] Cell. 1987 Jul 31;50(3):347-59 [3607873] Proc Natl Acad Sci U S A. 1988 Apr;85(8):2548-52 [3357880] Nucleic Acids Res. 1988 May 25;16(10):4419-35 [3380685] Proc Natl Acad Sci U S A. 1988 Aug;85(16):5976-80 [3413070] Mol Cell Biol. 1989 Mar;9(3):893-901 [2725505] Genes Dev. 1989 Dec;3(12A):1845-59 [2620825] Genes Dev. 1989 Dec;3(12A):1860-73 [2620826] Nucleic Acids Res. 1990 May 11;18(9):2607-16 [2339052] Proc Natl Acad Sci U S A. 1990 Nov;87(22):9028-32 [2247479] Annu Rev Cell Biol. 1990;6:95-124 [2275826] Mol Cell Biol. 1991 Feb;11(2):843-53 [1990287] Cell. 1991 May 3;65(3):493-505 [1850324] Proc Natl Acad Sci U S A. 1980 May;77(5):2596-600 [6248855] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Deletion of the vaccinia virus B5R gene encoding a 42-kilodalton membrane glycoprotein inhibits extracellular virus envelope formation and dissemination. AN - 75847946; 8331727 AB - The structure, formation, and function of the virion membranes are among the least well understood aspects of vaccinia virus replication. In this study, we investigated the role of gp42, a glycoprotein component of the extracellular enveloped form of vaccinia virus (EEV) encoded by the B5R gene. The B5R gene was deleted by homologous recombination from vaccinia virus strains IHD-J and WR, which produce high and low levels of EEV, respectively. Isolation of recombinant viruses was facilitated by the insertion into the genome of a cassette containing the Escherichia coli gpt and lacZ genes flanked by the ends of the B5R gene to provide simultaneous antibiotic selection and color screening. Deletion mutant viruses of both strains formed tiny plaques, and those of the IHD-J mutant lacked the characteristic comet shape caused by release of EEV. Nevertheless, similar yields of intracellular infectious virus were obtained whether cells were infected with the B5R deletion mutants or their parental strains. In the case of IHD-J, however, this deletion severely reduced the amount of infectious extracellular virus. Metabolic labeling studies demonstrated that the low extracellular infectivity corresponded with a decrease in EEV particles in the medium. Electron microscopic examination revealed that mature intracellular naked virions (INV) were present in cells infected with mutant virus, but neither membrane-wrapped INV nor significant amounts of plasma membrane-associated virus were observed. Syncytium formation, which occurs in cells infected with wild-type WR and IHD-J virus after brief low-pH treatment, did not occur in cells infected with the B5R deletion mutants. By contrast, syncytium formation induced by antibody to the viral hemagglutinin occurred, suggesting that different mechanisms are involved. When assayed by intracranial injection into weanling mice, both IHD-J and WR mutant viruses were found to be significantly attenuated. These findings demonstrate that the 42-kDa glycoprotein of the EEV is required for efficient membrane enwrapment of INV, externalization of the virus, and transmission and that gp42 contributes to viral virulence in strains producing both low and high levels of EEV. JF - Journal of virology AU - Wolffe, E J AU - Isaacs, S N AU - Moss, B AD - Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 4732 EP - 4741 VL - 67 IS - 8 SN - 0022-538X, 0022-538X KW - B5R KW - gpt KW - lacZ KW - DNA, Viral KW - 0 KW - Gene Products, env KW - Membrane Glycoproteins KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Genes, Bacterial KW - Viral Plaque Assay KW - Virion -- genetics KW - HeLa Cells KW - Humans KW - Escherichia coli -- genetics KW - Virion -- metabolism KW - Plasmids KW - Virion -- ultrastructure KW - Blotting, Southern KW - Giant Cells -- physiology KW - Restriction Mapping KW - Recombination, Genetic KW - DNA, Viral -- isolation & purification KW - Giant Cells -- cytology KW - Microscopy, Electron KW - DNA, Viral -- genetics KW - Mutagenesis, Insertional KW - Cell Line KW - Sequence Deletion KW - Gene Products, env -- metabolism KW - Vaccinia virus -- genetics KW - Vaccinia virus -- ultrastructure KW - Vaccinia virus -- metabolism KW - Genes, Viral KW - Gene Products, env -- biosynthesis KW - Membrane Glycoproteins -- metabolism KW - Membrane Glycoproteins -- genetics KW - Gene Deletion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75847946?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Deletion+of+the+vaccinia+virus+B5R+gene+encoding+a+42-kilodalton+membrane+glycoprotein+inhibits+extracellular+virus+envelope+formation+and+dissemination.&rft.au=Wolffe%2C+E+J%3BIsaacs%2C+S+N%3BMoss%2C+B&rft.aulast=Wolffe&rft.aufirst=E&rft.date=1993-08-01&rft.volume=67&rft.issue=8&rft.spage=4732&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-16 N1 - Date created - 1993-08-16 N1 - Date revised - 2017-01-13 N1 - Gene symbol - B5R; gpt; lacZ N1 - SuppNotes - Cited By: J Virol. 1992 Dec;66(12):7217-24 [1433514] Virology. 1990 Nov;179(1):247-66, 517-63 [2219722] J Virol. 1993 Jun;67(6):3319-25 [8497053] J Gen Virol. 1971 Oct;13(1):19-25 [5130569] J Gen Virol. 1971 Oct;13(1):9-17 [4108676] Virology. 1971 Dec;46(3):507-32 [4944855] Virology. 1971 Dec;46(3):533-43 [4109523] J Clin Invest. 1973 Mar;52(3):535-42 [4685079] Prog Med Virol. 1973;16:86-108 [4356899] J Gen Virol. 1974 May;23(2):197-200 [4833605] J Gen Virol. 1976 Jul;32(1):63-72 [986420] Virology. 1976 Aug;73(1):43-58 [960564] J Virol. 1978 Jul;27(1):28-37 [691112] J Virol. 1979 Jul;31(1):147-55 [501796] J Cell Biol. 1993 May;121(3):521-41 [8486734] Virology. 1991 Mar;181(1):158-64 [1994573] J Virol. 1991 Jul;65(7):3435-42 [2041074] J Gen Virol. 1991 Jun;72 ( Pt 6):1349-76 [2045793] J Virol. 1991 Nov;65(11):5910-20 [1920620] Virology. 1992 Mar;187(1):251-60 [1736527] J Virol. 1992 Mar;66(3):1610-21 [1738204] J Virol. 1992 May;66(5):2617-30 [1560521] Virology. 1992 Jun;188(2):801-10 [1585649] J Virol. 1992 Jul;66(7):4170-9 [1602540] J Gen Virol. 1980 Sep;50(1):89-100 [7441216] J Virol. 1981 Sep;39(3):903-13 [7288920] J Gen Virol. 1985 Mar;66 ( Pt 3):643-6 [3973566] Nature. 1985 Oct 31-Nov 6;317(6040):813-5 [4058585] Virology. 1986 Apr 30;150(2):451-62 [3008418] J Virol. 1986 Jun;58(3):757-64 [3701927] J Virol. 1987 Feb;61(2):395-404 [3806791] J Virol. 1987 Nov;61(11):3550-4 [2822962] J Virol. 1988 Mar;62(3):866-74 [3339716] Virology. 1988 Mar;163(1):133-44 [2450423] J Virol. 1988 Jun;62(6):1849-54 [3130492] Virology. 1990 Apr;175(2):372-84 [2183466] Virology. 1990 Sep;178(1):81-91 [2389560] J Virol. 1990 Oct;64(10):4884-92 [2398531] Erratum In: J Virol 1993 Sep;67(9):5709-11 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Prevention of tobacco use during childhood and adolescence. Five steps to prevent the onset of smoking. AN - 75847184; 8334651 AB - Most tobacco users become addicted during childhood and adolescence. To reduce the prevalence of tobacco-related illnesses, more emphasis must be placed on preventing the onset of tobacco use. Physicians can play a major role. Based on a series of clinical trials, the National Cancer Institute (NCI) developed recommendations to help patients stop smoking. Behavioral and developmental research have identified factors that contribute to the onset of smoking. The American Academy of Pediatrics (AAP) has developed guidelines for health supervision from birth to adulthood, including engaging parents and children as partners in health care. The NCI recommendations, behavioral research results, and AAP guidelines were integrated to develop a strategy to prevent the onset of tobacco use. The NCI proposes five steps to prevent tobacco use during childhood and adolescence. There are five physician activities, beginning with the letter A, including anticipatory guidance, ask, advise, assist, and arrange follow-up. Anticipatory guidance, the practice of counseling for potential problems, is a key part of health care for the young. The nature of these steps varies, depending on the child's age, developmental stage, and behavior, as well as smoking habits of family members. Despite the long-term consequences of smoking, onset and addiction to tobacco use usually begins in childhood. Therefore, physicians who care for children have a major role in eliminating tobacco use by preventing its onset. JF - Cancer AU - Epps, R P AU - Manley, M W AD - National Cancer Institute, Bethesda, Maryland. Y1 - 1993/08/01/ PY - 1993 DA - 1993 Aug 01 SP - 1002 EP - 1004 VL - 72 IS - 3 Suppl SN - 0008-543X, 0008-543X KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Health Behavior KW - Child KW - Adolescent KW - Child, Preschool KW - Health Promotion -- methods KW - Tobacco Use Disorder -- prevention & control KW - Smoking -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75847184?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=Prevention+of+tobacco+use+during+childhood+and+adolescence.+Five+steps+to+prevent+the+onset+of+smoking.&rft.au=Epps%2C+R+P%3BManley%2C+M+W&rft.aulast=Epps&rft.aufirst=R&rft.date=1993-08-01&rft.volume=72&rft.issue=3+Suppl&rft.spage=1002&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-23 N1 - Date created - 1993-08-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - A major transactivator of varicella-zoster virus, the immediate-early protein IE62, contains a potent N-terminal activation domain. AN - 75846223; 8392592 AB - Accumulating evidence indicates that the product of the putative immediate-early gene ORF62 (IE62) activates varicella-zoster virus (VZV) genes thought to represent all three kinetic classes, namely, immediate-early (alpha), early (beta), and late (gamma) classes, of VZV genes as well as a variety heterologous gene promoters. However, the mechanism(s) by which IE62 protein mediates transactivation of these diverse VZV and heterologous gene promoters remains to be elucidated. In this study, by using yeast GAL4 protein chimeras, the coding regions of VZV ORF62 possessing activation domains have been assessed. We demonstrate that the VZV IE62 protein contains a potent activation domain in the N-terminal portion of the molecule, encoded within the first 86 codons of ORF62. The predicted secondary structure profile and the acid-base composition of this IE62 domain resemble those of other transregulatory proteins whose activation is mediated through acidic, hydrophobic elements. In addition, we show that deletion of this activation domain from the 1,310-residue native IE62 protein results in ablation of the transactivator function of IE62. We also present evidence that the mutant IE62 protein lacking the activation domain, though devoid of transactivation ability, was still capable of interfering with the activation of target promoters by the native, full-length IE62. JF - Journal of virology AU - Perera, L P AU - Mosca, J D AU - Ruyechan, W T AU - Hayward, G S AU - Straus, S E AU - Hay, J AD - Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 4474 EP - 4483 VL - 67 IS - 8 SN - 0022-538X, 0022-538X KW - IE62 KW - ORF62 KW - Codon KW - 0 KW - DNA-Binding Proteins KW - Fungal Proteins KW - GAL4 protein, S cerevisiae KW - IE62 protein, Human herpesvirus 3 KW - Immediate-Early Proteins KW - Oligodeoxyribonucleotides KW - Recombinant Fusion Proteins KW - Saccharomyces cerevisiae Proteins KW - Trans-Activators KW - Transcription Factors KW - Viral Envelope Proteins KW - Index Medicus KW - Codon -- genetics KW - Humans KW - Amino Acid Sequence KW - Fungal Proteins -- genetics KW - Plasmids KW - Recombinant Fusion Proteins -- metabolism KW - Mutagenesis, Site-Directed KW - Promoter Regions, Genetic KW - Base Sequence KW - Fungal Proteins -- metabolism KW - Restriction Mapping KW - Molecular Sequence Data KW - Cell Line KW - T-Lymphocytes KW - Trans-Activators -- metabolism KW - Herpesvirus 3, Human -- genetics KW - Gene Expression Regulation, Viral KW - Trans-Activators -- genetics KW - Genes, Viral KW - Viral Envelope Proteins -- metabolism KW - Herpesvirus 3, Human -- metabolism KW - Transcriptional Activation KW - Viral Envelope Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75846223?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=A+major+transactivator+of+varicella-zoster+virus%2C+the+immediate-early+protein+IE62%2C+contains+a+potent+N-terminal+activation+domain.&rft.au=Perera%2C+L+P%3BMosca%2C+J+D%3BRuyechan%2C+W+T%3BHayward%2C+G+S%3BStraus%2C+S+E%3BHay%2C+J&rft.aulast=Perera&rft.aufirst=L&rft.date=1993-08-01&rft.volume=67&rft.issue=8&rft.spage=4474&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-16 N1 - Date created - 1993-08-16 N1 - Date revised - 2017-01-13 N1 - Gene symbol - IE62; ORF62 N1 - SuppNotes - Cited By: Virology. 1987 Feb;156(2):423-6 [3027986] J Virol. 1987 Jan;61(1):225-8 [3023701] Microbiol Rev. 1987 Dec;51(4):458-76 [2830478] J Virol. 1988 Jun;62(6):2076-82 [2835512] J Gen Virol. 1988 Jul;69 ( Pt 7):1531-74 [2839594] Cell. 1988 Aug 26;54(5):659-64 [3044607] Nature. 1988 Oct 6;335(6190):563-4 [3047590] Nature. 1988 Oct 20;335(6192):683-9 [3050531] Cell. 1988 Dec 23;55(6):1137-45 [2849508] Nature. 1989 Mar 2;338(6210):39-44 [2521923] Nucleic Acids Res. 1989 Jun 26;17(12):4637-46 [2546124] Science. 1989 Jul 28;245(4916):371-8 [2667136] Virology. 1989 Sep;172(1):223-36 [2549711] Annu Rev Biochem. 1989;58:799-839 [2673023] Nucleic Acids Res. 1989 Sep 25;17(18):7539 [2798115] Virology. 1989 Dec;173(2):700-9 [2556848] Science. 1990 Feb 9;247(4943):710-2 [2405489] Cell. 1990 Jun 29;61(7):1199-208 [2163758] Cell. 1990 Jun 29;61(7):1209-15 [2163759] J Gen Virol. 1990 Nov;71 ( Pt 11):2681-9 [2174959] J Bacteriol. 1991 Feb;173(3):1151-60 [1991714] J Virol. 1991 Mar;65(3):1149-59 [1847444] J Virol. 1991 Jul;65(7):3839-52 [1645794] J Virol. 1992 Jan;66(1):359-66 [1309252] J Virol. 1992 Jun;66(6):3811-22 [1316484] Virology. 1992 Jul;189(1):304-16 [1318606] J Virol. 1992 Sep;66(9):5298-304 [1323696] Virology. 1992 Nov;191(1):346-54 [1329324] J Exp Med. 1958 Dec 1;108(6):945-56 [13598821] J Virol. 1974 Jul;14(1):8-19 [4365321] Virology. 1974 Jul;60(1):302-7 [4366499] Proc Natl Acad Sci U S A. 1975 Apr;72(4):1276-80 [165503] J Virol. 1977 Mar;21(3):996-1001 [191658] Cell. 1977 Sep;12(1):275-85 [198141] J Virol. 1979 Jan;29(1):275-84 [219222] J Virol. 1979 Aug;31(2):447-62 [225564] J Virol. 1979 Nov;32(2):357-69 [228063] Nature. 1980 May 29;285(5763):329-30 [6246451] J Virol. 1980 Oct;36(1):189-203 [6255206] J Virol. 1982 Dec;44(3):939-49 [6294341] Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] J Virol. 1983 May;46(2):371-7 [6302308] Proc Natl Acad Sci U S A. 1984 Jul;81(13):4065-9 [6330737] J Mol Biol. 1984 Nov 25;180(1):1-19 [6096556] Cell. 1985 Apr;40(4):767-74 [3886158] Proc Natl Acad Sci U S A. 1985 Jul;82(13):4539-43 [2989831] Proc Natl Acad Sci U S A. 1985 Sep;82(17):5870-4 [2994050] J Virol. 1985 Nov;56(2):558-70 [2997476] J Virol. 1985 Dec;56(3):723-33 [2999428] Nucleic Acids Res. 1986 Feb 25;14(4):1727-45 [3005980] J Gen Virol. 1986 Sep;67 ( Pt 9):1759-816 [3018124] Nature. 1986 Aug 21-27;322(6081):697-701 [3018583] Nucleic Acids Res. 1987 Jun 11;15(11):4491-511 [3035496] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Inhibition of endogenous phosphatase in a postsynaptic density fraction allows extensive phosphorylation of the major postsynaptic density protein. AN - 75836729; 8393087 AB - The major postsynaptic density protein, proposed to be a calcium/calmodulin-dependent protein kinase, becomes phosphorylated when a postsynaptic density preparation from rat cerebral cortex is incubated in medium containing calcium and calmodulin. Upon longer incubation, however, the level of phosphorylation declines, suggesting the presence of a phosphatase activity. When Microcystin-LR, a phosphatase inhibitor, is included in the phosphorylation medium, the decline in phosphorylation is prevented and a higher maximal level of phosphorylation can be achieved. Under these conditions, the maximal phosphorylation of major postsynaptic density protein is accompanied by a nearly complete shift in its electrophoretic mobility from 50 kDa to 54 kDa, similar to that described for the alpha subunit of the soluble calcium/calmodulin-dependent protein kinase II. Of the four major groups of serine/threonine protein phosphatases, the enzyme responsible for the dephosphorylation of major postsynaptic density protein is neither type 2C, which is insensitive to Microcystin-LR, nor type 2B, which is calcium-dependent. As Microcystin-LR is much more potent than okadaic acid in inhibiting the dephosphorylation of major postsynaptic density protein, it is likely that the postsynaptic density-associated phosphatase is a type 1. The above results indicate that the relatively low level of phosphorylation of the major postsynaptic density protein observed in preparations containing postsynaptic densities is not due to a difference between the cytoplasmic and postsynaptic density-associated calcium/calmodulin-dependent kinases as previously proposed, but to a phosphatase activity, presumably belonging to the type 1 group. JF - Journal of neurochemistry AU - Dosemeci, A AU - Reese, T S AD - Laboratory of Neurobiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/08// PY - 1993 DA - August 1993 SP - 550 EP - 555 VL - 61 IS - 2 SN - 0022-3042, 0022-3042 KW - Calmodulin KW - 0 KW - Ethers, Cyclic KW - Microcystins KW - Nerve Tissue Proteins KW - Peptides, Cyclic KW - postsynaptic density proteins KW - Okadaic Acid KW - 1W21G5Q4N2 KW - Egtazic Acid KW - 526U7A2651 KW - Phosphoric Monoester Hydrolases KW - EC 3.1.3.2 KW - cyanoginosin LR KW - EQ8332842Y KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Rats KW - Cell Fractionation KW - Animals KW - Rats, Sprague-Dawley KW - Phosphorylation KW - Microscopy, Electron KW - Calcium -- pharmacology KW - Ethers, Cyclic -- pharmacology KW - Peptides, Cyclic -- pharmacology KW - Egtazic Acid -- pharmacology KW - Calmodulin -- pharmacology KW - Cerebral Cortex -- metabolism KW - Synaptosomes -- ultrastructure KW - Cerebral Cortex -- ultrastructure KW - Nerve Tissue Proteins -- metabolism KW - Synaptosomes -- metabolism KW - Phosphoric Monoester Hydrolases -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75836729?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neurochemistry&rft.atitle=Inhibition+of+endogenous+phosphatase+in+a+postsynaptic+density+fraction+allows+extensive+phosphorylation+of+the+major+postsynaptic+density+protein.&rft.au=Dosemeci%2C+A%3BReese%2C+T+S&rft.aulast=Dosemeci&rft.aufirst=A&rft.date=1993-08-01&rft.volume=61&rft.issue=2&rft.spage=550&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurochemistry&rft.issn=00223042&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-24 N1 - Date created - 1993-08-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Community nutrition intervention strategies for cancer risk reduction AN - 1434033920; 18537524 AB - As the accumulated evidence continues to indicate a need for Americans to modify current eating patterns and other lifestyle factors to reduce the risk of chronic diseases, the demand for community nutrition interventions will accelerate. All interventions require certain basic elements, such as measurable objectives and robust evaluation designs. However, there are other overarching strategies whose application will contribute to the research knowledge base for community interventions. This article focuses on three such strategies: use of the national health objectives, use of community channels, and development of interventions based on theories of health behavior. The application of these strategies to the National 5 A Day for Better Health Program is illustrated. JF - Cancer AU - Heimendinger, Jerianne AD - National Cancer Institute, National Institutes of Health, Division of Cancer Prevention and Control, 9000 Rockville Pike, EPN 330, Bethesda, MD 20892. Y1 - 1993/08// PY - 1993 DA - Aug 1993 SP - 1019 EP - 1023 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 72 IS - S3 SN - 0008-543X, 0008-543X KW - Risk Abstracts; Health & Safety Science Abstracts KW - intervention KW - nutrition KW - risk reduction KW - cancer KW - Health risks KW - Intervention KW - Nutrition KW - Cancer KW - H 11000:Diseases/Injuries/Trauma KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434033920?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=Community+nutrition+intervention+strategies+for+cancer+risk+reduction&rft.au=Heimendinger%2C+Jerianne&rft.aulast=Heimendinger&rft.aufirst=Jerianne&rft.date=1993-08-01&rft.volume=72&rft.issue=S3&rft.spage=1019&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/10.1002%2F1097-0142%2819930801%2972%3A3%2B3.0.CO%3B2+-B LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-09-01 N1 - Last updated - 2015-08-05 N1 - SubjectsTermNotLitGenreText - Health risks; Intervention; Nutrition; Cancer DO - http://dx.doi.org/10.1002/1097-0142(19930801)72:3+<1019::AID-CNCR2820721313>3.0.CO;2 ER - TY - JOUR T1 - The canadian national breast screening study. An appraisal and implications for early detection policy AN - 1434022341; 18537543 AB - The recent reports from the Canadian National Breast Screening Study (CNBSS) address the effectiveness of breast cancer screening for women in the 40-49 age group and the benefit of adding mammography to standard clinical breast examination in women aged 50-59. Overall, the CNBSS results do not show reductions in breast cancer mortality after seven years of follow-up in either age group. The CNBSS is an important study that includes a large number of women, rigorous procedures, and thorough follow-up, but there are several caveats to interpreting these results. The study results reported to date are based on small numbers of end point events. There are questions about the effectiveness of the randomization procedures in creating cohorts that initially were at equal risk of breast cancer-related death. It also has been observed that the quality level of mammographic screens obtained at the beginning of the study were not as high as those obtained later. Future reports from the CNBSS are planned and may provide additional data helpful in interpreting the results. JF - Cancer AU - Mettlin, Curtis J AU - Smart, Charles R AD - Retired Chief, Early Detection Branch, NCI, HHS. Y1 - 1993/08// PY - 1993 DA - Aug 1993 SP - 1461 EP - 1465 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 72 IS - S4 SN - 0008-543X, 0008-543X KW - Risk Abstracts; Health & Safety Science Abstracts KW - Health risks KW - Mortality KW - Age KW - Breast cancer KW - H 8000:Radiation Safety/Electrical Safety KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434022341?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=The+canadian+national+breast+screening+study.+An+appraisal+and+implications+for+early+detection+policy&rft.au=Mettlin%2C+Curtis+J%3BSmart%2C+Charles+R&rft.aulast=Mettlin&rft.aufirst=Curtis&rft.date=1993-08-01&rft.volume=72&rft.issue=S4&rft.spage=1461&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/10.1002%2F1097-0142%2819930815%2972%3A4%2B3.0.CO%3B2+-S LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-09-01 N1 - Last updated - 2013-10-21 N1 - SubjectsTermNotLitGenreText - Mortality; Health risks; Age; Breast cancer DO - http://dx.doi.org/10.1002/1097-0142(19930815)72:4+<1461::AID-CNCR2820721408>3.0.CO;2 ER - TY - JOUR T1 - Data monitoring in the cardiac arrhythmia suppression trial. AN - 76203731; 8306012 AB - This report discusses practical aspects of data monitoring in a clinical trial which stopped ahead of schedule due to adverse findings. A review of the considerations and decisions made by the data-monitoring committee of the Cardiac Arrhythmia Suppression Trial (CAST), a randomized, double-blind clinical trial. CAST consisted of men and women with a recent myocardial infarction, asymptomatic or minimally symptomatic ventricular arrhythmias, and reduced left ventricular ejection fraction. In CAST, 3 antiarrhythmic agents, encainide, flecainide, and moricizine, were compared against placebo. The main outcome measures in CAST were arrhythmic death and total mortality. CAST found the 3 agents to be harmful. Encainide and flecainide were stopped first. Subsequently, moricizine was discontinued ahead of schedule. The complexity of the study design and a midcourse protocol modification raise several data-monitoring issues not previously discussed. These include how to handle apparently dramatic yet unexpected results, the need for flexibility in modifying study design and goals, and the conflict between existing study data and both conventional wisdom and medical practice. JF - The Online journal of current clinical trials AU - Friedman, L M AU - Bristow, J D AU - Hallstrom, A AU - Schron, E AU - Proschan, M AU - Verter, J AU - DeMets, D AU - Fisch, C AU - Nies, A S AU - Ruskin, J AD - National Heart, Lung, and Blood Institute, Bethesda, MD 20892. Y1 - 1993/07/31/ PY - 1993 DA - 1993 Jul 31 VL - Doc No 79 KW - Anti-Arrhythmia Agents KW - 0 KW - Index Medicus KW - Multicenter Studies as Topic KW - Randomized Controlled Trials as Topic KW - Myocardial Infarction -- complications KW - Humans KW - Data Interpretation, Statistical KW - Research Design KW - Male KW - Female KW - Professional Staff Committees KW - Clinical Trials as Topic KW - Arrhythmias, Cardiac -- drug therapy KW - Decision Making KW - Anti-Arrhythmia Agents -- adverse effects KW - Anti-Arrhythmia Agents -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76203731?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Online+journal+of+current+clinical+trials&rft.atitle=Data+monitoring+in+the+cardiac+arrhythmia+suppression+trial.&rft.au=Friedman%2C+L+M%3BBristow%2C+J+D%3BHallstrom%2C+A%3BSchron%2C+E%3BProschan%2C+M%3BVerter%2C+J%3BDeMets%2C+D%3BFisch%2C+C%3BNies%2C+A+S%3BRuskin%2C+J&rft.aulast=Friedman&rft.aufirst=L&rft.date=1993-07-31&rft.volume=Doc+No+79&rft.issue=&rft.spage=%5B5870+words%3B+53+paragraphs%5D&rft.isbn=&rft.btitle=&rft.title=The+Online+journal+of+current+clinical+trials&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-03-17 N1 - Date created - 1994-03-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Alterations in populations of GST-p-immunoreactive single hepatocytes and hepatocellular foci after a single injection of N-nitrosodiethylamine with or without phenobarbital promotion in male F344/NCr rats. AN - 75942353; 8364903 AB - The fate of placental glutathione S-transferase (GST-P)-immunoreactive hepatocytes, detectable in livers of rats soon after treatment with N-nitrosodiethylamine (DEN), was examined sequentially with or without phenobarbital (PB) promotion. Group 1 male F344/NCr rats were administered a single i.p. injection of 200 mg DEN per kg body weight at 5 weeks of age. Group 2 rats were given 500 ppm PB in the diet two weeks after the DEN treatment. Groups of six rats were sequentially sacrificed 16, 42, 70, 126 and 238 days after DEN injection. In DEN-treated rats, GST-P immunoreactive hepatocytes (single cells and multiple cell foci) were detectable 16 days after DEN, the total numbers decreasing by day 70 and thereafter rising again. In the early stages the proportion of single immunoreactive hepatocytes was prominent, but with time a gradual increase in small GST-P+ hepatocellular foci and larger foci became evident. Feeding of PB to rats for 16-238 days after a single DEN injection resulted in increases of both single cells and foci, especially foci composed of more than three hepatocytes. The growth response was increasingly pronounced with time. Adenomas or carcinomas were only observed at 126 or 238 days. Numbers of GST-P+ foci far exceeded the numbers of foci visible in hematoxylin-eosin (H & E) stained sections, and a few H & E foci were negative for GST-P. Many GST-P+ foci smaller than ten cells were composed of histologically normal hepatocytes. Almost all GST-P+ foci identifiable in H&E stained sections were larger than ten cells, consisted of clear cells (in both groups) or mixed (clear-eosinophilic) cells in PB-exposed rats, and appeared to be evenly distributed throughout the three zones of the liver. These results suggest that the promotive effect of PB is most evident as an increase in larger hepatocyte populations composed of more than three GST-P+ hepatocytes, rather than in increasing the populations of single GST-P immunoreactive cells. PB may cause clonal expansion of these single GST-P reactive hepatocytes. This study provides evidence for the hypothesis that some of the GST-P reactive hepatocytes are initiated cells. JF - Cancer letters AU - Jang, J J AU - Henneman, J R AU - Kurata, Y AU - Uno, H AU - Ward, J M AD - Tumor Pathology and Pathogenesis Section, NCI-FCRDC, Frederick, Maryland 21702-1201. Y1 - 1993/07/30/ PY - 1993 DA - 1993 Jul 30 SP - 89 EP - 95 VL - 71 IS - 1-3 SN - 0304-3835, 0304-3835 KW - Diethylnitrosamine KW - 3IQ78TTX1A KW - Glutathione Transferase KW - EC 2.5.1.18 KW - Phenobarbital KW - YQE403BP4D KW - Index Medicus KW - Rats KW - Body Weight KW - Animals KW - Rats, Inbred F344 KW - Placenta -- enzymology KW - Cells, Cultured KW - Time Factors KW - Organ Size KW - Male KW - Diethylnitrosamine -- toxicity KW - Liver -- enzymology KW - Liver -- cytology KW - Liver -- drug effects KW - Glutathione Transferase -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75942353?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+letters&rft.atitle=Alterations+in+populations+of+GST-p-immunoreactive+single+hepatocytes+and+hepatocellular+foci+after+a+single+injection+of+N-nitrosodiethylamine+with+or+without+phenobarbital+promotion+in+male+F344%2FNCr+rats.&rft.au=Jang%2C+J+J%3BHenneman%2C+J+R%3BKurata%2C+Y%3BUno%2C+H%3BWard%2C+J+M&rft.aulast=Jang&rft.aufirst=J&rft.date=1993-07-30&rft.volume=71&rft.issue=1-3&rft.spage=89&rft.isbn=&rft.btitle=&rft.title=Cancer+letters&rft.issn=03043835&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-06 N1 - Date created - 1993-10-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Mutations at the mouse microphthalmia locus are associated with defects in a gene encoding a novel basic-helix-loop-helix-zipper protein. AN - 75854920; 8343963 AB - Mice with mutations at the microphthalmia (mi) locus have some or all of the following defects: loss of pigmentation, reduced eye size, failure of secondary bone resorption, reduced numbers of mast cells, and early onset of deafness. Using a transgenic insertional mutation at this locus, we have identified a gene whose expression is disrupted in transgenic animals. This gene encodes a novel member of the basic-helix-loop-helix-leucine zipper (bHLH-ZIP) protein family of transcription factors, is altered in mice carrying two independent mi alleles (mi and miws), and is expressed in the developing eye, ear, and skin, all anatomical sites affected by mi. The multiple spontaneous and induced mutations available at mi provide a unique biological resource for studying the role of a bHLH-ZIP protein in mammalian development. JF - Cell AU - Hodgkinson, C A AU - Moore, K J AU - Nakayama, A AU - Steingrímsson, E AU - Copeland, N G AU - Jenkins, N A AU - Arnheiter, H AD - Laboratory of Viral and Molecular Pathogenesis, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/07/30/ PY - 1993 DA - 1993 Jul 30 SP - 395 EP - 404 VL - 74 IS - 2 SN - 0092-8674, 0092-8674 KW - mi KW - DNA-Binding Proteins KW - 0 KW - MITF protein, human KW - Microphthalmia-Associated Transcription Factor KW - Mitf protein, mouse KW - Transcription Factors KW - Index Medicus KW - Animals KW - Protein Structure, Secondary KW - Mice, Transgenic -- embryology KW - Humans KW - Gene Expression KW - Amino Acid Sequence KW - Mice KW - Tissue Distribution KW - Transcription Factors -- genetics KW - Cloning, Molecular KW - Alleles KW - Base Sequence KW - Molecular Sequence Data KW - Genetic Complementation Test KW - Mice, Inbred C3H KW - Mice, Inbred C57BL KW - Sequence Homology, Amino Acid KW - Waardenburg Syndrome -- genetics KW - Vitiligo -- genetics KW - Mutagenesis, Insertional KW - Protein Conformation KW - DNA-Binding Proteins -- genetics KW - Microphthalmos -- genetics KW - Leucine Zippers UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75854920?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cell&rft.atitle=Mutations+at+the+mouse+microphthalmia+locus+are+associated+with+defects+in+a+gene+encoding+a+novel+basic-helix-loop-helix-zipper+protein.&rft.au=Hodgkinson%2C+C+A%3BMoore%2C+K+J%3BNakayama%2C+A%3BSteingr%C3%ADmsson%2C+E%3BCopeland%2C+N+G%3BJenkins%2C+N+A%3BArnheiter%2C+H&rft.aulast=Hodgkinson&rft.aufirst=C&rft.date=1993-07-30&rft.volume=74&rft.issue=2&rft.spage=395&rft.isbn=&rft.btitle=&rft.title=Cell&rft.issn=00928674&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-03 N1 - Date created - 1993-09-03 N1 - Date revised - 2017-01-13 N1 - Gene symbol - mi N1 - Genetic sequence - L19248; GENBANK; L19249; S60905; S60904; S60902; Z23066; S60903; L33709; S60924; L14569 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Ascorbic acid recycling in human neutrophils. AN - 75863259; 8340380 AB - Ascorbic acid (vitamin C) accumulation in activated human neutrophils is increased as much as 10-fold above the mM concentrations present in normal neutrophils. Internal concentrations as high as 14 mM are achieved when external vitamin is at physiologic concentration. The mechanism is by oxidation of external vitamin to dehydroascorbic acid, preferential transmembrane translocation of dehydroascorbic acid, and intracellular reduction to ascorbic acid within minutes. These data indicate that vitamin C accumulation is enhanced in activated human neutrophils and that human neutrophils utilize and recycle oxidized external vitamin C under physiologic conditions. JF - The Journal of biological chemistry AU - Washko, P W AU - Wang, Y AU - Levine, M AD - Section of Cell Biology and Biochemistry, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/07/25/ PY - 1993 DA - 1993 Jul 25 SP - 15531 EP - 15535 VL - 268 IS - 21 SN - 0021-9258, 0021-9258 KW - Antioxidants KW - 0 KW - Xanthines KW - Xanthine KW - 1AVZ07U9S7 KW - N-Formylmethionine Leucyl-Phenylalanine KW - 59880-97-6 KW - Sodium Fluoride KW - 8ZYQ1474W7 KW - Catalase KW - EC 1.11.1.6 KW - Superoxide Dismutase KW - EC 1.15.1.1 KW - Xanthine Oxidase KW - EC 1.17.3.2 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Ascorbic Acid KW - PQ6CK8PD0R KW - Dehydroascorbic Acid KW - Y2Z3ZTP9UM KW - Index Medicus KW - Xanthine Oxidase -- metabolism KW - Humans KW - Superoxide Dismutase -- metabolism KW - Xanthines -- metabolism KW - Catalase -- metabolism KW - N-Formylmethionine Leucyl-Phenylalanine -- pharmacology KW - Oxidation-Reduction KW - Dehydroascorbic Acid -- metabolism KW - Antioxidants -- pharmacology KW - Cells, Cultured KW - Adult KW - Sodium Fluoride -- pharmacology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Male KW - Neutrophils -- metabolism KW - Neutrophils -- drug effects KW - Ascorbic Acid -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75863259?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Ascorbic+acid+recycling+in+human+neutrophils.&rft.au=Washko%2C+P+W%3BWang%2C+Y%3BLevine%2C+M&rft.aulast=Washko&rft.aufirst=P&rft.date=1993-07-25&rft.volume=268&rft.issue=21&rft.spage=15531&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-30 N1 - Date created - 1993-08-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Electroporation enhances c-myc antisense oligodeoxynucleotide efficacy. AN - 19713586; 8734186 AB - Obtaining high transfection efficiencies and achieving appropriate intracellular concentrations and localization are two of the most important barriers to the implementation of gene targeted therapy. The efficiency of endogenous uptake of oligodeoxynucleotides (ODNs) varies from cell type to cell type and may be a limiting factor of antisense efficacy. The use of electroporation to obtain high intracellular concentrations of a synthetic ODN in essentially 100% of viable cells is described. It is also shown that the transfected ODNs initially localize to the nucleus and remain there for at least 48 hours. The cellular trafficking of electroporated ODNs is shown to be an energy dependent process. Targeting of the c-myc proto-oncogene of U937 cells by electroporation of phosphorothioate-modified ODNs results in rapid and specific suppression of this gene at ODN concentrations much lower than would otherwise be required. This technique appears to be applicable to a variety of cell types and may represent a powerful new investigate tool as well as a promising approach to the ex vivo treatment of hematologic disorders. Images JF - Nucleic Acids Research AU - Bergan, R AU - Connell, Y AU - Fahmy, B AU - Neckers, L AD - Clinical Pharmacology Branch, NCI, NIH, Bethesda, MD 20892. Y1 - 1993/07/25/ PY - 1993 DA - 1993 Jul 25 SP - 3567 EP - 3573 PB - Oxford University Press, Oxford Journals, Great Clarendon Street VL - 21 IS - 15 SN - 0305-1048, 0305-1048 KW - Biotechnology and Bioengineering Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - Antisense oligonucleotides KW - Electroporation KW - Transfection KW - Energy KW - Limiting factors KW - Nuclei KW - Oligonucleotides KW - c-Myc protein KW - Proto-oncogenes KW - W 30905:Medical Applications KW - N 14840:Antisense, Nucleotide Analogs UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/19713586?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+Acids+Research&rft.atitle=Electroporation+enhances+c-myc+antisense+oligodeoxynucleotide+efficacy.&rft.au=Bergan%2C+R%3BConnell%2C+Y%3BFahmy%2C+B%3BNeckers%2C+L&rft.aulast=Bergan&rft.aufirst=R&rft.date=1993-07-25&rft.volume=21&rft.issue=15&rft.spage=3567&rft.isbn=&rft.btitle=&rft.title=Nucleic+Acids+Research&rft.issn=03051048&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2008-12-01 N1 - Last updated - 2015-03-27 N1 - SubjectsTermNotLitGenreText - Antisense oligonucleotides; Electroporation; Transfection; Energy; Limiting factors; Nuclei; Oligonucleotides; Proto-oncogenes; c-Myc protein ER - TY - JOUR T1 - Sympathetic nerves, but not the adrenal gland, contribute to elevated plasma levels of met-enkephalin in rats with acute cholestatic hepatitis. AN - 76029802; 8210512 AB - Met-enkephalin is known to circulate in human and animal plasma in low levels. However, the source(s) of plasma met-enkephalin have not been completely elucidated. It has been proposed that the adrenal gland, sympathetic nerves, pancreas and the gut might be implicated. Recently, markedly elevated levels of met-enkephalin have been documented in the presence of liver disease. To investigate potential sources of met-enkephalin in liver disease, rats with acute cholestatic hepatitis 24 h after gavage with alpha naphthylisothiocyanate (ANIT) 100 mg/kg were studied. Plasma met-enkephalin levels were determined by radioimmunoassay in plasma samples from normal, adrenalectomized, or chemically sympathectomized animals. In control rats, ANIT treatment resulted in a striking 8.7-fold increase in systemic venous met-enkephalin levels (inferior vena cava) (P < or = 0.0005) and a significant increase in peptidase-derived met-enkephalin levels (determined after trypsin/carboxypeptidase B digestion of plasma samples) (P < or = 0.05). ANIT-treatment also resulted in a 5.6-fold increase in portal vein met-enkephalin levels (P < or = 0.005). Portal vein met-enkephalin levels were only 1.2-fold higher than IVC levels in ANIT-treated rats (P < or = 0.05). Plasma activities of the two main enkephalin degrading enzymes, aminopeptidase and enkephalinase, were similar in control and ANIT-treated rats. Chemical sympathectomy, prior to ANIT treatment, decreased the elevation in inferior vena caval met-enkephalin levels by 35% (P < or = 0.005). Adrenalectomy did not alter ANIT-induced increases in circulating met-enkephalin levels (pNS).(ABSTRACT TRUNCATED AT 250 WORDS) JF - Regulatory peptides AU - Swain, M G AU - Vergalla, J AU - Bergasa, N V AU - Jones, E A AD - Liver Diseases Section, NIDDK, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/07/23/ PY - 1993 DA - 1993 Jul 23 SP - 535 EP - 542 VL - 46 IS - 3 SN - 0167-0115, 0167-0115 KW - 1-Naphthylisothiocyanate KW - 551-06-4 KW - Enkephalin, Methionine KW - 58569-55-4 KW - Aminopeptidases KW - EC 3.4.11.- KW - Neprilysin KW - EC 3.4.24.11 KW - Index Medicus KW - Animals KW - Portal Vein -- metabolism KW - Aminopeptidases -- blood KW - Sympathectomy, Chemical KW - Disease Models, Animal KW - Adrenalectomy KW - Radioimmunoassay KW - Chromatography, High Pressure Liquid KW - Rats KW - Rats, Sprague-Dawley KW - Neprilysin -- blood KW - Male KW - Enkephalin, Methionine -- blood KW - Sympathetic Nervous System -- secretion KW - Hepatitis, Animal -- chemically induced KW - Hepatitis, Animal -- blood KW - Adrenal Glands -- secretion KW - Cholestasis, Intrahepatic -- chemically induced KW - Cholestasis, Intrahepatic -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76029802?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Regulatory+peptides&rft.atitle=Sympathetic+nerves%2C+but+not+the+adrenal+gland%2C+contribute+to+elevated+plasma+levels+of+met-enkephalin+in+rats+with+acute+cholestatic+hepatitis.&rft.au=Swain%2C+M+G%3BVergalla%2C+J%3BBergasa%2C+N+V%3BJones%2C+E+A&rft.aulast=Swain&rft.aufirst=M&rft.date=1993-07-23&rft.volume=46&rft.issue=3&rft.spage=535&rft.isbn=&rft.btitle=&rft.title=Regulatory+peptides&rft.issn=01670115&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-01 N1 - Date created - 1993-11-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Genetic risk and carcinogen exposure: a common inherited defect of the carcinogen-metabolism gene glutathione S-transferase M1 (GSTM1) that increases susceptibility to bladder cancer. AN - 75827798; 8320745 AB - Numerous studies have associated bladder cancer with exposure to carcinogens present in tobacco smoke and other environmental or occupational exposures. Approximately 50% of all humans inherit two deleted copies of the GSTM1 gene which encodes for the carcinogen-detoxification enzyme glutathione S-transferase M1. Recent findings suggest that the GSTM1 gene may modulate the internal dose of environmental carcinogens and thereby affect the risk of developing bladder cancer. We investigated whether the absence of the GSTM1 gene affects bladder cancer risk and whether there are racial differences in GSTM1 genotype frequency. Using a polymerase chain reaction (PCR)-based method, we examined the frequency of the homozygous deleted genotype (GSTM1 0/0) in 229 patients with transitional cell carcinoma of the bladder and 211 control subjects who were enrolled from the Urology Clinics at Duke University Medical Center and the University of North Carolina Hospitals. Control subjects were urology clinic patients who primarily presented with benign prostatic hypertrophy or impotence, who had no history of any cancer other than nonmelanoma skin cancer, and who were frequency matched to case patients on race, sex, and age (10-year age intervals). In order to explore racial differences in GSTM1 gene frequency, genotype was also determined in a community-based sample of 466 paid, healthy, unrelated volunteers from Durham and Chapel Hill, N.C. The presence or absence of the GSTM1 gene locus was determined by using a differential PCR, a semiquantitative technique in which multiple genes are coamplified. Overall, the GSTM1 0/0 genotype conferred a 70% increased risk of bladder cancer (odds ratio [OR] = 1.7; 95% confidence interval [CI] = 1.2-2.5; P = .004). Absence of the GSTM1 gene encoding the glutathione S-transferase M1 enzyme significantly increased risk to persons with exposure to the carcinogens in tobacco smoke (OR = 1.8; 95% CI = 1.2-3.0; P = .01) but poses little increased risk to persons without such exposure. Persons with smoking exposure of more than 50 pack-years who had the GSTM1 0/0 genotype had a sixfold greater risk relative to persons in the lowest risk group (i.e., nonsmokers who were GSTM1 +/+ or +/0). In the pooled clinic control and community sample groups (677 individuals), the GSTM1 0/0 genotype occurred less frequently among Blacks (35%) than among Whites (49%, P < .001). These findings support a protective role for the GSTM1 gene in bladder cancer. From these findings, it is estimated that 25% of all bladder cancer may be attributable to the at-risk GSTM1 0/0 genotype. JF - Journal of the National Cancer Institute AU - Bell, D A AU - Taylor, J A AU - Paulson, D F AU - Robertson, C N AU - Mohler, J L AU - Lucier, G W AD - Laboratory of Biochemical Risk Analysis, National Institute of Environmental Health-Sciences (NIEHS), Research Triangle Park, N.C. 27709. Y1 - 1993/07/21/ PY - 1993 DA - 1993 Jul 21 SP - 1159 EP - 1164 VL - 85 IS - 14 SN - 0027-8874, 0027-8874 KW - GSTM1 KW - Isoenzymes KW - 0 KW - Glutathione Transferase KW - EC 2.5.1.18 KW - Index Medicus KW - Genotype KW - Polymerase Chain Reaction KW - Continental Population Groups -- genetics KW - Base Sequence KW - Humans KW - Molecular Sequence Data KW - Smoking -- adverse effects KW - Genetic Predisposition to Disease KW - Male KW - Female KW - Urinary Bladder Neoplasms -- genetics KW - Urinary Bladder Neoplasms -- enzymology KW - Glutathione Transferase -- genetics KW - Isoenzymes -- genetics KW - Carcinoma, Transitional Cell -- genetics KW - Carcinoma, Transitional Cell -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75827798?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Genetic+risk+and+carcinogen+exposure%3A+a+common+inherited+defect+of+the+carcinogen-metabolism+gene+glutathione+S-transferase+M1+%28GSTM1%29+that+increases+susceptibility+to+bladder+cancer.&rft.au=Bell%2C+D+A%3BTaylor%2C+J+A%3BPaulson%2C+D+F%3BRobertson%2C+C+N%3BMohler%2C+J+L%3BLucier%2C+G+W&rft.aulast=Bell&rft.aufirst=D&rft.date=1993-07-21&rft.volume=85&rft.issue=14&rft.spage=1159&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-05 N1 - Date created - 1993-08-05 N1 - Date revised - 2017-01-13 N1 - Gene symbol - GSTM1 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Crystal structures of native and inhibited forms of human cathepsin D: implications for lysosomal targeting and drug design. AN - 75862919; 8393577 AB - Cathepsin D (EC 3.4.23.5) is a lysosomal protease suspected to play important roles in protein catabolism, antigen processing, degenerative diseases, and breast cancer progression. Determination of the crystal structures of cathepsin D and a complex with pepstatin at 2.5 A resolution provides insights into inhibitor binding and lysosomal targeting for this two-chain, N-glycosylated aspartic protease. Comparison with the structures of a complex of pepstatin bound to rhizopuspepsin and with a human renin-inhibitor complex revealed differences in subsite structures and inhibitor-enzyme interactions that are consistent with affinity differences and structure-activity relationships and suggest strategies for fine-tuning the specificity of cathepsin D inhibitors. Mutagenesis studies have identified a phosphotransferase recognition region that is required for oligosaccharide phosphorylation but is 32 A distant from the N-domain glycosylation site at Asn-70. Electron density for the crystal structure of cathepsin D indicated the presence of an N-linked oligosaccharide that extends from Asn-70 toward Lys-203, which is a key component of the phosphotransferase recognition region, and thus provides a structural explanation for how the phosphotransferase can recognize apparently distant sites on the protein surface. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Baldwin, E T AU - Bhat, T N AU - Gulnik, S AU - Hosur, M V AU - Sowder, R C AU - Cachau, R E AU - Collins, J AU - Silva, A M AU - Erickson, J W AD - Structural Biochemistry Program, Program Resources Inc./DynCorp, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702. Y1 - 1993/07/15/ PY - 1993 DA - 1993 Jul 15 SP - 6796 EP - 6800 VL - 90 IS - 14 SN - 0027-8424, 0027-8424 KW - Pepstatins KW - 0 KW - Streptomyces pepsin inhibitor KW - 11076-29-2 KW - Phosphotransferases KW - EC 2.7.- KW - Aspartic Acid Endopeptidases KW - EC 3.4.23.- KW - Renin KW - EC 3.4.23.15 KW - rhizopuspepsin KW - EC 3.4.23.21 KW - Cathepsin D KW - EC 3.4.23.5 KW - pepstatin KW - V6Y2T27Q1U KW - Index Medicus KW - Renin -- chemistry KW - X-Ray Diffraction KW - Models, Molecular KW - Humans KW - Biological Transport KW - Amino Acid Sequence KW - Aspartic Acid Endopeptidases -- chemistry KW - Glycosylation KW - Drug Design KW - Molecular Sequence Data KW - Lysosomes KW - Protein Conformation KW - Cathepsin D -- antagonists & inhibitors KW - Pepstatins -- chemistry KW - Cathepsin D -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75862919?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Crystal+structures+of+native+and+inhibited+forms+of+human+cathepsin+D%3A+implications+for+lysosomal+targeting+and+drug+design.&rft.au=Baldwin%2C+E+T%3BBhat%2C+T+N%3BGulnik%2C+S%3BHosur%2C+M+V%3BSowder%2C+R+C%3BCachau%2C+R+E%3BCollins%2C+J%3BSilva%2C+A+M%3BErickson%2C+J+W&rft.aulast=Baldwin&rft.aufirst=E&rft.date=1993-07-15&rft.volume=90&rft.issue=14&rft.spage=6796&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-30 N1 - Date created - 1993-08-30 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Biochem Biophys Res Commun. 1967 Apr 20;27(2):157-62 [6035483] J Mol Biol. 1990 Jul 5;214(1):143-70 [2115087] Proteins. 1990;8(1):62-81 [2217165] Nature. 1991 Feb 21;349(6311):669-76 [1847504] Semin Cancer Biol. 1990 Apr;1(2):153-60 [2103491] Semin Cancer Biol. 1990 Apr;1(2):99-106 [2103492] Science. 1991 Nov 8;254(5033):862-6 [1948067] J Biol Chem. 1991 Dec 5;266(34):23365-72 [1660471] Sci Am. 1992 Feb;266(2):54-9, 62-3 [1373003] Proteins. 1992 Jul;13(3):195-205 [1603809] Nature. 1992 Jun 11;357(6378):466-72 [1608447] J Mol Biol. 1992 Jul 20;226(2):555-7 [1640466] J Mol Biol. 1992 Sep 5;227(1):265-70 [1522590] J Biol Chem. 1992 Nov 15;267(32):23342-8 [1331081] J Biol Chem. 1992 Nov 15;267(32):23349-56 [1331082] J Biol Chem. 1992 Nov 15;267(32):23357-63 [1331083] J Mol Biol. 1992 Oct 20;227(4):1265-8 [1433300] Protein Sci. 1993 Feb;2(2):264-76 [8443603] J Mol Biol. 1977 May 25;112(3):535-42 [875032] Methods Enzymol. 1979;63:437-67 [502865] Annu Rev Biochem. 1986;55:167-93 [2943218] J Med Chem. 1986 Dec;29(12):2519-24 [3783611] Can J Physiol Pharmacol. 1987 Feb;65(2):124-9 [3552162] Biochemistry. 1987 Dec 15;26(25):8083-6 [3327517] J Biol Chem. 1988 Nov 5;263(31):16504-11 [3182800] Science. 1989 Mar 10;243(4896):1346-51 [2493678] J Biol Chem. 1989 Aug 25;264(24):14159-64 [2474542] J Neurosci Res. 1989 Aug;23(4):454-6 [2769800] EMBO J. 1989 Aug;8(8):2179-88 [2676515] Annu Rev Cell Biol. 1989;5:483-525 [2557062] Nature. 1990 Jan 11;343(6254):133-9 [2404209] Biochem J. 1990 Feb 1;265(3):871-8 [2407237] Proc Natl Acad Sci U S A. 1990 May;87(10):3861-5 [1692625] Annu Rev Biophys Biophys Chem. 1990;19:189-215 [2194475] Cell. 1990 Oct 19;63(2):281-91 [2170024] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Fidelity of DNA replication by extracts of normal and malignantly transformed human cells. AN - 75861597; 8391921 AB - To test the hypothesis that a mutator phenotype may be associated with carcinogenesis (L. A. Loeb, Cancer Res., 51: 3074-3079, 1991), we have compared the fidelity of double-stranded DNA replication and the efficiency of mismatch repair in extracts from normal diploid and malignantly transformed human cells. Included was a diploid fibroblast strain and its transformed derivative, as well as a second diploid fibroblast strain and HeLa cells. The fidelity of DNA replication by cytoplasmic extracts in the presence of simian virus 40 large tumor antigen (SV40 T-antigen) was measured using a forward mutagenesis assay. The replicated DNA consisted of double-stranded M13 mp2 DNA containing the SV40 origin of replication and the lacZ alpha complementation gene as a target sequence for scoring mutations. T-antigen-dependent replication was detected in all cell extracts, with those from transformed cells having the greatest activity. No differences in replication fidelity were detected between normal and transformed cell extracts. Using a heteroduplex containing a G.G mispair, we also detected mismatch repair activity in the cell extracts, including efficient repair in extracts from malignantly transformed cells. While these data do not eliminate the possibility that a mutator phenotype may be associated with carcinogenesis, they do suggest that genetic instability associated with transformation does not involve reduced fidelity of replication of undamaged DNA or reduced mismatch repair efficiency. JF - Cancer research AU - Boyer, J C AU - Thomas, D C AU - Maher, V M AU - McCormick, J J AU - Kunkel, T A AD - Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993/07/15/ PY - 1993 DA - 1993 Jul 15 SP - 3270 EP - 3275 VL - 53 IS - 14 SN - 0008-5472, 0008-5472 KW - DNA, Neoplasm KW - 0 KW - Index Medicus KW - Phenotype KW - HeLa Cells KW - Simian virus 40 -- genetics KW - Humans KW - Escherichia coli -- genetics KW - Cell Line, Transformed KW - Male KW - Fibroblasts KW - DNA Repair KW - Mutation -- genetics KW - Neoplasms -- genetics KW - DNA Replication UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75861597?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Fidelity+of+DNA+replication+by+extracts+of+normal+and+malignantly+transformed+human+cells.&rft.au=Boyer%2C+J+C%3BThomas%2C+D+C%3BMaher%2C+V+M%3BMcCormick%2C+J+J%3BKunkel%2C+T+A&rft.aulast=Boyer&rft.aufirst=J&rft.date=1993-07-15&rft.volume=53&rft.issue=14&rft.spage=3270&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-10 N1 - Date created - 1993-08-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Functionally anergic lpr and gld B220+ T cell receptor (TCR)-alpha/beta+ double-negative T cells express CD28 and respond to costimulation with phorbol myristate acetate and antibodies to CD28 and the TCR. AN - 75859253; 7687618 AB - Mice homozygous for lpr and gld develop lymphadenopathy characterized by the progressive accumulation of an unusual population of CD4-, CD8-, CD2-, IL-2R- double-negative (DN) T cells that express reduced levels of TCR-alpha/beta, high levels of CD45 (B220) and Ly-6C and variable levels of CD69. These cells are refractory to most stimuli, including staphylococcal entertoxins and cross-linking of the TCR, Ly-6C, and CD69. For normal T cells, the binding of ligand to the TCR alone is insufficient to induce a proliferative response and can result in the induction of a state of prolonged anergy. Efficient stimulation is dependent on the delivery of a second or costimulatory signal. Recently it was reported that CD28 can provide costimulatory signals to T cells and, that these signals can prevent anergy induction in T cell clones. We investigated the possibility that lpr and gld DN T cells are unresponsive because they fail to transduce signals via CD28. These studies showed that highly purified B220+ TCR-alpha/beta+ DN T cells expressed high levels of CD28, responded weakly to stimulation with PMA and anti-CD28 mAb and quite strongly to PMA, anti-CD28 antibody and high concentrations of immobilized anti-TCR-alpha/beta antibodies. The latter stimulus also induced low levels of expression of CD2 and IL-2R and secretion of modest amounts of IL-2. Although DN T cells proliferated and secreted IL-2, these responses differed qualitatively and quantitatively from those of +/+ and lprB220- T cells. Consistent with its effects on normal T cells, cyclosporin A partially inhibited the response of DN T cells to TCR cross-linking and CD28 ligation. Studies of synergism between CD28-, Ly-6C-, and CD69-mediated signals revealed that ligation of CD28 enhanced the proliferative response induced by cross-linking of Ly-6C or CD69 on +/+, lpr and gld B220- T cells but had no effect on the unresponsiveness of DN T cells to these stimuli. Ligation of CD28 did not reverse the unresponsiveness of DN T cells to SEB and had only a weak synergistic effect on the response of B220- T cells. Together, these observations suggest that the mechanisms leading to immunosuppression of DN T cells are complex and appear to involve abnormalities in signal transduction via the TCR and CD28 and possibly via Ly-6C and CD69 as well. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Giese, T AU - Allison, J P AU - Davidson, W F AD - Laboratory of Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/07/15/ PY - 1993 DA - 1993 Jul 15 SP - 597 EP - 609 VL - 151 IS - 2 SN - 0022-1767, 0022-1767 KW - gld KW - lpr KW - Antibodies, Monoclonal KW - 0 KW - Antigens, CD KW - Antigens, CD28 KW - Antigens, CD4 KW - Antigens, CD8 KW - Antigens, Differentiation, T-Lymphocyte KW - Antigens, Surface KW - Enterotoxins KW - Interleukin-2 KW - Receptors, Antigen, T-Cell, alpha-beta KW - enterotoxin B, staphylococcal KW - 39424-53-8 KW - Cyclosporine KW - 83HN0GTJ6D KW - Antigens, CD45 KW - EC 3.1.3.48 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Enterotoxins -- immunology KW - Animals KW - Cyclosporine -- pharmacology KW - Mice, Inbred C3H KW - Mice KW - Interleukin-2 -- secretion KW - Antibodies, Monoclonal -- immunology KW - Antigens, CD -- analysis KW - Antigens, CD -- physiology KW - Antigens, CD8 -- analysis KW - Lymphoproliferative Disorders -- immunology KW - Immune Tolerance KW - Receptors, Antigen, T-Cell, alpha-beta -- physiology KW - Lymphocyte Activation KW - Antigens, Differentiation, T-Lymphocyte -- analysis KW - Antigens, CD4 -- analysis KW - Antigens, Differentiation, T-Lymphocyte -- physiology KW - T-Lymphocyte Subsets -- immunology KW - Receptors, Antigen, T-Cell, alpha-beta -- analysis KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Antigens, Surface -- analysis KW - Autoimmune Diseases -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75859253?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=Functionally+anergic+lpr+and+gld+B220%2B+T+cell+receptor+%28TCR%29-alpha%2Fbeta%2B+double-negative+T+cells+express+CD28+and+respond+to+costimulation+with+phorbol+myristate+acetate+and+antibodies+to+CD28+and+the+TCR.&rft.au=Giese%2C+T%3BAllison%2C+J+P%3BDavidson%2C+W+F&rft.aulast=Giese&rft.aufirst=T&rft.date=1993-07-15&rft.volume=151&rft.issue=2&rft.spage=597&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.issn=00221767&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-25 N1 - Date created - 1993-08-25 N1 - Date revised - 2017-01-13 N1 - Gene symbol - gld; lpr N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Oxygen tension distributions are sufficient to explain the local response of human breast tumors treated with radiation alone. AN - 75845023; 8330993 AB - Several factors are known to influence the probability of tumor control after radiation. These include tumor oxygen tension distribution, glutathione content, intrinsic radiation sensitivity, rate of repopulation, tumor size, physician skill, etc. The relative impact of oxygen on human tumor response is unknown. The purpose of this analysis is to determine to what extent the observed shape of the radiation response curve for human tumors can be predicted by the tumor oxygenation status. The radiation dose response curve for patients treated with radiation alone for breast cancer was calculated based on pooled data. Tumor control rates as a function of radiation dose were fitted to a probit curve. Twenty-two women with breast cancer in Mainz (Germany) and at Stanford University had pO2 measurements made of their tumors. An average of 87 +/- 58 (range 21 to 300) measurements were made from each patient. Hypoxia was assumed to be a purely dose modifying factor with a maximum oxygen enhancement ratio of 2.5. Assuming patients are treated with daily radiation doses of 2 Gy, the breast cancer alpha/beta ratio is 10 Gy, tumors have a mean of 10(8) stem cells, and using the linear quadratic formula for modelling surviving fraction, it was possible to estimate tumor control probability. Tumor oxygenation was an extremely important modifier of the shape of the dose response curve and alone was sufficient to account for the slope of the observed dose response curve for human breast carcinoma. Tumor size distribution had a smaller effect on the shape and the slope of the dose response curve. Two models of radiation induced reoxygenation were tested, one that allowed full reoxygenation to the baseline state between the daily radiation fractions and another with no reoxygenation between fractions. The clinical data fell between these two models in accordance with the expected incomplete reoxygenation between treatments. The results support the conclusion that in human breast carcinoma, oxygen tension distribution is a critical modifier of radiation treatment response. JF - International journal of radiation oncology, biology, physics AU - Okunieff, P AU - Hoeckel, M AU - Dunphy, E P AU - Schlenger, K AU - Knoop, C AU - Vaupel, P AD - Radiation Oncology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/07/15/ PY - 1993 DA - 1993 Jul 15 SP - 631 EP - 636 VL - 26 IS - 4 SN - 0360-3016, 0360-3016 KW - Oxygen KW - S88TT14065 KW - Index Medicus KW - Humans KW - Dose-Response Relationship, Radiation KW - Partial Pressure KW - Female KW - Breast Neoplasms -- physiopathology KW - Breast Neoplasms -- radiotherapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75845023?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+radiation+oncology%2C+biology%2C+physics&rft.atitle=Oxygen+tension+distributions+are+sufficient+to+explain+the+local+response+of+human+breast+tumors+treated+with+radiation+alone.&rft.au=Okunieff%2C+P%3BHoeckel%2C+M%3BDunphy%2C+E+P%3BSchlenger%2C+K%3BKnoop%2C+C%3BVaupel%2C+P&rft.aulast=Okunieff&rft.aufirst=P&rft.date=1993-07-15&rft.volume=26&rft.issue=4&rft.spage=631&rft.isbn=&rft.btitle=&rft.title=International+journal+of+radiation+oncology%2C+biology%2C+physics&rft.issn=03603016&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-19 N1 - Date created - 1993-08-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The fifth transmembrane segment of the neuromedin B receptor is critical for high affinity neuromedin B binding. AN - 75834306; 8392057 AB - The two bombesin receptor subtypes, neuromedin B (NMB-R) and gastrin releasing peptide (GRP-R) receptors, bind their respective ligands with high affinity. To identify molecular components mediating high affinity NMB binding, four mutant receptors were constructed, in which different parts of the NMB-R were replaced with the corresponding regions of the GRP-R. When stably expressed in Balb 3T3 fibroblasts, all four NMB-R/GRP-R chimeras were functional and showed NMB-induced stimulation of inositol phosphate (IP) formation. Results of 125I-[D-Tyr0]NMB displacement assays using unlabeled NMB for competition indicated that high affinity NMB binding was determined by amino acid sequences in transmembrane domain V (TM-V) of the NMB-R. To identify which amino acid(s) in TM-V of NMB-R contributed to high affinity NMB binding, four additional NMB-R mutants were constructed where non-conserved amino acids in TM-V of NMB-R were replaced by the corresponding GRP-R amino acids. Three of the mutations, TyrPheLeu220-222-->PheTyrVal, Ile230-->Val, and His234-->Phe, did not affect high affinity NMB binding. The Ile216-->Ser substitution, however, abolished high affinity NMB binding and severely impaired the ability of the mutant receptor to stimulate NMB-dependent inositol phosphate formation. These results suggest that ILe216 in TM-V of NMB-R may be critical for high affinity NMB binding. JF - The Journal of biological chemistry AU - Fathi, Z AU - Benya, R V AU - Shapira, H AU - Jensen, R T AU - Battey, J F AD - Laboratory of Biological Chemistry, Development Therapeutics Program, Division of Cancer Treatment, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1993/07/15/ PY - 1993 DA - 1993 Jul 15 SP - 14622 EP - 14626 VL - 268 IS - 20 SN - 0021-9258, 0021-9258 KW - Receptors, Bombesin KW - 0 KW - Receptors, Neurotransmitter KW - Neurokinin B KW - 86933-75-7 KW - neuromedin B KW - 87096-84-2 KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Animals KW - 3T3 Cells KW - Sequence Alignment KW - Humans KW - Molecular Sequence Data KW - Cell Membrane -- chemistry KW - Mice KW - Amino Acid Sequence KW - Cell Membrane -- metabolism KW - Mice, Inbred BALB C KW - Binding Sites KW - Receptors, Neurotransmitter -- chemistry KW - Neurokinin B -- genetics KW - Receptors, Neurotransmitter -- metabolism KW - Receptors, Neurotransmitter -- genetics KW - Neurokinin B -- metabolism KW - Neurokinin B -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75834306?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=The+fifth+transmembrane+segment+of+the+neuromedin+B+receptor+is+critical+for+high+affinity+neuromedin+B+binding.&rft.au=Fathi%2C+Z%3BBenya%2C+R+V%3BShapira%2C+H%3BJensen%2C+R+T%3BBattey%2C+J+F&rft.aulast=Fathi&rft.aufirst=Z&rft.date=1993-07-15&rft.volume=268&rft.issue=20&rft.spage=14622&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-12 N1 - Date created - 1993-08-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - A wide range of human cancers express interleukin 4 (IL4) receptors that can be targeted with chimeric toxin composed of IL4 and Pseudomonas exotoxin. AN - 75807973; 8314773 AB - A chimeric toxin has been constructed by fusion of a gene encoding human interleukin 4 (hIL4) to a gene encoding a mutant form of Pseudomonas exotoxin A (PE) which cannot bind to its receptors (PE4E). The chimeric gene was expressed in Escherichia coli where large amounts of the chimeric toxin, hIL4-PE4E, was produced. Purified hIL4-PE4E was very cytotoxic to cancer cell lines of both hematopoietic and solid tumor origin. In the HUT 102 T cell leukemia and Daudi B cell lymphoma cell lines, protein synthesis was inhibited by 50% (ID50) at a hIL4-PE4E concentration of 2 and 7 ng/ml (25 and 86 pM, respectively). hIL4-PE4E was also very cytotoxic to cell lines derived from carcinomas of the colon, breast, stomach, liver, adrenals, and prostate, as well as melanoma and epidermoid carcinoma, indicating that hIL4 receptors are widely expressed on human malignancies. We also found that human phytohemagglutinin-activated peripheral blood lymphocytes were extremely sensitive to hIL4-PE4E with an ID50 of 0.2 ng/ml (2.5 pM). The cytotoxic action of hIL4-PE4E was specific because it was blocked by an excess of hIL4 and not of human interleukin 2. In addition, hIL4-PE4ED553, an enzymatically inactive form of the chimeric toxin, was not cytotoxic. These results suggest that the hIL4 receptor may be a target for therapy in malignant and immunologic disorders using hIL4 chimeric toxin. JF - The Journal of biological chemistry AU - Debinski, W AU - Puri, R K AU - Kreitman, R J AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/07/05/ PY - 1993 DA - 1993 Jul 05 SP - 14065 EP - 14070 VL - 268 IS - 19 SN - 0021-9258, 0021-9258 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - Oligodeoxyribonucleotides KW - Protein Synthesis Inhibitors KW - Receptors, Interleukin-4 KW - Receptors, Mitogen KW - Recombinant Fusion Proteins KW - Virulence Factors KW - Interleukin-4 KW - 207137-56-2 KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - Humans KW - Escherichia coli -- genetics KW - Cloning, Molecular KW - Base Sequence KW - Protein Synthesis Inhibitors -- toxicity KW - Tumor Cells, Cultured KW - Cell Survival -- drug effects KW - Binding, Competitive KW - Molecular Sequence Data KW - Pseudomonas aeruginosa KW - Female KW - Male KW - Receptors, Mitogen -- drug effects KW - Interleukin-4 -- toxicity KW - Receptors, Mitogen -- metabolism KW - Exotoxins -- toxicity KW - Recombinant Fusion Proteins -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75807973?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=A+wide+range+of+human+cancers+express+interleukin+4+%28IL4%29+receptors+that+can+be+targeted+with+chimeric+toxin+composed+of+IL4+and+Pseudomonas+exotoxin.&rft.au=Debinski%2C+W%3BPuri%2C+R+K%3BKreitman%2C+R+J%3BPastan%2C+I&rft.aulast=Debinski&rft.aufirst=W&rft.date=1993-07-05&rft.volume=268&rft.issue=19&rft.spage=14065&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-27 N1 - Date created - 1993-07-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Characterization of upstream activation elements essential for the expression of germ cell alkaline phosphatase in human choriocarcinoma cells. AN - 75807942; 8314767 AB - Expression of the germ cell alkaline phosphatase is a highly regulated process tied to malignant transformation of the human placenta. Human choriocarcinoma cells (malignant trophoblasts) express primarily the germ cell alkaline phosphatase gene and only low or nondetectable levels of the placental alkaline phosphatase normally found in the human placenta. Here, we show that nucleotides -156 to -1 region relative to the gene transcription start site (+1) contain cis-acting DNA elements that direct germ cell alkaline phosphatase expression in choriocarcinoma cells. Within the minimal activator region, at least three nuclear protein-binding sites, I (-63/-44), II (-87/-67), and III (-136/-103), were identified by DNase I footprinting analysis. All three sites are GC-rich. Sites I and II contain a sequence known to bind the transcription factor AP-2; the AP-2 site in site II overlaps a consensus motif for the transcription factor Sp1. Gel retardation experiments showed that similar nuclear protein factor(s) in JEG-3 choriocarcinoma cells bind to all three sites, with highest affinity to sites I and II. Site-directed mutagenesis that prevents binding of nuclear proteins to either site I or II, or both sites I and II, resulted in the loss of factor binding and reduced activator activity. The germ cell alkaline phosphatase promoter that contains an intact binding site III but altered sites I and II had little activator activity, suggesting that protein-protein interaction is important for germ cell alkaline phosphatase gene activation. JF - The Journal of biological chemistry AU - Wada, N AU - Chou, J Y AD - Human Genetics Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/07/05/ PY - 1993 DA - 1993 Jul 05 SP - 14003 EP - 14010 VL - 268 IS - 19 SN - 0021-9258, 0021-9258 KW - Nuclear Proteins KW - 0 KW - Oligodeoxyribonucleotides KW - Alkaline Phosphatase KW - EC 3.1.3.1 KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Base Sequence KW - Tumor Cells, Cultured KW - Cell Nucleus -- metabolism KW - Humans KW - Molecular Sequence Data KW - Choriocarcinoma KW - Uterine Neoplasms KW - Transcriptional Activation KW - Female KW - Pregnancy KW - Binding Sites KW - Gene Expression Regulation, Neoplastic KW - Promoter Regions, Genetic KW - Gene Expression Regulation, Enzymologic KW - Alkaline Phosphatase -- biosynthesis KW - Alkaline Phosphatase -- genetics KW - Ovum -- enzymology KW - Nuclear Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75807942?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Characterization+of+upstream+activation+elements+essential+for+the+expression+of+germ+cell+alkaline+phosphatase+in+human+choriocarcinoma+cells.&rft.au=Wada%2C+N%3BChou%2C+J+Y&rft.aulast=Wada&rft.aufirst=N&rft.date=1993-07-05&rft.volume=268&rft.issue=19&rft.spage=14003&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-27 N1 - Date created - 1993-07-27 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - L12591; GENBANK N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Nucleolar targeting signal of Rex protein of human T-cell leukemia virus type I specifically binds to nucleolar shuttle protein B-23. AN - 75806863; 8314759 AB - Rex protein, the post-transcriptional regulator of human T-cell leukemia virus type I, is located predominantly in the cell nucleolus and is associated with the cytoplasmic accumulation of unspliced and singly spliced viral mRNAs. The N-terminal 19-amino acid segment of Rex has been identified as the nucleolar targeting signal (NOS) and shown to be important for Rex function. To study the molecular interaction between the NOS region of Rex and its binding host protein(s) in the nucleolus, we chemically synthesized a functional NOS peptide (wild type) and mutant NOS peptides. Fluorescein isothiocyanate-conjugated functional NOS peptide was rapidly taken up by human cells and was transported to the nucleolus. Using affinity chromatography, we identified nucleolar protein B-23 as the major protein that binds to NOS. We also identified two highly acidic regions of B-23 (amino acids 120-132 and 161-188) as acceptor regions for NOS. Previous experiments have suggested that B-23 functions as a shuttle protein for the nucleolar transport of ribosomal components. Our results suggest that B-23 may also serve as a shuttle for the import of Rex from the cytoplasm to the nucleolus coupled to the export of viral mRNAs containing the Rex-responsive element. JF - The Journal of biological chemistry AU - Adachi, Y AU - Copeland, T D AU - Hatanaka, M AU - Oroszlan, S AD - Laboratory of Molecular Virology and Carcinogenesis, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, Maryland 21702-1201. Y1 - 1993/07/05/ PY - 1993 DA - 1993 Jul 05 SP - 13930 EP - 13934 VL - 268 IS - 19 SN - 0021-9258, 0021-9258 KW - Gene Products, rex KW - 0 KW - Immune Sera KW - Nuclear Proteins KW - Peptides KW - nucleophosmin KW - 117896-08-9 KW - Index Medicus KW - AIDS/HIV KW - Chromatography, Affinity KW - Tumor Cells, Cultured KW - HeLa Cells KW - Cell Nucleus -- metabolism KW - Humans KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Protein Binding KW - Peptides -- chemical synthesis KW - Gene Products, rex -- metabolism KW - Nuclear Proteins -- isolation & purification KW - Peptides -- metabolism KW - Human T-lymphotropic virus 1 -- metabolism KW - Nuclear Proteins -- metabolism KW - Cell Nucleolus -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75806863?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Nucleolar+targeting+signal+of+Rex+protein+of+human+T-cell+leukemia+virus+type+I+specifically+binds+to+nucleolar+shuttle+protein+B-23.&rft.au=Adachi%2C+Y%3BCopeland%2C+T+D%3BHatanaka%2C+M%3BOroszlan%2C+S&rft.aulast=Adachi&rft.aufirst=Y&rft.date=1993-07-05&rft.volume=268&rft.issue=19&rft.spage=13930&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-27 N1 - Date created - 1993-07-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Regional specificity of membrane instability in Alzheimer's disease brain. AN - 75934396; 8364743 AB - We report an inherent tendency towards the destabilisation of cellular membranes in Alzheimer's disease (AD) brain. This tendency is a natural consequence of abnormal membrane lipid composition, which has previously been documented in AD. Membrane destabilisation may contribute to AD pathogenesis in its own right and may also facilitate amyloid beta-protein deposition, which is potentially neurotoxic. The instability was found to co-localise selectively with areas of neurodegeneration in AD brain, thereby possibly accounting for the focal pathology observed in this disorder. JF - Brain research AU - Ginsberg, L AU - Atack, J R AU - Rapoport, S I AU - Gershfeld, N L AD - Laboratory of Physical Biology, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/07/02/ PY - 1993 DA - 1993 Jul 02 SP - 355 EP - 357 VL - 615 IS - 2 SN - 0006-8993, 0006-8993 KW - Membrane Lipids KW - 0 KW - Index Medicus KW - Nerve Degeneration KW - Aged, 80 and over KW - Humans KW - Membrane Lipids -- metabolism KW - Temperature KW - Aged KW - Cell Membrane -- physiology KW - Cell Membrane -- metabolism KW - Male KW - Female KW - Brain -- pathology KW - Brain -- metabolism KW - Alzheimer Disease -- metabolism KW - Alzheimer Disease -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75934396?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research&rft.atitle=Regional+specificity+of+membrane+instability+in+Alzheimer%27s+disease+brain.&rft.au=Ginsberg%2C+L%3BAtack%2C+J+R%3BRapoport%2C+S+I%3BGershfeld%2C+N+L&rft.aulast=Ginsberg&rft.aufirst=L&rft.date=1993-07-02&rft.volume=615&rft.issue=2&rft.spage=355&rft.isbn=&rft.btitle=&rft.title=Brain+research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-04 N1 - Date created - 1993-10-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Interleukin-7: a cofactor for V(D)J rearrangement of the T cell receptor beta gene. AN - 75806660; 7686307 AB - The diversity of the T cell receptor repertoire is generated by rearrangement of gene elements in immature thymocytes. To identify a thymic signal that induces this rearrangement, a variety of agents were tested for their ability to induce rearrangement of the T cell receptor beta gene in suspensions of thymocytes from mouse embryos at day 14 of gestation. Of 16 agents tested, only interleukin-7 (IL-7) induced V(D)J gene rearrangement and sustained expression of the RAG-1 and RAG-2 genes, which are known to control rearrangement. These data implicate IL-7, a cytokine that is abundantly expressed in embryonic thymus, in driving gene rearrangement during early T cell development. JF - Science (New York, N.Y.) AU - Muegge, K AU - Vila, M P AU - Durum, S K AD - Biological Carcinogenesis and Development Program, Program Resources Inc./Dyncorp, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702. Y1 - 1993/07/02/ PY - 1993 DA - 1993 Jul 02 SP - 93 EP - 95 VL - 261 IS - 5117 SN - 0036-8075, 0036-8075 KW - RAG-1 KW - RAG-2 KW - DNA-Binding Proteins KW - 0 KW - Hematopoietic Cell Growth Factors KW - Interleukin-7 KW - Proteins KW - Rag2 protein, mouse KW - Stem Cell Factor KW - V(D)J recombination activating protein 2 KW - Ionomycin KW - 56092-81-0 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Gene Expression KW - Hematopoietic Cell Growth Factors -- pharmacology KW - Ionomycin -- pharmacology KW - Mice KW - Proteins -- genetics KW - Thymus Gland -- immunology KW - Base Sequence KW - Tumor Cells, Cultured KW - Cell Survival -- drug effects KW - Cells, Cultured KW - Genes, RAG-1 KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Thymus Gland -- embryology KW - Organ Culture Techniques KW - Cell Line KW - T-Lymphocytes -- cytology KW - Gene Rearrangement, beta-Chain T-Cell Antigen Receptor KW - Interleukin-7 -- pharmacology KW - T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75806660?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science+%28New+York%2C+N.Y.%29&rft.atitle=Interleukin-7%3A+a+cofactor+for+V%28D%29J+rearrangement+of+the+T+cell+receptor+beta+gene.&rft.au=Muegge%2C+K%3BVila%2C+M+P%3BDurum%2C+S+K&rft.aulast=Muegge&rft.aufirst=K&rft.date=1993-07-02&rft.volume=261&rft.issue=5117&rft.spage=93&rft.isbn=&rft.btitle=&rft.title=Science+%28New+York%2C+N.Y.%29&rft.issn=00368075&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-27 N1 - Date created - 1993-07-27 N1 - Date revised - 2017-01-13 N1 - Gene symbol - RAG-1; RAG-2 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Visual and auditory evoked potentials in early onset Parkinson's disease and their relationship to cerebrospinal fluid monoamine metabolites. AN - 85277265; pmid-7688076 AB - We studied visual (VEP) and brainstem auditory (BAEP) evoked potential changes in 23 patients with early onset Parkinson's disease (EOPD) to establish the nature of the changes as well as their relationship to dopaminergic (DA) and serotonergic (5-HT) disturbances, as determined by cerebrospinal fluid levels of homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA). We also compared these parameters between the young onset (YOPD) and juvenile Parkinsonism (JP), the two subgroups of EOPD, to look for any possible differences between the two. In EOPD, the mean P100 latency of the VEP was significantly prolonged compared to controls (p < 0.001). However, within EOPD the evoked potential parameters were not significantly different between YOPD and the JP subgroups. P100 latency was abnormal in six patients (YOPD: 5, JP: 1) (26%). Six patients (YOPD: 3, JP:3) (26%) had abnormal BAEP. A significant negative correlation (r: -0.89, p < 1%) was observed between the P100 latency and CSF HVA levels. No correlation was observed between the BAEP interpeak latencies and either CSF HVA or 5-HIAA levels. This study suggests that VEP and BAEP abnormalities do occur in EOPD (in both YOPD and JP), and that the prolongation of P100 latency is secondary to DA deficiency as in PD. The cause of BAEP abnormalities is probably independent of DA and 5-HT disturbances. The only difference between EOPD and classical PD was the higher incidence of BAEP abnormalities in EOPD. There was no correlation between the VEP or BAEP changes to either the age at onset or duration of EOPD. JF - Movement Disorders AU - Muthane, U B AU - Satishchandra, P AU - Subhash, M N AD - Department of Neurology, National Institute of Mental Health and Neurosciences, Bangalore, India. PY - 1993 SP - 344 EP - 348 VL - 8 IS - 3 SN - 0885-3185, 0885-3185 KW - Hydroxyindoleacetic Acid KW - Human KW - Aged KW - Photic Stimulation KW - Comparative Study KW - Parkinson Disease KW - Adult KW - Middle Age KW - Acoustic Stimulation KW - Adolescent KW - Homovanillic Acid KW - Male KW - Female KW - Evoked Potentials, Visual KW - Evoked Potentials, Auditory, Brain Stem UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85277265?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Movement+Disorders&rft.atitle=Visual+and+auditory+evoked+potentials+in+early+onset+Parkinson%27s+disease+and+their+relationship+to+cerebrospinal+fluid+monoamine+metabolites.&rft.au=Muthane%2C+U+B%3BSatishchandra%2C+P%3BSubhash%2C+M+N&rft.aulast=Muthane&rft.aufirst=U&rft.date=1993-07-01&rft.volume=8&rft.issue=3&rft.spage=344&rft.isbn=&rft.btitle=&rft.title=Movement+Disorders&rft.issn=08853185&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Inhibition of outer hair cell electromotility by sulfhydryl specific reagents. AN - 85260265; pmid-8233059 AB - Mammalian outer hair cells can change length at acoustic frequencies when they are electrically stimulated. It was postulated that these length changes depend on electromechanical transduction based on voltage dependent conformational changes in a membrane motor protein. In this report, we describe the effect of various sulfhydryl (SH)-specific reagents on the OHC electromotility. p-Chloromercuriphenylsulfonate (pCMPS), in addition to other mercurials that can react with well-protected SH-groups in proteins, inhibits this electromechanical transduction process. In contrast, N-ethylmaleimide and diamide, SH-reagents that only react with exposed SH-groups, showed no effect. These results suggest that one or more reactive SH-groups are present in a functionally important and protected region of the electromechanical transduction protein. Such reactivity can be utilized to identify and characterize this novel membrane motor. JF - Neuroscience Letters AU - Kalinec, F AU - Kachar, B AD - Laboratory of Cellular Biology, National Institute on Deafness and other Communication Disorders, NIDCD-NIH, Bethesda, MD 20892. PY - 1993 SP - 231 EP - 234 VL - 157 IS - 2 SN - 0304-3940, 0304-3940 KW - Cell Movement KW - Ethylmaleimide KW - 4-Chloromercuribenzenesulfonate KW - Sulfhydryl Reagents KW - Ethacrynic Acid KW - Diamide KW - Cysteine KW - Guinea Pigs KW - Hair Cells, Outer KW - Animal KW - Cystine KW - Mersalyl KW - Electric Stimulation KW - Membrane Proteins KW - Nerve Tissue Proteins KW - Protein Conformation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85260265?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroscience+Letters&rft.atitle=Inhibition+of+outer+hair+cell+electromotility+by+sulfhydryl+specific+reagents.&rft.au=Kalinec%2C+F%3BKachar%2C+B&rft.aulast=Kalinec&rft.aufirst=F&rft.date=1993-07-01&rft.volume=157&rft.issue=2&rft.spage=231&rft.isbn=&rft.btitle=&rft.title=Neuroscience+Letters&rft.issn=03043940&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Effect of stress on the membrane capacitance of the auditory outer hair cell. AN - 85253923; pmid-8369452 AB - The membrane capacitance of the outer hair cell, which has unique membrane potential-dependent motility, was monitored during application of membrane tension. It was found that the membrane capacitance of the cell decreased when stress was applied to the membrane. This result is the opposite of stretching the lipid bilayer in the plasma membrane. It thus indicates the importance of some other capacitance component that decreases on stretching. It has been known that charge movement across the membrane can appear to be a nonlinear capacitance. If membrane stress at the resting potential restricts the movement of the charge associated with force generation, the nonlinear capacitance will decrease. Furthermore, less capacitance reduction by membrane stretching is expected when the membrane is already extended by the (hyperpolarizing) membrane potential. Indeed, it was found that at hyperpolarized potentials, the reduction of the membrane capacitance due to stretching is less. The capacitance change can be described by a two state model of a force-producing unit in which the free energy difference between the contracted and stretched states has both electrical and mechanical components. From the measured change in capacitance, the estimated difference in the membrane area of the unit between the two states is about 2 nm2. JF - Biophysical Journal AU - Iwasa, Kuni H AD - National Institute on Deafness and Other Communication Disorders PY - 1993 SP - 492 EP - 498 VL - 65 IS - 1 SN - 0006-3495, 0006-3495 KW - Cell Movement KW - In Vitro KW - Hair Cells KW - Guinea Pigs KW - Stress, Mechanical KW - Cell Membrane KW - Electric Impedance KW - Animal KW - Membrane Potentials KW - Models, Neurological KW - Electrophysiology KW - Biomechanics KW - Biophysics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85253923?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biophysical+Journal&rft.atitle=Effect+of+stress+on+the+membrane+capacitance+of+the+auditory+outer+hair+cell.&rft.au=Iwasa%2C+Kuni+H&rft.aulast=Iwasa&rft.aufirst=Kuni&rft.date=1993-07-01&rft.volume=65&rft.issue=1&rft.spage=492&rft.isbn=&rft.btitle=&rft.title=Biophysical+Journal&rft.issn=00063495&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - How independent are the messages carried by adjacent inferior temporal cortical neurons? AN - 85235845; pmid-8331371 AB - There are at least three possibilities for encoding information in a small area of cortex. First, neurons could have identical characteristics, thus conveying redundant information; second, neurons could give different responses to the same stimuli, thus conveying independent information; or third, neurons could cooperate with each other to encode more information jointly than they do separately, that is, synergistically. We recorded from 28 pairs of neurons in inferior temporal cortex of behaving rhesus monkeys. Each pair was recorded from a single microelectrode. Both the magnitude and the temporal modulation of the responses were quantified. We separated the responses into signal (average response to each stimulus) and noise (deviation of each response from the average). Linear regression showed that an average of only 18.7% of the magnitude of the signal carried by one neuron could be predicted from the magnitude of the other, and only 22.0% could be predicted by including the temporal modulation. For the noise, the figures were 5.5% and 6.3%, respectively, even less than for the signal. Information theoretic analysis shows that the pairs of neurons we studied carried an average of 20% redundant information. However, even this relatively small amount of redundancy places a severe upper limit on the information that can be transmitted by a neuronal pool. A pool of neurons for which each pair is mutually redundant to extent y can only carry a maximum of 1/y, here five times, as much information as one neuron alone. Information theoretic analysis gave no evidence for the presence of information as a function of both neurons considered together, that is, synergistic codes. Cross-correlation showed that at least 61% of the neuronal pairs shared connections in some manner. Given these shared connections, if adjacent neurons had had identical characteristics, then the noise on the outputs of these neurons would have been highly correlated, and it would not be possible to separate the signal and noise. The severe impact of correlated noise and information redundancy leads us to propose that the processing carried out by these neurons evolved both to provide a rich description of many stimulus properties and simultaneously to minimize the redundancy in a local group of neurons. These two principles appear to be a major constraint on the organization of inferior temporal, and possibly all, cortex. JF - The Journal of Neuroscience AU - Gawne, T J AU - Richmond, B J AD - Laboratory of Neuropsychology, National Institute of Mental Health, Bethesda, MD 20892. PY - 1993 SP - 2758 EP - 2771 VL - 13 IS - 7 SN - 0270-6474, 0270-6474 KW - Regression Analysis KW - Animal KW - Reward KW - Neurons KW - Temporal Lobe KW - Conditioning, Operant KW - Membrane Potentials KW - Support, U.S. Gov't, Non-P.H.S. KW - Macaca mulatta KW - Models, Neurological KW - Visual Perception KW - Stereotaxic Techniques KW - Microelectrodes KW - Pattern Recognition, Visual UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85235845?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+Neuroscience&rft.atitle=How+independent+are+the+messages+carried+by+adjacent+inferior+temporal+cortical+neurons%3F&rft.au=Gawne%2C+T+J%3BRichmond%2C+B+J&rft.aulast=Gawne&rft.aufirst=T&rft.date=1993-07-01&rft.volume=13&rft.issue=7&rft.spage=2758&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+Neuroscience&rft.issn=02706474&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Appearance of wave III of auditory brainstem response after removal of a cerebellar tumor. AN - 85221447; pmid-8250155 AB - Findings for auditory brainstem response (ABR) before and after surgical removal of a cerebellar tumor in a 10-year-old female are presented. ABR improved markedly, although the tumor showed no direct invasion to the brainstem. The cause of the ABR change and the origin of wave III are discussed. JF - Brain and Development AU - Kaga, M AU - Nihei, K AD - National Institute of Mental Health, National Center of Neurology and Psychiatry, Chiba, Japan. PY - 1993 SP - 305 EP - 307 VL - 15 IS - 4 SN - 0387-7604, 0387-7604 KW - Cerebellar Neoplasms KW - Human KW - Tomography, X-Ray Computed KW - Case Report KW - Child KW - Postoperative Period KW - Female KW - Evoked Potentials, Auditory, Brain Stem UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85221447?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+and+Development&rft.atitle=Appearance+of+wave+III+of+auditory+brainstem+response+after+removal+of+a+cerebellar+tumor.&rft.au=Kaga%2C+M%3BNihei%2C+K&rft.aulast=Kaga&rft.aufirst=M&rft.date=1993-07-01&rft.volume=15&rft.issue=4&rft.spage=305&rft.isbn=&rft.btitle=&rft.title=Brain+and+Development&rft.issn=03877604&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Carcinogenicity of TCDD in laboratory animals: implications for risk assessment. AN - 76174673; 8296316 JF - Toxicology and industrial health AU - Lucier, G AU - Clark, G AU - Hiermath, C AU - Tritscher, A AU - Sewall, C AU - Huff, J AD - Laboratory of Biochemical Risk Analysis, N.I.E.H.S., Research Triangle Park, NC 27709. PY - 1993 SP - 631 EP - 668 VL - 9 IS - 4 SN - 0748-2337, 0748-2337 KW - Polychlorinated Dibenzodioxins KW - 0 KW - Index Medicus KW - Rats KW - Animals KW - Risk Factors KW - Humans KW - Carcinogenicity Tests KW - Biological Assay KW - Mice KW - Male KW - Female KW - Cricetinae KW - Polychlorinated Dibenzodioxins -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76174673?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+industrial+health&rft.atitle=Carcinogenicity+of+TCDD+in+laboratory+animals%3A+implications+for+risk+assessment.&rft.au=Lucier%2C+G%3BClark%2C+G%3BHiermath%2C+C%3BTritscher%2C+A%3BSewall%2C+C%3BHuff%2C+J&rft.aulast=Lucier&rft.aufirst=G&rft.date=1993-07-01&rft.volume=9&rft.issue=4&rft.spage=631&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+industrial+health&rft.issn=07482337&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-03-01 N1 - Date created - 1994-03-01 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Toxicol Ind Health 1994 May-Jun;10(3):247 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Stigma or legitimation? A historical examination of the social potentials of addiction disease models. AN - 76105623; 8258758 AB - This article presents a historical discussion of disease models of opiate addiction in the United States in the twentieth century. First, several approaches to defining disease are discussed. Then, the shifts in formulations of opiate addiction as a disease in the twentieth century in the U.S. are analysed in light of the preceding theoretical discussion. The period before 1920 is described as heterodox, as researchers attempted to develop scientific models of opiate addiction, while various medically legitimate and quasi-legitimate treatment approaches flourished in an unregulated marketplace. After 1920, a stigmatizing disease model of opiate addiction was based on a psychiatric formulation that linked chronic addiction with psychoneurotic deficits in certain individuals. After 1940, this model dominated medical and scientific thinking about opiate addiction for several decades. After 1970, enormous changes in the demographics of drug use forced changes to the prevailing model of addiction. A new focus on behavioral aspects of addiction allowed the creation of a nonstigmatizing Parsonian disease model. JF - Journal of psychoactive drugs AU - Acker, C J AD - National Institutes of Health Historical Office, National Institutes of Health, Bethesda, Maryland 20892. PY - 1993 SP - 193 EP - 205 VL - 25 IS - 3 SN - 0279-1072, 0279-1072 KW - Index Medicus KW - History of medicine KW - United States KW - Models, Psychological KW - History, 20th Century KW - Legislation, Drug -- history KW - Humans KW - Opioid-Related Disorders -- psychology KW - Opioid-Related Disorders -- history UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76105623?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+psychoactive+drugs&rft.atitle=Stigma+or+legitimation%3F+A+historical+examination+of+the+social+potentials+of+addiction+disease+models.&rft.au=Acker%2C+C+J&rft.aulast=Acker&rft.aufirst=C&rft.date=1993-07-01&rft.volume=25&rft.issue=3&rft.spage=193&rft.isbn=&rft.btitle=&rft.title=Journal+of+psychoactive+drugs&rft.issn=02791072&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-01-19 N1 - Date created - 1994-01-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Is there any relationship between aluminum and Alzheimer's disease? AN - 76052819; 8224045 AB - The controversial role of aluminum in Alzheimer's disease (AD) is reviewed. While current data would suggest the lack of a causative role, alterations in the brain and other organ systems caused by AD might increase the penetration of aluminum as well as other metals into the brain and lead to their contribution to such pathological features as neurofibrillar tangles (NFTs). JF - Experimental gerontology AU - Eichhorn, G L AD - National Institutes of Health, National Institute on Aging, Laboratory of Cellular and Molecular Biology, Baltimore, Maryland 21224. PY - 1993 SP - 493 EP - 498 VL - 28 IS - 4-5 SN - 0531-5565, 0531-5565 KW - Aluminum KW - CPD4NFA903 KW - Silicon KW - Z4152N8IUI KW - Index Medicus KW - Humans KW - Brain -- drug effects KW - Aged KW - Silicon -- toxicity KW - Brain -- metabolism KW - Neurofibrillary Tangles -- drug effects KW - Aluminum -- adverse effects KW - Alzheimer Disease -- chemically induced KW - Alzheimer Disease -- metabolism KW - Aluminum -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76052819?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Experimental+gerontology&rft.atitle=Is+there+any+relationship+between+aluminum+and+Alzheimer%27s+disease%3F&rft.au=Eichhorn%2C+G+L&rft.aulast=Eichhorn&rft.aufirst=G&rft.date=1993-07-01&rft.volume=28&rft.issue=4-5&rft.spage=493&rft.isbn=&rft.btitle=&rft.title=Experimental+gerontology&rft.issn=05315565&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-22 N1 - Date created - 1993-12-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Reduced interleukin-2 (IL-2) production in common variable immunodeficiency is due to a primary abnormality of CD4+ T cell differentiation. AN - 76042624; 7901231 AB - Common variable immunodeficiency (CVI) is a condition characterized by hypogammaglobulinemia and impaired antibody responses, resulting in recurrent bacterial infections in untreated patients. In addition, affected individuals exhibit an increased incidence of autoimmunity, malignancy, and certain viral infections, suggesting the presence of an underlying generalized immune dysregulation. We have previously described a subgroup of CVI patients in whom T cells within PBMC populations exhibit a selective defect in lymphokine production. IL-2, IL-4, and IL-5 mRNA production was impaired in these patients, while proliferation, IL-2R expression, and c-myc mRNA production were normal. In the present series of experiments, using highly purified CD4+ T cells prepared by negative selection, we show that this lymphokine production defect is a primary abnormality of CVI CD4+ T cells: whereas CD4+ T cells from CVI patients proliferate normally in response to stimulation by PHA, staphylococcal enterotoxin B (SEB), or anti-CD2 antibodies, these stimuli induce significantly less IL-2 production than observed with CD4+ T cells from normal individuals. Furthermore, we show that this IL-2 production defect is not due to an accessory cell abnormality, since it was seen in the presence of normal (allogeneic) accessory cells, and patient accessory cells supported normal amounts of IL-2 production by PHA-stimulated CD4+ T cells obtained from normal individuals. Of interest, we also found that while IL-2 production by CD4+ T cells from CVI patients induced by stimulation with immobilized anti-CD3 antibody was reduced compared to CD4+ T cells from normal control individuals, this reduction was not statistically significant. Furthermore, stimulation of both CVI patient and normal CD4+ T cells with either ionomycin+phorbol myristate acetate or a combination of immobilized anti-CD3 antibody plus anti-CD28 antibody resulted in a 50-fold increase in IL-2 production compared to stimulation with immobilized anti-CD3 antibody alone, and, under these conditions, CVI and normal CD4+ T cells produced equivalent amounts of IL-2. Finally, minor defects in interferon-gamma production by CD4+ T cells from CVI donors were observed, but these were less severe than the IL-2 production defects and were not statistically significant. We conclude that a primary abnormality of lymphokine production exists in the CD4+ T cells of a subset of patients with CVI.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Journal of clinical immunology AU - Eisenstein, E M AU - Jaffe, J S AU - Strober, W AD - Mucosal Immunity Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 247 EP - 258 VL - 13 IS - 4 SN - 0271-9142, 0271-9142 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, CD28 KW - Antigens, CD3 KW - Interleukin-2 KW - Lectins KW - Ionomycin KW - 56092-81-0 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Antigens, CD3 -- immunology KW - Humans KW - Ionomycin -- immunology KW - Enzyme-Linked Immunosorbent Assay KW - Lymphocyte Subsets KW - Antigens, CD28 -- immunology KW - Lymphocyte Activation KW - Common Variable Immunodeficiency -- immunology KW - Interleukin-2 -- biosynthesis KW - CD4-Positive T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76042624?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+human+genetics&rft.atitle=Functional+studies+of+a+germ-line+polymorphism+at+codon+47+within+the+p53+gene.&rft.au=Felley-Bosco%2C+E%3BWeston%2C+A%3BCawley%2C+H+M%3BBennett%2C+W+P%3BHarris%2C+C+C&rft.aulast=Felley-Bosco&rft.aufirst=E&rft.date=1993-09-01&rft.volume=53&rft.issue=3&rft.spage=752&rft.isbn=&rft.btitle=&rft.title=American+journal+of+human+genetics&rft.issn=00029297&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-01 N1 - Date created - 1993-12-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Anticonvulsant activity of AMPA/kainate antagonists: comparison of GYKI 52466 and NBOX in maximal electroshock and chemoconvulsant seizure models. AN - 76027104; 7693450 AB - The anticonvulsant activities of a noncompetitive (GYKI 52466) and a competitive (NBQX) AMPA/kainate antagonist were compared in the maximal electroshock (MES) seizure test and various chemoconvulsant models. Both antagonists were protective in the MES and pentylenetetrazol tests. GYKI 52466 was also protective against seizures and lethality induced by 4-aminopyridine, kainate and AMPA, but not by NMDA, whereas NBQX was ineffective in these chemoconvulsant tests. Both GYKI 52466 and NBQX produced motor impairment at doses similar to those that were protective in the MES test. Under some circumstances, noncompetitive AMPA/kainate antagonists could offer advantages over competitive antagonists in seizure therapy. However, neurological toxicity is an obstacle to the potential clinical use of both classes of agents. JF - Epilepsy research AU - Yamaguchi, S AU - Donevan, S D AU - Rogawski, M A AD - Neuronal Excitability Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 29892. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 179 EP - 184 VL - 15 IS - 3 SN - 0920-1211, 0920-1211 KW - Anti-Anxiety Agents KW - 0 KW - Anticonvulsants KW - Quinoxalines KW - Receptors, AMPA KW - Receptors, Kainic Acid KW - GYKI 52466 KW - 102771-26-6 KW - 2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline KW - 118876-58-7 KW - Benzodiazepines KW - 12794-10-4 KW - alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid KW - 77521-29-0 KW - 4-Aminopyridine KW - BH3B64OKL9 KW - Kainic Acid KW - SIV03811UC KW - Pentylenetetrazole KW - WM5Z385K7T KW - Index Medicus KW - Animals KW - Receptors, AMPA -- antagonists & inhibitors KW - Hindlimb -- physiology KW - Dose-Response Relationship, Drug KW - 4-Aminopyridine -- pharmacology KW - Disease Models, Animal KW - Binding, Competitive -- drug effects KW - Mice KW - Receptors, Kainic Acid -- antagonists & inhibitors KW - Electroshock KW - Male KW - Seizures -- chemically induced KW - Anticonvulsants -- pharmacology KW - Kainic Acid -- antagonists & inhibitors KW - alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid -- antagonists & inhibitors KW - Seizures -- prevention & control KW - Benzodiazepines -- pharmacology KW - Quinoxalines -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76027104?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Epilepsy+research&rft.atitle=Anticonvulsant+activity+of+AMPA%2Fkainate+antagonists%3A+comparison+of+GYKI+52466+and+NBOX+in+maximal+electroshock+and+chemoconvulsant+seizure+models.&rft.au=Yamaguchi%2C+S%3BDonevan%2C+S+D%3BRogawski%2C+M+A&rft.aulast=Yamaguchi&rft.aufirst=S&rft.date=1993-07-01&rft.volume=15&rft.issue=3&rft.spage=179&rft.isbn=&rft.btitle=&rft.title=Epilepsy+research&rft.issn=09201211&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-06 N1 - Date created - 1993-12-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Generation of isogenic K54 capsule-deficient Escherichia coli strains through TnphoA-mediated gene disruption. AN - 76008484; 8412686 AB - Transposon mutagenesis, using IS50L::phoA(Tn-phoA), was performed in a K54/O4/H5 blood isolate of Escherichia coli (CP9), to generate a library of random mutants. Five hundred and twenty-six independent CP9 TnphoA mutants were isolated with active gene fusions to alkaline phosphatase. From this mutant library, eight capsule-deficient strains were detected and were found to have a single copy of TnphoA. Sixteen additional capsule deficient mutants with TnphoA inserts were subsequently obtained that did not possess active PhoA fusions. In conjunction with the initial eight capsule-deficient isolates we have defined genes on three different XbaI fragments as being involved in capsule production. Generalized transduction with the bacteriophage T4 established that these insertions were responsible for the loss of capsule and that they are linked. These capsule-deficient strains can be used to assess the pathogenic role of the K54 capsular polysaccharide. JF - Molecular microbiology AU - Russo, T A AU - Guenther, J E AU - Wenderoth, S AU - Frank, M M AD - Bacterial Pathogenesis Unit, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 357 EP - 364 VL - 9 IS - 2 SN - 0950-382X, 0950-382X KW - Antigens, Bacterial KW - 0 KW - Antigens, Surface KW - DNA, Bacterial KW - K antigens KW - Recombinant Fusion Proteins KW - Alkaline Phosphatase KW - EC 3.1.3.1 KW - Index Medicus KW - Genes, Bacterial KW - Transduction, Genetic KW - Alkaline Phosphatase -- genetics KW - Plasmids KW - Escherichia coli Infections -- microbiology KW - DNA, Bacterial -- genetics KW - Chromosomes, Bacterial KW - T-Phages -- genetics KW - Carbohydrate Sequence KW - Molecular Sequence Data KW - Recombinant Fusion Proteins -- genetics KW - Sepsis -- microbiology KW - Mutagenesis, Insertional KW - Gene Library KW - Escherichia coli -- immunology KW - Escherichia coli -- isolation & purification KW - Escherichia coli -- genetics KW - Antigens, Surface -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76008484?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+microbiology&rft.atitle=Generation+of+isogenic+K54+capsule-deficient+Escherichia+coli+strains+through+TnphoA-mediated+gene+disruption.&rft.au=Russo%2C+T+A%3BGuenther%2C+J+E%3BWenderoth%2C+S%3BFrank%2C+M+M&rft.aulast=Russo&rft.aufirst=T&rft.date=1993-07-01&rft.volume=9&rft.issue=2&rft.spage=357&rft.isbn=&rft.btitle=&rft.title=Molecular+microbiology&rft.issn=0950382X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-15 N1 - Date created - 1993-11-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Fish, in and out of water; food, toxins, allergens. AN - 76000371; 8224836 JF - Allergy proceedings : the official journal of regional and state allergy societies AU - Cohen, S G AD - National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD. PY - 1993 SP - 287 EP - 316 VL - 14 IS - 4 SN - 1046-9354, 1046-9354 KW - Allergens KW - 0 KW - Toxins, Biological KW - Index Medicus KW - History of medicine KW - Animals KW - History, 20th Century KW - Fishes, Poisonous KW - History, 18th Century KW - History, 19th Century KW - Europe KW - Israel KW - History, 17th Century KW - History, Medieval KW - Egypt KW - Philately KW - History, 15th Century KW - History, Ancient KW - China KW - History, 16th Century KW - Fishes -- immunology KW - Fish Products -- history KW - Toxins, Biological -- history KW - Allergens -- history UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76000371?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Allergy+proceedings+%3A+the+official+journal+of+regional+and+state+allergy+societies&rft.atitle=Fish%2C+in+and+out+of+water%3B+food%2C+toxins%2C+allergens.&rft.au=Cohen%2C+S+G&rft.aulast=Cohen&rft.aufirst=S&rft.date=1993-07-01&rft.volume=14&rft.issue=4&rft.spage=287&rft.isbn=&rft.btitle=&rft.title=Allergy+proceedings+%3A+the+official+journal+of+regional+and+state+allergy+societies&rft.issn=10469354&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-07 N1 - Date created - 1993-12-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Analysis of Mdr50: a Drosophila P-glycoprotein/multidrug resistance gene homolog. AN - 75997730; 7691715 AB - Using degenerate oligonucleotides from conserved portions of the ATP-binding domain of the active transporter genes, a new member of this gene superfamily has been cloned from Drosophila DNA. The gene contains two sets of transmembrane domains and two ATP-binding domains and shows a high degree of similarity to the mammalian P-glycoprotein/multidrug resistance (MDR) genes. The gene is adjacent to Hsc5, a locus mapped to chromosome 2, band 50, and is named Mdr50. Mdr50 represents the third MDR homolog identified in Drosophila. Conservation in the position of intervening sequences between Mdr50 and the human MDR genes provides further evidence for their common origin. JF - Genomics AU - Gerrard, B AU - Stewart, C AU - Dean, M AD - Biological Carcinogenesis and Development Program, National Cancer Institute, Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 83 EP - 88 VL - 17 IS - 1 SN - 0888-7543, 0888-7543 KW - CFTR KW - MDR KW - MDR1 KW - Mdr50 KW - CFTR protein, human KW - 0 KW - Carrier Proteins KW - Drosophila Proteins KW - Insect Hormones KW - Membrane Glycoproteins KW - Membrane Proteins KW - P-Glycoprotein KW - P-Glycoproteins KW - multidrug resistance protein 50, Drosophila KW - Cystic Fibrosis Transmembrane Conductance Regulator KW - 126880-72-6 KW - Index Medicus KW - Animals KW - Carrier Proteins -- genetics KW - Humans KW - Open Reading Frames KW - Amino Acid Sequence KW - Membrane Proteins -- genetics KW - Polymerase Chain Reaction KW - Base Sequence KW - Sequence Alignment KW - Molecular Sequence Data KW - Consensus Sequence KW - Sequence Homology, Amino Acid KW - Species Specificity KW - Membrane Glycoproteins -- genetics KW - Biological Transport, Active -- genetics KW - Drosophila melanogaster -- genetics KW - Multigene Family KW - Insect Hormones -- genetics KW - Genes, Insect UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75997730?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Genomics&rft.atitle=Analysis+of+Mdr50%3A+a+Drosophila+P-glycoprotein%2Fmultidrug+resistance+gene+homolog.&rft.au=Gerrard%2C+B%3BStewart%2C+C%3BDean%2C+M&rft.aulast=Gerrard&rft.aufirst=B&rft.date=1993-07-01&rft.volume=17&rft.issue=1&rft.spage=83&rft.isbn=&rft.btitle=&rft.title=Genomics&rft.issn=08887543&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-22 N1 - Date created - 1993-10-22 N1 - Date revised - 2017-01-13 N1 - Gene symbol - CFTR; MDR; MDR1; Mdr50 N1 - Genetic sequence - L07065; GENBANK N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Environmental risks to the health of American children. AN - 75996989; 8415509 AB - The major environmental health issue for children today is the extremely high prevalence of unacceptable exposure to lead, especially in inner cities, but occurring throughout the country. It is now generally accepted that lead is toxic to the developing nervous system at levels that were thought only a decade ago to be without effect. Children are more susceptible to the effects of lead than the adults who live in the same environments. Although lead-based paint is no longer used and lead is now removed from gasoline, children will continue to live in housing with the potential for lead poisoning for perhaps another generation. Research into the prevention of exposure and prevention of the consequences of unavoidable exposure is now under way. JF - Preventive medicine AU - Olden, K AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709-2233. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 576 EP - 578 VL - 22 IS - 4 SN - 0091-7435, 0091-7435 KW - Dust KW - 0 KW - Lead KW - 2P299V784P KW - Index Medicus KW - Urban Population -- statistics & numerical data KW - Humans KW - Child KW - Cross-Sectional Studies KW - Mass Screening KW - Adult KW - Incidence KW - Adolescent KW - Dust -- adverse effects KW - Lead -- pharmacokinetics KW - United States -- epidemiology KW - Female KW - Male KW - Lead Poisoning -- prevention & control KW - Lead Poisoning -- epidemiology KW - Environmental Exposure -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75996989?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Preventive+medicine&rft.atitle=Environmental+risks+to+the+health+of+American+children.&rft.au=Olden%2C+K&rft.aulast=Olden&rft.aufirst=K&rft.date=1993-07-01&rft.volume=22&rft.issue=4&rft.spage=576&rft.isbn=&rft.btitle=&rft.title=Preventive+medicine&rft.issn=00917435&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-09 N1 - Date created - 1993-11-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Activation of hepatic stem cell compartment in the rat: role of transforming growth factor alpha, hepatocyte growth factor, and acidic fibroblast growth factor in early proliferation. AN - 75986214; 7691152 AB - We have demonstrated previously a pronounced increase in the expression of hepatocyte growth factor (HGF) (Z. Hu, R. P. Evarts, K. Fujio, E. R. Marsden, and S. S. Thorgeirsson, Am. J. Pathol., 142: 1823-1830, 1993), transforming growth factor alpha (TGF-alpha) (R. P. Evarts, H. Nakatsukasa, E. R. Marsden, Z. Hu, and S. S. Thorgeirsson, Mol. Carcinog., 5: 25-31, 1992), and acidic fibroblast growth factor (aFGF) (E. R. Marsden, Z. Hu, K. Fujio, H. Nakatsukasa, S. S. Thorgeirsson, and R. P. Evarts, Lab. Invest., 67: 427-433, 1992) that coincided with the proliferation and differentiation of putative hepatic stem cells and perisinusoidal stellate (Ito) cells. Here, we examine the earliest stages of stem cell activation in rat liver using an experimental model involving treatment with acetylaminofluorene and partial hepatectomy (R. P. Evarts, P. Nagy, E. Marsden, and S. S. Thorgeirsson, Carcinogenesis (Lond.), 8: 1737-1740, 1987). Histochemical identification of stem cell progeny and Ito cells was accomplished by OV6 and desmin antibodies, respectively. Expression of the 2.1-kilobase alpha-fetoprotein transcripts and the concomitant DNA synthesis ([3H]thymidine label) were used as indicators for the activation of the stem cell compartment. Expression of HGF, TGF-alpha, and aFGF was analyzed at the time of partial hepatectomy and 4, 12, 24, 48, 72, and 92 h after the operation. [3H]-Thymidine-labeled OV6- and desmin-positive cells were present in the portal space and in the Glisson capsule 4 h after partial hepatectomy.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research AU - Evarts, R P AU - Hu, Z AU - Fujio, K AU - Marsden, E R AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 555 EP - 561 VL - 4 IS - 7 SN - 1044-9523, 1044-9523 KW - RNA, Messenger KW - 0 KW - Transforming Growth Factor alpha KW - alpha-Fetoproteins KW - Fibroblast Growth Factor 1 KW - 104781-85-3 KW - Hepatocyte Growth Factor KW - 67256-21-7 KW - Thymidine KW - VC2W18DGKR KW - Index Medicus KW - Thymidine -- metabolism KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Blotting, Northern KW - alpha-Fetoproteins -- biosynthesis KW - Cell Division -- physiology KW - Time Factors KW - Immunohistochemistry KW - RNA, Messenger -- biosynthesis KW - Male KW - Hepatocyte Growth Factor -- physiology KW - Hepatocyte Growth Factor -- biosynthesis KW - Liver -- cytology KW - Transforming Growth Factor alpha -- physiology KW - Transforming Growth Factor alpha -- biosynthesis KW - Liver -- metabolism KW - Fibroblast Growth Factor 1 -- physiology KW - Cell Compartmentation -- physiology KW - Stem Cells -- physiology KW - Fibroblast Growth Factor 1 -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75986214?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cell+growth+%26+differentiation+%3A+the+molecular+biology+journal+of+the+American+Association+for+Cancer+Research&rft.atitle=Activation+of+hepatic+stem+cell+compartment+in+the+rat%3A+role+of+transforming+growth+factor+alpha%2C+hepatocyte+growth+factor%2C+and+acidic+fibroblast+growth+factor+in+early+proliferation.&rft.au=Evarts%2C+R+P%3BHu%2C+Z%3BFujio%2C+K%3BMarsden%2C+E+R%3BThorgeirsson%2C+S+S&rft.aulast=Evarts&rft.aufirst=R&rft.date=1993-07-01&rft.volume=4&rft.issue=7&rft.spage=555&rft.isbn=&rft.btitle=&rft.title=Cell+growth+%26+differentiation+%3A+the+molecular+biology+journal+of+the+American+Association+for+Cancer+Research&rft.issn=10449523&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-05 N1 - Date created - 1993-11-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Characterization of 2',3'-dideoxycytidine diphosphocholine and 2',3'-dideoxycytidine diphosphoethanolamine. Prominent phosphodiester metabolites of the anti-HIV nucleoside 2',3'-dideoxycytidine. AN - 75963792; 7690699 AB - 2',3'-Dideoxycytidine (ddCyd) is among the most potent of the anti-human immunodeficiency virus (HIV) agents of the dideoxynucleoside class. Its pharmacologically active metabolite 2',3'-dideoxycytidine 5'-triphosphate (ddCTP) is an effective inhibitor of HIV reverse transcriptase and thus of HIV replication. ddCyd differs, however, from other dideoxynucleoside agents such as 3'-azido-3'-deoxythymidine and 2',3'-dideoxyinosine in its capacity to generate phosphodiester metabolites (i.e. ddCDP choline and ddCDP ethanolamine). We have synthesized and characterized these two diesters, and established their identity with the metabolites formed in ddCyd-treated Molt-4 cells. Toward this end, the biologically generated metabolites have been isolated on a preparative scale and compared with the synthetic compounds mass spectroscopically, chromatographically, and enzymatically (i.e. their relative susceptibility to the catabolic enzymes alkaline phosphatase and venom phosphodiesterase). The concentration reached by each of these two phosphodiesters within cells can, under certain conditions, equal or exceed that of ddCTP, and their half-times of disappearance are long, indicating that they may serve as depot forms of ddCyd. The possible role of these phosphodiesters in contributing to the unusual toxicity of ddCyd is discussed. JF - Drug metabolism and disposition: the biological fate of chemicals AU - Hao, Z AU - Stowe, E E AU - Ahluwalia, G AU - Baker, D C AU - Hebbler, A K AU - Chisena, C AU - Musser, S M AU - Kelley, J A AU - Perno, C F AU - Johns, D G AD - Laboratory of Medicinal Chemistry, National Cancer Institute/National Institutes of Health, Bethesda, MD 20892. PY - 1993 SP - 738 EP - 744 VL - 21 IS - 4 SN - 0090-9556, 0090-9556 KW - Deoxycytosine Nucleotides KW - 0 KW - Dideoxynucleotides KW - Ethanolamines KW - Reverse Transcriptase Inhibitors KW - 2',3'-dideoxycytidine diphosphoethanolamine KW - 130036-23-6 KW - 2',3'-dideoxycytidine diphosphocholine KW - 130036-24-7 KW - Cytidine Diphosphate Choline KW - 536BQ2JVC7 KW - Ethanolamine KW - 5KV86114PT KW - Cytidine Diphosphate KW - 63-38-7 KW - Zalcitabine KW - 6L3XT8CB3I KW - HIV Reverse Transcriptase KW - EC 2.7.7.49 KW - Choline KW - N91BDP6H0X KW - Index Medicus KW - AIDS/HIV KW - Molecular Structure KW - Chromatography, Paper KW - Cells, Cultured KW - Cytidine Diphosphate -- analogs & derivatives KW - Choline -- metabolism KW - Spectrometry, Mass, Fast Atom Bombardment KW - Zalcitabine -- metabolism KW - Deoxycytosine Nucleotides -- metabolism KW - HIV -- drug effects KW - Ethanolamines -- metabolism KW - Cytidine Diphosphate Choline -- analogs & derivatives KW - Cytidine Diphosphate Choline -- chemistry KW - Cytidine Diphosphate Choline -- metabolism KW - Ethanolamines -- chemistry KW - Deoxycytosine Nucleotides -- chemistry KW - Zalcitabine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75963792?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Drug+metabolism+and+disposition%3A+the+biological+fate+of+chemicals&rft.atitle=Characterization+of+2%27%2C3%27-dideoxycytidine+diphosphocholine+and+2%27%2C3%27-dideoxycytidine+diphosphoethanolamine.+Prominent+phosphodiester+metabolites+of+the+anti-HIV+nucleoside+2%27%2C3%27-dideoxycytidine.&rft.au=Hao%2C+Z%3BStowe%2C+E+E%3BAhluwalia%2C+G%3BBaker%2C+D+C%3BHebbler%2C+A+K%3BChisena%2C+C%3BMusser%2C+S+M%3BKelley%2C+J+A%3BPerno%2C+C+F%3BJohns%2C+D+G&rft.aulast=Hao&rft.aufirst=Z&rft.date=1993-07-01&rft.volume=21&rft.issue=4&rft.spage=738&rft.isbn=&rft.btitle=&rft.title=Drug+metabolism+and+disposition%3A+the+biological+fate+of+chemicals&rft.issn=00909556&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-15 N1 - Date created - 1993-10-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Multistep carcinogenesis. AN - 75947646; 8396563 JF - Japanese journal of cancer research : Gann AU - Harris, C C AD - Laboratory of Human Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/07// PY - 1993 DA - July 1993 VL - 84 IS - 7 SN - 0910-5050, 0910-5050 KW - Index Medicus KW - Precancerous Conditions -- genetics KW - Liver Neoplasms -- pathology KW - Carcinoma, Hepatocellular -- etiology KW - Carcinoma, Hepatocellular -- genetics KW - Chromosome Aberrations KW - Carcinoma, Hepatocellular -- pathology KW - Liver Neoplasms -- etiology KW - Precancerous Conditions -- pathology KW - Liver Neoplasms -- genetics KW - Neoplasms -- pathology KW - Neoplasms -- genetics KW - Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75947646?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Japanese+journal+of+cancer+research+%3A+Gann&rft.atitle=Multistep+carcinogenesis.&rft.au=Harris%2C+C+C&rft.aulast=Harris&rft.aufirst=C&rft.date=1993-07-01&rft.volume=84&rft.issue=7&rft.spage=inside+front+cover&rft.isbn=&rft.btitle=&rft.title=Japanese+journal+of+cancer+research+%3A+Gann&rft.issn=09105050&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-08 N1 - Date created - 1993-10-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - ADP-ribosylation factors, 20,000 M(r) guanine nucleotide-binding protein activators of cholera toxin and components of intracellular vesicular transport systems. AN - 75945039; 8373721 JF - Cellular signalling AU - Moss, J AU - Vaughan, M AD - Laboratory of Cellular Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 367 EP - 379 VL - 5 IS - 4 SN - 0898-6568, 0898-6568 KW - Cholera Toxin KW - 9012-63-9 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - ADP-Ribosylation Factors KW - EC 3.6.5.2 KW - Adenylyl Cyclases KW - EC 4.6.1.1 KW - Index Medicus KW - Animals KW - Conserved Sequence KW - Humans KW - Molecular Sequence Data KW - Biological Transport KW - Adenylyl Cyclases -- metabolism KW - Amino Acid Sequence KW - Sequence Homology, Amino Acid KW - Signal Transduction KW - Molecular Weight KW - Organelles -- metabolism KW - GTP-Binding Proteins -- metabolism KW - GTP-Binding Proteins -- genetics KW - Cholera Toxin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75945039?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cellular+signalling&rft.atitle=ADP-ribosylation+factors%2C+20%2C000+M%28r%29+guanine+nucleotide-binding+protein+activators+of+cholera+toxin+and+components+of+intracellular+vesicular+transport+systems.&rft.au=Moss%2C+J%3BVaughan%2C+M&rft.aulast=Moss&rft.aufirst=J&rft.date=1993-07-01&rft.volume=5&rft.issue=4&rft.spage=367&rft.isbn=&rft.btitle=&rft.title=Cellular+signalling&rft.issn=08986568&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-19 N1 - Date created - 1993-10-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Are mouse strains differentially susceptible to the reproductive toxicity of ethylene glycol monomethyl ether? A study of three strains. AN - 75931428; 8365589 AB - Most rodent reproductive toxicology studies utilize strains of high fecundity. These studies were conducted to examine the possibility that mouse strains of differing fecundity would respond differently to a known reproductive toxicant. Thirty pairs each of Swiss CD-1, C57B1, and C3H mice were cohabited for 14 weeks while consuming 0, 0.03, 0.10, or 0.30% EGME in the drinking water. Litter data were collected during cohabitation. Body and organ weights, and various sperm data, were collected at necropsy, and second-generation fertility was evaluated. The data show that the most fecund strain (Swiss) was affected the least by exposure to EGME, while the least fecund strain (C3H) suffered the greatest declines in fertility. These differences might alter interspecies extrapolation factors, or the permissible exposure levels for humans. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Chapin, R E AU - Morrissey, R E AU - Gulati, D K AU - Hope, E AU - Barnes, L H AU - Russell, S A AU - Kennedy, S R AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 8 EP - 14 VL - 21 IS - 1 SN - 0272-0590, 0272-0590 KW - Ethylene Glycols KW - 0 KW - methyl cellosolve KW - EK1L6XWI56 KW - Index Medicus KW - Mice, Inbred Strains KW - Litter Size -- drug effects KW - Animals KW - Body Weight -- drug effects KW - Mice KW - Sperm Motility -- drug effects KW - Species Specificity KW - Male KW - Female KW - Organ Size -- drug effects KW - Ethylene Glycols -- toxicity KW - Fertility -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75931428?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.atitle=Are+mouse+strains+differentially+susceptible+to+the+reproductive+toxicity+of+ethylene+glycol+monomethyl+ether%3F+A+study+of+three+strains.&rft.au=Chapin%2C+R+E%3BMorrissey%2C+R+E%3BGulati%2C+D+K%3BHope%2C+E%3BBarnes%2C+L+H%3BRussell%2C+S+A%3BKennedy%2C+S+R&rft.aulast=Chapin&rft.aufirst=R&rft.date=1993-07-01&rft.volume=21&rft.issue=1&rft.spage=8&rft.isbn=&rft.btitle=&rft.title=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.issn=02720590&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-05 N1 - Date created - 1993-10-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Risk assessment in immunotoxicology. II. Relationships between immune and host resistance tests. AN - 75931388; 8365588 AB - We have reported on the design and content of a screening battery using a "tier" approach for detecting potential immunotoxic compounds in mice (Luster et al., Fundam. Appl. Toxicol., 10, 2-19, 1988). The data base generated from these studies, which consists of over 50 selected compounds, has been collected and analyzed in an attempt to improve future testing strategies and provide information to aid in developing future quantitative risk assessment for immunotoxicity. In a recent study it was shown that as few as two or three immune parameters were needed to predict immunotoxicants in mice (Luster et al., Fundam. Appl. Toxicol., 18, 200-210, 1992). In particular, enumeration of lymphocyte populations and quantitation of the T-dependent antibody response were particularly beneficial. Furthermore, commonly employed apical measures (e.g., leukocyte counts, lymphoid organ weights) were fairly insensitive. The present analyses focus on the use of this data base to develop statistical models that examine the qualitative and quantitative relationship(s) between the immune function and host resistance tests. The conclusion derived from these analyses are: (1) A good correlation exists between changes in the immune tests and altered host resistance in that there were no instances where host resistance was altered without affecting an immune test(s). However, in some instances immune changes occurred without corresponding changes in host resistance. (2) No single immune test could be identified which was fully predictive for altered host resistance, although most assays were relatively good indicators (i.e., > 70%). Several others, such as proliferative response to lipopolysaccharide and leukocyte counts, were found to be relatively poor indicators for host resistance changes. (3) The ability to resist infectious agent challenge is dependent upon the degrees of immunosuppression and the quantity of infectious agent administered. (4) Logistic and standard regression modeling using one extensive chemical data set from the immunosuppressive agent, cyclophosphamide, indicated that most immune function-host resistance relationships followed linear rather than linear-quadratic (threshold-like) models. For most of the relationships this could not be confirmed using a large chemical data set and, thus, a more mechanistically based approach for modeling will need to be developed. (5) Using this limited data set, methods were developed for modeling the precise quantitative relationships between changes in selected immune tests and host resistance tests. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Luster, M I AU - Portier, C AU - Pait, D G AU - Rosenthal, G J AU - Germolec, D R AU - Corsini, E AU - Blaylock, B L AU - Pollock, P AU - Kouchi, Y AU - Craig, W AD - Environmental Immunology and Neurobiology Section, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 71 EP - 82 VL - 21 IS - 1 SN - 0272-0590, 0272-0590 KW - Cyclophosphamide KW - 8N3DW7272P KW - Index Medicus KW - Regression Analysis KW - Animals KW - Dose-Response Relationship, Drug KW - Mice, Inbred C57BL KW - Models, Statistical KW - Mice KW - Immunity, Innate KW - Cyclophosphamide -- toxicity KW - Female KW - Immune System -- drug effects KW - Risk Factors KW - Toxicology -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75931388?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.atitle=Risk+assessment+in+immunotoxicology.+II.+Relationships+between+immune+and+host+resistance+tests.&rft.au=Luster%2C+M+I%3BPortier%2C+C%3BPait%2C+D+G%3BRosenthal%2C+G+J%3BGermolec%2C+D+R%3BCorsini%2C+E%3BBlaylock%2C+B+L%3BPollock%2C+P%3BKouchi%2C+Y%3BCraig%2C+W&rft.aulast=Luster&rft.aufirst=M&rft.date=1993-07-01&rft.volume=21&rft.issue=1&rft.spage=71&rft.isbn=&rft.btitle=&rft.title=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.issn=02720590&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-05 N1 - Date created - 1993-10-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Non-conservation of a catalytic residue in a dipeptidyl aminopeptidase IV-related protein encoded by a gene on human chromosome 7. AN - 75929119; 8103397 JF - Human molecular genetics AU - Yokotani, N AU - Doi, K AU - Wenthold, R J AU - Wada, K AD - Laboratory of Neurochemistry, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 1037 EP - 1039 VL - 2 IS - 7 SN - 0964-6906, 0964-6906 KW - DPPX KW - DNA KW - 9007-49-2 KW - Dipeptidyl-Peptidases and Tripeptidyl-Peptidases KW - EC 3.4.14.- KW - Dipeptidyl Peptidase 4 KW - EC 3.4.14.5 KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Base Sequence KW - Conserved Sequence KW - Humans KW - DNA -- genetics KW - Molecular Sequence Data KW - Hybrid Cells KW - Binding Sites -- genetics KW - Chromosome Mapping KW - Dipeptidyl-Peptidases and Tripeptidyl-Peptidases -- genetics KW - Chromosomes, Human, Pair 7 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75929119?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Human+molecular+genetics&rft.atitle=Non-conservation+of+a+catalytic+residue+in+a+dipeptidyl+aminopeptidase+IV-related+protein+encoded+by+a+gene+on+human+chromosome+7.&rft.au=Yokotani%2C+N%3BDoi%2C+K%3BWenthold%2C+R+J%3BWada%2C+K&rft.aulast=Yokotani&rft.aufirst=N&rft.date=1993-07-01&rft.volume=2&rft.issue=7&rft.spage=1037&rft.isbn=&rft.btitle=&rft.title=Human+molecular+genetics&rft.issn=09646906&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-04 N1 - Date created - 1993-10-04 N1 - Date revised - 2017-01-13 N1 - Gene symbol - DPPX N1 - Genetic sequence - M96859; GENBANK; M96860 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Heterogeneity in the concerted evolution process of a tandem satellite array in meadow mice (Microtus). AN - 75913635; 8360918 AB - The evolutionary history of a 160-bp tandem satellite array, originally described from Microtus chrotorrhinus and called MSAT-160, was examined in related species of arvicolid rodents by sequence analyses, quantitative dot blotting, and Southern blotting. Results indicate that MSAT-160 is present in 12 of the 20 species and subspecies of Microtus assayed, but not in species belonging to any of the eight other genera examined. DNA from each species containing MSAT-160 was digested with 12 restriction endonucleases and restriction patterns were obtained reflecting the variable extent of homogenization of any given variant in different species. For example, with MboI digestion, M. chrotorrhinus produced a type A ladder pattern where most monomers contain the restriction site, M. ochrogaster generated a type B pattern where most monomers lack the site, and M. agrestis yielded a pattern intermediate between the A and B types. Further, dot blotting revealed copy-number differences between species. These findings indicate that changes in the periodic structure and amount of satellite DNA have occurred since these species last shared a common ancestor. In addition, various species-specific patterns were documented, illustrating that mechanisms other than genome-wide homogenization, such as stochastic mutation, out-of-register crossing over, deletion, and random amplification also play a role in structuring tandem arrays. Stochastic mutation and homogenization rates in satellite DNA, levels of species diversity, and magnitudes of chromosomal divergence differ significantly in Microtus, Mus and Ctenomys, the three rodent lineages examined. JF - Journal of molecular evolution AU - Modi, W S AD - Biological Carcinogenesis Development Program, Program Resources Inc./DynCorp, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702-1201. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 48 EP - 56 VL - 37 IS - 1 SN - 0022-2844, 0022-2844 KW - DNA, Satellite KW - 0 KW - Index Medicus KW - Animals KW - Base Sequence KW - Sequence Homology, Nucleic Acid KW - Blotting, Southern KW - Molecular Sequence Data KW - Rodentia -- genetics KW - Species Specificity KW - Cell Line KW - DNA, Satellite -- genetics KW - Biological Evolution KW - Arvicolinae -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75913635?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+molecular+evolution&rft.atitle=Heterogeneity+in+the+concerted+evolution+process+of+a+tandem+satellite+array+in+meadow+mice+%28Microtus%29.&rft.au=Modi%2C+W+S&rft.aulast=Modi&rft.aufirst=W&rft.date=1993-07-01&rft.volume=37&rft.issue=1&rft.spage=48&rft.isbn=&rft.btitle=&rft.title=Journal+of+molecular+evolution&rft.issn=00222844&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-24 N1 - Date created - 1993-09-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - A dose escalation study to determine the toxicity and maximally tolerated dose of foscarnet. AN - 75907261; 8357555 AB - To determine the maximum tolerated dose of intravenous foscarnet (trisodium phosphonoformate hexahydrate); and to examine antiviral activity at plasma levels shown to inhibit HIV-1. Dose escalation study in three male subjects with AIDS who received foscarnet by continuous intravenous infusion at a dose of 200 mg/kg per day, after a 20 mg/kg loading dose. The dose was increased until a plasma level > 150 micrograms/ml was attained. Foscarnet was discontinued due to progressive renal insufficiency in all three patients (days 11, 19, and 21). Renal function normalized in all three, and no adverse sequelae due to foscarnet were observed at 1 year of follow-up. A seizure was observed in one patient on day 19. Maximum daily doses of foscarnet achieved were 395 mg/kg, 389 mg/kg, and 523 mg/kg. No changes in serum Ca2+, Mg2+, or PO4- were observed. Renal effects and toxicity of foscarnet in evolving renal insufficiency is self-limiting and reversible when the drug is discontinued. Incremental increases in dose can result in rapid rises in the plasma level with renal failure and may be compounded by concomitant medications and underlying illnesses. JF - AIDS (London, England) AU - Seidel, E A AU - Koenig, S AU - Polis, M A AD - Laboratory of Immunoregulation, NIAID, NIH, Bethesda, MD 20892. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 941 EP - 945 VL - 7 IS - 7 SN - 0269-9370, 0269-9370 KW - Foscarnet KW - 364P9RVW4X KW - Creatinine KW - AYI8EX34EU KW - Index Medicus KW - AIDS/HIV KW - Seizures -- complications KW - Infusions, Intravenous KW - Dose-Response Relationship, Drug KW - Humans KW - Adult KW - Middle Aged KW - Renal Insufficiency -- complications KW - Creatinine -- blood KW - Male KW - Acquired Immunodeficiency Syndrome -- complications KW - Foscarnet -- toxicity KW - Foscarnet -- administration & dosage KW - Acquired Immunodeficiency Syndrome -- drug therapy KW - HIV-1 -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75907261?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS+%28London%2C+England%29&rft.atitle=A+dose+escalation+study+to+determine+the+toxicity+and+maximally+tolerated+dose+of+foscarnet.&rft.au=Seidel%2C+E+A%3BKoenig%2C+S%3BPolis%2C+M+A&rft.aulast=Seidel&rft.aufirst=E&rft.date=1993-07-01&rft.volume=7&rft.issue=7&rft.spage=941&rft.isbn=&rft.btitle=&rft.title=AIDS+%28London%2C+England%29&rft.issn=02699370&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-27 N1 - Date created - 1993-09-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Managing occupational exposures to HIV-1 in the healthcare workplace. AN - 75902475; 8354872 JF - Infection control and hospital epidemiology AU - Fahey, B J AU - Beekmann, S E AU - Schmitt, J M AU - Fedio, J M AU - Henderson, D K AD - Hospital Epidemiology Service, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 405 EP - 412 VL - 14 IS - 7 SN - 0899-823X, 0899-823X KW - Index Medicus KW - Nursing KW - AIDS/HIV KW - Coitus -- psychology KW - Risk Factors KW - Humans KW - Pregnancy Complications, Infectious KW - First Aid KW - Counseling KW - Occupational Health Services KW - Male KW - Female KW - Pregnancy KW - Occupational Exposure -- prevention & control KW - Personnel, Hospital -- psychology KW - Occupational Diseases -- drug therapy KW - Acquired Immunodeficiency Syndrome -- transmission KW - Occupational Diseases -- etiology KW - Acquired Immunodeficiency Syndrome -- drug therapy KW - HIV-1 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75902475?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+control+and+hospital+epidemiology&rft.atitle=Managing+occupational+exposures+to+HIV-1+in+the+healthcare+workplace.&rft.au=Fahey%2C+B+J%3BBeekmann%2C+S+E%3BSchmitt%2C+J+M%3BFedio%2C+J+M%3BHenderson%2C+D+K&rft.aulast=Fahey&rft.aufirst=B&rft.date=1993-07-01&rft.volume=14&rft.issue=7&rft.spage=405&rft.isbn=&rft.btitle=&rft.title=Infection+control+and+hospital+epidemiology&rft.issn=0899823X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-23 N1 - Date created - 1993-09-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Occupational risks for primary liver cancer in Shanghai, China. AN - 75891436; 8352295 AB - Using occupational data for over 3,400 primary liver cancer cases diagnosed between 1980 and 1984 reported to the Shanghai Cancer Registry, and employment information from the 1982 census for the Shanghai population, standardized incidence ratios were computed to generate leads to occupational risks of liver cancer. Among men, a statistically significant excess number of cases was observed for chemical processors, textile workers, wood workers, blacksmiths and machine-tool operators, and material handlers and dock workers. Increased incidence of liver cancer also was observed among female transport equipment operators. These findings indicate that a number of similar occupations are associated with increased risk of primary liver cancer in western countries and China. Although causal inferences cannot be drawn from these data, our study adds to the limited evidence of the potential role of occupational exposures in liver carcinogenesis. JF - American journal of industrial medicine AU - Chow, W H AU - McLaughlin, J K AU - Zheng, W AU - Blot, W J AU - Gao, Y T AD - Division of Cancer Etiology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 93 EP - 100 VL - 24 IS - 1 SN - 0271-3586, 0271-3586 KW - Index Medicus KW - Risk Factors KW - Humans KW - China -- epidemiology KW - Adult KW - Incidence KW - Male KW - Female KW - Occupational Diseases -- etiology KW - Occupations -- statistics & numerical data KW - Occupational Diseases -- epidemiology KW - Liver Neoplasms -- epidemiology KW - Liver Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75891436?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+industrial+medicine&rft.atitle=Occupational+risks+for+primary+liver+cancer+in+Shanghai%2C+China.&rft.au=Chow%2C+W+H%3BMcLaughlin%2C+J+K%3BZheng%2C+W%3BBlot%2C+W+J%3BGao%2C+Y+T&rft.aulast=Chow&rft.aufirst=W&rft.date=1993-07-01&rft.volume=24&rft.issue=1&rft.spage=93&rft.isbn=&rft.btitle=&rft.title=American+journal+of+industrial+medicine&rft.issn=02713586&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-14 N1 - Date created - 1993-09-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Contribution of occupation and diet to white blood cell polycyclic aromatic hydrocarbon-DNA adducts in wildland firefighters. AN - 75886115; 8348057 AB - Wildland (forest) firefighters are exposed to a wide range of carcinogenic polycyclic aromatic hydrocarbons (PAH) in forest fire smoke. PAH undergo metabolic activation and can subsequently bind to DNA. In this study, we investigated the association between occupational and dietary PAH exposures and the formation of WBC PAH-DNA adducts in a population of wildland firefighters. An enzyme-linked immunosorbent assay using an antiserum elicited against benzo(a)pyrene-modified DNA was used to measure PAH-DNA adducts in WBC obtained from 47 California firefighters at two time points, early and late in the 1988 forest fire season. PAH-DNA adduct levels were not associated with cumulative hours of recent firefighting activity. However, firefighters who consumed charbroiled food within the previous week had elevated PAH-DNA adduct levels, which were related to frequency of charbroiled food intake. These findings suggest that dietary sources of PAH contribute to PAH-DNA adduct levels in peripheral WBC and should be evaluated when using this assay to assess occupational and environmental PAH exposure. JF - Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology AU - Rothman, N AU - Correa-Villaseñor, A AU - Ford, D P AU - Poirier, M C AU - Haas, R AU - Hansen, J A AU - O'Toole, T AU - Strickland, P T AD - Environmental Epidemiology Branch, National Cancer Institute, NIH, Bethesda, Maryland 20892. PY - 1993 SP - 341 EP - 347 VL - 2 IS - 4 SN - 1055-9965, 1055-9965 KW - Polycyclic Compounds KW - 0 KW - Smoke KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Food KW - Humans KW - Retrospective Studies KW - Protein Binding KW - California KW - Prospective Studies KW - Adult KW - Cooking KW - Middle Aged KW - Adolescent KW - Time Factors KW - Female KW - Male KW - Occupational Exposure KW - Leukocytes -- metabolism KW - Fires KW - Trees KW - DNA -- metabolism KW - Polycyclic Compounds -- metabolism KW - Diet UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75886115?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain%2C+behavior%2C+and+immunity&rft.atitle=Immunocompetence+in+the+long+sleep+and+short+sleep+mouse+lines%3A+baseline+versus+primed+responses.&rft.au=Fride%2C+E%3BMcIntyre%2C+T%3BSkolnick%2C+P%3BArora%2C+P+K&rft.aulast=Fride&rft.aufirst=E&rft.date=1993-09-01&rft.volume=7&rft.issue=3&rft.spage=231&rft.isbn=&rft.btitle=&rft.title=Brain%2C+behavior%2C+and+immunity&rft.issn=08891591&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-16 N1 - Date created - 1993-09-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Clinical and laboratory adverse effects associated with long-term, low-dose isotretinoin: incidence and risk factors. The Isotretinoin-Basal Cell Carcinomas Study Group. AN - 75881810; 8348061 AB - Adverse effects associated with the long-term low-dose regimens of retinoids used in cancer chemoprevention studies are not well described. In order to examine the clinical and laboratory adverse effects of 3 years of intervention with isotretinoin (10 mg/day) and to assess potential risk factors for developing these, we collected adverse effect data on patients participating in a randomized, placebo-controlled trial designed to evaluate the effectiveness of isotretinoin in preventing the subsequent occurrence of new basal cell carcinoma. Our results showed a significantly higher incidence of adverse mucocutaneous effects and serum triglyceride elevations in the isotretinoin group (P < 0.001). Associated risk factors included male gender, very fair skin, and elevated pretreatment triglyceride levels. The toxicity observed, although less severe and less frequent, was similar to that seen with higher doses and should be weighed with adverse skeletal effects when considering long-term treatment of patients with moderate cancer risk. JF - Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology AU - Tangrea, J A AU - Adrianza, E AU - Helsel, W E AU - Taylor, P R AU - Hartman, A M AU - Peck, G L AU - Edwards, B K AD - Division of Cancer Prevention and Control, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. PY - 1993 SP - 375 EP - 380 VL - 2 IS - 4 SN - 1055-9965, 1055-9965 KW - Placebos KW - 0 KW - Triglycerides KW - Cholesterol KW - 97C5T2UQ7J KW - Isotretinoin KW - EH28UP18IF KW - Index Medicus KW - Triglycerides -- blood KW - Double-Blind Method KW - Humans KW - Skin -- pathology KW - Aged KW - Pain KW - Joints -- drug effects KW - Cholesterol -- blood KW - Risk Factors KW - Hypertriglyceridemia -- chemically induced KW - Adult KW - Incidence KW - Middle Aged KW - Follow-Up Studies KW - Hypercholesterolemia -- chemically induced KW - Male KW - Female KW - Muscles -- drug effects KW - Cheilitis -- chemically induced KW - Isotretinoin -- administration & dosage KW - Carcinoma, Basal Cell -- prevention & control KW - Isotretinoin -- adverse effects KW - Skin Neoplasms -- prevention & control KW - Isotretinoin -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75881810?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+epidemiology%2C+biomarkers+%26+prevention+%3A+a+publication+of+the+American+Association+for+Cancer+Research%2C+cosponsored+by+the+American+Society+of+Preventive+Oncology&rft.atitle=Clinical+and+laboratory+adverse+effects+associated+with+long-term%2C+low-dose+isotretinoin%3A+incidence+and+risk+factors.+The+Isotretinoin-Basal+Cell+Carcinomas+Study+Group.&rft.au=Tangrea%2C+J+A%3BAdrianza%2C+E%3BHelsel%2C+W+E%3BTaylor%2C+P+R%3BHartman%2C+A+M%3BPeck%2C+G+L%3BEdwards%2C+B+K&rft.aulast=Tangrea&rft.aufirst=J&rft.date=1993-07-01&rft.volume=2&rft.issue=4&rft.spage=375&rft.isbn=&rft.btitle=&rft.title=Cancer+epidemiology%2C+biomarkers+%26+prevention+%3A+a+publication+of+the+American+Association+for+Cancer+Research%2C+cosponsored+by+the+American+Society+of+Preventive+Oncology&rft.issn=10559965&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-16 N1 - Date created - 1993-09-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Increased sensitivity for determination of polycyclic aromatic hydrocarbon-DNA adducts in human DNA samples by dissociation-enhanced lanthanide fluoroimmunoassay (DELFIA). AN - 75877395; 8348058 AB - A competitive enzyme-linked immunosorbent assay (ELISA), the most frequently used immunoassay for the determination of polycyclic aromatic hydrocarbon-DNA adducts in human tissues, has been modified to achieve approximately a 6-fold increase in sensitivity. The new assay, a competitive dissociation-enhanced lanthanide fluoroimmunoassay (DELFIA) has utilized the same rabbit antiserum as the ELISA, antiserum elicited against DNA modified with benzo[a]pyrene. However, the alkaline phosphatase conjugate has been replaced with a biotin-europium-labeled streptavidin signal amplification system, and the release of europium into the solution forms a highly fluorescent chelate complex that is measured by time-resolved fluorometry. The DELFIA has achieved a 5- to 6-fold increase in sensitivity for measurement of DNA samples modified in vitro with benzo[a]pyrene, for cultured cells exposed to radiolabeled benzo[a]pyrene, and for human samples from occupationally exposed workers. The assay has been validated by comparison of adduct levels determined by DELFIA, ELISA, and radioactivity in DNA from mouse keratinocytes exposed to radiolabeled benzo[a]pyrene. Human lymphocyte DNA samples from 104 Hungarian aluminum plant workers were assayed by ELISA and compared to blood cell DNA samples from 69 Italian coke oven workers assayed by DELFIA. The standard curves demonstrated that the limit of detection of 4.0 adducts in 10(8) nucleotides for polycyclic aromatic hydrocarbon-DNA adducts by ELISA, using 35 micrograms of DNA/microtiter plate well, has been decreased to 1.3 adducts in 10(8) nucleotides by DELFIA, using 20 micrograms of DNA/microtiter well. If 35 micrograms of DNA were used in the DELFIA, the calculated detection limit would be 0.7 adducts in 10(8) nucleotides.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology AU - Schoket, B AU - Doty, W A AU - Vincze, I AU - Strickland, P T AU - Ferri, G M AU - Assennato, G AU - Poirier, M C AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, NIH Bethesda, Maryland 20892. PY - 1993 SP - 349 EP - 353 VL - 2 IS - 4 SN - 1055-9965, 1055-9965 KW - Bacterial Proteins KW - 0 KW - Coke KW - Metals, Rare Earth KW - Polycyclic Compounds KW - Benzo(a)pyrene KW - 3417WMA06D KW - Europium KW - 444W947O8O KW - DNA KW - 9007-49-2 KW - Streptavidin KW - 9013-20-1 KW - Aluminum KW - CPD4NFA903 KW - Deoxyguanosine KW - G9481N71RO KW - Index Medicus KW - Fluorescence KW - Humans KW - Lymphocytes -- metabolism KW - Italy KW - Hungary KW - Enzyme-Linked Immunosorbent Assay KW - Fluorometry KW - Deoxyguanosine -- analysis KW - Chemical Industry KW - Polycyclic Compounds -- analysis KW - DNA -- analysis KW - Fluoroimmunoassay -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75877395?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+epidemiology%2C+biomarkers+%26+prevention+%3A+a+publication+of+the+American+Association+for+Cancer+Research%2C+cosponsored+by+the+American+Society+of+Preventive+Oncology&rft.atitle=Increased+sensitivity+for+determination+of+polycyclic+aromatic+hydrocarbon-DNA+adducts+in+human+DNA+samples+by+dissociation-enhanced+lanthanide+fluoroimmunoassay+%28DELFIA%29.&rft.au=Schoket%2C+B%3BDoty%2C+W+A%3BVincze%2C+I%3BStrickland%2C+P+T%3BFerri%2C+G+M%3BAssennato%2C+G%3BPoirier%2C+M+C&rft.aulast=Schoket&rft.aufirst=B&rft.date=1993-07-01&rft.volume=2&rft.issue=4&rft.spage=349&rft.isbn=&rft.btitle=&rft.title=Cancer+epidemiology%2C+biomarkers+%26+prevention+%3A+a+publication+of+the+American+Association+for+Cancer+Research%2C+cosponsored+by+the+American+Society+of+Preventive+Oncology&rft.issn=10559965&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-16 N1 - Date created - 1993-09-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Prior medical conditions and the risk of adult leukemia in Shanghai, People's Republic of China. AN - 75877199; 8347786 AB - A population-based case-control interview study of 486 adult leukemia cases and 502 healthy controls was carried out in Shanghai, People's Republic of China during 1987-89 to evaluate the etiologic role of prior medical conditions, medications, and diagnostic X-rays. Risks were examined separately for 236 cases with acute non-lymphocytic leukemia (ANLL), 79 with chronic myeloid leukemia (CML), 81 with acute lymphocytic leukemia (ALL), and 21 with chronic lymphocytic leukemia (CLL). Little difference was found between cases and controls for prior history of diabetes, hypertension, allergic conditions, most medications, and diagnostic X-rays. A few significant associations were observed for appendectomy, tuberculosis, and for several other chronic disorders with specific leukemia cell types, but the odds ratio estimates for most of these ranged from two to three and, with the exception of the two specified above, were based generally on five or fewer exposed controls. In contrast to an association with childhood leukemia in Shanghai, prior use of chloramphenicol was not linked with ANLL or other forms of adult leukemia. Further research is needed to clarify the relation of specific medical conditions and exposures with particular subtypes of leukemia, and to examine reasons for the low incidence of CLL in China and other Asian populations. JF - Cancer causes & control : CCC AU - Zheng, W AU - Linet, M S AU - Shu, X O AU - Pan, R P AU - Gao, Y T AU - Fraumeni, J F AD - Epidemiology and Biostatistics Program, National Cancer Institute, Bethesda, MD. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 361 EP - 368 VL - 4 IS - 4 SN - 0957-5243, 0957-5243 KW - Salicylates KW - 0 KW - Index Medicus KW - Age Factors KW - Leukemia, Lymphocytic, Chronic, B-Cell -- epidemiology KW - Humans KW - Hyperthyroidism -- epidemiology KW - Aged KW - Tuberculosis -- epidemiology KW - Population Surveillance KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma -- epidemiology KW - Salicylates -- adverse effects KW - Risk Factors KW - Leukemia, Myeloid, Acute -- epidemiology KW - Appendectomy -- statistics & numerical data KW - China -- epidemiology KW - Adult KW - Case-Control Studies KW - Middle Aged KW - Leukemia, Myelogenous, Chronic, BCR-ABL Positive -- epidemiology KW - Adolescent KW - Male KW - Female KW - Disease KW - Leukemia -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75877199?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+causes+%26+control+%3A+CCC&rft.atitle=Prior+medical+conditions+and+the+risk+of+adult+leukemia+in+Shanghai%2C+People%27s+Republic+of+China.&rft.au=Zheng%2C+W%3BLinet%2C+M+S%3BShu%2C+X+O%3BPan%2C+R+P%3BGao%2C+Y+T%3BFraumeni%2C+J+F&rft.aulast=Zheng&rft.aufirst=W&rft.date=1993-07-01&rft.volume=4&rft.issue=4&rft.spage=361&rft.isbn=&rft.btitle=&rft.title=Cancer+causes+%26+control+%3A+CCC&rft.issn=09575243&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-16 N1 - Date created - 1993-09-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Retroviral mediated expression of human cytochrome P450 2A6 in C3H/10T1/2 cells confers transformability by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). AN - 75869299; 8330360 AB - In order to develop more efficient in vitro systems for the study of pro-mutagenic or pro-carcinogenic chemicals, we have produced transgenic C3H/10T1/2 cell lines expressing human cytochrome P450 (CYP) 2A6. A retroviral vector containing the cDNA was packaged in psi-2 cells, and used to infect C3H/10T1/2 cells. From 100 G418-resistant clones initially isolated, three cell lines were chosen for further study based upon their morphologies, growth rates and CYP2A6-dependent coumarin 7-hydroxylase activities. Infected clone 10T1/2-04, like the 10T1/2 cells, had no detectable CYP2A6 enzyme activity, while clones 10T1/2-10 and 10T1/2-29 had microsomal CYP2A6 enzyme activities within the range found in human liver microsomes. CYP2A6 protein levels were in agreement with the observed enzyme activities. Southern blots revealed that cells from clone 10T1/2-04 contained a vector lacking the CYP2A6 cDNA, while cells from clones 10T1/2-10 and 10T1/2-29 contained multiple full-length inserts. Southern analysis also indicated the presence of an endogenous CYP2A6 ortholog in the four cell lines. All cell lines exhibited about equal sensitivity to induction of cytotoxicity and conversion to ouabain resistance by the direct acting mutagen N-methyl-N'-nitro-N-nitrosoguanidine. The four lines were also about equally sensitive to transformation by benzo[a]pyrene, a chemical requiring metabolic activation. However, only clones 10T1/2-10 and 10T1/2-29, which express CYP2A6 activity, were mutated and morphologically transformed by the tobacco specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone. JF - Carcinogenesis AU - Tiano, H F AU - Hosokawa, M AU - Chulada, P C AU - Smith, P B AU - Wang, R L AU - Gonzalez, F J AU - Crespi, C L AU - Langenbach, R AD - National Institute of Environmental Health Sciences, Laboratory of Environmental Carcinogenesis and Mutagenesis, Research Triangle Park, NC 27709. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 1421 EP - 1427 VL - 14 IS - 7 SN - 0143-3334, 0143-3334 KW - Nitrosamines KW - 0 KW - 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone KW - 7S395EDO61 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Mixed Function Oxygenases KW - EC 1.- KW - Aryl Hydrocarbon Hydroxylases KW - EC 1.14.14.1 KW - CYP2A6 protein, human KW - Cytochrome P-450 CYP2A6 KW - Index Medicus KW - Animals KW - Blotting, Western KW - Cell Survival -- drug effects KW - Blotting, Southern KW - Biotransformation KW - Humans KW - Genetic Vectors KW - Mice, Inbred C3H KW - Mice KW - Cell Line KW - Cloning, Molecular KW - Nitrosamines -- toxicity KW - Mixed Function Oxygenases -- metabolism KW - Cytochrome P-450 Enzyme System -- genetics KW - Nitrosamines -- metabolism KW - Cytochrome P-450 Enzyme System -- metabolism KW - Nitrosamines -- pharmacokinetics KW - Retroviridae -- genetics KW - Cell Transformation, Neoplastic -- genetics KW - Mixed Function Oxygenases -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75869299?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Retroviral+mediated+expression+of+human+cytochrome+P450+2A6+in+C3H%2F10T1%2F2+cells+confers+transformability+by+4-%28methylnitrosamino%29-1-%283-pyridyl%29-1-butanone+%28NNK%29.&rft.au=Tiano%2C+H+F%3BHosokawa%2C+M%3BChulada%2C+P+C%3BSmith%2C+P+B%3BWang%2C+R+L%3BGonzalez%2C+F+J%3BCrespi%2C+C+L%3BLangenbach%2C+R&rft.aulast=Tiano&rft.aufirst=H&rft.date=1993-07-01&rft.volume=14&rft.issue=7&rft.spage=1421&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-18 N1 - Date created - 1993-08-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Electron spin resonance evidence for free radical generation in copper-treated vitamin E- and selenium-deficient rats: in vivo spin-trapping investigation. AN - 75866436; 8393522 AB - The ESR spin-trapping technique has been used to investigate free radical generation in copper-challenged rats deficient in vitamin E and/or selenium. Radical adduct excreted in the bile was detected only from copper-challenged rats deficient in both vitamin E and selenium. The phenyl-N-t-butylnitrone radical adduct has hyperfine coupling constants of aN = 15.36 G and a beta H = 2.50 G and arises from the trapping of a radical formed from an endogenous molecular species. The induction of this radical species in vivo may be important in the increased toxicity of copper in rats deficient in both vitamin E and selenium. These findings support the proposal that dietary selenium and vitamin E can protect against lipid peroxidation and copper toxicity. The results obtained suggest that the presence of only one of these nutrients in the diet is enough to prevent the formation of this radical adduct at ESR-detectable levels, and they provide the most direct ESR evidence yet obtained for the involvement of in vivo lipid peroxidation in the toxicity of copper. JF - Molecular pharmacology AU - Kadiiska, M B AU - Hanna, P M AU - Jordan, S J AU - Mason, R P AD - National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 222 EP - 227 VL - 44 IS - 1 SN - 0026-895X, 0026-895X KW - Free Radicals KW - 0 KW - Copper KW - 789U1901C5 KW - Glutathione Peroxidase KW - EC 1.11.1.9 KW - Selenium KW - H6241UJ22B KW - Index Medicus KW - Rats KW - Animals KW - Rats, Sprague-Dawley KW - Liver -- enzymology KW - Glutathione Peroxidase -- metabolism KW - Liver -- drug effects KW - Electron Spin Resonance Spectroscopy KW - Lipid Peroxidation -- drug effects KW - Models, Chemical KW - Male KW - Selenium -- deficiency KW - Vitamin E Deficiency -- metabolism KW - Copper -- pharmacology KW - Free Radicals -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75866436?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+pharmacology&rft.atitle=Electron+spin+resonance+evidence+for+free+radical+generation+in+copper-treated+vitamin+E-+and+selenium-deficient+rats%3A+in+vivo+spin-trapping+investigation.&rft.au=Kadiiska%2C+M+B%3BHanna%2C+P+M%3BJordan%2C+S+J%3BMason%2C+R+P&rft.aulast=Kadiiska&rft.aufirst=M&rft.date=1993-07-01&rft.volume=44&rft.issue=1&rft.spage=222&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmacology&rft.issn=0026895X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-27 N1 - Date created - 1993-08-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Neutrophil-specific granule deficiency includes eosinophils. AN - 75865544; 8324226 AB - Neutrophil-specific granule deficiency is a disorder of leukocyte maturation associated with decreased levels of mRNA for a distinct subset of granule proteins. Our work indicates that this disorder, previously thought to be limited to the neutrophil lineage, can also include eosinophils. Immunofluorescence staining led to the discovery of a small but distinct population of peripheral white blood cells containing eosinophil peroxidase (EPO). Unlike normal eosinophils, these EPO+ cells do not have large, eosin-staining cytoplasmic granules, and are indistinguishable from granule-deficient neutrophils by light microscopy. The EPO+ cell lineage did resemble the normal eosinophil lineage in its ability to respond dramatically to granulocyte-macrophage colony-stimulating factor (GM-CSF); the size of the EPO+ peripheral cell population increased approximately 70-fold over baseline in response to GM-CSF administration. The EPO+ cells contained eosinophil Charcot-Leyden crystal protein, but were deficient in three eosinophil-specific granule proteins; neither eosinophil cationic protein, eosinophil-derived neurotoxin, nor major basic protein could be detected in these EPO+ cells, despite the presence of mRNA transcripts for each of the three absent proteins. JF - Blood AU - Rosenberg, H F AU - Gallin, J I AD - Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/07/01/ PY - 1993 DA - 1993 Jul 01 SP - 268 EP - 273 VL - 82 IS - 1 SN - 0006-4971, 0006-4971 KW - ECP KW - EDN KW - MPB KW - Blood Proteins KW - 0 KW - Eosinophil Granule Proteins KW - Neurotoxins KW - Oligodeoxyribonucleotides KW - RNA, Messenger KW - Peroxidases KW - EC 1.11.1.- KW - Eosinophil-Derived Neurotoxin KW - EC 3.1.- KW - Ribonucleases KW - Abridged Index Medicus KW - Index Medicus KW - Neurotoxins -- metabolism KW - Humans KW - Gene Expression KW - RNA, Messenger -- genetics KW - Base Sequence KW - Genes KW - Oligodeoxyribonucleotides -- chemistry KW - Molecular Sequence Data KW - Blood Proteins -- metabolism KW - Fluorescent Antibody Technique KW - Peroxidases -- metabolism KW - Hematologic Diseases -- genetics KW - Cytoplasmic Granules -- ultrastructure KW - Eosinophils -- metabolism KW - Hematologic Diseases -- metabolism KW - Cytoplasmic Granules -- metabolism KW - Eosinophils -- ultrastructure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75865544?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Blood&rft.atitle=Neutrophil-specific+granule+deficiency+includes+eosinophils.&rft.au=Rosenberg%2C+H+F%3BGallin%2C+J+I&rft.aulast=Rosenberg&rft.aufirst=H&rft.date=1993-07-01&rft.volume=82&rft.issue=1&rft.spage=268&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=00064971&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-11 N1 - Date created - 1993-08-11 N1 - Date revised - 2017-01-13 N1 - Gene symbol - ECP; EDN; MPB N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Comparison of the toxicity of citral in F344 rats and B6C3F1 mice when administrated by microencapsulation in feed or by corn-oil gavage. AN - 75865188; 8340024 AB - A study of the potential effects of microencapsulation on the toxicity of citral was conducted in 14-day continuous feeding studies with both sexes of F344 rats and B6C3F1 mice. Toxicity by the feeding route was compared with that from bolus doses of the neat chemical in corn oil administrated by gavage. Both sexes of rats and mice were given diet containing 0, 0.63, 1.25, 2.5, 5 and 10% citral microcapsules. These feed formulations were equivalent to daily doses of 0, 142, 285, 570, 1140 and 2280 mg citral/kg body weight for rats and 0, 534, 1068, 2137, 4275 and 8550 mg citral/kg body weight for mice. The daily gavage doses were 0, 570, 1140 and 2280 mg citral/kg body weight for both sexes of rats, and 0, 534, 1068 and 2137 mg citral/kg body weight for both sexes of mice. Citral microcapsules administered in the diet did not cause mortality in mice or rats. Toxicity was confined to decreases in body weight at the 10% concentration in mice, at the 5 and 10% concentrations in rats, and decreases in absolute weights of the liver, kidney and spleen at the 10% concentration in rats. The only histopathological change observed was minimal to mild hyperplasia and/or squamous metaplasia of the respiratory epithelium in the anterior portion of the nasal passages of rats fed 5 or 10% citral microcapsules. By contrast, citral gavage caused mortality in five out of five male and female mice at 2137 mg/kg body weight, and in two out of five male mice at 1068 mg/kg body weight. There were dose-related increases in absolute liver weights of male and female mice. Cytoplasmic vacuolization of hepatocytes occurred in all female mice gavaged with 1068 and 2137 mg citral/kg body weight, and in male mice from the 2137 mg/kg dose group. Necrosis, ulceration and/or acute inflammation of the forestomach occurred in the high-dose mice of both sexes. Inflammation and/or hyperplasia of the forestomach occurred in about half of the male and female mice dosed with 1068 mg citral/kg. Citral gavage at doses that were equivalent to up to 10% in the diet (2280 mg/kg body weight) did not cause toxicity in rats, except for minimal hyperplasia of the squamous epithelium of the forestomach in high-dose males.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association AU - Dieter, M P AU - Goehl, T J AU - Jameson, C W AU - Elwell, M R AU - Hildebrandt, P K AU - Yuan, J H AD - National Institutes of Health, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 463 EP - 474 VL - 31 IS - 7 SN - 0278-6915, 0278-6915 KW - Monoterpenes KW - 0 KW - Terpenes KW - Vitamin A KW - 11103-57-4 KW - Corn Oil KW - 8001-30-7 KW - citral KW - T7EU0O9VPP KW - Index Medicus KW - Administration, Oral KW - Eating -- drug effects KW - Animals KW - Drug Compounding KW - Dose-Response Relationship, Drug KW - Vitamin A -- antagonists & inhibitors KW - Mice KW - Drug Administration Routes KW - Rats KW - Mice, Inbred Strains KW - Rats, Inbred F344 KW - Animal Feed KW - Body Weight -- drug effects KW - Toxicology -- methods KW - Species Specificity KW - Female KW - Male KW - Terpenes -- toxicity KW - Terpenes -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75865188?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Food+and+chemical+toxicology+%3A+an+international+journal+published+for+the+British+Industrial+Biological+Research+Association&rft.atitle=Comparison+of+the+toxicity+of+citral+in+F344+rats+and+B6C3F1+mice+when+administrated+by+microencapsulation+in+feed+or+by+corn-oil+gavage.&rft.au=Dieter%2C+M+P%3BGoehl%2C+T+J%3BJameson%2C+C+W%3BElwell%2C+M+R%3BHildebrandt%2C+P+K%3BYuan%2C+J+H&rft.aulast=Dieter&rft.aufirst=M&rft.date=1993-07-01&rft.volume=31&rft.issue=7&rft.spage=463&rft.isbn=&rft.btitle=&rft.title=Food+and+chemical+toxicology+%3A+an+international+journal+published+for+the+British+Industrial+Biological+Research+Association&rft.issn=02786915&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-30 N1 - Date created - 1993-08-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Population characteristics of DNA fingerprints in humpback whales (Megaptera novaeangliae). AN - 75861502; 8340617 AB - Humpback whales exhibit a remarkable social organization that is characterized by seasonal long-distance migration (> 10,000 km/year) between summer feeding grounds in high latitudes and winter calving and breeding grounds in tropical or near-tropical waters. All populations are currently considered endangered as a result of intensive commercial exploitation during the last 200 years. Using three hypervariable minisatellite DNA probes (33.15, 3'HVR, and M13) originally developed for studies of human genetic variation, we examined genetic variation within and among three regional subpopulations of humpback whales from the North Pacific and one from the North Atlantic oceans. Analysis of DNA extracted from skin tissues collected by biopsy darting from free-ranging whales revealed considerable variation in each subpopulation. The extent of this variation argues against a recent history of inbreeding among humpback whales as a result of nineteenth- and twentieth-century hunting. A canonical variate analysis suggested a relationship between scaled genetic distance, based on similarities of DNA fingerprints, and geographic distance (i.e., longitude of regional subpopulation). Significant categorical differences were found between the two oceanic populations using a multivariate analysis of variance (MANOVA) with a modification of the Mantel nonparametric permutation test. The relationship between DNA fingerprint similarities and geographic distance suggests that nuclear gene flow between regional subpopulations within the North Pacific is restricted by relatively low rates of migratory interchange between breeding grounds or assortative mating on common wintering grounds. JF - The Journal of heredity AU - Baker, C S AU - Gilbert, D A AU - Weinrich, M T AU - Lambertsen, R AU - Calambokidis, J AU - McArdle, B AU - Chambers, G K AU - O'Brien, S J AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick, MD 21701-1013. PY - 1993 SP - 281 EP - 290 VL - 84 IS - 4 SN - 0022-1503, 0022-1503 KW - DNA Probes KW - 0 KW - DNA, Satellite KW - Index Medicus KW - Animals KW - Electrophoresis, Agar Gel KW - Genetic Variation KW - Whales -- genetics KW - DNA Fingerprinting UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75861502?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+heredity&rft.atitle=Population+characteristics+of+DNA+fingerprints+in+humpback+whales+%28Megaptera+novaeangliae%29.&rft.au=Baker%2C+C+S%3BGilbert%2C+D+A%3BWeinrich%2C+M+T%3BLambertsen%2C+R%3BCalambokidis%2C+J%3BMcArdle%2C+B%3BChambers%2C+G+K%3BO%27Brien%2C+S+J&rft.aulast=Baker&rft.aufirst=C&rft.date=1993-07-01&rft.volume=84&rft.issue=4&rft.spage=281&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+heredity&rft.issn=00221503&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-02 N1 - Date created - 1993-09-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Chemically induced skin carcinogenesis in a transgenic mouse line (TG.AC) carrying a v-Ha-ras gene. AN - 75847672; 8330346 AB - A transgenic mouse line (TG.AC) created in the FVB/N strain, carries a v-Ha-ras gene fused to a zeta-globin promoter gene. These trangenic mice have the properties of genetically initiated skin and have been shown to be sensitive to 12-O-tetradecanoylphorbol-13-acetate (TPA), a well-described promoter of skin papillomas in the two-stage mouse skin tumorigenesis model. It was of interest to determine whether the TG.AC mouse strain was also responsive to other known promoters. Groups of heterozygous or homozygous TG.AC mice were treated topically, 2x/week, for up to 20 weeks with benzoyl peroxide (BPO), 2-butanol peroxide (2-BUP), phenol (PH), acetic acid (AA), TPA and acetone (ACN), the vehicle control. Skin papillomas were induced in all groups treated with TPA, BPO and 2-BUP. Papillomas were observed in some treatment groups as early as 3 weeks. The relative activity of the promoters was TPA > 2-BUP > BPO > PH = AA = ACN. No papillomas were observed in any of the uninitiated FVB/N mice treated in a similar manner and which served as treatment control groups. Studies to determine the sensitivity of TG.AC mice to TPA, indicated that a total dose of 25-30 micrograms of TPA administered in 3 or 10 applications, was sufficient to induce an average incidence of 11-15 papillomas per mouse. The papilloma incidence continued to increase and was maintained up to 15 weeks after TPA treatment was terminated. The short latency period and high incidence of papilloma induction indicate that TG.AC mice have a high sensitivity to known skin promoters. The TG.AC line should prove to be a sensitive model for identifying putative tumor promoters or complete carcinogens. JF - Carcinogenesis AU - Spalding, J W AU - Momma, J AU - Elwell, M R AU - Tennant, R W AD - Laboratory of Experimental Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 1335 EP - 1341 VL - 14 IS - 7 SN - 0143-3334, 0143-3334 KW - v-Ha-ras KW - Acetates KW - 0 KW - Butanols KW - Carcinogens KW - Phenols KW - Phenol KW - 339NCG44TV KW - 2-butanol peroxide KW - 37364-67-3 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Acetic Acid KW - Q40Q9N063P KW - Benzoyl Peroxide KW - W9WZN9A0GM KW - Index Medicus KW - Animals KW - Homozygote KW - Dose-Response Relationship, Drug KW - Mice KW - Mice, Transgenic KW - Promoter Regions, Genetic KW - Heterozygote KW - Skin Neoplasms -- genetics KW - Genes, ras KW - Skin Neoplasms -- chemically induced KW - Papilloma -- genetics KW - Papilloma -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75847672?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Chemically+induced+skin+carcinogenesis+in+a+transgenic+mouse+line+%28TG.AC%29+carrying+a+v-Ha-ras+gene.&rft.au=Spalding%2C+J+W%3BMomma%2C+J%3BElwell%2C+M+R%3BTennant%2C+R+W&rft.aulast=Spalding&rft.aufirst=J&rft.date=1993-07-01&rft.volume=14&rft.issue=7&rft.spage=1335&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-18 N1 - Date created - 1993-08-18 N1 - Date revised - 2017-01-13 N1 - Gene symbol - v-Ha-ras N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Infiltrating angiolipoma of skeletal muscle. Transplacental induction in nonhuman primates by N-nitrosoethylurea. AN - 75846388; 8331894 AB - In humans, relatively little is known on the association of prenatal exposure to cancer-causing agents and the development of specific tumors later in life as a consequence. Therefore, the effects on the offspring of carcinogen exposure during gestation and the development of tumors later in life were studied in nonhuman primates. Pregnancy was confirmed in Erythrocebus patas (patas) and Macaca mulatta (rhesus) by palpation at 27 to 40 days of gestation. Pregnant animals were treated once weekly intravenously from that time with N-nitrosoethylurea according to different dosing regimens for 6 to 19 weeks with 0.05 to 0.2 mmol/kg/injection. A common lesion developing in only the offspring of mothers treated early in pregnancy was identical with the human condition referred to as intramuscular angioma, hemangioma, or infiltrating angiolipoma of skeletal muscle. In the rhesus, one of 7 animals, and in the patas, 18 of 78 monkeys developed these processes (10 to 40% per group). The lesions typically arose within, infiltrated and displaced skeletal muscle. They occurred most commonly in the lower extremities, followed by the upper extremities and the head; they recurred in three cases of incomplete resection but did not metastasize. The tumors were seen mainly in young adults of both sexes (latency range: 4 to 76 months) and consisted of vessels of variable caliber, and to varying degrees, mature adipose and connective tissue, undifferentiated mesenchymal cells, and lymphoid cell aggregates. Ultrastructurally, the endothelium possessed numerous Weibel-Palade bodies and showed strong immunoreactivity for von Willebrand factor by immunohistochemistry and immunoelectron microscopy. The present investigation suggests a classification of these lesions as infiltrating angiolipoma of skeletal muscle originating from a pluripotent mesenchymal stem cell, caused by exposure to carcinogens during early pregnancy. The great clinical and morphologic similarity of this condition with that observed in humans suggests that it may likewise be caused by exposure to an agent during pregnancy. JF - Laboratory investigation; a journal of technical methods and pathology AU - Rehm, S AU - Palmer, A E AU - Harbaugh, S W AU - Rice, J M AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, National Institutes of Health, Frederick, Maryland. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 111 EP - 120 VL - 69 IS - 1 SN - 0023-6837, 0023-6837 KW - Ethylnitrosourea KW - P8M1T4190R KW - Index Medicus KW - Animals KW - Microscopy, Electron KW - Macaca mulatta KW - Erythrocebus patas KW - Microscopy, Immunoelectron KW - Immunohistochemistry KW - Male KW - Female KW - Pregnancy KW - Muscular Diseases -- pathology KW - Muscular Diseases -- metabolism KW - Hemangioma -- pathology KW - Muscular Diseases -- chemically induced KW - Hemangioma -- chemically induced KW - Lipoma -- pathology KW - Hemangioma -- metabolism KW - Lipoma -- metabolism KW - Lipoma -- chemically induced KW - Prenatal Exposure Delayed Effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75846388?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Laboratory+investigation%3B+a+journal+of+technical+methods+and+pathology&rft.atitle=Infiltrating+angiolipoma+of+skeletal+muscle.+Transplacental+induction+in+nonhuman+primates+by+N-nitrosoethylurea.&rft.au=Fu%2C+Y+M%3BMesri%2C+E+A%3BYu%2C+Z+X%3BKreitman%2C+R+J%3BPastan%2C+I%3BEpstein%2C+S+E&rft.aulast=Fu&rft.aufirst=Y&rft.date=1993-09-01&rft.volume=27&rft.issue=9&rft.spage=1691&rft.isbn=&rft.btitle=&rft.title=Cardiovascular+research&rft.issn=00086363&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-16 N1 - Date created - 1993-08-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Loss of expression of transforming growth factor beta in skin and skin tumors is associated with hyperproliferation and a high risk for malignant conversion. AN - 75840809; 7687059 AB - Mouse skin carcinomas arise from a small subpopulation of benign papillomas with an increased risk of malignant conversion. These papillomas arise with limited stimulation by tumor promoters, appear rapidly, and do not regress, suggesting that they differ in growth properties from the majority of benign tumors. The transforming growth factor beta (TGF-beta) proteins are expressed in the epidermis and are growth inhibitors for mouse keratinocytes in vitro; altered TGF-beta expression could influence the growth properties of high-risk papillomas. Normal epidermis, tumor promoter-treated epidermis, and skin papillomas at low risk for malignant conversion express TGF-beta 1 in the basal cell compartment and TGF-beta 2 in the suprabasal strata. In low-risk tumors, 90% of the proliferating cells are confined to the basal compartment. In contrast, the majority of high-risk papillomas are devoid of both TGF-beta 1 and TGF-beta 2 as soon as they arise; these tumors have up to 40% of the proliferating cells in the suprabasal layers. Squamous cell carcinomas are also devoid of TGF-beta, suggesting that they arise from the TGF-beta-deficient high-risk papillomas. In some high-risk papillomas, TGF-beta 1 loss can occur first and correlates with basal cell hyperproliferation, while TGF-beta 2 loss correlates with suprabasal hyperproliferation. Similarly, TGF-beta 1-null transgenic mice, which express wild-type levels of TGF-beta 2 in epidermis but no TGF-beta 1 in the basal layer, have a hyperproliferative basal cell layer without suprabasal proliferation. In tumors, loss of TGF-beta is controlled at the posttranscriptional level and is associated with expression of keratin 13, a documented marker of malignant progression. These results show that TGF-beta expression and function are compartmentalized in epidermis and epidermal tumors and that loss of TGF-beta is an early, biologically relevant risk factor for malignant progression. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Glick, A B AU - Kulkarni, A B AU - Tennenbaum, T AU - Hennings, H AU - Flanders, K C AU - O'Reilly, M AU - Sporn, M B AU - Karlsson, S AU - Yuspa, S H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/07/01/ PY - 1993 DA - 1993 Jul 01 SP - 6076 EP - 6080 VL - 90 IS - 13 SN - 0027-8424, 0027-8424 KW - Transforming Growth Factor beta KW - 0 KW - Keratins KW - 68238-35-7 KW - Index Medicus KW - Animals KW - Carcinoma, Squamous Cell -- etiology KW - Papilloma -- pathology KW - Mice KW - Keratins -- analysis KW - Mice, Transgenic KW - Risk KW - Base Sequence KW - Papilloma -- etiology KW - Carcinoma, Squamous Cell -- pathology KW - Molecular Sequence Data KW - Papilloma -- chemistry KW - Carcinoma, Squamous Cell -- chemistry KW - Female KW - Cell Division KW - Transforming Growth Factor beta -- analysis KW - Skin Neoplasms -- etiology KW - Epidermis -- cytology KW - Skin Neoplasms -- pathology KW - Skin Neoplasms -- chemistry KW - Epidermis -- chemistry KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75840809?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Loss+of+expression+of+transforming+growth+factor+beta+in+skin+and+skin+tumors+is+associated+with+hyperproliferation+and+a+high+risk+for+malignant+conversion.&rft.au=Glick%2C+A+B%3BKulkarni%2C+A+B%3BTennenbaum%2C+T%3BHennings%2C+H%3BFlanders%2C+K+C%3BO%27Reilly%2C+M%3BSporn%2C+M+B%3BKarlsson%2C+S%3BYuspa%2C+S+H&rft.aulast=Glick&rft.aufirst=A&rft.date=1993-07-01&rft.volume=90&rft.issue=13&rft.spage=6076&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-06 N1 - Date created - 1993-08-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Development. 1990 Jul;109(3):585-95 [2401212] Growth Factors. 1990;3(1):45-52 [2383401] J Cell Physiol. 1991 Jul;148(1):157-73 [1907288] Carcinogenesis. 1991 Nov;12(11):2063-7 [1718620] Proc Natl Acad Sci U S A. 1991 Nov 1;88(21):9613-7 [1946376] J Cell Biol. 1992 Jan;116(1):187-96 [1730743] Proc Natl Acad Sci U S A. 1993 Jan 15;90(2):770-4 [8421714] Carcinogenesis. 1983;4(4):369-74 [6839411] Nature. 1983 May 5-11;303(5912):72-4 [6843661] Nature. 1983 Jul 7-13;304(5921):67-9 [6866091] Nature. 1984 Feb 16-22;307(5952):658-60 [6694757] Carcinogenesis. 1985 Nov;6(11):1607-10 [2414025] Cancer Res. 1986 Apr;46(4 Pt 2):2068-71 [2418960] Methods Enzymol. 1986;124:497-510 [3754925] Proc Natl Acad Sci U S A. 1992 Jun 15;89(12):5408-12 [1608949] Cancer Res. 1992 Jul 15;52(14):4042-5 [1319836] J Biol Chem. 1992 Jul 5;267(19):13702-7 [1618868] Cell Growth Differ. 1992 Feb;3(2):81-91 [1504019] Carcinogenesis. 1992 Dec;13(12):2367-73 [1473246] Environ Health Perspect. 1986 Sep;68:69-74 [3780634] Proc Natl Acad Sci U S A. 1987 Apr;84(7):2029-32 [3104907] J Cell Biol. 1987 Aug;105(2):965-75 [2887577] J Cell Biol. 1987 Dec;105(6 Pt 2):2861-76 [3320058] Nature. 1988 Jan 28;331(6154):363-5 [3422343] Cancer Res. 1988 Jun 1;48(11):3245-52 [2452688] Int J Cancer. 1989 May 15;43(5):915-21 [2714898] Mol Carcinog. 1988;1(3):171-9 [2471536] Mol Carcinog. 1989;2(1):22-6 [2499343] Mol Carcinog. 1988;1(2):96-108 [3076454] Cancer Res. 1990 Feb 1;50(3):653-7 [2105160] Proc Natl Acad Sci U S A. 1990 Jan;87(2):643-7 [2153961] Mol Endocrinol. 1990 Jan;4(1):46-52 [2157977] Cell. 1990 May 4;61(3):407-17 [2185890] Mol Carcinog. 1991;4(3):210-9 [2064727] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Mutations induced by saturated aqueous nitric oxide in the pSP189 supF gene in human Ad293 and E. coli MBM7070 cells. AN - 75838879; 8330336 AB - Nitric oxide is an important bioregulatory agent that may also be an endogenous and exogenous human mutagen. In order to study mutations generated following exposure of a shuttle vector-borne target gene to nitric oxide, mutations were induced in the supF gene of the pSP189 shuttle vector by treatment with nitric oxide in aerobic buffered solution followed by replication of the plasmid in either human Ad293 or Escherichia coli MBM7070 cells. The induced mutation frequency, which increased with nitric oxide dose, was 44-fold greater than the spontaneous background in human cells and > 15-fold greater than background in the bacterial cells when a total of 100 mmol of nitric oxide was oxidatively absorbed/I of pH 7.4 buffer containing the plasmid. The majority of point mutations analysed (61 and 75% for human and E. coli cells respectively) were AT-->GC transitions with GC-->AT transitions (29 and 23%) being the next most prevalent. The overall frequencies of the various point mutations seen in the supF gene were similar in the two cell types, although the distribution of hotspots showed differences. The results are consistent with a mutational mechanism initiated by deamination of DNA bases. JF - Carcinogenesis AU - Routledge, M N AU - Wink, D A AU - Keefer, L K AU - Dipple, A AD - Chemistry of Carcinogenesis Laboratory, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 1251 EP - 1254 VL - 14 IS - 7 SN - 0143-3334, 0143-3334 KW - supF KW - DNA, Bacterial KW - 0 KW - Mutagens KW - Water KW - 059QF0KO0R KW - Nitric Oxide KW - 31C4KY9ESH KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Base Sequence KW - Cells, Cultured KW - Humans KW - Water -- chemistry KW - Molecular Sequence Data KW - Plasmids KW - DNA, Bacterial -- drug effects KW - DNA Replication -- drug effects KW - DNA -- drug effects KW - Nitric Oxide -- toxicity KW - Point Mutation KW - Escherichia coli -- drug effects KW - Mutagens -- toxicity KW - Escherichia coli -- genetics KW - Genes, Bacterial -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75838879?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Mutations+induced+by+saturated+aqueous+nitric+oxide+in+the+pSP189+supF+gene+in+human+Ad293+and+E.+coli+MBM7070+cells.&rft.au=Routledge%2C+M+N%3BWink%2C+D+A%3BKeefer%2C+L+K%3BDipple%2C+A&rft.aulast=Routledge&rft.aufirst=M&rft.date=1993-07-01&rft.volume=14&rft.issue=7&rft.spage=1251&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-18 N1 - Date created - 1993-08-18 N1 - Date revised - 2017-01-13 N1 - Gene symbol - supF N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - 32P-postlabeling analysis of IQ, MeIQx and PhIP adducts formed in vitro in DNA and polynucleotides and found in vivo in hepatic DNA from IQ-, MeIQx- and PhIP-treated monkeys. AN - 75838668; 8330355 AB - The 32P-postlabeling method was used to examine the adducts in DNA, polynucleotides, and mononucleotides reacted in vitro with the N-hydroxy and N-acetoxy derivatives of 2-amino-3-methylimidazo[4,5-f]quinoline (IQ), 2-amino-3, 8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) or 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP). Adduct profiles were compared to those found in vivo in liver of cynomolgus monkeys fed IQ, MeIQx or PhIP. The N-acetoxy derivatives of IQ, MeIQx and PhIP (generated in situ from the corresponding N-hydroxylamine in the presence of acetic anhydride) each formed three principal adducts in DNA. Adduct 1 of IQ, MeIQx and PhIP was chromatographically identical to the 32P-labeled bis(phosphate) derivative of N-(deoxyguanosin-8-yl)-IQ, N-(deoxyguanosin-8-yl)-MeIQx, and N-(deoxyguanosin-8-yl)-PhIP respectively, and this adduct comprised approximately 65% of total adduct levels found in DNA in vitro. The C8-guanine adduct and the two minor adducts were also found in poly(dG-dC). poly(dG-dC), suggesting that the two minor adducts of IQ, MeIQx and PhIP are also formed on the guanine base. The N-acetoxy derivatives of IQ, MeIQx, and to a much lesser extent PhIP, also formed adducts with adenine-containing polynucleotides including poly(dA), poly(dA).poly(dT) and poly(dA-dT).poly(dA-dT), but these adenine adducts were chromatographically different from those found in DNA. The three guanine adducts of N-acetoxy-IQ, -MeIQx and -PhIP found in vitro in DNA and in guanine-containing polynucleotides were also found in the liver of monkeys fed IQ, MeIQx or PhIP respectively, indicating that metabolic activation via N-hydroxylation and esterification occurred in vivo in monkeys. With each compound, the C8-guanine adduct was the predominant adduct found in vivo. The results indicate similarities among IQ, MeIQx and PhIP in the DNA adducts formed in vitro and in vivo and substantiate the use of the 32P-postlabeling method for comparative adduct studies. JF - Carcinogenesis AU - Snyderwine, E G AU - Davis, C D AU - Nouso, K AU - Roller, P P AU - Schut, H A AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, MD. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 1389 EP - 1395 VL - 14 IS - 7 SN - 0143-3334, 0143-3334 KW - Imidazoles KW - 0 KW - Mutagens KW - Phosphorus Radioisotopes KW - Polynucleotides KW - Quinolines KW - Quinoxalines KW - 2-amino-3-methylimidazo(4,5-f)quinoline KW - 30GL3D3T0G KW - 2-amino-3,8-dimethylimidazo(4,5-f)quinoxaline KW - 77500-04-0 KW - DNA KW - 9007-49-2 KW - 2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine KW - 909C6UN66T KW - Index Medicus KW - Quinolines -- toxicity KW - Animals KW - Imidazoles -- toxicity KW - DNA Damage KW - Quinoxalines -- analysis KW - Quinoxalines -- toxicity KW - Imidazoles -- analysis KW - Autoradiography KW - Quinolines -- analysis KW - Haplorhini KW - Chromatography, High Pressure Liquid KW - Polynucleotides -- chemistry KW - Mutagens -- analysis KW - Liver -- drug effects KW - Mutagens -- toxicity KW - Liver -- metabolism KW - DNA -- chemistry KW - DNA -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75838668?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=32P-postlabeling+analysis+of+IQ%2C+MeIQx+and+PhIP+adducts+formed+in+vitro+in+DNA+and+polynucleotides+and+found+in+vivo+in+hepatic+DNA+from+IQ-%2C+MeIQx-+and+PhIP-treated+monkeys.&rft.au=Snyderwine%2C+E+G%3BDavis%2C+C+D%3BNouso%2C+K%3BRoller%2C+P+P%3BSchut%2C+H+A&rft.aulast=Snyderwine&rft.aufirst=E&rft.date=1993-07-01&rft.volume=14&rft.issue=7&rft.spage=1389&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-18 N1 - Date created - 1993-08-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - MK-801 impairs recognition memory in rhesus monkeys: comparison with cholinergic drugs. AN - 75836789; 8331575 AB - Both N-methyl-D-aspartate (NMDA) and cholinergic receptors are thought to participate in processes of learning and memory. The effects of the noncompetitive NMDA antagonist ((+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine) MK-801 on recognition memory in rhesus monkeys performing a computer-automated version of delayed nonmatching-to-sample DNMS were compared to those of the cholinergic compounds physostigmine and scopolamine. In the sample phase of the test, 20 symbols were presented sequentially every 30 sec on a color monitor fitted with a touch-sensitive screen. These symbols were then presented again in the same order as before, but each symbol was now paired with a different novel symbol. A monkey was rewarded with a food pellet if it touched the symbol in the sample phase and the previously unseen symbol in the choice phase. Physostigmine (3.2, 10 and 32 micrograms/kg), scopolamine (3.2, 10, 17.8 and 32 micrograms/kg) or MK-801 (3.2, 10 and 32 micrograms/kg) was injected i.m. 20, 20 and 30 min before testing, respectively. The highest doses of both MK-801 and scopolamine significantly impaired performance. In addition, scopolamine, but not MK-801, prolonged response latency, whereas MK-801, but not scopolamine, increased response bias. Physostigmine produced a small but significant increase in correct responses at the intermediate dose, but not at the highest dose. These results suggest that both the glutamatergic and the cholinergic systems participate in visual recognition memory in monkeys, though probably by different mechanisms. JF - The Journal of pharmacology and experimental therapeutics AU - Ogura, H AU - Aigner, T G AD - Laboratory of Neuropsychology, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 60 EP - 64 VL - 266 IS - 1 SN - 0022-3565, 0022-3565 KW - Scopolamine Hydrobromide KW - 451IFR0GXB KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - Physostigmine KW - 9U1VM840SP KW - Index Medicus KW - Animals KW - Memory Disorders -- chemically induced KW - Dose-Response Relationship, Drug KW - Macaca mulatta KW - Male KW - Learning Disorders -- chemically induced KW - Scopolamine Hydrobromide -- pharmacology KW - Memory -- drug effects KW - Physostigmine -- pharmacology KW - Learning -- drug effects KW - Dizocilpine Maleate -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75836789?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.atitle=MK-801+impairs+recognition+memory+in+rhesus+monkeys%3A+comparison+with+cholinergic+drugs.&rft.au=Ogura%2C+H%3BAigner%2C+T+G&rft.aulast=Ogura&rft.aufirst=H&rft.date=1993-07-01&rft.volume=266&rft.issue=1&rft.spage=60&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.issn=00223565&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-19 N1 - Date created - 1993-08-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Leukemia, lymphoma, and multiple myeloma after pelvic radiotherapy for benign disease. AN - 75836442; 8327655 AB - The relationship between exposure to sparsely ionizing radiation and mortality due to cancers of hematopoietic and lymphopoietic tissues was studied among 12,955 women treated for benign gynecological disorders at any of 17 hospitals in New England or New York State and followed for an average of 25 years; 9770 women were treated by radiation (intracavitary 226Ra, external-beam X rays), while 3185 were treated by other methods, including curettage, surgery, and hormones. The average age at treatment was 46.5 years, and the mean dose to active bone marrow among irradiated women was 119 cGy. Forty deaths due to acute, myelocytic, or monocytic leukemia were observed among irradiated women. This number was 70% higher than expected based on U.S. mortality rates [standardized mortality ratio (SMR) = 1.7; 90% confidence interval (CI) 1.3-2.3]. A deficit was recorded among nonirradiated women, based on three observed deaths (SMR = 0.5; 90% CI 0.1-1.2). A well-defined gradient in the SMR with dose among exposed women was not detected. The SMR was highest within 5 years after irradiation but remained elevated even after 30 years. The temporal pattern differed by subtype of leukemia: excess mortality due to chronic myelocytic leukemia occurred almost exclusively within the first 15 years, whereas the SMR for acute leukemia, though also elevated, varied little over time. Cancers of lymphoreticular tissue occurred more often than expected based on U.S. mortality rates, but not appreciably differently for irradiated and nonirradiated women. There was little or no evidence of effects attributable to radiotherapy for chronic lymphocytic leukemia [relative risk (RR) = 1.1; 90% CI 0.5-3.0], Hodgkin's disease (RR = 0.9; 90% CI 0.3-3.2), non-Hodgkin's lymphoma (RR = 0.9; 90% CI 0.6-1.6), or multiple myeloma (RR = 0.6; 90% CI 0.3-1.4). These results corroborate previous findings indicating that acute and myelocytic leukemias are the most prominent malignancies after exposure to sparsely ionizing radiation, occurring in excess shortly after irradiation, and that lymphomas are either not caused by radiation or are induced only rarely. JF - Radiation research AU - Inskip, P D AU - Kleinerman, R A AU - Stovall, M AU - Cookfair, D L AU - Hadjimichael, O AU - Moloney, W C AU - Monson, R R AU - Thompson, W D AU - Wactawski-Wende, J AU - Wagoner, J K AD - Radiation Epidemiology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 108 EP - 124 VL - 135 IS - 1 SN - 0033-7587, 0033-7587 KW - Index Medicus KW - Space life sciences KW - Radiotherapy Dosage KW - Humans KW - Middle Aged KW - Hematology KW - Follow-Up Studies KW - Bone Marrow -- radiation effects KW - Female KW - Cause of Death KW - Lymphoma -- etiology KW - Leukemia, Radiation-Induced -- blood KW - Neoplasms, Radiation-Induced KW - Radiotherapy -- methods KW - Radiotherapy -- adverse effects KW - Genital Diseases, Female -- radiotherapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75836442?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Radiation+research&rft.atitle=Leukemia%2C+lymphoma%2C+and+multiple+myeloma+after+pelvic+radiotherapy+for+benign+disease.&rft.au=Inskip%2C+P+D%3BKleinerman%2C+R+A%3BStovall%2C+M%3BCookfair%2C+D+L%3BHadjimichael%2C+O%3BMoloney%2C+W+C%3BMonson%2C+R+R%3BThompson%2C+W+D%3BWactawski-Wende%2C+J%3BWagoner%2C+J+K&rft.aulast=Inskip&rft.aufirst=P&rft.date=1993-07-01&rft.volume=135&rft.issue=1&rft.spage=108&rft.isbn=&rft.btitle=&rft.title=Radiation+research&rft.issn=00337587&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-11 N1 - Date created - 1993-08-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Regulation of hair follicle development: an in vitro model for hair follicle invasion of dermis and associated connective tissue remodeling. AN - 75836306; 8326151 AB - During embryonic development presumptive hair follicle cells of epithelial and mesenchymal origin are determined in defined body locations. This is followed by rapid proliferation of epithelial cells and associated penetration into the dermis in response to as yet undetermined signals. A collagen matrix culture system, which maintains the three-dimensional relationships of hair follicle cells to each other, was developed to study the regulation of the enlargement of immature hair follicles and the accompanying remodeling of the dermis. In studies with a heterogeneous dermis-derived preparation of murine hair follicles, ranging in size from the earliest down-growing budding cell mass to hair-forming follicles, we had previously shown that cell proliferation was stimulated by cholera toxin and epidermal growth factor, but only the epidermal growth factor-stimulated proliferation was accompanied by digestion of the collagen matrix due to release of collagenolytic enzymes. Further studies revealed that transforming growth factor-alpha also stimulated hair follicle cell proliferation and collagenase release. However, although transforming growth factor-beta inhibited the transforming growth factor-alpha-stimulated proliferation, it enhanced the release and activation of collagenases and other gelatin-degrading enzymes detectable by gelatin zymography. Stimulation of collagenolytic activity depended on the three-dimensional hair follicle structure and did not occur in monolayer cultures of hair follicle cells. Comparison of hair follicle buds with more developed dermis-derived hair follicles, plated at the same cell density (based on DNA content), suggested that a greater fraction of cells in the bud-stage follicle responded to the growth factors by release of collagenases. Possibly only the cells in the advancing portion of growing hair follicles that are closest to the dermal papilla cell cluster produce the collagenases in response to growth factors. To examine the participation of dermal papilla cells in collagenase release and activation, several immortalized rat whisker dermal papilla cell lines were co-cultured with mouse hair follicle buds. Co-culture resulted in a marked enlargement of follicles as well as activation of the 92-kDa type IV collagenase, produced by hair follicle buds, that correlated with ability of the dermal papilla cells to stimulate hair formation in grafts of hair follicle buds on nude mice. Dermal papilla cells cultured alone produced the 72-kDa type IV collagenase, which was also activated during co-culture with hair follicle buds. Thus, two activities, both relevant for hair follicle development, namely, cell proliferation and release and activation of collagenases, have been stimulated in immature hair follicle buds by either growth-factor supplementation or interaction with dermal papilla cells.(ABSTRACT TRUNCATED AT 400 WORDS) JF - The Journal of investigative dermatology AU - Yuspa, S H AU - Wang, Q AU - Weinberg, W C AU - Goodman, L AU - Ledbetter, S AU - Dooley, T AU - Lichti, U AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 27S EP - 32S VL - 101 IS - 1 Suppl SN - 0022-202X, 0022-202X KW - Growth Substances KW - 0 KW - Collagenases KW - EC 3.4.24.- KW - Index Medicus KW - Animals KW - Cells, Cultured KW - Growth Substances -- pharmacology KW - Epidermis -- cytology KW - Enzyme Activation -- drug effects KW - Mice KW - Mice, Inbred BALB C KW - 3T3 Cells -- enzymology KW - Collagenases -- metabolism KW - Hair -- growth & development KW - Connective Tissue -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75836306?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+investigative+dermatology&rft.atitle=Regulation+of+hair+follicle+development%3A+an+in+vitro+model+for+hair+follicle+invasion+of+dermis+and+associated+connective+tissue+remodeling.&rft.au=Yuspa%2C+S+H%3BWang%2C+Q%3BWeinberg%2C+W+C%3BGoodman%2C+L%3BLedbetter%2C+S%3BDooley%2C+T%3BLichti%2C+U&rft.aulast=Yuspa&rft.aufirst=S&rft.date=1993-07-01&rft.volume=101&rft.issue=1+Suppl&rft.spage=27S&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+investigative+dermatology&rft.issn=0022202X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-11 N1 - Date created - 1993-08-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Chrysotile asbestos upregulates gene expression and production of alpha-receptors for platelet-derived growth factor (PDGF-AA) on rat lung fibroblasts. AN - 75833234; 8392089 AB - PDGF isoforms have been postulated to serve as mediators of fibroblast proliferation and chemotaxis during lung fibrogenesis induced by asbestos inhalation. We have studied the interaction of chrysotile asbestos fibers with rat lung fibroblasts (RLF) in vitro and the consequent changes in PDGF receptor mRNA expression, PDGF binding, and mitogenic activity of PDGF isoforms. Northern blot analysis revealed that mRNA for the PDGF-receptor alpha subtype (PDGF-R alpha) on RLF was upregulated after a 24-h exposure to asbestos in culture (0.5-15 micrograms fibers/cm2). [125I]PDGF-BB receptor assays showed that normal RLF possess mainly PDGF-R beta and a paucity of PDGF-R alpha. In agreement with the Northern data, saturation binding of [125I]PDGF-BB to RLF exposed to asbestos demonstrated an approximately 40% increase in binding sites accompanied by a twofold decrease in receptor affinity. Treating asbestos-exposed RLF with PDGF-AA, which binds only PDGF-R alpha, blocked the PDGF binding sites that were upregulated by fiber exposure. PDGF-AA had increased mitogenic potency for fiber-exposed RLF, but PDGF-BB was a less potent mitogen for these RLF. Nonfibrogenic carbonyl iron spheres induced similar changes in PDGF growth responses. These data show that inorganic particulates alter the PDGF-R alpha population on RLF without significant change in PDGF-R beta. JF - The Journal of clinical investigation AU - Bonner, J C AU - Goodell, A L AU - Coin, P G AU - Brody, A R AD - Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 425 EP - 430 VL - 92 IS - 1 SN - 0021-9738, 0021-9738 KW - Asbestos, Serpentine KW - 0 KW - Platelet-Derived Growth Factor KW - RNA, Messenger KW - Asbestos KW - 1332-21-4 KW - Receptors, Platelet-Derived Growth Factor KW - EC 2.7.10.1 KW - Abridged Index Medicus KW - Index Medicus KW - Rats KW - Gene Expression -- drug effects KW - Animals KW - Cells, Cultured KW - In Vitro Techniques KW - Cell Division -- drug effects KW - Up-Regulation KW - RNA, Messenger -- genetics KW - Fibroblasts KW - Receptors, Platelet-Derived Growth Factor -- metabolism KW - Receptors, Platelet-Derived Growth Factor -- classification KW - Platelet-Derived Growth Factor -- metabolism KW - Lung -- cytology KW - Asbestos -- pharmacology KW - Receptors, Platelet-Derived Growth Factor -- genetics KW - Platelet-Derived Growth Factor -- classification KW - Lung -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75833234?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+clinical+investigation&rft.atitle=Chrysotile+asbestos+upregulates+gene+expression+and+production+of+alpha-receptors+for+platelet-derived+growth+factor+%28PDGF-AA%29+on+rat+lung+fibroblasts.&rft.au=Bonner%2C+J+C%3BGoodell%2C+A+L%3BCoin%2C+P+G%3BBrody%2C+A+R&rft.aulast=Bonner&rft.aufirst=J&rft.date=1993-07-01&rft.volume=92&rft.issue=1&rft.spage=425&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+clinical+investigation&rft.issn=00219738&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-12 N1 - Date created - 1993-08-12 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Am J Pathol. 1988 Apr;131(1):156-70 [2833103] J Biol Chem. 1992 Sep 5;267(25):18032-9 [1325456] Am J Med. 1981 Mar;70(3):542-68 [7011012] J Cell Biol. 1982 Feb;92(2):584-8 [7061598] N Engl J Med. 1982 Jun 17;306(24):1446-55 [7043267] Am J Pathol. 1982 Oct;109(1):107-14 [7124904] J Cell Physiol. 1982 Nov;113(2):261-6 [6184376] Proc Natl Acad Sci U S A. 1983 Apr;80(7):1919-23 [6300879] Cell. 1985 Nov;43(1):277-86 [2416458] N Engl J Med. 1986 Feb 20;314(8):488-500 [3511384] Cell. 1986 Jul 18;46(2):155-69 [3013421] N Engl J Med. 1987 Jul 23;317(4):202-9 [3600711] Anal Biochem. 1987 Apr;162(1):156-9 [2440339] J Cell Biol. 1988 Feb;106(2):403-13 [2828383] Exp Lung Res. 1988;14(1):51-66 [2830106] FASEB J. 1988 Apr;2(7):2272-7 [3280379] Science. 1988 Jun 10;240(4858):1529-31 [2836952] EMBO J. 1988 May;7(5):1387-93 [2842148] Science. 1989 Jan 20;243(4889):393-6 [2783498] Am J Pathol. 1989 Jan;134(1):133-40 [2913821] J Biol Chem. 1989 May 15;264(14):8120-5 [2542264] J Biol Chem. 1989 May 25;264(15):8771-8 [2542288] J Biol Chem. 1989 May 25;264(15):8905-12 [2542295] Proc Natl Acad Sci U S A. 1989 Jul;86(13):4917-21 [2544881] J Cell Physiol. 1989 Aug;140(2):295-304 [2745564] J Clin Invest. 1990 Mar;85(3):916-20 [2155930] Am J Pathol. 1990 Mar;136(3):695-705 [2156434] J Clin Invest. 1990 Jun;85(6):2023-7 [2347924] J Biol Chem. 1990 Jun 25;265(18):10238-43 [2162342] Proc Natl Acad Sci U S A. 1990 Oct;87(19):7385-9 [2170975] Cell. 1990 Nov 2;63(3):515-24 [2171777] Am J Respir Cell Mol Biol. 1990 Dec;3(6):595-602 [1701306] J Biol Chem. 1991 Jun 5;266(16):10143-7 [1709926] Carcinogenesis. 1991 Aug;12(8):1499-502 [1650293] Am J Respir Cell Mol Biol. 1991 Dec;5(6):539-47 [1958381] J Exp Med. 1992 May 1;175(5):1227-34 [1314885] Proc Natl Acad Sci U S A. 1988 Apr;85(8):2810-4 [3282240] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - In vivo regulation of murine hair growth: insights from grafting defined cell populations onto nude mice. AN - 75830570; 8326145 AB - The nude mouse graft model for testing the hair-forming ability of selected cell populations has considerable potential for providing insights into factors that are important for hair follicle development and proper hair formation. We have developed a minimal component system consisting of immature hair follicle buds from newborn pigmented C57BL/6 mice and adenovirus E1A-immortalized rat vibrissa dermal papilla cells. Hair follicle buds contribute to formation of hairless skin when grafted alone or with Swiss 3T3 cells, but produce densely haired skin when grafted with a fresh dermal cell preparation. The fresh dermal cell preparation represents the single cell fraction after hair follicles have been removed from a collagenase digest of newborn mouse dermis. It provides dermal papilla cells, fibroblasts, and possibly other important growth factor-producing cell types. Rat vibrissa dermal papilla cells supported dense hair growth at early passage in culture but progressively lost this potential during repeated passage in culture. Of 19 E1A-immortalized, clonally derived rat vibrissa dermal papilla cell lines, the four most positive clones supported hair growth to the extent of approximately 200 to 300 hairs per 1-2 cm2 graft area. The remaining clones were moderately positive (five clones), weakly positive (three clones), or negative (seven clones). Swiss 3T3 cells prevented contraction of the graft area but did not appear to affect the number of hairs in the graft site produced by dermal papilla cells plus hair follicle buds alone. The relatively low hair density (estimated 1-5% of normal) resulting from grafts of hair follicle buds with the most positive of the immortalized dermal papilla cell clones compared to fresh dermal cells suggests that optimal reconstitution of hair growth requires some function of dermal papilla cells partially lost during the immortalization process and possibly the contribution of other cell types present in the fresh dermal cell preparation, which is not supplied by the Swiss 3T3 cells. The current graft system, comprising hair follicle buds and immortalized dermal papilla cell clones, provides an assay for positive or negative influences on hair growth exerted by added selected cell types, growth factors, or other substances. Characterization of the phenotype of the dermal papilla cell lines, which differ in their ability to support hair growth when grafted with hair follicle buds, may provide insight into specific dermal papilla cell properties important for their function in this system. JF - The Journal of investigative dermatology AU - Lichti, U AU - Weinberg, W C AU - Goodman, L AU - Ledbetter, S AU - Dooley, T AU - Morgan, D AU - Yuspa, S H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, NIH, Bethesda, MD 20892. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 124S EP - 129S VL - 101 IS - 1 Suppl SN - 0022-202X, 0022-202X KW - Index Medicus KW - Evaluation Studies as Topic KW - Animals KW - Cells, Cultured KW - Skin Transplantation -- physiology KW - Mice, Nude KW - Mice KW - Mice, Inbred BALB C KW - Hair -- growth & development KW - Skin -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75830570?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+investigative+dermatology&rft.atitle=In+vivo+regulation+of+murine+hair+growth%3A+insights+from+grafting+defined+cell+populations+onto+nude+mice.&rft.au=Lichti%2C+U%3BWeinberg%2C+W+C%3BGoodman%2C+L%3BLedbetter%2C+S%3BDooley%2C+T%3BMorgan%2C+D%3BYuspa%2C+S+H&rft.aulast=Lichti&rft.aufirst=U&rft.date=1993-07-01&rft.volume=101&rft.issue=1+Suppl&rft.spage=124S&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+investigative+dermatology&rft.issn=0022202X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-11 N1 - Date created - 1993-08-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Interleukin 4 suppresses interleukin 2 and interferon gamma production by naive T cells stimulated by accessory cell-dependent receptor engagement. AN - 75830334; 8100998 AB - Interleukin 2 (IL-2) and interferon gamma (IFN-gamma) production by CD4+ T cells and IFN-gamma production by CD8+ T cells from naive mice in response to soluble anti-CD3 and antigen-presenting cells (APCs) were strikingly inhibited by culture in the presence of IL-4. IL-4 decreased IL-2 and IFN-gamma mRNA levels after 15-24 hr but gave relatively little decrease in these mRNAs at 6-12 hr after stimulation with soluble anti-CD3. A 16-hr preculture of T cells with anti-CD3, APCs, and IL-4 was sufficient to inhibit subsequent production of IL-2 and IFN-gamma in response to restimulation in the absence of IL-4. Furthermore, IL-4 treatment of T cells purified 24 hr after stimulation inhibited their capacity to subsequently produce IL-2 in response to anti-CD3 and APCs, indicating that T cells were targets of IL-4-mediated inhibition. IL-4 blocked acute IL-2 production in response to a cytochrome c peptide of T cells derived from transgenic mice expressing T-cell receptors specific for cytochrome c but it did not block IL-2 production by such cells after they had been primed in vitro. Nor did IL-4 inhibit production of IFN-gamma by cloned T cells in response to antigen and APCs or production of IL-2 and IFN-gamma by naive T cells in response to phorbol ester and calcium ionophore. These results indicate that IL-4 strikingly inhibits IL-2 and IFN-gamma production by naive T cells in response to accessory cell-dependent, receptor-mediated stimulation (i.e., soluble anti-CD3 and APCs or antigen and APCs) but does not inhibit accessory cell-independent stimulation of naive T cells or accessory cell-dependent receptor-mediated stimulation of recently primed T cells or cloned T-cell lines. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Tanaka, T AU - Hu-Li, J AU - Seder, R A AU - Fazekas de St Groth, B AU - Paul, W E AD - Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/07/01/ PY - 1993 DA - 1993 Jul 01 SP - 5914 EP - 5918 VL - 90 IS - 13 SN - 0027-8424, 0027-8424 KW - Interleukin-2 KW - 0 KW - Interleukin-4 KW - 207137-56-2 KW - Ionomycin KW - 56092-81-0 KW - Interferon-gamma KW - 82115-62-6 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - CD4-Positive T-Lymphocytes -- metabolism KW - Cells, Cultured KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Mice KW - Ionomycin -- pharmacology KW - Mice, Inbred BALB C KW - CD4-Positive T-Lymphocytes -- drug effects KW - Female KW - Lymphocyte Activation KW - T-Lymphocytes -- metabolism KW - Antigen-Presenting Cells -- physiology KW - Interleukin-4 -- pharmacology KW - Interleukin-2 -- biosynthesis KW - Interferon-gamma -- biosynthesis KW - T-Lymphocytes -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75830334?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Interleukin+4+suppresses+interleukin+2+and+interferon+gamma+production+by+naive+T+cells+stimulated+by+accessory+cell-dependent+receptor+engagement.&rft.au=Tanaka%2C+T%3BHu-Li%2C+J%3BSeder%2C+R+A%3BFazekas+de+St+Groth%2C+B%3BPaul%2C+W+E&rft.aulast=Tanaka&rft.aufirst=T&rft.date=1993-07-01&rft.volume=90&rft.issue=13&rft.spage=5914&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-06 N1 - Date created - 1993-08-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Immunol Rev. 1979;47:63-90 [398327] J Immunol. 1993 Mar 15;150(6):2112-20 [7680682] Immunol Rev. 1982;69:5-23 [6984001] Nature. 1985 Mar 7-13;314(6006):98-100 [3919312] Nature. 1985 May 23-29;315(6017):333-6 [2582266] J Exp Med. 1985 Nov 1;162(5):1695-708 [3877141] Proc Natl Acad Sci U S A. 1987 Mar;84(5):1374-8 [2950524] J Immunol Methods. 1987 Nov 23;104(1-2):137-42 [3119723] J Exp Med. 1987 Nov 1;166(5):1229-44 [2960769] J Exp Med. 1987 Dec 1;166(6):1774-87 [2960773] Immunol Rev. 1988 Feb;102:77-105 [2966763] J Immunol Methods. 1989 Jan 17;116(2):151-8 [2642947] J Immunol. 1989 Feb 1;142(3):800-7 [2783601] Eur J Immunol. 1989 Apr;19(4):617-23 [2567241] J Exp Med. 1989 Nov 1;170(5):1751-6 [2530302] J Exp Med. 1990 Jan 1;171(1):115-27 [2104918] J Exp Med. 1990 Sep 1;172(3):921-9 [2117636] J Immunol. 1990 Dec 1;145(11):3796-806 [2147202] J Immunol. 1991 Jun 1;146(11):3831-9 [1827817] J Immunol. 1991 Jun 15;146(12):4209-14 [1674955] J Immunol. 1992 Feb 15;148(4):1182-7 [1531351] J Immunol. 1992 Mar 15;148(6):1652-6 [1347305] J Exp Med. 1992 Jul 1;176(1):19-25 [1535368] Proc Natl Acad Sci U S A. 1992 Jul 1;89(13):6065-9 [1385868] J Exp Med. 1992 Oct 1;176(4):1091-8 [1328464] J Exp Med. 1980 Aug 1;152(2):280-95 [6156984] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Evidence that the SKI antiviral system of Saccharomyces cerevisiae acts by blocking expression of viral mRNA. AN - 75822622; 8321235 AB - The SKI2 gene is part of a host system that represses the copy number of the L-A double-stranded RNA (dsRNA) virus and its satellites M and X dsRNA, of the L-BC dsRNA virus, and of the single-stranded replicon 20S RNA. We show that SKI2 encodes a 145-kDa protein with motifs characteristic of helicases and nucleolar proteins and is essential only in cells carrying M dsRNA. Unexpectedly, Ski2p does not repress M1 dsRNA copy number when M1 is supported by aN L-A cDNA clone; nonetheless, it did lower the levels of M1 dsRNA-encoded toxin produced. Since toxin secretion from cDNA clones of M1 is unaffected by Ski2p, these data suggest that Ski2p acts by specifically blocking translation of viral mRNAs, perhaps recognizing the absence of cap or poly(A). In support of this idea, we find that Ski2p represses production of beta-galactosidase from RNA polymerase I [no cap and no poly(A)] transcripts but not from RNA polymerase II (capped) transcripts. JF - Molecular and cellular biology AU - Widner, W R AU - Wickner, R B AD - Section on Genetics of Simple Eukaryotes, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 4331 EP - 4341 VL - 13 IS - 7 SN - 0270-7306, 0270-7306 KW - SKI2 KW - Antiviral Agents KW - 0 KW - DNA, Fungal KW - Fungal Proteins KW - Multienzyme Complexes KW - Nuclear Proteins KW - RNA, Double-Stranded KW - RNA, Messenger KW - RNA, Viral KW - SKI2 protein, S cerevisiae KW - Saccharomyces cerevisiae Proteins KW - RNA Polymerase II KW - EC 2.7.7.- KW - RNA Polymerase I KW - EC 2.7.7.6 KW - beta-Galactosidase KW - EC 3.2.1.23 KW - Index Medicus KW - RNA Polymerase I -- metabolism KW - Multienzyme Complexes -- metabolism KW - RNA Polymerase II -- metabolism KW - Gene Expression Regulation, Viral KW - Amino Acid Sequence KW - RNA, Double-Stranded -- antagonists & inhibitors KW - Cloning, Molecular KW - RNA, Messenger -- antagonists & inhibitors KW - Mutagenesis, Site-Directed KW - Base Sequence KW - Promoter Regions, Genetic KW - Restriction Mapping KW - beta-Galactosidase -- antagonists & inhibitors KW - Molecular Sequence Data KW - beta-Galactosidase -- genetics KW - Nuclear Proteins -- metabolism KW - Saccharomyces cerevisiae -- genetics KW - Fungal Proteins -- metabolism KW - RNA, Viral -- antagonists & inhibitors KW - Genes, Fungal KW - Saccharomyces cerevisiae -- growth & development KW - Fungal Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75822622?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+cellular+biology&rft.atitle=Evidence+that+the+SKI+antiviral+system+of+Saccharomyces+cerevisiae+acts+by+blocking+expression+of+viral+mRNA.&rft.au=Widner%2C+W+R%3BWickner%2C+R+B&rft.aulast=Widner&rft.aufirst=W&rft.date=1993-07-01&rft.volume=13&rft.issue=7&rft.spage=4331&rft.isbn=&rft.btitle=&rft.title=Molecular+and+cellular+biology&rft.issn=02707306&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-30 N1 - Date created - 1993-07-30 N1 - Date revised - 2017-01-13 N1 - Gene symbol - SKI2 N1 - Genetic sequence - L13469; GENBANK N1 - SuppNotes - Cited By: Yeast. 1993 Jan;9(1):43-51 [8442386] Yeast. 1992 Dec;8(12):1007-14 [1284101] Mol Cell Biol. 1984 Apr;4(4):761-70 [6371496] Cell. 1984 Dec;39(3 Pt 2):663-73 [6096018] Proc Natl Acad Sci U S A. 1985 Jan;82(2):488-92 [3881765] Virology. 1986 Apr 15;150(1):299-303 [3006342] Mol Cell Biol. 1985 Nov;5(11):2913-23 [3018486] Proc Natl Acad Sci U S A. 1986 Oct;83(20):7826-30 [3463999] Mol Cell Biol. 1986 Feb;6(2):674-87 [3023862] Gene. 1986;45(3):299-310 [3026915] Virology. 1987 Mar;157(1):252-6 [3029964] Gene. 1987;52(2-3):225-33 [3038686] Mol Cell Biol. 1987 Aug;7(8):2947-55 [2823109] Genetics. 1987 Nov;117(3):399-408 [3319767] Methods Enzymol. 1987;155:156-65 [3323819] J Virol. 1988 Apr;62(4):1278-85 [3279233] Methods Cell Biol. 1975;11:221-33 [1102849] Nucleic Acids Res. 1976 Oct;3(10):2427-36 [792814] J Biol Chem. 1977 Dec 25;252(24):9010-7 [336627] Proc Natl Acad Sci U S A. 1978 Sep;75(9):4224-8 [360211] J Bacteriol. 1978 Dec;136(3):1002-7 [363683] Cell. 1978 Dec;15(4):1439-46 [215328] Nucleic Acids Res. 1979 Jan;6(1):27-39 [106368] J Mol Biol. 1979 Jan 25;127(3):297-308 [372542] J Virol. 1993 May;67(5):2764-71 [8474174] Yeast. 1993 Mar;9(3):251-66 [8488726] Mol Cell Biol. 1984 Jan;4(1):92-100 [6366515] Cell. 1980 Feb;19(2):403-14 [6986991] Proc Natl Acad Sci U S A. 1980 Jan;77(1):527-30 [6987655] J Bacteriol. 1980 Jul;143(1):463-70 [6995444] Cell. 1980 Aug;21(1):217-26 [6996833] J Bacteriol. 1983 Jan;153(1):163-8 [6336730] Nucleic Acids Res. 1983 Feb 25;11(4):1077-97 [6338480] Methods Enzymol. 1983;101:181-91 [6310321] Mol Cell Biol. 1984 Jan;4(1):101-9 [6199660] Mol Cell Biol. 1984 Jan;4(1):181-7 [6366509] Gene. 1987;60(2-3):237-43 [3327750] Nature. 1988 May 5;333(6168):22-3 [3362205] J Mol Biol. 1988 Apr 20;200(4):627-38 [3137346] Cell. 1988 Nov 18;55(4):663-71 [2460245] Genetics. 1988 Sep;120(1):95-108 [2851484] J Biol Chem. 1989 Apr 25;264(12):6716-23 [2651431] Mol Cell Biol. 1989 Mar;9(3):1243-54 [2657388] Dev Biol. 1989 Jul;134(1):246-57 [2567251] Genetics. 1989 May;122(1):19-27 [2659436] Yeast. 1989 May-Jun;5(3):149-58 [2660461] Nucleic Acids Res. 1989 Jun 26;17(12):4713-30 [2546125] EMBO J. 1989 Dec 20;8(13):4015-24 [2686980] Curr Genet. 1989 Sep;16(3):139-43 [2557163] J Biol Chem. 1990 Feb 5;265(4):2209-15 [2298745] Experientia. 1990 Feb 15;46(2):193-200 [2406163] Proc Natl Acad Sci U S A. 1990 Oct;87(19):7628-32 [1699230] J Mol Biol. 1990 Oct 5;215(3):403-10 [2231712] J Virol. 1991 Jan;65(1):155-61 [1985195] Proc Natl Acad Sci U S A. 1991 Jan 1;88(1):174-8 [1986362] J Biol Chem. 1991 Jul 5;266(19):12772-8 [2061340] J Biol Chem. 1991 Jul 5;266(19):12779-83 [1648104] Nucleic Acids Res. 1991 Sep 25;19(18):4949-53 [1656383] EMBO J. 1992 Feb;11(2):673-82 [1531632] Proc Natl Acad Sci U S A. 1992 Mar 15;89(6):2185-9 [1549580] DNA Seq. 1992;2(4):203-10 [1352711] EMBO J. 1992 Jul;11(7):2655-64 [1628625] Mol Cell Biol. 1992 Aug;12(8):3390-8 [1630453] J Biol Chem. 1992 Aug 15;267(23):16252-8 [1644811] Mol Cell Biol. 1992 Sep;12(9):3865-71 [1508189] Nature. 1992 Oct 22;359(6397):746-9 [1436038] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Induction of cellular p53 activity by DNA-damaging agents and growth arrest. AN - 75811602; 8321226 AB - The tumor suppressor p53 can function as a sequence-specific transcription factor and is required for activation by ionizing radiation (IR) of one or more downstream effector genes, such as the human GADD45 gene. One important consequence of IR that is probably mediated by these downstream effector genes is activation of the p53-mediated G1 cell cycle checkpoint. While the induction of reporter constructs containing p53-binding sites has already been demonstrated with p53 expression vectors, we have now demonstrated the direct activation of such a construct after treatment of the human RKO line, which has a normal p53 phenotype, with various types of DNA-damaging agents and also after growth arrest produced by medium depletion (starvation). IR, UV radiation, and methylmethane sulfonate were found to induce p53 activity when a stably integrated reporter construct containing functional p53-binding sites was used and also in mobility shift assays with a p53-binding site from the GADD45 gene, and IR-inducible gene previously associated with growth arrest. The same cell treatments that induced this p53 activity also caused an increase in cellular p53 protein levels. The response in cells lacking normal p53 or in RKO cells expressing a dominant negative mutant p53 was markedly reduced. Interestingly, the spectrum of effective inducing agents for the above-described experiments was similar to that which induces GADD45 either in cells with a normal p53 status or, with the exception of IR, in cells lacking normal p53. These results indicate a role for p53 in the IR pathway, which is completely p53 dependent, and in other genotoxic stress responses, in which p53 has a cooperative effect but is not required. JF - Molecular and cellular biology AU - Zhan, Q AU - Carrier, F AU - Fornace, A J AD - Laboratory of Molecular Pharmacology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 4242 EP - 4250 VL - 13 IS - 7 SN - 0270-7306, 0270-7306 KW - GADD45 KW - Mutagens KW - 0 KW - Tumor Suppressor Protein p53 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Ultraviolet Rays KW - Humans KW - Cell Division -- drug effects KW - Transcription, Genetic KW - Binding Sites KW - Cloning, Molecular KW - Base Sequence KW - Chickens KW - Promoter Regions, Genetic KW - Tumor Cells, Cultured KW - Molecular Sequence Data KW - Suppression, Genetic KW - Signal Transduction KW - Cell Division -- radiation effects KW - DNA Damage KW - Mutagens -- pharmacology KW - Tumor Suppressor Protein p53 -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75811602?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+cellular+biology&rft.atitle=Induction+of+cellular+p53+activity+by+DNA-damaging+agents+and+growth+arrest.&rft.au=Zhan%2C+Q%3BCarrier%2C+F%3BFornace%2C+A+J&rft.aulast=Zhan&rft.aufirst=Q&rft.date=1993-07-01&rft.volume=13&rft.issue=7&rft.spage=4242&rft.isbn=&rft.btitle=&rft.title=Molecular+and+cellular+biology&rft.issn=02707306&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-30 N1 - Date created - 1993-07-30 N1 - Date revised - 2017-01-13 N1 - Gene symbol - GADD45 N1 - SuppNotes - Cited By: Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] Nat Genet. 1992 Apr;1(1):45-9 [1301998] Nucleic Acids Res. 1983 Mar 11;11(5):1475-89 [6828386] Mol Cell Biol. 1984 Sep;4(9):1689-94 [6092932] Virology. 1987 Mar;157(1):211-9 [3029959] Mol Cell Biol. 1987 Aug;7(8):2745-52 [3670292] Cancer Res. 1989 Apr 1;49(7):1687-92 [2466559] J Biol Chem. 1989 Jun 5;264(16):9539-46 [2722849] Lab Invest. 1989 Aug;61(2):143-61 [2666742] Mol Cell Biol. 1989 Oct;9(10):4196-203 [2573827] Proc Natl Acad Sci U S A. 1989 Dec;86(24):10104-7 [2602359] Science. 1990 Aug 24;249(4971):912-5 [2144057] J Biol Chem. 1990 Sep 5;265(25):15211-8 [1697587] Mol Cell Biol. 1991 Feb;11(2):1009-16 [1990262] New Biol. 1990 Aug;2(8):712-8 [2282368] J Natl Cancer Inst. 1991 Apr 3;83(7):480-4 [2005631] New Biol. 1991 Sep;3(9):825-33 [1931825] Cancer Res. 1991 Dec 1;51(23 Pt 1):6304-11 [1933891] Virology. 1992 Jan;186(1):133-47 [1727595] Mol Cell Biol. 1992 Apr;12(4):1856-63 [1312672] Mol Cell Biol. 1992 Jun;12(6):2866-71 [1588974] Science. 1992 May 8;256(5058):827-30 [1589764] J Virol. 1992 Aug;66(8):4757-62 [1352831] Proc Natl Acad Sci U S A. 1992 Aug 15;89(16):7491-5 [1323840] Cell. 1992 Aug 21;70(4):523-6 [1505019] Cell. 1992 Nov 13;71(4):587-97 [1423616] Proc Natl Acad Sci U S A. 1992 Dec 15;89(24):12028-32 [1465435] Cell. 1992 Dec 24;71(7):1081-91 [1473146] Science. 1993 Jan 1;259(5091):84-7 [8418500] Ann N Y Acad Sci. 1992 Nov 21;663:139-53 [1482047] Proc Natl Acad Sci U S A. 1993 May 1;90(9):3988-92 [8387205] Erratum In: Mol Cell Biol 1993 Sep;13(9):5928 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Pharmacokinetics of the 9-amino and 10,11-methylenedioxy derivatives of camptothecin in mice. AN - 75809818; 8319213 AB - Although 20(S)-camptothecin (CA) exhibited potent cytotoxicity against a broad spectrum of tumor models, clinical trials with the sodium salt of its opened lactone ring form were discontinued due to highly variable and severe toxicity. Recently, the 9-amino (AC) and 10,11-methylenedioxy (MC) derivatives of CA were selected for preclinical evaluation by the National Cancer Institute. In the present investigation, the pharmacokinetic behavior of CA, its sodium salt CA, AC, and MC in mice was characterized using specific liquid chromatographic assays which permitted determination of the intact lactone and opened ring carboxylate forms of these compounds. CA disposition was triexponential with a prolonged terminal phase that had a 24.6-h half-life (t1/2,z) that comprised only 14.6% of the area under the concentration-time profile. The relative magnitudes of the total body apparent volume of distribution (Vz) and terminal phase rate constant suggest that the high observed total plasma clearance (CL, 104 ml/min/kg) may be associated with extensive accumulation in peripheral tissue regions from which the drug is slowly released. In comparison, the terminal disposition phase of MC accounted for 49.7% of the area under the curve profile. It also had a shorter t1/2,z (15.2 h) and appreciably greater CL (526 ml/min/kg) and Vz (694 liters/kg). This suggested that the degree of binding to tissues relative to plasma proteins was enhanced by the methylenedioxy moiety. In contrast, the 9-amino substituent profoundly diminished the apparent extent of tissue distribution, as indicated by the magnitude of Vz (7.7 liters/kg), effecting an enhanced rate of elimination (t1/2,z, 1.4 h). Comparison of the CL of CA and its two derivatives provided an inaccurate indication of drug elimination due to the influence of their unusually large Vz values. For these compounds, the relative ease of elimination from the body was best represented by mean residence times, which were 0.55, 7.24, and 11.2 h for AC, CA, and MC, respectively. Intact lactone plasma levels achieved after dosing with the lactone form of CA and its 9-amino and 10,11-methylenedioxy derivatives exceeded the far less active carboxylate at all times. In summary, these studies indicate that considerable alterations in pharmacokinetic behavior result from structural modification of the A ring of CA. JF - Cancer research AU - Supko, J G AU - Malspeis, L AD - Laboratory of Pharmaceutical Chemistry, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1993/07/01/ PY - 1993 DA - 1993 Jul 01 SP - 3062 EP - 3069 VL - 53 IS - 13 SN - 0008-5472, 0008-5472 KW - 10,11-methylenedioxy-20-camptothecin KW - 104155-89-7 KW - 9-aminocamptothecin KW - 5MB77ICE2Q KW - Camptothecin KW - XT3Z54Z28A KW - Index Medicus KW - Animals KW - Mice KW - Tissue Distribution KW - Mice, Inbred BALB C KW - Male KW - Structure-Activity Relationship KW - Mice, Inbred DBA KW - Camptothecin -- pharmacokinetics KW - Camptothecin -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75809818?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Pharmacokinetics+of+the+9-amino+and+10%2C11-methylenedioxy+derivatives+of+camptothecin+in+mice.&rft.au=Supko%2C+J+G%3BMalspeis%2C+L&rft.aulast=Supko&rft.aufirst=J&rft.date=1993-07-01&rft.volume=53&rft.issue=13&rft.spage=3062&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-30 N1 - Date created - 1993-07-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Physical methods for the detection of carcinogen-DNA adducts in humans. AN - 75805796; 7686262 AB - This report has attempted to summarize the principles, advantages, limitations and the source of data derived in the use of physical detection techniques for DNA-adduct measurement in human biomonitoring. Each method, although inherently chemically-specific, has advantages and limitations depending on the adduct type under study. These methods have a niche that is at least consistent with corroborative technology, and are being applied to dosimetry problems in the field. JF - Mutation research AU - Weston, A AD - Molecular Epidemiology Section, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 19 EP - 29 VL - 288 IS - 1 SN - 0027-5107, 0027-5107 KW - Carcinogens KW - 0 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Spectrometry, Fluorescence -- methods KW - Humans KW - Mass Spectrometry -- methods KW - Spectrophotometry, Atomic KW - Conductometry KW - Chromatography, Gas -- methods KW - Carcinogens -- metabolism KW - DNA Damage KW - DNA Mutational Analysis -- methods KW - DNA -- metabolism KW - DNA -- analysis KW - Carcinogens -- analysis KW - Environmental Monitoring -- methods KW - DNA -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75805796?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutation+research&rft.atitle=Physical+methods+for+the+detection+of+carcinogen-DNA+adducts+in+humans.&rft.au=Weston%2C+A&rft.aulast=Weston&rft.aufirst=A&rft.date=1993-07-01&rft.volume=288&rft.issue=1&rft.spage=19&rft.isbn=&rft.btitle=&rft.title=Mutation+research&rft.issn=00275107&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-26 N1 - Date created - 1993-07-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Role of omega-conotoxin GVIA-sensitive Ca2+ entry in angiotensin II-stimulated [3H]phorbol 12,13-dibutyrate binding in bovine adrenal medullary cells. AN - 75800292; 8515289 AB - The relative contributions of Ca2+ influx and intracellular Ca2+ mobilization were examined for angiotensin II-stimulated [3H]phorbol 12,13-dibutyrate binding, which reflects the level of activated protein kinase C in bovine chromaffin cells. Angiotensin II receptors activate phospholipase C in chromaffin cells, leading to a short-lived mobilization of intracellular Ca2+. Angiotensin II-stimulated [3H]phorbol 12,13-dibutyrate binding was largely blocked in Ca(2+)-free buffer and by pretreatment with the Ca(2+)-channel blocker omega-conotoxin GVIA. The [3H]phorbol 12,13-dibutyrate binding response to [Sar1]angiotensin II also appeared to be voltage sensitive, as no additivity was observed with the response to the depolarizing agent 4-aminopyridine (3 mM). Threshold sensitivities of the extra- and intracellular Ca(2+)-mobilizing pathways to angiotensin II were similar, and all examined effects of angiotensin II in these cells were apparently mediated by losartan-sensitive (AT1-like) receptors. The dependence of angiotensin II-stimulated [3H]phorbol 12,13-dibutyrate binding on extracellular Ca2+ entry, in contrast to stimulation by other phospholipase C-linked receptor agonists (bradykinin and methacholine), suggests that angiotensin II preferentially stimulates protein kinase C translocation to the plasma membrane, rather than to internal membranes, in bovine adrenal medullary cells. JF - Journal of neurochemistry AU - McMillian, M K AU - Hudson, P M AU - Suh, H H AU - Ye, H AU - Tuominen, R K AU - Hong, J S AD - Laboratory of Molecular and Integrative Neuroscience, National Institute of Environmental Health Sciences, National Institute of Health, Research Triangle Park, North Carolina 27709. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 93 EP - 99 VL - 61 IS - 1 SN - 0022-3042, 0022-3042 KW - Peptides, Cyclic KW - 0 KW - Tritium KW - 10028-17-8 KW - Angiotensin II KW - 11128-99-7 KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - angiotensin II, Sar(1)- KW - 59680-38-5 KW - omega-Conotoxin GVIA KW - 92078-76-7 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Osmolar Concentration KW - Animals KW - Cattle KW - Differential Threshold KW - Cells, Cultured KW - Membrane Potentials KW - Calcium -- metabolism KW - Angiotensin II -- analogs & derivatives KW - Angiotensin II -- metabolism KW - Phorbol 12,13-Dibutyrate -- metabolism KW - Adrenal Medulla -- physiology KW - Adrenal Medulla -- cytology KW - Adrenal Medulla -- metabolism KW - Peptides, Cyclic -- pharmacology KW - Angiotensin II -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75800292?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neurochemistry&rft.atitle=Role+of+omega-conotoxin+GVIA-sensitive+Ca2%2B+entry+in+angiotensin+II-stimulated+%5B3H%5Dphorbol+12%2C13-dibutyrate+binding+in+bovine+adrenal+medullary+cells.&rft.au=McMillian%2C+M+K%3BHudson%2C+P+M%3BSuh%2C+H+H%3BYe%2C+H%3BTuominen%2C+R+K%3BHong%2C+J+S&rft.aulast=McMillian&rft.aufirst=M&rft.date=1993-07-01&rft.volume=61&rft.issue=1&rft.spage=93&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurochemistry&rft.issn=00223042&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-22 N1 - Date created - 1993-07-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Analysis of a segment of the human glial fibrillary acidic protein gene that directs astrocyte-specific transcription. AN - 75799131; 8515262 AB - To understand astrocyte-specific transcription, we have been studying the human gfa gene. This gene encodes glial fibrillary acidic protein (GFAP), an intermediate filament protein expressed primarily in astrocytes. A survey of the gfa 5' flanking region showed it to contain several segments that contribute to expression of a chloramphenicol acetyltransferase reporter gene in transfected cells. The most active of these was the 124-bp B region, which spans bp -1612 to -1489. We have now used site-directed mutagenesis to analyze this region in greater detail, and show that the B region itself contains several important elements. The most crucial of these is a consensus AP-1 sequence, the binding site for the Fos and Jun families of transcription factors. The presence of members of both these families in the glial fibrillary acidic protein-expressing U251 cell line used for our transfection studies was verified by gel mobility-shift experiments. This is the first demonstration of the functioning of a specific transcription factor site for astrocytes, and provides a focus for future studies of glial fibrillary acidic protein regulation during development and reactive gliosis. JF - Journal of neurochemistry AU - Masood, K AU - Besnard, F AU - Su, Y AU - Brenner, M AD - Laboratory of Molecular Biology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 160 EP - 166 VL - 61 IS - 1 SN - 0022-3042, 0022-3042 KW - Glial Fibrillary Acidic Protein KW - 0 KW - Oligonucleotide Probes KW - Proto-Oncogene Proteins c-fos KW - Proto-Oncogene Proteins c-jun KW - Index Medicus KW - Base Sequence KW - Proto-Oncogene Proteins c-fos -- metabolism KW - Oligonucleotide Probes -- genetics KW - Humans KW - Molecular Sequence Data KW - Proto-Oncogene Proteins c-jun -- metabolism KW - Consensus Sequence KW - Binding Sites KW - Genes KW - Astrocytes -- physiology KW - Transcription, Genetic KW - Glial Fibrillary Acidic Protein -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75799131?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neurochemistry&rft.atitle=Analysis+of+a+segment+of+the+human+glial+fibrillary+acidic+protein+gene+that+directs+astrocyte-specific+transcription.&rft.au=Masood%2C+K%3BBesnard%2C+F%3BSu%2C+Y%3BBrenner%2C+M&rft.aulast=Masood&rft.aufirst=K&rft.date=1993-07-01&rft.volume=61&rft.issue=1&rft.spage=160&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurochemistry&rft.issn=00223042&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-22 N1 - Date created - 1993-07-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - A phase II evaluation of thiotepa in pediatric central nervous system malignancies. AN - 75789680; 8508417 AB - Both thiotepa and its active metabolite, tepa, efficiently cross the blood-brain barrier. After intravenous administration, the cerebrospinal fluid concentrations achieved are nearly identical to those in plasma. This provides a strong rationale for testing this agent against brain tumors. Sixty pediatric patients with recurrent primary brain tumors were treated on a multiinstitutional Phase II study of intravenous thiotepa at a dose of 65 mg/m2 administered every 3 weeks. This dose is the result of a prior pediatric Phase I trial and is significantly higher than those previously recommended. Three of 13 assessable patients with medulloblastoma had partial responses lasting 22, 25, and 54 weeks. Although no objective responses were observed in 16 assessable patients with malignant gliomas and 14 with brain stem gliomas, 5 of 16 and 4 of 14 patients in these respective strata had prolonged periods of stable disease (SD) lasting from 12 to more than 33 weeks. Nine assessable patients with ependymoma had no objective response, but two had SD, both for more than 33 weeks. Myelosuppression was the principle toxic effect encountered and appeared to be more severe in patients who had received prior craniospinal radiation therapy or nitrosourea therapy. By conventional Phase II criteria, thiotepa appears to have activity in medulloblastoma. Based on several patients with prolonged SD, it also may possess some limited activity in brain stem and malignant gliomas. The steep in vitro dose-response curve of thiotepa and the long durations of response or SD observed with the dose reported here suggest that moderate-dose to high-dose thiotepa with cytokine support or autologous bone marrow rescue may be associated with an improved response rate to this agent. JF - Cancer AU - Heideman, R L AU - Packer, R J AU - Reaman, G H AU - Allen, J C AU - Lange, B AU - Horowitz, M E AU - Steinberg, S M AU - Gillespie, A AU - Kovnar, E H AU - Balis, F M AD - Pediatric Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1993/07/01/ PY - 1993 DA - 1993 Jul 01 SP - 271 EP - 275 VL - 72 IS - 1 SN - 0008-543X, 0008-543X KW - Thiotepa KW - 905Z5W3GKH KW - Abridged Index Medicus KW - Index Medicus KW - Drug Administration Schedule KW - Ependymoma -- drug therapy KW - Medulloblastoma -- drug therapy KW - Humans KW - Child KW - Child, Preschool KW - Infant KW - Cerebellar Neoplasms -- drug therapy KW - Glioma -- drug therapy KW - Adult KW - Adolescent KW - Female KW - Male KW - Brain Neoplasms -- drug therapy KW - Neoplasm Recurrence, Local -- drug therapy KW - Thiotepa -- administration & dosage KW - Thiotepa -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75789680?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=A+phase+II+evaluation+of+thiotepa+in+pediatric+central+nervous+system+malignancies.&rft.au=Heideman%2C+R+L%3BPacker%2C+R+J%3BReaman%2C+G+H%3BAllen%2C+J+C%3BLange%2C+B%3BHorowitz%2C+M+E%3BSteinberg%2C+S+M%3BGillespie%2C+A%3BKovnar%2C+E+H%3BBalis%2C+F+M&rft.aulast=Heideman&rft.aufirst=R&rft.date=1993-07-01&rft.volume=72&rft.issue=1&rft.spage=271&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-13 N1 - Date created - 1993-07-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Albendazole in human loiasis: results of a double-blind, placebo-controlled trial. AN - 75783556; 8515109 AB - To assess the filaricidal activity and clinical safety of albendazole in human loiasis, a double-blind, placebo-controlled study was conducted in an endemic area in Benin, Africa. Twenty-three men with microfilaremia (100-30,000/mL) were randomly assigned to receive albendazole (200 mg; n = 11) or placebo (n = 12) twice daily for 21 days; 1 patient from each group withdrew from the study. There were no clinical adverse effects and no observed hepatotoxicity, renal toxicity, or hematologic abnormalities attributable to the drug. In the albendazole group, microfilarial levels began to decrease at day 14 after treatment and by 6 months had fallen to a geometric mean of 20% of pretreatment levels (vs. 84.8% in the placebo group). Blood eosinophil levels and anti-filarial IgG and IgG4 also fell significantly in response to albendazole. Taken together, these data suggest that albendazole has a primary (possibly embryotoxic) effect on the adult parasite, resulting in a slow decrease in microfilaremia. JF - The Journal of infectious diseases AU - Klion, A D AU - Massougbodji, A AU - Horton, J AU - Ekoué, S AU - Lanmasso, T AU - Ahouissou, N L AU - Nutman, T B AD - Laboratory of Parasitic Diseases, National Institutes of Health, Bethesda, Maryland. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 202 EP - 206 VL - 168 IS - 1 SN - 0022-1899, 0022-1899 KW - Albendazole KW - F4216019LN KW - Abridged Index Medicus KW - Index Medicus KW - Double-Blind Method KW - Humans KW - Africa, Western KW - Adult KW - Aged KW - Middle Aged KW - Adolescent KW - Male KW - Female KW - Albendazole -- adverse effects KW - Loiasis -- drug therapy KW - Albendazole -- pharmacokinetics KW - Albendazole -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75783556?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+infectious+diseases&rft.atitle=Albendazole+in+human+loiasis%3A+results+of+a+double-blind%2C+placebo-controlled+trial.&rft.au=Klion%2C+A+D%3BMassougbodji%2C+A%3BHorton%2C+J%3BEkou%C3%A9%2C+S%3BLanmasso%2C+T%3BAhouissou%2C+N+L%3BNutman%2C+T+B&rft.aulast=Klion&rft.aufirst=A&rft.date=1993-07-01&rft.volume=168&rft.issue=1&rft.spage=202&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+infectious+diseases&rft.issn=00221899&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-20 N1 - Date created - 1993-07-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Susceptibility and resistance to J3V1 retrovirus-induced murine plasmacytomagenesis in reconstituted severe combined immunodeficient mice. AN - 75772029; 7685514 AB - To date much is known about the genetics of susceptibility and resistance to plasmacytoma induction in mice, however little is known about the cellular aspects of these phenotypes. The complexity of plasmacytomagenesis allows for susceptibility and resistance to reflect differences in B cells, T cells, accessory cells and/or stromal elements contributing to the disease process. Alternatively, these phenotypes may result from differential abilities to affect events critical to plasmacytomagenesis, such as myc deregulation. To address these possibilities, the v-myc-raf-containing retrovirus, J3V1, was used to induce plasmacytomas (PCTs) in severe combined immunodeficient (SCID) mice reconstituted with susceptible (Balb/c) and/or resistant (DBA/2) cells. The results demonstrate that Balb/c bone marrow (BM)-reconstituted SCID mice yielded PCTs of donor origin, while DBA/2 BM-reconstituted mice did not. Mice reconstituted with both DBA/2 BM and Balb/c peripheral lymphocytes, as well as those reconstituted with Balb/c peripheral lymphocytes alone, also yielded only Balb/c PCTs. These results indicate that: (1) a microenvironment supportive of plasmacytomagenesis is insufficient to allow PCT development among resistant cells; (2) DBA/2 BM-derived cells do not suppress plasmacytomagenesis by target cell elimination or microenvironment destruction; (3) resistance is not solely attributable to the inability of DBA/2 B cells to deregulate myc; and (4) potential PCT targets reside in a number of lymphoid tissues. Taken together, these results demonstrate that a major aspect of resistance/susceptibility to plasmacytomagenesis is dictated by the genotype of the target B cell. JF - Oncogene AU - Hilbert, D M AU - Pumphrey, J G AU - Troppmair, J AU - Rapp, U R AU - Rudikoff, S AD - Laboratory of Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 1993 EP - 2000 VL - 8 IS - 7 SN - 0950-9232, 0950-9232 KW - Antigens, CD KW - 0 KW - Antigens, CD5 KW - Terpenes KW - pristane KW - 26HZV48DT1 KW - Index Medicus KW - Animals KW - Antigens, CD -- analysis KW - Disease Susceptibility KW - Genes, myc KW - B-Lymphocytes -- immunology KW - Mice KW - Mice, Inbred BALB C KW - Mice, Inbred DBA KW - Terpenes -- pharmacology KW - Mice, SCID KW - Species Specificity KW - Female KW - Plasmacytoma -- genetics KW - Plasmacytoma -- immunology KW - Retroviridae -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75772029?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncogene&rft.atitle=Susceptibility+and+resistance+to+J3V1+retrovirus-induced+murine+plasmacytomagenesis+in+reconstituted+severe+combined+immunodeficient+mice.&rft.au=Hilbert%2C+D+M%3BPumphrey%2C+J+G%3BTroppmair%2C+J%3BRapp%2C+U+R%3BRudikoff%2C+S&rft.aulast=Hilbert&rft.aufirst=D&rft.date=1993-07-01&rft.volume=8&rft.issue=7&rft.spage=1993&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=09509232&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-09 N1 - Date created - 1993-07-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Human immunodeficiency virus type 1 Vpu protein induces degradation of CD4 in vitro: the cytoplasmic domain of CD4 contributes to Vpu sensitivity. AN - 75771964; 8510209 AB - CD4 is an integral membrane glycoprotein which functions as the human immunodeficiency virus (HIV) receptor for infection of human host cells. We have recently demonstrated that Vpu, an HIV type 1 (HIV-1) encoded integral membrane phosphoprotein, induces rapid degradation of CD4 in the endoplasmic reticulum. In this report, we describe an in vitro model system that allowed us to define important parameters for Vpu-dependent CD4 degradation. The rate of CD4 decay in rabbit reticulocyte lysate was approximately one-third of that observed previously in tissue culture experiments in the presence of Vpu (40 versus 12 min) and required no other HIV-1 encoded proteins. Degradation was contingent on the presence of microsomal membranes in the assay and the coexpression of Vpu and CD4 in the same membrane compartment. By using the in vitro degradation assay, the effects of specific mutations in CD4, including C-terminal truncations and glycosylation mutants, were analyzed. The results of these experiments indicate that Vpu has the capacity to induce degradation of glycosylated as well as nonglycosylated membrane-associated CD4. Truncation of 13 C-terminal amino acids of CD4 did not affect the ability of Vpu to induce its degradation. However, the removal of 32 amino acids from the C-terminus of CD4 completely abolished sensitivity to Vpu. This suggests that Vpu targets specific sequences in the cytoplasmic domain of CD4 to induce its degradation. We also analyzed the effects of mutations in Vpu on its biological activity in the in vitro CD4 degradation assay. The results of these experiments suggest that sequences critical for this function of Vpu are located in its hydrophilic C-terminal domain. JF - Journal of virology AU - Chen, M Y AU - Maldarelli, F AU - Karczewski, M K AU - Willey, R L AU - Strebel, K AD - Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 3877 EP - 3884 VL - 67 IS - 7 SN - 0022-538X, 0022-538X KW - Antigens, CD4 KW - 0 KW - Human Immunodeficiency Virus Proteins KW - Oligodeoxyribonucleotides KW - Recombinant Proteins KW - Viral Regulatory and Accessory Proteins KW - vpu protein, Human immunodeficiency virus 1 KW - Hexosaminidases KW - EC 3.2.1.- KW - Index Medicus KW - AIDS/HIV KW - Protein Biosynthesis KW - Animals KW - Solubility KW - Transcription, Genetic KW - Rabbits KW - Amino Acid Sequence KW - Glycosylation KW - Structure-Activity Relationship KW - Mutagenesis, Site-Directed KW - Base Sequence KW - Recombinant Proteins -- metabolism KW - Cytoplasm -- metabolism KW - Hexosaminidases -- pharmacology KW - Microsomes -- metabolism KW - Oligodeoxyribonucleotides -- chemistry KW - In Vitro Techniques KW - Molecular Sequence Data KW - HIV-1 -- metabolism KW - Viral Regulatory and Accessory Proteins -- metabolism KW - Antigens, CD4 -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75771964?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Human+immunodeficiency+virus+type+1+Vpu+protein+induces+degradation+of+CD4+in+vitro%3A+the+cytoplasmic+domain+of+CD4+contributes+to+Vpu+sensitivity.&rft.au=Chen%2C+M+Y%3BMaldarelli%2C+F%3BKarczewski%2C+M+K%3BWilley%2C+R+L%3BStrebel%2C+K&rft.aulast=Chen&rft.aufirst=M&rft.date=1993-07-01&rft.volume=67&rft.issue=7&rft.spage=3877&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-12 N1 - Date created - 1993-07-12 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Methods Enzymol. 1983;96:84-93 [6656655] Proc Natl Acad Sci U S A. 1977 Aug;74(8):3278-82 [198778] J Virol. 1986 Aug;59(2):284-91 [3016298] Cell. 1986 Nov 7;47(3):333-48 [3094962] Science. 1986 Nov 28;234(4780):1123-7 [3095925] Science. 1988 Sep 2;241(4870):1221-3 [3261888] Proc Natl Acad Sci U S A. 1989 Jul;86(13):5163-7 [2472639] J Virol. 1989 Sep;63(9):3784-91 [2788224] J Virol. 1990 Feb;64(2):621-9 [2404139] Nature. 1990 May 24;345(6273):356-9 [2188136] Cell. 1990 Aug 24;62(4):611-4 [2201450] J Virol. 1990 Nov;64(11):5448-56 [2214021] J Virol. 1990 Nov;64(11):5585-93 [2214026] J Virol. 1990 Dec;64(12):6297-304 [2243395] Cell. 1990 Dec 21;63(6):1129-36 [2175676] Virology. 1991 Feb;180(2):617-24 [1989386] J Biol Chem. 1991 Mar 5;266(7):4500-7 [1825655] Proc Natl Acad Sci U S A. 1991 Mar 1;88(5):1918-22 [2000396] J Biol Chem. 1991 Jun 5;266(16):10658-65 [1674746] J Virol. 1991 Dec;65(12):6387-96 [1942241] J Virol. 1992 Jan;66(1):226-34 [1727486] Curr Opin Cell Biol. 1991 Aug;3(4):592-600 [1772654] J Biol Chem. 1992 Feb 15;267(5):3268-73 [1737783] Eur J Biochem. 1992 Mar 1;204(2):875-83 [1541298] Cell. 1992 May 1;69(3):517-28 [1374685] J Virol. 1992 Dec;66(12):7193-200 [1433512] Cell. 1985 Aug;42(1):93-104 [2990730] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The PU.1/Spi-1 proto-oncogene is a transcriptional regulator of a lentivirus promoter. AN - 75771577; 8389910 AB - The enhancer unit present in the retrovirus equine infectious anemia virus (EIAV) was previously shown to contain binding sites for proteins belonging to MDBP, PEA2, AP-1, and ets families. The EIAV ets motif matches the consensus sequence for both PEA3- and PU.1-binding sites. Here, we show by gel shift analysis that PU.1, present in nuclear extracts from monocyte and B-lymphocyte cell lines, binds to oligonucleotides containing the EIAV ets element. HeLa cells transiently transfected with a PU.1 expression plasmid expressed nuclear factors that formed complexes indistinguishable from those seen with monocyte extracts. Antibodies to PU.1 protein either supershifted or abolished formation of these complexes, depending on the PU.1 epitopes recognized. The binding of PU.1 to the EIAV ets motif in vitro correlated with transcriptional activity of the EIAV promoter in transfected monocyte cell lines. In HeLa cells, the product of PU.1 cDNA bound to the EIAV ets motif and activated transcription from the EIAV promoter. The PU.1-binding site was the primary determinant of EIAV promoter activity in cell lines that express PU.1. Nucleotide determinants of PU.1 binding and a consensus PU.1 binding sequence were defined in gel shift assays using a panel of mutated oligonucleotides. To our knowledge, this is the first report of a retroviral promoter controlled by PU.1. JF - Journal of virology AU - Carvalho, M AU - Derse, D AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick, Maryland 21702-1201. Y1 - 1993/07// PY - 1993 DA - July 1993 SP - 3885 EP - 3890 VL - 67 IS - 7 SN - 0022-538X, 0022-538X KW - AP-1 KW - PEA2 KW - ets KW - DNA-Binding Proteins KW - 0 KW - Proto-Oncogene Proteins KW - RNA, Messenger KW - Retroviridae Proteins, Oncogenic KW - Transcription Factors KW - v-Spi-1 protein, Friend spleen focus-forming virus KW - Index Medicus KW - Base Sequence KW - Multigene Family KW - Humans KW - Enhancer Elements, Genetic KW - In Vitro Techniques KW - Molecular Sequence Data KW - Transcription, Genetic KW - RNA, Messenger -- genetics KW - Proto-Oncogenes KW - Proto-Oncogene Proteins -- physiology KW - Cell Line KW - Binding Sites KW - Transcription Factors -- physiology KW - Promoter Regions, Genetic KW - Gene Expression Regulation, Viral KW - Infectious Anemia Virus, Equine -- genetics KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75771577?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=The+PU.1%2FSpi-1+proto-oncogene+is+a+transcriptional+regulator+of+a+lentivirus+promoter.&rft.au=Carvalho%2C+M%3BDerse%2C+D&rft.aulast=Carvalho&rft.aufirst=M&rft.date=1993-07-01&rft.volume=67&rft.issue=7&rft.spage=3885&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-12 N1 - Date created - 1993-07-12 N1 - Date revised - 2017-01-13 N1 - Gene symbol - AP-1; PEA2; ets N1 - SuppNotes - Cited By: Cell Growth Differ. 1992 May;3(5):327-34 [1633115] Mol Cell Biol. 1992 Jul;12(7):2967-75 [1620109] J Virol. 1993 Apr;67(4):2064-74 [8383228] Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] Nucleic Acids Res. 1983 Mar 11;11(5):1475-89 [6828386] Rev Infect Dis. 1985 Jan-Feb;7(1):83-8 [2984759] Proc Natl Acad Sci U S A. 1986 Nov;83(22):8550-4 [3022296] Nature. 1988 Jan 21;331(6153):277-80 [2827041] J Virol. 1988 Sep;62(9):3522-6 [2841502] J Virol. 1989 Jan;63(1):398-402 [2535740] Mol Cell Biol. 1989 Apr;9(4):1804-9 [2725524] EMBO J. 1989 Nov;8(11):3371-8 [2555163] Cell. 1990 Apr 6;61(1):113-24 [2180582] J Virol. 1990 Apr;64(4):1616-24 [2157047] Oncogene. 1990 May;5(5):663-8 [1693183] EMBO J. 1990 Jul;9(7):2241-6 [2162765] J Virol. 1991 Jul;65(7):3468-74 [1645778] Genes Dev. 1991 Jun;5(6):908-18 [2044959] J Virol. 1991 Oct;65(10):5391-400 [1654447] Mol Cell Biol. 1992 Jan;12(1):368-78 [1729611] Mol Cell Biol. 1992 Mar;12(3):1043-53 [1545787] J Exp Med. 1992 May 1;175(5):1391-9 [1569404] Genes Dev. 1992 Jun;6(6):965-74 [1592263] J Virol. 1992 Oct;66(10):5906-13 [1382143] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Aberrant expression of high mobility group chromosomal protein 14 affects cellular differentiation. AN - 75793539; 8514795 AB - High mobility group (HMG) 14 is a ubiquitous chromosomal protein that binds specifically to nucleosomal DNA and may be involved in a process that confers distinct properties to the chromatin structure of transcriptionally active genes. To explore the involvement of this protein in regulation of gene expression, we studied the effect of aberrant expression of HMG-14 protein on cellular differentiation. We produced stably transfected C2C12 mouse myoblasts expressing the human HMG-14 protein under the control of the mouse mammary tumor virus promoter. Transformed colonies retained their potential do differentiate into myotubes. Induction of human HMG-14 expression by dexamethasone inhibited the myogenic process. Revertant colonies, which lost the ability to express human HMG-14, regained the ability to differentiate into myotubes. Inhibition of myoblast differentiation by aberrantly expressed HMG-14 correlated with down-regulation of myogenic determination factors. The results suggest that proper cellular differentiation requires regulated expression of HMG-14 protein and are consistent with the possibility that this protein may be involved in gene regulation. JF - The Journal of biological chemistry AU - Pash, J M AU - Alfonso, P J AU - Bustin, M AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/06/25/ PY - 1993 DA - 1993 Jun 25 SP - 13632 EP - 13638 VL - 268 IS - 18 SN - 0021-9258, 0021-9258 KW - Biomarkers KW - 0 KW - High Mobility Group Proteins KW - RNA, Messenger KW - Dexamethasone KW - 7S5I7G3JQL KW - Index Medicus KW - Muscles -- cytology KW - Animals KW - Gene Expression Regulation -- physiology KW - RNA, Messenger -- metabolism KW - Transfection KW - Cells, Cultured KW - Humans KW - Dexamethasone -- pharmacology KW - RNA, Messenger -- drug effects KW - Muscles -- metabolism KW - Mice KW - High Mobility Group Proteins -- physiology KW - High Mobility Group Proteins -- biosynthesis KW - Cell Differentiation -- physiology KW - Cell Differentiation -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75793539?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Aberrant+expression+of+high+mobility+group+chromosomal+protein+14+affects+cellular+differentiation.&rft.au=Pash%2C+J+M%3BAlfonso%2C+P+J%3BBustin%2C+M&rft.aulast=Pash&rft.aufirst=J&rft.date=1993-06-25&rft.volume=268&rft.issue=18&rft.spage=13632&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-22 N1 - Date created - 1993-07-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Pseudomonas exotoxin and recombinant immunotoxins derived from it. AN - 75936509; 8363279 AB - Pseudomonas exotoxin (PE) is a bacterial toxin that kills mammalian cells by gaining entry to the cytosol and inactivating protein synthesis. The toxin binds and enters cells via the alpha 2-macroglobulin receptors. Within cells, the toxin is processed in several steps to produce an enzymatically active 37-kDa C-terminal fragment which translocates to the cytosol and ADP-ribosylates elongation factor 2. Because PE is a very potent toxin, derivatives of it have been produced which, when joined to various binding ligands, are capable of killing specific target cells. It is hoped that this strategy will lead to the development of effective therapeutic agents for the treatment of human diseases such as cancer, AIDS, and various immunologic disorders. JF - Annals of the New York Academy of Sciences AU - Fitzgerald, D AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1993/06/23/ PY - 1993 DA - 1993 Jun 23 SP - 740 EP - 745 VL - 685 SN - 0077-8923, 0077-8923 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - Immunotoxins KW - Recombinant Fusion Proteins KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - Animals KW - Humans KW - Exotoxins -- pharmacology KW - Recombinant Fusion Proteins -- pharmacology KW - Bacterial Toxins -- pharmacology KW - Pseudomonas aeruginosa KW - Immunotoxins -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75936509?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+the+New+York+Academy+of+Sciences&rft.atitle=Pseudomonas+exotoxin+and+recombinant+immunotoxins+derived+from+it.&rft.au=Fitzgerald%2C+D%3BPastan%2C+I&rft.aulast=Fitzgerald&rft.aufirst=D&rft.date=1993-06-23&rft.volume=685&rft.issue=&rft.spage=740&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+New+York+Academy+of+Sciences&rft.issn=00778923&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-24 N1 - Date created - 1993-09-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Immune dysfunction related to drug-metabolizing enzymes. AN - 75931727; 8395782 JF - Annals of the New York Academy of Sciences AU - Albright, J F AD - Division of Allergy, Immunology and Transplantation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/06/23/ PY - 1993 DA - 1993 Jun 23 SP - 620 EP - 623 VL - 685 SN - 0077-8923, 0077-8923 KW - Pharmaceutical Preparations KW - 0 KW - Polychlorinated Dibenzodioxins KW - Receptors, Aryl Hydrocarbon KW - Receptors, Drug KW - Index Medicus KW - Animals KW - Mice, Inbred C57BL KW - Mice KW - Receptors, Drug -- physiology KW - Mice, Inbred DBA KW - Pharmaceutical Preparations -- metabolism KW - Immune System -- drug effects KW - Polychlorinated Dibenzodioxins -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75931727?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+the+New+York+Academy+of+Sciences&rft.atitle=Immune+dysfunction+related+to+drug-metabolizing+enzymes.&rft.au=Albright%2C+J+F&rft.aulast=Albright&rft.aufirst=J&rft.date=1993-06-23&rft.volume=685&rft.issue=&rft.spage=620&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+New+York+Academy+of+Sciences&rft.issn=00778923&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-24 N1 - Date created - 1993-09-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The interleukin-2 receptor: a target for immunotherapy. AN - 75931688; 8363269 JF - Annals of the New York Academy of Sciences AU - Waldmann, T A AU - Goldman, C AU - Top, L AU - Grant, A AU - Burton, J AU - Bamford, R AU - Roessler, E AU - Horak, I AU - Zaknoen, S AU - Kasten-Sportes, C AD - Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/06/23/ PY - 1993 DA - 1993 Jun 23 SP - 603 EP - 610 VL - 685 SN - 0077-8923, 0077-8923 KW - Antibodies, Monoclonal KW - 0 KW - Immunotoxins KW - Receptors, Interleukin-2 KW - Index Medicus KW - AIDS/HIV KW - HTLV-I Infections -- therapy KW - Animals KW - Leukemia, T-Cell -- therapy KW - Humans KW - Immunotoxins -- therapeutic use KW - HTLV-I Infections -- immunology KW - Leukemia, T-Cell -- immunology KW - Neoplasms -- immunology KW - Antibodies, Monoclonal -- therapeutic use KW - Receptors, Interleukin-2 -- physiology KW - Receptors, Interleukin-2 -- analysis KW - Immunotherapy KW - Receptors, Interleukin-2 -- chemistry KW - Receptors, Interleukin-2 -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75931688?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+the+New+York+Academy+of+Sciences&rft.atitle=The+interleukin-2+receptor%3A+a+target+for+immunotherapy.&rft.au=Waldmann%2C+T+A%3BGoldman%2C+C%3BTop%2C+L%3BGrant%2C+A%3BBurton%2C+J%3BBamford%2C+R%3BRoessler%2C+E%3BHorak%2C+I%3BZaknoen%2C+S%3BKasten-Sportes%2C+C&rft.aulast=Waldmann&rft.aufirst=T&rft.date=1993-06-23&rft.volume=685&rft.issue=&rft.spage=603&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+New+York+Academy+of+Sciences&rft.issn=00778923&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-24 N1 - Date created - 1993-09-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Evaluation of 'cypenhymustine', a new anticancer compound, in murine tumour models. AN - 75851488; 8330289 AB - 'Cypenhymustine', 3-[2-[bis(2'-chloroethyl)-amino] ethyl]-5,5- tetramethylenehydantoin, has been synthesised as a potential analog of spiromustine (NSC 172112). The LD50 value was determined in Swiss male mice and found to be 65.0 mg/kg by single i.p. injection. In in vivo screening experiments, three parameters, namely, ascites cell count, ascites fluid measurement and increase in life span (ILS) of drug-treated over control Swiss mice were studied in three murine ascites tumours namely Ehrlich ascites carcinoma (EAC), sarcoma-180 (S-180) and Dalton's lymphoma (DL). Cypenhymustine exhibited a very high percentage of inhibition of both the ascites cell and fluid in these models and also displayed excellent reproducible ILS activity (ILS values of 151 in EAC, 157 in S-180 and 181 in DL at the optimum dose of 3 mg/kg for days 1-7 treatment following tumour transplant on day 0) having a 'curative' effect (1-2 animals: 6 having > 60 days survival rate). The chemical alkylating activity has been compared with spiromustine and another antitumour agent namely nor-HN2. JF - Cancer letters AU - Sanyal, U AU - Bhattacharya, S AU - Sadhu, U AU - Dutta, S AU - Das, H AU - Ghosh, M AD - Department of Chemotherapy, Chittaranjan National Cancer Institute, Calcutta, India. Y1 - 1993/06/15/ PY - 1993 DA - 1993 Jun 15 SP - 1 EP - 6 VL - 70 IS - 1-2 SN - 0304-3835, 0304-3835 KW - Antineoplastic Agents KW - 0 KW - Hydantoins KW - Nitrogen Mustard Compounds KW - cypenhymustine KW - 150380-35-1 KW - Index Medicus KW - Mice, Inbred Strains KW - Drug Screening Assays, Antitumor KW - Animals KW - Dose-Response Relationship, Drug KW - Sarcoma 180 -- drug therapy KW - Carcinoma, Ehrlich Tumor -- drug therapy KW - Lethal Dose 50 KW - Lymphoma -- drug therapy KW - Mice KW - Male KW - Hydantoins -- chemical synthesis KW - Nitrogen Mustard Compounds -- therapeutic use KW - Hydantoins -- therapeutic use KW - Nitrogen Mustard Compounds -- chemical synthesis KW - Antineoplastic Agents -- chemical synthesis KW - Antineoplastic Agents -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75851488?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+letters&rft.atitle=Evaluation+of+%27cypenhymustine%27%2C+a+new+anticancer+compound%2C+in+murine+tumour+models.&rft.au=Sanyal%2C+U%3BBhattacharya%2C+S%3BSadhu%2C+U%3BDutta%2C+S%3BDas%2C+H%3BGhosh%2C+M&rft.aulast=Sanyal&rft.aufirst=U&rft.date=1993-06-15&rft.volume=70&rft.issue=1-2&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Cancer+letters&rft.issn=03043835&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-17 N1 - Date created - 1993-08-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Variation in colorectal cancer incidence in the United States by subsite of origin. AN - 75796585; 8508350 AB - Colorectal cancer incidence rates vary widely internationally, by race and gender, and have changed over time. Investigation of the patterns by subsite within the colorectum may suggest clues of possible etiologic significance for further study. Using population-based data on more than 120,000 cases diagnosed 1976-1987 in the United States Surveillance, Epidemiology, and End Results program, colorectal cancer incidence was evaluated by subsite of origin. Little racial variation was evident for cecum and ascending colon cancers; rates were higher among blacks than whites for transverse and descending colon cancers but lower for sigmoid, rectosigmoid, and rectal cancers. Rates generally increased over time for most colon sites, especially sigmoid colon among white men, but declined slightly for rectal cancer among whites. The sex ratio increased among whites monotonically from 1.12 for cecum to 1.71 for rectal cancers. The distal colon cancer excess among men was most notable at older ages, contrasting with slightly higher rates among women at younger ages. Geographic differences were particularly notable for transverse and rectosigmoid colon cancers. It may be fruitful for future studies to evaluate factors affecting colorectal carcinogenesis by subsite of origin. JF - Cancer AU - Devesa, S S AU - Chow, W H AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1993/06/15/ PY - 1993 DA - 1993 Jun 15 SP - 3819 EP - 3826 VL - 71 IS - 12 SN - 0008-543X, 0008-543X KW - Abridged Index Medicus KW - Index Medicus KW - New Mexico -- epidemiology KW - Age Factors KW - Sex Factors KW - Humans KW - Utah -- epidemiology KW - African Americans KW - Aged KW - Sigmoid Neoplasms -- epidemiology KW - Aged, 80 and over KW - Cecal Neoplasms -- epidemiology KW - European Continental Ancestry Group KW - Adult KW - Connecticut -- epidemiology KW - Incidence KW - Middle Aged KW - United States -- epidemiology KW - Male KW - Female KW - Iowa -- epidemiology KW - Colonic Neoplasms -- epidemiology KW - Rectal Neoplasms -- pathology KW - Rectal Neoplasms -- epidemiology KW - Colonic Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75796585?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=Variation+in+colorectal+cancer+incidence+in+the+United+States+by+subsite+of+origin.&rft.au=Devesa%2C+S+S%3BChow%2C+W+H&rft.aulast=Devesa&rft.aufirst=S&rft.date=1993-06-15&rft.volume=71&rft.issue=12&rft.spage=3819&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-09 N1 - Date created - 1993-07-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - A brief history of opiates, opioid peptides, and opioid receptors. AN - 75794049; 8390660 JF - Proceedings of the National Academy of Sciences of the United States of America AU - Brownstein, M J AD - Laboratory of Cell Biology, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1993/06/15/ PY - 1993 DA - 1993 Jun 15 SP - 5391 EP - 5393 VL - 90 IS - 12 SN - 0027-8424, 0027-8424 KW - Endorphins KW - 0 KW - Narcotics KW - Receptors, Opioid KW - Opium KW - 8008-60-4 KW - Index Medicus KW - History of medicine KW - Opium -- history KW - History, 20th Century KW - Humans KW - Molecular Sequence Data KW - History, Ancient KW - History, 19th Century KW - Amino Acid Sequence KW - History, Medieval KW - Receptors, Opioid -- history KW - Receptors, Opioid -- metabolism KW - Endorphins -- metabolism KW - Narcotics -- therapeutic use KW - Narcotics -- adverse effects KW - Endorphins -- history KW - Narcotics -- history UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75794049?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=A+brief+history+of+opiates%2C+opioid+peptides%2C+and+opioid+receptors.&rft.au=Brownstein%2C+M+J&rft.aulast=Brownstein&rft.aufirst=M&rft.date=1993-06-15&rft.volume=90&rft.issue=12&rft.spage=5391&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-22 N1 - Date created - 1993-07-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1971 Aug;68(8):1742-7 [5288759] Science. 1992 Dec 18;258(5090):1952-5 [1335167] Proc Natl Acad Sci U S A. 1973 Jul;70(7):1947-9 [4516196] Nature. 1973 Oct 26;245(5426):447-50 [4127185] Res Commun Chem Pathol Pharmacol. 1973 Nov;6(3):1052-62 [4760880] Acta Pharmacol Toxicol (Copenh). 1973;33(5):377-84 [4801083] Annu Rev Pharmacol. 1975;15:29-47 [238462] Nature. 1975 Dec 18;258(5536):577-80 [1207728] Nature. 1976 Apr 29;260(5554):793-5 [1264258] J Pharmacol Exp Ther. 1976 Jun;197(3):517-32 [945347] Nature. 1977 Jun 9;267(5611):495-9 [195217] Nature. 1979 Mar 29;278(5703):423-7 [221818] Hoppe Seylers Z Physiol Chem. 1979 Sep;360(9):1211-6 [511110] Proc Natl Acad Sci U S A. 1981 Nov;78(11):7219-23 [6118870] Nature. 1982 Jan 21;295(5846):202-6 [6276759] Nature. 1982 Jul 15;298(5871):245-9 [6123953] J Biol Chem. 1983 Feb 10;258(3):1435-8 [6130091] Proc Natl Acad Sci U S A. 1986 Dec;83(24):9832-6 [2432604] Proc Natl Acad Sci U S A. 1987 Aug;84(15):5487-91 [2440052] J Pharmacol Exp Ther. 1987 Aug;242(2):583-7 [3497260] Proc Natl Acad Sci U S A. 1989 Jul;86(13):5188-92 [2544892] Annu Rev Pharmacol Toxicol. 1990;30:123-47 [2160790] Proc Natl Acad Sci U S A. 1992 Dec 15;89(24):12048-52 [1334555] Science. 1973 Mar 9;179(4077):1011-4 [4687585] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Directed mutagenesis and barnase-barstar recognition. AN - 75784308; 8507637 AB - Directed mutagenesis has been applied to the cloned genes of barnase and barstar, the extracellular ribonuclease of Bacillus amyloliquefaciens and its intracellular inhibitor, to locate residues involved in the mutual recognition of these two proteins. Arg59 and His102 of barnase and Asp35 and Asp39 of barstar have been so identified. With both Cys40 and Cys82 mutated to alanines, barstar is still produced in high yield and is functional both in vitro and in vivo. Methods devised for determining relative and absolute dissociation coefficients for various combinations of mutant and wild-type proteins have allowed us to determine a dissociation coefficient for the complex of wild-type barnase and barstar of about 10(-13) M, with off and on rate constants of 10(-5) s-1 and 10(8) M-1 s-1, respectively. JF - Biochemistry AU - Hartley, R W AD - Laboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/06/15/ PY - 1993 DA - 1993 Jun 15 SP - 5978 EP - 5984 VL - 32 IS - 23 SN - 0006-2960, 0006-2960 KW - Bacterial Proteins KW - 0 KW - Recombinant Proteins KW - barstar protein, Bacillus amyloliquefaciens KW - 37328-61-3 KW - Ribonucleases KW - EC 3.1.- KW - Bacillus amyloliquefaciens ribonuclease KW - EC 3.1.4.- KW - Index Medicus KW - Base Sequence KW - Kinetics KW - Protein Denaturation KW - Molecular Sequence Data KW - Models, Chemical KW - Recombinant Proteins -- chemistry KW - Protein Binding KW - Structure-Activity Relationship KW - Mutagenesis, Site-Directed KW - Bacterial Proteins -- genetics KW - Ribonucleases -- antagonists & inhibitors KW - Bacterial Proteins -- chemistry KW - Bacterial Proteins -- metabolism KW - Ribonucleases -- genetics KW - Ribonucleases -- chemistry KW - Ribonucleases -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75784308?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemistry&rft.atitle=Directed+mutagenesis+and+barnase-barstar+recognition.&rft.au=Hartley%2C+R+W&rft.aulast=Hartley&rft.aufirst=R&rft.date=1993-06-15&rft.volume=32&rft.issue=23&rft.spage=5978&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-09 N1 - Date created - 1993-07-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - An insert of seven amino acids confers functional differences between smooth muscle myosins from the intestines and vasculature. AN - 75771227; 8509418 AB - The molecular mechanisms underlying the heterogeneity in contractile properties observed among smooth muscle tissues are unknown. We examined whether part of this diversity might be intrinsic to myosin by comparing structural and enzymatic properties of myosins from two physiologically diverse tissues. Using the reverse transcriptase polymerase chain reaction, we compared avian intestinal smooth muscle and vascular smooth muscle myosin heavy chain (MHC) mRNA. We found that intestinal, but not vascular, MHC mRNA contains an insert of 21 nucleotides, encoding 7 amino acids, in a region near the ATP binding site in the myosin head. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis of purified myosin revealed that the relative mobilities of the previously described intestinal MHC isoforms SM1 (204 kDa) and SM2 (200 kDa) were slower than the corresponding vascular SM1 and SM2 isoforms. Furthermore, antibodies raised against a synthetic peptide corresponding to the deduced amino acid sequence of the intestinal insert strongly recognized intestinal SM1 and SM2 but only weakly recognized the vascular isoforms. The presence of the insert in intestinal myosin correlated with a higher velocity of movement of actin filaments in vitro and a higher actin-activated Mg(2+)-ATPase activity, compared with vascular myosin. Other than the MHC insert, one other structural difference distinguished intestinal and vascular myosins: two isoforms of the 17-kDa myosin light chain were found in vascular myosin, whereas a single isoform was found in intestinal myosin. Exchange of the intestinal myosin light chains onto the vascular MHC did not alter its activity in the in vitro motility assay, suggesting that the 7-amino acid MHC insert is responsible for the different enzymatic activities of vascular and intestinal myosins. JF - The Journal of biological chemistry AU - Kelley, C A AU - Takahashi, M AU - Yu, J H AU - Adelstein, R S AD - Laboratory of Molecular Cardiology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/06/15/ PY - 1993 DA - 1993 Jun 15 SP - 12848 EP - 12854 VL - 268 IS - 17 SN - 0021-9258, 0021-9258 KW - Oligodeoxyribonucleotides KW - 0 KW - RNA, Messenger KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Ca(2+) Mg(2+)-ATPase KW - EC 3.6.1.- KW - Myosins KW - EC 3.6.4.1 KW - Index Medicus KW - Animals KW - Turkeys KW - Gizzard, Avian -- metabolism KW - Amino Acid Sequence KW - Organ Specificity KW - Binding Sites KW - Polymerase Chain Reaction KW - Base Sequence KW - Chickens KW - RNA, Messenger -- metabolism KW - Adenosine Triphosphate -- metabolism KW - Molecular Sequence Data KW - Aorta -- embryology KW - Mutagenesis, Insertional KW - Myosins -- metabolism KW - Myosins -- biosynthesis KW - Myosins -- genetics KW - Muscle, Smooth, Vascular -- metabolism KW - Ca(2+) Mg(2+)-ATPase -- metabolism KW - Muscle, Smooth -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75771227?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=An+insert+of+seven+amino+acids+confers+functional+differences+between+smooth+muscle+myosins+from+the+intestines+and+vasculature.&rft.au=Kelley%2C+C+A%3BTakahashi%2C+M%3BYu%2C+J+H%3BAdelstein%2C+R+S&rft.aulast=Kelley&rft.aufirst=C&rft.date=1993-06-15&rft.volume=268&rft.issue=17&rft.spage=12848&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-13 N1 - Date created - 1993-07-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Functional redundancy of the DE-1 and alpha A-CRYBP1 regulatory sites of the mouse alpha A-crystallin promoter. AN - 19353014; 8733159 AB - Previous studies have implicated the DE-1 (-111/-106) and alpha A-CRYBP1 (-66/-57) sites for activity of the mouse alpha A-crystallin promoter in transiently transfected lens cells. Here we have used the bacterial chloramphenicol acetyltransferase (CAT) reporter gene to test the functional importance of the putative DE-1 and alpha A-CRYBP1 regulatory elements by site-specific and deletion mutagenesis in stably transformed alpha TN4-1 lens cells and in transgenic mice. FVB/N and C57BL/6 x SJL F2 hybrid transgenic mice were assayed for CAT activity in the lens, heart, lung, kidney, spleen, liver, cerebrum, and muscle. F0, F1, and F2 mice from multiple lines carrying single mutations of the DE-1 or alpha A-CRYBP1 sites showed high levels of CAT activity in the lens, but not in any of the non-lens tissues. By contrast, despite activity of the wild-type promoter, none of the mutant promoter/CAT constructs were active in the transiently transfected and stably transformed lens cells. The mice carrying transgenes with either site-specific mutations in both the DE-1 and alpha A-CRYBP1 sites or a deletion of the entire DE-1 and part of the alpha A-CRYBP1 site (-60/+46) fused to the CAT gene did not exhibit CAT activity above background in any of the tissues examined, including the lens. Our results thus indicate that the DE-1 and alpha A-CRYBP1 sites are functionally redundant in transgenic mice. Moreover, the present data coupled with previous transfection and transgenic mouse experiments suggest that this functional redundancy is confined to lens expression within the mouse and is not evident in transiently transfected and stably transformed lens cells, making the cultured lens cells sensitive indicators of functional elements of crystallin genes. Images JF - Nucleic Acids Research AU - Sax, C M AU - Ilagan, J G AU - Piatigorsky, J AD - Laboratory of Molecular and Developmental Biology, NEI, NIH, Bethesda, MD 20892. Y1 - 1993/06/11/ PY - 1993 DA - 1993 Jun 11 SP - 2633 EP - 2640 PB - Oxford University Press, Oxford Journals, Great Clarendon Street VL - 21 IS - 11 SN - 0305-1048, 0305-1048 KW - Microbiology Abstracts B: Bacteriology; Biochemistry Abstracts 2: Nucleic Acids KW - Crystallin KW - Data processing KW - Cerebrum KW - Regulatory sequences KW - Transgenes KW - Muscles KW - Cardiac muscle KW - Spleen KW - Transgenic mice KW - alpha -Crystallin KW - Mutagenesis KW - Promoters KW - Gene deletion KW - Chloramphenicol O-acetyltransferase KW - Lung KW - Reporter gene KW - Transfection KW - Hybrids KW - CAT gene KW - Kidney KW - Liver KW - Mutation KW - J 02310:Genetics & Taxonomy KW - N 14845:Miscellaneous UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/19353014?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+Acids+Research&rft.atitle=Functional+redundancy+of+the+DE-1+and+alpha+A-CRYBP1+regulatory+sites+of+the+mouse+alpha+A-crystallin+promoter.&rft.au=Sax%2C+C+M%3BIlagan%2C+J+G%3BPiatigorsky%2C+J&rft.aulast=Sax&rft.aufirst=C&rft.date=1993-06-11&rft.volume=21&rft.issue=11&rft.spage=2633&rft.isbn=&rft.btitle=&rft.title=Nucleic+Acids+Research&rft.issn=03051048&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2008-12-01 N1 - Last updated - 2015-03-27 N1 - SubjectsTermNotLitGenreText - Crystallin; Data processing; Cerebrum; Regulatory sequences; Transgenes; Muscles; Spleen; Cardiac muscle; Transgenic mice; alpha -Crystallin; Mutagenesis; Promoters; Chloramphenicol O-acetyltransferase; Gene deletion; Transfection; Reporter gene; Lung; Hybrids; CAT gene; Liver; Kidney; Mutation ER - TY - JOUR T1 - GABAergic cells and signals appear together in the early post-mitotic period of telencephalic and striatal development. AN - 75902341; 8394789 AB - Single cell suspensions derived from embryonic telencephala taken from embryos of gestational day 13 (E13) as well as rat striatal tissue from E14, 15 and 17 were prepared by tissue digestion with papain. Cell suspensions were analyzed by flow cytometry or plated onto poly-D-lysine-coated culture dishes for either nuclear staining or immunocytochemistry. Experiments on functional Na+ channels and GABAA receptor expression were carried out using a fluorescence-activated cell sorter (FACS) and a negatively charged fluorescent indicator dye (oxonol). FACS analysis of embryonic cell suspensions at E13-17 consistently revealed one major subpopulation accounting for 85-90% of the events and one minor subpopulation (10-15% of the total). When sorted, the major subpopulation consisted of phase-bright cells of 5-7 microns diameter some of which had neurites. The minor population consisted of phase-dark cells and resealed membranes of 0.5-4 microns diameter as well as debris. Almost all the cells obtained in the high FALS (forward-angle light scatter) subpopulation at E17 expressed 200-kDa neurofilament and tetanus toxin antigens while the small diameter cells seldom expressed tetanus toxin and particles never did. A small number of GABA-containing neurons were detected in the telencephalon at E13 (3%) and in the developing striatum at E14 (6%). All of the GABA-containing neurons expressed neurofilament. In the embryonic rat striatum, nanomolar concentrations of muscimol (GABAA agonist) induced depolarizing responses. A small number of cells in the high FALS subpopulation were responsive to muscimol starting at embryonic day 14, and the number of responsive cells increased at E15.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Brain research. Developmental brain research AU - Fiszman, M L AU - Behar, T AU - Lange, G D AU - Smith, S V AU - Novotny, E A AU - Barker, J L AD - Laboratory of Neurophysiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/06/08/ PY - 1993 DA - 1993 Jun 08 SP - 243 EP - 251 VL - 73 IS - 2 SN - 0165-3806, 0165-3806 KW - Fluorescent Dyes KW - 0 KW - Isoxazoles KW - Neuromuscular Depolarizing Agents KW - Sodium Channels KW - oxonol dyes (isoxazole) KW - Muscimol KW - 2763-96-4 KW - gamma-Aminobutyric Acid KW - 56-12-2 KW - Acridine Orange KW - F30N4O6XVV KW - Index Medicus KW - Animals KW - Intermediate Filaments -- metabolism KW - Sodium Channels -- physiology KW - Neuromuscular Depolarizing Agents -- pharmacology KW - Pregnancy KW - Rats KW - Phenotype KW - Rats, Sprague-Dawley KW - Flow Cytometry KW - Immunohistochemistry KW - Muscimol -- pharmacology KW - Female KW - Signal Transduction -- physiology KW - Corpus Striatum -- cytology KW - Telencephalon -- embryology KW - gamma-Aminobutyric Acid -- physiology KW - Telencephalon -- cytology KW - Mitosis -- physiology KW - Corpus Striatum -- embryology KW - Telencephalon -- enzymology KW - Corpus Striatum -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75902341?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research.+Developmental+brain+research&rft.atitle=GABAergic+cells+and+signals+appear+together+in+the+early+post-mitotic+period+of+telencephalic+and+striatal+development.&rft.au=Fiszman%2C+M+L%3BBehar%2C+T%3BLange%2C+G+D%3BSmith%2C+S+V%3BNovotny%2C+E+A%3BBarker%2C+J+L&rft.aulast=Fiszman&rft.aufirst=M&rft.date=1993-06-08&rft.volume=73&rft.issue=2&rft.spage=243&rft.isbn=&rft.btitle=&rft.title=Brain+research.+Developmental+brain+research&rft.issn=01653806&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-22 N1 - Date created - 1993-09-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Excitatory amino acid regulation of the enkephalin phenotype in mouse embryonic spinal cord cultures. AN - 75902096; 8353931 AB - Expression of the preproenkephalin gene in developing spinal cord-dorsal root ganglia (SC-DRG) cultures was determined by Northern analysis following treatments with different agonists and antagonists of the glutamate receptor. Cultures (10-12 days old) were treated with various concentrations (10(-7)-10(-3) M) of N-methyl-D-aspartate (NMDA), quisqualate, kainic acid (KA), 2-amino-5-phosphonovaleric acid (APV) and 5-methyl-10,11-dihydro-5H-dibenzo[a, d]cyclohepten-5,10-imine maleate (MK801) either with or without blocking spontaneous electrical activity with 1 microM tetrodotoxin (TTX). In electrically active cultures, treatments with NMDA and KA increased preproenkephalin transcripts (mRNAppENK), showing maximum effects at 1 microM (4-fold and 2-fold, respectively), while treatments with quisqualate and MK801 caused concentration-dependent down-regulation in mRNAppENK. The most effective concentrations of NMDA (1 microM) and quisqualate (10 microM) altered mRNAppENK levels within 4 h of treatment and peaked after 24 h for NMDA and 48 h for quisqualate treatment. Co-treatment with APV completely blocked the NMDA-induced rise of mRNAppENK. During electrical blockade, none of the concentrations of NMDA tested showed any effect on enkephalin expression, neither could NMDA pre-treatment prevent the TTX-induced down-regulation of mRNAppENK. Our results indicate that the activity-dependent establishment of the enkephalin phenotype is modulated through the selective activation of the NMDA-glutamate receptor. JF - Brain research. Developmental brain research AU - Summers, R W AU - Wu, X R AU - Fitzgerald, S C AU - Brenneman, D E AU - von Agoston, D AD - Laboratory of Developmental Neurobiology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/06/08/ PY - 1993 DA - 1993 Jun 08 SP - 185 EP - 192 VL - 73 IS - 2 SN - 0165-3806, 0165-3806 KW - Amino Acids KW - 0 KW - Enkephalins KW - Ligands KW - Protein Precursors KW - RNA, Messenger KW - Receptors, Glutamate KW - Tetrodotoxin KW - 4368-28-9 KW - N-Methylaspartate KW - 6384-92-5 KW - preproenkephalin KW - 93443-35-7 KW - Index Medicus KW - Animals KW - Blotting, Northern KW - Receptors, Glutamate -- drug effects KW - Receptors, Glutamate -- metabolism KW - Protein Precursors -- genetics KW - Mice KW - Electric Stimulation KW - RNA, Messenger -- biosynthesis KW - Pregnancy KW - Phenotype KW - Ganglia, Spinal -- cytology KW - RNA, Messenger -- metabolism KW - N-Methylaspartate -- pharmacology KW - Cells, Cultured KW - Protein Precursors -- biosynthesis KW - Mice, Inbred C57BL KW - N-Methylaspartate -- antagonists & inhibitors KW - Ganglia, Spinal -- drug effects KW - Tetrodotoxin -- pharmacology KW - Down-Regulation -- drug effects KW - Female KW - Enkephalins -- genetics KW - Enkephalins -- biosynthesis KW - Spinal Cord -- metabolism KW - Enkephalins -- metabolism KW - Spinal Cord -- embryology KW - Amino Acids -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75902096?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research.+Developmental+brain+research&rft.atitle=Excitatory+amino+acid+regulation+of+the+enkephalin+phenotype+in+mouse+embryonic+spinal+cord+cultures.&rft.au=Summers%2C+R+W%3BWu%2C+X+R%3BFitzgerald%2C+S+C%3BBrenneman%2C+D+E%3Bvon+Agoston%2C+D&rft.aulast=Summers&rft.aufirst=R&rft.date=1993-06-08&rft.volume=73&rft.issue=2&rft.spage=185&rft.isbn=&rft.btitle=&rft.title=Brain+research.+Developmental+brain+research&rft.issn=01653806&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-22 N1 - Date created - 1993-09-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Brefeldin A blocks the response of cultured cells to cholera toxin. Implications for intracellular trafficking in toxin action. AN - 75766440; 8389369 AB - Cholera toxin (CT) consists of a pentameric B subunit which binds to ganglioside GM1 on the cell surface and an A subunit which activates adenylylcyclase. The latter process involves the reduction of A to the A1 peptide which ADP-ribosylates the stimulatory G protein, Gs of adenylylcyclase. There is a distinct lag phase between toxin binding and activation of adenylylcyclase. Little is known about the events during this lag including where A1 is generated and how it gains access to Gs on the cytoplasmic side of the plasma membrane. We explored the effects of several inhibitors of intracellular trafficking on the response of human SK-N-MC neurotumor and Caco-2 intestinal tumor cells to CT. Whereas chloroquine or monensin had little or no effect on CT stimulation of cyclic AMP accumulation, brefeldin A (BFA) totally inhibited the response to CT in a time- and dose-dependent and reversible manner. BFA was effective when added at the same time as CT and had an IC50 of 30 ng/ml. BFA did not alter cell surface GM1 as cells treated with BFA for 30 min bound as much 125I-CT as control cells. Furthermore, BFA inhibited CT stimulation of GM1-treated rat glioma C6 cells. BFA treatment did not affect beta-adrenergic agonist stimulation of cyclic AMP. In addition, adenylylcyclase was activated by A1 peptide and NAD+ to the same extent in membranes from control and BFA-treated cells, or when BFA was added directly to the assay. Whereas control cells generated small amounts of A1 from bound CT with time, no A1 was detected in BFA-treated cells. BFA treatment did not prevent the internalization of CT but did inhibit its degradation. BFA is known to disrupt the organization of the Golgi complex, resulting in inhibition of protein transport from the endoplasmic reticulum and redistribution of Golgi enzymes to the endoplasmic reticulum. BFA also prevents the formation of non-clathrin-coated vesicles from Golgi membranes and thus vesicular transport between Golgi cisternae. We confirmed that BFA caused the morphological disruption of the Golgi apparatus in Caco-2 cells. The data support a role for a functional Golgi apparatus with its associated vesicular routing in CT action. JF - The Journal of biological chemistry AU - Orlandi, P A AU - Curran, P K AU - Fishman, P H AD - Membrane Biochemistry Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/06/05/ PY - 1993 DA - 1993 Jun 05 SP - 12010 EP - 12016 VL - 268 IS - 16 SN - 0021-9258, 0021-9258 KW - Cyclopentanes KW - 0 KW - Mycotoxins KW - Brefeldin A KW - 20350-15-6 KW - Chloroquine KW - 886U3H6UFF KW - Cholera Toxin KW - 9012-63-9 KW - Monensin KW - 906O0YJ6ZP KW - Cyclic AMP KW - E0399OZS9N KW - Adenylyl Cyclases KW - EC 4.6.1.1 KW - Isoproterenol KW - L628TT009W KW - Index Medicus KW - Animals KW - Mycotoxins -- pharmacology KW - Enzyme Activation KW - Golgi Apparatus -- drug effects KW - Humans KW - Monensin -- pharmacology KW - Isoproterenol -- pharmacology KW - Biological Transport -- drug effects KW - Rats KW - Tumor Cells, Cultured KW - Chloroquine -- pharmacology KW - Kinetics KW - Golgi Apparatus -- ultrastructure KW - Glioma KW - Adenocarcinoma KW - Time Factors KW - Colonic Neoplasms KW - Cell Line KW - Cyclopentanes -- pharmacology KW - Cyclic AMP -- metabolism KW - Cholera Toxin -- pharmacology KW - Adenylyl Cyclases -- metabolism KW - Cholera Toxin -- antagonists & inhibitors KW - Cholera Toxin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75766440?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Brefeldin+A+blocks+the+response+of+cultured+cells+to+cholera+toxin.+Implications+for+intracellular+trafficking+in+toxin+action.&rft.au=Orlandi%2C+P+A%3BCurran%2C+P+K%3BFishman%2C+P+H&rft.aulast=Orlandi&rft.aufirst=P&rft.date=1993-06-05&rft.volume=268&rft.issue=16&rft.spage=12010&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-07 N1 - Date created - 1993-07-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Differential effects of chronic dopamine D1 and D2 receptor agonists on rotational behavior and dopamine receptor binding. AN - 75924537; 8102970 AB - The effects of chronic continuous and intermittent administration of the dopamine D1 receptor agonist SKF 38393 or the D2 receptor agonist quinpirole on rotational behavior and dopamine receptor binding were examined in rats with a unilateral 6-hydroxydopamine lesion of the nigrostriatal pathway. Continuous and intermittent SKF 38393 both decreased the rotational response to subsequent challenge with SKF 38393. Intermittent SKF 38393 increased quinpirole rotation, while continuous SKF 38393 had no effect. Continuous administration of quinpirole did not affect rotation elicited by either SKF 38393 or quinpirole. Intermittent quinpirole, however, increased both SKF 38393- and quinpirole-induced rotation. Autoradiographic techniques were used to measure D1 receptor binding in striatum and substantia nigra pars reticulata and D2 receptor binding in striatum and nucleus accumbens. Intermittent SKF 38393 reduced D1 receptor Bmax and increased D1 Kd in the striatum, while both continuous and intermittent treatment with the D1 agonist decreased D1 binding in the substantia nigra pars reticulata. Intermittent quinpirole decreased D1 receptor Kd in striatum, and continuous quinpirole reduced D1 binding slightly in substantia nigra pars reticulata. Striatal D2 receptor binding was unaffected by treatment with either SKF 38393 or quinpirole. Intermittent SKF 38393 and continuous quinpirole both reversed the lesioned-induced elevation in D2 binding in the nucleus accumbens, while intermittent quinpirole decreased D2 binding in the accumbens on both the intact and denervated sides. Thus, the effects of chronic treatment with D1 and D2 agonists on behavioral responses to D1 and D2 receptor stimulation differed considerably and were dependent on the treatment regimen employed.(ABSTRACT TRUNCATED AT 250 WORDS) JF - European journal of pharmacology AU - Engber, T M AU - Marin, C AU - Susel, Z AU - Chase, T N AD - Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/06/04/ PY - 1993 DA - 1993 Jun 04 SP - 385 EP - 393 VL - 236 IS - 3 SN - 0014-2999, 0014-2999 KW - Dopamine Agents KW - 0 KW - Ergolines KW - Receptors, Dopamine D1 KW - Receptors, Dopamine D2 KW - Quinpirole KW - 20OP60125T KW - 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine KW - 67287-49-4 KW - Oxidopamine KW - 8HW4YBZ748 KW - Index Medicus KW - Animals KW - Substantia Nigra -- injuries KW - Corpus Striatum -- metabolism KW - Autoradiography KW - Denervation KW - Binding Sites KW - Substantia Nigra -- metabolism KW - Rats KW - Rats, Sprague-Dawley KW - Oxidopamine -- toxicity KW - Nucleus Accumbens -- metabolism KW - Male KW - Ergolines -- administration & dosage KW - Ergolines -- pharmacology KW - Dopamine Agents -- pharmacology KW - Receptors, Dopamine D2 -- drug effects KW - Receptors, Dopamine D1 -- drug effects KW - Motor Activity -- drug effects KW - 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine -- pharmacology KW - 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine -- administration & dosage KW - Receptors, Dopamine D1 -- metabolism KW - Receptors, Dopamine D2 -- metabolism KW - Dopamine Agents -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75924537?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+pharmacology&rft.atitle=Differential+effects+of+chronic+dopamine+D1+and+D2+receptor+agonists+on+rotational+behavior+and+dopamine+receptor+binding.&rft.au=Engber%2C+T+M%3BMarin%2C+C%3BSusel%2C+Z%3BChase%2C+T+N&rft.aulast=Engber&rft.aufirst=T&rft.date=1993-06-04&rft.volume=236&rft.issue=3&rft.spage=385&rft.isbn=&rft.btitle=&rft.title=European+journal+of+pharmacology&rft.issn=00142999&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-30 N1 - Date created - 1993-09-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - NMDA receptor-mediated glutamate toxicity of cultured cerebellar, cortical and mesencephalic neurons: neuroprotective properties of amantadine and memantine. AN - 75894671; 8102306 AB - Effects of amantadine and memantine on NMDA receptor-mediated glutamate toxicity were studied in cultured cerebellar, cortical and mesencephalic neurons. Both drugs protected cerebellar and cortical neurons against glutamate toxicity, memantine being consistently more effective than amantadine but less effective than MK-801. Glutamate toxicity of dopaminergic neurons in mesencephalic cultures was only mildly attenuated by memantine but was also only incompletely blocked by MK-801. These findings suggest that adamantanamines act by inhibiting NMDA receptor-mediated excitatory neurotransmission. However, since non-NMDA receptors appear to be principal mediators of glutamate toxicity of dopaminergic mesencephalic neurons, adamantanamines may fail to protect the nigrostriatal neurons which specifically degenerate in Parkinson's disease. JF - Brain research AU - Weller, M AU - Finiels-Marlier, F AU - Paul, S M AD - Section on Molecular Pharmacology, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1993/06/04/ PY - 1993 DA - 1993 Jun 04 SP - 143 EP - 148 VL - 613 IS - 1 SN - 0006-8993, 0006-8993 KW - Excitatory Amino Acid Antagonists KW - 0 KW - Glutamates KW - Receptors, N-Methyl-D-Aspartate KW - Glutamic Acid KW - 3KX376GY7L KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - Amantadine KW - BF4C9Z1J53 KW - Memantine KW - W8O17SJF3T KW - Index Medicus KW - Rats KW - Mesencephalon -- drug effects KW - Animals KW - Rats, Sprague-Dawley KW - Cerebral Cortex -- drug effects KW - Cell Survival -- drug effects KW - Cells, Cultured KW - Cerebellum -- drug effects KW - Dizocilpine Maleate -- pharmacology KW - Receptors, N-Methyl-D-Aspartate -- physiology KW - Neurons -- drug effects KW - Memantine -- pharmacology KW - Glutamates -- toxicity KW - Amantadine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75894671?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research&rft.atitle=NMDA+receptor-mediated+glutamate+toxicity+of+cultured+cerebellar%2C+cortical+and+mesencephalic+neurons%3A+neuroprotective+properties+of+amantadine+and+memantine.&rft.au=Weller%2C+M%3BFiniels-Marlier%2C+F%3BPaul%2C+S+M&rft.aulast=Weller&rft.aufirst=M&rft.date=1993-06-04&rft.volume=613&rft.issue=1&rft.spage=143&rft.isbn=&rft.btitle=&rft.title=Brain+research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-15 N1 - Date created - 1993-09-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Restoration of interferon alpha potentiation of a recombinant ricin A chain immunotoxin following cytoreduction of xenografts of advanced ovarian tumors. AN - 75741059; 8492319 AB - We have demonstrated that, in the human ovarian carcinoma cell line (OVCAR-3), recombinant human interferon alpha (rHuIFN-alpha) potentiated in vitro inhibition of protein synthesis by immunotoxins. The antitumor activity of intracavitary immunotoxin administered to nude mice 5 days after tumor cell injection was enhanced by a nontherapeutic dose of rHuIFN-alpha, as evidenced by increased survival time. Our purpose was to determine the outcome of treatment with immunotoxin and rHuIFN-alpha in xenografts of more advanced tumors. At 10 or 15 days after tumor cell injection, nude mice with peritoneal OVCAR-3 xenografts were treated intraperitoneally with immunotoxin or with 454A12 monoclonal antibody (MAb) recombinant ricin A chain (rRA), alone or combined with a nontherapeutic dose of rHuIFN-alpha. The immunotoxin was composed of rRA covalently bound to an anti-CD71 (transferrin receptor) MAb. In other experiments, mice were treated intraperitoneally with cyclophosphamide and cisplatin to reduce tumor size on days 20 and 27 after tumor cell inoculation and then, beginning on day 40, with immunotoxin alone or combined with rHuIFN-alpha. Initiation of treatment 10 days after OVCAR-3 transplantation significantly increased median survival from 41 to 89 days (10% survivors on day 120) with 454A12 MAb rRA alone and to more than 120 days (70% survivors) with 454A12 MAb rRA combined with rHuIFN-alpha (P < .0001). The increase in survival time between tumor-bearing mice treated with immunotoxin combined with rHuIFN-alpha and those treated with immunotoxin alone was statistically significant (P = .017). In contrast, the 15-day transplant tumors were not curable with immunotoxin therapy (survival, 72 days; 0% survivors) and were refractory to rHuIFN-alpha potentiation (survival, 75 days; 0% survivors). After the second course of chemotherapy to reduce the size of the advanced tumors (day 40), during the ascites cell count nadir, initiation of treatment with 454A12 MAb rRA alone or combined with rHuIFN-alpha resulted in significantly different survival times of 129 and 162 days, respectively (P = .0037). Pathologic examination of surviving mice treated with chemotherapy and 454A12 MAb rRA alone or in combination with rHuIFN-alpha revealed that one (17%) of six mice and 11 (65%) of 17 were tumor free, respectively. The synergy between immunotoxins and IFN-alpha is dependent on tumor burden. These agents are less effective against large tumor burdens (i.e., advanced stage disease), but their beneficial effects re-emerge after cytoreduction by combination chemotherapy. The ideal setting for testing the efficacy of intracavitary immunotoxin combined with rHuIFN-alpha after front-line chemotherapy is in patients with residual tumor refractory to additional chemotherapy or in those with toxic effects that prevent delivery of effective doses. JF - Journal of the National Cancer Institute AU - Pearson, J W AU - Fogler, W E AU - Volker, K AU - Riggs, C W AU - Gruys, E AU - Groves, E S AU - Wiltrout, R H AU - Longo, D L AD - Biological Response Modifiers Program, National Cancer Institute (NCI), NCI-Frederick Cancer Research and Development Center FCRDC, Md 21702-1201. Y1 - 1993/06/02/ PY - 1993 DA - 1993 Jun 02 SP - 907 EP - 912 VL - 85 IS - 11 SN - 0027-8874, 0027-8874 KW - Antibodies, Monoclonal KW - 0 KW - Immunotoxins KW - Interferon Type I KW - Recombinant Proteins KW - Ricin KW - 9009-86-3 KW - Index Medicus KW - Neoplasm Transplantation KW - Animals KW - Humans KW - Mice, Nude KW - Mice KW - Drug Synergism KW - Female KW - Antibodies, Monoclonal -- therapeutic use KW - Ricin -- therapeutic use KW - Ovarian Neoplasms -- pathology KW - Interferon Type I -- therapeutic use KW - Immunotoxins -- therapeutic use KW - Ovarian Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75741059?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Restoration+of+interferon+alpha+potentiation+of+a+recombinant+ricin+A+chain+immunotoxin+following+cytoreduction+of+xenografts+of+advanced+ovarian+tumors.&rft.au=Pearson%2C+J+W%3BFogler%2C+W+E%3BVolker%2C+K%3BRiggs%2C+C+W%3BGruys%2C+E%3BGroves%2C+E+S%3BWiltrout%2C+R+H%3BLongo%2C+D+L&rft.aulast=Pearson&rft.aufirst=J&rft.date=1993-06-02&rft.volume=85&rft.issue=11&rft.spage=907&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-16 N1 - Date created - 1993-06-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Neuropsychiatric effects of anabolic steroids in male normal volunteers. AN - 75734884; 8492402 AB - To evaluate the acute effects of anabolic steroids on mood and behavior in male normal volunteers. A 2-week, double-blind (subject and rater), fixed-order, placebo-controlled crossover trial of methyltestosterone. An inpatient research unit at the National Institutes of Health. A volunteer sample of 20 men who were medication free, free of medical and psychiatric illness, not involved in athletic training, and had no prior history of anabolic steroid use. A sequential trial for 3 days each of the following four drug conditions: placebo baseline, low-dose methyltestosterone (40 mg/d), high-dose methyltestosterone (240 mg/d), and placebo withdrawal. Mood and behavioral ratings were completed during each drug condition and included both subjective and objective measures. Significant (P < .05) albeit subtle increases in symptom scores were observed during high-dose methyltestosterone administration compared with baseline in positive mood (euphoria, energy, and sexual arousal), negative mood (irritability, mood swings, violent feelings, and hostility), and cognitive impairment (distractibility, forgetfulness, and confusion). An acute manic episode was observed in one of the 20 subjects, representing a 5% incidence, even under these conservative conditions. An additional subject became hypomanic. Baseline characteristics including family psychiatric history or previous drug abuse did not predict symptom changes. This is the first placebo-controlled prospective study demonstrating the adverse and activating mood and behavioral effects of anabolic steroids. JF - JAMA AU - Su, T P AU - Pagliaro, M AU - Schmidt, P J AU - Pickar, D AU - Wolkowitz, O AU - Rubinow, D R AD - Section on Behavioral Endocrinology, National Institute of Mental Health/NIH, Bethesda, MD 20892. Y1 - 1993/06/02/ PY - 1993 DA - 1993 Jun 02 SP - 2760 EP - 2764 VL - 269 IS - 21 SN - 0098-7484, 0098-7484 KW - Anabolic Agents KW - 0 KW - Methyltestosterone KW - V9EFU16ZIF KW - Abridged Index Medicus KW - Index Medicus KW - Prospective Studies KW - Double-Blind Method KW - Humans KW - Adult KW - Anabolic Agents -- metabolism KW - Adolescent KW - Male KW - Psychological Tests KW - Anabolic Agents -- adverse effects KW - Behavior -- drug effects KW - Affect -- drug effects KW - Cognition -- drug effects KW - Methyltestosterone -- metabolism KW - Methyltestosterone -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75734884?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=JAMA&rft.atitle=Neuropsychiatric+effects+of+anabolic+steroids+in+male+normal+volunteers.&rft.au=Su%2C+T+P%3BPagliaro%2C+M%3BSchmidt%2C+P+J%3BPickar%2C+D%3BWolkowitz%2C+O%3BRubinow%2C+D+R&rft.aulast=Su&rft.aufirst=T&rft.date=1993-06-02&rft.volume=269&rft.issue=21&rft.spage=2760&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-17 N1 - Date created - 1993-06-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Cancer in developing countries: opportunity and challenge. AN - 75730715; 8492315 AB - Epidemiologic observations indicate that environment and lifestyle are the major determinants of the geographical patterns of cancer. The developing countries, which account for 75% of the world's population, have lower incidence rates of cancer compared with the industrialized nations but bear more than half the global cancer burden. Demographic trends resulting from economic progress (decreasing incidence of infectious diseases, population growth, aging, and urbanization), coupled with increased tobacco consumption and dietary changes, indicate that developing countries will bear a continually increasing proportion of the world's cancer burden and its accompanying demand for the provision of costly treatment programs. Yet the developing countries command only 5% of the world's economic resources, and health care programs are already fully extended and frequently inadequate. Thus, cancer control in the developing countries, including preemptive prevention of the anticipated increases in cancers presently more common in the industrialized nations (e.g., lung, breast, and colon), should include much greater emphasis on cancer prevention than is presently the case. But there is another perspective. The developing countries, with their dramatic contrasts in lifestyles and environments and equally diverse patterns of cancer, provide an unparalleled, and often neglected, opportunity for studies directed toward understanding the mechanisms of environmental carcinogenesis. Such an understanding should eventually lead to the development of novel intervention approaches. Unfortunately, cancer research is much more difficult to conduct in the developing countries because of the lack of population-based registries, poor communication and transportation systems, and deficiencies in infrastructure, financial support, and the training of health professionals. These difficulties could be overcome, to the benefit of all, if the extent of collaboration in cancer research between the developing and industrialized nations were to be greatly expanded. JF - Journal of the National Cancer Institute AU - Magrath, I AU - Litvak, J AD - Clinical Oncology Program, National Cancer Institute, Bethesda, Md. 20892. Y1 - 1993/06/02/ PY - 1993 DA - 1993 Jun 02 SP - 862 EP - 874 VL - 85 IS - 11 SN - 0027-8874, 0027-8874 KW - Index Medicus KW - Humans KW - Incidence KW - Developing Countries -- statistics & numerical data KW - International Cooperation KW - Neoplasms -- epidemiology KW - Neoplasms -- prevention & control KW - Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75730715?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Cancer+in+developing+countries%3A+opportunity+and+challenge.&rft.au=Magrath%2C+I%3BLitvak%2C+J&rft.aulast=Magrath&rft.aufirst=I&rft.date=1993-06-02&rft.volume=85&rft.issue=11&rft.spage=862&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-16 N1 - Date created - 1993-06-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Fully automated segmentation of cerebrospinal fluid in computed tomography. AN - 75975705; 8378487 AB - A method is presented for automated delineation and measurement of cerebrospinal fluid (CSF) regions in computed tomographic (CT) sections. Regions of skull and scalp are removed by using a linear discriminant analysis approach. Beam-hardening artifact is reduced by subtracting from each section the average radial intensity profile, characterized by a polynomial function. Remaining intensity gradients are suppressed by implementing CSF segmentation with a local thresholding technique based on maximum-entropy principles. CSF fractions from 12 regions of interest (ROIs) were measured in 10 patients with alcoholic Korsakoff syndrome and 9 normal volunteers. The same ROIs were also assessed by an interactive segmentation method, which enabled the operator to compensate for beam-hardening distortions by selecting suitable threshold values for each ROI. Both methods identified the same ROIs as displaying statistically significant differences between the two subject groups. However, interactive segmentation underestimated sulcal CSF by 20-70%, which was confirmed by applying both methods to CT scans of an anthropomorphic phantom. Hence, in contrast to interactive thresholding, unsupervised segmentation relies on firmly fixed criteria that reduce the influence of beam-hardening distortions and provide more objective results. JF - Psychiatry research AU - Ruttimann, U E AU - Joyce, E M AU - Rio, D E AU - Eckardt, M J AD - Laboratory of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD 20892. Y1 - 1993/06// PY - 1993 DA - June 1993 SP - 101 EP - 119 VL - 50 IS - 2 SN - 0165-1781, 0165-1781 KW - Index Medicus KW - Artifacts KW - Humans KW - Aged KW - Middle Aged KW - Cerebral Ventriculography KW - Technology, Radiologic KW - Male KW - Tomography, X-Ray Computed -- methods KW - Tomography, X-Ray Computed -- statistics & numerical data KW - Cerebrospinal Fluid -- diagnostic imaging KW - Alcohol Amnestic Disorder -- diagnostic imaging KW - Brain -- diagnostic imaging KW - Tomography, X-Ray Computed -- instrumentation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75975705?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychiatry+research&rft.atitle=Fully+automated+segmentation+of+cerebrospinal+fluid+in+computed+tomography.&rft.au=Ruttimann%2C+U+E%3BJoyce%2C+E+M%3BRio%2C+D+E%3BEckardt%2C+M+J&rft.aulast=Ruttimann&rft.aufirst=U&rft.date=1993-06-01&rft.volume=50&rft.issue=2&rft.spage=101&rft.isbn=&rft.btitle=&rft.title=Psychiatry+research&rft.issn=01651781&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-15 N1 - Date created - 1993-10-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Higher levels of nicotine in arterial than in venous blood after cigarette smoking. AN - 75971483; 8370337 AB - We examined differences between arterial and venous concentrations of nicotine in human subjects. Shortly after smoking a cigarette, levels of nicotine in arterial plasma were more than double those in venous plasma. The time course of the rise in arterial nicotine levels and the magnitude of the arteriovenous difference varied considerably among subjects. For some subjects, arterial nicotine concentrations after one cigarette were similar to venous concentrations typically observed after 20 cigarettes and were nearly 10 times greater than venous concentrations. Our findings have implications for understanding the high degree of addictiveness and cardiovascular toxicity of smoked forms of drugs. JF - Drug and alcohol dependence AU - Henningfield, J E AU - Stapleton, J M AU - Benowitz, N L AU - Grayson, R F AU - London, E D AD - Addiction Research Center, National Institute on Drug Abuse, Balitmore, MD 21224. Y1 - 1993/06// PY - 1993 DA - June 1993 SP - 23 EP - 29 VL - 33 IS - 1 SN - 0376-8716, 0376-8716 KW - Nicotine KW - 6M3C89ZY6R KW - Index Medicus KW - Veins KW - Humans KW - Arteries KW - Metabolic Clearance Rate -- physiology KW - Adult KW - Male KW - Smoking -- blood KW - Nicotine -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75971483?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Drug+and+alcohol+dependence&rft.atitle=Higher+levels+of+nicotine+in+arterial+than+in+venous+blood+after+cigarette+smoking.&rft.au=Henningfield%2C+J+E%3BStapleton%2C+J+M%3BBenowitz%2C+N+L%3BGrayson%2C+R+F%3BLondon%2C+E+D&rft.aulast=Henningfield&rft.aufirst=J&rft.date=1993-06-01&rft.volume=33&rft.issue=1&rft.spage=23&rft.isbn=&rft.btitle=&rft.title=Drug+and+alcohol+dependence&rft.issn=03768716&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-14 N1 - Date created - 1993-10-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Comorbid psychopathy is not associated with increased D2 dopamine receptor TaqI A or B gene marker frequencies in incarcerated substance abusers. AN - 75939542; 8104042 JF - Biological psychiatry AU - Smith, S S AU - Newman, J P AU - Evans, A AU - Pickens, R AU - Wydeven, J AU - Uhl, G R AU - Newlin, D B AD - National Institute on Drug Abuse, Addiction Research Center, Baltimore, MD. PY - 1993 SP - 845 EP - 848 VL - 33 IS - 11-12 SN - 0006-3223, 0006-3223 KW - Genetic Markers KW - 0 KW - Receptors, Dopamine D2 KW - DNA KW - 9007-49-2 KW - Deoxyribonucleases, Type II Site-Specific KW - EC 3.1.21.4 KW - TCGA-specific type II deoxyribonucleases KW - Index Medicus KW - Genetic Linkage KW - Analysis of Variance KW - Psychiatric Status Rating Scales KW - Gene Frequency KW - Polymorphism, Restriction Fragment Length KW - Humans KW - Adult KW - DNA -- analysis KW - Prisoners KW - Male KW - Personality Disorders -- genetics KW - Substance-Related Disorders -- complications KW - Receptors, Dopamine D2 -- genetics KW - Personality Disorders -- psychology KW - Substance-Related Disorders -- psychology KW - Personality Disorders -- complications KW - Substance-Related Disorders -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75939542?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biological+psychiatry&rft.atitle=Comorbid+psychopathy+is+not+associated+with+increased+D2+dopamine+receptor+TaqI+A+or+B+gene+marker+frequencies+in+incarcerated+substance+abusers.&rft.au=Smith%2C+S+S%3BNewman%2C+J+P%3BEvans%2C+A%3BPickens%2C+R%3BWydeven%2C+J%3BUhl%2C+G+R%3BNewlin%2C+D+B&rft.aulast=Smith&rft.aufirst=S&rft.date=1993-06-01&rft.volume=33&rft.issue=11-12&rft.spage=845&rft.isbn=&rft.btitle=&rft.title=Biological+psychiatry&rft.issn=00063223&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-21 N1 - Date created - 1993-10-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Glucocorticoids synergize with tumor necrosis factor alpha in the induction of HIV expression from a chronically infected promonocytic cell line. AN - 75906717; 8347399 AB - In this study we have investigated the effects of glucocorticoids (GCs) on the expression of human immunodeficiency virus (HIV) in a chronically infected promonocytic cell line, U1. Although no increase in virus production was observed in U1 cells stimulated with physiological concentrations of GC alone, costimulation with dexamethasone plus tumor necrosis factor alpha (TNF-alpha) synergistically enhanced TNF-alpha-dependent HIV expression. Molecular analysis demonstrated that GCs plus TNF-alpha resulted in an accumulation of steady state HIV RNA secondary to either an increase in transcription or an increase in message stability. These findings may be of physiological relevance because GCs are used in the treatment of certain disorders associated with HIV infection and TNF-alpha levels have been reported to be elevated in the plasma and cerebrospinal fluid of certain HIV-infected individuals. JF - AIDS research and human retroviruses AU - Bressler, P AU - Poli, G AU - Justement, J S AU - Biswas, P AU - Fauci, A S AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/06// PY - 1993 DA - June 1993 SP - 547 EP - 551 VL - 9 IS - 6 SN - 0889-2229, 0889-2229 KW - HIV Antigens KW - 0 KW - RNA, Messenger KW - Tumor Necrosis Factor-alpha KW - Dexamethasone KW - 7S5I7G3JQL KW - Index Medicus KW - AIDS/HIV KW - Virus Replication -- drug effects KW - HIV Antigens -- biosynthesis KW - Transcription, Genetic KW - Monocytes -- microbiology KW - Stem Cells -- microbiology KW - Drug Synergism KW - RNA, Messenger -- biosynthesis KW - Cell Line KW - HIV -- growth & development KW - HIV -- drug effects KW - Dexamethasone -- pharmacology KW - Tumor Necrosis Factor-alpha -- pharmacology KW - Gene Expression Regulation, Viral -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75906717?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS+research+and+human+retroviruses&rft.atitle=Glucocorticoids+synergize+with+tumor+necrosis+factor+alpha+in+the+induction+of+HIV+expression+from+a+chronically+infected+promonocytic+cell+line.&rft.au=Bressler%2C+P%3BPoli%2C+G%3BJustement%2C+J+S%3BBiswas%2C+P%3BFauci%2C+A+S&rft.aulast=Bressler&rft.aufirst=P&rft.date=1993-06-01&rft.volume=9&rft.issue=6&rft.spage=547&rft.isbn=&rft.btitle=&rft.title=AIDS+research+and+human+retroviruses&rft.issn=08892229&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-10 N1 - Date created - 1993-09-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Immunotherapy and neuropsychiatric toxicity. Nursing clinical management consideration. AN - 75879078; 8348526 AB - Ensuring the safety of patients who receive immunotherapy is an essential element of nursing care. Communicating changes in mental status to the medical team is important feedback for modifying or discontinuing the cycle of immunotherapy. These observations are even more crucial if neuropsychiatric toxicity (NPT) has been exhibited in a previous cycle of treatment. If nurses are aware of associative factors of NPT they can be more alert for emerging cognitive dysfunction. Early intervention will also mean the nurse will take additional measures to ensure patient safety, such as suggesting possible pharmacological alternatives and closer observation, and encouraging family members to help with orientation. The nurse can further assist by helping alleviate the patient's or family's feelings of helplessness by assuring them that the NPT will begin to subside once treatment has been terminated. JF - Cancer nursing AU - Sparber, A G AU - Biller-Sparber, K AD - National Institutes of Health, Clinical Center, Bethesda, MD. Y1 - 1993/06// PY - 1993 DA - June 1993 SP - 188 EP - 192 VL - 16 IS - 3 SN - 0162-220X, 0162-220X KW - Immunologic Factors KW - 0 KW - Interleukin-2 KW - Index Medicus KW - Nursing KW - Humans KW - Middle Aged KW - Male KW - Family -- psychology KW - Confusion -- psychology KW - Interleukin-2 -- adverse effects KW - Akathisia, Drug-Induced -- nursing KW - Substance-Related Disorders -- nursing KW - Substance-Related Disorders -- etiology KW - Akathisia, Drug-Induced -- psychology KW - Akathisia, Drug-Induced -- etiology KW - Substance-Related Disorders -- psychology KW - Confusion -- nursing KW - Confusion -- chemically induced KW - Immunologic Factors -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75879078?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+nursing&rft.atitle=Immunotherapy+and+neuropsychiatric+toxicity.+Nursing+clinical+management+consideration.&rft.au=Sparber%2C+A+G%3BBiller-Sparber%2C+K&rft.aulast=Sparber&rft.aufirst=A&rft.date=1993-06-01&rft.volume=16&rft.issue=3&rft.spage=188&rft.isbn=&rft.btitle=&rft.title=Cancer+nursing&rft.issn=0162220X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-10 N1 - Date created - 1993-09-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Suspended judgment. The 1953 clinical trial of diethylstilbestrol during pregnancy: could it have stopped DES use? AN - 75861820; 8339548 JF - Controlled clinical trials AU - Berendes, H W AU - Lee, Y J AD - Division of Epidemiology, Statistics and Prevention Research, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/06// PY - 1993 DA - June 1993 SP - 179 EP - 182 VL - 14 IS - 3 SN - 0197-2456, 0197-2456 KW - Diethylstilbestrol KW - 731DCA35BT KW - Index Medicus KW - History of medicine KW - United States KW - History, 20th Century KW - Adenocarcinoma -- chemically induced KW - Vaginal Neoplasms -- chemically induced KW - Humans KW - Drug Monitoring -- history KW - Vaginal Neoplasms -- history KW - United States Food and Drug Administration -- history KW - Adenocarcinoma -- history KW - Female KW - Pregnancy KW - Diethylstilbestrol -- adverse effects KW - Clinical Trials as Topic -- history KW - Clinical Trials as Topic -- standards KW - Diethylstilbestrol -- history KW - Prenatal Exposure Delayed Effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75861820?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Controlled+clinical+trials&rft.atitle=Suspended+judgment.+The+1953+clinical+trial+of+diethylstilbestrol+during+pregnancy%3A+could+it+have+stopped+DES+use%3F&rft.au=Berendes%2C+H+W%3BLee%2C+Y+J&rft.aulast=Berendes&rft.aufirst=H&rft.date=1993-06-01&rft.volume=14&rft.issue=3&rft.spage=179&rft.isbn=&rft.btitle=&rft.title=Controlled+clinical+trials&rft.issn=01972456&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-02 N1 - Date created - 1993-09-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Thromboxane and prostacyclin differentially regulate murine extracellular matrix gene expression. AN - 75812841; 8315934 AB - Alterations in the arachidonic acid metabolites thromboxane and prostacyclin are known to contribute to hemodynamic changes observed in certain models of acute and chronic renal failure. We have previously shown that thromboxane may have an important role in mediating glomerulosclerosis by stimulating the expression of certain extracellular matrix proteins. In the present study, we compared the effects of thromboxane and prostacyclin on the expression of genes encoding basement membrane proteins using a murine teratocarcinoma cell line, that when differentiated to an endodermal phenotype synthesizes abundant extracellular matrix. Incubation of these cells with stable analogs of thromboxane and prostacyclin for four hours resulted in changes in basement membrane gene expression. Thromboxane increased steady-state mRNA levels for all three laminin chains, type IV collagen, and fibronectin, but decreased the level of mRNA for heparan sulfate proteoglycan. In contrast, incubation with carbo-prostacyclin, a stable analog of prostacyclin, decreased the steady-state mRNA level for the laminin A and B1 chains, type IV collagen and fibronectin, and increased the mRNA level for heparan sulfate proteoglycan and laminin B2. Carbo-prostacyclin did not affect cellular proliferation or thymidine incorporation. These results indicate that eicosanoids directly modulate matrix gene expression independently of hemodynamic influence, and independently of effects mediated by platelets, or mitogenesis. Furthermore, these findings suggest that the alterations in renal eicosanoid metabolism may directly participate in the pathogenesis of glomerulosclerosis and thus provide a rationale for therapy directed toward the specific inhibition of thromboxane in the treatment of progressive glomerular sclerosis. JF - Kidney international AU - Bruggeman, L A AU - Pellicoro, J A AU - Horigan, E A AU - Klotman, P E AD - Molecular Medicine Section, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland. Y1 - 1993/06// PY - 1993 DA - June 1993 SP - 1219 EP - 1225 VL - 43 IS - 6 SN - 0085-2538, 0085-2538 KW - Extracellular Matrix Proteins KW - 0 KW - Fibronectins KW - Heparan Sulfate Proteoglycans KW - Laminin KW - Proteoglycans KW - RNA, Messenger KW - Thromboxane A2 KW - 57576-52-0 KW - Collagen KW - 9007-34-5 KW - Heparitin Sulfate KW - 9050-30-0 KW - Epoprostenol KW - DCR9Z582X0 KW - Index Medicus KW - Collagen -- genetics KW - Animals KW - Proteoglycans -- genetics KW - Tumor Cells, Cultured KW - Laminin -- genetics KW - RNA, Messenger -- analysis KW - Mice KW - Fibronectins -- genetics KW - Heparitin Sulfate -- genetics KW - Epoprostenol -- pharmacology KW - Extracellular Matrix Proteins -- genetics KW - Gene Expression Regulation -- drug effects KW - Thromboxane A2 -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75812841?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Kidney+international&rft.atitle=Thromboxane+and+prostacyclin+differentially+regulate+murine+extracellular+matrix+gene+expression.&rft.au=Bruggeman%2C+L+A%3BPellicoro%2C+J+A%3BHorigan%2C+E+A%3BKlotman%2C+P+E&rft.aulast=Bruggeman&rft.aufirst=L&rft.date=1993-06-01&rft.volume=43&rft.issue=6&rft.spage=1219&rft.isbn=&rft.btitle=&rft.title=Kidney+international&rft.issn=00852538&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-27 N1 - Date created - 1993-07-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Immunohistochemical localization of transforming growth factor-beta 1 in rats with experimental silicosis, alveolar type II hyperplasia, and lung cancer. AN - 75783349; 8389528 AB - Immunohistochemical localization of transforming growth factor-beta 1 (TGF-beta 1) was studied in the lungs of rats given crystalline silica or ferric oxide by single intratracheal instillation. Ferric oxide elicited no progressive granulomatous reaction, no epithelial hyperplasia, and no lung tumors; no demonstrable reactivity to TGF-beta 1 was observed. Silica induced a granulomatous reaction with progressive fibrosis, adjacent alveolar type II hyperplasia, and alveolar carcinomas. Rabbit polyclonal antibodies to synthetic peptides corresponding to the first 30 amino acids of mature TGF-beta 1, anti-LC (1-30), and anti-CC (1-30) were used for the localization of intracellular and extracellular TGF-beta 1. An antibody to a peptide corresponding to amino acids 266-278 of the TGF-beta 1 precursor sequence, anti-Pre (266-278), was used to detect the TGF-beta precursor and the latency-associated peptide. Intracellular mature TGF-beta (anti-LC) was demonstrated in fibroblasts and macrophages located at the periphery of silicotic granulomas and in fibroblasts adjacent to hyperplastic type II cells. Extracellular mature TGF-beta 1 was localized in the connective tissue matrix of the granulomas and in the stroma of both hyperplastic type II cells and well-differentiated adenocarcinomas. Immunoreactivity to anti-Pre was localized, intracellularly, in hyperplastic alveolar type II cells and their proliferative lesions adjacent to granulomas, in adenomas, but not in adenocarcinomas. The hyperplastic type II cells appear to be the sites of production and secretion of TGF-beta 1, which may regulate their own growth and differentiation and mediate the production of extracellular TGF-beta 1-associated matrix. The lack of reactivity to TGF-beta 1 precursor in the adenocarcinomas is consistent with the loss of normal cellular differentiation and function. TGF-beta 1 appears to have a pathogenetic role in silica-induced mesenchymal and epithelial lesions. The role of TGF-beta 1 and other cytokines in silica-induced carcinogenesis requires further investigation. JF - The American journal of pathology AU - Williams, A O AU - Flanders, K C AU - Saffiotti, U AD - Laboratory of Experimental Pathology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/06// PY - 1993 DA - June 1993 SP - 1831 EP - 1840 VL - 142 IS - 6 SN - 0002-9440, 0002-9440 KW - Ferric Compounds KW - 0 KW - Protein Precursors KW - Transforming Growth Factor beta KW - ferric oxide KW - 1K09F3G675 KW - Silicon Dioxide KW - 7631-86-9 KW - Abridged Index Medicus KW - Index Medicus KW - Rats KW - Hyperplasia -- pathology KW - Animals KW - Rats, Inbred F344 KW - Protein Precursors -- metabolism KW - Hyperplasia -- etiology KW - Hyperplasia -- metabolism KW - Disease Models, Animal KW - Male KW - Female KW - Silicosis -- metabolism KW - Pulmonary Alveoli -- pathology KW - Adenocarcinoma -- metabolism KW - Silicosis -- pathology KW - Lung -- chemistry KW - Lung -- metabolism KW - Lung -- pathology KW - Adenocarcinoma -- pathology KW - Transforming Growth Factor beta -- analysis KW - Adenoma -- metabolism KW - Lung Neoplasms -- etiology KW - Transforming Growth Factor beta -- physiology KW - Adenocarcinoma -- etiology KW - Adenoma -- etiology KW - Adenoma -- pathology KW - Transforming Growth Factor beta -- metabolism KW - Silicosis -- etiology KW - Lung Neoplasms -- metabolism KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75783349?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+journal+of+pathology&rft.atitle=Immunohistochemical+localization+of+transforming+growth+factor-beta+1+in+rats+with+experimental+silicosis%2C+alveolar+type+II+hyperplasia%2C+and+lung+cancer.&rft.au=Williams%2C+A+O%3BFlanders%2C+K+C%3BSaffiotti%2C+U&rft.aulast=Williams&rft.aufirst=A&rft.date=1993-06-01&rft.volume=142&rft.issue=6&rft.spage=1831&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+pathology&rft.issn=00029440&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-08 N1 - Date created - 1993-07-08 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Am J Respir Cell Mol Biol. 1991 May;4(5):455-62 [2021482] N Engl J Med. 1991 Apr 4;324(14):933-40 [1900574] Hum Pathol. 1992 Jan;23(1):13-20 [1544664] Microbiol Immunol. 1986;30(11):1189-98 [3027514] Br J Cancer. 1980 Jun;41(6):908-17 [6252921] Fed Proc. 1983 Jun;42(9):2621-6 [6303865] Cancer Res. 1984 May;44(5):2170-80 [6324999] J Clin Invest. 1984 May;73(5):1462-72 [6325504] J Leukoc Biol. 1986 Feb;39(2):123-32 [3001212] J Biol Chem. 1986 Mar 25;261(9):4337-45 [3456347] Proc Natl Acad Sci U S A. 1986 Jun;83(12):4167-71 [2424019] Cancer Res. 1986 Sep;46(9):4665-71 [3089593] Exp Cell Res. 1986 Dec;167(2):539-49 [3464447] Am J Ind Med. 1987;11(1):93-107 [3028139] Lab Invest. 1987 Nov;57(5):546-54 [2824924] J Cell Biol. 1987 Dec;105(6 Pt 2):2861-76 [3320058] Biochem J. 1987 Nov 1;247(3):597-604 [3501287] Proc Natl Acad Sci U S A. 1988 Mar;85(5):1539-43 [3422749] Nature. 1988 Mar 17;332(6161):217-9 [2831460] J Biol Chem. 1988 Jun 5;263(16):7646-54 [3163692] J Pharmacol Exp Ther. 1988 Aug;246(2):765-71 [2457084] Br J Cancer. 1988 Jun;57(6):594-600 [3044431] Recent Prog Horm Res. 1988;44:157-97 [3064207] J Cell Biol. 1989 Feb;108(2):653-60 [2465297] Am J Ind Med. 1989;15(3):343-6 [2539015] J Clin Invest. 1989 May;83(5):1661-6 [2708527] J Mol Cell Cardiol. 1989 Feb;21 Suppl 1:151-9 [2733025] Proc Natl Acad Sci U S A. 1989 Jun;86(12):4544-8 [2734305] J Cell Biol. 1989 Jun;108(6):2477-82 [2500447] J Exp Med. 1989 Sep 1;170(3):727-37 [2475572] Postgrad Med J. 1988;64 Suppl 4:26-34 [3076931] J Clin Invest. 1989 Dec;84(6):1836-42 [2480367] Nature. 1990 Mar 15;344(6263):245-7 [2156165] Am J Respir Cell Mol Biol. 1990 Apr;2(4):381-90 [2157474] Ann N Y Acad Sci. 1990;580:225-32 [2186691] J Cell Biol. 1990 Aug;111(2):757-63 [1696270] Am J Respir Cell Mol Biol. 1991 Aug;5(2):155-62 [1892646] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Expression of hepatocyte growth factor and c-met genes during hepatic differentiation and liver development in the rat. AN - 75783323; 8506951 AB - Hepatocyte growth factor (HGF) is a potent mitogen for mature hepatocytes in vitro. The receptor for HGF has recently been characterized as the product of the proto-oncogene c-met. We have examined the possible involvement of HGF in hepatic growth and differentiation in the rat. The experimental systems used were acetylaminofluorene treatment combined with partial hepatectomy to induce proliferation and differentiation of oval cells in adult liver and the pre- and postnatal liver. In the acetylaminofluorene model, Northern blot analysis showed that level of HGF transcripts increased one day after partial hepatectomy, reached a peak by day 6, were maintained at that level until day 13, and then declined, reaching normal level at 20 days. The expression of c-met also increased gradually, reached a peak around 9 to 13 days after partial hepatectomy, at which time oval cell proliferation was most prominent. In the developing liver, an elevated level of HGF transcripts was found between 4 and 21 days after birth. The expression of c-met also slightly increased at the same time. In situ hybridization showed that the transcripts for HGF were localized in desmin-positive Ito cells, whereas the transcripts for c-met were strongly expressed by oval cells. We have shown earlier that Ito cells and oval cells proliferate simultaneously and exist in close proximity in the acetylaminofluorene model and that Ito cells are a primary source of growth factors such as transforming growth factor-alpha and acidic fibroblast growth factors. The data presented here suggest that HGF is, in combination with other growth factors, involved in the proliferation and differentiation of oval cells via a paracrine mechanism. JF - The American journal of pathology AU - Hu, Z AU - Evarts, R P AU - Fujio, K AU - Marsden, E R AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-0037. Y1 - 1993/06// PY - 1993 DA - June 1993 SP - 1823 EP - 1830 VL - 142 IS - 6 SN - 0002-9440, 0002-9440 KW - Proto-Oncogene Proteins KW - 0 KW - Hepatocyte Growth Factor KW - 67256-21-7 KW - 2-Acetylaminofluorene KW - 9M98QLJ2DL KW - Proto-Oncogene Proteins c-met KW - EC 2.7.10.1 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Blotting, Northern KW - Cell Division -- drug effects KW - Transcription, Genetic KW - Rats KW - In Situ Hybridization KW - Rats, Inbred F344 KW - 2-Acetylaminofluorene -- pharmacology KW - Hepatectomy KW - Cell Differentiation -- drug effects KW - Time Factors KW - Immunohistochemistry KW - Male KW - Hepatocyte Growth Factor -- analysis KW - Hepatocyte Growth Factor -- physiology KW - Liver -- cytology KW - Gene Expression -- genetics KW - Proto-Oncogene Proteins -- analysis KW - Proto-Oncogenes -- genetics KW - Hepatocyte Growth Factor -- genetics KW - Proto-Oncogene Proteins -- metabolism KW - Liver -- metabolism KW - Proto-Oncogene Proteins -- genetics KW - Liver -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75783323?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+journal+of+pathology&rft.atitle=Expression+of+hepatocyte+growth+factor+and+c-met+genes+during+hepatic+differentiation+and+liver+development+in+the+rat.&rft.au=Hu%2C+Z%3BEvarts%2C+R+P%3BFujio%2C+K%3BMarsden%2C+E+R%3BThorgeirsson%2C+S+S&rft.aulast=Hu&rft.aufirst=Z&rft.date=1993-06-01&rft.volume=142&rft.issue=6&rft.spage=1823&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+pathology&rft.issn=00029440&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-08 N1 - Date created - 1993-07-08 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nature. 1989 May 11;339(6220):155-6 [2541345] Proc Natl Acad Sci U S A. 1989 Oct;86(19):7432-6 [2477840] Nature. 1989 Nov 23;342(6248):440-3 [2531289] Mol Carcinog. 1989;2(6):345-54 [2619882] Proc Natl Acad Sci U S A. 1990 Apr;87(8):3200-4 [2139229] Curr Opin Cell Biol. 1990 Feb;2(1):121-30 [2183836] J Clin Invest. 1990 Jun;85(6):1833-43 [1693377] Cancer Res. 1990 Jul 1;50(13):3811-5 [1693878] Ann N Y Acad Sci. 1990;593:231-42 [2165377] Biochem Biophys Res Commun. 1990 Nov 30;173(1):42-7 [2147853] Biochem Biophys Res Commun. 1991 Jan 15;174(1):331-7 [1846541] Science. 1991 Feb 15;251(4995):802-4 [1846706] Biochem Biophys Res Commun. 1991 Jan 31;174(2):831-8 [1704229] Hepatology. 1991 Apr;13(4):743-50 [1826282] Biochem Biophys Res Commun. 1991 Apr 15;176(1):45-51 [1708252] Oncogene. 1991 Apr;6(4):501-4 [1827664] Biochem Biophys Res Commun. 1991 May 31;177(1):330-5 [1828341] Biochem Biophys Res Commun. 1991 May 31;177(1):559-65 [1828343] Proc Natl Acad Sci U S A. 1991 Aug 15;88(16):7001-5 [1831266] Hepatology. 1991 Sep;14(3):488-94 [1831438] Mol Cell Biol. 1991 Sep;11(9):4405-14 [1875930] Exp Cell Res. 1991 Sep;196(1):114-20 [1879464] EMBO J. 1991 Oct;10(10):2867-78 [1655405] FEBS Lett. 1991 Sep 23;290(1-2):9-12 [1915898] Biochem Biophys Res Commun. 1991 Oct 31;180(2):765-73 [1835386] Cell. 1991 Nov 29;67(5):901-8 [1835669] Hepatology. 1992 Jan;15(1):149-55 [1530787] Mol Carcinog. 1992;5(1):25-31 [1543539] Biochem Biophys Res Commun. 1992 Mar 16;183(2):739-42 [1532309] Crit Rev Oncog. 1992;3(1-2):27-54 [1312869] Lab Invest. 1992 Oct;67(4):427-33 [1279268] Br J Cancer. 1979 Nov;40(5):782-90 [41564] Cancer Res. 1984 Oct;44(10):4414-9 [6235912] Biochem Biophys Res Commun. 1984 Aug 16;122(3):1450-9 [6477569] J Cell Sci. 1985 Aug;77:209-23 [3841349] Cancer Res. 1987 Oct 15;47(20):5469-75 [2443240] Carcinogenesis. 1987 Nov;8(11):1737-40 [3664968] Proc Natl Acad Sci U S A. 1989 Mar;86(5):1558-62 [2922399] Cancer Res. 1989 Mar 15;49(6):1541-7 [2466557] Blood. 1989 May 15;73(7):1794-800 [2469500] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Identification of a binding site for the human immunodeficiency virus type 1 nucleocapsid protein. AN - 75773355; 8506369 AB - The nucleocapsid (NC) protein NCp7 of human immunodeficiency virus type 1 (HIV-1) is important for encapsidation of the virus genome, RNA dimerization, and primer tRNA annealing in vitro. Here we present evidence from gel mobility-shift experiments indicating that NCp7 binds specifically to an RNA sequence. Two complexes were identified in native gels. The more slowly migrating complex contained two RNA molecules and one peptide, while the more rapidly migrating one is composed of one RNA and one peptide. Further, mutational analysis of the RNA shows that the predicted stem and loop structure of stem-loop 1 plays a critical role. Our results show that NCp7 binds to a unique RNA structure within the psi region; in addition, this structure is necessary for RNA dimerization. We propose that NCp7 binds to the RNA via a direct interaction of one zinc-binding motif to stem-loop 1 followed by binding of the other zinc-binding motif to stem-loop 1, stem-loop 2, or the linker region of the second RNA molecule, forming a bridge between the two RNAs. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Sakaguchi, K AU - Zambrano, N AU - Baldwin, E T AU - Shapiro, B A AU - Erickson, J W AU - Omichinski, J G AU - Clore, G M AU - Gronenborn, A M AU - Appella, E AD - Laboratory of Cell Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/06/01/ PY - 1993 DA - 1993 Jun 01 SP - 5219 EP - 5223 VL - 90 IS - 11 SN - 0027-8424, 0027-8424 KW - gag KW - Cross-Linking Reagents KW - 0 KW - Peptide Fragments KW - RNA, Viral KW - Viral Core Proteins KW - Bromodeoxyuridine KW - G34N38R2N1 KW - Index Medicus KW - AIDS/HIV KW - Peptide Fragments -- metabolism KW - Ultraviolet Rays KW - Nucleic Acid Conformation KW - Binding Sites KW - Mutagenesis KW - Peptide Fragments -- chemical synthesis KW - Zinc Fingers -- physiology KW - Base Sequence KW - Zinc Fingers -- genetics KW - Molecular Sequence Data KW - Protein Folding KW - Genes, gag KW - Sequence Deletion KW - HIV-1 -- metabolism KW - HIV-1 -- genetics KW - Capsid -- genetics KW - RNA, Viral -- chemistry KW - Viral Core Proteins -- genetics KW - Capsid -- metabolism KW - RNA, Viral -- genetics KW - Viral Core Proteins -- metabolism KW - RNA, Viral -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75773355?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Identification+of+a+binding+site+for+the+human+immunodeficiency+virus+type+1+nucleocapsid+protein.&rft.au=Sakaguchi%2C+K%3BZambrano%2C+N%3BBaldwin%2C+E+T%3BShapiro%2C+B+A%3BErickson%2C+J+W%3BOmichinski%2C+J+G%3BClore%2C+G+M%3BGronenborn%2C+A+M%3BAppella%2C+E&rft.aulast=Sakaguchi&rft.aufirst=K&rft.date=1993-06-01&rft.volume=90&rft.issue=11&rft.spage=5219&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-07 N1 - Date created - 1993-07-07 N1 - Date revised - 2017-01-13 N1 - Gene symbol - gag N1 - SuppNotes - Cited By: Nucleic Acids Res. 1990 Dec 25;18(24):7287-92 [2259624] J Mol Biol. 1990 Dec 5;216(3):689-99 [2124274] Int J Pept Protein Res. 1990 Dec;36(6):551-8 [1708745] J Virol. 1992 Feb;66(2):632-40 [1309906] J Virol. 1992 Jul;66(7):4144-53 [1602537] Proc Natl Acad Sci U S A. 1992 Jul 15;89(14):6472-6 [1631144] Pept Res. 1988 Nov-Dec;1(2):74-80 [2856555] J Virol. 1981 Jan;37(1):109-16 [6260966] J Biol Chem. 1981 Aug 25;256(16):8400-6 [6267042] J Virol. 1985 May;54(2):401-7 [3989912] Anal Biochem. 1987 Nov 1;166(2):368-79 [2449095] EMBO J. 1988 Jun;7(6):1777-83 [2458920] Science. 1989 Apr 7;244(4900):48-52 [2468181] Proc Natl Acad Sci U S A. 1989 Oct;86(20):7706-10 [2479010] J Virol. 1990 Jan;64(1):450-2 [2152832] J Virol. 1990 Feb;64(2):774-83 [2153242] Methods Enzymol. 1989;180:51-62 [2482430] Biochemistry. 1990 Jan 16;29(2):329-40 [2105740] J Mol Biol. 1990 Jan 20;211(2):447-63 [2407856] J Virol. 1990 Jul;64(7):3207-11 [2191147] Comput Appl Biosci. 1990 Oct;6(4):309-18 [1701685] J Biol Chem. 1991 Apr 15;266(11):7306-11 [2016331] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Oxidative stress and thiol modification induced by chronic administration of haloperidol. AN - 75773018; 8509999 AB - Haloperidol, a widely used neuroleptic, acts through blockade of dopamine receptors leading to increased turnover of dopamine. Increased turnover of dopamine could lead to excessive production of hydrogen peroxide and, thus, generate oxidative stress. The effect of chronic administration of haloperidol on glutathione (GSH)-protein thiol homeostasis and lipid peroxidation was examined in rat brain regions. The oxidized GSH levels increased significantly, though not substantially, in cortex (CT, 15%), striatum (ST, 28%) and midbrain (MB, 27%). Maximal decreases in GSH levels were noted in CT (23%), ST (28%) and MB (20%) after 1 month of haloperidol administration. The GSH levels recovered thereafter, and after 6 months of haloperidol treatment, the GSH levels were not significantly different from control in ST and MB. The depleted GSH was recovered essentially as protein-GSH mixed disulfide with a concomitant decrease in the protein thiol concentration in all the three regions of the brain. The increase in oxidized GSH concentration represented only 1.8, 2.0 and 3.5% of the depleted GSH in the CT, ST and MB after 1 month of haloperidol administration. The concentration of thiobarbituric acid-reactive products increased significantly up to 3 months of haloperidol treatment, but at the end of 6 months, the levels were substantially decreased. The present study demonstrates that haloperidol administration for 1 month results in significant oxidative stress in CT, ST and MB regions of the brain, as demonstrated by alterations in GSH-protein thiol homeostasis and increased lipid peroxidation products. However, after prolonged administration of haloperidol for 6 months, the GSH-protein thiol homeostasis is restored to a large extent, concomitant with the decrease in the concentration of lipid peroxidation products. Administration of haloperidol leads to development of tolerance (supersensitivity of the dopamine autoreceptors) to neuroleptics, which is associated with decreased turnover of dopamine; this may result in overcoming the oxidative stress generated initially due to increased dopamine turnover. JF - The Journal of pharmacology and experimental therapeutics AU - Shivakumar, B R AU - Ravindranath, V AD - Department of Neurochemistry, National Institute of Mental Health and Neuro Sciences, Bangalore, India. Y1 - 1993/06// PY - 1993 DA - June 1993 SP - 1137 EP - 1141 VL - 265 IS - 3 SN - 0022-3565, 0022-3565 KW - Sulfhydryl Compounds KW - 0 KW - Malondialdehyde KW - 4Y8F71G49Q KW - Glutathione KW - GAN16C9B8O KW - Haloperidol KW - J6292F8L3D KW - Index Medicus KW - Rats KW - Oxidation-Reduction KW - Malondialdehyde -- metabolism KW - Animals KW - Rats, Sprague-Dawley KW - Sulfhydryl Compounds -- metabolism KW - Brain -- drug effects KW - Brain -- metabolism KW - Homeostasis -- drug effects KW - Haloperidol -- adverse effects KW - Glutathione -- metabolism KW - Haloperidol -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75773018?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.atitle=Oxidative+stress+and+thiol+modification+induced+by+chronic+administration+of+haloperidol.&rft.au=Shivakumar%2C+B+R%3BRavindranath%2C+V&rft.aulast=Shivakumar&rft.aufirst=B&rft.date=1993-06-01&rft.volume=265&rft.issue=3&rft.spage=1137&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.issn=00223565&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-14 N1 - Date created - 1993-07-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Mutagenesis of EIAV TAT reveals structural features essential for transcriptional activation and TAR element recognition. AN - 75772969; 8389074 AB - Certain members of the lentivirus subfamily of retroviruses encode unique transcriptional activator (Tat) proteins that modify the transcription complex after binding to the 5' end of nascent viral mRNA. The Tat proteins are modular, containing RNA-binding and activation domains that can be exchanged between different Tat proteins or replaced with heterologous protein fragments. While there is considerable sequence conservation among the divergent Tat proteins, there are also some structural differences that might be informative. For example, a cluster of basic amino acids in HIV-1 Tat is sufficient for RNA binding in vivo and in vitro. The homologous region of EIAV Tat is necessary but not sufficient for recognition of its cognate cis-acting RNA element; the entire C-terminal 26 amino acids of EIAV Tat, including the basic patch, are required. To better understand the structure-function relationships in EIAV Tat, we have generated a battery of expression plasmids encoding insertion, deletion, and missense mutations in the carboxy-terminal region of the tat gene. The plasmids were tested for their ability to trans-activate the EIAV promoter or to trans-inhibit a heterologous Tat protein. A mutation of a glutamine to an arginine in the cluster of basic residues generated a potent trans-dominant inhibitor of both EIAV and HIV-1 Tat, indicating that the mutation abolished RNA binding but did not alter the activation domain. Mutations at the extreme C-terminus of EIAV Tat impaired both RNA binding and activation domain functions, suggesting effects on secondary or tertiary structure. JF - Virology AU - Derse, D AU - Newbold, S H AD - Laboratory of Viral Carcinogenesis, NCI-Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1993/06// PY - 1993 DA - June 1993 SP - 530 EP - 536 VL - 194 IS - 2 SN - 0042-6822, 0042-6822 KW - Gene Products, tat KW - 0 KW - RNA-Binding Proteins KW - Recombinant Fusion Proteins KW - tat Gene Products, Human Immunodeficiency Virus KW - Index Medicus KW - AIDS/HIV KW - HIV-1 -- genetics KW - DNA Mutational Analysis KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Sequence Homology, Amino Acid KW - Precipitin Tests KW - Transcriptional Activation KW - Structure-Activity Relationship KW - Mutagenesis KW - Promoter Regions, Genetic KW - RNA-Binding Proteins -- genetics KW - Gene Expression Regulation, Viral KW - RNA-Binding Proteins -- immunology KW - Infectious Anemia Virus, Equine -- genetics KW - Transcription, Genetic KW - Gene Products, tat -- immunology KW - Gene Products, tat -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75772969?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Virology&rft.atitle=Mutagenesis+of+EIAV+TAT+reveals+structural+features+essential+for+transcriptional+activation+and+TAR+element+recognition.&rft.au=Derse%2C+D%3BNewbold%2C+S+H&rft.aulast=Derse&rft.aufirst=D&rft.date=1993-06-01&rft.volume=194&rft.issue=2&rft.spage=530&rft.isbn=&rft.btitle=&rft.title=Virology&rft.issn=00426822&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-25 N1 - Date created - 1993-06-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - 2B and 2C mutations are essential but mutations throughout the genome of HAV contribute to adaptation to cell culture. AN - 75771337; 8389072 AB - Chimeric viruses constructed from various portions of two infectious cDNA clones representing the genomes of the wild-type and cell culture-adapted mutants of the HM-175 strain of hepatitis A virus were compared for their ability to replicate in cultures of fetal rhesus kidney cells. Mutations located in either the 5' or 3' third of the genome could markedly enhance growth in vitro but only when they were combined with mutations in the P2 region within either the 2B or the 2C gene. Therefore, mutations in 2B and 2C are essential for cell culture adaptation but mutations elsewhere in the genome also contribute significantly to the enhanced growth rate. JF - Virology AU - Emerson, S U AU - Huang, Y K AU - Purcell, R H AD - Hepatitis Viruses Section, National Institutes of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/06// PY - 1993 DA - June 1993 SP - 475 EP - 480 VL - 194 IS - 2 SN - 0042-6822, 0042-6822 KW - 2B KW - 2C KW - Capsid Proteins KW - 0 KW - DNA, Recombinant KW - DNA, Viral KW - Viral Nonstructural Proteins KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Animals KW - Transfection KW - Cells, Cultured KW - Capsid -- genetics KW - Macaca mulatta KW - DNA, Viral -- genetics KW - Adaptation, Biological KW - Cloning, Molecular KW - Viral Nonstructural Proteins -- genetics KW - Hepatovirus -- growth & development KW - Mutation -- genetics KW - Genome, Viral KW - Hepatovirus -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75771337?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Virology&rft.atitle=2B+and+2C+mutations+are+essential+but+mutations+throughout+the+genome+of+HAV+contribute+to+adaptation+to+cell+culture.&rft.au=Emerson%2C+S+U%3BHuang%2C+Y+K%3BPurcell%2C+R+H&rft.aulast=Emerson&rft.aufirst=S&rft.date=1993-06-01&rft.volume=194&rft.issue=2&rft.spage=475&rft.isbn=&rft.btitle=&rft.title=Virology&rft.issn=00426822&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-25 N1 - Date created - 1993-06-25 N1 - Date revised - 2017-01-13 N1 - Gene symbol - 2B; 2C N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Regulation of gonadotropin-releasing hormone by protein kinase-A and -C in immortalized hypothalamic neurons. AN - 75770896; 8504741 AB - As major signal transduction cascades, the protein kinase-A and -C (PKA and PKC) pathways have been implicated in the regulation of GnRH synthesis and secretion in the hypothalamus. We have investigated the roles of these pathways in the regulation of GnRH transcription, mRNA levels, propeptide processing, and secretion in GT1-7 cells, a mouse hypothalamic GnRH neuronal cell line. Forskolin, which activates adenylate cyclase to raise cAMP levels, had no effect on GnRH mRNA levels at 10 microM, but induced c-fos mRNA at 30 min. An activator of PKC, 12-O-tetradecanoylphorbol-13-acetate (TPA; 100 nM), also induced c-fos at 30 min, but produced a progressive decline in GnRH mRNA, resulting in a 70% decrease by 16 h. Coadministration of 10 nM TPA and 20 microM of a PKC inhibitor, NPC 15437 [2,6-diamino-N-([1-(1-oxotridecyl)2-piperidinyl]methyl)hexanami de], prevented c-fos induction, but did not antagonize GnRH repression. Instead, the inhibitor itself reduced GnRH mRNA levels by 56% at 16 h (with no effect on c-fos mRNA). Thus, since extended exposure to TPA can down-regulate PKC, suppression of GnRH mRNA by TPA may be due to decreased PKC activity, indicating a role for PKC in the maintenance of the GnRH gene expression (a role that is unlikely to involve c-fos). In transient transfections, the transcriptional activity from 3 kilobases of GnRH 5'-flanking sequence was repressed 2-fold by either 100 nM TPA or 20 microM NPC 15437 at 24 h, demonstrating that suppression of GnRH mRNA is at least, in part, at the level of transcription. In contrast, both TPA (100 nM) and forskolin (10 microM) stimulated secretion. Enhancement of GnRH secretion by TPA was robust and rapid (2.5 min), while the response to forskolin was relatively delayed (2 h). Over a 24-h period, unstimulated cells released primarily unprocessed prohormone, whereas forskolin and TPA stimulated the secretion of processed products. These data indicate that PKC and PKA may influence propeptide processing and/or the route of GnRH secretion. These data demonstrate that the PKA and PKC pathways regulate GnRH at the multiple levels of transcription, pro-GnRH processing, and GnRH secretion. JF - Endocrinology AU - Wetsel, W C AU - Eraly, S A AU - Whyte, D B AU - Mellon, P L AD - Laboratory of Molecular and Integrative Neuroscience, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993/06// PY - 1993 DA - June 1993 SP - 2360 EP - 2370 VL - 132 IS - 6 SN - 0013-7227, 0013-7227 KW - Oligonucleotide Probes KW - 0 KW - Piperidines KW - Protein Precursors KW - RNA, Messenger KW - progonadoliberin I KW - NPC 15437 KW - 136449-85-9 KW - Colforsin KW - 1F7A44V6OU KW - Gonadotropin-Releasing Hormone KW - 33515-09-2 KW - Protein Kinases KW - EC 2.7.- KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Piperidines -- pharmacology KW - Protein Processing, Post-Translational -- drug effects KW - Animals KW - Colforsin -- pharmacology KW - Base Sequence KW - Transcription, Genetic -- drug effects KW - Protein Precursors -- metabolism KW - Oligonucleotide Probes -- genetics KW - RNA, Messenger -- metabolism KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Cell Line, Transformed KW - Gonadotropin-Releasing Hormone -- metabolism KW - Protein Kinase C -- antagonists & inhibitors KW - Protein Kinases -- physiology KW - Neurons -- metabolism KW - Neurons -- drug effects KW - Hypothalamus -- metabolism KW - Neurons -- cytology KW - Hypothalamus -- cytology KW - Protein Kinase C -- physiology KW - Gonadotropin-Releasing Hormone -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75770896?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Endocrinology&rft.atitle=Regulation+of+gonadotropin-releasing+hormone+by+protein+kinase-A+and+-C+in+immortalized+hypothalamic+neurons.&rft.au=Wetsel%2C+W+C%3BEraly%2C+S+A%3BWhyte%2C+D+B%3BMellon%2C+P+L&rft.aulast=Wetsel&rft.aufirst=W&rft.date=1993-06-01&rft.volume=132&rft.issue=6&rft.spage=2360&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=00137227&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-02 N1 - Date created - 1993-07-02 N1 - Date revised - 2017-01-24 N1 - Last updated - 2017-01-25 ER - TY - JOUR T1 - Mechanisms of nitric oxide-mediated neurotoxicity in primary brain cultures. AN - 75756910; 7684776 AB - In addition to mediating several physiological functions, nitric oxide (NO) has been implicated in the cytotoxicities observed following activation of macrophages or excess stimulation of neurons by glutamate. We extend our previous observations of glutamate-stimulated, NO-mediated neurotoxicity in primary cultures of rat fetal cortical, striatal, and hippocampal neurons. Neurotoxicity elicited by either NMDA or sodium nitroprusside (SNP) exhibits a similar concentration-effect relationship and time course. The concentration-effect curve of NMDA-induced neurotoxicity is shifted to the right in the presence of nitro-L-arginine and farther to the right in arginine-free media. The rank order of potency of several NO synthase (NOS) inhibitors in preventing neurotoxicity is the same as the rank order of these compounds in inhibiting NOS, and this inhibition is stereospecific. NMDA neurotoxicity is also prevented by flavoprotein inhibitors and calmodulin inhibitors, fitting with the roles of flavoproteins and calmodulin as NOS regulators. 8-Bromo-cGMP and guanylyl cyclase inhibitors do not affect neurotoxicity, while superoxide dismutase attenuates neurotoxicity. NOS neurons appear to be the source of neurotoxic NO in culture, as lesions of these neurons with 20 microM quisqualate diminish subsequent NMDA neurotoxicity. Moreover, NMDA neurotoxicity develops over time in culture coincident with the expression of NOS. Immunohistochemical localization of NOS in cultures and intact brain demonstrates widespread distribution of the cell processes suggesting that NOS neurons contact the majority of cortical neurons and so could mediate widespread neurotoxicity. JF - The Journal of neuroscience : the official journal of the Society for Neuroscience AU - Dawson, V L AU - Dawson, T M AU - Bartley, D A AU - Uhl, G R AU - Snyder, S H AD - National Institute on Drug Abuse, Addiction Research Center, Laboratory of Molecular Neurobiology, Baltimore, Maryland 21224. Y1 - 1993/06// PY - 1993 DA - June 1993 SP - 2651 EP - 2661 VL - 13 IS - 6 SN - 0270-6474, 0270-6474 KW - Neurotoxins KW - 0 KW - Superoxides KW - 11062-77-4 KW - Nitric Oxide KW - 31C4KY9ESH KW - N-Methylaspartate KW - 6384-92-5 KW - Nitric Oxide Synthase KW - EC 1.14.13.39 KW - Amino Acid Oxidoreductases KW - EC 1.4.- KW - Cyclic GMP KW - H2D2X058MU KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Rats KW - Animals KW - Superoxides -- pharmacology KW - Amino Acid Oxidoreductases -- metabolism KW - N-Methylaspartate -- pharmacology KW - Cells, Cultured KW - Amino Acid Oxidoreductases -- antagonists & inhibitors KW - Cyclic GMP -- physiology KW - Calcium -- physiology KW - Neurons -- enzymology KW - Brain -- cytology KW - Brain -- drug effects KW - Nitric Oxide -- metabolism KW - Neurotoxins -- pharmacology KW - Brain -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75756910?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+neuroscience+%3A+the+official+journal+of+the+Society+for+Neuroscience&rft.atitle=Mechanisms+of+nitric+oxide-mediated+neurotoxicity+in+primary+brain+cultures.&rft.au=Dawson%2C+V+L%3BDawson%2C+T+M%3BBartley%2C+D+A%3BUhl%2C+G+R%3BSnyder%2C+S+H&rft.aulast=Dawson&rft.aufirst=V&rft.date=1993-06-01&rft.volume=13&rft.issue=6&rft.spage=2651&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+neuroscience+%3A+the+official+journal+of+the+Society+for+Neuroscience&rft.issn=02706474&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-28 N1 - Date created - 1993-06-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Parameters affecting the development of non-Hodgkin's lymphoma in patients with severe human immunodeficiency virus infection receiving antiretroviral therapy. AN - 75754273; 8099121 AB - To investigate the occurrence of non-Hodgkin's lymphoma (NHL) in human immunodeficiency virus (HIV)-infected patients receiving long-term antiretroviral therapy and factors associated with the development of these lymphomas. The charts of 55 patients with advanced HIV infection receiving zidovudine (formerly known as azidothymidine [AZT])-based therapy and 61 patients receiving dideoxyinosine (ddI) were examined for the occurrence of NHL. Stored samples from the AZT-based treatment cohort were examined retrospectively for parameters predictive of the subsequent development of lymphoma. Eight of 55 patients receiving AZT-based therapy developed NHL, yielding an estimated probability of 12% (95% confidence interval [CI], 4.7% to 27.1%) after 24 months, and 29.2% (95% CI, 15.2% to 48.7%) after 36 months. Four of 61 patients receiving ddI developed NHL, yielding a 6.2% (95% CI, 2.1% to 17%) estimated probability after 24 months, and 9.5% (95% CI, 3.6% to 22.8%) after 36 months. The difference between these cohorts was not significant (two-tailed P [P2] = .13). Patients with less than 50 CD4 cells/microL developed NHL at a significantly higher rate (P2 = .0085). This was particularly true for patients who presented with primary CNS lymphoma (PCNSL). For patients receiving AZT-based therapy, pretreatment serum interleukin-6 (IL-6) levels were somewhat higher in those who subsequently developed NHL than in those who did not (P2 = .048). HIV-infected patients with profound immunodeficiency, especially those with less than 50 CD4 cells/microL, are at substantial risk of developing NHL and particularly PCNSL. Additional studies are needed to define the role of other factors such as IL-6 in the pathogenesis of these opportunistic tumors. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Pluda, J M AU - Venzon, D J AU - Tosato, G AU - Lietzau, J AU - Wyvill, K AU - Nelson, D L AU - Jaffe, E S AU - Karp, J E AU - Broder, S AU - Yarchoan, R AD - Medicine Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/06// PY - 1993 DA - June 1993 SP - 1099 EP - 1107 VL - 11 IS - 6 SN - 0732-183X, 0732-183X KW - Interleukin-6 KW - 0 KW - Zidovudine KW - 4B9XT59T7S KW - Didanosine KW - K3GDH6OH08 KW - Index Medicus KW - AIDS/HIV KW - Interleukin-6 -- blood KW - Risk Factors KW - Humans KW - Leukocyte Count KW - CD4-Positive T-Lymphocytes KW - Zidovudine -- therapeutic use KW - Didanosine -- therapeutic use KW - Lymphoma, AIDS-Related -- immunology KW - Zidovudine -- adverse effects KW - HIV Infections -- complications KW - HIV Infections -- immunology KW - HIV Infections -- drug therapy KW - Lymphoma, Non-Hodgkin -- etiology KW - Didanosine -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75754273?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=Parameters+affecting+the+development+of+non-Hodgkin%27s+lymphoma+in+patients+with+severe+human+immunodeficiency+virus+infection+receiving+antiretroviral+therapy.&rft.au=Pluda%2C+J+M%3BVenzon%2C+D+J%3BTosato%2C+G%3BLietzau%2C+J%3BWyvill%2C+K%3BNelson%2C+D+L%3BJaffe%2C+E+S%3BKarp%2C+J+E%3BBroder%2C+S%3BYarchoan%2C+R&rft.aulast=Pluda&rft.aufirst=J&rft.date=1993-06-01&rft.volume=11&rft.issue=6&rft.spage=1099&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=0732183X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-29 N1 - Date created - 1993-06-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - cDNA cloning, chromosomal mapping, and functional characterization of the human peroxisome proliferator activated receptor. AN - 75752033; 7684926 AB - The human peroxisome proliferator activated receptor (hPPAR) was cloned from a human liver cDNA library. The cDNA exhibited 85% and 91% DNA and deduced amino acid sequence identity with mouse PPAR (mPPAR), respectively. The hPPAR gene was mapped on human chromosome 22 slightly telomeric to a linkage group of six genes and genetic markers that are located in the general region 22q12-q13.1. Cotransfection assays of mouse Hepa 1 cells were used to roughly compare the ability of hPPAR- and mPPAR-expressed cDNAs to trans-activate the acyl CoA oxidase (ACO) PPAR response element located 5' upstream to the minimal thymidine kinase promoter driving the expression of the chloramphenicol acetyl transferase (CAT) reporter gene. Both receptors elicited a response with the prototypical peroxisome proliferators nafenopin, clofibrate, and WY-14,643. Moreover, using cotransfection assays in which the CAT reporter plasmid contained the CYP4 A6 gene response element rather than the ACO element, it was shown that hPPAR is capable of very efficiently trans-activating a second PPAR response element. These results indicate that the PPAR is present in humans in a form that is functional and can trans-activate response elements derived from two different genes, the rat ACO and the rabbit CYP4A6. JF - Biochemistry AU - Sher, T AU - Yi, H F AU - McBride, O W AU - Gonzalez, F J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1993/06/01/ PY - 1993 DA - 1993 Jun 01 SP - 5598 EP - 5604 VL - 32 IS - 21 SN - 0006-2960, 0006-2960 KW - Oligodeoxyribonucleotides KW - 0 KW - Pyrimidines KW - Receptors, Cell Surface KW - Receptors, Cytoplasmic and Nuclear KW - Transcription Factors KW - Nafenopin KW - 093W78U96W KW - pirinixic acid KW - 86C4MRT55A KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Mixed Function Oxygenases KW - EC 1.- KW - Oxidoreductases KW - Cytochrome P-450 CYP4A KW - EC 1.14.15.3 KW - Acyl-CoA Oxidase KW - EC 1.3.3.6 KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Thymidine Kinase KW - EC 2.7.1.21 KW - Deoxyribonuclease HpaII KW - EC 3.1.21.- KW - Deoxyribonucleases, Type II Site-Specific KW - EC 3.1.21.4 KW - TCGA-specific type II deoxyribonucleases KW - Clofibrate KW - HPN91K7FU3 KW - Index Medicus KW - Genetic Linkage KW - Animals KW - Humans KW - Chromosome Mapping KW - Rats KW - Promoter Regions, Genetic KW - Lod Score KW - Molecular Sequence Data KW - Microbodies -- ultrastructure KW - Microbodies -- drug effects KW - Microbodies -- metabolism KW - Gene Library KW - Cytochrome P-450 Enzyme System -- genetics KW - Nafenopin -- pharmacology KW - Pyrimidines -- pharmacology KW - Rabbits KW - Amino Acid Sequence KW - Mice KW - Chloramphenicol O-Acetyltransferase -- metabolism KW - Transcription Factors -- genetics KW - Cloning, Molecular KW - Clofibrate -- pharmacology KW - Polymerase Chain Reaction KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Base Sequence KW - Oxidoreductases -- genetics KW - Thymidine Kinase -- genetics KW - Mixed Function Oxygenases -- genetics KW - Chromosomes, Human, Pair 22 KW - Polymorphism, Restriction Fragment Length KW - DNA -- genetics KW - Receptors, Cell Surface -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75752033?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemistry&rft.atitle=cDNA+cloning%2C+chromosomal+mapping%2C+and+functional+characterization+of+the+human+peroxisome+proliferator+activated+receptor.&rft.au=Sher%2C+T%3BYi%2C+H+F%3BMcBride%2C+O+W%3BGonzalez%2C+F+J&rft.aulast=Sher&rft.aufirst=T&rft.date=1993-06-01&rft.volume=32&rft.issue=21&rft.spage=5598&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-06 N1 - Date created - 1993-07-06 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - S60099; GENBANK; L16878; L02932; L16873; L11867; L11866; L11865; L16876; L16875; L16874 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Dissociation of progeny vaccinia virus from the cell membrane is regulated by a viral envelope glycoprotein: effect of a point mutation in the lectin homology domain of the A34R gene. AN - 75751129; 8497053 AB - Vaccinia virus strains vary considerably in the amounts of extracellular enveloped virus (EEV) that they release from infected cells. The IHD-J strain produces up to 40 times more EEV than does the related WR strain and consequently generates elongated comet-shaped virus plaques instead of sharply defined round ones in susceptible monolayer cells under liquid medium. The difference in EEV formation is due to the retention of enveloped WR virions on the cell surface (R. Blasco and B. Moss, J. Virol. 66:4170-4179, 1992). By using WR and IHD-J DNA fragments for marker transfer and analyzing the progeny virus by the comet formation assay, we determined that gene A34R and at least one other gene regulate the release of cell-associated virions. Replacement of the A34R gene of WR with the corresponding gene from IHD-J increased the amount of EEV produced by 10-fold and conferred the ability to form distinctive comet-shaped plaques. Gene A34R encodes an EEV-specific glycoprotein with homology to C-type animal lectins (S.A. Duncan and G.L. Smith, J. Virol. 66:1610-1621, 1992). The nucleotide sequences of the A34R genes of WR and IHD-J strains differed in six positions, of which four were silent. One of the codon mutations (Lys-151-->Glu), which is located in the putative carbohydrate recognition domain, was sufficient to transfer a comet-forming phenotype to WR virus. These data indicate that the A34R-encoded glycoprotein is involved, through its lectin homology domain, in the retention of progeny virus on the surface of parental cells and raise the possibility that the protein also has a role in virus attachment to uninfected cells. JF - Journal of virology AU - Blasco, R AU - Sisler, J R AU - Moss, B AD - Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1993/06// PY - 1993 DA - June 1993 SP - 3319 EP - 3325 VL - 67 IS - 6 SN - 0022-538X, 0022-538X KW - A34R KW - A34R protein, Vaccina virus KW - 0 KW - Glycoproteins KW - Viral Envelope Proteins KW - Index Medicus KW - Phenotype KW - Mutagenesis, Site-Directed KW - Animals KW - Base Sequence KW - Viral Plaque Assay KW - DNA Mutational Analysis KW - Molecular Sequence Data KW - Biological Transport KW - Cosmids KW - Sequence Analysis, DNA KW - Chromosome Mapping KW - Vaccinia virus -- genetics KW - Genes, Viral -- genetics KW - Vaccinia virus -- growth & development KW - Point Mutation KW - Cell Membrane -- metabolism KW - Glycoproteins -- genetics KW - Viral Envelope Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75751129?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Dissociation+of+progeny+vaccinia+virus+from+the+cell+membrane+is+regulated+by+a+viral+envelope+glycoprotein%3A+effect+of+a+point+mutation+in+the+lectin+homology+domain+of+the+A34R+gene.&rft.au=Blasco%2C+R%3BSisler%2C+J+R%3BMoss%2C+B&rft.aulast=Blasco&rft.aufirst=R&rft.date=1993-06-01&rft.volume=67&rft.issue=6&rft.spage=3319&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-21 N1 - Date created - 1993-06-21 N1 - Date revised - 2017-01-13 N1 - Gene symbol - A34R N1 - SuppNotes - Cited By: Virology. 1971 Dec;46(3):507-32 [4944855] J Gen Virol. 1991 Jun;72 ( Pt 6):1349-76 [2045793] Virology. 1976 Aug;73(1):43-58 [960564] J Virol. 1978 Jul;27(1):28-37 [691112] J Virol. 1991 Nov;65(11):5910-20 [1920620] Virology. 1992 Mar;187(1):251-60 [1736527] J Virol. 1992 Mar;66(3):1610-21 [1738204] Virology. 1992 Jun;188(2):801-10 [1585649] J Virol. 1992 Jul;66(7):4170-9 [1602540] J Gen Virol. 1992 Nov;73 ( Pt 11):2887-902 [1331292] J Virol. 1992 Dec;66(12):7217-24 [1433514] Nature. 1992 Nov 12;360(6400):127-34 [1436090] J Virol. 1979 Jul;31(1):147-55 [501796] J Virol. 1979 Nov;32(2):614-22 [501802] J Gen Virol. 1980 Sep;50(1):89-100 [7441216] J Virol. 1981 Sep;39(3):903-13 [7288920] J Virol. 1982 Jul;43(1):136-49 [6286993] J Gen Virol. 1985 Mar;66 ( Pt 3):643-6 [3973566] Virology. 1986 Apr 30;150(2):451-62 [3008418] J Virol. 1986 Jun;58(3):757-64 [3701927] Virology. 1986 Nov;155(1):97-105 [3465088] J Virol. 1987 Jun;61(6):1765-71 [3033308] J Biol Chem. 1988 Jul 15;263(20):9557-60 [3290208] Nucleic Acids Res. 1990 Sep 25;18(18):5347-51 [2216706] Virology. 1990 Nov;179(1):247-66, 517-63 [2219722] J Virol. 1991 Jul;65(7):3435-42 [2041074] Prog Med Virol. 1973;16:86-108 [4356899] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Pharmacokinetics of piroxantrone in a phase I trial of piroxantrone and granulocyte-colony stimulating factor. AN - 75746091; 7684320 AB - Piroxantrone is an anthrapyrazole derivative with broad antitumor activity in vitro. In previous phase I trials, the dose-limiting toxicity of this agent was myelosuppression. Therefore, a phase I and pharmacokinetic study of a 1-h infusion of piroxantrone in combination with granulocyte-colony stimulating factor was conducted. In this article, we report the results of the pharmacokinetic analysis. Thirty-seven patients were studied over a dosage range of 150 to 555 mg/m2. The plasma elimination of piroxantrone was biexponential with a mean (+/- SD) t1/2 alpha of 3.2 +/- 2.7 min and a mean (+/- SD) t1/2 beta of 82 +/- 92 min. Clearance was 840 +/- 230 ml/min/m2. A limited sampling strategy was developed to allow the estimation of total drug exposure (area under the plasma concentration-time curve) from the plasma piroxantrone concentrations at 30, 60, and 120 min after the start of the infusion. The pharmacokinetic behavior of a presumed piroxantrone metabolite not previously described in plasma was also characterized. Based on in vitro cytotoxicity studies with partially purified extract of this compound, we do not believe that it contributes to the antitumor effects of piroxantrone at the concentrations observed in plasma. Finally, piroxantrone elimination was linear over the nearly 4-fold dose range studied, indicating that when dose adjustments are made, systemic drug exposure will remain predictable. JF - Cancer research AU - Berg, S L AU - Savarese, D M AU - Balis, F M AU - Denicoff, A M AU - Hillig, M AU - O'Shaughnessy, J A AU - Poplack, D G AU - Cowan, K H AD - Pediatric Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1993/06/01/ PY - 1993 DA - 1993 Jun 01 SP - 2587 EP - 2590 VL - 53 IS - 11 SN - 0008-5472, 0008-5472 KW - Anthraquinones KW - 0 KW - Antineoplastic Agents KW - Pyrazoles KW - Granulocyte Colony-Stimulating Factor KW - 143011-72-7 KW - piroxantrone KW - YL4TY9WH22 KW - Index Medicus KW - Humans KW - Adult KW - Pyrazoles -- administration & dosage KW - Neoplasms -- drug therapy KW - Pyrazoles -- urine KW - Antineoplastic Agents -- administration & dosage KW - Antineoplastic Agents -- pharmacokinetics KW - Anthraquinones -- administration & dosage KW - Anthraquinones -- pharmacokinetics KW - Granulocyte Colony-Stimulating Factor -- administration & dosage KW - Antineoplastic Agents -- blood KW - Anthraquinones -- urine KW - Anthraquinones -- blood KW - Antineoplastic Agents -- urine KW - Pyrazoles -- blood KW - Pyrazoles -- pharmacokinetics KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75746091?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Pharmacokinetics+of+piroxantrone+in+a+phase+I+trial+of+piroxantrone+and+granulocyte-colony+stimulating+factor.&rft.au=Berg%2C+S+L%3BSavarese%2C+D+M%3BBalis%2C+F+M%3BDenicoff%2C+A+M%3BHillig%2C+M%3BO%27Shaughnessy%2C+J+A%3BPoplack%2C+D+G%3BCowan%2C+K+H&rft.aulast=Berg&rft.aufirst=S&rft.date=1993-06-01&rft.volume=53&rft.issue=11&rft.spage=2587&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-21 N1 - Date created - 1993-06-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Nonpromoting 12-deoxyphorbol 13-esters inhibit phorbol 12-myristate 13-acetate induced tumor promotion in CD-1 mouse skin. AN - 75746033; 8495413 AB - Prostratin and 12-deoxyphorbol 13-phenylacetate (dPP) form a new class of protein kinase C activators of unique biological activity. Although they bind to and activate protein kinase C, in mouse skin they either fail to induce typical phorbol ester (PMA) effects (e.g., hyperplasia) or induce only partial response (e.g., inflammation). Furthermore, pretreatment with these agents inhibits a range of PMA induced effects (acute and chronic hyperplasia, inflammation, etc.) These observations suggested that prostratin and dPP would function as inhibitors of phorbol ester tumor promotion. Here we verify that prediction. We report that both compounds reduced both the average number of papillomas and the tumor incidence in a tumor promotion schedule in CD-1 mouse skin, in which each PMA application was preceded by 12-deoxyphorbol 13-monoester pretreatment. The highest dose of prostratin used (2.56 mumol or 1 mg/pretreatment) caused a 96% (23-fold) reduction in the average number of papillomas with a decrease of tumor incidence from 97 to 40%. The highest dose of dPP used (21.4 nmol or 10 micrograms/pretreatment) induced an 86% (7-fold) reduction in the average number of papillomas with a 53% reduction of tumor incidence from 100 to 47%. The inhibitory effect was dose dependent. The dose causing 50% inhibition was 11 nmol/pretreatment for prostratin and 0.8 nmol/pretreatment for dPP. Maximal inhibition of tumor promotion was accompanied by a block of epidermal hyperplasia; however, significant inhibition of tumor induction was observed at doses without any apparent effect on the PMA induced hyperplasia. JF - Cancer research AU - Szallasi, Z AU - Krsmanovic, L AU - Blumberg, P M AD - Molecular Mechanisms of Tumor Promotion Section, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1993/06/01/ PY - 1993 DA - 1993 Jun 01 SP - 2507 EP - 2512 VL - 53 IS - 11 SN - 0008-5472, 0008-5472 KW - Phorbol Esters KW - 0 KW - 9,10-Dimethyl-1,2-benzanthracene KW - 57-97-6 KW - 12-deoxyphorbolphenylacetate KW - 58821-98-0 KW - prostratin KW - 60857-08-1 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Drug Administration Schedule KW - Dose-Response Relationship, Drug KW - Mice KW - Female KW - Phorbol Esters -- pharmacology KW - Papilloma -- prevention & control KW - Skin Neoplasms -- chemically induced KW - Phorbol Esters -- administration & dosage KW - Skin Neoplasms -- prevention & control KW - Papilloma -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75746033?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Nonpromoting+12-deoxyphorbol+13-esters+inhibit+phorbol+12-myristate+13-acetate+induced+tumor+promotion+in+CD-1+mouse+skin.&rft.au=Szallasi%2C+Z%3BKrsmanovic%2C+L%3BBlumberg%2C+P+M&rft.aulast=Szallasi&rft.aufirst=Z&rft.date=1993-06-01&rft.volume=53&rft.issue=11&rft.spage=2507&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-21 N1 - Date created - 1993-06-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Kinetics of serum and cellular interleukin-5 in posttreatment eosinophilia of patients with lymphatic filariasis. AN - 75744893; 8501330 AB - Peripheral blood eosinophil counts and serum levels and in vitro production of eosinophilopoietic cytokines were assessed before and at frequent intervals after diethylcarbamazine treatment of Bancroftian filariasis. Eosinophil counts peaked at day 7 after the start of treatment (359% +/- 118% of pretreatment levels) and declined to pretreatment levels by day 17. Serum interleukin (IL)-5, undetectable in 14 of 15 patients before treatment, rose sharply but transiently, with peak levels (32 +/- 7 pg/mL) 2 days after diethylcarbamazine treatment. Granulocyte-macrophage colony-stimulating factor and IL-3 were not detectable in serum at any time. In vitro mitogen-induced IL-5 levels decreased significantly in 7 of 9 patients 3 days after treatment when serum IL-5 was at near-peak levels. By day 10 IL-5 values increased in 8 of 9 patients compared with treatment values (P < .02). These data define the temporal relation between serum IL-5 levels and the subsequent development of eosinophilia and suggest that lymphocytes are the source of IL-5. JF - The Journal of infectious diseases AU - Limaye, A P AU - Ottesen, E A AU - Kumaraswami, V AU - Abrams, J S AU - Regunathan, J AU - Vijayasekaran, V AU - Jayaraman, K AU - Nutman, T B AD - Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/06// PY - 1993 DA - June 1993 SP - 1396 EP - 1400 VL - 167 IS - 6 SN - 0022-1899, 0022-1899 KW - Interleukin-5 KW - 0 KW - Ionomycin KW - 56092-81-0 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Diethylcarbamazine KW - V867Q8X3ZD KW - Abridged Index Medicus KW - Index Medicus KW - Kinetics KW - Humans KW - Adult KW - Eosinophils -- metabolism KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Ionomycin -- pharmacology KW - Adolescent KW - Diethylcarbamazine -- therapeutic use KW - Male KW - Interleukin-5 -- metabolism KW - Elephantiasis, Filarial -- immunology KW - Interleukin-5 -- blood KW - Eosinophilia -- immunology KW - Elephantiasis, Filarial -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75744893?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+infectious+diseases&rft.atitle=Kinetics+of+serum+and+cellular+interleukin-5+in+posttreatment+eosinophilia+of+patients+with+lymphatic+filariasis.&rft.au=Limaye%2C+A+P%3BOttesen%2C+E+A%3BKumaraswami%2C+V%3BAbrams%2C+J+S%3BRegunathan%2C+J%3BVijayasekaran%2C+V%3BJayaraman%2C+K%3BNutman%2C+T+B&rft.aulast=Limaye&rft.aufirst=A&rft.date=1993-06-01&rft.volume=167&rft.issue=6&rft.spage=1396&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+infectious+diseases&rft.issn=00221899&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-29 N1 - Date created - 1993-06-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Topical application of T-2 toxin inhibits the contact hypersensitivity response in BALB/c mice. AN - 75744606; 8496607 AB - T-2 toxin, a trichothecene mycotoxin, has previously been shown to alter immune functions and promote skin tumors. We demonstrate that topically applied T-2 toxin reduces the ear swelling response to oxazolone challenge in BALB/c mice. For this reduction in ear swelling to occur, toxin application must be at, or within, 1 h after challenge. Dose-response studies showed a 44% reduction in ear swelling with 30 ng of T-2 toxin as compared with a similar reduction with 300 ng of dexamethasone. T-2 toxin did not affect Ag transport from the challenge site to the draining lymph nodes as measured by FITC transport. However, T-2 toxin significantly reduced both MHC class II (Ia) expression and Ag presentation at the same concentrations. Because T-2 toxin, a known protein synthesis inhibitor, was found to inhibit protein synthesis in epidermal cell cultures as measured by [3H]-leucine incorporation, cycloheximide was also examined. Cycloheximide reduced both oxazolone-induced ear swelling and Ag presentation in a similar manner to T-2 toxin. One mechanism of action for T-2 toxin in reducing the contact hypersensitivity response is via inhibition of protein synthesis and effective Ag presentation by epidermal Langerhans cells. This may involve alterations in Ia Ag expression, although a role for class II in the induction phase of the contact hypersensitivity response has not been established definitively. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Blaylock, B L AU - Kouchi, Y AU - Comment, C E AU - Pollock, P L AU - Luster, M I AD - Environmental Immunology Section, National Institute of Environmental Health Sciences/NIH, Research Triangle Park, NC 27709. Y1 - 1993/06/01/ PY - 1993 DA - 1993 Jun 01 SP - 5135 EP - 5143 VL - 150 IS - 11 SN - 0022-1767, 0022-1767 KW - Histocompatibility Antigens Class II KW - 0 KW - Protein Synthesis Inhibitors KW - Oxazolone KW - 15646-46-5 KW - Cycloheximide KW - 98600C0908 KW - T-2 Toxin KW - I3FL5NM3MO KW - Abridged Index Medicus KW - Index Medicus KW - Protein Biosynthesis KW - Animals KW - Langerhans Cells -- drug effects KW - Oxazolone -- toxicity KW - Cell Movement -- immunology KW - Mice KW - Histocompatibility Antigens Class II -- analysis KW - Langerhans Cells -- metabolism KW - Mice, Inbred BALB C KW - Langerhans Cells -- immunology KW - Protein Synthesis Inhibitors -- toxicity KW - Biological Transport -- immunology KW - Cells, Cultured KW - Cycloheximide -- pharmacology KW - Kinetics KW - Administration, Topical KW - Female KW - Dermatitis, Allergic Contact -- immunology KW - Dermatitis, Allergic Contact -- prevention & control KW - T-2 Toxin -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75744606?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=Topical+application+of+T-2+toxin+inhibits+the+contact+hypersensitivity+response+in+BALB%2Fc+mice.&rft.au=Blaylock%2C+B+L%3BKouchi%2C+Y%3BComment%2C+C+E%3BPollock%2C+P+L%3BLuster%2C+M+I&rft.aulast=Blaylock&rft.aufirst=B&rft.date=1993-06-01&rft.volume=150&rft.issue=11&rft.spage=5135&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.issn=00221767&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-22 N1 - Date created - 1993-06-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Growth regulation of primary rat tracheal epithelial cell cultures by endogenous transforming growth factor-beta s. AN - 75741714; 8491788 AB - Primary rat tracheal epithelial (RTE) cell cultures have previously been shown to secrete transforming growth factor-beta (TGF beta) and to be growth inhibited by exogenous TGF beta. The purpose of the present studies was to determine whether the endogenous TGF beta(s) were regulating the growth of RTE cell cultures and, if so, which isoforms were involved. Neutralizing antibodies specific to TGF beta 1 and TGF beta 2 were added to cultures, and their effects on several growth parameters were measured. Addition of antibodies to early cultures (day 1), resulted in 1.8- and 3-fold increases in colony formation and cell number, respectively, above control IgG-treated cultures. Antibody dose-response experiments revealed that TGF beta 2 was the predominant isoform inhibiting early RTE cell growth. The antibody treatments resulted in similar stimulation of early growth at low and high seeding densities, suggesting that the endogenous TGF beta s were acting locally. Anti-TGF beta 1 treatment of cultures at various stages of growth resulted in 1.2-1.7-fold increases in DNA synthesis above controls, whereas anti-TGF beta 2 treatment resulted in increased DNA synthesis only in early and late cultures (1.7- and 2.5-fold, respectively), but not during midlogarithmic growth. Continuous treatment with a combination of both antibodies resulted in increased growth and decreased exfoliation in early cultures, but had no effect on the slow down of growth in late cultures. Thus endogenous TGF beta s inhibited primarily early growth and contributed to, but did not appear to be responsible for, plateau of growth in late stage cultures. Antibody treatment of secondary cultures resulted in 4-70-fold increases in colony formation, depending on the age of the primary cultures when replated, indicating that endogenous production of both TGF beta 1 and TGF beta 2 greatly inhibits the subculturability of primary RTE cells. Other experiments suggested that cholera toxin enhances RTE cell growth in part by counteracting the inhibitory effects of endogenous TGF beta s. JF - Journal of cellular physiology AU - Rundhaug, J E AU - Nettesheim, P AD - Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993/06// PY - 1993 DA - June 1993 SP - 483 EP - 493 VL - 155 IS - 3 SN - 0021-9541, 0021-9541 KW - Antibodies KW - 0 KW - Transforming Growth Factor beta KW - DNA KW - 9007-49-2 KW - Cholera Toxin KW - 9012-63-9 KW - Index Medicus KW - Animals KW - Cell Count KW - Cholera Toxin -- pharmacology KW - DNA -- biosynthesis KW - Rats KW - Rats, Inbred F344 KW - Epithelial Cells KW - Cells, Cultured KW - Cell Death KW - Epithelium -- metabolism KW - Male KW - Cell Division KW - Transforming Growth Factor beta -- biosynthesis KW - Transforming Growth Factor beta -- pharmacology KW - Trachea -- metabolism KW - Trachea -- cytology KW - Transforming Growth Factor beta -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75741714?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+cellular+physiology&rft.atitle=Growth+regulation+of+primary+rat+tracheal+epithelial+cell+cultures+by+endogenous+transforming+growth+factor-beta+s.&rft.au=Rundhaug%2C+J+E%3BNettesheim%2C+P&rft.aulast=Rundhaug&rft.aufirst=J&rft.date=1993-06-01&rft.volume=155&rft.issue=3&rft.spage=483&rft.isbn=&rft.btitle=&rft.title=Journal+of+cellular+physiology&rft.issn=00219541&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-17 N1 - Date created - 1993-06-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Mutation of the serine 15 phosphorylation site of human p53 reduces the ability of p53 to inhibit cell cycle progression. AN - 75737894; 8502477 AB - Overexpression of wild-type p53 prevents cells from entering the S phase of the cell cycle. The amino-terminal transactivation region of p53 is phosphorylated by several protein kinases, including DNA-PK, a nuclear serine/threonine protein kinase that in vitro requires DNA for activity. DNA-PK was recently shown to phosphorylate serines 15 and 37 of human p53 (Lees-Miller et al., 1992. Mol. Cell. Biol., 12, 5041-5049). To prevent phosphorylation at these sites, mutants were constructed that changed the codons for serine 15 or serine 37 to alanine codons. Expression of p53-Ala-37 in stably transformed T98G cells blocked progression of the cells into S phase as well as did the expression of wild-type p53. In contrast, p53-Ala-15 was partially defective in blocking cell cycle progression. Several cell clones transformed with the mutant p53-Ala-15 gene expressed normal levels of p53 mRNA but accumulated little or no detectable p53 protein. However, by using a transient expression system driven by a strong cytomegalovirus promoter, we showed that the inability of p53-Ala-15 to fully block cell cycle progression was not due to inadequate levels of expression or to a failure of the mutant protein to accumulate in the nucleus. These results suggest that phosphorylation of Ser-15 may affect p53 function. JF - Oncogene AU - Fiscella, M AU - Ullrich, S J AU - Zambrano, N AU - Shields, M T AU - Lin, D AU - Lees-Miller, S P AU - Anderson, C W AU - Mercer, W E AU - Appella, E AD - Laboratory of Cell Biology, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/06// PY - 1993 DA - June 1993 SP - 1519 EP - 1528 VL - 8 IS - 6 SN - 0950-9232, 0950-9232 KW - p53 KW - Antibodies, Monoclonal KW - 0 KW - Oligodeoxyribonucleotides KW - Peptides KW - RNA, Messenger KW - Tumor Suppressor Protein p53 KW - Serine KW - 452VLY9402 KW - Protein Kinases KW - EC 2.7.- KW - Index Medicus KW - Peptides -- chemical synthesis KW - Immunoblotting KW - Blotting, Northern KW - Humans KW - Peptides -- immunology KW - Amino Acid Sequence KW - Mutagenesis, Site-Directed KW - Protein Kinases -- metabolism KW - Polymerase Chain Reaction KW - Base Sequence KW - RNA, Messenger -- metabolism KW - Phosphorylation KW - Transfection KW - Kinetics KW - Molecular Sequence Data KW - Cell Line KW - Tumor Suppressor Protein p53 -- analysis KW - Genes, p53 KW - Cell Cycle -- physiology KW - Tumor Suppressor Protein p53 -- genetics KW - Tumor Suppressor Protein p53 -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75737894?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncogene&rft.atitle=Mutation+of+the+serine+15+phosphorylation+site+of+human+p53+reduces+the+ability+of+p53+to+inhibit+cell+cycle+progression.&rft.au=Fiscella%2C+M%3BUllrich%2C+S+J%3BZambrano%2C+N%3BShields%2C+M+T%3BLin%2C+D%3BLees-Miller%2C+S+P%3BAnderson%2C+C+W%3BMercer%2C+W+E%3BAppella%2C+E&rft.aulast=Fiscella&rft.aufirst=M&rft.date=1993-06-01&rft.volume=8&rft.issue=6&rft.spage=1519&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=09509232&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-29 N1 - Date created - 1993-06-29 N1 - Date revised - 2017-01-13 N1 - Gene symbol - p53 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Salvage trial of trimetrexate-leucovorin for the treatment of cerebral toxoplasmosis in patients with AIDS. AN - 75735742; 8501335 AB - The clinical efficacy of trimetrexate, a dihydrofolate reductase inhibitor with potent in vitro antitoxoplasma activity, was assessed in 9 sulfonamide-intolerant patients with AIDS and biopsy-proven cerebral toxoplasmosis. The 9 patients were treated for 28-149 days with trimetrexate (30-280 mg/m2/day) plus leucovorin (20-90 mg/m2 every 6 h). Radiographic responses were documented in 8 patients, and clinical responses in 5 patients. Despite continued therapy, all patients deteriorated clinically and radiographically within 13-109 days of their initial improvement. Trimetrexate at very high doses for extended periods was not associated with serious toxicity. Trimetrexate alone had dramatic but transient activity in sulfonamide-intolerant patients and thus is not adequate as single-agent therapy for AIDS-associated toxoplasmosis. JF - The Journal of infectious diseases AU - Masur, H AU - Polis, M A AU - Tuazon, C U AU - Ogata-Arakaki, D AU - Kovacs, J A AU - Katz, D AU - Hilt, D AU - Simmons, T AU - Feuerstein, I AU - Lundgren, B AD - National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/06// PY - 1993 DA - June 1993 SP - 1422 EP - 1426 VL - 167 IS - 6 SN - 0022-1899, 0022-1899 KW - Leucovorin KW - Q573I9DVLP KW - Trimetrexate KW - UPN4ITI8T4 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Drug Evaluation KW - Humans KW - Adult KW - Tomography, X-Ray Computed KW - Adolescent KW - Male KW - Female KW - Acquired Immunodeficiency Syndrome -- complications KW - Toxoplasmosis, Cerebral -- drug therapy KW - Toxoplasmosis, Cerebral -- complications KW - Trimetrexate -- therapeutic use KW - Toxoplasmosis, Cerebral -- diagnostic imaging KW - Leucovorin -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75735742?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+infectious+diseases&rft.atitle=Salvage+trial+of+trimetrexate-leucovorin+for+the+treatment+of+cerebral+toxoplasmosis+in+patients+with+AIDS.&rft.au=Masur%2C+H%3BPolis%2C+M+A%3BTuazon%2C+C+U%3BOgata-Arakaki%2C+D%3BKovacs%2C+J+A%3BKatz%2C+D%3BHilt%2C+D%3BSimmons%2C+T%3BFeuerstein%2C+I%3BLundgren%2C+B&rft.aulast=Masur&rft.aufirst=H&rft.date=1993-06-01&rft.volume=167&rft.issue=6&rft.spage=1422&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+infectious+diseases&rft.issn=00221899&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-29 N1 - Date created - 1993-06-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Child-care debate - transformed or distorted? AN - 39047130; 1253926 JF - American psychologist Y1 - 1993/06// PY - 1993 DA - Jun 1993 SP - 692 VL - 48 IS - 6 SN - 0003-066X, 0003-066X KW - Sociology KW - Child care UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/39047130?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+psychologist&rft.atitle=Child-care+debate+-+transformed+or+distorted%3F&rft.au=&rft.aulast=&rft.aufirst=&rft.date=1993-06-01&rft.volume=48&rft.issue=6&rft.spage=692&rft.isbn=&rft.btitle=&rft.title=American+psychologist&rft.issn=0003066X&rft_id=info:doi/ LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2013-06-12 N1 - Last updated - 2013-09-16 N1 - SubjectsTermNotLitGenreText - 2192 ER - TY - JOUR T1 - State-dependent radial elasticity of attached cross-bridges in single skinned fibres of rabbit psoas muscle. AN - 1647020020; 21249423 AB - 1. In a single skinned fibre of rabbit psoas muscle, upon attachment of cross bridges to actin in the presence of ADP or pyrophosphate (PPi), the separation between the contractile filaments, as determined by equatorial X-ray diffraction, is found to decrease, suggesting that force is generated in the radial direction. 2. The single muscle fibres were subjected to compression by 0-8% of dextran T500. The changes in lattice spacings by dextran compression were compared with changes induced by cross-bridge attachment to actin. Based on this comparison, the magnitude and the direction of the radial force generated by the attached cross-bridges were estimated. The radial cross-bridge force varied with filament separation, and the magnitude of the radial cross-bridge force reached as high as the maximal axial force produced during isometric contraction. 3. One key parameter of the radial elasticity, i.e. the equilibrium spacing where the radial force is zero, was found to depend on the ligand bound to the myosin head. In the presence of ADP, the equilibrium spacing was 36 nm. In the presence of MgPPi the equilibrium spacing shifted to 35 nm and Ca2+ had little effect on the equilibrium spacing. 4. The equilibrium spacing was independent of the fraction of cross-bridges attached to actin. The fraction of cross-bridges attached in rigor was modulated from 100% to close to 0% by adding up to 10 mM of ATP gamma S in the rigor solution. The lattice spacing remained at 38 nm, the equilibrium spacing for nucleotide-free cross-bridges at mu = 170 mM. 5. Radial force generated by cross-bridges in rigor at large lattice spacings (38 nm < or = d10 < or = 46 nm) appeared to vary linearly with lattice spacing. 6. The titration of ATP gamma S to fibres in rigor provided a correlation between the radial stiffness of the nucleotide-free cross-bridges and the equatorial intensities. The relation between the equatorial intensity ratio I11/I10 and radial stiffness appeared to be approximately linear. 7. The fibres under different conditions showed a wide range of radial stiffness, which was not proportional to the apparent axial stiffness of the fibre. If the apparent axial stiffness is a measure of the fraction of cross-bridges bound to actin, it follows that the radial elastic constant is state dependent; or vice versa.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Journal of Physiology (London) AU - Xu, S AU - Brenner, B AU - Yu, L C AD - National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/06/01/ PY - 1993 DA - 1993 Jun 01 SP - 749 EP - 765 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 465 IS - 1 SN - 0022-3751, 0022-3751 KW - Physical Education Index KW - X-Ray KW - Biochemistry KW - Animal subjects KW - Muscles KW - Isometrics KW - Balance KW - PE 090:Sports Medicine & Exercise Sport Science UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647020020?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Physiology+%28London%29&rft.atitle=State-dependent+radial+elasticity+of+attached+cross-bridges+in+single+skinned+fibres+of+rabbit+psoas+muscle.&rft.au=Xu%2C+S%3BBrenner%2C+B%3BYu%2C+L+C&rft.aulast=Xu&rft.aufirst=S&rft.date=1993-06-01&rft.volume=465&rft.issue=1&rft.spage=749&rft.isbn=&rft.btitle=&rft.title=Journal+of+Physiology+%28London%29&rft.issn=00223751&rft_id=info:doi/10.1113%2Fjphysiol.1993.sp019704 LA - English DB - Physical Education Index N1 - Date revised - 2015-01-01 N1 - Document feature - figure 0 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - X-Ray; Biochemistry; Animal subjects; Muscles; Isometrics; Balance DO - http://dx.doi.org/10.1113/jphysiol.1993.sp019704 ER - TY - JOUR T1 - Child-Care Debate: Transformed or Distorted? AN - 1289903466 JF - American Psychologist Y1 - 1993/06/01/ PY - 1993 DA - 1993 Jun 01 SP - 692 CY - Arlington, Va. PB - American Psychological Association VL - 48 IS - 6 SN - 0003-066X KW - Psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1289903466?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Apio&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Psychologist&rft.atitle=Child-Care+Debate%3A+Transformed+or+Distorted%3F&rft.au=&rft.aulast=&rft.aufirst=&rft.date=1993-06-01&rft.volume=48&rft.issue=6&rft.spage=692&rft.isbn=&rft.btitle=&rft.title=American+Psychologist&rft.issn=0003066X&rft_id=info:doi/ DB - Periodicals Index Online N1 - Last updated - 2013-02-21 ER - TY - JOUR T1 - Trophic factor production by reactive astrocytes in injured brain. AN - 75785218; 8099771 JF - Annals of the New York Academy of Sciences AU - Schwartz, J P AU - Sheng, J G AU - Mitsuo, K AU - Shirabe, S AU - Nishiyama, N AD - Clinical Neuroscience Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/05/28/ PY - 1993 DA - 1993 May 28 SP - 226 EP - 234 VL - 679 SN - 0077-8923, 0077-8923 KW - Biomarkers KW - 0 KW - Enkephalins KW - Glial Fibrillary Acidic Protein KW - Nerve Growth Factors KW - Neuropeptides KW - Neurotoxins KW - Protein Precursors KW - RNA, Messenger KW - proenkephalin KW - Somatostatin KW - 51110-01-1 KW - Enkephalin, Methionine KW - 58569-55-4 KW - Oxidopamine KW - 8HW4YBZ748 KW - Index Medicus KW - Enkephalin, Methionine -- analysis KW - Aging -- metabolism KW - Animals KW - Fetus KW - Mice KW - Somatostatin -- biosynthesis KW - Cerebellum -- metabolism KW - Rats KW - Rats, Sprague-Dawley KW - Enkephalins -- biosynthesis KW - RNA, Messenger -- metabolism KW - Cerebellum -- growth & development KW - Oxidopamine -- toxicity KW - Cells, Cultured KW - Protein Precursors -- biosynthesis KW - MPTP Poisoning KW - Mice, Inbred C57BL KW - Enkephalin, Methionine -- metabolism KW - Male KW - Nerve Growth Factors -- biosynthesis KW - Glial Fibrillary Acidic Protein -- metabolism KW - Glial Fibrillary Acidic Protein -- analysis KW - Neuropeptides -- biosynthesis KW - Neurotoxins -- toxicity KW - Astrocytes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75785218?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+the+New+York+Academy+of+Sciences&rft.atitle=Trophic+factor+production+by+reactive+astrocytes+in+injured+brain.&rft.au=Schwartz%2C+J+P%3BSheng%2C+J+G%3BMitsuo%2C+K%3BShirabe%2C+S%3BNishiyama%2C+N&rft.aulast=Schwartz&rft.aufirst=J&rft.date=1993-05-28&rft.volume=679&rft.issue=&rft.spage=226&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+New+York+Academy+of+Sciences&rft.issn=00778923&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-15 N1 - Date created - 1993-07-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Nutrient and food group intake by tobacco use status: the 1987 National Health Interview Survey. AN - 75784323; 8512257 JF - Annals of the New York Academy of Sciences AU - Subar, A F AU - Harlan, L C AD - Applied Research Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/05/28/ PY - 1993 DA - 1993 May 28 SP - 310 EP - 21; discussion 321-2 VL - 686 SN - 0077-8923, 0077-8923 KW - Index Medicus KW - United States KW - Regression Analysis KW - Sex Factors KW - Humans KW - Adult KW - Aged KW - Nutrition Surveys KW - Middle Aged KW - Male KW - Female KW - Plants, Toxic KW - Smoking KW - Diet -- trends KW - Diet -- statistics & numerical data KW - Tobacco, Smokeless UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75784323?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+the+New+York+Academy+of+Sciences&rft.atitle=Nutrient+and+food+group+intake+by+tobacco+use+status%3A+the+1987+National+Health+Interview+Survey.&rft.au=Subar%2C+A+F%3BHarlan%2C+L+C&rft.aulast=Subar&rft.aufirst=A&rft.date=1993-05-28&rft.volume=686&rft.issue=&rft.spage=310&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+New+York+Academy+of+Sciences&rft.issn=00778923&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-15 N1 - Date created - 1993-07-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The goldfish as a drug discovery vehicle for Parkinson's disease and other neurodegenerative disorders. AN - 75782545; 8512193 JF - Annals of the New York Academy of Sciences AU - Pollard, H B AU - Adeyemo, M AU - Dhariwal, K AU - Levine, M AU - Caohuy, H AU - Markey, S AU - Markey, C J AU - Youdim, M B AD - Laboratory of Cell Biology and Genetics, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/05/28/ PY - 1993 DA - 1993 May 28 SP - 317 EP - 320 VL - 679 SN - 0077-8923, 0077-8923 KW - Neurotoxins KW - 0 KW - Index Medicus KW - Rats KW - Animals KW - Humans KW - Disease Models, Animal KW - Mice KW - Primates KW - Parkinson Disease, Secondary -- chemically induced KW - MPTP Poisoning KW - Alzheimer Disease -- drug therapy KW - Goldfish KW - Alzheimer Disease -- chemically induced KW - Neurotoxins -- toxicity KW - Parkinson Disease, Secondary -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75782545?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+the+New+York+Academy+of+Sciences&rft.atitle=The+goldfish+as+a+drug+discovery+vehicle+for+Parkinson%27s+disease+and+other+neurodegenerative+disorders.&rft.au=Pollard%2C+H+B%3BAdeyemo%2C+M%3BDhariwal%2C+K%3BLevine%2C+M%3BCaohuy%2C+H%3BMarkey%2C+S%3BMarkey%2C+C+J%3BYoudim%2C+M+B&rft.aulast=Pollard&rft.aufirst=H&rft.date=1993-05-28&rft.volume=679&rft.issue=&rft.spage=317&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+New+York+Academy+of+Sciences&rft.issn=00778923&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-15 N1 - Date created - 1993-07-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Induction of a neuroprotective state in cerebellar granule cells following activation of N-methyl-D-aspartate receptors. AN - 75781704; 8099772 JF - Annals of the New York Academy of Sciences AU - Marini, A M AU - Paul, S M AD - Section on Molecular Pharmacology, National Institutes of Health, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1993/05/28/ PY - 1993 DA - 1993 May 28 SP - 253 EP - 259 VL - 679 SN - 0077-8923, 0077-8923 KW - Glutamates KW - 0 KW - Neurotoxins KW - Pyridinium Compounds KW - Receptors, N-Methyl-D-Aspartate KW - Dactinomycin KW - 1CC1JFE158 KW - Glutamic Acid KW - 3KX376GY7L KW - 1-(4-methoxyphenyl)pyridinium KW - 42850-10-2 KW - N-Methylaspartate KW - 6384-92-5 KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - Cycloheximide KW - 98600C0908 KW - Index Medicus KW - Dactinomycin -- pharmacology KW - Animals KW - Cell Survival -- drug effects KW - Cells, Cultured KW - Cycloheximide -- pharmacology KW - Dizocilpine Maleate -- pharmacology KW - Pyridinium Compounds -- antagonists & inhibitors KW - Neurons -- metabolism KW - Pyridinium Compounds -- toxicity KW - Neurons -- drug effects KW - Cerebellum -- pathology KW - Receptors, N-Methyl-D-Aspartate -- metabolism KW - Neurotoxins -- toxicity KW - Cerebellum -- metabolism KW - Neurons -- pathology KW - Receptors, N-Methyl-D-Aspartate -- drug effects KW - Glutamates -- pharmacology KW - N-Methylaspartate -- pharmacology KW - Cerebellum -- drug effects KW - N-Methylaspartate -- toxicity KW - Glutamates -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75781704?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+the+New+York+Academy+of+Sciences&rft.atitle=Induction+of+a+neuroprotective+state+in+cerebellar+granule+cells+following+activation+of+N-methyl-D-aspartate+receptors.&rft.au=Marini%2C+A+M%3BPaul%2C+S+M&rft.aulast=Marini&rft.aufirst=A&rft.date=1993-05-28&rft.volume=679&rft.issue=&rft.spage=253&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+New+York+Academy+of+Sciences&rft.issn=00778923&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-15 N1 - Date created - 1993-07-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Preliminary observations on the in vitro toxicity of N-butylbenzenesulfonamide: a newly discovered neurotoxin. AN - 75771604; 8512189 JF - Annals of the New York Academy of Sciences AU - Nerurkar, V R AU - Wakayama, I AU - Rowe, T AU - Yanagihara, R AU - Garruto, R M AD - Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/05/28/ PY - 1993 DA - 1993 May 28 SP - 280 EP - 287 VL - 679 SN - 0077-8923, 0077-8923 KW - Biomarkers KW - 0 KW - Neurotoxins KW - Plasticizers KW - Sulfonamides KW - Tritium KW - 10028-17-8 KW - N-butylbenzenesulfonamide KW - 3622-84-2 KW - L-Lactate Dehydrogenase KW - EC 1.1.1.27 KW - Thymidine KW - VC2W18DGKR KW - Index Medicus KW - Thymidine -- metabolism KW - Rats KW - Animals KW - Tumor Cells, Cultured KW - L-Lactate Dehydrogenase -- analysis KW - Kinetics KW - Cell Division -- drug effects KW - Glioma KW - Cell Death -- drug effects KW - Plasticizers -- toxicity KW - DNA Replication -- drug effects KW - Cell Line KW - Sulfonamides -- toxicity KW - Neurotoxins -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75771604?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+the+New+York+Academy+of+Sciences&rft.atitle=Preliminary+observations+on+the+in+vitro+toxicity+of+N-butylbenzenesulfonamide%3A+a+newly+discovered+neurotoxin.&rft.au=Nerurkar%2C+V+R%3BWakayama%2C+I%3BRowe%2C+T%3BYanagihara%2C+R%3BGarruto%2C+R+M&rft.aulast=Nerurkar&rft.aufirst=V&rft.date=1993-05-28&rft.volume=679&rft.issue=&rft.spage=280&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+New+York+Academy+of+Sciences&rft.issn=00778923&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-15 N1 - Date created - 1993-07-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Synergistic antiproliferative effects of interleukin-1 alpha and doxorubicin against the human ovarian carcinoma cell line (NIH:OVCAR-3). AN - 75781769; 8512591 AB - Interleukin-1 alpha (IL-1 alpha) exerts antiproliferative effects on a human ovarian carcinoma cell line, NIH:OVCAR-3, which is resistant to clinically relevant concentrations of doxorubicin (DOX) and other chemotherapeutic agents. This action of IL-1 alpha depends on the presence of type I (80 kDa) receptors, although no quantitative relationship has been established between receptor occupancy and inhibition of cell growth. When NIH:OVCAR-3 cells were exposed to IL-1 alpha and DOX in combination, a mutual potentiation of the antiproliferative effects of the two agents was observed. This synergistic effect was not due to IL-1 receptor expression up-regulation by DOX, and receptor-dependent internalization of the cytokine was also unaffected. The involvement of IL-1 receptors is supported by the observation that synergism between the two agents was diminished (but not abolished) in the presence of a specific IL-1 receptor antagonist at concentrations blocking more than 75% of IL-1 alpha binding. DOX was found to significantly increase IL-1 alpha accumulation by NIH:OVCAR-3 cells after long-term (48 hr) exposure to the cytokine at 37 degrees, which might be due to increased nonspecific fluid phase uptake or to interference with cytokine degradation and/or release processes. The potent synergy of IL-1 alpha and DOX against ovarian carcinoma cells in vitro suggests that this drug combination may be effective against this disease in the clinic. JF - Biochemical pharmacology AU - Monti, E AU - Mimnaugh, E G AU - Sinha, B K AD - Biochemical and Molecular Pharmacology Section, National Cancer Institute, NIH, Bethesda, MD 20892. Y1 - 1993/05/25/ PY - 1993 DA - 1993 May 25 SP - 2099 EP - 2107 VL - 45 IS - 10 SN - 0006-2952, 0006-2952 KW - Interleukin-1 KW - 0 KW - Iodine Radioisotopes KW - Receptors, Interleukin-1 KW - Doxorubicin KW - 80168379AG KW - Index Medicus KW - Drug Interactions KW - Interleukin-1 -- administration & dosage KW - Tumor Cells, Cultured -- drug effects KW - Humans KW - Cell Division -- drug effects KW - Intracellular Fluid -- metabolism KW - Doxorubicin -- administration & dosage KW - Protein Binding KW - Receptors, Interleukin-1 -- drug effects KW - Up-Regulation -- physiology KW - Interleukin-1 -- metabolism KW - Doxorubicin -- pharmacology KW - Interleukin-1 -- pharmacokinetics KW - Up-Regulation -- drug effects KW - Receptors, Interleukin-1 -- metabolism KW - Receptors, Interleukin-1 -- physiology KW - Drug Synergism KW - Female KW - Ovarian Neoplasms -- metabolism KW - Ovarian Neoplasms -- pathology KW - Antineoplastic Combined Chemotherapy Protocols -- pharmacology KW - Ovarian Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75781769?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+pharmacology&rft.atitle=Synergistic+antiproliferative+effects+of+interleukin-1+alpha+and+doxorubicin+against+the+human+ovarian+carcinoma+cell+line+%28NIH%3AOVCAR-3%29.&rft.au=Monti%2C+E%3BMimnaugh%2C+E+G%3BSinha%2C+B+K&rft.aulast=Monti&rft.aufirst=E&rft.date=1993-05-25&rft.volume=45&rft.issue=10&rft.spage=2099&rft.isbn=&rft.btitle=&rft.title=Biochemical+pharmacology&rft.issn=00062952&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-09 N1 - Date created - 1993-07-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The human papillomavirus E7 protein as a transforming and transactivating factor. AN - 75768444; 8389201 AB - The HPV proteins encoded by the early viral genes, including E6 and E7, are thought to subvert the normal regulatory pathways of infected cells to accommodate viral replication. Mechanistically some of this is accomplished by protein-protein interactions between viral proteins and a number of key cellular regulatory proteins that include tumor suppressor gene products. By undermining cellular regulatory pathways the HPV oncogenes cause hyperproliferation and the perturbation of normal cellular differentiation pathways. Although expression of the high-risk HPV-encoded E6 and E7 oncoproteins may be important prerequisites for cellular transformation, it is very likely that additional cellular changes are necessary for carcinogenic progression. The elucidation of the role of the early HPV genes in the initiation and/or maintenance of carcinogenic progression will continue to be a fascinating area of investigation and may reveal new opportunities for antiviral therapy and antitumor intervention. JF - Biochimica et biophysica acta AU - Münger, K AU - Phelps, W C AD - Laboratory of Tumor Virus Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/05/25/ PY - 1993 DA - 1993 May 25 SP - 111 EP - 123 VL - 1155 IS - 1 SN - 0006-3002, 0006-3002 KW - Oncogene Proteins, Viral KW - 0 KW - Papillomavirus E7 Proteins KW - oncogene protein E7, Human papillomavirus type 16 KW - Index Medicus KW - Animals KW - Genes, Retinoblastoma KW - Humans KW - Molecular Sequence Data KW - Uterine Cervical Neoplasms -- genetics KW - Amino Acid Sequence KW - Female KW - Oncogene Proteins, Viral -- chemistry KW - Papillomaviridae KW - Transcriptional Activation KW - Oncogene Proteins, Viral -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75768444?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochimica+et+biophysica+acta&rft.atitle=The+human+papillomavirus+E7+protein+as+a+transforming+and+transactivating+factor.&rft.au=M%C3%BCnger%2C+K%3BPhelps%2C+W+C&rft.aulast=M%C3%BCnger&rft.aufirst=K&rft.date=1993-05-25&rft.volume=1155&rft.issue=1&rft.spage=111&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+biophysica+acta&rft.issn=00063002&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-07 N1 - Date created - 1993-07-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Assessment of the carcinogenic potential of chlorinated water: experimental studies of chlorine, chloramine, and trihalomethanes. AN - 75717628; 8487327 AB - Water chlorination has been one of the major disease prevention treatments of this century. While epidemiologic studies suggest an association between cancer in humans and consumption of chlorination byproducts in drinking water, these studies have not been adequate to draw definite conclusions about the carcinogenic potential of the individual byproducts. The purpose of this study was to investigate the carcinogenic potential of chlorinated or chloraminated drinking water and of four organic trihalomethane byproducts of chlorination (chloroform, bromodichloromethane, chlorodibromomethane, and bromoform) in rats and mice. Bromodichloromethane, chlorodibromomethane, bromoform, chlorine, or chloramine was administered to both sexes of F344/N rats and (C57BL/6 x C3H)F1 mice (hereafter called B6C3F1 mice). Chloroform was given to both sexes of Osborne-Mendel rats and B6C3F1 mice. Chlorine or chloramine was administered daily in the drinking water for 2 years at doses ranging from 0.05 to 0.3 mmol/kg per day. The trihalomethanes were administered by gavage in corn oil at doses ranging from 0.15 to 4.0 mmol/kg per day for 2 years, with the exception of chloroform, which was given for 78 weeks. The trihalomethanes were carcinogenic in the liver, kidney, and/or intestine of rodents. There was equivocal evidence for carcinogenicity in female rats that received chlorinated or chloraminated drinking water; this evidence was based on a marginal increase in the incidence of mononuclear cell leukemia. Rodents were generally exposed to lower doses of chlorine and chloramine than to the trihalomethanes, but the doses in these studies were the maximum that the animals would consume in the drinking water. The highest doses used in the chlorine and chloramine studies were equivalent to a daily gavage dose of bromodichloromethane that induced neoplasms of the large intestine in rats. In contrast to the results with the trihalomethanes, administration of chlorine or chloramine did not cause a clear carcinogenic response in rats or mice after long-term exposure. These results suggest that organic byproducts of chlorination are the chemicals of greatest concern in assessment of the carcinogenic potential of chlorinated drinking water. JF - Journal of the National Cancer Institute AU - Dunnick, J K AU - Melnick, R L AD - National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, N.C. 27709. Y1 - 1993/05/19/ PY - 1993 DA - 1993 May 19 SP - 817 EP - 822 VL - 85 IS - 10 SN - 0027-8874, 0027-8874 KW - Chloramines KW - 0 KW - Chlorofluorocarbons, Methane KW - Chlorine KW - 4R7X1O2820 KW - chloramine KW - KW8K411A1P KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Liver -- drug effects KW - Kidney Neoplasms -- chemically induced KW - Dose-Response Relationship, Drug KW - Mice, Inbred C57BL KW - Mice, Inbred C3H KW - Intestinal Neoplasms -- chemically induced KW - Liver Neoplasms, Experimental -- chemically induced KW - Mice KW - Male KW - Female KW - Chlorine -- toxicity KW - Chloramines -- toxicity KW - Water Supply -- standards KW - Neoplasms, Experimental -- chemically induced KW - Chlorofluorocarbons, Methane -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75717628?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Assessment+of+the+carcinogenic+potential+of+chlorinated+water%3A+experimental+studies+of+chlorine%2C+chloramine%2C+and+trihalomethanes.&rft.au=Dunnick%2C+J+K%3BMelnick%2C+R+L&rft.aulast=Dunnick&rft.aufirst=J&rft.date=1993-05-19&rft.volume=85&rft.issue=10&rft.spage=817&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-10 N1 - Date created - 1993-06-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Pitfalls inherent in retrospective time-to-event studies: the example of time to pregnancy. AN - 75826062; 8327803 AB - Retrospective studies of time from initiation of risk (for example, transfusion of HIV-infected blood) to the occurrence of an endpoint of interest are useful in epidemiology. One example is studies of time to pregnancy, which have evaluated exposures that may affect human fertility. One can reconstruct the non-contracepting interval required for each woman's most recent pregnancy and then treat the data as if the couples had been studied prospectively. As we illustrate, however, failure-time models can be dangerously misleading when there have been trends over calendar time in exposures under study. We propose an ad hoc method for evaluating possible effects on fertility despite this bias, by making use of external data on trends in the exposure over time. This approach applies a prospective model and generates an empirical p-value, based on comparing the data-based estimated exposure coefficient with its null distribution estimated by simulation. A second method maximizes a conditional likelihood, and we show that this is equivalent to logistically modelling the relative odds for the subject's exposure as related to the reported time she required to achieve pregnancy. JF - Statistics in medicine AU - Weinberg, C R AU - Baird, D D AU - Rowland, A S AD - Statistics and Biomathematics Branch, National Institute of Environmental Health Sciences, NC 27709. Y1 - 1993/05/15/ PY - 1993 DA - 1993 May 15 SP - 867 EP - 879 VL - 12 IS - 9 SN - 0277-6715, 0277-6715 KW - Nitrous Oxide KW - K50XQU1029 KW - Index Medicus KW - Nitrous Oxide -- adverse effects KW - Cross-Sectional Studies KW - Infertility, Female -- epidemiology KW - Humans KW - Retrospective Studies KW - Occupational Exposure -- adverse effects KW - Dental Assistants -- statistics & numerical data KW - Bias (Epidemiology) KW - California -- epidemiology KW - Female KW - Infertility, Female -- chemically induced KW - Models, Statistical KW - Pregnancy -- statistics & numerical data UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75826062?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Statistics+in+medicine&rft.atitle=Pitfalls+inherent+in+retrospective+time-to-event+studies%3A+the+example+of+time+to+pregnancy.&rft.au=Weinberg%2C+C+R%3BBaird%2C+D+D%3BRowland%2C+A+S&rft.aulast=Weinberg&rft.aufirst=C&rft.date=1993-05-15&rft.volume=12&rft.issue=9&rft.spage=867&rft.isbn=&rft.btitle=&rft.title=Statistics+in+medicine&rft.issn=02776715&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-06 N1 - Date created - 1993-08-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Stability, clearance, and disposition of intraventricularly administered oligodeoxynucleotides: implications for therapeutic application within the central nervous system. AN - 75784065; 8506315 AB - We report experiments in the rat demonstrating the feasibility of intraventricular administration of oligodeoxynucleotides (ODNs) as a regional treatment approach to disorders within the central nervous system (CNS). Although we find little intrinsic nuclease activity in cerebrospinal fluid (CSF), phosphodiester ODNs are rapidly degraded by brain-associated alpha-exonuclease activity. Phosphorothioate ODNs, however, appear resistant to degradation in the CNS and, after intraventricular administration, we find they are cleared in a manner consistent with CSF bulk flow. Continuous infusion of ODN at 1.5 nmol/hr by miniosmotic pump can maintain micromolar concentrations of intact phosphorothioate ODN in CSF for at least 1 week without obvious neurologic or systemic toxicity. After infusion, extensive brain penetration and marked cellular uptake, especially by astrocytic cells, is demonstrated. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Whitesell, L AU - Geselowitz, D AU - Chavany, C AU - Fahmy, B AU - Walbridge, S AU - Alger, J R AU - Neckers, L M AD - Tumor Cell Biology Section, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/05/15/ PY - 1993 DA - 1993 May 15 SP - 4665 EP - 4669 VL - 90 IS - 10 SN - 0027-8424, 0027-8424 KW - Oligodeoxyribonucleotides KW - 0 KW - Thionucleotides KW - Index Medicus KW - Rats KW - Microscopy, Fluorescence KW - Animals KW - Rats, Sprague-Dawley KW - Base Sequence KW - Molecular Sequence Data KW - Tissue Distribution KW - Thionucleotides -- chemistry KW - Female KW - Injections, Intraventricular KW - Oligodeoxyribonucleotides -- pharmacokinetics KW - Oligodeoxyribonucleotides -- chemistry KW - Oligodeoxyribonucleotides -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75784065?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Stability%2C+clearance%2C+and+disposition+of+intraventricularly+administered+oligodeoxynucleotides%3A+implications+for+therapeutic+application+within+the+central+nervous+system.&rft.au=Whitesell%2C+L%3BGeselowitz%2C+D%3BChavany%2C+C%3BFahmy%2C+B%3BWalbridge%2C+S%3BAlger%2C+J+R%3BNeckers%2C+L+M&rft.aulast=Whitesell&rft.aufirst=L&rft.date=1993-05-15&rft.volume=90&rft.issue=10&rft.spage=4665&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-02 N1 - Date created - 1993-07-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Brain Res. 1973 Mar 30;52:323-32 [4739806] Differentiation. 1983;25(2):193-203 [6198232] J Neurochem. 1985 Aug;45(2):508-13 [2409231] Nature. 1992 Sep 3;359(6390):67-70 [1522889] Crit Rev Oncog. 1992;3(1-2):175-231 [1312868] Antisense Res Dev. 1991 Winter;1(4):343-50 [1821655] Proc Natl Acad Sci U S A. 1991 Sep 1;88(17):7595-9 [1881900] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Oxygen toxicity in a polyamine-depleted spe2 delta mutant of Saccharomyces cerevisiae. AN - 75781978; 8506320 AB - When a mutant of Saccharomyces cerevisiae (spe2 delta) that cannot make spermidine or spermine was incubated in a polyamine-deficient medium in oxygen, there was a rapid cessation of cell growth and associated cell death. In contrast, when the mutant cells were incubated in the polyamine-deficient medium in air or anaerobically, the culture stopped growing more gradually, and there was no significant loss of cell viability. We also found that the polyamine-deficient cells grown in air, but not those grown anaerobically, showed a permanent loss of functional mitochondria ("respiratory competency"), as evidenced by their inability to grow on glycerol as the sole carbon source. These data support the postulation that polyamines act, in part, by protecting cell components from damage resulting from oxidation. However, since the mutant cells still required spermidine or spermine for growth when incubated under strictly anaerobic conditions, polyamines must also have other essential functions. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Balasundaram, D AU - Tabor, C W AU - Tabor, H AD - Section on Pharmacology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/05/15/ PY - 1993 DA - 1993 May 15 SP - 4693 EP - 4697 VL - 90 IS - 10 SN - 0027-8424, 0027-8424 KW - SOD1 KW - SPE2 KW - Polyamines KW - 0 KW - Superoxide Dismutase KW - EC 1.15.1.1 KW - Adenosylmethionine Decarboxylase KW - EC 4.1.1.50 KW - Oxygen KW - S88TT14065 KW - Index Medicus KW - Space life sciences KW - Phenotype KW - Superoxide Dismutase -- metabolism KW - Mitochondria -- metabolism KW - Anaerobiosis KW - Adenosylmethionine Decarboxylase -- physiology KW - Saccharomyces cerevisiae -- physiology KW - Oxygen -- toxicity KW - Polyamines -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75781978?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Oxygen+toxicity+in+a+polyamine-depleted+spe2+delta+mutant+of+Saccharomyces+cerevisiae.&rft.au=Balasundaram%2C+D%3BTabor%2C+C+W%3BTabor%2C+H&rft.aulast=Balasundaram&rft.aufirst=D&rft.date=1993-05-15&rft.volume=90&rft.issue=10&rft.spage=4693&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-02 N1 - Date created - 1993-07-02 N1 - Date revised - 2017-01-13 N1 - Gene symbol - SOD1; SPE2 N1 - SuppNotes - Cited By: Comp Biochem Physiol B. 1989;93(3):647-51 [2758801] J Bacteriol. 1980 Jun;142(3):791-9 [6991493] Proc Natl Acad Sci U S A. 1990 Apr;87(7):2851-5 [2181453] Arch Biochem Biophys. 1990 May 1;278(2):386-91 [2139316] J Biol Chem. 1990 Dec 25;265(36):22321-8 [2266128] Proc Natl Acad Sci U S A. 1991 Jul 1;88(13):5872-6 [2062864] J Bacteriol. 1991 Sep;173(18):5918-20 [1885557] Eur J Biochem. 1981 May;116(1):1-6 [7018900] J Bacteriol. 1983 Jan;153(1):163-8 [6336730] CRC Crit Rev Biochem. 1983;14(1):47-92 [6340956] Annu Rev Biochem. 1984;53:749-90 [6206782] Microbiol Rev. 1985 Mar;49(1):81-99 [3157043] Biochem Biophys Res Commun. 1985 Jul 31;130(2):533-9 [2992473] Proc Natl Acad Sci U S A. 1986 Jun;83(11):3820-4 [3520557] Biochem J. 1988 Jan 1;249(1):33-6 [3124824] Proc Natl Acad Sci U S A. 1988 Jul;85(13):4789-93 [3290902] Yeast. 1986 Sep;2(3):163-7 [3333305] J Biol Chem. 1989 May 15;264(14):7761-4 [2542241] Microbiol Rev. 1992 Jun;56(2):280-90 [1620066] Proc Natl Acad Sci U S A. 1992 Dec 1;89(23):11426-7 [1454830] Proc Natl Acad Sci U S A. 1992 Dec 1;89(23):11428-30 [1454831] Yeast. 1992 Dec;8(12):1033-41 [1293883] J Mol Biol. 1970 Sep 14;52(2):323-35 [5485912] J Biol Chem. 1978 Mar 25;253(6):1838-45 [204632] J Bacteriol. 1978 Apr;134(1):208-13 [348678] J Bacteriol. 1978 Apr;134(1):214-20 [348679] Biochem J. 1989 May 15;260(1):1-10 [2673211] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Generation of free radicals in reactions of Ni(II)-thiol complexes with molecular oxygen and model lipid hydroperoxides. AN - 75763630; 8388916 AB - The generation of free radicals from reactions of nickel(II)-thiol complexes with molecular oxygen and model lipid hydroperoxides was investigated by electron spin resonance (ESR) utilizing 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) as a spin trap. Incubation of nickel(II) [Ni(II)] with cysteine in an aerobic environment generated hydroxyl (.OH) radical, which then reacted with cysteine to generate a carbon-centered alkyl (.R) radical. Radical generation was inhibited under a nitrogen atmosphere. Model lipid hydroperoxides, cumene hydroperoxide, and t-butyl hydroperoxide enhanced the yield of these radicals and also generated an alkoxyl (.OR) radical. Radical yield decreased by approximately half under a nitrogen atmosphere. Although histidine did not cause radical formation in the reaction between Ni(II) and cumene hydroperoxide under aerobic conditions, the addition of histidine to a mixture containing Ni(II), cysteine, and cumene hydroperoxide under the same experimental conditions increased the yield of .R radical but lowered the yield of .OR and .OH radical adducts. It thus appears that histidine caused the .OH attack to be more site-specific. Similar results were obtained utilizing t-butyl hydroperoxide. Penicillamine or N-acetylcysteine yielded similar results except that under aerobic conditions, reaction between Ni(II) and N-acetylcysteine without hydroperoxide did not generate a significant concentration of free radicals. Under the same experimental conditions, cystine did not generate any detectable free radicals, suggesting an important role of the -SH group in Ni(II)-mediated free radical generation. The results indicate that free radical generation from the reaction of Ni(II)-thiol complexes and molecular oxygen, and/or lipid hydroperoxides, may play an important role in the mechanism(s) of Ni(II) toxicity and carcinogenesis. JF - Journal of inorganic biochemistry AU - Shi, X AU - Dalal, N S AU - Kasprzak, K S AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick Cancer Research and Development Center, Maryland 21702. Y1 - 1993/05/15/ PY - 1993 DA - 1993 May 15 SP - 211 EP - 225 VL - 50 IS - 3 SN - 0162-0134, 0162-0134 KW - Benzene Derivatives KW - 0 KW - Free Radicals KW - Lipid Peroxides KW - Peroxides KW - Sulfhydryl Compounds KW - Histidine KW - 4QD397987E KW - Nickel KW - 7OV03QG267 KW - tert-Butylhydroperoxide KW - 955VYL842B KW - Penicillamine KW - GNN1DV99GX KW - Cysteine KW - K848JZ4886 KW - cumene hydroperoxide KW - PG7JD54X4I KW - Oxygen KW - S88TT14065 KW - Acetylcysteine KW - WYQ7N0BPYC KW - Index Medicus KW - Cysteine -- metabolism KW - Peroxides -- metabolism KW - Electron Spin Resonance Spectroscopy KW - Benzene Derivatives -- metabolism KW - Acetylcysteine -- metabolism KW - Penicillamine -- metabolism KW - Histidine -- pharmacology KW - Sulfhydryl Compounds -- metabolism KW - Oxygen -- metabolism KW - Nickel -- metabolism KW - Lipid Peroxides -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75763630?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+inorganic+biochemistry&rft.atitle=Generation+of+free+radicals+in+reactions+of+Ni%28II%29-thiol+complexes+with+molecular+oxygen+and+model+lipid+hydroperoxides.&rft.au=Shi%2C+X%3BDalal%2C+N+S%3BKasprzak%2C+K+S&rft.aulast=Shi&rft.aufirst=X&rft.date=1993-05-15&rft.volume=50&rft.issue=3&rft.spage=211&rft.isbn=&rft.btitle=&rft.title=Journal+of+inorganic+biochemistry&rft.issn=01620134&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-29 N1 - Date created - 1993-06-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Retinoid status controls the appearance of reserve cells and keratin expression in mouse cervical epithelium. AN - 75722629; 7683571 AB - We describe an animal model to induce the histogenesis of squamous metaplasia of the cervical columnar epithelium, a condition usually preceding cervical neoplasia. This model is based on dietary retinoid depletion in female mice. Control sibling mice fed the same diet but with all-trans-retinoic acid (at 3 micrograms/g diet) showed the normal endocervical epithelial and glandular columnar morphology, typical of a simple epithelium without subcolumnar reserve cells. The stratified squamous ectocervical epithelium of these mice fed all-trans retinoic acid showed intense immunohistochemical staining in basal and suprabasal cells with mono-specific antibodies against keratins K5, K14, K6, K13, and, suprabasally, with antibodies specific for K1 and K10. At the squamocolumnar junction, the adjacent columnar epithelium (termed "suprajunctional") did not show staining for K5, K14, K6, K13, K1, and K10 but specifically stained for keratin K8, typical of simple epithelia and absent from the adjacent ectocervical squamous stratified lining (termed "subjunctional"), in striking contrast. Sections of the squamocolumnar junction from mice kept on the vitamin A-deficient diet for 10 weeks showed suprajunctional isolated patches of reserve cells, proximal and distal to the junction. These cells were detected prior to any symptoms of vitamin A deficiency, such as loss of body weight or respiratory discomfort. The subcolumnar reserve cells induced by vitamin A deficiency displayed positive staining for K5 and K14. As deficiency became severe, the reserve cells occupied the entirety of the suprajunctional basement membrane. This epithelium eventually became stratified and squamous metaplastic, the squamocolumnar junction was no longer discernible, and the entire endocervical epithelium and the endometrial glands lost K8 positivity, while acquiring K5, K14, K6, K13, K1, and K10 keratins typical of the ectocervix under normal conditions of vitamin A nutriture. Vitamin A deficiency also altered keratin expression and localization in squamous subjunctional epithelium. In situ hybridization studies for K1 and K5 mRNA showed their major site of expression at the basal (K5) and immediately suprabasal (K1) cell layers. The localization of both K5 and K1 proteins in these same cell layers, and above, is consistent with transcriptional regulation of these keratins. Early vitamin A deficiency caused the appearance of single subcolumnar reserve cells expressing K5 mRNA. After these cells grew into a squamous focus, K1 mRNA became expressed suprabasally. We conclude that retinoid status plays a key role in maintaining differentiative characteristics of the cervical and glandular epithelia and, as such, may be a modulating factor in the development of cervical cancer. JF - Cancer research AU - Darwiche, N AU - Celli, G AU - Sly, L AU - Lancillotti, F AU - De Luca, L M AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1993/05/15/ PY - 1993 DA - 1993 May 15 SP - 2287 EP - 2299 VL - 53 IS - 10 Suppl SN - 0008-5472, 0008-5472 KW - RNA, Messenger KW - 0 KW - Retinoids KW - Tretinoin KW - 5688UTC01R KW - Keratins KW - 68238-35-7 KW - Index Medicus KW - Animals KW - Carcinoma, Squamous Cell -- etiology KW - Disease Models, Animal KW - Mice, Nude KW - Mice KW - Vitamin A Deficiency -- pathology KW - RNA, Messenger -- genetics KW - Mice, Inbred BALB C KW - Metaplasia -- etiology KW - Phenotype KW - In Situ Hybridization KW - Carcinoma, Squamous Cell -- pathology KW - Metaplasia -- pathology KW - Diet KW - Epithelium -- pathology KW - Vitamin A Deficiency -- complications KW - Immunohistochemistry KW - Female KW - Uterine Cervical Neoplasms -- etiology KW - Keratins -- genetics KW - Cervix Uteri -- pathology KW - Cervix Uteri -- drug effects KW - Tretinoin -- pharmacology KW - Cervix Uteri -- physiology KW - Retinoids -- metabolism KW - Keratins -- physiology KW - Precancerous Conditions -- etiology KW - Uterine Cervical Neoplasms -- pathology KW - Precancerous Conditions -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75722629?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Retinoid+status+controls+the+appearance+of+reserve+cells+and+keratin+expression+in+mouse+cervical+epithelium.&rft.au=Darwiche%2C+N%3BCelli%2C+G%3BSly%2C+L%3BLancillotti%2C+F%3BDe+Luca%2C+L+M&rft.aulast=Darwiche&rft.aufirst=N&rft.date=1993-05-15&rft.volume=53&rft.issue=10+Suppl&rft.spage=2287&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-10 N1 - Date created - 1993-06-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - A masked, randomized, dose-response study between cyclosporine A and G in the treatment of sight-threatening uveitis of noninfectious origin. AN - 75718999; 8488909 AB - Thirty-two patients with sight-threatening uveitis and a decrease in visual acuity requiring systemic therapy were randomly assigned to either cyclosporine A or G in a dose-escalation study. Groups received from 2.5 mg/kg of body weight/day to 10 mg/kg of body weight/day of either drug along with low-dose prednisone. More patients taking cyclosporine G had improved visual acuity and a decrease in macular edema, which occurred more rapidly than in the other group, even at the lower doses tested. No difference in renal function was noted between groups at any doses tested. Four patients receiving cyclosporine G had hepatic alterations, but only one required cessation of the drug. The study indicates the potential usefulness of cyclosporine G, particularly at lower doses (4 mg/kg of body weight/day), which could lower the potential for serious renal complications. JF - American journal of ophthalmology AU - Nussenblatt, R B AU - de Smet, M D AU - Rubin, B AU - Freidlin, V AU - Whitcup, S M AU - Davis, J AU - Herman, D AU - Bloom, J N AU - Sran, P K AU - Whitcher, S AD - Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/05/15/ PY - 1993 DA - 1993 May 15 SP - 583 EP - 591 VL - 115 IS - 5 SN - 0002-9394, 0002-9394 KW - Cyclosporins KW - 0 KW - Immunosuppressive Agents KW - cyclosporin G KW - 74436-00-3 KW - Cyclosporine KW - 83HN0GTJ6D KW - Prednisone KW - VB0R961HZT KW - Abridged Index Medicus KW - Index Medicus KW - Double-Blind Method KW - Dose-Response Relationship, Drug KW - Humans KW - Visual Acuity -- drug effects KW - Adult KW - Prednisone -- administration & dosage KW - Male KW - Female KW - Cyclosporins -- adverse effects KW - Cyclosporine -- administration & dosage KW - Cyclosporine -- adverse effects KW - Vision Disorders -- etiology KW - Vision Disorders -- prevention & control KW - Uveitis -- complications KW - Uveitis -- physiopathology KW - Cyclosporins -- administration & dosage KW - Uveitis -- drug therapy KW - Immunosuppressive Agents -- adverse effects KW - Immunosuppressive Agents -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75718999?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+ophthalmology&rft.atitle=A+masked%2C+randomized%2C+dose-response+study+between+cyclosporine+A+and+G+in+the+treatment+of+sight-threatening+uveitis+of+noninfectious+origin.&rft.au=Nussenblatt%2C+R+B%3Bde+Smet%2C+M+D%3BRubin%2C+B%3BFreidlin%2C+V%3BWhitcup%2C+S+M%3BDavis%2C+J%3BHerman%2C+D%3BBloom%2C+J+N%3BSran%2C+P+K%3BWhitcher%2C+S&rft.aulast=Nussenblatt&rft.aufirst=R&rft.date=1993-05-15&rft.volume=115&rft.issue=5&rft.spage=583&rft.isbn=&rft.btitle=&rft.title=American+journal+of+ophthalmology&rft.issn=00029394&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-08 N1 - Date created - 1993-06-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - A cytotoxic ribonuclease. Study of the mechanism of onconase cytotoxicity. AN - 75715251; 8486718 AB - Onconase, or P-30, is a protein initially purified from extracts of Rana pipiens oocytes and early embryos based upon its anticancer activity both in vitro and in vivo. It is a basic single-chain protein with an apparent molecular mass of 12,000 daltons and is homologous to RNase A. In cultured 9L glioma cells, onconase inhibits protein synthesis with an IC50 of about 10(-7) M. The inhibition of protein synthesis correlates with cell death determined by clonogenic assays. 125I-Labeled onconase binds to specific sites on cultured 9L glioma cells. Scatchard analysis of the binding data shows that onconase appears to bind to cells with two different affinities, one with a Kd of 6.2 x 10(-8) and another of 2.5 x 10(-7) M. Each cell could bind about 3 x 10(5) molecules of onconase at each of the two affinity sites. The low affinity Kd is similar to the IC50 for onconase toxicity. Onconase also demonstrates a saturability of cytotoxicity at a concentration that would saturate the low affinity binding site. Incubation at 4 degrees C increased the binding of onconase to cells relative to 37 degrees C binding and also increased the sensitivity of cells to onconase toxicity, indicating that receptor binding may be an initial step in cell toxicity. Onconase cytotoxicity can be blocked by metabolic inhibitors, NaN3 and 2-deoxyglucose, and cytotoxicity is potentiated 10-fold by monensin. Ribonuclease activity appears necessary for onconase toxicity because alkylated onconase, which only retains 2% of the ribonuclease activity, was at least 100-fold less potent in inhibiting protein synthesis in cells. Onconase inhibition of protein synthesis in 9L cells coincides with the degradation of cellular 28 S and 18 S rRNA. In contrast to RNase A, onconase is resistant to two RNase inhibitors, placental ribonuclease inhibitor and Inhibit-Ace. Northern hybridization with placental ribonuclease inhibitor cDNA probe indicates that 9L glioma cells contain endogenous placental ribonuclease inhibitor mRNA. Based on these results, we propose that onconase toxicity results from onconase binding to cell surface receptors, internalization to the cell cytosol where it degrades ribosomal RNA, inhibiting protein synthesis and causing cell death. JF - The Journal of biological chemistry AU - Wu, Y AU - Mikulski, S M AU - Ardelt, W AU - Rybak, S M AU - Youle, R J AD - Biochemistry Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/05/15/ PY - 1993 DA - 1993 May 15 SP - 10686 EP - 10693 VL - 268 IS - 14 SN - 0021-9258, 0021-9258 KW - Antineoplastic Agents KW - 0 KW - Cyclopentanes KW - Egg Proteins KW - Neoplasm Proteins KW - Placental Hormones KW - Protein Synthesis Inhibitors KW - RNA, Messenger KW - placental ribonuclease inhibitor KW - 120178-77-0 KW - Brefeldin A KW - 20350-15-6 KW - Ribonucleases KW - EC 3.1.- KW - Ribonuclease, Pancreatic KW - EC 3.1.27.5 KW - Leucine KW - GMW67QNF9C KW - ranpirnase KW - ZE15FIT23E KW - Index Medicus KW - Rana pipiens KW - Animals KW - Neoplasm Proteins -- biosynthesis KW - Blotting, Northern KW - Dose-Response Relationship, Drug KW - Ribonuclease, Pancreatic -- toxicity KW - RNA, Messenger -- genetics KW - Autoradiography KW - Embryo, Nonmammalian KW - Ribonuclease, Pancreatic -- metabolism KW - Placental Hormones -- biosynthesis KW - Cyclopentanes -- pharmacology KW - Tumor Cells, Cultured KW - RNA, Messenger -- metabolism KW - Kinetics KW - Leucine -- metabolism KW - Oocytes KW - Glioma KW - Tumor Stem Cell Assay KW - Ribonucleases -- toxicity KW - Ribonucleases -- antagonists & inhibitors KW - Protein Synthesis Inhibitors -- pharmacology KW - Cell Survival -- drug effects KW - Antineoplastic Agents -- metabolism KW - Antineoplastic Agents -- toxicity KW - Egg Proteins -- metabolism KW - Egg Proteins -- toxicity KW - Ribonucleases -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75715251?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=A+cytotoxic+ribonuclease.+Study+of+the+mechanism+of+onconase+cytotoxicity.&rft.au=Wu%2C+Y%3BMikulski%2C+S+M%3BArdelt%2C+W%3BRybak%2C+S+M%3BYoule%2C+R+J&rft.aulast=Wu&rft.aufirst=Y&rft.date=1993-05-15&rft.volume=268&rft.issue=14&rft.spage=10686&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-08 N1 - Date created - 1993-06-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Multiple myeloma. New approaches to therapy. AN - 75699286; 7683062 JF - JAMA AU - Dunbar, C E AU - Nienhuis, A W AD - Hematology Branch, National Heart, Lung, and Blood Institute, Bethesda, Md, National Institutes of Health 20892. Y1 - 1993/05/12/ PY - 1993 DA - 1993 May 12 SP - 2412 EP - 2416 VL - 269 IS - 18 SN - 0098-7484, 0098-7484 KW - Genetic Markers KW - 0 KW - Interferon-alpha KW - Interleukin-6 KW - Granulocyte Colony-Stimulating Factor KW - 143011-72-7 KW - Cyclophosphamide KW - 8N3DW7272P KW - Melphalan KW - Q41OR9510P KW - Fluorouracil KW - U3P01618RT KW - Abridged Index Medicus KW - Index Medicus KW - Interferon-alpha -- therapeutic use KW - Granulocyte Colony-Stimulating Factor -- therapeutic use KW - Interleukin-6 -- secretion KW - Combined Modality Therapy KW - Humans KW - Transplantation, Autologous KW - Fluorouracil -- therapeutic use KW - Whole-Body Irradiation KW - Cyclophosphamide -- therapeutic use KW - Genetic Therapy -- methods KW - Middle Aged KW - Melphalan -- therapeutic use KW - Research KW - Bone Marrow Transplantation KW - Female KW - Multiple Myeloma -- genetics KW - Multiple Myeloma -- therapy KW - Multiple Myeloma -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75699286?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=proceeding&rft.jtitle=JAMA&rft.atitle=Multiple+myeloma.+New+approaches+to+therapy.&rft.au=Dunbar%2C+C+E%3BNienhuis%2C+A+W&rft.aulast=Dunbar&rft.aufirst=C&rft.date=1993-05-12&rft.volume=269&rft.issue=18&rft.spage=2412&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-25 N1 - Date created - 1993-05-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Prediction of alternative RNA secondary structures based on fluctuating thermodynamic parameters. AN - 19797125; 8739496 AB - In this paper we present a new method for predicting a set of RNA secondary structures that are thermodynamically favored in RNA folding simulations. This method uses a large number of 'simulated energy rules' (SER) generated by perturbing the free energy parameters derived experimentally within the range of the experimental errors. The structure with the lowest free energy is computed for each SER. Structural comparisons are used to avoid multiple generation of similar structures. Computed structures are evaluated using the energy distribution of the lowest free energy structures derived in the simulation. Predicted be graphically displayed with their occurring frequencies in the simulation by dot-plot representations. On average, about 90% of phylogenetic helixes in the known models of tRNA, Group I self-splicing intron, and Escherichia coli 16 S rRNA, were predicted using the method. JF - Nucleic Acids Research AU - Le, S Y AU - Chen, J H AU - Maizel, J V AD - Laboratory of Mathematical Biology, National Cancer Institute, NIH, Frederick, MD 21702. Y1 - 1993/05/11/ PY - 1993 DA - 1993 May 11 SP - 2173 EP - 2178 PB - Oxford University Press, Oxford Journals, Great Clarendon Street VL - 21 IS - 9 SN - 0305-1048, 0305-1048 KW - Microbiology Abstracts B: Bacteriology; Biochemistry Abstracts 2: Nucleic Acids KW - Protein structure KW - Phylogeny KW - rRNA KW - Thermodynamics KW - tRNA KW - Secondary structure KW - Escherichia coli KW - Introns KW - Free energy KW - Models KW - J 02310:Genetics & Taxonomy KW - N 14810:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/19797125?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+Acids+Research&rft.atitle=Prediction+of+alternative+RNA+secondary+structures+based+on+fluctuating+thermodynamic+parameters.&rft.au=Le%2C+S+Y%3BChen%2C+J+H%3BMaizel%2C+J+V&rft.aulast=Le&rft.aufirst=S&rft.date=1993-05-11&rft.volume=21&rft.issue=9&rft.spage=2173&rft.isbn=&rft.btitle=&rft.title=Nucleic+Acids+Research&rft.issn=03051048&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2008-12-01 N1 - Last updated - 2015-03-27 N1 - SubjectsTermNotLitGenreText - Phylogeny; Protein structure; rRNA; Thermodynamics; tRNA; Secondary structure; Introns; Free energy; Models; Escherichia coli ER - TY - JOUR T1 - A method to increase the cumulative cleavage efficiency of ribozymes: thermal cycling. AN - 19713290; 8733210 AB - Images JF - Nucleic Acids Research AU - Dropulic, B AU - Lin, N H AU - Jeang, K T AD - Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/05/11/ PY - 1993 DA - 1993 May 11 SP - 2273 EP - 2274 PB - Oxford University Press, Oxford Journals, Great Clarendon Street VL - 21 IS - 9 SN - 0305-1048, 0305-1048 KW - Biotechnology and Bioengineering Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - Ribozymes KW - W 30940:Products KW - N 14810:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/19713290?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+Acids+Research&rft.atitle=A+method+to+increase+the+cumulative+cleavage+efficiency+of+ribozymes%3A+thermal+cycling.&rft.au=Dropulic%2C+B%3BLin%2C+N+H%3BJeang%2C+K+T&rft.aulast=Dropulic&rft.aufirst=B&rft.date=1993-05-11&rft.volume=21&rft.issue=9&rft.spage=2273&rft.isbn=&rft.btitle=&rft.title=Nucleic+Acids+Research&rft.issn=03051048&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2008-12-01 N1 - Last updated - 2015-03-27 N1 - SubjectsTermNotLitGenreText - Ribozymes ER - TY - JOUR T1 - Activation of ADP-ribosylation factor by Golgi membranes. Evidence for a brefeldin A- and protease-sensitive activating factor on Golgi membranes. AN - 75730021; 8486645 AB - Recent evidence has implicated ADP-ribosylation factor (ARF) proteins as critical regulators of the protein secretory pathway, particularly in the endoplasmic reticulum-Golgi pathway. We have examined whether Golgi membranes contain activators of ARF and the consequences of ARF activation and acylation on its membrane association. Two means were used to assess ARF activation. First, guanosine 5'-3-O-(thio)triphosphate (GTP gamma S) binding to protein was found to be greater when ARF and Golgi were incubated together than when either was incubated alone. These data suggested that ARF GTP gamma S was formed. This was confirmed by showing that the GTP gamma S-bound protein functioned as a cofactor for cholera toxin-stimulated ADP-ribosylation of Gs alpha, a reaction for which activated ARF is a necessary cofactor. Trypsin treatment of Golgi, an inhibitory ARF peptide, and brefeldin A each inhibited Golgi-mediated activation by approximately 70%, demonstrating that a specific protein interaction is required for the majority of the ARF activation. This ARF-activating protein is a strong candidate for the molecular target for brefeldin A. The ubiquitous nature of ARF proteins and their importance in both the exocytic and endocytic pathways may explain the effects of brefeldin A on both exocytic and endocytic membrane traffic in animal cells. A protease-insensitive activation of ARF by Golgi could also be demonstrated and was the dominant activity observed in submicromolar concentrations of magnesium. We believe this to be the lipid-mediated process described previously for purified ARF proteins. ARF activation resulted in tight association of ARF with phospholipid vesicles. Vesicle association required amino-terminal myristoylation of ARF whereas activation did not. These studies indicate that the brefeldin A-sensitive ARF-activating protein and other factors that determine the level of activation of ARF in animal cells are fundamental regulators of membrane traffic in animal cells. JF - The Journal of biological chemistry AU - Randazzo, P A AU - Yang, Y C AU - Rulka, C AU - Kahn, R A AD - Section of Regulatory Mechanisms, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/05/05/ PY - 1993 DA - 1993 May 05 SP - 9555 EP - 9563 VL - 268 IS - 13 SN - 0021-9258, 0021-9258 KW - Carrier Proteins KW - 0 KW - Cyclopentanes KW - Myristic Acids KW - Peptides KW - Recombinant Proteins KW - Myristic Acid KW - 0I3V7S25AW KW - NAD KW - 0U46U6E8UK KW - Guanosine Diphosphate KW - 146-91-8 KW - Brefeldin A KW - 20350-15-6 KW - Guanosine 5'-O-(3-Thiotriphosphate) KW - 37589-80-3 KW - Guanosine Triphosphate KW - 86-01-1 KW - Cholera Toxin KW - 9012-63-9 KW - Endopeptidases KW - EC 3.4.- KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - ADP-Ribosylation Factors KW - EC 3.6.5.2 KW - Dimyristoylphosphatidylcholine KW - U86ZGC74V5 KW - Index Medicus KW - Peptides -- chemical synthesis KW - Animals KW - Guanosine Diphosphate -- metabolism KW - Humans KW - Cholera Toxin -- pharmacology KW - Brain -- metabolism KW - Guanosine Triphosphate -- metabolism KW - Rats KW - NAD -- metabolism KW - Recombinant Proteins -- metabolism KW - Molecular Sequence Data KW - CHO Cells KW - Dimyristoylphosphatidylcholine -- metabolism KW - Centrifugation, Density Gradient KW - Endoplasmic Reticulum -- metabolism KW - Carrier Proteins -- metabolism KW - Amino Acid Sequence KW - Myristic Acids -- metabolism KW - Cyclopentanes -- pharmacology KW - Cattle KW - Kinetics KW - Guanosine 5'-O-(3-Thiotriphosphate) -- metabolism KW - Cricetinae KW - GTP-Binding Proteins -- metabolism KW - GTP-Binding Proteins -- isolation & purification KW - Endopeptidases -- metabolism KW - Liver -- metabolism KW - Golgi Apparatus -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75730021?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Activation+of+ADP-ribosylation+factor+by+Golgi+membranes.+Evidence+for+a+brefeldin+A-+and+protease-sensitive+activating+factor+on+Golgi+membranes.&rft.au=Randazzo%2C+P+A%3BYang%2C+Y+C%3BRulka%2C+C%3BKahn%2C+R+A&rft.aulast=Randazzo&rft.aufirst=P&rft.date=1993-05-05&rft.volume=268&rft.issue=13&rft.spage=9555&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-04 N1 - Date created - 1993-06-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Role of the fusion peptide sequence in initial stages of influenza hemagglutinin-induced cell fusion. AN - 75726655; 8387488 AB - The fusion activity of influenza hemagglutinin (HA) and of HA proteins altered in the amino terminus of HA2 (fusion peptide) by site-directed mutagenesis (Gething, M.-J., Doms, R. W., York, D., and White, J. (1986) J. Cell Biol. 102, 11-23) was analyzed following expression in CV-1 cells using SV40-HA recombinant virus vectors. Fusion was monitored by the redistribution of lipid and cytoplasmic dyes between fluorescently labeled erythrocytes and HA-expressing CV-1 cells using spectrofluorometry and fluorescence microscopy. The kinetics of lipid redistribution after lowering the pH showed the same pattern for wild type HA and nonlethal mutants, although there were shifts in the pH threshold. The time for commitment to the fusogenic state and the temperature dependence of the processes leading to HA-mediated fusion were also the same for wild type and nonlethal mutants. However, striking differences were observed between wild type HA and the nonlethal mutants in their ability to induce pH-dependent redistribution from erythrocytes to HA-expressing cells of large molecular weight (M(r) > 10,000) fluorescently labeled dextran molecules. The data indicate that the kinetic processes which are measurable in the time range of seconds are insensitive to the structure of the fusion peptide. Surprisingly, however, the fusion peptide plays an important role in later processes related to pore widening which eventually results in delivery of the nucleocapsid into the cell. JF - The Journal of biological chemistry AU - Schoch, C AU - Blumenthal, R AD - Section on Membrane Structure and Function, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/05/05/ PY - 1993 DA - 1993 May 05 SP - 9267 EP - 9274 VL - 268 IS - 13 SN - 0021-9258, 0021-9258 KW - Hemagglutinin Glycoproteins, Influenza Virus KW - 0 KW - Hemagglutinins, Viral KW - Viral Envelope Proteins KW - Index Medicus KW - Animals KW - Simian virus 40 -- genetics KW - Humans KW - Hydrogen-Ion Concentration KW - Amino Acid Sequence KW - Mutagenesis, Site-Directed KW - Kinetics KW - Cercopithecus aethiops KW - Kidney KW - Molecular Sequence Data KW - Viral Envelope Proteins -- metabolism KW - Cell Line KW - Erythrocyte Membrane -- metabolism KW - Hemagglutinins, Viral -- metabolism KW - Cell Fusion KW - Hemagglutinins, Viral -- genetics KW - Erythrocytes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75726655?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Role+of+the+fusion+peptide+sequence+in+initial+stages+of+influenza+hemagglutinin-induced+cell+fusion.&rft.au=Schoch%2C+C%3BBlumenthal%2C+R&rft.aulast=Schoch&rft.aufirst=C&rft.date=1993-05-05&rft.volume=268&rft.issue=13&rft.spage=9267&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-04 N1 - Date created - 1993-06-04 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - J02127; GENBANK N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Mutational analysis of the Golgi retention signal of bovine beta-1,4-galactosyltransferase. AN - 75726494; 8387508 AB - To examine the role of the NH2-terminal region of the 402-residue-long beta-1,4-galactosyltransferase (beta-1,4-GT), a series of mutants and chimeric cDNA were constructed by polymerase chain reaction and transiently expressed in COS-7 cells, the enzyme activities were measured, and the protein was localized in the cells by subcellular fractionation or indirect immunofluorescence microscopy. We showed earlier that the deletion of the amino-terminal cytoplasmic tail and transmembrane domain from GT abolishes the stable expression of this protein in mammalian cells (Masibay, A.S., Boeggeman, E., and Qasba, P.K. (1992) Mol. Biol. Rep. 16, 99-104). Further deletion analyses of the amino-terminal region show that the first 21 amino acids of beta-1,4-GT are not essential for the stable production of the protein and are consistently localized in the Golgi apparatus. In addition, analysis of hybrid constructs showed that residues 1-25 of alpha-1,3-galactosyltransferase can functionally replace the beta-1,4-GT amino-terminal domain (residues 1-43). This fusion protein also showed Golgi localization. On the other hand, the alpha-2,6-sialyltransferase/beta-1,4-GT fusion protein (alpha-2,6-ST/beta-1,4-GT) needed additional COOH-terminal sequences flanking the transmembrane domain of the alpha-2,6-ST for stability and Golgi localization. Substitution of Arg-24, Leu-25, Leu-26, and His-33 of the beta-1,4-GT transmembrane by Ile (pLFM) or substitution of Tyr by Ile at positions 40 and 41 coupled with the insertion of 4 Ile residues at position 43 (pLB) released the mutant proteins from the Golgi and was detected on the cell surface. Our results show that (a) the transmembrane domains of beta-1,4-GT, alpha-1,3-galactosyltransferase, and alpha-2,6-ST, along with its stem region, all play a role in Golgi targeting and participate in a common mechanism that allows the protein to be processed properly and not be degraded in vivo; (b) increasing the length of the transmembrane domain overrides the Golgi retention signal and directs the enzyme to the plasma membrane; and (c) the length of the hydrophobic region of the transmembrane domain of beta-1,4-GT is an important parameter but is not sufficient by itself for Golgi retention. JF - The Journal of biological chemistry AU - Masibay, A S AU - Balaji, P V AU - Boeggeman, E E AU - Qasba, P K AD - Laboratory of Mathematical Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/05/05/ PY - 1993 DA - 1993 May 05 SP - 9908 EP - 9916 VL - 268 IS - 13 SN - 0021-9258, 0021-9258 KW - DNA, Recombinant KW - 0 KW - Oligodeoxyribonucleotides KW - Protein Sorting Signals KW - Recombinant Proteins KW - N-Acetyllactosamine Synthase KW - EC 2.4.1.90 KW - Sodium-Potassium-Exchanging ATPase KW - EC 3.6.3.9 KW - Index Medicus KW - Animals KW - Immunoblotting KW - Cell Membrane -- enzymology KW - Amino Acid Sequence KW - Mutagenesis KW - Base Sequence KW - Cattle KW - Sodium-Potassium-Exchanging ATPase -- metabolism KW - DNA, Recombinant -- metabolism KW - Transfection KW - Recombinant Proteins -- metabolism KW - Molecular Sequence Data KW - Recombinant Proteins -- analysis KW - Cell Line KW - Sequence Deletion KW - Protein Conformation KW - Protein Sorting Signals -- metabolism KW - N-Acetyllactosamine Synthase -- genetics KW - N-Acetyllactosamine Synthase -- analysis KW - N-Acetyllactosamine Synthase -- metabolism KW - Golgi Apparatus -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75726494?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Mutational+analysis+of+the+Golgi+retention+signal+of+bovine+beta-1%2C4-galactosyltransferase.&rft.au=Masibay%2C+A+S%3BBalaji%2C+P+V%3BBoeggeman%2C+E+E%3BQasba%2C+P+K&rft.aulast=Masibay&rft.aufirst=A&rft.date=1993-05-05&rft.volume=268&rft.issue=13&rft.spage=9908&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-04 N1 - Date created - 1993-06-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Binding of mutants of human insulin-like growth factor II to insulin-like growth factor binding proteins 1-6. AN - 75721283; 7683646 AB - A family of six specific insulin-like growth factor binding proteins (IGFBPs) modulates the biological actions of the insulin-like growth factors, IGF-I and IGF-II. In the present study, we determined the binding affinity of purified human IGFBPs 1-6 for recombinant human IGF-II mutants whose binding to IGF-I, IGF-II/mannose 6-phosphate, and insulin receptors was previously reported (Sakano, K., Enjoh, T., Numata, F., Fujiwara, H., Marumoto, Y., Higashihashi, N., Sato, Y., Perdue, J. F., and Fujita-Yamaguchi, Y. (1991) J. Biol. Chem. 266, 20626-20635). Of the regions studied, the most important determinants of IGF-II binding to the IGFBPs were A-domain residues 48-50 and B-domain residue 26. Substitution of residues 48-50 with the analogous residues from human insulin (Thr-Ser-Ile) reduced binding to IGFBP-1, -5, and -6 more than 50-fold and to IGFBP-4 by 15-50-fold; binding to IGFBP-2 and -3 was reduced 6-12-fold. The same substitution markedly reduced binding to the IGF-II/mannose 6-phosphate receptor but not to IGF-I or insulin receptors. Although substitution of residues 54 and 55 with the analogous residues from IGF-I (Arg-Arg) abolished binding to the IGF-II/mannose 6-phosphate receptor, binding to IGFBPs was not substantially affected. Substitution of Phe26 with Ser or Leu, which decreased binding to the IGF-I and insulin receptors, reduced binding to IGFBP-1 and -6 up to 80-fold, but had lesser effects on the other IGFBPs. [Leu27]IGF-II and [Leu43]IGF-II, which had a more markedly reduced affinity for the IGF-I and insulin receptors than did [Ser26]IGF-II, were bound by the IGFBPs with relatively unchanged affinity compared with IGF-II. Thus, the determinants of IGF-II binding to IGFBPs partially overlap those for the IGF-II/mannose 6-phosphate receptor and overlap those for the IGF-I receptor to a lesser extent. IGFBP-1 and IGFBP-6 are most sensitive to changes in IGF-II structure, although IGFBP-1 binds IGF-I and IGF-II with equal affinity, whereas IGFBP-6 has a marked preferential binding affinity for IGF-II. IGF-II mutants with selective impairment in recognition by specific IGFBPs or receptors will provide a useful tool for dissecting the role of the different IGF binding macromolecules in the mediation of IGF-II actions. JF - The Journal of biological chemistry AU - Bach, L A AU - Hsieh, S AU - Sakano, K AU - Fujiwara, H AU - Perdue, J F AU - Rechler, M M AD - Growth and Development Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/05/05/ PY - 1993 DA - 1993 May 05 SP - 9246 EP - 9254 VL - 268 IS - 13 SN - 0021-9258, 0021-9258 KW - Carrier Proteins KW - 0 KW - Insulin-Like Growth Factor Binding Protein 1 KW - Insulin-Like Growth Factor Binding Protein 2 KW - Insulin-Like Growth Factor Binding Protein 4 KW - Insulin-Like Growth Factor Binding Protein 5 KW - Insulin-Like Growth Factor Binding Protein 6 KW - Insulin-Like Growth Factor Binding Proteins KW - Recombinant Proteins KW - Insulin-Like Growth Factor I KW - 67763-96-6 KW - Insulin-Like Growth Factor II KW - 67763-97-7 KW - Index Medicus KW - Animals KW - Humans KW - Liver -- metabolism KW - Insulin-Like Growth Factor I -- metabolism KW - Amino Acid Sequence KW - Pregnancy KW - Rats KW - Mutagenesis, Site-Directed KW - Recombinant Proteins -- isolation & purification KW - Amniotic Fluid -- metabolism KW - Recombinant Proteins -- metabolism KW - Kinetics KW - Binding, Competitive KW - Molecular Sequence Data KW - Sequence Homology, Amino Acid KW - Female KW - Sequence Deletion KW - Carrier Proteins -- metabolism KW - Carrier Proteins -- cerebrospinal fluid KW - Insulin-Like Growth Factor II -- genetics KW - Insulin-Like Growth Factor II -- metabolism KW - Carrier Proteins -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75721283?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Binding+of+mutants+of+human+insulin-like+growth+factor+II+to+insulin-like+growth+factor+binding+proteins+1-6.&rft.au=Bach%2C+L+A%3BHsieh%2C+S%3BSakano%2C+K%3BFujiwara%2C+H%3BPerdue%2C+J+F%3BRechler%2C+M+M&rft.aulast=Bach&rft.aufirst=L&rft.date=1993-05-05&rft.volume=268&rft.issue=13&rft.spage=9246&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-04 N1 - Date created - 1993-06-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - A controlled trial of HA-1A in a canine model of gram-negative septic shock. AN - 75671326; 8474201 AB - To investigate the therapeutic efficacy and microbiological and physiological effects of a human IgM monoclonal antibody (HA-1A) directed against the lipid A component of endotoxin in a canine model of sepsis that simulates the cardiovascular abnormalities of human septic shock. Blinded, placebo-controlled 28-day trial. Purpose-bred beagles were implanted with an intraperitoneal clot infected with Escherichia coli O111:B4. At clot placement, animals received HA-1A (10 mg.kg-1), control human IgM antibody (10 mg.kg-1), or control human serum albumin intravenously. All animals were given antibiotic and fluid therapy. Survival and microbiological and physiological events. Only two (15%) of 13 animals in the HA-1A group, compared with eight (57%) of 14 control animals (combined control human IgM antibody and control human serum albumin groups) (P = .05), survived 28 days. At 24 hours, the HA-1A group had lower mean arterial pressure (P = .04) and cardiac index (P = .004) and higher lactate levels (P = .05) compared with the combined-controls group. In addition, these parameters in the HA-1A group were significantly more predictive of death. The HA-1A and combined-controls groups had similar significant increases in the level of endotoxemia and bacteremia. Studies of toxic effects showed no harmful effects of control human IgM antibody in infected animals or HA-1A in non-infected animals. In a canine model of E coli sepsis, HA-1A did not alter levels of bacteremia or endotoxemia and actually decreased survival. If these data are relevant to human septic shock, HA-1A therapy should be limited until the conditions under which this monoclonal antibody has beneficial or deleterious effects are more completely defined. JF - JAMA AU - Quezado, Z M AU - Natanson, C AU - Alling, D W AU - Banks, S M AU - Koev, C A AU - Elin, R J AU - Hosseini, J M AU - Bacher, J D AU - Danner, R L AU - Hoffman, W D AD - Department of Critical Care Medicine, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/05/05/ PY - 1993 DA - 1993 May 05 SP - 2221 EP - 2227 VL - 269 IS - 17 SN - 0098-7484, 0098-7484 KW - Antibodies, Monoclonal KW - 0 KW - Endotoxins KW - Immunoglobulin M KW - Serum Albumin KW - nebacumab KW - 138330-99-1 KW - Abridged Index Medicus KW - Index Medicus KW - Serum Albumin -- pharmacology KW - Immunoglobulin M -- pharmacology KW - Animals KW - Humans KW - Escherichia coli Infections -- drug therapy KW - Dogs KW - Disease Models, Animal KW - Male KW - Female KW - Survival Analysis KW - Gram-Negative Bacterial Infections -- mortality KW - Shock, Septic -- immunology KW - Shock, Septic -- drug therapy KW - Gram-Negative Bacterial Infections -- immunology KW - Gram-Negative Bacterial Infections -- drug therapy KW - Endotoxins -- immunology KW - Antibodies, Monoclonal -- pharmacology KW - Shock, Septic -- mortality KW - Antibodies, Monoclonal -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75671326?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=JAMA&rft.atitle=A+controlled+trial+of+HA-1A+in+a+canine+model+of+gram-negative+septic+shock.&rft.au=Quezado%2C+Z+M%3BNatanson%2C+C%3BAlling%2C+D+W%3BBanks%2C+S+M%3BKoev%2C+C+A%3BElin%2C+R+J%3BHosseini%2C+J+M%3BBacher%2C+J+D%3BDanner%2C+R+L%3BHoffman%2C+W+D&rft.aulast=Quezado&rft.aufirst=Z&rft.date=1993-05-05&rft.volume=269&rft.issue=17&rft.spage=2221&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-20 N1 - Date created - 1993-05-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: JAMA. 1993 May 5;269(17):2266-7 [8474207] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Cognitive and behavioral profile of the oculocerebrorenal syndrome of Lowe. AN - 85274336; pmid-8488875 AB - BACKGROUND: The oculocerebrorenal syndrome of Lowe (OCRL) is an X-linked disorder characterized by congenital cataracts, cognitive impairment, and renal tubular dysfunction. Significant behavioral difficulties have been reported, but no formal study of intelligence or behavior has been described. METHODS: We surveyed IQ and behavior using archival data and standardized instruments in 47 affected males. RESULTS: Mean IQ was in the moderate mental retardation range (40 or = 70). The OCRL population was comparable to a normative population with mental retardation in language, communication, and socialization skills, but lower in independent living skills than means of either populations of individuals with mental retardation or visual impairment. Maladaptive behaviors, particularly stubbornness, temper tantrums, and stereotypic behaviors, were very frequent (> 80%). CONCLUSIONS: The diagnosis of OCRL is compatible with normal intelligence. Maladaptive behaviors significantly interfere with adaptive functions. These behaviors appear to define a characteristic behavioral phenotype in OCRL. JF - American Journal of Medical Genetics AU - Kenworthy, L AU - Park, T AU - Charnas, L R AD - Human Genetics Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. PY - 1993 SP - 297 EP - 303 VL - 46 IS - 3 SN - 0148-7299, 0148-7299 KW - Mental Retardation KW - Intelligence KW - Support, U.S. Gov't, P.H.S. KW - Human KW - Adult KW - Stereotyped Behavior KW - Oculocerebrorenal Syndrome KW - Child KW - Aggression KW - Adolescent KW - Male KW - Rage KW - Mental Disorders UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85274336?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Medical+Genetics&rft.atitle=Cognitive+and+behavioral+profile+of+the+oculocerebrorenal+syndrome+of+Lowe.&rft.au=Kenworthy%2C+L%3BPark%2C+T%3BCharnas%2C+L+R&rft.aulast=Kenworthy&rft.aufirst=L&rft.date=1993-05-01&rft.volume=46&rft.issue=3&rft.spage=297&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Medical+Genetics&rft.issn=01487299&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Expression of AMPA-selective glutamate receptor subunits in morphologically defined neurons of the mammalian cochlear nucleus. AN - 85241299; pmid-7683046 AB - Glutamate and related amino acids mediate fast excitatory neurotransmission in the vertebrate CNS via ligand-gated cationic channels in the neuronal membrane. These channels are composed of different subunits that assemble into a functional receptor/channel complex. Although studies have shown that these subunits are differentially expressed in neurons, few studies have quantitatively addressed the cell-specific expression of glutamate subunits in relation to known glutamatergic pathways. In the vertebrate auditory system, glutamate is the proposed neurotransmitter of the auditory nerve and parallel fiber pathways. In situ hybridization histochemistry was used to localize AMPA-selective glutamate receptor subunit mRNAs in seven cell types of the rat cochlear nucleus. GluR1-GluR4 AMPA-selective subunits were all expressed in cochlear nucleus neurons; however, the subunits expressed in identified cells varied with the cell type. Granule cells, previously not known to receive glutamatergic input, expressed GluR2 and GluR4 subunits. Cartwheel and stellate interneurons in the dorsal cochlear nucleus, which receive parallel fiber input, expressed all four subunits. Neurons receiving synaptic input from the auditory nerve, including globular, round, spherical, and fusiform cells, expressed GluR2, GluR3, and GluR4 subunits. Furthermore, a subpopulation of round cells in the ventral cochlear nucleus, and fusiform cells in the dorsal cochlear nucleus, expressed the GluR3 subunit at greatly reduced levels compared to neighboring cells. The results confirm the auditory nerve and parallel fiber pathways as glutamatergic and identify a third synaptic population, projecting to granule cells, which is likely glutamatergic. The data suggest that the composition of GluR1-GluR4 subunits on neurons in the cochlear nucleus may be related to presynaptic input; moreover, heterogeneous patterns of expression of the GluR3 subunit, in addition, suggest that variability in mRNA levels within one population of morphologically defined cells is present. JF - The Journal of Neuroscience AU - Hunter, C AU - Petralia, R S AU - Vu T AU - Wenthold, R J AD - Section on Neurotransmitter Receptor Biology, NIDCD, National Institutes of Health, Bethesda, Maryland 20892. PY - 1993 SP - 1932 EP - 1946 VL - 13 IS - 5 SN - 0270-6474, 0270-6474 KW - Rats KW - RNA, Messenger KW - Granulocytes KW - In Situ Hybridization KW - Auditory Pathways KW - Neurons KW - alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid KW - Receptors, Glutamate KW - Animal KW - Cochlear Nerve KW - Ibotenic Acid KW - Tissue Distribution KW - Silver UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85241299?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+Neuroscience&rft.atitle=Expression+of+AMPA-selective+glutamate+receptor+subunits+in+morphologically+defined+neurons+of+the+mammalian+cochlear+nucleus.&rft.au=Hunter%2C+C%3BPetralia%2C+R+S%3BVu+T%3BWenthold%2C+R+J&rft.aulast=Hunter&rft.aufirst=C&rft.date=1993-05-01&rft.volume=13&rft.issue=5&rft.spage=1932&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+Neuroscience&rft.issn=02706474&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Cerebrospinal fluid pharmacokinetics and toxicology of intraventricular and intrathecal arabinosyl-5-azacytosine (fazarabine, NSC 281272) in the nonhuman primate. AN - 76144203; 7505267 AB - Arabinosyl-5-azacytosine (AAC), a new nucleoside antimetabolite, is broadly active in preclinical tumor screening evaluations. To assess the potential for intrathecal use of this drug, we studied the toxicity and pharmacokinetics of intrathecal and intraventricular administration in nonhuman primates. Four adult male rhesus monkeys were given single 10 mg intrathecal (n = 1) or intraventricular (n = 3) doses of AAC to determine its acute toxicity and pharmacokinetic parameters. An additional 3 animals were given four weekly 10 mg intrathecal doses to assess the systemic and neurologic toxicity associated with chronic administration. Disappearance from the cerebrospinal fluid (CSF) was biexponential, and CSF clearance was 0.2 ml/min, which exceeds the rate of CSF bulk flow by 5-fold. The peak CSF concentration and area under the concentration x time curve achieved with the intraventricular administration of 10 mg were one hundred, and fifty fold greater, respectively, than those achieved after an intravenous dose of 200 mg/kg (1500-2400 mg) in prior experiments. No clinically evident neurotoxicity was observed in either the single or the weekly x 4 dose groups. A slight, transient CSF pleocytosis and increased CSF protein was observed. Systemic toxicity was limited to one animal in the weekly x 4 dose group who demonstrated a mild and transient decrease in his peripheral leukocyte count unassociated with a change in his hematocrit or platelet count. These studies in nonhuman primates demonstrate a clear pharmacokinetic advantage for intrathecal vs systemic administration of AAC. This is demonstrated by a 50-fold greater CSF drug exposure with an intrathecal or intraventricular dose 1/200th of that which can be given systemically.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Investigational new drugs AU - Heideman, R L AU - McCully, C AU - Balis, F M AU - Poplack, D G AD - Pediatric Branch, National Cancer Institute, Bethesda, Maryland 20892. PY - 1993 SP - 135 EP - 140 VL - 11 IS - 2-3 SN - 0167-6997, 0167-6997 KW - Antineoplastic Agents KW - 0 KW - fazarabine KW - 5V71D8JOKK KW - Azacitidine KW - M801H13NRU KW - Index Medicus KW - Animals KW - Injections, Spinal KW - Macaca mulatta KW - Male KW - Injections, Intraventricular KW - Azacitidine -- pharmacokinetics KW - Antineoplastic Agents -- cerebrospinal fluid KW - Azacitidine -- cerebrospinal fluid KW - Azacitidine -- toxicity KW - Antineoplastic Agents -- pharmacokinetics KW - Antineoplastic Agents -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76144203?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Investigational+new+drugs&rft.atitle=Cerebrospinal+fluid+pharmacokinetics+and+toxicology+of+intraventricular+and+intrathecal+arabinosyl-5-azacytosine+%28fazarabine%2C+NSC+281272%29+in+the+nonhuman+primate.&rft.au=Heideman%2C+R+L%3BMcCully%2C+C%3BBalis%2C+F+M%3BPoplack%2C+D+G&rft.aulast=Heideman&rft.aufirst=R&rft.date=1993-05-01&rft.volume=11&rft.issue=2-3&rft.spage=135&rft.isbn=&rft.btitle=&rft.title=Investigational+new+drugs&rft.issn=01676997&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-01-24 N1 - Date created - 1994-01-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Multiple effects of spermine on N-methyl-D-aspartic acid receptor responses of rat cultured hippocampal neurones. AN - 76046679; 8229795 AB - 1. The modulation by polyamines of responses to N-methyl-D-aspartic acid (NMDA) was studied using a rapid perfusion system and whole-cell voltage-clamp recording from rat hippocampal neurons in dissociated culture. 2. Concentration jump responses to 100 microM NMDA in the presence of 10 microM glycine revealed potentiation by 3 mM spermine at a membrane potential of +60 mV, but depression at -120 mV; the degree of potentiation at +60 mV was variable from cell to cell while marked depression at -120 mV was observed in all cells. The depression of responses to NMDA by spermine was highly voltage dependent (z delta = 1.17) with an apparent equilibrium dissociation constant for block at 0 mV of 27 mM. 3. Analysis of spermine dose-potentiation curves for responses recorded at +60 mV in the presence of 10 microM glycine revealed a half-maximal effect at 125 microM. Under the same conditions, but at -60 mV, analysis of spermine-evoked depression was performed for cells with less than 5% potentiation at +60 mV, and revealed half-maximal inhibition at 344 microM. 4. Dose-response analysis for the glycine-sensitive activation of NMDA receptors at +60 mV revealed a 3.5-fold increase in apparent affinity for glycine in the presence of 1 mM spermine. This increase in affinity for glycine was accompanied by a 3.3-fold decrease in the rate of development of glycine-sensitive desensitization, and a 2.4-fold decrease in the rate of dissociation of glycine from NMDA receptors, while the rate constant for dissociation of NMDA was not reduced. 5. In the presence of non-saturating concentrations of glycine, spermine-induced potentiation at +60 mV developed with two exponential components: a slow glycine-sensitive component, the amplitude and time constant of which decreased with increasing glycine concentration (30 nM glycine, amplitude = 80.2 +/- 5.1%, tau = 780 +/- 79 ms; 3 microM glycine, amplitude = 22.6 +/- 7.1%, tau = 45 +/- 13 ms), and a faster component (tau < 20 ms at all concentrations of glycine), the amplitude of which varied from cell to cell, and which became larger with increase in concentration of glycine. When responses to the application of spermine were measured in the presence 10 microM L-alanine instead of 100 nM glycine, the slow component of potentiation was absent.(ABSTRACT TRUNCATED AT 400 WORDS) JF - The Journal of physiology AU - Benveniste, M AU - Mayer, M L AD - Laboratory of Cellular and Molecular Neurophysiology, NICHD, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 131 EP - 163 VL - 464 SN - 0022-3751, 0022-3751 KW - Receptors, N-Methyl-D-Aspartate KW - 0 KW - Spermine KW - 2FZ7Y3VOQX KW - N-Methylaspartate KW - 6384-92-5 KW - Glycine KW - TE7660XO1C KW - Index Medicus KW - Rats KW - Animals KW - N-Methylaspartate -- pharmacology KW - Glycine -- pharmacology KW - Dose-Response Relationship, Drug KW - Cells, Cultured KW - Kinetics KW - Glycine -- metabolism KW - N-Methylaspartate -- antagonists & inhibitors KW - Membrane Potentials KW - Drug Synergism KW - Neurons -- metabolism KW - Spermine -- pharmacology KW - Receptors, N-Methyl-D-Aspartate -- drug effects KW - Hippocampus -- metabolism KW - Hippocampus -- cytology KW - Neurons -- physiology KW - Receptors, N-Methyl-D-Aspartate -- metabolism KW - Hippocampus -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76046679?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+physiology&rft.atitle=Multiple+effects+of+spermine+on+N-methyl-D-aspartic+acid+receptor+responses+of+rat+cultured+hippocampal+neurones.&rft.au=Benveniste%2C+M%3BMayer%2C+M+L&rft.aulast=Benveniste&rft.aufirst=M&rft.date=1993-05-01&rft.volume=464&rft.issue=&rft.spage=131&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+physiology&rft.issn=00223751&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-26 N1 - Date created - 1993-11-26 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Neuron. 1992 Feb;8(2):343-52 [1531415] Science. 1992 Jan 24;255(5043):470-2 [1346477] Mol Pharmacol. 1992 Apr;41(4):727-35 [1373801] Science. 1992 May 22;256(5060):1217-21 [1350383] Proc Natl Acad Sci U S A. 1992 Oct 1;89(19):9359-63 [1409641] J Physiol. 1992 May;450:643-72 [1359126] J Physiol. 1990 Sep;428:313-31 [2172523] J Gen Physiol. 1973 Jun;61(6):687-708 [4541078] Pflugers Arch. 1981 Aug;391(2):85-100 [6270629] J Physiol. 1983 Jun;339:663-78 [6310093] Nature. 1984 Feb 2-8;307(5950):462-5 [6320006] Nature. 1984 May 17-23;309(5965):261-3 [6325946] Biophys J. 1986 Mar;49(3):607-18 [2421791] J Physiol. 1987 Dec;394:501-27 [2451020] J Physiol. 1988 May;399:247-66 [2457089] Science. 1988 Aug 12;241(4867):835-7 [2841759] J Neurochem. 1988 Sep;51(3):830-6 [2457653] J Physiol. 1988 Jan;395:131-59 [2457675] Neurosci Lett. 1988 Jul 8;89(3):313-8 [2458553] Nature. 1989 Mar 30;338(6214):425-7 [2538755] Science. 1989 Mar 24;243(4898):1611-3 [2467381] Mol Pharmacol. 1989 Oct;36(4):575-81 [2554112] Mol Pharmacol. 1989 Nov;36(5):758-65 [2555674] Mol Pharmacol. 1989 Dec;36(6):836-9 [2557533] J Neurosci. 1990 Jan;10(1):1-10 [1688928] Neuron. 1990 May;4(5):725-31 [2160836] J Physiol. 1990 Mar;422:203-25 [1972190] J Neurophysiol. 1990 Jun;63(6):1373-84 [1972740] Synapse. 1990;5(4):294-8 [1972818] Eur J Pharmacol. 1990 Apr 25;179(3):477-8 [1694770] J Physiol. 1989 Aug;415:329-50 [2561788] Nature. 1990 Aug 9;346(6284):565-7 [1974037] Neuron. 1990 Aug;5(2):199-208 [2166545] Trends Pharmacol Sci. 1990 Jul;11(7):290-6 [2167544] J Physiol. 1990 Sep;428:333-57 [2146385] Mol Pharmacol. 1990 Oct;38(4):554-61 [2172769] J Pharmacol Exp Ther. 1990 Dec;255(3):1001-7 [2148185] Proc Natl Acad Sci U S A. 1990 Dec;87(24):9971-4 [1702227] Life Sci. 1991;48(6):469-98 [1825128] Neurosci Lett. 1990 Nov 27;120(1):17-20 [2149877] Biophys J. 1991 Mar;59(3):560-73 [1710938] J Neurochem. 1991 Sep;57(3):811-8 [1830614] Neuron. 1991 Oct;7(4):605-13 [1681832] Mol Pharmacol. 1992 Jan;41(1):83-8 [1370709] J Neurosci. 1992 Feb;12(2):635-43 [1346806] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Studies of binding and internalization of human recombinant monocyte chemotactic and activating factor (MCAF) by monocytic cells. AN - 76036060; 8218939 AB - Recombinant human monocyte chemotactic and activating factor (MCAF) was iodinated and specific binding sites for this cytokine were detected on human peripheral blood monocytes, the monocytic leukemia cell line THP-1, and on PMA-differentiated HL60 and U937 cell lines. The binding sites were specific for MCAF since other polypeptide cytokines and the chemotactic peptide formyl-methionyl-leucyl-phenylalanine (fMLP) failed to compete for 125I-rhMCAF binding. Steady-state binding experiments at 4 degrees C revealed the presence of 13,000 and 18,000 receptor sites/cell on monocytes and THP-1 cells with Kd values of 22.5 nM and 25.7 nM, respectively. Compared to a human natural MCAF, rhMCAF was less potent in inducing maximal monocyte migration. Human natural MCAF similarly competed more efficiently for 125I-rhMCAF binding than unlabelled rhMCAF. The ligand-receptor association was highly temperature-dependent, with maximal ligand uptake at 37 degrees C accompanied by internalization of the ligand-receptor complexes. The internalized 125I-MCAF was progressively degraded and released into the culture medium starting at 30 min. Lysosomotropic ammonium chloride could inhibit the degradation of this ligand suggesting the involvement of lysosomal enzymes in the proteolytic digestion. Incubation with cycloheximide did not block the rapid reappearance of MCAF receptors within 20 min on the cell surface indicative of receptor recycling rather than new protein synthesis. These data indicate that monocytic cells express specific receptors for rhMCAF which can be dynamically regulated by MCAF. JF - Cytokine AU - Wang, J M AU - Hishinuma, A AU - Oppenheim, J J AU - Matsushima, K AD - Laboratory of Molecular Immunoregulation, National Cancer Institute, Frederick Cancer Research and Development Center, Maryland 21702. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 264 EP - 275 VL - 5 IS - 3 SN - 1043-4666, 1043-4666 KW - Chemokine CCL2 KW - 0 KW - Chemotactic Factors KW - Cytokines KW - Receptors, CCR2 KW - Receptors, Chemokine KW - Receptors, Cytokine KW - Recombinant Proteins KW - Cycloheximide KW - 98600C0908 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Leukemia, Monocytic, Acute KW - Tumor Cells, Cultured KW - Recombinant Proteins -- metabolism KW - Kinetics KW - Humans KW - Cycloheximide -- pharmacology KW - In Vitro Techniques KW - Biological Transport KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Cell Line KW - Neutrophils -- metabolism KW - Receptors, Cytokine -- biosynthesis KW - Monocytes -- metabolism KW - Cytokines -- metabolism KW - Chemotactic Factors -- metabolism KW - Receptors, Cytokine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76036060?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cytokine&rft.atitle=Studies+of+binding+and+internalization+of+human+recombinant+monocyte+chemotactic+and+activating+factor+%28MCAF%29+by+monocytic+cells.&rft.au=Wang%2C+J+M%3BHishinuma%2C+A%3BOppenheim%2C+J+J%3BMatsushima%2C+K&rft.aulast=Wang&rft.aufirst=J&rft.date=1993-05-01&rft.volume=5&rft.issue=3&rft.spage=264&rft.isbn=&rft.btitle=&rft.title=Cytokine&rft.issn=10434666&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-15 N1 - Date created - 1993-12-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Liver carcinogenesis is not a predicted outcome of chemically induced hepatocyte proliferation. AN - 75944606; 8367884 AB - Cell proliferation has long been recognized as a basic component of multistage carcinogenesis. Based largely on the finding that certain nongenotoxic chemical carcinogens induce cell proliferation in the same organ that develops tumors after long-term exposure, some suggest that the increased rates of cell division account for the carcinogenicity of these chemicals. This paper examines relationships between chemically induced liver toxicity, cell proliferation, and liver carcinogenesis; major factors include consistency, transient vs. sustained dose-response correspondence, and scientific plausibility. For a presumed mechanism to be valid, a sustained proliferative response is critical, largely because transient increases in hepatocyte proliferation are not sufficient to induce cancer or promote liver tumor development. A consistent association between liver toxicity and carcinogenicity has not been established. Our evaluation of studies on purported relationships between chemically induced cell proliferation and liver carcinogenesis shows: 1) that inconsistencies in sex and species specificity exist, 2) that a large percentage of proliferative responses are transient, 3) that inconsistencies in response to various hepatic peroxisome proliferators are common, and 4) that dose-response and duration relationships have not been sufficiently examined. Studies of proliferative responses of putative preneoplastic cells in the liver indicate that these cells divide faster than normal hepatocytes and also have higher death rates. Chemicals that induce cell proliferation in preneoplastic foci do not always provide a persistent increase in replication rates, even with continuous exposure. A selective growth advantage to preneoplastic cells in the liver may be provided either by an enhancement of the replication rates of these cells compared to the surrounding normal hepatocytes, by inhibition of cell loss, or by inhibition of the growth rate of normal cells. More work is needed to understand how chemical carcinogens and noncarcinogens affect cell division and cell loss of normal hepatocytes and of preneoplastic cells; measurements of hepatocyte proliferation alone are not sufficient to elucidate mechanisms of liver tumor development or to predict liver carcinogenesis. Because of our limited knowledge of the complex molecular changes occurring during liver cancer, it would be inappropriate and far too premature to amend scientific risk assessment procedures for nongenotoxic chemical carcinogens based on oversimplified or incompletely tested speculations. JF - Toxicology and industrial health AU - Melnick, R L AU - Huff, J AD - National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. PY - 1993 SP - 415 EP - 438 VL - 9 IS - 3 SN - 0748-2337, 0748-2337 KW - Carcinogens KW - 0 KW - Hydrocarbons, Halogenated KW - Index Medicus KW - Rats KW - Animals KW - Hydrocarbons, Halogenated -- toxicity KW - Cell Transformation, Neoplastic -- pathology KW - Dose-Response Relationship, Drug KW - Chemical and Drug Induced Liver Injury KW - Cell Transformation, Neoplastic -- chemically induced KW - Cell Division -- drug effects KW - Carcinogenicity Tests KW - Mice KW - Male KW - Female KW - Liver -- drug effects KW - Liver Diseases -- pathology KW - Liver Neoplasms -- chemically induced KW - Carcinogens -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75944606?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+industrial+health&rft.atitle=Liver+carcinogenesis+is+not+a+predicted+outcome+of+chemically+induced+hepatocyte+proliferation.&rft.au=Melnick%2C+R+L%3BHuff%2C+J&rft.aulast=Melnick&rft.aufirst=R&rft.date=1993-05-01&rft.volume=9&rft.issue=3&rft.spage=415&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+industrial+health&rft.issn=07482337&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-01 N1 - Date created - 1993-10-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Palpebral amelanotic melanomas in F344 rats. AN - 75854128; 8333109 AB - Spontaneous amelanotic melanomas in the eyelids of F344 rats were found in one of 1/926 (0.11%) male and 5/925 (0.54%) female F344 rats that were used as control and treated animals in five different carcinogenicity studies conducted by the National Toxicology Program (Research Triangle Park, NC). These melanomas were grossly recognized as single, tan or white, well-circumscribed masses of the right or left eyelid. These melanomas primarily occurred in the dermis of the skin of the eyelids and consisted of poorly differentiated spindle cells characteristically arranged in interlacing fascicles. Rarely, epithelioid tumor cells were also observed, and these tumor cells showed a negative histochemical reaction for melanin. The epidermis and dermal-epidermal junction were usually uninvolved. The diagnosis of amelanotic melanoma could only be established by electron microscopic examination. The most striking ultrastructural feature of the tumor cells was a large number of intracytoplasmic premelanosomes (stage II melanosomes without melanin), which nearly filled the cytoplasm of most tumor cells. Giant premelanosomes and melanophagosomes were also seen. The tumor cells did not possess the ultrastructural features characteristics of Schwann cells (thin, long cell processes and pericytoplasmic basal laminae). The histologic and ultrastructural features of these palpebral tumors were similar to those of cutaneous amelanotic melanomas of the pinna in F344 rats. JF - Veterinary pathology AU - Yoshitomi, K AU - Boorman, G A AD - Experimental Pathology Laboratory, National Institute of Environmental Health Sciences, Research Triangle Park, NC. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 280 EP - 286 VL - 30 IS - 3 SN - 0300-9858, 0300-9858 KW - Index Medicus KW - Rats KW - Animals KW - Carcinogenicity Tests KW - Microscopy, Electron KW - Male KW - Female KW - Rats, Inbred F344 KW - Eyelid Neoplasms -- pathology KW - Melanoma -- pathology KW - Melanoma -- chemically induced KW - Eyelid Neoplasms -- chemically induced KW - Melanocytes -- ultrastructure KW - Rodent Diseases -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75854128?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Veterinary+pathology&rft.atitle=Palpebral+amelanotic+melanomas+in+F344+rats.&rft.au=Yoshitomi%2C+K%3BBoorman%2C+G+A&rft.aulast=Yoshitomi&rft.aufirst=K&rft.date=1993-05-01&rft.volume=30&rft.issue=3&rft.spage=280&rft.isbn=&rft.btitle=&rft.title=Veterinary+pathology&rft.issn=03009858&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-16 N1 - Date created - 1993-08-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Proconvulsant action of diethyldithiocarbamate in stimulation of the perforant path. AN - 75851788; 8393131 AB - The ability of diethyldithiocarbamate (DEDTC) to prolong electrical afterdischarge (AD) and lower the threshold for behavioral seizures elicited by stimulation of the perforant path (PPS) was examined. DEDTC was given in doses of 25, 50, and 100 mg/kg, IP. The effects of DEDTC on the threshold for wet dog shakes (WDS) and the number of WDS elicited by PPS were inconsistent. It had no effect on the duration of AD accompanied with WDS. However, DEDTC, at both 50 and 100 mg/kg, significantly lowered the threshold for rearing accompanied with forelimb clonus. At 100 mg/kg, it also prolonged the duration of AD occurring with these seizures. The effects of DEDTC were transitory and coincided with the time course for its ability to chelate the mossy fiber intravesicular pool of zinc (i.e., that which is released by activation of dentate granule cells). It is suggested that release of zinc from the mossy fibers may serve to protect the hippocampus from paroxysmal seizure activity. JF - Neurotoxicology and teratology AU - Mitchell, C L AU - Barnes, M I AD - Laboratory of Molecular and Integrative Neuroscience, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. PY - 1993 SP - 165 EP - 171 VL - 15 IS - 3 SN - 0892-0362, 0892-0362 KW - Chelating Agents KW - 0 KW - Convulsants KW - Ditiocarb KW - 99Z2744345 KW - Zinc KW - J41CSQ7QDS KW - Index Medicus KW - Seizures -- chemically induced KW - Animals KW - Dose-Response Relationship, Drug KW - Neural Pathways -- physiology KW - Zinc -- blood KW - Seizures -- prevention & control KW - Histocytochemistry KW - Neural Pathways -- drug effects KW - Hippocampus -- drug effects KW - Rats KW - Chelating Agents -- pharmacology KW - Rats, Inbred F344 KW - Zinc -- physiology KW - Male KW - Hippocampus -- anatomy & histology KW - Ditiocarb -- toxicity KW - Behavior, Animal -- drug effects KW - Convulsants -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75851788?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurotoxicology+and+teratology&rft.atitle=Proconvulsant+action+of+diethyldithiocarbamate+in+stimulation+of+the+perforant+path.&rft.au=Mitchell%2C+C+L%3BBarnes%2C+M+I&rft.aulast=Mitchell&rft.aufirst=C&rft.date=1993-05-01&rft.volume=15&rft.issue=3&rft.spage=165&rft.isbn=&rft.btitle=&rft.title=Neurotoxicology+and+teratology&rft.issn=08920362&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-23 N1 - Date created - 1993-08-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Trends in cirrhosis morbidity and mortality: United States, 1979-1988. AN - 75848700; 8337600 JF - Seminars in liver disease AU - Dufour, M C AU - Stinson, F S AU - Caces, M F AD - Division of Biometry and Epidemiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20857. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 109 EP - 125 VL - 13 IS - 2 SN - 0272-8087, 0272-8087 KW - Index Medicus KW - Humans KW - Death Certificates KW - Adult KW - Incidence KW - Aged KW - Middle Aged KW - Hospitalization -- statistics & numerical data KW - Adolescent KW - United States -- epidemiology KW - Morbidity KW - Male KW - Female KW - Prevalence KW - Liver Cirrhosis -- epidemiology KW - Liver Cirrhosis, Alcoholic -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75848700?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Seminars+in+liver+disease&rft.atitle=Trends+in+cirrhosis+morbidity+and+mortality%3A+United+States%2C+1979-1988.&rft.au=Dufour%2C+M+C%3BStinson%2C+F+S%3BCaces%2C+M+F&rft.aulast=Dufour&rft.aufirst=M&rft.date=1993-05-01&rft.volume=13&rft.issue=2&rft.spage=109&rft.isbn=&rft.btitle=&rft.title=Seminars+in+liver+disease&rft.issn=02728087&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-26 N1 - Date created - 1993-08-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Chronic inhibition of monoamine oxidase type A increases noradrenaline release in rat frontal cortex. AN - 75833094; 8391652 AB - Chronic but not acute treatment of rats with MAO inhibitors, as with other antidepressant drugs, has been shown to down-regulate the number of cerebro-cortical beta-adrenoceptors. In order to establish whether this effect is associated with an increase in cortical noradrenaline release, rats were treated for 1, 3 or 21 days with clorgyline (2 mg/kg i.p. single injection; 1 mg/kg i.p. repeated injections), and the frontal cortex was then perfused by microdialysis in the awake animal. Control animals were injected with saline. The concentration of noradrenaline in the microdialysate increased only slightly after 1 or 3 days of clorgyline treatment but increased fourfold over control levels after 21 days treatment. Yohimbine (20 mumol/l) added to the perfusing solution caused a similar degree of enhancement in microdialysate noradrenaline concentration in all groups of rats. Tetrodotoxin (10 mumol/l) reduced noradrenaline concentration to low levels in all groups of animals, but noradrenaline was still detectable in the microdialysate in rats treated with clorgyline for 21 days. Concentrations of the deaminated metabolites dihydroxyphenylacetic acid, dihydroxyphenylglycol and methoxy-hydroxyphenylglycol were lowest after the 21 day clorgyline treatment. Determination of enzyme activity ex vivo showed that MAO-A was inhibited more than 95% by all clorgyline treatments with less than 10% inhibition of MAO-B. The results indicate that cerebrocortical noradrenaline release increases gradually during chronic MAO inhibition. This may be the result of more complete inhibition of the enzyme with time, not detectable by the ex vivo assay, but shown by the progressive reduction in metabolite levels.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Naunyn-Schmiedeberg's archives of pharmacology AU - Finberg, J P AU - Pacak, K AU - Kopin, I J AU - Goldstein, D S AD - Clinical Neurochemistry Section, N.I.N.D.S., N.I.H., Bethesda, MD 20892. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 500 EP - 505 VL - 347 IS - 5 SN - 0028-1298, 0028-1298 KW - Monoamine Oxidase Inhibitors KW - 0 KW - Receptors, Adrenergic, alpha KW - Yohimbine KW - 2Y49VWD90Q KW - Tetrodotoxin KW - 4368-28-9 KW - Monoamine Oxidase KW - EC 1.4.3.4 KW - Clorgyline KW - LYJ16FZU9Q KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Rats KW - Animals KW - Rats, Sprague-Dawley KW - Dialysis KW - Clorgyline -- administration & dosage KW - Yohimbine -- pharmacology KW - Receptors, Adrenergic, alpha -- metabolism KW - Tetrodotoxin -- pharmacology KW - Monoamine Oxidase -- metabolism KW - Male KW - Frontal Lobe -- drug effects KW - Norepinephrine -- metabolism KW - Frontal Lobe -- enzymology KW - Monoamine Oxidase Inhibitors -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75833094?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Naunyn-Schmiedeberg%27s+archives+of+pharmacology&rft.atitle=Chronic+inhibition+of+monoamine+oxidase+type+A+increases+noradrenaline+release+in+rat+frontal+cortex.&rft.au=Finberg%2C+J+P%3BPacak%2C+K%3BKopin%2C+I+J%3BGoldstein%2C+D+S&rft.aulast=Finberg&rft.aufirst=J&rft.date=1993-05-01&rft.volume=347&rft.issue=5&rft.spage=500&rft.isbn=&rft.btitle=&rft.title=Naunyn-Schmiedeberg%27s+archives+of+pharmacology&rft.issn=00281298&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-05 N1 - Date created - 1993-08-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Psychometric instruments to assist in alcoholism treatment planning. AN - 75809000; 8315703 AB - The clinical practice of alcoholism treatment can be enhanced by the judicious use of standardized psychometric instruments to characterize clients during the course of treatment. Knowledge of key behavioral, personality, and alcohol-specific factors will increase the clinician's ability to select the most appropriate treatment option, or, even if treatment options are limited, at least to develop a treatment plant with the patient's unique needs in mind. Monitoring of progress towards treatment goals can also be facilitated by the use of selected assessment tools. Seven examples of well-validated instruments are discussed, with suggestions on how data derived from them may be applied in the treatment planning process. JF - Journal of substance abuse treatment AU - Allen, J P AU - Mattson, M E AD - National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20857. PY - 1993 SP - 289 EP - 296 VL - 10 IS - 3 SN - 0740-5472, 0740-5472 KW - Index Medicus KW - Motivation KW - Personality Inventory -- statistics & numerical data KW - Combined Modality Therapy KW - Humans KW - Alcohol Drinking -- psychology KW - Psychometrics KW - Alcoholism -- rehabilitation KW - Personality Assessment -- statistics & numerical data KW - Patient Care Planning KW - Alcoholism -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75809000?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+substance+abuse+treatment&rft.atitle=Psychometric+instruments+to+assist+in+alcoholism+treatment+planning.&rft.au=Allen%2C+J+P%3BMattson%2C+M+E&rft.aulast=Allen&rft.aufirst=J&rft.date=1993-05-01&rft.volume=10&rft.issue=3&rft.spage=289&rft.isbn=&rft.btitle=&rft.title=Journal+of+substance+abuse+treatment&rft.issn=07405472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-29 N1 - Date created - 1993-07-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Paternal lineage of alcoholism, cohort effects, and alcoholism criteria. AN - 75798496; 8518712 AB - Adoption studies have led to the suggestion that there may be two distinct subgroups of alcoholics with differing genetic contributions. Among 249 male alcoholics we used discriminant analysis to relate the features of type 1 and type 2 alcoholism to the presence or absence of a family history of alcoholism in male paternal relatives. We found that guilt and binging, features usually attributed to type 1 (milieu-limited) alcoholism, were in fact more prevalent in the family history positive group. An additional cohort analysis found cohort-related variations in type 1/type 2 characteristics. The possible implications of these findings are discussed. JF - Addiction (Abingdon, England) AU - De Jong, J A AU - Roy, A AD - Laboratory of Clinical Studies, DICBR, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 623 EP - 629 VL - 88 IS - 5 SN - 0965-2140, 0965-2140 KW - Index Medicus KW - Risk Factors KW - Models, Genetic KW - Humans KW - Cohort Studies KW - Adult KW - Alcohol Drinking -- psychology KW - Middle Aged KW - Follow-Up Studies KW - Alcohol Drinking -- genetics KW - Male KW - Child of Impaired Parents -- psychology KW - Alcoholism -- classification KW - Alcoholism -- genetics KW - Alcoholism -- psychology KW - Social Environment UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75798496?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Addiction+%28Abingdon%2C+England%29&rft.atitle=Paternal+lineage+of+alcoholism%2C+cohort+effects%2C+and+alcoholism+criteria.&rft.au=De+Jong%2C+J+A%3BRoy%2C+A&rft.aulast=De+Jong&rft.aufirst=J&rft.date=1993-05-01&rft.volume=88&rft.issue=5&rft.spage=623&rft.isbn=&rft.btitle=&rft.title=Addiction+%28Abingdon%2C+England%29&rft.issn=09652140&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-28 N1 - Date created - 1993-07-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Improved protein detection with a polyvinylidene fluoride transfer membrane for two-dimensional gel electrophoresis. AN - 75789847; 7685610 JF - BioTechniques AU - Patterson, R M AU - Witcher, L L AU - He, C AU - Selkirk, J K AU - Merrick, B A AD - National Institute of Environmental Health Sciences, Laboratory of Molecular Carcinogenesis, Research Triangle Park, NC 27709. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 752 EP - 753 VL - 14 IS - 5 SN - 0736-6205, 0736-6205 KW - Membranes, Artificial KW - 0 KW - Polyvinyls KW - Proteins KW - polyvinylidene fluoride KW - 24937-79-9 KW - Index Medicus KW - Animals KW - Fibroblasts -- chemistry KW - Mice KW - Staining and Labeling KW - Biotechnology KW - Electrophoresis, Gel, Two-Dimensional -- methods KW - Proteins -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75789847?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BioTechniques&rft.atitle=Improved+protein+detection+with+a+polyvinylidene+fluoride+transfer+membrane+for+two-dimensional+gel+electrophoresis.&rft.au=Patterson%2C+R+M%3BWitcher%2C+L+L%3BHe%2C+C%3BSelkirk%2C+J+K%3BMerrick%2C+B+A&rft.aulast=Patterson&rft.aufirst=R&rft.date=1993-05-01&rft.volume=14&rft.issue=5&rft.spage=752&rft.isbn=&rft.btitle=&rft.title=BioTechniques&rft.issn=07366205&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-20 N1 - Date created - 1993-07-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - D1 and D2 dopamine receptor-mediated mechanisms and behavioral supersensitivity. AN - 75782351; 8516358 AB - The contribution of D1 and D2 dopamine (DA) receptor mechanisms to the behavioral supersensitivity and receptor upregulation induced by chronic DA antagonist administration were compared. Rats received either the selective D1 DA receptor antagonist SCH23390, the selective D2 DA receptor antagonist raclopride, their combination, or haloperidol, a predominantly D2 antagonist, for 21 days. Equivalent cataleptogenic doses of all drugs and drug combinations were employed. Tolerance to the cataleptic response was observed only in the haloperidol-treated group. Apomorphine-induced stereotypies were significantly enhanced in SCH23390-, raclopride-, and haloperidol-treated rats. In contrast, coadministration of both SCH23390 and raclopride had no effect on apomorphine-induced stereotypy. These findings suggest that neuroleptics blocking in equal proportion D1 and D2 receptor sites might be less likely to induce tardive dyskinesia and drug tolerance than those acting selectively on one or the other of these receptor subtypes. JF - Pharmacology, biochemistry, and behavior AU - Marin, C AU - Parashos, S A AU - Kapitzoglou-Logothetis, V AU - Peppe, A AU - Chase, T N AD - Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 195 EP - 200 VL - 45 IS - 1 SN - 0091-3057, 0091-3057 KW - Benzazepines KW - 0 KW - Dopamine D2 Receptor Antagonists KW - Receptors, Dopamine D1 KW - Salicylamides KW - Raclopride KW - 430K3SOZ7G KW - Haloperidol KW - J6292F8L3D KW - Apomorphine KW - N21FAR7B4S KW - Index Medicus KW - Rats KW - Animals KW - Rats, Sprague-Dawley KW - Catalepsy -- chemically induced KW - Benzazepines -- pharmacology KW - Apomorphine -- pharmacology KW - Up-Regulation -- drug effects KW - Haloperidol -- pharmacology KW - Salicylamides -- pharmacology KW - Stereotyped Behavior -- drug effects KW - Male KW - Behavior, Animal -- drug effects KW - Receptors, Dopamine D1 -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75782351?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacology%2C+biochemistry%2C+and+behavior&rft.atitle=D1+and+D2+dopamine+receptor-mediated+mechanisms+and+behavioral+supersensitivity.&rft.au=Marin%2C+C%3BParashos%2C+S+A%3BKapitzoglou-Logothetis%2C+V%3BPeppe%2C+A%3BChase%2C+T+N&rft.aulast=Marin&rft.aufirst=C&rft.date=1993-05-01&rft.volume=45&rft.issue=1&rft.spage=195&rft.isbn=&rft.btitle=&rft.title=Pharmacology%2C+biochemistry%2C+and+behavior&rft.issn=00913057&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-19 N1 - Date created - 1993-07-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Biosynthesis of dopamine and serotonin in the rat brain after repeated cocaine injections: a microdissection mapping study. AN - 75779490; 8511717 AB - The purpose of the present study was to examine the effects of chronic cocaine on dopamine (DA) and serotonin (5-HT) synthesis in several rat brain regions implicated in drug reinforcement. Male rats were treated twice daily with cocaine (15 mg/kg, ip) or saline for 1 week. After 42 hr of abstinence, rats were challenged with either cocaine (15 mg/kg, ip) or saline, followed by the aromatic L-amino acid decarboxylase inhibitor 3-hydroxybenzylhydrazine (NSD-1015; 100 mg/kg, ip). Animals were decapitated 30 min after NSD-1015 and discrete brain regions were microdisected from 300 microns frozen sections. Postmortem tissue levels of 3,4-dihydroxyphenylalanine (DOPA) and 5-hyroxytryptophan (5-HTP) were quantified by HPLC with electrochemical detection and used to estimate biosynthesis of DA and 5-HT, respectively. In chronic saline-treated rats, cocaine dramatically suppressed DA and 5-HT synthesis in all forebrain regions examined, including: medial prefrontal cortex, nucleus accumbens, caudate nucleus, olfactory tubercle, and basolateral amygdala. The degree of inhibition ranged from 35-65% and was more pronounced in 5-HT neurons compared to DA neurons in the same tissue sample. In general, chronic cocaine did not significantly alter basal levels of DOPA or 5-HTP; a notable exception was lateral hypothalamus, where chronic cocaine reduced basal DA synthesis to 75% of control. After repeated cocaine injections, the synthesis-inhibiting effect of a challenge injection of cocaine was attenuated in many brain areas. These data suggest that whereas acute cocaine decreases DA and 5-HT synthesis in forebrain, chronic cocaine is not neurotoxic to DA and 5-HT neurons. In addition, the mechanism(s) mediating cocaine-induced suppression of monoamine synthesis may become desensitized by chronic exposure to the drug. JF - Synapse (New York, N.Y.) AU - Baumann, M H AU - Raley, T J AU - Partilla, J S AU - Rothman, R B AD - Clinical Psychopharmacology Section, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland 21224. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 40 EP - 50 VL - 14 IS - 1 SN - 0887-4476, 0887-4476 KW - Serotonin KW - 333DO1RDJY KW - Dihydroxyphenylalanine KW - 63-84-3 KW - 5-Hydroxytryptophan KW - C1LJO185Q9 KW - Cocaine KW - I5Y540LHVR KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Rats KW - Electrochemistry -- methods KW - Animals KW - Rats, Sprague-Dawley KW - Dihydroxyphenylalanine -- metabolism KW - 5-Hydroxytryptophan -- metabolism KW - Injections KW - Male KW - Dissection KW - Chromatography, High Pressure Liquid KW - Serotonin -- biosynthesis KW - Dopamine -- biosynthesis KW - Brain -- metabolism KW - Cocaine -- pharmacology KW - Cocaine -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75779490?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Synapse+%28New+York%2C+N.Y.%29&rft.atitle=Biosynthesis+of+dopamine+and+serotonin+in+the+rat+brain+after+repeated+cocaine+injections%3A+a+microdissection+mapping+study.&rft.au=Baumann%2C+M+H%3BRaley%2C+T+J%3BPartilla%2C+J+S%3BRothman%2C+R+B&rft.aulast=Baumann&rft.aufirst=M&rft.date=1993-05-01&rft.volume=14&rft.issue=1&rft.spage=40&rft.isbn=&rft.btitle=&rft.title=Synapse+%28New+York%2C+N.Y.%29&rft.issn=08874476&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-15 N1 - Date created - 1993-07-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - A mechanistic model of effects of dioxin on gene expression in the rat liver. AN - 75779124; 8511776 AB - Improved methods for estimating the shape of the response curve for effects of exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) are needed in order to evaluate possible adverse health effects of TCDD. A mathematical model has been constructed to describe TCDD-mediated alterations in hepatic proteins in the rat. In this model it was assumed that TCDD mediates increases in the liver concentration of transforming growth factor-alpha (TGF-alpha) by a mechanism which requires the aryl hydrocarbon (Ah) receptor. TGF-alpha subsequently binds to the epidermal growth factor (EGF) receptor, a process which is known to cause internalization of this receptor in hepatocytes. This action is thought to be an early event in the generation of a mitogenic signal. Because TCDD decreases binding of EGF in the livers of intact female rats but not in ovariectomized rats, this effect was further assumed to be dependent on estrogen action. The model postulates Ah receptor-dependent effects on the concentration of cytochrome P450 1A2 (CYP1A2), which is involved in the metabolism of estradiol, and on the concentration of the estrogen receptor. The model also incorporates information on induction of cytochrome P450 1A1 (CYP1A1) by TCDD. The biochemical response curves for all these proteins were hyperbolic (Hill exponents in the equations for their expression were found to be 1), indicating a proportional relationship between target tissue dose and protein concentration at low administered doses of TCDD. The model successfully reproduced the observed tissue distribution of TCDD, the concentrations of CYP1A1 and CYP1A2, and the effects of TCDD on the Ah, estrogen, and EGF receptors over a wide dose range. JF - Toxicology and applied pharmacology AU - Kohn, M C AU - Lucier, G W AU - Clark, G C AU - Sewall, C AU - Tritscher, A M AU - Portier, C J AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 138 EP - 154 VL - 120 IS - 1 SN - 0041-008X, 0041-008X KW - Estrogens KW - 0 KW - Polychlorinated Dibenzodioxins KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Index Medicus KW - Receptor, Epidermal Growth Factor -- drug effects KW - Rats KW - Animals KW - Estrogens -- metabolism KW - Dose-Response Relationship, Drug KW - Cell Division -- drug effects KW - Cytochrome P-450 Enzyme System -- metabolism KW - Tissue Distribution KW - Female KW - Gene Expression -- drug effects KW - Polychlorinated Dibenzodioxins -- pharmacokinetics KW - Liver -- drug effects KW - Polychlorinated Dibenzodioxins -- toxicity KW - Models, Biological UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75779124?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+applied+pharmacology&rft.atitle=A+mechanistic+model+of+effects+of+dioxin+on+gene+expression+in+the+rat+liver.&rft.au=Kohn%2C+M+C%3BLucier%2C+G+W%3BClark%2C+G+C%3BSewall%2C+C%3BTritscher%2C+A+M%3BPortier%2C+C+J&rft.aulast=Kohn&rft.aufirst=M&rft.date=1993-05-01&rft.volume=120&rft.issue=1&rft.spage=138&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=0041008X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-09 N1 - Date created - 1993-07-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Quantification of axotomy-induced alteration of neuropeptide mRNAs in dorsal root ganglion neurons with special reference to neuropeptide Y mRNA and the effects of neonatal capsaicin treatment. AN - 75772334; 7685398 AB - Alteration in mRNA expression in dorsal root ganglia (DRG) neurons encoding 5 neuropeptides was quantitatively compared in normal rats and in those neonatally treated with capsaicin, a selective neurotoxin which destroys a subpopulation of DRG neurons with unmyelinated axons. Adult rats received a unilateral transection of the sciatic nerve and were killed 7 days later. Oligonucleotide probes specific for the genes encoding neuropeptide Y (NPY), vasoactive intestinal polypeptide (VIP), galanin (GAL), somatostatin (SOM), and calcitonin gene-related peptide (CGRP) were used for in situ hybridization and RNA blot analysis. Following the nerve cut, RNA blot analysis demonstrated a dramatic induction of NPY, VIP, and GAL mRNA levels from the undetectable constitutive level of expression. Conversely, CGRP and SOM mRNAs, which are constitutively expressed, were reduced 55% and 70%, respectively, following the nerve cut. A unimodal size distribution for neurons expressing NPY mRNA was determined, with a mean cross-sectional area of 1700 microns2 representing 24.4% of DRG neurons ipsilateral to the nerve cut. Neurons expressing VIP mRNA were mainly small sized, with a cross-sectional area of approximately 700 microns2, while those expressing GAL mRNA were both small (approximately 700 microns2) and medium (approximately 1,300 microns2) sized. The percentages of neurons expressing VIP or GAL mRNA were 19.9% and 33.7%, respectively. In neonatal capsaicin-treated rats, there was a 10% reduction in neurons expressing NPY mRNA, a 37% reduction for VIP, and a 27% for GAL mRNA compared to vehicle-treated rats after nerve cut. Capsaicin-sensitive neurons comprised 37% of CGRP neurons and 83% of SOM neurons. These observations suggest that NPY is primarily induced in myelinated primary afferent neurons, while VIP and GAL mRNA induction occurs in a mixed population, a sizeable percentage of which has unmyelinated axons. Additionally, SOM mRNA expression is associated mainly with unmyelinated primary afferents. JF - Journal of neuroscience research AU - Noguchi, K AU - De León, M AU - Nahin, R L AU - Senba, E AU - Ruda, M A AD - Neurobiology and Anesthesiology Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/05/01/ PY - 1993 DA - 1993 May 01 SP - 54 EP - 66 VL - 35 IS - 1 SN - 0360-4012, 0360-4012 KW - Neuropeptide Y KW - 0 KW - Neuropeptides KW - Oligonucleotide Probes KW - Peptides KW - RNA, Messenger KW - Sulfur Radioisotopes KW - Vasoactive Intestinal Peptide KW - 37221-79-7 KW - Somatostatin KW - 51110-01-1 KW - Calcitonin Gene-Related Peptide KW - 83652-28-2 KW - Galanin KW - 88813-36-9 KW - Capsaicin KW - S07O44R1ZM KW - Index Medicus KW - Vasoactive Intestinal Peptide -- biosynthesis KW - Gene Expression -- drug effects KW - Somatostatin -- genetics KW - Animals KW - Calcitonin Gene-Related Peptide -- genetics KW - Peptide Biosynthesis KW - Autoradiography KW - Somatostatin -- biosynthesis KW - Neuropeptide Y -- genetics KW - Rats KW - Neuropeptide Y -- biosynthesis KW - Animals, Newborn KW - Rats, Sprague-Dawley KW - In Situ Hybridization KW - Calcitonin Gene-Related Peptide -- biosynthesis KW - Peptides -- genetics KW - Vasoactive Intestinal Peptide -- genetics KW - Male KW - Ganglia, Spinal -- cytology KW - Neurons -- metabolism KW - RNA, Messenger -- metabolism KW - Neurons -- drug effects KW - Ganglia, Spinal -- metabolism KW - Neurons -- cytology KW - Sciatic Nerve -- physiology KW - Neuropeptides -- biosynthesis KW - Ganglia, Spinal -- drug effects KW - Neuropeptides -- genetics KW - Capsaicin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75772334?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neuroscience+research&rft.atitle=Quantification+of+axotomy-induced+alteration+of+neuropeptide+mRNAs+in+dorsal+root+ganglion+neurons+with+special+reference+to+neuropeptide+Y+mRNA+and+the+effects+of+neonatal+capsaicin+treatment.&rft.au=Noguchi%2C+K%3BDe+Le%C3%B3n%2C+M%3BNahin%2C+R+L%3BSenba%2C+E%3BRuda%2C+M+A&rft.aulast=Noguchi&rft.aufirst=K&rft.date=1993-05-01&rft.volume=35&rft.issue=1&rft.spage=54&rft.isbn=&rft.btitle=&rft.title=Journal+of+neuroscience+research&rft.issn=03604012&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-15 N1 - Date created - 1993-07-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Cancer and other causes of death among male and female farmers from twenty-three states. AN - 75771679; 8506851 AB - Occupation and industry codes on death certificates from 23 states for 1984-1988 were used to evaluate mortality risks among white and nonwhite, male and female farmers. Proportionate mortality and proportionate cancer mortality ratios were calculated using deaths among nonfarmers from the same states to generate expected numbers. Among farmers there were 119,648 deaths among white men, 2,400 among white women, 11,446 among nonwhite men, and 2,066 among nonwhite women. Deficits occurred in all race-sex groups for infective and parasitic diseases, all cancer combined, lung cancer, liver cancer, diseases of the nervous system, multiple sclerosis, hypertension, and emphysema. As reported in other studies, white male farmers had excesses of cancer of the lymphatic and hematopoietic system, lip, eye, brain, and prostate. Excesses of cancers of the pancreas, kidney, bone, and thyroid were new findings. Regional patterns were evident, particularly among white men. Significant excesses for accidents, vascular lesions of the central nervous system (CNS), and cancers of the prostate tended to occur in most geographic regions, while excesses for mechanical suffocation, non-Hodgkin's lymphoma, and cancers of the lip, brain, and the lymphatic and hematopoietic system were limited to the Central states. Increases among nonwhite men were similar to those in white men for some causes of death (vascular lesions of the CNS and cancers of the pancreas and prostate), but were absent for others (lymphatic and hematopoietic system, lip, eye, kidney, and brain). Women (white and nonwhite) had excesses for vascular lesions of the CNS, disease of the genitourinary system (white women only), and cancers of the stomach and cervix (nonwhite women only). Cancer of the buccal cavity and pharynx was slightly elevated among women, and white women had nonsignificant excesses of multiple myeloma and leukemia. Excesses for leukemia and non-Hodgkin's lymphoma occurred among white men and women, but not among nonwhites. Excesses for several types of accidental deaths were seen among all race-sex groups. JF - American journal of industrial medicine AU - Blair, A AU - Dosemeci, M AU - Heineman, E F AD - Occupational Studies Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 729 EP - 742 VL - 23 IS - 5 SN - 0271-3586, 0271-3586 KW - Index Medicus KW - Humans KW - Continental Population Groups KW - United States -- epidemiology KW - Male KW - Female KW - Cause of Death KW - Agricultural Workers' Diseases -- mortality KW - Agricultural Workers' Diseases -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75771679?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+industrial+medicine&rft.atitle=Cancer+and+other+causes+of+death+among+male+and+female+farmers+from+twenty-three+states.&rft.au=Blair%2C+A%3BDosemeci%2C+M%3BHeineman%2C+E+F&rft.aulast=Blair&rft.aufirst=A&rft.date=1993-05-01&rft.volume=23&rft.issue=5&rft.spage=729&rft.isbn=&rft.btitle=&rft.title=American+journal+of+industrial+medicine&rft.issn=02713586&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-07 N1 - Date created - 1993-07-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - p53 mutations in human immortalized epithelial cell lines. AN - 75769231; 8504475 AB - Although rodent cells have been immortalized following transfection with a mutant p53 gene, the role of p53 in the immortalization of human cells is unknown. Therefore, human epithelial cell lines were examined for p53 mutations in exons 4-9 which include the evolutionarily conserved regions. A spontaneously immortalized skin keratinocyte cell line, HaCat, and three ras-transfected clones, have a p53 mutational spectrum that is typical of ultraviolet light induced mutations. A normal finite lifespan cell strain (184) and two benzo[a]pyrene immortalized mammary epithelial cell lines derived from 184 (184A1 and 184B5) contain wild type p53 sequences in exons 4-9, although elevated levels of nuclear p53 indicate an alteration in the stability of the normally transient protein. Wild type p53 was found in human bronchial, esophageal and hepatic epithelial cells immortalized by SV40 T antigen gene and human renal epithelial cells immortalized by adenovirus 5. BEAS-2B, an SV40 T antigen immortalized bronchial epithelial cell line and two subclones, have a germline polymorphism at codon 47. Inactivation of p53 by mechanisms such as mutation or complexing with proteins of DNA tumor viruses appears to be important in the immortalization of human epithelial cells. JF - Carcinogenesis AU - Lehman, T A AU - Modali, R AU - Boukamp, P AU - Stanek, J AU - Bennett, W P AU - Welsh, J A AU - Metcalf, R A AU - Stampfer, M R AU - Fusenig, N AU - Rogan, E M AD - Laboratory of Human Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 833 EP - 839 VL - 14 IS - 5 SN - 0143-3334, 0143-3334 KW - p53 KW - ras KW - Oligodeoxyribonucleotides KW - 0 KW - Tumor Suppressor Protein p53 KW - Benzo(a)pyrene KW - 3417WMA06D KW - Index Medicus KW - Benzo(a)pyrene -- pharmacology KW - Tumor Suppressor Protein p53 -- biosynthesis KW - Exons KW - Humans KW - Breast KW - Respiratory System KW - Epithelium -- drug effects KW - Genes, ras KW - Polymerase Chain Reaction KW - Tumor Suppressor Protein p53 -- analysis KW - Base Sequence KW - Molecular Sequence Data KW - Kidney KW - Introns KW - Epithelium -- metabolism KW - Cell Line, Transformed KW - Immunohistochemistry KW - Cell Transformation, Neoplastic KW - Female KW - Genes, p53 KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75769231?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=p53+mutations+in+human+immortalized+epithelial+cell+lines.&rft.au=Lehman%2C+T+A%3BModali%2C+R%3BBoukamp%2C+P%3BStanek%2C+J%3BBennett%2C+W+P%3BWelsh%2C+J+A%3BMetcalf%2C+R+A%3BStampfer%2C+M+R%3BFusenig%2C+N%3BRogan%2C+E+M&rft.aulast=Lehman&rft.aufirst=T&rft.date=1993-05-01&rft.volume=14&rft.issue=5&rft.spage=833&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-06 N1 - Date created - 1993-07-06 N1 - Date revised - 2017-01-13 N1 - Gene symbol - p53; ras N1 - SuppNotes - Erratum In: Carcinogenesis 1993 Jul;14(7):1491 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Inhalation exposure to a hepatocarcinogenic concentration of methylene chloride does not induce sustained replicative DNA synthesis in hepatocytes of female B6C3F1 mice. AN - 75768087; 8099314 AB - We have used methylene chloride as a model to study cellular and molecular processes responsible for liver tumor induction by chlorinated hydrocarbons. Because of current interest in the role of enhanced cell proliferation in tumor induction, measurement of S-phase hepatocytes was incorporated into recently conducted toxicity and carcinogenicity studies. In prechronic studies, female B6C3F1 mice were exposed to 0, 1000, 2000 or 8000 p.p.m. methylene chloride by inhalation, 5 days per week, for up to 4 weeks followed by a 1 and 2 week recovery period. Mice exposed to concentrations of 2000, 4000 or 8000 p.p.m. methylene chloride had sustained increased liver weight commencing after 1 week of exposure and returning to normal after the 1 or 2 week recovery period. The increased liver weight was attributed to hepatocellular hypertrophy secondary to intracellular glycogen accumulation. Tritiated thymidine was administered by osmotic minipumps to label S-phase hepatocytes over a 6 day period. At most intervals examined there was decreased hepatocyte labeling in mice exposed to methylene chloride. However, there was a transitory increased number of S-phase hepatocytes observed at the 2 week interval in the 1000, 4000 and 8000 p.p.m. methylene chloride groups. In a chronic study, female mice were exposed to 2000 p.p.m. methylene chloride for up to two years. Following labeling with BRDU using 6 day minipumps, a statistically significant decrease in S-phase hepatocytes was observed after 13 weeks of methylene chloride exposure. A minor increased labeling index (LI) observed at 52 weeks was not considered to be a methylene chloride treatment-related effect. Retrospective immunohistochemical staining for proliferating cell nuclear antigen (PCNA) in liver sections containing foci of cellular alteration allowed demonstration of S-phase hepatocytes in these clonally expanded preneoplastic lesions. While foci frequently had higher LI's than surrounding normal hepatocytes, there was no difference in the mean LI of foci from methylene chloride-treated mice versus foci occurring spontaneously in control mice. The absence of a sustained increase in S-phase hepatocytes in female B6C3F1 mice suggests that enhanced cell proliferation is not a major mechanistic factor associated with the observed hepatocarcinogenicity of methylene chloride. JF - Carcinogenesis AU - Foley, J F AU - Tuck, P D AU - Ton, T V AU - Frost, M AU - Kari, F AU - Anderson, M W AU - Maronpot, R R AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 811 EP - 817 VL - 14 IS - 5 SN - 0143-3334, 0143-3334 KW - Antigens, Neoplasm KW - 0 KW - Carcinogens KW - Liver Glycogen KW - Nuclear Proteins KW - Proliferating Cell Nuclear Antigen KW - Methylene Chloride KW - 588X2YUY0A KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Mitotic Index -- drug effects KW - Antigens, Neoplasm -- analysis KW - Cell Division -- drug effects KW - Mice KW - Nuclear Proteins -- analysis KW - Mice, Inbred Strains KW - Hypertrophy KW - Liver Glycogen -- metabolism KW - Administration, Inhalation KW - Cell Cycle -- drug effects KW - Female KW - Liver -- pathology KW - Carcinogens -- administration & dosage KW - Methylene Chloride -- toxicity KW - Liver -- drug effects KW - Carcinogens -- toxicity KW - Liver -- metabolism KW - Methylene Chloride -- administration & dosage KW - DNA -- biosynthesis KW - DNA Replication -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75768087?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Inhalation+exposure+to+a+hepatocarcinogenic+concentration+of+methylene+chloride+does+not+induce+sustained+replicative+DNA+synthesis+in+hepatocytes+of+female+B6C3F1+mice.&rft.au=Foley%2C+J+F%3BTuck%2C+P+D%3BTon%2C+T+V%3BFrost%2C+M%3BKari%2C+F%3BAnderson%2C+M+W%3BMaronpot%2C+R+R&rft.aulast=Foley&rft.aufirst=J&rft.date=1993-05-01&rft.volume=14&rft.issue=5&rft.spage=811&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-06 N1 - Date created - 1993-07-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Carcinogenesis. 1993 May;14(5):787-8 [8504469] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Characterization of p53 mutations in methylene chloride-induced lung tumors from B6C3F1 mice. AN - 75767114; 8504472 AB - Mutations of the p53 tumor suppressor gene are the most common defined genetic alterations seen in a wide variety of human cancers. In contrast, little is known about the importance of the p53 gene in chemically induced tumors of rodents, which are widely used as models for the evaluation of human health risks. In this study we examined 54 methylene chloride-induced and seven spontaneously arising lung tumors from female B6C3F1 mice for losses of heterozygosity (LOH) at markers near the p53 gene on chromosome 11. LOH was detected in seven methylene chloride-induced lung carcinomas by Southern analysis of a restriction fragment length polymorphism and PCR analysis of five simple sequence length polymorphisms. In each case allele loss was observed at all six markers; thus, these chromosomal alterations were likely to have resulted from mitotic nondisjunction. In contrast, LOH was not detected in 20 liver tumors from methylene chloride-treated mice at the Acrb locus, which is tightly linked to the p53 gene on chromosome 11. In addition single strand conformation polymorphism analysis was performed to screen for mutations in the most conserved regions of the p53 gene (exons 5 to 8). Consequently, potential mutations identified by direct sequencing, were only detected in four of the seven tumor samples with LOH, but not in any of the remaining lung tumors. Overexpression of the p53 protein by immunohistochemical staining was detected only in the four tumors that contained p53 point mutations and in a focal area of another tumor. Finally, using a simple sequence length polymorphism within the retinoblastoma tumor suppressor gene, LOH on mouse chromosome 14 was also detected in three lung carcinomas and one liver tumor. Inactivation of p53 and possibly the retinoblastoma tumor suppressor gene appear to be infrequent events in lung and liver tumors from methylene chloride treated mice. JF - Carcinogenesis AU - Hegi, M E AU - Söderkvist, P AU - Foley, J F AU - Schoonhoven, R AU - Swenberg, J A AU - Kari, F AU - Maronpot, R AU - Anderson, M W AU - Wiseman, R W AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 803 EP - 810 VL - 14 IS - 5 SN - 0143-3334, 0143-3334 KW - Acrb KW - Csfgm KW - Hpg KW - Krt-1 KW - Myla KW - p53 KW - Carcinogens KW - 0 KW - DNA, Neoplasm KW - Genetic Markers KW - Oligodeoxyribonucleotides KW - Tumor Suppressor Protein p53 KW - Methylene Chloride KW - 588X2YUY0A KW - Index Medicus KW - Animals KW - Polymorphism, Genetic KW - Exons KW - Mice KW - DNA, Neoplasm -- isolation & purification KW - Chromosome Mapping KW - Mice, Inbred Strains KW - Tumor Suppressor Protein p53 -- analysis KW - Base Sequence KW - Heterozygote KW - Molecular Sequence Data KW - DNA, Neoplasm -- genetics KW - Immunohistochemistry KW - Female KW - Methylene Chloride -- toxicity KW - Genes, p53 KW - Carcinogens -- toxicity KW - Lung Neoplasms -- genetics KW - Lung Neoplasms -- chemically induced KW - Mutagenesis KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75767114?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Characterization+of+p53+mutations+in+methylene+chloride-induced+lung+tumors+from+B6C3F1+mice.&rft.au=Hegi%2C+M+E%3BS%C3%B6derkvist%2C+P%3BFoley%2C+J+F%3BSchoonhoven%2C+R%3BSwenberg%2C+J+A%3BKari%2C+F%3BMaronpot%2C+R%3BAnderson%2C+M+W%3BWiseman%2C+R+W&rft.aulast=Hegi&rft.aufirst=M&rft.date=1993-05-01&rft.volume=14&rft.issue=5&rft.spage=803&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-06 N1 - Date created - 1993-07-06 N1 - Date revised - 2017-01-13 N1 - Gene symbol - Acrb; Csfgm; Hpg; Krt-1; Myla; p53 N1 - SuppNotes - Comment In: Carcinogenesis. 1993 May;14(5):787-8 [8504469] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Detection of metabolites of polycyclic aromatic hydrocarbons in human urine. AN - 75767084; 8504465 AB - A non-invasive assay has been developed for the recovery of r-7,t-8,t-9,c-10-tetrahydroxy-7,8,9,10-tetrahydrobenzo[alpha]-pyrene (BP-7,10/8,9-tetrol) from human urine. This tetrol is excreted as a metabolite of benzo[alpha]pyrene (BP) in a process catalyzed by cytochrome P450 enzymes and epoxide hydrolases. Urine was hydrolysed to release activated benzo[alpha]-pyrene-diol-epoxides covalently bound to macromolecular species or conjugated tetrols. The relatively non-polar organic molecules from urine hydrolysates were collected on octadecasilane chromatography columns (Sep-Paks). Materials eluted in solvent (80% CH3OH), were further purified on immunoaffinity columns with antibodies raised against anti-N2-[10(7,8,9-trihydroxy-7,8,9,10-tetrahydrobenzo [alpha]pyrenyl)]-guanosine. HPLC was then used to isolate BP-7,10/8,9-tetrol, which was quantitated by synchronous fluorescence spectroscopy (SFS). This assay detected 0.24-3.12 pmol BP-7,10/8,9-tetrol per ml urine (limit of detection 0.01 pmol/ml, given 10 ml urine), in four study subjects. Reproducibility was assessed by adding tritium labeled BP-7,10/8,9-tetrol (1500 fmol) to a urine sample previously identified to contain the tetrol at levels below the limit of detection of the fluorescence assay; a recovery of > 30% of the added radioactivity was achieved (510 +/- 64 fmol, mean +/- SD, n = 3). Because HPLC alone was not sufficient to isolate materials for quantitation by SFS directly from human urine, immunoaffinity chromatography was found to be a necessary preparatory step in BP-7,10/8,9-tetrol isolation. These data demonstrate the presence of tetrahydrotetrol metabolites of BP in human urine and suggest that measurement of BP-7,10/8,9-tetrol and other polycyclic aromatic hydrocarbon-tetrols may prove to be valuable dosimeters of human internal exposure to polycyclic aromatic hydrocarbons. JF - Carcinogenesis AU - Weston, A AU - Bowman, E D AU - Carr, P AU - Rothman, N AU - Strickland, P T AD - Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 1053 EP - 1055 VL - 14 IS - 5 SN - 0143-3334, 0143-3334 KW - Benzopyrenes KW - 0 KW - Tritium KW - 10028-17-8 KW - Benzo(a)pyrene KW - 3417WMA06D KW - 7,8,9,10-tetrahydroxytetrahydrobenzo(a)pyrene KW - 59957-91-4 KW - Index Medicus KW - Reference Values KW - Spectrometry, Fluorescence -- methods KW - Lung Neoplasms -- urine KW - Biotransformation KW - Humans KW - Benzopyrenes -- analysis KW - Benzo(a)pyrene -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75767084?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Detection+of+metabolites+of+polycyclic+aromatic+hydrocarbons+in+human+urine.&rft.au=Weston%2C+A%3BBowman%2C+E+D%3BCarr%2C+P%3BRothman%2C+N%3BStrickland%2C+P+T&rft.aulast=Weston&rft.aufirst=A&rft.date=1993-05-01&rft.volume=14&rft.issue=5&rft.spage=1053&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-06 N1 - Date created - 1993-07-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Deficient gene specific repair of cisplatin-induced lesions in Xeroderma pigmentosum and Fanconi's anemia cell lines. AN - 75761168; 8504485 AB - Cisplatin is a chemotherapeutic agent known to cause DNA damage. The cytotoxicity of this drug is believed to result from the formation of DNA intrastrand adducts (IA) and DNA interstrand crosslinks (ICL). While there are many studies on DNA repair of cisplatin damage at the overall level of the genome in various human cell lines, there is little information on the gene-specific repair. In this report, we have measured the formation and repair of cisplatin induced DNA adducts in the dihydrofolate reductase (DHFR) and ribosomal RNA (rRNA) genes in three cell lines: normal human fibroblasts, Fanconi's anemia complementation group A (FAA) and Xeroderma pigmentosum complementation group A (XPA). It is generally thought that XPA cells lack nucleotide excision repair and that FAA cells are deficient in the repair of DNA ICL. We find that normal human fibroblast cells repair 84% of the ICL in the DHFR gene after 24 h, whereas XPA and FAA cell lines only repaired 32 and 50% of the ICL respectively. Furthermore, 69% of the cisplatin IA in the DHFR gene were repaired in 24 h in normal human fibroblasts compared to 22% for XPA and 24% for FAA cells. The repair of the rRNA gene was less efficient than in the DHFR gene, but the relative pattern between the different cell lines was similar to that of the DHFR gene. We thus find that FAA cells are deficient not only in the gene specific repair of cisplatin ICL, but also in the gene specific repair of the more common cisplatin IA. XPA cells are normally thought to be without any nucleotide excision repair capacity, but our data could support a slight ICL unhooking activity. JF - Carcinogenesis AU - Zhen, W AU - Evans, M K AU - Haggerty, C M AU - Bohr, V A AD - Laboratory of Molecular Pharmacology, National Cancer Institute, NIH, Bethesda, MD 20892. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 919 EP - 924 VL - 14 IS - 5 SN - 0143-3334, 0143-3334 KW - DHFR KW - DNA, Ribosomal KW - 0 KW - DNA KW - 9007-49-2 KW - Tetrahydrofolate Dehydrogenase KW - EC 1.5.1.3 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Fibroblasts -- drug effects KW - Kinetics KW - Humans KW - Genetic Complementation Test KW - DNA, Ribosomal -- drug effects KW - Time Factors KW - Fibroblasts -- metabolism KW - DNA, Ribosomal -- genetics KW - Chromosome Mapping KW - Cell Line KW - Tetrahydrofolate Dehydrogenase -- genetics KW - DNA Repair KW - DNA Damage KW - Cisplatin -- toxicity KW - DNA -- genetics KW - Xeroderma Pigmentosum -- genetics KW - Fanconi Anemia -- genetics KW - DNA -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75761168?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Deficient+gene+specific+repair+of+cisplatin-induced+lesions+in+Xeroderma+pigmentosum+and+Fanconi%27s+anemia+cell+lines.&rft.au=Zhen%2C+W%3BEvans%2C+M+K%3BHaggerty%2C+C+M%3BBohr%2C+V+A&rft.aulast=Zhen&rft.aufirst=W&rft.date=1993-05-01&rft.volume=14&rft.issue=5&rft.spage=919&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-06 N1 - Date created - 1993-07-06 N1 - Date revised - 2017-01-13 N1 - Gene symbol - DHFR N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Effect of varying exposure regimens on methylene chloride-induced lung and liver tumors in female B6C3F1 mice. AN - 75761084; 8504473 AB - Methylene chloride is a high production chemical used in a variety of applications resulting in estimated occupational and consumer exposures of at least one million people per day. Results of previously reported chronic evaluations of inhaled methylene chloride indicated that it caused mammary tumors in Fischer 344 rats and neoplasia in the lungs and liver of B6C3F1 mice. Mechanism(s) for methylene chloride-induced carcinogenesis have not been adequately elucidated. In this paper we describe the histologic evaluation of animals at a number of intermittent times for the purposes of assessing the progressive development of liver and lung neoplasia. Additionally, a series of stop-exposure treatments was conducted to evaluate the role of different methylene chloride exposure durations on the induction of hepatic and pulmonary neoplasia in female mice. Inhalation exposure to 2000 p.p.m. methylene chloride for 6 h per day, 5 days per week, for 104 weeks resulted in an 8-fold increase in the incidence of exposed animals having a lung adenoma or carcinoma (63 versus 7.5%; P < 0.01) and a 13-fold increase in the total number of pulmonary adenomas and carcinomas per animal at risk (0.97 versus 0.075; P < 0.01). This exposure also caused a 2.5-fold increase in the incidence of mice having liver tumors (69 versus 27%; P < 0.01) and a 3-fold increase in the total number of hepatic adenomas and carcinomas per animal at risk (1.34 versus 0.46; P < 0.01). Methylene chloride exposure hastened the first appearance of lung tumors (by 1 year) compared to that observed in control animals; chemical-induced and spontaneous liver tumors first occurred simultaneously. A shorter exposure duration was sufficient to attain maximal numbers of lung tumors than that needed for a maximal liver tumor burden. Lung tumor multiplicity was substantially increased by having additional time after cessation of the chemical treatment. This contrasts with the findings in liver, where additional post-exposure latency time did not effect tumor multiplicity compared to that of mice evaluated immediately after cessation of exposure. The incidence of lung alveolar hyperplasia in methylene chloride exposed animals was very low, even in tumor-bearing animals and the hyperplasias were not seen until at least 13 weeks after appearance of adenomas and carcinomas. Thus, the genesis of methylene chloride induced lung tumors in B6C3F1 mice is not preceded by overt cytotoxicity, enhanced cell proliferation nor observed hyperplasia.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Carcinogenesis AU - Kari, F W AU - Foley, J F AU - Seilkop, S K AU - Maronpot, R R AU - Anderson, M W AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 819 EP - 826 VL - 14 IS - 5 SN - 0143-3334, 0143-3334 KW - Carcinogens KW - 0 KW - Methylene Chloride KW - 588X2YUY0A KW - Index Medicus KW - Mice, Inbred Strains KW - Animals KW - Hyperplasia KW - Drug Administration Schedule KW - Carcinoma -- pathology KW - Adenoma -- chemically induced KW - Mice KW - Adenoma -- pathology KW - Time Factors KW - Female KW - Carcinoma -- chemically induced KW - Liver Neoplasms -- pathology KW - Liver -- pathology KW - Carcinogens -- administration & dosage KW - Methylene Chloride -- toxicity KW - Liver -- drug effects KW - Lung -- drug effects KW - Liver Neoplasms -- chemically induced KW - Carcinogens -- toxicity KW - Methylene Chloride -- administration & dosage KW - Lung Neoplasms -- chemically induced KW - Lung -- pathology KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75761084?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Effect+of+varying+exposure+regimens+on+methylene+chloride-induced+lung+and+liver+tumors+in+female+B6C3F1+mice.&rft.au=Kari%2C+F+W%3BFoley%2C+J+F%3BSeilkop%2C+S+K%3BMaronpot%2C+R+R%3BAnderson%2C+M+W&rft.aulast=Kari&rft.aufirst=F&rft.date=1993-05-01&rft.volume=14&rft.issue=5&rft.spage=819&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-06 N1 - Date created - 1993-07-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Carcinogenesis. 1993 May;14(5):787-8 [8504469] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Ras proto-oncogene activation in liver and lung tumors from B6C3F1 mice exposed chronically to methylene chloride. AN - 75761036; 8504471 AB - Methylene chloride has been the subject of recent toxicological and carcinogenesis studies because of significant human exposure and widespread use in industrial processing, food preparation and agriculture. In this study, liver and lung tumors, induced in female B6C3F1 mice by inhalation of 2000 p.p.m. methylene chloride (6 h/day, 5 days/week continuous exposure), were examined for the presence of activated ras proto-oncogenes. DNA was isolated from 49 spontaneous and 50 methylene chloride-induced liver tumors and screened by oligonucleotide hybridization of PCR amplified H-ras gene fragments for codon 61 mutations. In the chemically induced tumors, 38 mutations were detected, 16 C to A transversions in base 1, 16 A to G transitions in base 2 and 6 A to T transversions in base 2. This mutation profile was similar to that identified for the H-ras gene in the spontaneous liver tumors and suggests that methylene chloride acts in liver by promoting cells with spontaneous lesions. Tumors in which H-ras codon 61 mutations were not detected were examined for the presence of transforming genes by the nude mouse tumorigenicity assay. Except for activated K-ras genes detected in DNA from two methylene chloride induced tumors and one spontaneous tumor, no other transforming genes were identified. DNA from 54 lung tumors was screened by direct sequencing of PCR amplified DNA fragments of the K-ras gene for first and second exon mutations, and 12 mutations were identified, 5 in exon one and 7 in exon 2. The low number of spontaneous tumors available in this study limits the interpretation of the data, and thus the frequency and spectrum of K-ras activation in the methylene chloride induced tumors was not significantly different from that in the seven spontaneous tumors analyzed. Since K-ras activation was not detected in 80% of the tumors, the nude mouse tumorigenicity assay was used to examine the lung tumors for the presence of other transforming genes. At present no transforming genes other than ras genes were identified in either liver or lung tumors. JF - Carcinogenesis AU - Devereux, T R AU - Foley, J F AU - Maronpot, R R AU - Kari, F AU - Anderson, M W AD - Laboratory of Molecular Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 795 EP - 801 VL - 14 IS - 5 SN - 0143-3334, 0143-3334 KW - H-ras KW - K-ras KW - ras KW - Carcinogens KW - 0 KW - Codon KW - DNA, Neoplasm KW - Oligodeoxyribonucleotides KW - Methylene Chloride KW - 588X2YUY0A KW - Index Medicus KW - 3T3 Cells KW - Animals KW - Polymorphism, Genetic KW - Exons KW - Mice, Nude KW - Mice KW - DNA, Neoplasm -- isolation & purification KW - Chromosome Mapping KW - Polymerase Chain Reaction KW - Mice, Inbred Strains KW - Base Sequence KW - Blotting, Southern KW - Adenoma -- chemically induced KW - Molecular Sequence Data KW - DNA, Neoplasm -- genetics KW - Adenoma -- genetics KW - Female KW - Carcinoma -- chemically induced KW - Carcinoma -- genetics KW - Genes, ras KW - Methylene Chloride -- toxicity KW - Point Mutation KW - Liver Neoplasms -- chemically induced KW - Carcinogens -- toxicity KW - Lung Neoplasms -- genetics KW - Lung Neoplasms -- chemically induced KW - Gene Expression Regulation, Neoplastic -- drug effects KW - Liver Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75761036?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Ras+proto-oncogene+activation+in+liver+and+lung+tumors+from+B6C3F1+mice+exposed+chronically+to+methylene+chloride.&rft.au=Devereux%2C+T+R%3BFoley%2C+J+F%3BMaronpot%2C+R+R%3BKari%2C+F%3BAnderson%2C+M+W&rft.aulast=Devereux&rft.aufirst=T&rft.date=1993-05-01&rft.volume=14&rft.issue=5&rft.spage=795&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-06 N1 - Date created - 1993-07-06 N1 - Date revised - 2017-01-13 N1 - Gene symbol - H-ras; K-ras; ras N1 - SuppNotes - Comment In: Carcinogenesis. 1993 May;14(5):787-8 [8504469] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Relative performance of the MAST, VAST, and CAGE versus DSM-III-R criteria for alcohol dependence. AN - 75759551; 8501469 AB - A number of instruments have been developed to screen for alcoholism. With the advent of DSM-III and lay administered psychiatric diagnostic instruments, a test of the performance of these screens relative to diagnostic instruments is critical. In this paper, we document the relative effectiveness in a general medical clinic of the Michigan Alcoholism Screening Test (MAST), the Veterans Alcoholism Screening Test (VAST), and the CAGE questions in comparison to the DSM-III-R criteria for alcohol dependence as measured in the Composite International Diagnostic Interview (CIDI). All of the screens performed at acceptable levels, but the MAST and VAST tended to have higher performance characteristics. At the recommended cut points, they had higher sensitivity for lifetime alcohol dependence (VAST 95.1%, MAST 90.2%, CAGE 78.0%) as well as higher specificity (VAST 80.3%, MAST 81.7%, CAGE 76.1%). For present alcohol dependence only, at the recommended cut points the MAST and CAGE had sensitivity of 100% but specificity of 62.0 and 61.0% respectively. The VAST had sensitivity of 83.3% and specificity of 89.0%. We conclude that all three perform well relative to DSM-III-R criteria. JF - Journal of clinical epidemiology AU - Magruder-Habib, K AU - Stevens, H A AU - Alling, W C AD - National Institute of Mental Health, Rockville, MD 20857. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 435 EP - 441 VL - 46 IS - 5 SN - 0895-4356, 0895-4356 KW - Index Medicus KW - Sensitivity and Specificity KW - Psychiatric Status Rating Scales KW - Humans KW - Surveys and Questionnaires KW - Predictive Value of Tests KW - Middle Aged KW - Mass Screening -- methods KW - Male KW - Prevalence KW - Alcoholism -- diagnosis KW - Psychological Tests -- statistics & numerical data KW - Alcoholism -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75759551?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+epidemiology&rft.atitle=Relative+performance+of+the+MAST%2C+VAST%2C+and+CAGE+versus+DSM-III-R+criteria+for+alcohol+dependence.&rft.au=Magruder-Habib%2C+K%3BStevens%2C+H+A%3BAlling%2C+W+C&rft.aulast=Magruder-Habib&rft.aufirst=K&rft.date=1993-05-01&rft.volume=46&rft.issue=5&rft.spage=435&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+epidemiology&rft.issn=08954356&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-01 N1 - Date created - 1993-07-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Hepatic stem cells. AN - 75745511; 8494039 JF - The American journal of pathology AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute. National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 1331 EP - 1333 VL - 142 IS - 5 SN - 0002-9440, 0002-9440 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Humans KW - Cell Differentiation KW - Liver Neoplasms -- etiology KW - Cell Line KW - Liver -- cytology KW - Stem Cells -- cytology KW - Stem Cells -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75745511?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+journal+of+pathology&rft.atitle=Hepatic+stem+cells.&rft.au=Thorgeirsson%2C+S+S&rft.aulast=Thorgeirsson&rft.aufirst=S&rft.date=1993-05-01&rft.volume=142&rft.issue=5&rft.spage=1331&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+pathology&rft.issn=00029440&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-14 N1 - Date created - 1993-06-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Biochem Cell Biol. 1986 Aug;64(8):788-802 [2429680] Lab Invest. 1985 Apr;52(4):354-62 [2858600] Cancer Res. 1985 Feb;45(2):673-81 [2578305] Cancer Res. 1984 Dec;44(12 Pt 1):5463-74 [6388826] Am J Pathol. 1983 Jan;110(1):70-4 [6185004] Cancer Res. 1984 Jan;44(1):332-8 [6690044] Exp Cell Res. 1984 Sep;154(1):38-52 [6468534] Ann N Y Acad Sci. 1980;349:165-82 [6784634] Ann N Y Acad Sci. 1980;349:138-52 [6939360] Carcinogenesis. 1987 Nov;8(11):1737-40 [3664968] In Vitro Cell Dev Biol. 1987 May;23(5):339-48 [3294781] Am J Pathol. 1987 Apr;127(1):168-81 [3031986] Gastroenterology. 1987 Dec;93(6):1414-9 [3315827] J Pathol Bacteriol. 1958 Oct;76(2):441-9 [13588479] Hepatology. 1992 Dec;16(6):1327-33 [1280243] Am J Physiol. 1992 Aug;263(2 Pt 1):G139-48 [1325126] Hepatology. 1991 Jul;14(1):144-9 [2066062] Proc Natl Acad Sci U S A. 1991 Feb 15;88(4):1217-21 [1899924] Lab Invest. 1990 Jul;63(1):4-20 [2197504] Pathobiology. 1990;58(2):65-77 [2193646] Cancer Res. 1988 Jan 15;48(2):368-78 [2446746] Mol Carcinog. 1988;1(3):189-95 [3074814] Prog Clin Biol Res. 1990;331:325-34 [2315345] Biochem Pharmacol. 1990 Jun 15;39(12):1837-46 [2191651] Cancer Res. 1990 Jul 1;50(13):3811-5 [1693878] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Induction of multidrug resistance gene expression during cholestasis in rats and nonhuman primates. AN - 75736053; 8098315 AB - P-glycoprotein, an energy-dependent plasma membrane drug-efflux pump capable of reducing the intracellular concentration of a variety of hydrophobic xenobiotics, is encoded by mdr1, a member of the multidrug-resistant (mdr) gene family. The physiological function of this protein is unknown. Because of its location on the bile canalicular domain of the hepatocyte, we and others have hypothesized that P-glycoprotein may have a physiological role as a biliary transporter of xenobiotics and endobiotics and that its expression may therefore be altered in cholestasis. Both obstructive and alpha-naphthylisothiocyanate-induced cholestasis increased mdr1a and 1b gene expression in rat liver. Hepatic P-glycoprotein levels were also increased, and the protein remained localized at the biliary hepatocyte domain. Induction of mdr1a and mdr1b gene expression in rat liver was accomplished by means of increased transcription. alpha-Naphthylisothiocyanate-induced cholestasis in cynomolgus monkeys increased hepatic expression of both the mdr1 and 2 genes. To investigate the possible role of P-glycoprotein as a biliary efflux transporter, biliary excretion of vinblastine, a representative substrate of P-glycoprotein, was studied in rats. Increased hepatic mdr messenger RNA and P-glycoprotein levels, mediated by the xenobiotic inducer 2-acetylaminofluorene, resulted in a significant increase in biliary excretion of vinblastine, which was antagonized by the P-glycoprotein inhibitor verapamil. These findings suggest that P-glycoprotein functions as a biliary efflux pump for xenobiotics and, possibly, for unidentified physiological inducers that may mediate increased transcription of the mdr gene observed during cholestasis. JF - Hepatology (Baltimore, Md.) AU - Schrenk, D AU - Gant, T W AU - Preisegger, K H AU - Silverman, J A AU - Marino, P A AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 854 EP - 860 VL - 17 IS - 5 SN - 0270-9139, 0270-9139 KW - mdr KW - Carrier Proteins KW - 0 KW - Membrane Glycoproteins KW - P-Glycoprotein KW - Vinblastine KW - 5V9KLZ54CY KW - Index Medicus KW - Rats KW - Animals KW - Vinblastine -- metabolism KW - Rats, Inbred F344 KW - Blotting, Western KW - Macaca fascicularis KW - Blotting, Northern KW - Bile -- metabolism KW - Immunohistochemistry KW - Male KW - Female KW - Drug Resistance -- genetics KW - Membrane Glycoproteins -- physiology KW - Carrier Proteins -- genetics KW - Carrier Proteins -- physiology KW - Gene Expression Regulation KW - Cholestasis -- genetics KW - Membrane Glycoproteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75736053?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hepatology+%28Baltimore%2C+Md.%29&rft.atitle=Induction+of+multidrug+resistance+gene+expression+during+cholestasis+in+rats+and+nonhuman+primates.&rft.au=Schrenk%2C+D%3BGant%2C+T+W%3BPreisegger%2C+K+H%3BSilverman%2C+J+A%3BMarino%2C+P+A%3BThorgeirsson%2C+S+S&rft.aulast=Schrenk&rft.aufirst=D&rft.date=1993-05-01&rft.volume=17&rft.issue=5&rft.spage=854&rft.isbn=&rft.btitle=&rft.title=Hepatology+%28Baltimore%2C+Md.%29&rft.issn=02709139&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-15 N1 - Date created - 1993-06-15 N1 - Date revised - 2017-01-13 N1 - Gene symbol - mdr N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Comparison of lead bioavailability in F344 rats fed lead acetate, lead oxide, lead sulfide, or lead ore concentrate from Skagway, Alaska. AN - 75729992; 8492331 AB - An animal model using rats was developed to initiate investigations on the bioavailability of different sources of environmental lead. Lead must be absorbed and transported to target organs like brain, liver, kidney, and bone, before susceptible cells can be harmed. The bioavailability and therefore the toxicity of lead are dependent upon the route of exposure, dose, chemical structure, solubility, particle size, matrix incorporation, and other physiological and physicochemical factors. In the present study male F344 rats were fed < or = 38 microns size particles of lead sulfide, lead oxide, lead acetate, and a lead ore concentrate from Skagway, Alaska, mixed into the diet at doses of 0, 10, 30, and 100 ppm as lead for 30 d. No mortality or overt symptoms of lead toxicity were observed during the course of the study. Maximum blood lead concentrations attained in the 100 ppm groups were approximately 80 micrograms/dl in rats fed lead acetate and lead oxide, and were approximately 10 micrograms/dl in those fed lead sulfide and lead ore concentrate. Maximum bone lead levels in rats fed soluble lead oxide and lead acetate were much higher (approximately 200 micrograms/g) than those seen in rats fed the less soluble lead sulfide and lead ore (approximately 10 micrograms); kidney lead concentrations were also about 10-fold greater in rats fed the more soluble compared to the less soluble lead compounds. However, strong correlations between dose and tissue lead concentrations were observed in rats fed each of the four different lead compounds. Kidney lesions graded as minimal occurred in 7/10 rats fed 30 ppm and in 10/10 rats fed 100 ppm lead acetate, but not at lower doses or from other lead compounds. Similarly, urinary aminolevulinic acid excretion, a biomarker for lead toxicity, was increased in rats fed 100 ppm lead acetate or lead oxide, but was unaffected at lower doses or by the less soluble lead compounds. Although the histological and biochemical responses to lead toxicity were restricted to the more soluble lead compounds in this study, lead from Skagway lead ore concentrate and lead sulfide was also bioavailable, and accumulated in proportion to dose in vulnerable target organs such as bone and kidney. Longer-term studies with different mining materials are being conducted to determine if tissue lead continues to increase, and whether the levels attained are toxic. Data from such studies can be used to compare the toxicity and bioavailability of lead from different sources in the environment. JF - Journal of toxicology and environmental health AU - Dieter, M P AU - Matthews, H B AU - Jeffcoat, R A AU - Moseman, R F AD - National Institute of Environmental Health Sciences, Research Triangle Institute, NC 27709. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 79 EP - 93 VL - 39 IS - 1 SN - 0098-4108, 0098-4108 KW - Organometallic Compounds KW - 0 KW - Oxides KW - Sulfides KW - lead sulfide KW - 2425D15SYM KW - Lead KW - 2P299V784P KW - lead oxide KW - 4IN6FN8492 KW - lead acetate KW - RX077P88RY KW - Index Medicus KW - Rats KW - Administration, Oral KW - Animals KW - Rats, Inbred F344 KW - Kidney Tubules -- pathology KW - Bone and Bones -- chemistry KW - Kidney Tubules -- drug effects KW - Environmental Exposure KW - Intestinal Absorption KW - Alaska KW - Tissue Distribution KW - Male KW - Biological Availability KW - Oxides -- pharmacokinetics KW - Organometallic Compounds -- toxicity KW - Oxides -- toxicity KW - Lead -- blood KW - Organometallic Compounds -- pharmacokinetics KW - Sulfides -- pharmacokinetics KW - Lead -- toxicity KW - Oxides -- blood KW - Sulfides -- blood KW - Organometallic Compounds -- blood KW - Sulfides -- toxicity KW - Mining KW - Lead -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75729992?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+toxicology+and+environmental+health&rft.atitle=Comparison+of+lead+bioavailability+in+F344+rats+fed+lead+acetate%2C+lead+oxide%2C+lead+sulfide%2C+or+lead+ore+concentrate+from+Skagway%2C+Alaska.&rft.au=Dieter%2C+M+P%3BMatthews%2C+H+B%3BJeffcoat%2C+R+A%3BMoseman%2C+R+F&rft.aulast=Dieter&rft.aufirst=M&rft.date=1993-05-01&rft.volume=39&rft.issue=1&rft.spage=79&rft.isbn=&rft.btitle=&rft.title=Journal+of+toxicology+and+environmental+health&rft.issn=00984108&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-17 N1 - Date created - 1993-06-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Selective growth arrest and phenotypic reversion of prostate cancer cells in vitro by nontoxic pharmacological concentrations of phenylacetate. AN - 75723973; 8486788 AB - Differentiation therapy may provide an alternative for treatment of cancers that do not respond to cytotoxic chemotherapy or hormonal manipulations. This hypothesis led us to evaluate the effect of a nontoxic differentiation inducer, sodium phenylacetate (NaPA), on hormone-refractory prostate cancer, the second most common cause of cancer deaths in men. NaPA treatment of androgen-independent PC3 and DU145 prostate cell lines, like that of hormone-responsive LNCaP cultures, resulted in dose-dependent inhibition of cell proliferation. Similar treatments were not significantly inhibitory to replicating normal endothelial cells and skin fibroblasts. In addition to the selective cytostatic effect, NaPA induced reversion of the prostatic cells to a nonmalignant phenotype, evidenced by their reduced invasiveness and loss of tumorigenicity in athymic mice. Phenotypic reversion was accompanied by alterations in gene expression, including selective reduction in tumor growth factor-beta 2 mRNA levels and increased amounts of class I major histocompatibility complex HLA transcripts. Furthermore, there was a decrease in tumor-associated proteolysis mediated by urokinase plasminogen activator, a molecular marker of disease progression in humans. When tumor cells were treated with NaPA together with suramin, a drug with demonstrable activity in patients, there was complete abrogation of cell growth under conditions in which each treatment alone produced only a partial effect. The in vitro antineoplastic activity was observed with drug concentrations that have been achieved in humans with no significant toxicities, suggesting that PA, used alone or in combination with other antitumor agents, warrants evaluation in the treatment of advanced prostatic cancer. JF - The Journal of clinical investigation AU - Samid, D AU - Shack, S AU - Myers, C E AD - Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 2288 EP - 2295 VL - 91 IS - 5 SN - 0021-9738, 0021-9738 KW - HLA-A3 Antigen KW - 0 KW - Phenylacetates KW - RNA, Neoplasm KW - Transforming Growth Factor beta KW - Glutamine KW - 0RH81L854J KW - Suramin KW - 6032D45BEM KW - phenylacetic acid KW - ER5I1W795A KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - HLA-A3 Antigen -- genetics KW - Humans KW - Mice KW - Mice, Nude KW - RNA, Neoplasm -- genetics KW - Suramin -- pharmacology KW - DNA Replication -- drug effects KW - Phenotype KW - Neoplasm Transplantation KW - Glutamine -- pharmacology KW - RNA, Neoplasm -- isolation & purification KW - Tumor Cells, Cultured KW - Cell Survival -- drug effects KW - Neoplasm Invasiveness -- pathology KW - Transplantation, Heterologous KW - Transforming Growth Factor beta -- genetics KW - Female KW - Male KW - Prostatic Neoplasms -- pathology KW - Phenylacetates -- pharmacology KW - Cell Division -- drug effects KW - Prostatic Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75723973?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+clinical+investigation&rft.atitle=Selective+growth+arrest+and+phenotypic+reversion+of+prostate+cancer+cells+in+vitro+by+nontoxic+pharmacological+concentrations+of+phenylacetate.&rft.au=Samid%2C+D%3BShack%2C+S%3BMyers%2C+C+E&rft.aulast=Samid&rft.aufirst=D&rft.date=1993-05-01&rft.volume=91&rft.issue=5&rft.spage=2288&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+clinical+investigation&rft.issn=00219738&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-04 N1 - Date created - 1993-06-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Res. 1981 Apr;41(4):1324-8 [7214322] J Urol. 1989 Jul;142(1):193-8 [2659823] Br J Cancer. 1989 Sep;60(3):397-400 [2506920] Am Heart J. 1990 Sep;120(3):757-61; discussion 769-72 [2117846] Cancer Res. 1990 Nov 1;50(21):6827-9 [2119883] N Engl J Med. 1991 Jan 24;324(4):236-45 [1985245] J Urol. 1991 Feb;145(2):393-8 [1824865] Prog Clin Biol Res. 1990;359:155-64; discussion 177-80 [2284289] Cancer Res. 1991 May 1;51(9):2498-505 [2015610] Cancer Metastasis Rev. 1990 Dec;9(4):353-67 [2129023] In Vitro Cell Dev Biol. 1991 Apr;27A(4):327-36 [1856158] Cell Regul. 1991 Mar;2(3):241-9 [1859854] Semin Cancer Biol. 1990 Apr;1(2):117-26 [2151734] Cancer Commun. 1991 Aug;3(8):255-64 [1653586] Cancer Res. 1991 Sep 15;51(18):4948-54 [1654207] Cancer Res. 1991 Dec 15;51(24):6629-35 [1742736] Cancer Res. 1992 Apr 1;52(7):1988-92 [1372534] Cancer Res. 1992 Apr 15;52(8):2138-42 [1559217] J Neurosurg. 1992 May;76(5):799-804 [1373442] Leukemia. 1992;6 Suppl 2:24-7 [1349662] J Clin Oncol. 1992 Jun;10(6):881-9 [1375283] N Engl J Med. 1992 Aug 20;327(8):569-70 [1378939] Blood. 1992 Sep 15;80(6):1576-81 [1381630] Nature. 1970 Sep 12;227(5263):1136-7 [4915990] Proc R Soc Lond B Biol Sci. 1972 Jul 25;182(1066):25-35 [4403084] Can J Microbiol. 1972 Aug;18(8):1257-61 [5052893] J Bacteriol. 1976 Oct;128(1):182-91 [10273] Int J Cancer. 1978 Mar 15;21(3):274-81 [631930] Natl Cancer Inst Monogr. 1978 Dec;(49):17-21 [571045] Cancer Treat Rep. 1981;65 Suppl 4:61-5 [7346158] Arch Biochem Biophys. 1983 Apr 1;222(1):259-65 [6838224] Cancer Res. 1983 Aug;43(8):3466-92 [6305486] Cancer Metastasis Rev. 1983;2(1):5-23 [6616442] Cancer Res. 1984 Jan;44(1):311-8 [6197164] Cancer Treat Rep. 1984 Jan;68(1):199-205 [6692427] N Engl J Med. 1984 Jun 21;310(25):1630-4 [6427608] J Immunol. 1985 Oct;135(4):2835-41 [2993417] Invasion Metastasis. 1985;5(6):344-55 [4066206] Proc Natl Acad Sci U S A. 1986 Jun;83(12):4167-71 [2424019] Pediatr Res. 1986 Nov;20(11):1117-21 [3099249] Pharmacol Ther. 1985;30(3):277-86 [2433702] Cancer Res. 1987 Jun 15;47(12):3239-45 [2438036] Mol Cell Biol. 1987 Jun;7(6):2196-200 [2439904] Cancer Res. 1988 Jan 15;48(2):291-6 [3121170] Proc Natl Acad Sci U S A. 1988 Jan;85(1):79-82 [3277172] Biochem Int. 1988 Feb;16(2):339-47 [3365266] J Biol Chem. 1988 Sep 15;263(26):12805-8 [2843499] J Urol. 1988 Dec;140(6):1466-9 [3193516] Eur Urol. 1988;15(3-4):256-8 [3145889] Prog Clin Biol Res. 1980;37:115-32 [7384082] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Transmission-blocking activity of a chitinase inhibitor and activation of malarial parasite chitinase by mosquito protease. AN - 75719941; 8483942 AB - During development in the mosquito midgut, malarial parasites must traverse a chitin-containing peritrophic matrix (PM) that forms around the food bolus. Previously Huber et al. [Huber, M., Cabib, E. & Miller, L. H. (1991) Proc. Natl. Acad. Sci. USA 88, 2807-2810] reported that the parasite secretes a protein with chitinase activity, and they suggested that parasite chitinase (EC 3.2.1.14) plays an important role in the parasite's egress from the blood meal. We found that allosamidin, a specific inhibitor of chitinase, completely blocked oocyst development in vivo and thus blocked malaria parasite transmission. Addition of exogenous chitinase to the blood meal prevented the PM from forming and reversed the transmission-blocking activity of allosamidin. Using exogenous chitinase, we also found that the PM does not limit the number of parasites that develop into oocysts, suggesting that the parasite produces sufficient quantities of chitinase to penetrate this potential barrier. In addition, we found that treatment of parasite chitinase with a diisopropyl fluorophosphate-sensitive trypsinlike protease from the mosquito midgut or endoproteinase Lys-C increased its enzymatic activity. These results suggest that malaria parasite has evolved an intricate mechanism to adapt to the PM and the protease-rich environment of the mosquito midgut. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Shahabuddin, M AU - Toyoshima, T AU - Aikawa, M AU - Kaslow, D C AD - Molecular Vaccine Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/05/01/ PY - 1993 DA - 1993 May 01 SP - 4266 EP - 4270 VL - 90 IS - 9 SN - 0027-8424, 0027-8424 KW - Insecticides KW - 0 KW - Trisaccharides KW - allosamidin KW - 103782-08-7 KW - Chitinases KW - EC 3.2.1.14 KW - Endopeptidases KW - EC 3.4.- KW - Acetylglucosamine KW - V956696549 KW - Index Medicus KW - Animals KW - Chickens KW - Enzyme Activation KW - Kinetics KW - Streptomyces griseus -- enzymology KW - Aedes -- physiology KW - Trisaccharides -- pharmacology KW - Aedes -- drug effects KW - Plasmodium gallinaceum -- physiology KW - Acetylglucosamine -- pharmacology KW - Anopheles -- enzymology KW - Plasmodium gallinaceum -- enzymology KW - Endopeptidases -- metabolism KW - Aedes -- enzymology KW - Chitinases -- metabolism KW - Plasmodium gallinaceum -- drug effects KW - Insecticides -- pharmacology KW - Plasmodium falciparum -- drug effects KW - Plasmodium falciparum -- physiology KW - Acetylglucosamine -- analogs & derivatives KW - Chitinases -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75719941?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Transmission-blocking+activity+of+a+chitinase+inhibitor+and+activation+of+malarial+parasite+chitinase+by+mosquito+protease.&rft.au=Shahabuddin%2C+M%3BToyoshima%2C+T%3BAikawa%2C+M%3BKaslow%2C+D+C&rft.aulast=Shahabuddin&rft.aufirst=M&rft.date=1993-05-01&rft.volume=90&rft.issue=9&rft.spage=4266&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-01 N1 - Date created - 1993-06-01 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Annu Rev Entomol. 1977;22:219-40 [319739] Nature. 1981 Nov 26;294(5839):364-6 [7031476] J Immunol. 1983 Nov;131(5):2557-62 [6631012] Cell Tissue Res. 1986;245(1):19-27 [3524850] J Parasitol. 1986 Oct;72(5):723-7 [3806321] Acta Trop. 1965;22:148-54 [14319772] Biochim Biophys Acta. 1991 Jan 23;1073(1):177-82 [1991132] Exp Parasitol. 1991 Feb;72(2):145-56 [2009919] Proc Natl Acad Sci U S A. 1991 Apr 1;88(7):2807-10 [2011589] Proc Biol Sci. 1991 Aug 22;245(1313):121-6 [1682935] Science. 1992 Jan 24;255(5043):448-50 [1734521] Mol Biochem Parasitol. 1988 Jun;29(2-3):223-5 [3412376] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The spatial distribution of immunotoxins in solid tumors: assessment by quantitative autoradiography. AN - 75718914; 8481911 AB - The spatial distribution of i.v. administered immunotoxins in s.c. human rhabdomyosarcoma RD2 xenografts was studied. The toxin and immunotoxins were: (a) diphtheria toxin (DT); (b) a binding-deficient form of DT (CRM107) linked to a monoclonal IgG1 antibody (454A12) directed against the human transferrin receptor (454A12-107); (c) the binding-deficient form of DT linked to the Fab' fragment of 454A12 (Fab'-107); and (d) the binding-deficient form of DT coupled to MOPC21, a monoclonal IgG1 with no significant binding to RD2 cells. DT and the immunotoxins were radiolabeled with 125I and injected via the tail vein into tumor-bearing athymic mice (median tumor weight, 0.25 g). Tumors were removed 2, 6, and 24 h after injection of DT or immunotoxin. Film images of 20-microns frozen sections were digitized by video microscopy, and gray levels were converted to tissue concentrations based upon the film response to radioactivity standards and the specific activity of the radiolabeled toxins. Images of the tumors were characterized quantitatively by the kurtosis and the area above threshold; the kurtosis is a measure of the spatial heterogeneity of the radiolabeled immunotoxins, and the area above threshold is defined here as the fractional tumor area that reaches or exceeds 1.5% of the initial plasma concentration. The spatial distribution of DT in the tumors was extremely uniform, characterized by low kurtosis values. In contrast, the autoradiograms of 454A12-107 were punctate in appearance and were characterized by very high kurtosis values. Fab'-107, which has approximately one-half the molecular weight of the intact immunotoxin and binds only monovalently, also produced punctate images with kurtosis values similar to those for 454A12-107. The nonbinding immunotoxin distributed somewhat less uniformly than DT but much more homogeneously than either of the binding immunotoxins. DT, 454A12-107, and Fab'-107 have similar affinities for their respective receptors, but the concentration of binding sites for DT on RD2 cells (<3,000 receptors/cell) is much lower than the concentration of transferrin receptor (60,000 receptors/cell). Thus, the heterogeneous distribution of 454A12-107 and Fab'-107 probably reflects retarded penetration due to binding to the tumor cells. The area above threshold was greatest for DT and lowest for 454A12-107; the fragment and nonbinding immunotoxins had intermediate values. The lower area above threshold for the nonbinding immunotoxin as compared with DT may be due to the considerably large molecular weight and hence the lower capillary permeability and diffusion coefficient of the immunotoxin.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Cancer research AU - Sung, C AU - Dedrick, R L AU - Hall, W A AU - Johnson, P A AU - Youle, R J AD - Biomedical Engineering and Instrumentation Program, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, Maryland 20892. Y1 - 1993/05/01/ PY - 1993 DA - 1993 May 01 SP - 2092 EP - 2099 VL - 53 IS - 9 SN - 0008-5472, 0008-5472 KW - Diphtheria Toxin KW - 0 KW - Immunotoxins KW - Index Medicus KW - Animals KW - Tumor Cells, Cultured KW - Humans KW - In Vitro Techniques KW - Diphtheria Toxin -- metabolism KW - Mice, Nude KW - Mice KW - Tissue Distribution KW - Female KW - Sarcoma, Experimental -- metabolism KW - Immunotoxins -- metabolism KW - Autoradiography -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75718914?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=The+spatial+distribution+of+immunotoxins+in+solid+tumors%3A+assessment+by+quantitative+autoradiography.&rft.au=Sung%2C+C%3BDedrick%2C+R+L%3BHall%2C+W+A%3BJohnson%2C+P+A%3BYoule%2C+R+J&rft.aulast=Sung&rft.aufirst=C&rft.date=1993-05-01&rft.volume=53&rft.issue=9&rft.spage=2092&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-01 N1 - Date created - 1993-06-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Differences in the antibody response to human immunodeficiency virus-1 envelope glycoprotein (gp160) in infected laboratory workers and vaccinees. AN - 75716764; 7683694 AB - Studies of the immune response to the human immunodeficiency virus (HIV) have been hampered by the antigenic diversity of the HIV envelope protein. In an effort to predict the efficacy of vaccination we have compared the systemic anti-envelope antibody response in seronegative volunteers immunized with recombinant gp160 (either in vaccinia or as soluble protein produced in baculovirus) derived from the HTLV-IIIB strain of HIV-1 and in two laboratory workers accidentally infected with the same strain. 11 of 14 vaccinees responded to immunization by producing anti-gp160 of similar titer and the same isotype as that seen in the laboratory workers. Four vaccinees also had antibody to the principal neutralizing domain (V3 loop) that was comparable in titer with that seen in the laboratory workers, but the fine specificity of anti-V3 antibody was qualitatively different in the two groups. Antibody that can block the interaction between CD4 and gp120 was present at comparable levels in three vaccines and the lab workers. Neutralizing antibody titers were markedly lower in the vaccinees than in the laboratory workers. In seven of the vaccinees, an immunodominant epitope was at amino acid 720-740. Analyses of monoclonal antibodies to this region indicate that they do not neutralize, bind to infected cells, nor function as immunotoxins. Although the anti-gp160 antibody response was of similar magnitude in both infected and vaccinated individuals, there were important qualitative differences. JF - The Journal of clinical investigation AU - Pincus, S H AU - Messer, K G AU - Schwartz, D H AU - Lewis, G K AU - Graham, B S AU - Blattner, W A AU - Fisher, G AD - Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana 59840. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 1987 EP - 1996 VL - 91 IS - 5 SN - 0021-9738, 0021-9738 KW - AIDS Vaccines KW - 0 KW - Antibodies, Monoclonal KW - Antibodies, Viral KW - Antigens, CD4 KW - Epitopes KW - Gene Products, env KW - HIV Envelope Protein gp120 KW - HIV Envelope Protein gp160 KW - Immunoglobulin G KW - Peptides KW - Protein Precursors KW - Vaccines, Synthetic KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Reference Values KW - Antibodies, Monoclonal -- metabolism KW - Humans KW - Peptides -- immunology KW - Amino Acid Sequence KW - HIV Envelope Protein gp120 -- metabolism KW - Immunoglobulin G -- immunology KW - Antigens, CD4 -- metabolism KW - Antibodies, Viral -- blood KW - Immunoglobulin G -- blood KW - Epitopes -- analysis KW - Neutralization Tests KW - Molecular Sequence Data KW - Enzyme-Linked Immunosorbent Assay KW - Cell Line KW - HIV-1 -- immunology KW - Protein Precursors -- immunology KW - AIDS Vaccines -- immunology KW - Vaccines, Synthetic -- immunology KW - Protein Precursors -- genetics KW - Medical Laboratory Personnel KW - Gene Products, env -- immunology KW - Antibody Formation KW - HIV Seropositivity -- immunology KW - HIV Seropositivity -- blood KW - Gene Products, env -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75716764?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+clinical+investigation&rft.atitle=Differences+in+the+antibody+response+to+human+immunodeficiency+virus-1+envelope+glycoprotein+%28gp160%29+in+infected+laboratory+workers+and+vaccinees.&rft.au=Pincus%2C+S+H%3BMesser%2C+K+G%3BSchwartz%2C+D+H%3BLewis%2C+G+K%3BGraham%2C+B+S%3BBlattner%2C+W+A%3BFisher%2C+G&rft.aulast=Pincus&rft.aufirst=S&rft.date=1993-05-01&rft.volume=91&rft.issue=5&rft.spage=1987&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+clinical+investigation&rft.issn=00219738&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-04 N1 - Date created - 1993-06-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1989 Sep;86(17):6768-72 [2771954] Science. 1988 Jan 1;239(4835):68-71 [3336776] Science. 1988 Feb 26;239(4843):1021-3 [2830667] Proc Natl Acad Sci U S A. 1988 Mar;85(6):1932-6 [2450351] Proc Natl Acad Sci U S A. 1988 May;85(9):3198-202 [2452447] Virology. 1988 Jul;165(1):209-15 [2838959] Proc Natl Acad Sci U S A. 1988 Jul;85(14):5200-4 [2455898] Proc Natl Acad Sci U S A. 1988 Sep;85(18):6944-8 [3413127] J Virol. 1988 Oct;62(10):3779-88 [3047430] Nature. 1989 Jun 1;339(6223):385-8, 340 [2542797] Nature. 1989 Aug 10;340(6233):431-2 [2787895] J Virol. 1989 Sep;63(9):3579-85 [2474670] Ann Intern Med. 1991 Jan 15;114(2):119-27 [1984386] Proc Natl Acad Sci U S A. 1991 Jan 15;88(2):542-6 [1988952] Science. 1990 Dec 14;250(4987):1590-3 [1703322] Lancet. 1991 Mar 9;337(8741):567-72 [1671940] N Engl J Med. 1991 Jun 13;324(24):1677-84 [1674589] N Engl J Med. 1991 Jun 13;324(24):1733-5 [2034251] J Immunol. 1991 Jun 15;146(12):4315-24 [1710247] J Immunol. 1991 Jun 15;146(12):4325-32 [1710248] Science. 1991 Jul 5;253(5015):71-4 [1905842] Biotechniques. 1991 Mar;10(3):336-42 [2064772] J Virol. 1991 Sep;65(9):4832-8 [1714520] Immunol Today. 1991 Jul;12(7):211-3 [1716107] J Virol. 1991 Nov;65(11):5983-90 [1717712] Science. 1991 Oct 4;254(5028):105-8 [1718036] Science. 1991 Nov 1;254(5032):647 [1948042] Proc Natl Acad Sci U S A. 1992 Jan 15;89(2):461-5 [1370580] Nature. 1992 Feb 20;355(6362):728-30 [1741059] Science. 1992 Jun 19;256(5064):1687-90 [1609280] J Infect Dis. 1992 Aug;166(2):244-52 [1353102] Immunol Rev. 1980;49:79-91 [6154642] Science. 1986 Mar 28;231(4745):1556-9 [3006246] J Virol. 1986 Aug;59(2):284-91 [3016298] EMBO J. 1986 Nov;5(11):3065-71 [3466790] J Clin Microbiol. 1987 May;25(5):845-8 [2438302] Cell. 1987 Sep 11;50(6):975-85 [2441877] J Immunol Methods. 1987 Sep 24;102(2):259-74 [2443575] Nature. 1990 Jun 14;345(6276):622-5 [2190095] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Radiation-associated lung cancer: a comparison of the histology of lung cancers in uranium miners and survivors of the atomic bombings of Hiroshima and Nagasaki. AN - 75716335; 8387679 AB - A binational panel of Japanese and American pulmonary pathologists reviewed tissue slides of lung cancer cases diagnosed among Japanese A-bomb survivors and American uranium miners and classified the cases according to histological subtype. Blind reviews were completed on slides from 92 uranium miners and 108 A-bomb survivors, without knowledge of population, sex, age, smoking history, or level of radiation exposure. Consensus diagnoses were obtained with respect to principal subtype, including squamous-cell cancer, small-cell cancer, adenocarcinoma, and less frequent subtypes. The results were analyzed in terms of population, radiation dose, and smoking history. As expected, the proportion of squamous-cell cancer was positively related to smoking history in both populations. The relative frequencies of small-cell cancer and adenocarcinoma were very different in the two populations, but this difference was accounted for adequately by differences in radiation dose or, more specifically, dose-based relative risk estimates based on published data. Radiation-induced cancers appeared more likely to be of the small-cell subtype, and less likely to be adenocarcinomas, in both populations. The data appeared to require no additional explanation in terms of radiation quality (alpha particles vs gamma rays), uniform or local irradiation, inhaled vs external radiation source, or other population difference. JF - Radiation research AU - Land, C E AU - Shimosato, Y AU - Saccomanno, G AU - Tokuoka, S AU - Auerbach, O AU - Tateishi, R AU - Greenberg, S D AU - Nambu, S AU - Carter, D AU - Akiba, S AD - National Cancer Institute, Bethesda, Maryland. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 234 EP - 243 VL - 134 IS - 2 SN - 0033-7587, 0033-7587 KW - Uranium KW - 4OC371KSTK KW - Index Medicus KW - Space life sciences KW - Carcinoma, Squamous Cell -- etiology KW - Carcinoma, Small Cell -- etiology KW - Carcinoma, Squamous Cell -- epidemiology KW - Carcinoma, Small Cell -- epidemiology KW - Humans KW - Aged KW - Japan -- epidemiology KW - Smoking KW - Adenocarcinoma -- epidemiology KW - Adenocarcinoma -- etiology KW - Middle Aged KW - United States -- epidemiology KW - Female KW - Male KW - Occupational Exposure KW - Lung Neoplasms -- etiology KW - Lung Neoplasms -- epidemiology KW - Neoplasms, Radiation-Induced -- etiology KW - Neoplasms, Radiation-Induced -- pathology KW - Nuclear Warfare KW - Neoplasms, Radiation-Induced -- epidemiology KW - Mining KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75716335?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Radiation+research&rft.atitle=Radiation-associated+lung+cancer%3A+a+comparison+of+the+histology+of+lung+cancers+in+uranium+miners+and+survivors+of+the+atomic+bombings+of+Hiroshima+and+Nagasaki.&rft.au=Land%2C+C+E%3BShimosato%2C+Y%3BSaccomanno%2C+G%3BTokuoka%2C+S%3BAuerbach%2C+O%3BTateishi%2C+R%3BGreenberg%2C+S+D%3BNambu%2C+S%3BCarter%2C+D%3BAkiba%2C+S&rft.aulast=Land&rft.aufirst=C&rft.date=1993-05-01&rft.volume=134&rft.issue=2&rft.spage=234&rft.isbn=&rft.btitle=&rft.title=Radiation+research&rft.issn=00337587&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-10 N1 - Date created - 1993-06-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Recombination sequence-binding protein in thymocytes undergoing T-cell receptor gene rearrangement. AN - 75710347; 8483928 AB - Rearrangement of T-cell antigen receptor and immunoglobulin genes occurs in immature lymphoid cells by an unknown mechanism. To identify components of the rearrangement machinery, we isolated a population of murine thymocytes enriched for rearranging pre-T cells. In the nuclear fraction of these cells, we detected a protein that specifically bound the recombination sequences that flank T-cell receptor and immunoglobulin genes and are required for their rearrangement. This protein recognized both heptamer and nonamer motifs of the recombination sequence, separated by either 12 or 23 bp. The protein complexed with the recombination sequence oligonucleotide had an apparent molecular mass of 30 kDa. The binding characteristics of the protein and its presence in rearranging thymocytes and cell lines suggest that it could serve as the recognition unit of a recombinase complex. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Muegge, K AU - West, M AU - Durum, S K AD - Biological Carcinogenesis and Development Program, Program Resources, Inc.,/Dyncorp, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702-1201. Y1 - 1993/05/01/ PY - 1993 DA - 1993 May 01 SP - 4151 EP - 4155 VL - 90 IS - 9 SN - 0027-8424, 0027-8424 KW - DNA-Binding Proteins KW - 0 KW - Nuclear Proteins KW - Oligodeoxyribonucleotides KW - Receptors, Antigen, T-Cell, alpha-beta KW - Index Medicus KW - Animals KW - Nuclear Proteins -- isolation & purification KW - Cell Nucleus -- metabolism KW - Thymus Gland -- metabolism KW - Mice KW - Thymus Gland -- immunology KW - Mice, Inbred Strains KW - Base Sequence KW - T-Lymphocyte Subsets -- immunology KW - Mice, Inbred C57BL KW - Molecular Sequence Data KW - Substrate Specificity KW - Cell Line, Transformed KW - DNA-Binding Proteins -- isolation & purification KW - Nuclear Proteins -- metabolism KW - Time Factors KW - Radiation Chimera KW - DNA-Binding Proteins -- metabolism KW - Gene Rearrangement, T-Lymphocyte -- radiation effects KW - Recombination, Genetic KW - T-Lymphocytes -- radiation effects KW - Receptors, Antigen, T-Cell, alpha-beta -- genetics KW - T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75710347?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Recombination+sequence-binding+protein+in+thymocytes+undergoing+T-cell+receptor+gene+rearrangement.&rft.au=Muegge%2C+K%3BWest%2C+M%3BDurum%2C+S+K&rft.aulast=Muegge&rft.aufirst=K&rft.date=1993-05-01&rft.volume=90&rft.issue=9&rft.spage=4151&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-01 N1 - Date created - 1993-06-01 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Genes Dev. 1989 Jul;3(7):1053-61 [2777075] Genes Dev. 1987 Oct;1(8):751-61 [3428598] Cell. 1989 Nov 17;59(4):585-8 [2684413] Nature. 1989 Dec 21-28;342(6252):934-7 [2556644] Genes Dev. 1989 Nov;3(11):1801-13 [2606349] Science. 1990 Jun 22;248(4962):1517-23 [2360047] Cancer Cells. 1990 Jan;2(1):1-8 [2201335] J Immunogenet. 1990 Feb-Apr;17(1-2):67-75 [2212701] Nature. 1990 Oct 4;347(6292):479-82 [2215662] Annu Rev Immunol. 1991;9:323-50 [1910681] EMBO J. 1991 Oct;10(10):3025-32 [1915277] J Biol Chem. 1991 Dec 5;266(34):23334-40 [1744127] Eur J Immunol. 1992 Feb;22(2):505-10 [1537384] Cell. 1992 Mar 6;68(5):855-67 [1547487] Cell. 1992 Mar 6;68(5):869-77 [1547488] Cell. 1992 May 1;69(3):529-37 [1316241] Cell. 1984 Feb;36(2):357-69 [6537904] Proc Natl Acad Sci U S A. 1987 Oct;84(20):7019-23 [3118358] Science. 1987 Nov 20;238(4830):1134-8 [3120312] Science. 1989 Oct 13;246(4927):249-51 [2799385] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The N-methyl-D-aspartate antagonist MK-801 fails to protect dopaminergic neurons from 1-methyl-4-phenylpyridinium toxicity in vitro. AN - 75684862; 8473912 AB - Recent reports suggest that NMDA receptor antagonists when administered in vivo can protect dopaminergic neurons from the toxic actions of MPP+. In the present study the possible neuro-protective effects against MPP+ toxicity of the noncompetitive NMDA receptor antagonist MK-801 was studied in primary cultures of fetal rat mesencephalic dopamine neurons. MK-801 failed to protect dopaminergic neurons from MPP+ toxicity at concentrations that completely block NMDA-induced toxicity of these same neurons. In contrast to work carried out in cerebellar granule cells, MPP+ toxicity of mesencephalic dopamine neurons was unaffected by preexposure to subtoxic concentrations of either NMDA or cycloheximide. Our findings suggest that the toxic effects of MPP+ on dopaminergic neurons are not mediated through a direct interaction with the NMDA subtype of glutamate receptor. JF - Journal of neurochemistry AU - Finiels-Marlier, F AU - Marini, A M AU - Williams, P AU - Paul, S M AD - Section on Molecular Pharmacology, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 1968 EP - 1971 VL - 60 IS - 5 SN - 0022-3042, 0022-3042 KW - N-Methylaspartate KW - 6384-92-5 KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - Cycloheximide KW - 98600C0908 KW - 1-Methyl-4-phenylpyridinium KW - R865A5OY8J KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Mesencephalon -- drug effects KW - Animals KW - Cells, Cultured KW - Cycloheximide -- pharmacology KW - Mesencephalon -- cytology KW - Neurons -- metabolism KW - N-Methylaspartate -- pharmacology KW - Neurons -- drug effects KW - N-Methylaspartate -- antagonists & inhibitors KW - Dopamine -- metabolism KW - Dizocilpine Maleate -- pharmacology KW - 1-Methyl-4-phenylpyridinium -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75684862?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neurochemistry&rft.atitle=The+N-methyl-D-aspartate+antagonist+MK-801+fails+to+protect+dopaminergic+neurons+from+1-methyl-4-phenylpyridinium+toxicity+in+vitro.&rft.au=Finiels-Marlier%2C+F%3BMarini%2C+A+M%3BWilliams%2C+P%3BPaul%2C+S+M&rft.aulast=Finiels-Marlier&rft.aufirst=F&rft.date=1993-05-01&rft.volume=60&rft.issue=5&rft.spage=1968&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurochemistry&rft.issn=00223042&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-18 N1 - Date created - 1993-05-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Functional and molecular characterization of tumor-infiltrating lymphocytes transduced with tumor necrosis factor-alpha cDNA for the gene therapy of cancer in humans. AN - 75675601; 8473752 AB - TNF is effective in causing the regression of selected murine tumors when administered at high concentrations. Therapeutic levels in humans cannot be obtained systemically, however, because of dose-limiting toxicity. The development of immunotherapy with IL-2 and tumor-infiltrating lymphocytes (TIL), which can accumulate at tumor sites in some patients, and of efficient retroviral techniques for gene transfer into eukaryotic cells has allowed new therapeutic approaches using TNF. We have retrovirally transduced human TIL with the gene for TNF in an attempt to deliver high concentrations of TNF to the tumor site without dose-limiting systemic toxicity. Successful gene insertion was confirmed by Southern hybridization in 16 of 16 transduced and selected TIL cultures from 15 different patients, with an estimated 28 to 93% transduced cells within each culture. Transduced selected TIL cultures produced greater amounts of TNF, compared with nontransduced controls, in 11 of 16 cultures evaluated. However, overall production of TNF was > 30-fold lower, compared with a transduced and highly selected tumor cell line control (MEL-TNF). In addition, steady state levels of vector-derived transcript in nine of 10 transduced selected TIL cultures were < 14% of the amount seen in the MEL-TNF control line. In an attempt to increase TNF production, TIL were transduced with a mutated form of TNF containing the IFN-gamma signal peptide in place of the transmembranous region, to enhance secretion into the endoplasmic reticulum. By using this vector, TNF production increased by an average of fivefold. These studies demonstrate that TIL can be genetically modified to express and secrete a protein for use in targeted cancer therapy but that partial expression blockades exist that prevent maximal cytokine production by introduced genes in TIL. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Hwu, P AU - Yannelli, J AU - Kriegler, M AU - Anderson, W F AU - Perez, C AU - Chiang, Y AU - Schwarz, S AU - Cowherd, R AU - Delgado, C AU - Mulé, J AD - Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/05/01/ PY - 1993 DA - 1993 May 01 SP - 4104 EP - 4115 VL - 150 IS - 9 SN - 0022-1767, 0022-1767 KW - Tumor Necrosis Factor-alpha KW - 0 KW - DNA KW - 9007-49-2 KW - Abridged Index Medicus KW - Index Medicus KW - Tumor Cells, Cultured KW - Humans KW - Genetic Vectors KW - Transcription, Genetic KW - Repetitive Sequences, Nucleic Acid KW - Lymphocytes, Tumor-Infiltrating -- physiology KW - Transfection KW - DNA -- genetics KW - Tumor Necrosis Factor-alpha -- biosynthesis KW - Genetic Therapy KW - Neoplasms -- therapy KW - Tumor Necrosis Factor-alpha -- genetics KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75675601?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=Functional+and+molecular+characterization+of+tumor-infiltrating+lymphocytes+transduced+with+tumor+necrosis+factor-alpha+cDNA+for+the+gene+therapy+of+cancer+in+humans.&rft.au=Hwu%2C+P%3BYannelli%2C+J%3BKriegler%2C+M%3BAnderson%2C+W+F%3BPerez%2C+C%3BChiang%2C+Y%3BSchwarz%2C+S%3BCowherd%2C+R%3BDelgado%2C+C%3BMul%C3%A9%2C+J&rft.aulast=Hwu&rft.aufirst=P&rft.date=1993-05-01&rft.volume=150&rft.issue=9&rft.spage=4104&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.issn=00221767&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-20 N1 - Date created - 1993-05-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The RRE of human immunodeficiency virus type 1 contributes to cell-type-specific viral tropism. AN - 75675510; 8474177 AB - As part of a general program investigating the mechanism of the Rev axis of human immunodeficiency virus type 1 (HIV-1) autoregulation, a series of proviral HIV-1 mutants which differ from the parental HXB2 strain at selected positions within the RRE were constructed. All of the mutations were designed to perturb the RRE by introducing local helix disruptions without altering the coding potential of the overlapping envelope open reading frame. Viral replication in various cell types was monitored by a cell supernatant reverse transcriptase assay and Northern (RNA blot) analysis. All proviral RRE mutants displayed at least some impairment in replication. However, the relative impairment varied drastically among the various cell types tested. This suggests that the RRE may contribute to cell-type-specific viral tropism. JF - Journal of virology AU - Dayton, E T AU - Konings, D A AU - Lim, S Y AU - Hsu, R K AU - Butini, L AU - Pantaleo, G AU - Dayton, A I AD - National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 2871 EP - 2878 VL - 67 IS - 5 SN - 0022-538X, 0022-538X KW - Gene Products, rev KW - 0 KW - RNA, Viral KW - rev Gene Products, Human Immunodeficiency Virus KW - Index Medicus KW - AIDS/HIV KW - Virus Replication KW - Lymphocyte Activation KW - Base Sequence KW - Gene Products, rev -- metabolism KW - Sequence Alignment KW - Molecular Sequence Data KW - Databases, Factual KW - Cell Line -- microbiology KW - Virion -- isolation & purification KW - Nucleic Acid Conformation KW - Mutagenesis KW - HIV-1 -- genetics KW - HIV-1 -- pathogenicity KW - Proviruses -- genetics KW - HIV-1 -- growth & development KW - RNA, Viral -- genetics KW - Proviruses -- pathogenicity KW - Acquired Immunodeficiency Syndrome -- microbiology KW - Proviruses -- growth & development UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75675510?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft.genre=dissertations+%26+theses&rft.jtitle=&rft.atitle=&rft.au=Gratien%2C+Christopher&rft.aulast=Gratien&rft.aufirst=Christopher&rft.date=2015-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=9781339057934&rft.btitle=&rft.title=The+mountains+are+ours+Ecology+and+settlement+in+late+Ottoman+and+early+Republican+Cilicia%2C+1856-1956&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-17 N1 - Date created - 1993-05-17 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nature. 1984 Dec 20-1985 Jan 2;312(5996):763-7 [6096719] J Virol. 1992 Apr;66(4):2588-93 [1548785] Proc Natl Acad Sci U S A. 1985 Jul;82(13):4539-43 [2989831] J Immunol. 1985 Nov;135(5):3151-62 [2995487] Science. 1986 Mar 28;231(4745):1549-53 [3006244] Cell. 1986 Mar 28;44(6):941-7 [2420471] Nature. 1987 Aug 20-26;328(6132):728-30 [2441266] Science. 1987 Aug 21;237(4817):888-93 [3497453] Nature. 1989 Mar 16;338(6212):254-7 [2784194] Science. 1989 Apr 7;244(4900):48-52 [2468181] Science. 1989 Dec 22;246(4937):1625-9 [2688093] Nucleic Acids Res. 1990 Mar 25;18(6):1613-23 [2326200] J Immunol. 1990 Jun 15;144(12):4628-32 [1972163] J Virol. 1990 Sep;64(9):4390-8 [2384920] Nature. 1990 Nov 1;348(6296):69-73 [2172833] J Virol. 1990 Dec;64(12):5966-75 [2243382] EMBO J. 1990 Dec;9(12):4155-60 [2249669] Nature. 1991 Jan 10;349(6305):167-9 [1986308] J Virol. 1991 Feb;65(2):1041-5 [1987367] J Virol. 1991 Mar;65(3):1414-9 [1995951] J Exp Med. 1991 Mar 1;173(3):589-97 [1705278] Proc Natl Acad Sci U S A. 1991 Apr 15;88(8):3097-101 [2014229] Biochim Biophys Acta. 1991 Apr 16;1072(1):63-80 [2018779] Genes Dev. 1991 May;5(5):808-19 [1827422] Cell. 1991 May 17;65(4):651-62 [2032289] Science. 1991 Jul 5;253(5015):71-4 [1905842] J Virol. 1991 Aug;65(8):4350-8 [2072454] J Virol. 1991 Nov;65(11):5765-73 [1920615] J Virol. 1991 Dec;65(12):6931-41 [1658383] Annu Rev Microbiol. 1991;45:219-50 [1741615] J Virol. 1992 Feb;66(2):1139-51 [1731093] J Virol. 1992 Apr;66(4):2577-82 [1548783] Nature. 1984 Dec 20-1985 Jan 2;312(5996):767-8 [6083454] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Picolinic acid, a catabolite of L-tryptophan, is a costimulus for the induction of reactive nitrogen intermediate production in murine macrophages. AN - 75666806; 8473748 AB - In this study we investigated the effects of picolinic acid, a catabolite of L-tryptophan, on the production of L-arginine-derived reactive nitrogen intermediates in the murine macrophage cell line ANA-1. ANA-1 macrophages did not produce nitrite (NO2-) constitutively, but accumulated detectable levels of NO2- on exposure to IFN-gamma. Picolinic acid, although ineffective by itself, augmented IFN-gamma-induced NO2- production. The activity of picolinic acid was evident at 1 mM and reached its maximum at 4 mM. Picolinic acid also augmented the IFN-gamma-dependent expression of TNF-alpha mRNA, but did not appreciably affect the secretion of the TNF-alpha protein. Neutralizing concentrations of anti-TNF mAb completely abrogated IFN-gamma- and IFN-gamma plus rTNF-alpha-induced NO2- production in ANA-1 macrophages, but only decreased by approximately 50% the synergistic interaction between IFN-gamma and picolinic acid. Although IL-4 inhibited the expression of IFN-gamma plus picolinic acid-induced TNF-alpha mRNA and protein, it only partially suppressed picolinic acid-dependent NO2- production. Therefore, picolinic acid may affect NO2- production via both TNF-alpha-dependent and TNF-alpha-independent pathways. Overall, this study suggests that amino acid catabolites may be important for the activation and the expression of effector functions by murine macrophages, and provides the first evidence of a possible connection between tryptophan and arginine metabolism. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Melillo, G AU - Cox, G W AU - Radzioch, D AU - Varesio, L AD - Laboratory of Molecular Immunoregulation, National Cancer Institute-Frederick Cancer Research and Development Center, NIH, MD 21702-1201. Y1 - 1993/05/01/ PY - 1993 DA - 1993 May 01 SP - 4031 EP - 4040 VL - 150 IS - 9 SN - 0022-1767, 0022-1767 KW - Nitrites KW - 0 KW - Picolinic Acids KW - RNA, Messenger KW - Tumor Necrosis Factor-alpha KW - Interleukin-4 KW - 207137-56-2 KW - omega-N-Methylarginine KW - 27JT06E6GR KW - Interferon-gamma KW - 82115-62-6 KW - Tryptophan KW - 8DUH1N11BX KW - Arginine KW - 94ZLA3W45F KW - picolinic acid KW - QZV2W997JQ KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Interleukin-4 -- pharmacology KW - RNA, Messenger -- analysis KW - Interferon-gamma -- pharmacology KW - Tumor Necrosis Factor-alpha -- physiology KW - Mice KW - Tumor Necrosis Factor-alpha -- genetics KW - Arginine -- pharmacology KW - Macrophage Activation -- drug effects KW - Mice, Inbred C57BL KW - Drug Synergism KW - Arginine -- analogs & derivatives KW - Cell Line KW - Nitrites -- metabolism KW - Tryptophan -- metabolism KW - Macrophages -- drug effects KW - Picolinic Acids -- pharmacology KW - Macrophages -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75666806?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=Picolinic+acid%2C+a+catabolite+of+L-tryptophan%2C+is+a+costimulus+for+the+induction+of+reactive+nitrogen+intermediate+production+in+murine+macrophages.&rft.au=Melillo%2C+G%3BCox%2C+G+W%3BRadzioch%2C+D%3BVaresio%2C+L&rft.aulast=Melillo&rft.aufirst=G&rft.date=1993-05-01&rft.volume=150&rft.issue=9&rft.spage=4031&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.issn=00221767&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-20 N1 - Date created - 1993-05-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Fertility and pregnancy after treatment for cancer during childhood or adolescence AN - 1434023382; 18537369 AB - Because most children and adolescents with cancer now survive, issues regarding the late effects of therapy, including fertility and the health of offspring, are increasingly important. This article summarizes the literature regarding issues related to fertility in survivors of cancer, including actual fertility, gonadal function, menarche, menopause, and birth defects and cancer in the offspring. Radiation therapy to the gonads and alkylating agent chemotherapy, either alone or in combination, impair actual fertility in survivors of childhood and adolescent cancer. Males are particularly affected by alkylating agents, and females who have had radiation therapy to the abdomen have decreased fertility and an increased risk of adverse pregnancy outcomes. Consequently, these women should be followed up as high-risk obstetrical patients. Offspring of survivors of cancer appear to have little risk of childhood cancer or birth defects. Thus, in most instances, survivors of cancer should not be discouraged from having children and can expect a good outcome of pregnancy. This article concludes with advice to survivors and clinicians who counsel survivors. JF - Cancer AU - Nicholson, HStacy AU - Byrne, Julianne AD - Clinical Epidemiology Branch, EPN 400, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/05// PY - 1993 DA - May 1993 SP - 3392 EP - 3399 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 71 IS - S10 SN - 0008-543X, 0008-543X KW - Risk Abstracts KW - Radiation therapy KW - Health risks KW - Fertility KW - Congenital defects KW - Offspring KW - Children KW - Cancer KW - Adolescents KW - Pregnancy KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434023382?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=Fertility+and+pregnancy+after+treatment+for+cancer+during+childhood+or+adolescence&rft.au=Nicholson%2C+HStacy%3BByrne%2C+Julianne&rft.aulast=Nicholson&rft.aufirst=HStacy&rft.date=1993-05-01&rft.volume=71&rft.issue=S10&rft.spage=3392&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/10.1002%2F1097-0142%2819930515%2971%3A10%2B3.0.CO%3B+2-F LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-09-01 N1 - Last updated - 2013-10-04 N1 - SubjectsTermNotLitGenreText - Radiation therapy; Health risks; Fertility; Congenital defects; Offspring; Children; Adolescents; Cancer; Pregnancy DO - http://dx.doi.org/10.1002/1097-0142(19930515)71:10+<3392::AID-CNCR2820711743>3.0.CO; ER - TY - JOUR T1 - Phosphorylation of HIV-1 gag proteins by protein kinase C. AN - 75685009; 8473314 AB - We have demonstrated that the 17-kDa N-terminal matrix protein (p17gag) of HIV-1 Pr55gag is a substrate for protein kinase C (PKC). Phosphorylation of p17gag and Pr55gag was studied in vivo by infecting COS-7 cells with a recombinant vaccinia virus containing the HIV-1 gag-pol gene. Basal gag protein phosphorylation was inhibited up to 75% with the PKC inhibitor, H-7, and stimulated 3-4-fold with phorbol 12-myristate 13-acetate. In experiments using MCF-7 cell lines, p17gag and Pr55gag were dramatically phosphorylated only in clones with high PKC activity. Bacterially expressed and purified non-myristoylated and N-myristoylated p17gag were efficiently phosphorylated in a Ca2+ and phosphatidylserine-dependent manner by purified PKC. The N-myristoylated p17gag exhibited an apparent Km = 4 microM for PKC phosphorylation. Both in vitro and in vivo phosphorylated p17gag yielded identical V8 protease digestion phosphopeptide maps, indicating identical PKC phosphorylation sites. Phosphoamino acid analysis of the in vitro phosphorylated p17gag revealed only phosphoserine. These data are consistent with the identification of a highly conserved consensus PKC phosphorylation site motif in the HIV-1 gag protein at Ser111 and suggests that PKC phosphorylation plays an important role in gag protein function. JF - The Journal of biological chemistry AU - Burnette, B AU - Yu, G AU - Felsted, R L AD - Laboratory of Biological Chemistry, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/04/25/ PY - 1993 DA - 1993 Apr 25 SP - 8698 EP - 8703 VL - 268 IS - 12 SN - 0021-9258, 0021-9258 KW - Gene Products, gag KW - 0 KW - HIV Antigens KW - Protein Precursors KW - Viral Proteins KW - gag Gene Products, Human Immunodeficiency Virus KW - p17 protein, Human Immunodeficiency Virus Type 1 KW - p55 gag precursor protein, Human immunodeficiency virus 1 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - AIDS/HIV KW - Protein Precursors -- metabolism KW - Tumor Cells, Cultured KW - Phosphorylation KW - Peptide Mapping KW - Tetradecanoylphorbol Acetate -- pharmacology KW - HIV Antigens -- metabolism KW - Protein Kinase C -- metabolism KW - HIV-1 -- metabolism KW - Gene Products, gag -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75685009?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Phosphorylation+of+HIV-1+gag+proteins+by+protein+kinase+C.&rft.au=Burnette%2C+B%3BYu%2C+G%3BFelsted%2C+R+L&rft.aulast=Burnette&rft.aufirst=B&rft.date=1993-04-25&rft.volume=268&rft.issue=12&rft.spage=8698&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-14 N1 - Date created - 1993-05-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Lysine 87 in the beta subunit of tryptophan synthase that forms an internal aldimine with pyridoxal phosphate serves critical roles in transimination, catalysis, and product release. AN - 75684156; 8473317 AB - This study provides valuable insights into the functions of the lysine residue that forms an internal aldimine with pyridoxal phosphate in the beta subunit of tryptophan synthase from Salmonella typhimurium. Our spectroscopic and kinetic studies demonstrate that a mutant alpha 2 beta 2 complex having beta subunit lysine 87 replaced by threonine forms external aldimines with several amino acids including L-serine, beta-chloro-1-alanine, L-tryptophan, and D-tryptophan. Because the rates of aldimine formation are very slow, we conclude that one role of lysine 87 in the wild type enzyme is to facilitate formation of external aldimines by transimination. Lysine 87 is an essential catalytic residue because the mutant alpha 2 beta 2 complex has no measurable activity in reactions catalyzed by the beta subunit and does not convert external aldimines to products. The mutant enzyme carries out two slow partial beta-elimination reactions: the conversion of beta-chloro-L-alanine and L-serine to enzyme-bound aminoacrylate. The reaction with L-serine is catalyzed by ammonia, which partially replaces the deleted epsilon-amino group. Lysine 87 is important for substrate and product release because L-serine, L-tryptophan, and aminoacrylate dissociate very slowly from the mutant alpha 2 beta 2 complex. Our ability to prepare very stable derivatives of the mutant alpha 2 beta 2 complex containing tightly bound aldimines with a substrate, a product, or a reaction intermediate provides valuable materials for ongoing x-ray crystallographic investigations and future kinetic analyses of the allosteric activation of the alpha subunit by beta subunit ligands. JF - The Journal of biological chemistry AU - Lu, Z AU - Nagata, S AU - McPhie, P AU - Miles, E W AD - Laboratory of Biochemical Pharmacology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/04/25/ PY - 1993 DA - 1993 Apr 25 SP - 8727 EP - 8734 VL - 268 IS - 12 SN - 0021-9258, 0021-9258 KW - Imines KW - 0 KW - Pyridoxal Phosphate KW - 5V5IOJ8338 KW - Tryptophan Synthase KW - EC 4.2.1.20 KW - Lysine KW - K3Z4F929H6 KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Imines -- chemistry KW - Spectrum Analysis KW - Isomerism KW - Circular Dichroism KW - Imines -- metabolism KW - Salmonella typhimurium -- enzymology KW - Catalysis KW - Tryptophan Synthase -- metabolism KW - Tryptophan Synthase -- chemistry KW - Pyridoxal Phosphate -- chemistry KW - Tryptophan Synthase -- genetics KW - Pyridoxal Phosphate -- metabolism KW - Lysine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75684156?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Lysine+87+in+the+beta+subunit+of+tryptophan+synthase+that+forms+an+internal+aldimine+with+pyridoxal+phosphate+serves+critical+roles+in+transimination%2C+catalysis%2C+and+product+release.&rft.au=Lu%2C+Z%3BNagata%2C+S%3BMcPhie%2C+P%3BMiles%2C+E+W&rft.aulast=Lu&rft.aufirst=Z&rft.date=1993-04-25&rft.volume=268&rft.issue=12&rft.spage=8727&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-14 N1 - Date created - 1993-05-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Correlations between chemically related site-specific carcinogenic effects in long-term studies in rats and mice. AN - 75807609; 8513764 AB - We examined a database of 379 long-term carcinogenicity studies in rats and mice to evaluate sex and species correlations in site-specific carcinogenic responses. Within a species, most target sites showed a strong correlation between males and females. For example, chemicals producing forestomach or liver tumors in males were likely to produce these same types of tumors in females. There was also a significant correlation between species for certain site-specific carcinogenic effects, most notably tumors of the forestomach, liver, and thyroid gland. In contrast, adrenal pheochromocytoma, preputial/clitoral gland neoplasms, and lung tumors showed no significant interspecies correlation. Many chemicals produced a syndrome of carcinogenic effects involving tumors of the skin, Zymbal gland, preputial/clitoral gland, mammary gland, and/or oral cavity. Regarding different target sites, there appeared to be a correlation between thyroid and liver tumors both within and between species. Further, all chemicals producing mesotheliomas in male rats also produced mammary gland neoplasms in female rats. In contrast, kidney and urinary bladder tumors showed no significant association with any other tumor type in rats or mice. If a chemical produced a site-specific carcinogenic effect in female rats or mice, there was approximately a 65% probability that the chemical would also be carcinogenic at that same site in males. The interspecies correlation was somewhat lower: approximately 36% of the site-specific carcinogenic effects observed in one species (rats or mice) were also observed in the other species.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Environmental health perspectives AU - Haseman, J K AU - Lockhart, A M AD - Statistics and Biomathematics Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/04/22/ PY - 1993 DA - 1993 Apr 22 SP - 50 EP - 54 VL - 101 IS - 1 SN - 0091-6765, 0091-6765 KW - Carcinogens KW - 0 KW - Index Medicus KW - Rats KW - Mammary Neoplasms, Experimental -- chemically induced KW - Animals KW - Stomach Neoplasms -- chemically induced KW - Sex Characteristics KW - Databases, Factual KW - Carcinogenicity Tests KW - Liver Neoplasms, Experimental -- chemically induced KW - Mice KW - Species Specificity KW - Male KW - Female KW - Neoplasms -- chemically induced KW - Carcinogens -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75807609?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Correlations+between+chemically+related+site-specific+carcinogenic+effects+in+long-term+studies+in+rats+and+mice.&rft.au=Haseman%2C+J+K%3BLockhart%2C+A+M&rft.aulast=Haseman&rft.aufirst=J&rft.date=1993-04-22&rft.volume=101&rft.issue=1&rft.spage=50&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-19 N1 - Date created - 1993-07-19 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Annu Rev Pharmacol Toxicol. 1991;31:621-52 [2064387] Cancer Lett. 1987 Oct 30;37(2):125-32 [3677049] Environ Health Perspect. 1987 Oct;74:229-35 [3691430] Mutat Res. 1988 Jan;204(1):17-115 [3277047] Environ Health Perspect. 1991 Jun;93:247-70 [1773796] Environ Health Perspect. 1991 Jun;93:233-46 [1773795] Regul Toxicol Pharmacol. 1992 Oct;16(2):177-88 [1438997] Environ Health Perspect. 1989 May;81:211-9 [2759059] Fundam Appl Toxicol. 1992 Aug;19(2):207-13 [1516777] Regul Toxicol Pharmacol. 1986 Jun;6(2):155-70 [3726178] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Receptor mechanisms and dose-response models for the effects of dioxins. AN - 75796207; 8390353 AB - There is increasing evidence that receptor-mediated events impact one or more stages responsible for tumor development in experimental animals and humans. Although many chemicals and endogenous hormones require receptor interactions as a necessary event in their carcinogenic activity, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and its structural analogs are the most visible examples of receptor-mediated carcinogens. TCDD, or dioxin as it is frequently called, interacts with the Ah receptor (AhR), which functions in a manner analogous to receptors for steroids. TCDD produces a wide spectrum of biochemical and toxic responses in in vitro and in vivo systems, and the Ah receptor is generally considered necessary for most if not all of these responses. Risk assessments for dioxin made by the United States and other countries throughout the world have been based on its carcinogenecity in experimental animals. Recently, epidemiology studies have indicated that TCDD is a human carcinogen at high doses. Because TCDD appears to be acting like a potent and persistent hormone agonist, it appears reasonable to incorporate mechanistic information on receptor-mediated events in risk assessments for TCDD. This information may be obtained from steroid receptor action and from molecular data on the Ah receptor. In this paper, we evaluate the scientific foundation on which mechanistic models for estimating dioxin's risks should be based. These models need to recognize the mechanisms possible for the diversity of biological responses that are initiated by a single receptor interacting with a single ligand. The U.S. EPA is currently reevaluating dioxin's risks by examining the possibility of developing biologically based models.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Environmental health perspectives AU - Lucier, G W AU - Portier, C J AU - Gallo, M A AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/04/22/ PY - 1993 DA - 1993 Apr 22 SP - 36 EP - 44 VL - 101 IS - 1 SN - 0091-6765, 0091-6765 KW - CYP1A1 KW - Dioxins KW - 0 KW - Receptors, Aryl Hydrocarbon KW - Receptors, Drug KW - Index Medicus KW - Rats KW - Animals KW - Guinea Pigs KW - Dose-Response Relationship, Drug KW - Risk Factors KW - Humans KW - Male KW - Female KW - Cell Transformation, Neoplastic -- genetics KW - Dioxins -- metabolism KW - Receptors, Drug -- metabolism KW - Neoplasms -- chemically induced KW - Dioxins -- toxicity KW - Models, Biological UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75796207?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Receptor+mechanisms+and+dose-response+models+for+the+effects+of+dioxins.&rft.au=Lucier%2C+G+W%3BPortier%2C+C+J%3BGallo%2C+M+A&rft.aulast=Lucier&rft.aufirst=G&rft.date=1993-04-22&rft.volume=101&rft.issue=1&rft.spage=36&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-19 N1 - Date created - 1993-07-19 N1 - Date revised - 2017-01-13 N1 - Gene symbol - CYP1A1 N1 - SuppNotes - Cited By: Environ Health Perspect. 1987 Dec;76:125-31 [3447890] J Biol Chem. 1976 Aug 25;251(16):4936-46 [956169] Fed Proc. 1980 Jan;39(1):73-5 [7351247] Cancer Res. 1980 Oct;40(10):3616-20 [6108157] Nature. 1982 Nov 18;300(5889):271-3 [7144882] Environ Health Perspect. 1985 Feb;59:121-8 [2985378] Science. 1987 May 22;236(4804):933-41 [3554512] Environ Health Perspect. 1987 Dec;76:57-63 [3447904] J Biol Chem. 1988 Sep 25;263(27):13802-5 [2843537] Am J Ind Med. 1989;16(4):455-74 [2558567] Annu Rev Pharmacol Toxicol. 1990;30:251-77 [2188570] N Engl J Med. 1991 Jan 24;324(4):212-8 [1985242] Biochemistry. 1991 Mar 19;30(11):2909-16 [1848780] Cancer Res. 1991 Mar 1;51(5):1391-7 [1671757] Science. 1991 Apr 5;252(5002):9 [2011755] Science. 1991 May 17;252(5008):954-8 [1852076] Cell Biol Toxicol. 1991 Jan;7(1):67-94 [2054688] Science. 1991 Oct 18;254(5030):377 [1656528] Science. 1991 Oct 18;254(5030):415-8 [1925598] FASEB J. 1991 Dec;5(15):3092-9 [1743440] Science. 1992 Feb 21;255(5047):979-83 [1312255] Risk Anal. 1991 Dec;11(4):565-8 [1664119] Biochem Biophys Res Commun. 1992 Apr 15;184(1):246-53 [1314586] Cancer Res. 1992 Jun 15;52(12):3436-42 [1596902] Cancer Res. 1992 Jun 15;52(12):3478-82 [1596905] Carcinogenesis. 1992 Aug;13(8):1389-95 [1354083] Proc Natl Acad Sci U S A. 1992 Sep 1;89(17):8185-9 [1325649] Nucleic Acids Res. 1993 Jan 11;21(1):119-25 [8382788] Environ Health Perspect. 1992 Nov;98:125-32 [1336723] Fundam Appl Toxicol. 1993 Jan;20(1):48-56 [8381755] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Prospective randomized trial of high-dose interleukin-2 alone or in conjunction with lymphokine-activated killer cells for the treatment of patients with advanced cancer. AN - 75673918; 8468720 AB - Treatment using interleukin-2 (IL-2) alone or in conjunction with lymphokine-activated killer (LAK) cells has been shown to mediate disease regression in selected patients with advanced cancer. This prospective randomized trial was designed to determine whether the administration of LAK cells in conjunction with high-dose IL-2 alters response and survival rates, compared with those for IL-2 alone, in patients with advanced cancer. The 181 patients who had metastatic cancer that had failed to respond to standard therapy or who had disease for which no effective therapy existed received treatment with high-dose IL-2 alone or with LAK cells plus IL-2. Both treatment groups were to receive the same dose of IL-2 administered according to the same schedule. IL-2 doses were omitted depending on the tolerance of the patient. Of the 181 patients, 97 had renal cell cancer and 54 had melanoma. Median potential follow-up was 63.2 months. There were 10 complete responses among the 85 assessable patients who received IL-2 plus LAK cells, compared with four among the 79 who received IL-2 alone. There were 14 and 12 partial responses, respectively. Complete response continues in seven patients at 50-66 months. The 36-month actuarial survival with IL-2 plus LAK cells was 31%, compared with 17% with IL-2 alone (two-sided P value [P2] = .089). A trend toward improved survival was seen for patients with melanoma who received IL-2 plus LAK cells, compared with those who received IL-2 alone (24-month survival: 32% versus 15%; 48-month survival: 18% versus 4%; P2 = .064 [corrected]). None of 26 patients with melanoma who received IL-2 alone are alive; five of 28 who received IL-2 plus LAK cells are alive, and three continue in complete response. No difference in survival was seen in patients with renal cell cancer in the two treatment groups. There were six treatment-related deaths (3.3%); three were due to myocardial infarction. Other toxic effects resolved by discontinuation of IL-2. Many toxic effects were related to increased vascular permeability induced by IL-2. Some patients with metastatic cancer have prolonged remission when they are treated with high-dose IL-2 alone or in conjunction with LAK cells. Our results suggest a trend toward increased survival when IL-2 is given with LAK cells in patients with melanoma, but no trend was observed for patients with renal cell cancer. As these studies continue, efforts are underway to develop improved immunotherapies using tumor-infiltrating lymphocytes (TIL) and gene-modified TIL. JF - Journal of the National Cancer Institute AU - Rosenberg, S A AU - Lotze, M T AU - Yang, J C AU - Topalian, S L AU - Chang, A E AU - Schwartzentruber, D J AU - Aebersold, P AU - Leitman, S AU - Linehan, W M AU - Seipp, C A AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, Md 20892. Y1 - 1993/04/21/ PY - 1993 DA - 1993 Apr 21 SP - 622 EP - 632 VL - 85 IS - 8 SN - 0027-8874, 0027-8874 KW - Interleukin-2 KW - 0 KW - Index Medicus KW - Leukapheresis KW - Prospective Studies KW - Combined Modality Therapy KW - Humans KW - Adult KW - Treatment Outcome KW - Aged KW - Middle Aged KW - Child KW - Adolescent KW - Male KW - Female KW - Survival Analysis KW - Interleukin-2 -- adverse effects KW - Interleukin-2 -- administration & dosage KW - Neoplasms -- pathology KW - Interleukin-2 -- therapeutic use KW - Neoplasms -- therapy KW - Killer Cells, Lymphokine-Activated -- transplantation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75673918?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Prospective+randomized+trial+of+high-dose+interleukin-2+alone+or+in+conjunction+with+lymphokine-activated+killer+cells+for+the+treatment+of+patients+with+advanced+cancer.&rft.au=Rosenberg%2C+S+A%3BLotze%2C+M+T%3BYang%2C+J+C%3BTopalian%2C+S+L%3BChang%2C+A+E%3BSchwartzentruber%2C+D+J%3BAebersold%2C+P%3BLeitman%2C+S%3BLinehan%2C+W+M%3BSeipp%2C+C+A&rft.aulast=Rosenberg&rft.aufirst=S&rft.date=1993-04-21&rft.volume=85&rft.issue=8&rft.spage=622&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-07 N1 - Date created - 1993-05-07 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: J Natl Cancer Inst 1993 Jul 7;85(13):1091 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Effect of high-protein diet on pyrimidine synthesis and response to PALA in mouse tissues. AN - 75661101; 8468725 AB - High-protein diets have been found to protect mice from the lethal effects of cytotoxic pyrimidine analogues and to reduce the toxicity of the antipyrimidine fluorouracil (5-FU), but the biochemical explanation for these effects is not known. PALA potentiates the chemotherapeutic efficacy of 5-FU, and each of the two agents can produce dose-limiting intestinal toxic effects. We have shown that intraperitoneal infusion of ammonium chloride stimulates intestinal de novo pyrimidine synthesis. This stimulation with excess ammonia, which can also result from high-protein intake, is dependent on the presence of carbamoyl phosphate synthetase I, an enzyme in the liver and intestine but not in most tumors. These findings suggest that a high-protein diet can stimulate pyrimidine synthesis in the liver and intestine but leave it unchanged in tumor tissue. The purpose of this study was to determine whether varying dietary protein causes pharmacologically relevant and preferential changes in de novo pyrimidine synthesis. Mice were fed diets containing 18%, 35%, or 50% casein. Dietary effects on de novo pyrimidine synthesis were measured in the intestine, liver, and B16 mouse melanoma in mice treated with PALA and in untreated mice. De novo synthesis was measured by infusion of [15N]alanine into intact animals, determination of 15N incorporation into uracil by use of gas chromatography-mass spectrometry, and calculation of the fraction of the uracil nucleotide pool formed by de novo synthesis. In mice on a 50% casein diet (high protein), de novo pyrimidine synthesis increased substantially in the liver and intestine, compared with synthesis in mice receiving 18% casein. Increase in pyrimidine synthesis in B16 tumor tissue was negligible. The high-protein diet protected the intestine and liver from depletion of uracil nucleotide pools by PALA, and toxicity in tumor-free animals was reduced, as determined by mortality after PALA treatment. Sensitivity of the B16 tumor to the biochemical and cytotoxic effects of PALA was not diminished. We propose that the basis for these effects of a high-protein diet is the generation of excess carbamoyl phosphate in tissues containing carbamoyl phosphate synthetase I. This carbamoyl phosphate can stimulate de novo pyrimidine synthesis and compete with drugs that interact with enzymes of the de novo pathway, thereby selectively protecting the liver and intestine. These data provide a biochemical explanation for reported effects of high-protein diet on toxicity of antipyrimidines like 5-FU. Studies are underway to determine if stimulation of pyrimidine synthesis by excess ammonia improves therapy with 5-FU alone or combined with PALA. JF - Journal of the National Cancer Institute AU - Zaharevitz, D W AU - Grubb, M F AU - Hyman, R AU - Chisena, C AU - Cysyk, R L AD - Laboratory of Medicinal Chemistry, National Cancer Institute, Bethesda, Md 20892. Y1 - 1993/04/21/ PY - 1993 DA - 1993 Apr 21 SP - 662 EP - 666 VL - 85 IS - 8 SN - 0027-8874, 0027-8874 KW - Antimetabolites, Antineoplastic KW - 0 KW - Dietary Proteins KW - Pyrimidines KW - Aspartic Acid KW - 30KYC7MIAI KW - sparfosic acid KW - 78QVZ7RG8L KW - Phosphonoacetic Acid KW - N919E46723 KW - Index Medicus KW - Animals KW - Melanoma, Experimental -- metabolism KW - Intestines -- drug effects KW - Liver -- drug effects KW - Mice, Inbred C57BL KW - Liver -- metabolism KW - Mice KW - Intestines -- metabolism KW - Mice, Inbred BALB C KW - Male KW - Mice, Inbred DBA KW - Aspartic Acid -- pharmacology KW - Dietary Proteins -- administration & dosage KW - Aspartic Acid -- analogs & derivatives KW - Phosphonoacetic Acid -- analogs & derivatives KW - Phosphonoacetic Acid -- pharmacology KW - Pyrimidines -- biosynthesis KW - Antimetabolites, Antineoplastic -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75661101?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Effect+of+high-protein+diet+on+pyrimidine+synthesis+and+response+to+PALA+in+mouse+tissues.&rft.au=Zaharevitz%2C+D+W%3BGrubb%2C+M+F%3BHyman%2C+R%3BChisena%2C+C%3BCysyk%2C+R+L&rft.aulast=Zaharevitz&rft.aufirst=D&rft.date=1993-04-21&rft.volume=85&rft.issue=8&rft.spage=662&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-07 N1 - Date created - 1993-05-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Differential effects of activation of protein kinase C and cyclic-AMP-dependent protein kinase on sodium-dependent phosphate uptake in NIH 3T3 cells. AN - 75682506; 8471634 AB - Activation of protein kinase C (PKC) by phorbol ester (PMA), or by diacylglycerol analogue (OAG) treatment of NIH 3T3 cells resulted in the rapid (within 2-5 min) stimulation (approx. 2-fold) of sodium-dependent phosphate (Pi) transport. Conversely, preincubation of these cells with forskolin and cholera toxin, or incubation with 8-bromo-cAMP, to activate cAMP-dependent protein kinase (PKA), resulted in a decrease in Na+/Pi transport. Activation of either PKC or PKA did not change the Vmax of Pi uptake. However, activation of PKC did result in an increase, while activation of PKA caused a decrease, in the affinity for Pi. These results indicate that there is differential regulation of Na+/Pi uptake in NIH 3T3 cells by activators of PKC (stimulated) and PKA (inhibited) as a consequence of changes in the affinity of the transporter for Pi. JF - Biochimica et biophysica acta AU - Oláh, Z AU - Lehel, C AU - Anderson, W B AD - Laboratory of Cellular Oncology, National Cancer Institute, National Institutes of Health, Bethesda 20892. Y1 - 1993/04/16/ PY - 1993 DA - 1993 Apr 16 SP - 333 EP - 338 VL - 1176 IS - 3 SN - 0006-3002, 0006-3002 KW - Carrier Proteins KW - 0 KW - Phosphate-Binding Proteins KW - Phosphates KW - Protein Kinase Inhibitors KW - Colforsin KW - 1F7A44V6OU KW - 8-Bromo Cyclic Adenosine Monophosphate KW - 23583-48-4 KW - Cholera Toxin KW - 9012-63-9 KW - Sodium KW - 9NEZ333N27 KW - Protein Kinases KW - EC 2.7.- KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Carrier Proteins -- metabolism KW - 3T3 Cells -- drug effects KW - Cholera Toxin -- pharmacology KW - Mice KW - 8-Bromo Cyclic Adenosine Monophosphate -- pharmacology KW - Models, Biological KW - Colforsin -- pharmacology KW - Kinetics KW - 3T3 Cells -- metabolism KW - Enzyme Activation -- drug effects KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Time Factors KW - Signal Transduction KW - Protein Kinase C -- metabolism KW - Phosphates -- metabolism KW - Protein Kinases -- metabolism KW - Sodium -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75682506?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochimica+et+biophysica+acta&rft.atitle=Differential+effects+of+activation+of+protein+kinase+C+and+cyclic-AMP-dependent+protein+kinase+on+sodium-dependent+phosphate+uptake+in+NIH+3T3+cells.&rft.au=Ol%C3%A1h%2C+Z%3BLehel%2C+C%3BAnderson%2C+W+B&rft.aulast=Ol%C3%A1h&rft.aufirst=Z&rft.date=1993-04-16&rft.volume=1176&rft.issue=3&rft.spage=333&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+biophysica+acta&rft.issn=00063002&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-18 N1 - Date created - 1993-05-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Regulation of eukaryotic translation initiation factor expression during T-cell activation. AN - 75672348; 8471627 AB - Primary T-cells are metabolically quiescent, with little DNA, RNA or protein synthesis. Upon mitogenic stimulation the rate of protein synthesis increases 10-fold. We have studied the role of eIF-2 and eIF-4 alpha (eIF-4E) expression in the mechanism of translational activation. During this period, the levels of eIF-2 alpha and eIF-4 alpha mRNA increase some 50-fold. Similar to the increase in ribosomes and mRNA, the number of eIF-2 alpha, eIF-2 beta, and eIF-4 alpha molecules per cell also increase 2-3-fold. This suggests that in addition to an increase in the pool size of translational components, an additional mechanism exists which results in an increased efficiency of factor utilization. We have looked at initiation factor phosphorylation. We find that eIF-2 alpha does not undergo significant changes in its phosphorylation state nor is there a change in the efficiency of eIF-2 utilization. However, there is a rapid increase in the phosphorylation state of eIF-4 alpha which correlates with the rapid increase in translational activity. It thus appears there are 2 distinct components responsible for the translational activation of quiescent T-cells during mitogenic stimulation. The first is the phosphorylation of eIF-4 alpha, with a concomitant increase in the efficiency of eIF-4 alpha utilization. The second is an increase in the pool sizes of eIF-2 and eIF-4 alpha. JF - Biochimica et biophysica acta AU - Boal, T R AU - Chiorini, J A AU - Cohen, R B AU - Miyamoto, S AU - Frederickson, R M AU - Sonenberg, N AU - Safer, B AD - Molecular Hematology Branch, NHLBI, NIH, Bethesda, MD 20892. Y1 - 1993/04/16/ PY - 1993 DA - 1993 Apr 16 SP - 257 EP - 264 VL - 1176 IS - 3 SN - 0006-3002, 0006-3002 KW - Eukaryotic Initiation Factor-2 KW - 0 KW - Peptide Initiation Factors KW - Phytohemagglutinins KW - RNA, Messenger KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Protein Biosynthesis KW - Phosphorylation KW - Humans KW - RNA, Messenger -- analysis KW - Eukaryotic Initiation Factor-2 -- genetics KW - Gene Expression Regulation KW - T-Lymphocytes -- metabolism KW - Peptide Initiation Factors -- genetics KW - Lymphocyte Activation -- genetics KW - Peptide Initiation Factors -- biosynthesis KW - T-Lymphocytes -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75672348?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochimica+et+biophysica+acta&rft.atitle=Regulation+of+eukaryotic+translation+initiation+factor+expression+during+T-cell+activation.&rft.au=Boal%2C+T+R%3BChiorini%2C+J+A%3BCohen%2C+R+B%3BMiyamoto%2C+S%3BFrederickson%2C+R+M%3BSonenberg%2C+N%3BSafer%2C+B&rft.aulast=Boal&rft.aufirst=T&rft.date=1993-04-16&rft.volume=1176&rft.issue=3&rft.spage=257&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+biophysica+acta&rft.issn=00063002&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-18 N1 - Date created - 1993-05-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Site-directed mutagenesis of mouse steroid 7 alpha-hydroxylase (cytochrome P-450(7) alpha): role of residue-209 in determining steroid-cytochrome P-450 interaction. AN - 75718274; 8484736 AB - We have cloned a cDNA encoding mouse steroid 7 alpha-hydroxylase P450(7) alpha (cytochrome P-450(7) alpha) and expressed it in Saccharomyces cerevisiae. Mouse P450(7) alpha is 70% identical in its amino acid sequence with the mouse steroid 15 alpha-hydroxylase P450(15) alpha (2A4). The Leu at position 209 of P450(15) alpha is the most important residue to determine the steroid hydroxylase activity of the P450 [Lindberg and Negishi (1989) Nature (London) 339, 632-634]. The P450(7) alpha contains Asn at the position corresponding to the Leu-209 of P450(15) alpha, although both P450s hydroxylate testosterone. The CO-reduced P450(7) alpha complex is unstable, so that it is quickly converted into the inactive P420, whereas the P450(15) alpha is very stable. The P450(7) alpha, however, is stabilized either by addition of testosterone or by a mutation of Asn-209 to Leu. The mutant P450(7) alpha displays a 17-fold lower Vmax. value than the wild-type enzyme. Unexpectedly, it also has 3-fold lower Km and Kd values. Residue 209 in P450(7) alpha, therefore, appears to be located at a critical site of the haem-substrate-binding pocket. Corticosterone inhibits the testosterone 7 alpha-hydroxylase activity of the wild-type P450(7) alpha, whereas it does not inhibit the mutant P450(7) alpha. Conversely, the P450(15) alpha activity becomes inhibited by corticosterone upon the replacement of Leu-209 by Asn. In addition, this mutation increases the corticosterone 15 alpha-hydroxylase activity of P450(15) alpha at least 20-fold. Whereas the inhibition by corticosterone depends on the presence of Asn at position 209, deoxycorticosterone inhibits the activities of the P450s regardless of the type of residue at 209. The results indicate, therefore, that the identity of residue 209 determines the affinity as well as specificity of steroid binding to both P450(7) alpha and P450(15) alpha. JF - The Biochemical journal AU - Iwasaki, M AU - Lindberg, R L AU - Juvonen, R O AU - Negishi, M AD - Pharmacogenetics Section, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709. Y1 - 1993/04/15/ PY - 1993 DA - 1993 Apr 15 SP - 569 EP - 573 VL - 291 ( Pt 2) SN - 0264-6021, 0264-6021 KW - Coumarins KW - 0 KW - Hydroxyprogesterones KW - 11-hydroxyprogesterone KW - 312-90-3 KW - Desoxycorticosterone KW - 40GP35YQ49 KW - Progesterone KW - 4G7DS2Q64Y KW - Asparagine KW - 7006-34-0 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - coumarin KW - A4VZ22K1WT KW - Steroid Hydroxylases KW - EC 1.14.- KW - Aryl Hydrocarbon Hydroxylases KW - EC 1.14.14.1 KW - steroid hormone 7-alpha-hydroxylase KW - testosterone 7-alpha-hydroxylase, hamster KW - Leucine KW - GMW67QNF9C KW - Corticosterone KW - W980KJ009P KW - Index Medicus KW - Animals KW - Progesterone -- pharmacology KW - Amino Acid Sequence KW - Mice KW - Structure-Activity Relationship KW - Binding Sites KW - Base Sequence KW - Coumarins -- pharmacology KW - Molecular Sequence Data KW - Desoxycorticosterone -- pharmacology KW - Spectrophotometry KW - Corticosterone -- pharmacology KW - Mice, Inbred AKR KW - Hydroxyprogesterones -- pharmacology KW - Mutagenesis, Site-Directed KW - Cytochrome P-450 Enzyme System -- genetics KW - Cytochrome P-450 Enzyme System -- chemistry KW - Steroid Hydroxylases -- metabolism KW - Steroid Hydroxylases -- chemistry KW - Cytochrome P-450 Enzyme System -- metabolism KW - Steroid Hydroxylases -- genetics KW - Steroid Hydroxylases -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75718274?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Biochemical+journal&rft.atitle=Site-directed+mutagenesis+of+mouse+steroid+7+alpha-hydroxylase+%28cytochrome+P-450%287%29+alpha%29%3A+role+of+residue-209+in+determining+steroid-cytochrome+P-450+interaction.&rft.au=Iwasaki%2C+M%3BLindberg%2C+R+L%3BJuvonen%2C+R+O%3BNegishi%2C+M&rft.aulast=Iwasaki&rft.aufirst=M&rft.date=1993-04-15&rft.volume=291+%28+Pt+2%29&rft.issue=&rft.spage=569&rft.isbn=&rft.btitle=&rft.title=The+Biochemical+journal&rft.issn=02646021&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-01 N1 - Date created - 1993-06-01 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - L06463; GENBANK; D17642; X68677; X70243; D17801; D17800; D17802; D17798; D17799; D17797 N1 - SuppNotes - Cited By: DNA. 1985 Jun;4(3):203-10 [3159557] J Biol Chem. 1964 Jul;239:2370-8 [14209971] J Biol Chem. 1988 Dec 5;263(34):17995-8002 [3192524] Biochem Pharmacol. 1988 Dec 15;37(24):4778-80 [3202910] J Biol Chem. 1989 Jan 5;264(1):21-6 [2535839] Biochem Biophys Res Commun. 1989 Feb 15;158(3):717-22 [2493247] J Biol Chem. 1989 Apr 15;264(11):6465-71 [2703500] Biochemistry. 1989 Jan 24;28(2):656-60 [2713336] Nature. 1989 Jun 22;339(6226):632-4 [2733794] Biochemistry. 1989 May 16;28(10):4169-72 [2765478] Biochemistry. 1989 Aug 22;28(17):6848-57 [2819037] J Biol Chem. 1990 Oct 5;265(28):17197-201 [1976628] DNA Cell Biol. 1991 Jan-Feb;10(1):1-14 [1991046] J Biol Chem. 1991 Feb 25;266(6):3380-2 [1995602] J Biol Chem. 1991 Apr 5;266(10):6215-20 [1706711] Anal Biochem. 1976 May 7;72:248-54 [942051] Methods Enzymol. 1978;52:258-79 [209288] J Mol Biol. 1980 Oct 25;143(2):161-78 [6260957] Proc Natl Acad Sci U S A. 1983 Jul;80(13):3963-5 [6575390] Anal Biochem. 1984 Feb;136(2):390-6 [6426342] J Biol Chem. 1991 Jun 25;266(18):11939-46 [2050688] J Biol Chem. 1991 Sep 5;266(25):16431-5 [1885576] J Biol Chem. 1992 Jan 5;267(1):83-90 [1730627] Methods Enzymol. 1991;206:11-30 [1784202] J Biol Chem. 1993 Jan 15;268(2):759-62 [8419350] J Biol Chem. 1988 Mar 25;263(9):4166-71 [3346244] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Domains of the integrase protein of human immunodeficiency virus type 1 responsible for polynucleotidyl transfer and zinc binding. AN - 75692645; 8386373 AB - The integrase protein of human immunodeficiency virus type 1 carries out a set of polynucleotidyl transfer reactions that result in the covalent attachment of the retroviral cDNA to host DNA. We have analyzed the activities of a set of deletion derivatives of the integrase protein. The analysis reveals that a central domain of only 137 amino acids is sufficient in vitro to catalyze a subset of the reactions carried out by the complete protein. This polypeptide contains an amino acid sequence motif, Asp-Xaa39-58-Asp-Xaa35-Glu (DX39-58DX35E, where X and the subscript indicate the intervening amino acids between the invariant acidic residues), that is found in the integrases of retroviruses and retrotransposons and also the transposase proteins of some bacterial transposable elements. We also find that the integrase protein can bind Zn2+, and the histidine and cysteine residues of another conserved motif (HX3-7HX23-32CX2C) are required for efficient Zn2+ binding. The activities displayed by deletion mutants suggest to us possible functions for the various parts of integrase. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Bushman, F D AU - Engelman, A AU - Palmer, I AU - Wingfield, P AU - Craigie, R AD - Laboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/04/15/ PY - 1993 DA - 1993 Apr 15 SP - 3428 EP - 3432 VL - 90 IS - 8 SN - 0027-8424, 0027-8424 KW - Peptide Fragments KW - 0 KW - Recombinant Proteins KW - DNA Nucleotidyltransferases KW - EC 2.7.7.- KW - Integrases KW - Nucleotidyltransferases KW - Transposases KW - Zinc KW - J41CSQ7QDS KW - Index Medicus KW - AIDS/HIV KW - Peptide Fragments -- metabolism KW - Peptide Fragments -- isolation & purification KW - Escherichia coli -- genetics KW - Amino Acid Sequence KW - Binding Sites KW - Cloning, Molecular KW - Mutagenesis KW - Recombinant Proteins -- isolation & purification KW - Recombinant Proteins -- metabolism KW - Restriction Mapping KW - Molecular Sequence Data KW - Sequence Deletion KW - Nucleotidyltransferases -- metabolism KW - HIV-1 -- genetics KW - Zinc -- metabolism KW - DNA Nucleotidyltransferases -- isolation & purification KW - DNA Nucleotidyltransferases -- genetics KW - HIV-1 -- enzymology KW - DNA Nucleotidyltransferases -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75692645?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Domains+of+the+integrase+protein+of+human+immunodeficiency+virus+type+1+responsible+for+polynucleotidyl+transfer+and+zinc+binding.&rft.au=Bushman%2C+F+D%3BEngelman%2C+A%3BPalmer%2C+I%3BWingfield%2C+P%3BCraigie%2C+R&rft.aulast=Bushman&rft.aufirst=F&rft.date=1993-04-15&rft.volume=90&rft.issue=8&rft.spage=3428&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-17 N1 - Date created - 1993-05-17 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cell. 1985 Jul;41(3):867-76 [2988793] Proc Natl Acad Sci U S A. 1992 Oct 15;89(20):9598-602 [1409671] Gene. 1987;56(1):125-35 [3315856] EMBO J. 1987 Oct;6(10):3163-9 [2826132] Proc Natl Acad Sci U S A. 1988 Jun;85(12):4195-9 [3260031] Cell. 1988 Aug 12;54(4):497-504 [3401925] J Virol. 1989 Mar;63(3):1404-7 [2536841] Proc Natl Acad Sci U S A. 1989 Apr;86(8):2525-9 [2539592] Q Rev Biol. 1989 Mar;64(1):1-30 [2469098] Cell. 1989 Oct 20;59(2):373-83 [2553269] J Virol. 1989 Dec;63(12):5319-27 [2555556] Cell. 1990 Jan 12;60(1):3-4 [2403842] Genes Dev. 1990 Mar;4(3):324-30 [2159935] J Mol Biol. 1990 Jun 20;213(4):583-91 [2162963] J Bacteriol. 1990 Jul;172(7):4090-9 [2163395] Annu Rev Biophys Biophys Chem. 1990;19:405-21 [2114117] Proc Natl Acad Sci U S A. 1990 Jul;87(13):5119-23 [2164223] Cell. 1990 Aug 24;62(4):829-37 [2167180] Curr Top Microbiol Immunol. 1990;157:19-48 [2203610] Cell. 1990 Oct 5;63(1):87-95 [2170022] J Virol. 1990 Nov;64(11):5656-9 [2214031] Mol Microbiol. 1990 Jun;4(6):961-75 [2170815] Science. 1990 Sep 28;249(4976):1555-8 [2171144] Proc Natl Acad Sci U S A. 1991 Feb 15;88(4):1339-43 [1847518] Mol Microbiol. 1990 Oct;4(10):1771-7 [1963920] Nucleic Acids Res. 1991 Feb 25;19(4):851-60 [1850126] Cell. 1991 May 31;65(5):805-16 [1645619] J Virol. 1991 Sep;65(9):4636-44 [1870194] Cell. 1991 Dec 20;67(6):1211-21 [1760846] Nucleic Acids Res. 1991 Dec 25;19(24):6691-8 [1662361] Science. 1992 Feb 7;255(5045):723-6 [1738845] Proc Natl Acad Sci U S A. 1992 Apr 15;89(8):3458-62 [1533044] Mol Cell Biol. 1992 May;12(5):2331-8 [1314954] J Biol Chem. 1992 May 15;267(14):9639-44 [1577801] Virology. 1992 Jun;188(2):459-68 [1585629] J Biol Chem. 1992 Aug 15;267(23):16037-40 [1322888] J Biol Chem. 1992 Oct 25;267(30):21273-6 [1383220] J Virol. 1992 Nov;66(11):6361-9 [1404595] Proc Natl Acad Sci U S A. 1986 Oct;83(20):7648-52 [2429313] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Induction of neoplastic progression in Syrian hamster embryo cells treated with protein phosphatase inhibitors. AN - 75677451; 8385570 AB - In these studies, Syrian hamster embryo cells (SHE), which were isolated at different stages of neoplastic progression, were used to test the ability of the protein phosphatase inhibitors, okadaic acid and sodium orthovanadate (Na3VO4) to induce neoplastic progression. We observed that these chemicals can induce transition of the cells from one stage to the other at different points in the multistep process of neoplastic transformation. Three steps in this multistep process were studied: escape from cellular senescence, loss of a tumor suppressor gene function in immortal cells, and aquisition of anchorage-independent growth. Treatment of normal, primary SHE cells with okadaic acid or Na3VO4 allowed the cells to escape senescence and become immortal at a low frequency. The induction of immortality was associated with nonrandom chromosome changes, including trisomy 8 and 11 and monosomy 13 and Xq. The transition of preneoplastic cells to more advanced stages was also studied in immortal, nontumorigenic cells that either have retained (supB+) or have lost (supB-) the ability to suppress tumorigenicity of a transformed cell line in cell hybrids. SupB+ and supB- cells do not normally grow in agar, but supB- cells will grow in agar if additional growth factors are added. However, upon addition of protein phosphatase inhibitors, supB+ cells exhibited the supB- phenotype; for example, colony formation of supB+ cells was observed in agar supplemented with growth factors and protein phosphatase inhibitors. Following treatment, selection of these colonies showed that 89% of these cells heritably acquired the phenotype of cells that have lost the suppressor gene function (supB-). SupB- cells were also treated with protein phosphatase inhibitors in soft agar in the presence of additional growth factors. While the frequency of colonies in agar supplemented with growth factors in agar was not greatly enhanced, approximately 50% of the colonies acquired the ability to grow in agar autonomously without the supplemented growth factors, similar to tumorigenic cells. These studies suggest that Na3VO4 and okadaic acid induce progression of cells through various stages in this multistep system. JF - Cancer research AU - Afshari, C A AU - Kodama, S AU - Bivins, H M AU - Willard, T B AU - Fujiki, H AU - Barrett, J C AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina 27709. Y1 - 1993/04/15/ PY - 1993 DA - 1993 Apr 15 SP - 1777 EP - 1782 VL - 53 IS - 8 SN - 0008-5472, 0008-5472 KW - Ethers, Cyclic KW - 0 KW - Okadaic Acid KW - 1W21G5Q4N2 KW - Vanadates KW - 3WHH0066W5 KW - Phosphoprotein Phosphatases KW - EC 3.1.3.16 KW - Index Medicus KW - Phenotype KW - Karyotyping KW - Animals KW - Dose-Response Relationship, Drug KW - Cells, Cultured KW - Mutation KW - Embryo, Mammalian KW - Cricetinae KW - Cell Division KW - Phosphoprotein Phosphatases -- antagonists & inhibitors KW - Ethers, Cyclic -- toxicity KW - Vanadates -- toxicity KW - Cell Transformation, Neoplastic -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75677451?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Induction+of+neoplastic+progression+in+Syrian+hamster+embryo+cells+treated+with+protein+phosphatase+inhibitors.&rft.au=Afshari%2C+C+A%3BKodama%2C+S%3BBivins%2C+H+M%3BWillard%2C+T+B%3BFujiki%2C+H%3BBarrett%2C+J+C&rft.aulast=Afshari&rft.aufirst=C&rft.date=1993-04-15&rft.volume=53&rft.issue=8&rft.spage=1777&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-11 N1 - Date created - 1993-05-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Human immunodeficiency virus type 1 coat protein neurotoxicity mediated by nitric oxide in primary cortical cultures. AN - 75672887; 8097316 AB - The human immunodeficiency virus type 1 coat protein, gp120, kills neurons in primary cortical cultures at low picomolar concentrations. The toxicity requires external glutamate and calcium and is blocked by glutamate receptor antagonists. Nitric oxide (NO) contributes to gp120 toxicity, since nitroarginine, an inhibitor of NO synthase, prevents toxicity as does deletion of arginine from the incubation medium and hemoglobin, which binds NO. Superoxide dismutase also attenuates toxicity, implying a role for superoxide anions. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Dawson, V L AU - Dawson, T M AU - Uhl, G R AU - Snyder, S H AD - National Institute on Drug Abuse, Addiction Research Center, Baltimore, MD 21224. Y1 - 1993/04/15/ PY - 1993 DA - 1993 Apr 15 SP - 3256 EP - 3259 VL - 90 IS - 8 SN - 0027-8424, 0027-8424 KW - Excitatory Amino Acid Antagonists KW - 0 KW - Glutamates KW - HIV Envelope Protein gp120 KW - Hemoglobins KW - Inositol Phosphates KW - Neurotoxins KW - Quinoxalines KW - Nitroarginine KW - 2149-70-4 KW - Nitric Oxide KW - 31C4KY9ESH KW - Glutamic Acid KW - 3KX376GY7L KW - FG 9041 KW - 62T278S1MX KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - Arginine KW - 94ZLA3W45F KW - Dantrolene KW - F64QU97QCR KW - Cyclic GMP KW - H2D2X058MU KW - Nifedipine KW - I9ZF7L6G2L KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Fetus KW - Dantrolene -- pharmacology KW - Inositol Phosphates -- metabolism KW - Calcium -- pharmacology KW - Hemoglobins -- pharmacology KW - Cell Death -- drug effects KW - Dizocilpine Maleate -- pharmacology KW - Rats KW - Nifedipine -- pharmacology KW - Cyclic GMP -- metabolism KW - Hemoglobins -- metabolism KW - Cell Survival -- drug effects KW - Cells, Cultured KW - Glutamates -- pharmacology KW - Models, Neurological KW - Quinoxalines -- pharmacology KW - Cerebral Cortex -- cytology KW - Neurons -- metabolism KW - Cerebral Cortex -- metabolism KW - Neurons -- drug effects KW - Neurons -- cytology KW - Nitric Oxide -- metabolism KW - HIV Envelope Protein gp120 -- toxicity KW - Neurotoxins -- toxicity KW - HIV-1 KW - Arginine -- analogs & derivatives KW - Arginine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75672887?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Human+immunodeficiency+virus+type+1+coat+protein+neurotoxicity+mediated+by+nitric+oxide+in+primary+cortical+cultures.&rft.au=Dawson%2C+V+L%3BDawson%2C+T+M%3BUhl%2C+G+R%3BSnyder%2C+S+H&rft.aulast=Dawson&rft.aufirst=V&rft.date=1993-04-15&rft.volume=90&rft.issue=8&rft.spage=3256&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-17 N1 - Date created - 1993-05-17 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Brain Res. 1978 Jun 30;149(2):279-93 [27283] J Biol Chem. 1992 Jun 5;267(16):10976-81 [1375933] Ann Neurol. 1986 Jun;19(6):517-24 [3729308] Ann Neurol. 1986 Jun;19(6):525-35 [3014994] Science. 1986 Sep 5;233(4768):1089-93 [3016903] Ann Neurol. 1986 Sep;20(3):289-95 [3532930] N Engl J Med. 1987 Dec 24;317(26):1643-7 [3479685] Science. 1988 Feb 5;239(4840):586-92 [3277272] J Neurosci. 1988 Jun;8(6):2153-63 [3385492] Nature. 1988 Oct 13;335(6191):639-42 [2845276] Proc Natl Acad Sci U S A. 1989 Jan;86(2):621-5 [2536171] Neurosci Lett. 1992 Feb 3;135(2):227-30 [1625799] Science. 1992 Jul 24;257(5069):494-6 [1353273] J Neurochem. 1992 Sep;59(3):897-905 [1379633] FASEB J. 1992 Sep;6(12):3051-64 [1381691] Neuroreport. 1992 Jun;3(6):530-2 [1382661] J Immunol. 1992 Oct 15;149(8):2736-41 [1383325] Ann Neurol. 1992 Sep;32(3):297-311 [1384420] Neuroreport. 1992 Oct;3(10):913-5 [1421098] Neuroreport. 1992 Jul;3(7):645-8 [1384768] Mol Pharmacol. 1992 Oct;42(4):619-26 [1331753] Proc Natl Acad Sci U S A. 1992 Nov 15;89(22):10945-9 [1279698] Brain Res. 1992 Oct 30;594(2):189-96 [1450945] Biochem J. 1989 Mar 1;258(2):621-4 [2706006] Proc Natl Acad Sci U S A. 1990 Feb;87(4):1620-4 [2154753] Science. 1990 Apr 20;248(4953):364-7 [2326646] J Neurochem. 1990 Jul;55(1):114-21 [2162373] Science. 1990 Aug 3;249(4968):549-53 [2200125] J Exp Med. 1992 Dec 1;176(6):1703-18 [1460427] Brain Res. 1992 Dec 11;598(1-2):196-202 [1486480] Proc Natl Acad Sci U S A. 1990 Nov;87(21):8607-11 [1978327] Science. 1990 Dec 14;250(4987):1593-6 [2148832] J Biol Chem. 1991 Mar 5;266(7):4244-50 [1847917] Trends Neurosci. 1991 Feb;14(2):60-7 [1708538] Proc Natl Acad Sci U S A. 1991 Jul 15;88(14):6368-71 [1648740] Neuron. 1991 Jul;7(1):111-8 [1676893] Ion Channels. 1988;1:213-49 [2856492] Ann Neurol. 1991 Jun;29(6):651-7 [1909852] Arch Biochem Biophys. 1991 Aug 1;288(2):481-7 [1654835] Ann Neurol. 1991 Jul;30(1):110-4 [1656845] Eur J Pharmacol. 1991 Nov 12;204(3):339-40 [1773832] Nature. 1992 Feb 20;355(6362):722-5 [1371330] Proc Natl Acad Sci U S A. 1992 Apr 1;89(7):2590-4 [1372982] Trends Neurosci. 1992 Mar;15(3):75-9 [1373919] J Pharmacol Exp Ther. 1985 Mar;232(3):708-16 [2983068] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Dating the genetic bottleneck of the African cheetah. AN - 75670294; 8475057 AB - The cheetah is unusual among fields in exhibiting near genetic uniformity at a variety of loci previously screened to measure population genetic diversity. It has been hypothesized that a demographic crash or population bottleneck in the recent history of the species is causal to the observed monomorphic profiles for nuclear coding loci. The timing of a bottleneck is difficult to assess, but certain aspects of the cheetah's natural history suggest it may have occurred near the end of the last ice age (late Pleistocene, approximately 10,000 years ago), when a remarkable extinction of large vertebrates occurred on several continents. To further define the timing of such a bottleneck, the character of genetic diversity for two rapidly evolving DNA sequences, mitochondrial DNA and hypervariable minisatellite loci, was examined. Moderate levels of genetic diversity were observed for both of these indices in surveys of two cheetah subspecies, one from South Africa and one from East Africa. Back calculation from the extent of accumulation of DNA diversity based on observed mutation rates for VNTR (variable number of tandem repeats) loci and mitochondrial DNA supports a hypothesis of an ancient Pleistocene bottleneck that rendered the cheetah depauperate in genetic variation for nuclear coding loci but would allow sufficient time for partial reconstitution of more rapidly evolving genomic DNA segments. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Menotti-Raymond, M AU - O'Brien, S J AD - Biological Carcinogenesis and Development Program, National Cancer Institute, Frederick, MD 21702. Y1 - 1993/04/15/ PY - 1993 DA - 1993 Apr 15 SP - 3172 EP - 3176 VL - 90 IS - 8 SN - 0027-8424, 0027-8424 KW - DNA, Mitochondrial KW - 0 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Phylogeny KW - Animals KW - Restriction Mapping KW - DNA Fingerprinting KW - South Africa KW - Namibia KW - DNA, Mitochondrial -- genetics KW - Genetic Variation KW - Acinonyx -- genetics KW - DNA -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75670294?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Dating+the+genetic+bottleneck+of+the+African+cheetah.&rft.au=Menotti-Raymond%2C+M%3BO%27Brien%2C+S+J&rft.aulast=Menotti-Raymond&rft.aufirst=M&rft.date=1993-04-15&rft.volume=90&rft.issue=8&rft.spage=3172&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-17 N1 - Date created - 1993-05-17 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Genetics. 1981 Jan;97(1):145-63 [6266912] Mol Biol Evol. 1992 Jul;9(4):729-43 [1630309] Science. 1985 Mar 22;227(4693):1428-34 [2983425] Proc Natl Acad Sci U S A. 1987 Jan;84(2):508-11 [3467370] Biol Reprod. 1987 Mar;36(2):351-60 [3580457] Nature. 1988 Mar 17;332(6161):278-81 [3347271] Microb Pathog. 1987 Apr;2(4):269-82 [3507555] Hum Genet. 1989 Dec;84(1):75-8 [2558069] Proc Natl Acad Sci U S A. 1990 Jan;87(2):836-40 [1967831] Proc Natl Acad Sci U S A. 1990 Mar;87(5):1772-6 [1968637] Nature. 1990 Mar 15;344(6263):238-40 [1969116] Proc Natl Acad Sci U S A. 1990 Apr;87(7):2496-500 [2320570] Genomics. 1990 Mar;6(3):461-74 [1970327] Nature. 1990 Apr 19;344(6268):764-7 [1970419] Am J Hum Genet. 1990 Sep;47(3):499-514 [1975479] Am J Hum Genet. 1991 May;48(5):824-40 [2018036] Hum Genet. 1991 Sep;87(5):632-3 [1916768] J Hered. 1991 Sep-Oct;82(5):378-86 [1940281] Annu Rev Genet. 1991;25:45-69 [1667462] Proc Natl Acad Sci U S A. 1984 Apr;81(7):1991-5 [6326095] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Muscarinic receptor-mediated tyrosine phosphorylation of phospholipase C-gamma. An alternative mechanism for cholinergic-induced phosphoinositide breakdown. AN - 75668616; 7681827 AB - In Chinese hamster ovary cells transfected with m5 muscarinic receptors, carbachol stimulates both calcium influx and calcium release from intracellular stores. The marine toxin maitotoxin (MTX) elicits a similar response on calcium influx. Carbachol- and MTX-induced calcium influx can be inhibited by the proposed blockers of receptor-operated calcium channels (ROCC), CAI and SK&F 96365. Both carbachol and MTX induce a significant increase in total protein tyrosine phosphorylation, which is dependent on extracellular calcium and can be inhibited by CAI and SK&F 96365. Phospholipase C-gamma was identified as one of the substrates subject to calcium-dependent tyrosine phosphorylation following carbachol or MTX stimulation. Carbachol-induced [3H]inositol trisphosphate formation was partially inhibited by an inhibitor of tyrosine kinases, by removal of extracellular calcium, and by the inhibitor of receptor-operated calcium channels CAI suggesting that phosphorylation of phospholipase C-gamma plays a role in the muscarinic activation of phosphoinositide breakdown. Such an effect of carbachol is reminiscent of effects observed with peptide growth factors and represents a novel alternative signaling pathway for a muscarinic G protein-coupled receptor. JF - The Journal of biological chemistry AU - Gusovsky, F AU - Lueders, J E AU - Kohn, E C AU - Felder, C C AD - Laboratory of Bioorganic Chemistry, National Institute of Digestive Diseases and Kidney, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/04/15/ PY - 1993 DA - 1993 Apr 15 SP - 7768 EP - 7772 VL - 268 IS - 11 SN - 0021-9258, 0021-9258 KW - Calcium Channel Blockers KW - 0 KW - Isoenzymes KW - Marine Toxins KW - Oxocins KW - Phosphatidylinositols KW - Receptors, Muscarinic KW - Phosphotyrosine KW - 21820-51-9 KW - Tyrosine KW - 42HK56048U KW - Carbachol KW - 8Y164V895Y KW - maitotoxin KW - 9P59GES78D KW - Type C Phospholipases KW - EC 3.1.4.- KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Marine Toxins -- pharmacology KW - Animals KW - Phosphorylation KW - Calcium Channel Blockers -- pharmacology KW - Transfection KW - Kinetics KW - CHO Cells KW - Cricetinae KW - Calcium -- metabolism KW - Receptors, Muscarinic -- genetics KW - Phosphatidylinositols -- metabolism KW - Tyrosine -- analogs & derivatives KW - Carbachol -- pharmacology KW - Isoenzymes -- metabolism KW - Tyrosine -- analysis KW - Type C Phospholipases -- metabolism KW - Receptors, Muscarinic -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75668616?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Muscarinic+receptor-mediated+tyrosine+phosphorylation+of+phospholipase+C-gamma.+An+alternative+mechanism+for+cholinergic-induced+phosphoinositide+breakdown.&rft.au=Gusovsky%2C+F%3BLueders%2C+J+E%3BKohn%2C+E+C%3BFelder%2C+C+C&rft.aulast=Gusovsky&rft.aufirst=F&rft.date=1993-04-15&rft.volume=268&rft.issue=11&rft.spage=7768&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-06 N1 - Date created - 1993-05-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Transgenic mouse model for synergistic effects of nuclear oncogenes and growth factors in tumorigenesis: interaction of c-myc and transforming growth factor alpha in hepatic oncogenesis. AN - 75653923; 8467484 AB - Double transgenic mice bearing fusion genes consisting of mouse albumin enhancer/promoter-mouse c-myc complementary DNA and mouse metallothionein 1 promoter-human transforming growth factor alpha complementary DNA were generated to investigate the interaction of these genes in hepatic oncogenesis and to provide a general paradigm for characterizing the interaction of nuclear oncogenes and growth factors in tumorigenesis. Coexpression of c-myc and transforming growth factor alpha as transgenes in the mouse liver resulted in a tremendous acceleration of neoplastic development in this organ as compared to expression of either of these transgenes alone. The two distinct cellular reactions that occurred in the liver of the double transgenic mice prior to the appearance of liver tumors were dysplastic and apoptotic changes in the existing hepatocytes followed by emergence of multiple focal lesions composed of both hyperplastic and dysplastic cell populations. These observations suggest that the interaction of c-myc and transforming growth factor alpha, and possibly other combinations of nuclear oncogenes and growth factors, during development of hepatic neoplasia contributes to the selection and expansion of the preneoplastic cell populations which consequently increases the probability of malignant conversion. JF - Cancer research AU - Murakami, H AU - Sanderson, N D AU - Nagy, P AU - Marino, P A AU - Merlino, G AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1993/04/15/ PY - 1993 DA - 1993 Apr 15 SP - 1719 EP - 1723 VL - 53 IS - 8 SN - 0008-5472, 0008-5472 KW - c-myc KW - Transforming Growth Factor alpha KW - 0 KW - Zinc KW - J41CSQ7QDS KW - Index Medicus KW - Animals KW - Zinc -- pharmacology KW - Cell Nucleus -- metabolism KW - Gene Expression KW - Disease Models, Animal KW - Mice KW - Mice, Transgenic KW - Male KW - Cell Transformation, Neoplastic -- genetics KW - Liver Neoplasms, Experimental -- genetics KW - Cocarcinogenesis KW - Transforming Growth Factor alpha -- genetics KW - Genes, myc UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75653923?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Transgenic+mouse+model+for+synergistic+effects+of+nuclear+oncogenes+and+growth+factors+in+tumorigenesis%3A+interaction+of+c-myc+and+transforming+growth+factor+alpha+in+hepatic+oncogenesis.&rft.au=Murakami%2C+H%3BSanderson%2C+N+D%3BNagy%2C+P%3BMarino%2C+P+A%3BMerlino%2C+G%3BThorgeirsson%2C+S+S&rft.aulast=Murakami&rft.aufirst=H&rft.date=1993-04-15&rft.volume=53&rft.issue=8&rft.spage=1719&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-11 N1 - Date created - 1993-05-11 N1 - Date revised - 2017-01-13 N1 - Gene symbol - c-myc N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - G2 delay induced by nitrogen mustard in human cells affects cyclin A/cdk2 and cyclin B1/cdc2-kinase complexes differently. AN - 75636249; 8463339 AB - We investigated the temporal regulation of cyclin A- and B1-dependent kinases in human lymphoma cells treated with nitrogen mustard (HN2) and pentoxifylline, to determine whether the activity of these complexes correlated with cell cycle arrest induced by DNA damage. Cells were synchronized in G1/S, treated with HN2, and then postincubated with pentoxifylline. HN2-induced a protracted delay in G2 phase. This delay correlated with suppression of cyclin B1- and cdc2-kinase activities, and stabilization of hyperphosphorylated-cdc2 in the presence of similar cyclin B1 levels to those found in mitosis. HN2 had no discernible effect on the S phase activity of cyclin A- or cdk2-immune complexes. Entry of control cells into mitosis correlated with destruction of cyclin A, disappearance of cyclin A-bound cdk2 and decreased cdk2 kinase activity. G2 delay induced by HN2 was associated with stabilization of cyclin A, increased abundance of cyclin A-bound cdk2, and increased cdk2 activity. Cyclin A was also associated with cdc2, which, contrary to complexes containing cdk2, were only activated upon entry into mitosis. Pentoxifylline abrogated cell cycle arrest induced by aphidicolin and HN2 in human lymphoma cells. Pentoxifylline also reverted the activity of cyclin A- and B1-kinases in HN2-treated cells to approximately that observed in controls. Our findings suggest that delayed entry into mitosis following DNA damage correlates with suppression of cyclin B1/cdc2 and cyclin A/cdc2 complexes, while maintaining cyclin A/cdc2 complexes in an active state. Furthermore, we found that pentoxifylline disrupts the signal transduction pathway that regulates these complexes when damaged DNA is present, resulting in abrogation of cell cycle arrest. JF - The Journal of biological chemistry AU - O'Connor, P M AU - Ferris, D K AU - Pagano, M AU - Draetta, G AU - Pines, J AU - Hunter, T AU - Longo, D L AU - Kohn, K W AD - Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/04/15/ PY - 1993 DA - 1993 Apr 15 SP - 8298 EP - 8308 VL - 268 IS - 11 SN - 0021-9258, 0021-9258 KW - Antigen-Antibody Complex KW - 0 KW - Cyclins KW - Aphidicolin KW - 38966-21-1 KW - Mechlorethamine KW - 50D9XSG0VR KW - Protein Kinases KW - EC 2.7.- KW - Protein-Serine-Threonine Kinases KW - EC 2.7.11.1 KW - CDC2 Protein Kinase KW - EC 2.7.11.22 KW - CDC2-CDC28 Kinases KW - CDK2 protein, human KW - Cyclin-Dependent Kinase 2 KW - Cyclin-Dependent Kinases KW - Pentoxifylline KW - SD6QCT3TSU KW - Index Medicus KW - Aphidicolin -- pharmacology KW - Pentoxifylline -- pharmacology KW - Tumor Cells, Cultured KW - Mitotic Index -- drug effects KW - Kinetics KW - Humans KW - Flow Cytometry KW - Time Factors KW - Protein Binding KW - Lymphoma KW - Protein Kinases -- metabolism KW - Protein Kinases -- isolation & purification KW - G2 Phase -- drug effects KW - CDC2 Protein Kinase -- isolation & purification KW - CDC2 Protein Kinase -- metabolism KW - Cyclins -- isolation & purification KW - Cyclins -- metabolism KW - Mechlorethamine -- pharmacology KW - Cell Cycle -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75636249?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=G2+delay+induced+by+nitrogen+mustard+in+human+cells+affects+cyclin+A%2Fcdk2+and+cyclin+B1%2Fcdc2-kinase+complexes+differently.&rft.au=O%27Connor%2C+P+M%3BFerris%2C+D+K%3BPagano%2C+M%3BDraetta%2C+G%3BPines%2C+J%3BHunter%2C+T%3BLongo%2C+D+L%3BKohn%2C+K+W&rft.aulast=O%27Connor&rft.aufirst=P&rft.date=1993-04-15&rft.volume=268&rft.issue=11&rft.spage=8298&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-06 N1 - Date created - 1993-05-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Cross-talk between m1 muscarinic acetylcholine and beta 2-adrenergic receptors. cAMP and the third intracellular loop of m1 muscarinic receptors confer heterologous regulation. AN - 75635987; 8385129 AB - Genes encoding the m1 muscarinic (m1 mAChR) and beta 2-adrenergic receptors (beta 2AR) were stably co-expressed into Chinese hamster ovary (CHO) cells to study receptor regulation and cross-talk. Persistent activation of the beta 2AR/adenylate cyclase pathway by isoproterenol leads to heterologous desensitization, internalization, and down-regulation of the m1 mAChR which is comparable, but smaller in magnitude, with that seen with persistent activation of the m1 mAChR by carbachol. This heterologous effect was mimicked by dibutyryl cAMP and forskolin and antagonized by the protein kinase A (PKA) inhibitor H-8. A potential consensus sequence for phosphorylation by PKA (Lys351-Arg-Lys-Thr354) exists on the third intracellular loop of the m1 mAChR, suggesting that receptor phosphorylation by PKA may be involved in heterologous regulation. The loss of m1 mAChRs induced by carbachol was not reversed by H-8, indicating that homologous regulation is not dependent on PKA. Recent evidence suggests that muscarinic agonist-mediated internalization of the m1 mAChR involves the third intracellular loop (i3) (Maeda, S., Lameh, J., Mallet, W. G., Philip, M., Ramachandran, J., and Sadee, W. (1990) FEBS Lett. 269, 386-388). Three deletion mutant receptors were constructed in which the majority, or small regions, of i3 were eliminated but the membrane proximal portions of the loop were left intact. Each of the mutants was co-expressed with the beta 2AR in CHO cells. A small region in i3 was identified which is crucial for carbachol- and isoproterenol-promoted internalization and down-regulation. This region contains a series of 6 serine residues within an 8-amino acid stretch. A similar domain has been identified in the carboxyl tail of the beta 2AR and has been proposed to participate in receptor internalization (Hausdorff, W. P., Campbell, P. T., Ostrowski, J., Yu, S. S., Caron, M. G., and Lefkowitz, R. J. (1991) Proc. Natl. Acad. Sci. U.S.A. 88, 2979-2983). JF - The Journal of biological chemistry AU - Lee, N H AU - Fraser, C M AD - Section on Molecular Neurobiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20852. Y1 - 1993/04/15/ PY - 1993 DA - 1993 Apr 15 SP - 7949 EP - 7957 VL - 268 IS - 11 SN - 0021-9258, 0021-9258 KW - Isoquinolines KW - 0 KW - Oligodeoxyribonucleotides KW - Phosphatidylinositols KW - Protein Kinase Inhibitors KW - Receptors, Adrenergic, beta KW - Receptors, Muscarinic KW - Colforsin KW - 1F7A44V6OU KW - Bucladesine KW - 63X7MBT2LQ KW - Quinuclidinyl Benzilate KW - 6581-06-2 KW - N-(2-(methylamino)ethyl)-5-isoquinolinesulfonamide KW - 84478-11-5 KW - Carbachol KW - 8Y164V895Y KW - Cyclic AMP KW - E0399OZS9N KW - Adenylyl Cyclases KW - EC 4.6.1.1 KW - Isoproterenol KW - L628TT009W KW - Index Medicus KW - Phosphatidylinositols -- metabolism KW - Animals KW - Protein Structure, Secondary KW - Bucladesine -- pharmacology KW - Isoproterenol -- pharmacology KW - Mutagenesis KW - Carbachol -- metabolism KW - Isoquinolines -- pharmacology KW - Base Sequence KW - Colforsin -- pharmacology KW - Quinuclidinyl Benzilate -- metabolism KW - Transfection KW - Molecular Sequence Data KW - CHO Cells KW - Down-Regulation -- drug effects KW - Carbachol -- pharmacology KW - Sequence Deletion KW - Cricetinae KW - Receptors, Muscarinic -- genetics KW - Receptors, Adrenergic, beta -- metabolism KW - Receptors, Adrenergic, beta -- genetics KW - Cyclic AMP -- metabolism KW - Adenylyl Cyclases -- metabolism KW - Receptors, Muscarinic -- chemistry KW - Receptors, Muscarinic -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75635987?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Cross-talk+between+m1+muscarinic+acetylcholine+and+beta+2-adrenergic+receptors.+cAMP+and+the+third+intracellular+loop+of+m1+muscarinic+receptors+confer+heterologous+regulation.&rft.au=Lee%2C+N+H%3BFraser%2C+C+M&rft.aulast=Lee&rft.aufirst=N&rft.date=1993-04-15&rft.volume=268&rft.issue=11&rft.spage=7949&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-06 N1 - Date created - 1993-05-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Prevention of relapse of histoplasmosis with itraconazole in patients with the acquired immunodeficiency syndrome. AN - 75634887; 8383934 AB - To assess the efficacy and safety of itraconazole in preventing relapse of histoplasmosis after induction therapy with amphotericin B in patients with the acquired immunodeficiency syndrome (AIDS) and disseminated histoplasmosis. A prospective, multicenter, open-label clinical trial, with follow-up for at least 52 weeks. Tertiary care hospitals participating in a clinical investigation sponsored by the National Institutes of Allergy and Infectious Diseases (AIDS Clinical Trial Group and Mycoses Study Group). Forty-two patients with AIDS who had successfully completed induction therapy for disseminated histoplasmosis amphotericin B, at least 15 mg/kg body weight given over 4 to 12 weeks. Itraconazole, 200 mg given orally twice daily. Response to therapy, specifically prevention of histoplasmosis relapse, was the main outcome measure. Secondary end points were survival and the effect of therapy on Histoplasma capsulatum variety capsulatum antigen levels in urine and serum. Plasma itraconazole concentrations were measured to document drug absorption and compliance with therapy. The median follow-up was 109 weeks, and median survival was 98 weeks. Two relapses occurred (5%; 95% CI, 0.5% to 16%), one in a patient withdrawn from the study 18 weeks earlier and one in a patient who did not comply with the study therapy. Patients with elevated antigen levels at study entry showed clearance of antigen from urine and serum; urine specimens became negative in 43% of patients (CI, 26% to 59%), and serum specimens became negative in 75% of patients (CI, 56% to 94%). Only one patient discontinued treatment because of itraconazole toxicity (hypokalemia). Itraconazole, 200 mg twice daily, is safe and effective in preventing relapse of disseminated histoplasmosis in patients with AIDS. Antigen clearance from blood and urine correlates with clinical efficacy. JF - Annals of internal medicine AU - Wheat, J AU - Hafner, R AU - Wulfsohn, M AU - Spencer, P AU - Squires, K AU - Powderly, W AU - Wong, B AU - Rinaldi, M AU - Saag, M AU - Hamill, R AU - Murphy, R AU - Connolly-Stringfield, P AU - Briggs, N AU - Owens, S AU - National Institute of Allergy and Infectious Diseases Clinical Trials and Mycoses Study Group Collaborators AD - Indiana University School of Medicine, Wishard Memorial Hospital, Indianapolis 46202-2879. ; National Institute of Allergy and Infectious Diseases Clinical Trials and Mycoses Study Group Collaborators Y1 - 1993/04/15/ PY - 1993 DA - 1993 Apr 15 SP - 610 EP - 616 VL - 118 IS - 8 SN - 0003-4819, 0003-4819 KW - Antifungal Agents KW - 0 KW - Antigens, Fungal KW - Itraconazole KW - 304NUG5GF4 KW - Amphotericin B KW - 7XU7A7DROE KW - Ketoconazole KW - R9400W927I KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Humans KW - Recurrence KW - Prospective Studies KW - Patient Compliance KW - Adult KW - Middle Aged KW - Adolescent KW - Amphotericin B -- therapeutic use KW - Antigens, Fungal -- metabolism KW - Female KW - Male KW - Histoplasma -- immunology KW - AIDS-Related Opportunistic Infections -- drug therapy KW - Antifungal Agents -- adverse effects KW - Ketoconazole -- therapeutic use KW - Ketoconazole -- analogs & derivatives KW - Ketoconazole -- adverse effects KW - Histoplasmosis -- drug therapy KW - Ketoconazole -- blood KW - Antifungal Agents -- blood KW - Antifungal Agents -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75634887?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+internal+medicine&rft.atitle=Prevention+of+relapse+of+histoplasmosis+with+itraconazole+in+patients+with+the+acquired+immunodeficiency+syndrome.&rft.au=Wheat%2C+J%3BHafner%2C+R%3BWulfsohn%2C+M%3BSpencer%2C+P%3BSquires%2C+K%3BPowderly%2C+W%3BWong%2C+B%3BRinaldi%2C+M%3BSaag%2C+M%3BHamill%2C+R%3BMurphy%2C+R%3BConnolly-Stringfield%2C+P%3BBriggs%2C+N%3BOwens%2C+S%3BNational+Institute+of+Allergy+and+Infectious+Diseases+Clinical+Trials+and+Mycoses+Study+Group+Collaborators&rft.aulast=Wheat&rft.aufirst=J&rft.date=1993-04-15&rft.volume=118&rft.issue=8&rft.spage=610&rft.isbn=&rft.btitle=&rft.title=Annals+of+internal+medicine&rft.issn=00034819&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-15 N1 - Date created - 1993-04-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Protection of human endothelial cells from oxidant injury by adenovirus-mediated transfer of the human catalase cDNA. AN - 75700507; 8479912 AB - In a variety of disorders, endothelial cells are exposed to high levels of oxidants, generated within the cells and/or consequent to local inflammation. In the context of the sensitivity of endothelial cells to oxidant stress, particularly related to H2O2, we have designed a replication deficient recombinant adenovirus containing the human catalase cDNA (AdCL) to transfer the catalase cDNA to the endothelial cells, in order to augment intracellular anti-H2O2 protection. Human umbilical vein endothelial cells that were not infected or infected with control adenovirus maintained low levels of catalase mRNA. Endothelial cells infected with AdCL expressed AdCL-driven exogenous catalase mRNA, as early as 24 hr and at least for 7 days. Catalase protein levels were increased significantly over controls in cells infected with AdCL, as were catalase activity levels, with catalase activity correlated closely with levels of catalase protein. Importantly, when the endothelial cells were exposed to 500 microM H2O2, all the AdCL infected endothelial cells survived, compared to only 37% of the control cells. Thus, a recombinant adenovirus containing the human catalase cDNA is able to infect human endothelial cells in vitro and express high levels of functional intracellular catalase, protecting the cells against H2O2-mediated oxidant stress. These observations support the feasibility of the transfer of catalase cDNA to human endothelium to protect against oxidant injury. JF - Nucleic acids research AU - Erzurum, S C AU - Lemarchand, P AU - Rosenfeld, M A AU - Yoo, J H AU - Crystal, R G AD - Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/04/11/ PY - 1993 DA - 1993 Apr 11 SP - 1607 EP - 1612 VL - 21 IS - 7 SN - 0305-1048, 0305-1048 KW - RNA, Messenger KW - 0 KW - Hydrogen Peroxide KW - BBX060AN9V KW - Catalase KW - EC 1.11.1.6 KW - Index Medicus KW - Adenoviridae KW - Base Sequence KW - RNA, Messenger -- metabolism KW - Transfection KW - Cells, Cultured KW - Humans KW - Genetic Vectors KW - Molecular Sequence Data KW - Gene Expression KW - Hydrogen Peroxide -- toxicity KW - Catalase -- metabolism KW - Catalase -- biosynthesis KW - Endothelium, Vascular -- metabolism KW - Hydrogen Peroxide -- metabolism KW - Catalase -- genetics KW - Endothelium, Vascular -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75700507?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+acids+research&rft.atitle=Protection+of+human+endothelial+cells+from+oxidant+injury+by+adenovirus-mediated+transfer+of+the+human+catalase+cDNA.&rft.au=Erzurum%2C+S+C%3BLemarchand%2C+P%3BRosenfeld%2C+M+A%3BYoo%2C+J+H%3BCrystal%2C+R+G&rft.aulast=Erzurum&rft.aufirst=S&rft.date=1993-04-11&rft.volume=21&rft.issue=7&rft.spage=1607&rft.isbn=&rft.btitle=&rft.title=Nucleic+acids+research&rft.issn=03051048&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-25 N1 - Date created - 1993-05-25 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Am J Respir Cell Mol Biol. 1991 Apr;4(4):364-8 [1901719] Eur Respir J Suppl. 1990 Oct;11:482s-484s [2278607] Biochemistry. 1991 Sep 24;30(38):9305-13 [1654093] Pharmacol Ther. 1989;44(2):297-307 [2519346] J Clin Invest. 1992 Jan;89(1):197-202 [1370294] Cell. 1992 Jan 10;68(1):143-55 [1370653] Free Radic Biol Med. 1991;11(6):545-55 [1778501] Am J Respir Cell Mol Biol. 1992 Feb;6(2):175-82 [1540380] Circ Res. 1992 May;70(5):991-8 [1568306] Atherosclerosis. 1991 Nov;91(1-2):1-14 [1811545] Proc Natl Acad Sci U S A. 1992 Jul 15;89(14):6482-6 [1631146] Virology. 1973 Apr;52(2):456-67 [4705382] J Gen Virol. 1977 Jul;36(1):59-74 [886304] J Clin Invest. 1981 Sep;68(3):714-21 [6268662] Lab Invest. 1982 Nov;47(5):412-26 [6290784] Cell. 1982 Dec;31(3 Pt 2):543-51 [6297772] J Clin Invest. 1984 Jan;73(1):87-95 [6690485] J Immunol Methods. 1983 Dec 16;65(1-2):55-63 [6606682] J Clin Invest. 1984 Mar;73(3):706-13 [6707200] Circ Shock. 1984;12(4):229-39 [6327114] Methods Enzymol. 1984;105:121-6 [6727660] Am Rev Respir Dis. 1984 Aug;130(2):209-13 [6087699] Proc Natl Acad Sci U S A. 1984 Dec;81(23):7269-73 [6095281] N Engl J Med. 1985 Jan 17;312(3):159-63 [2981404] Nucleic Acids Res. 1986 Jul 11;14(13):5561-2 [3755526] J Lab Clin Med. 1986 Sep;108(3):190-8 [3091744] Am J Physiol. 1986 Nov;251(5 Pt 1):C671-80 [3777154] J Free Radic Biol Med. 1986;2(5-6):359-65 [3598065] Am Rev Respir Dis. 1987 Aug;136(2):483-5 [3619213] FASEB J. 1987 Nov;1(5):358-64 [2824268] J Clin Invest. 1988 Apr;81(4):1297-301 [3127425] J Biol Chem. 1988 May 15;263(14):6884-92 [3129432] J Clin Invest. 1988 May;81(5):1556-62 [3130395] J Clin Invest. 1988 Sep;82(3):1040-50 [2843565] N Engl J Med. 1989 Feb 9;320(6):365-76 [2536474] Free Radic Biol Med. 1988;5(5-6):409-19 [3076884] Biotechniques. 1988 Jul-Aug;6(7):616-29 [3078719] Free Radic Biol Med. 1990;8(2):201-9 [2185145] Science. 1991 Apr 19;252(5004):431-4 [2017680] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Report of the Cancer Therapy Evaluation Program monitoring plan for secondary acute myeloid leukemia following treatment with epipodophyllotoxins. AN - 75663389; 8455202 AB - Recent reports have documented the occurrence of treatment-related acute myeloid leukemia (AML) following therapy with epipodophyllotoxins. These reports have led to growing concern among oncologists, which could lead to premature abandonment of these agents at a time when the relationship between cumulative dose of epipodophyllotoxin and risk of treatment-related AML has not been determined. Because of the increasingly important role of epipodophyllotoxins in the treatment of several types of adult and pediatric tumors, the Cancer Therapy Evaluation Program (CTEP) of the National Cancer Institute (NCI) has developed a monitoring plan to obtain reliable estimates of the risk of treatment-related AML following epipodophyllotoxin treatment. We identified 12 NCI-supported Cooperative Group clinical trials in which patients with solid tumors are being treated with epipodophyllotoxins at different cumulative doses. One trial is using a moderate dose of teniposide (900 mg/m2), and 11 trials are using etoposide at a low dose ( or = 4000 mg/m2). Cases of treatment-related AML and treatment-related myelodysplastic syndrome (MDS) (hereafter referred to as treatment-related AML/MDS) occurring in these trials are reported to CTEP, with initial analysis for each cumulative dose group triggered by the reporting of four cases of treatment-related AML/MDS in that group. For each analysis, total patient follow-up for the group is determined and cumulative 6-year incidence rate is calculated. Three cases of treatment-related AML and one case of treatment-related MDS (with documented monosomy 7) were reported in a group of 207 patients who received etoposide at a low cumulative dose. The calculated 6-year rate of development of treatment-related AML/MDS was 3.2% (95% upper confidence interval bounded by 7.2%). The 6-year cumulative rate of treatment-related AML/MDS (3.2%) is within the range previously reported for alkylator-based regimens that did not include epipodophyllotoxins. Previous reports have suggested that higher cumulative doses of alkylators are associated with increased risk of treatment-related AML, and a critical goal of the monitoring plan is to determine whether a similar relationship exists for the epipodophyllotoxins. Estimates will be developed for leukemogenic risk for the moderate- and high-cumulative-dose groups when four cases of treatment-related AML/MDS have been identified within each group. JF - Journal of the National Cancer Institute AU - Smith, M A AU - Rubinstein, L AU - Cazenave, L AU - Ungerleider, R S AU - Maurer, H M AU - Heyn, R AU - Khan, F M AU - Gehan, E AD - Cancer Therapy Evaluation Program, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/04/07/ PY - 1993 DA - 1993 Apr 07 SP - 554 EP - 558 VL - 85 IS - 7 SN - 0027-8874, 0027-8874 KW - Etoposide KW - 6PLQ3CP4P3 KW - Podophyllotoxin KW - L36H50F353 KW - Index Medicus KW - Acute Disease KW - Humans KW - Adult KW - Clinical Trials as Topic KW - Incidence KW - Etoposide -- adverse effects KW - Child KW - Leukemia, Myeloid -- chemically induced KW - Podophyllotoxin -- adverse effects KW - Myelodysplastic Syndromes -- chemically induced KW - Neoplasms, Second Primary -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75663389?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Report+of+the+Cancer+Therapy+Evaluation+Program+monitoring+plan+for+secondary+acute+myeloid+leukemia+following+treatment+with+epipodophyllotoxins.&rft.au=Smith%2C+M+A%3BRubinstein%2C+L%3BCazenave%2C+L%3BUngerleider%2C+R+S%3BMaurer%2C+H+M%3BHeyn%2C+R%3BKhan%2C+F+M%3BGehan%2C+E&rft.aulast=Smith&rft.aufirst=M&rft.date=1993-04-07&rft.volume=85&rft.issue=7&rft.spage=554&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-16 N1 - Date created - 1993-04-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - In vivo inhibition of glucocorticoid-inducible gene expression by dimethylnitrosamine in rat liver. AN - 75679948; 8097092 AB - Sprague-Dawley rats were pretreated with a single i.p. injection of either 2.25 mL/kg of phosphate-buffered saline (PBS) or 22.5 mg/kg of dimethylnitrosamine (DMN) followed 2 hr later by a single i.p. injection of either 1.35 mg/kg of dexamethasone (DEX) or the vehicle, a 50% ethanol solution, both delivered in a volume of 3 mL/kg. RNA levels of the hormone-inducible, specialized liver function genes, tyrosine aminotransferase (TAT) and glutamine synthetase (GS), were monitored 4, 5, 6, 7, 8, and 10 hr after the DEX injection. Maximal induction of both the TAT (26-fold) and GS (6-fold) RNAs occurred 6 hr after DEX administration in PBS-pretreated animals. Pretreatment with DMN caused at least a 42% inhibition of DEX-induced RNA accumulation at every time point examined, with greater than 90% inhibition occurring when the genes were maximally induced at 6 hr. This inhibition was not due to any alterations of the glucocorticoid receptors as DMN had no effect on the binding affinity or amounts of glucocorticoid receptors present in rat hepatic cytosols. These results suggest that chemical carcinogens such as DMN may affect normal gene function in vivo by inhibiting the cellular response to hormone receptors mediating differentiation-associated, specialized cell functions. JF - Biochemical pharmacology AU - Miller, M S AU - Buzard, G S AU - McDowell, A E AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702. Y1 - 1993/04/06/ PY - 1993 DA - 1993 Apr 06 SP - 1465 EP - 1470 VL - 45 IS - 7 SN - 0006-2952, 0006-2952 KW - Carcinogens KW - 0 KW - RNA, Messenger KW - Receptors, Glucocorticoid KW - Dexamethasone KW - 7S5I7G3JQL KW - Tyrosine Transaminase KW - EC 2.6.1.5 KW - Glutamate-Ammonia Ligase KW - EC 6.3.1.2 KW - Dimethylnitrosamine KW - M43H21IO8R KW - Index Medicus KW - Gene Expression -- drug effects KW - Animals KW - Receptors, Glucocorticoid -- drug effects KW - Tyrosine Transaminase -- biosynthesis KW - Tyrosine Transaminase -- genetics KW - RNA, Messenger -- analysis KW - Receptors, Glucocorticoid -- metabolism KW - Glutamate-Ammonia Ligase -- genetics KW - Rats KW - Rats, Sprague-Dawley KW - Glutamate-Ammonia Ligase -- biosynthesis KW - Enzyme Induction KW - Time Factors KW - Dimethylnitrosamine -- pharmacology KW - Carcinogens -- pharmacology KW - Liver -- enzymology KW - Carcinogens -- administration & dosage KW - Dexamethasone -- metabolism KW - Liver -- drug effects KW - Dexamethasone -- antagonists & inhibitors KW - Dimethylnitrosamine -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75679948?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+pharmacology&rft.atitle=In+vivo+inhibition+of+glucocorticoid-inducible+gene+expression+by+dimethylnitrosamine+in+rat+liver.&rft.au=Miller%2C+M+S%3BBuzard%2C+G+S%3BMcDowell%2C+A+E&rft.aulast=Miller&rft.aufirst=M&rft.date=1993-04-06&rft.volume=45&rft.issue=7&rft.spage=1465&rft.isbn=&rft.btitle=&rft.title=Biochemical+pharmacology&rft.issn=00062952&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-10 N1 - Date created - 1993-05-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Tyrosine phosphorylation of pp125FAK by the aggregation of high affinity immunoglobulin E receptors requires cell adherence. AN - 75662936; 8463210 AB - The aggregation of the high affinity IgE receptor (Fc epsilon RI) in adherent rat basophilic leukemia (RBL-2H3) cells induces the tyrosine phosphorylation of several proteins. We examined whether focal adhesion-associated tyrosine kinase, pp125FAK, is one of these proteins. Anti-pp125FAK monoclonal antibody immunoblotted and precipitated a 115-kDa tyrosine-phosphorylated protein. In the absence of Fc epsilon RI aggregation, pp125FAK was tyrosine-phosphorylated only in adherent cells. Aggregating Fc epsilon RI in adherent cells markedly enhanced tyrosine phosphorylation of pp125FAK. This increase was detectable within 1 min of Fc epsilon RI aggregation and was maximal by 15 min. In contrast, in nonadherent cells Fc epsilon RI aggregation did not induce tyrosine phosphorylation of pp125FAK. The enhanced influx of calcium by calcium ionophore or the activation of protein kinase C by phorbol myristate acetate induced tyrosine phosphorylation of pp125FAK only in adherent cells. Thus, Fc epsilon RI-induced tyrosine phosphorylation of pp125FAK could be mediated by the activation of protein kinase C and/or the induction of calcium influx. The data indicate that cell adherence is essential for Fc epsilon RI-induced tyrosine phosphorylation of pp125FAK. JF - The Journal of biological chemistry AU - Hamawy, M M AU - Mergenhagen, S E AU - Siraganian, R P AD - Laboratory of Immunology, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/04/05/ PY - 1993 DA - 1993 Apr 05 SP - 6851 EP - 6854 VL - 268 IS - 10 SN - 0021-9258, 0021-9258 KW - Cell Adhesion Molecules KW - 0 KW - Receptors, IgE KW - Calcimycin KW - 37H9VM9WZL KW - Tyrosine KW - 42HK56048U KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Focal Adhesion Kinase 1 KW - EC 2.7.10.2 KW - Focal Adhesion Protein-Tyrosine Kinases KW - Ptk2 protein, rat KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Rats KW - Immunoblotting KW - Animals KW - Tumor Cells, Cultured KW - Phosphorylation KW - Kinetics KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Calcimycin -- pharmacology KW - Receptors, IgE -- metabolism KW - Cell Adhesion Molecules -- metabolism KW - Tyrosine -- metabolism KW - Receptor Aggregation KW - Protein-Tyrosine Kinases -- metabolism KW - Cell Adhesion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75662936?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Tyrosine+phosphorylation+of+pp125FAK+by+the+aggregation+of+high+affinity+immunoglobulin+E+receptors+requires+cell+adherence.&rft.au=Hamawy%2C+M+M%3BMergenhagen%2C+S+E%3BSiraganian%2C+R+P&rft.aulast=Hamawy&rft.aufirst=M&rft.date=1993-04-05&rft.volume=268&rft.issue=10&rft.spage=6851&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-05 N1 - Date created - 1993-05-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Toxicity of Bordetella avium beta-cystathionase toward MC3T3-E1 osteogenic cells. AN - 75659811; 8463265 AB - Bordetella avium is the etiological agent of an upper respiratory disease in birds which, symptomatically and pathologically, resembles bordetellosis in humans. Studies of the virulence of this organism revealed a novel cytotoxic protein, designated osteotoxin, that was lethal for MC3T3-E1 osteogenic cells, fetal bovine trabecular cells, UMR106-01(BSP) rat osteosarcoma cells, and embryonic bovine tracheal cells. The osteotoxin lacked dermonecrotic toxin activity, exhibited no cross-reactivity with antibody against B. avium dermonecrotic toxin, and was non-proteolytic. Osteotoxin (M(r) approximately 80,000 by gel filtration, pI 5.4) was purified to electrophoretic homogeneity from B. avium 197. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis and spectrophotometric analyses showed that the native protein was a homodimer and that each of the non-covalently linked subunits (M(r) approximately 41,000) contained one molecule of pyridoxal 5'-phosphate. Microsequencing of the first 32 amino acids from the NH2 terminus allowed the synthesis of two oligonucleotide probes, which, together with polyclonal antibody to the purified protein, facilitated cloning, sequencing, and expression of the osteotoxin gene product in Escherichia coli. The open reading frame encodes a polypeptide of 396 amino acid residues (M(r) = 42,606, calculated pI 5.9), whose sequence exhibits approximately 38% identity (approximately 60% similarity) to pyridoxal 5'-phosphate-dependent beta-cystathionase(s) from E. coli, Salmonella typhimurium, and rat liver. The characteristic motif, TKYXXGHSD, associated with binding the cofactor in these enzymes is also present in osteotoxin. Physicochemical and enzymatic analyses established the coidentity of osteotoxin with beta-cystathionase. The region upstream of the beta-cystathionase (metC) gene in B. avium 197 lacked regulatory sequences ("Met boxes") described for metC in enteric species, and enzyme production was not repressed by methionine. Incubation of MC3T3-E1 osteogenic cells in medium containing L-[35S]cystine and purified beta-cystathionase resulted in 35S-labeling of the enzyme and at least one major MC3T3-E1 cell protein (M(r) approximately 50,000). cytotoxicity can be attributed to: 1) beta-cystathionase-catalyzed cleavage of L-cystine in the medium and formation of reactive sulfane-containing derivative(s), and 2) transfer of sulfane sulfur to metabolically sensitive or structurally important proteins in the osteogenic cells. JF - The Journal of biological chemistry AU - Gentry-Weeks, C R AU - Keith, J M AU - Thompson, J AD - Laboratory of Microbial Ecology, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/04/05/ PY - 1993 DA - 1993 Apr 05 SP - 7298 EP - 7314 VL - 268 IS - 10 SN - 0021-9258, 0021-9258 KW - Bacterial Toxins KW - 0 KW - DNA, Bacterial KW - Virulence Factors, Bordetella KW - dermonecrotic toxin, Bordetella KW - Transglutaminases KW - EC 2.3.2.13 KW - Lyases KW - EC 4.- KW - cystathionine beta-lyase KW - EC 4.4.1.8 KW - Index Medicus KW - Swine KW - Animals KW - Turkeys KW - Electrophoresis, Polyacrylamide Gel KW - Guinea Pigs KW - Isoelectric Point KW - Rabbits KW - Amino Acid Sequence KW - Cloning, Molecular KW - Rats KW - Base Sequence KW - Blotting, Western KW - Cattle KW - Spectrum Analysis KW - Cells, Cultured KW - Kinetics KW - Restriction Mapping KW - Cell Death KW - Molecular Sequence Data KW - Substrate Specificity KW - Sequence Homology, Amino Acid KW - Cell Line KW - Osteoblasts -- drug effects KW - Bacterial Toxins -- genetics KW - Bacterial Toxins -- antagonists & inhibitors KW - Bacterial Toxins -- isolation & purification KW - Lyases -- toxicity KW - Lyases -- genetics KW - Lyases -- antagonists & inhibitors KW - Bacterial Toxins -- toxicity KW - Bordetella -- enzymology KW - Lyases -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75659811?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Toxicity+of+Bordetella+avium+beta-cystathionase+toward+MC3T3-E1+osteogenic+cells.&rft.au=Gentry-Weeks%2C+C+R%3BKeith%2C+J+M%3BThompson%2C+J&rft.aulast=Gentry-Weeks&rft.aufirst=C&rft.date=1993-04-05&rft.volume=268&rft.issue=10&rft.spage=7298&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-05 N1 - Date created - 1993-05-05 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - L10425; GENBANK N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Using the tolerable-dose diagram in the design of phase I combination chemotherapy trials. AN - 85276125; pmid-8478673 AB - PURPOSE: Choosing maximum-tolerated doses (MTDs) of agents to be administered in combination is more complicated than choosing the MTD for a single agent. This is because there are many combinations of doses that will be tolerated. We offer guidance in targeting specific MTD combinations, and suggest trial designs to achieve these targets. METHODS: A graphical method based on a simple, previously described mathematical model is used to guide the phase I trial design. The method involves constructing a tolerable-dose diagram, which displays the toxicities that are expected to occur at various dose combinations. The data required for the method are the single-agent toxicity profiles of the agents. Designs for combinations of taxol with fluorouracil, carboplatin, doxorubicin, cyclophosphamide, and cisplatin are used to demonstrate the methods. RESULTS: For all of the drugs considered here, leukopenia is dose-limiting or nearly dose-limiting. Consequently, no major improvement in total dose-intensity is achievable by combining these drugs. If leukopenia can be eliminated or substantially reduced by use of chemoprotective agents, then a cyclophosphamide/taxol combination appears promising from a dose-intensity point of view. For other combinations, the doses must be reduced from single-agent MTD levels. In the absence of biologic information such as concentrations needed for optimal modulation, it is suggested that single-agent MTDs be reduced approximately proportionately for each drug in the combination. CONCLUSION: Tolerable-dose diagrams are useful for planning phase I trials of combinations of agents. They can suggest which combinations are promising from a dose-intensity perspective, as well as dose-escalation schemes for combinations to be pursued for dose-intensity or other considerations. JF - Journal of Clinical Oncology AU - Korn, E L AU - Simon, R AD - Biometric Research Branch, National Cancer Institute, Bethesda, MD 20892. PY - 1993 SP - 794 EP - 801 VL - 11 IS - 4 SN - 0732-183X, 0732-183X KW - Antineoplastic Agents KW - Human KW - Carboplatin KW - Cyclophosphamide KW - Doxorubicin KW - Clinical Trials, Phase I UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85276125?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Clinical+Oncology&rft.atitle=Using+the+tolerable-dose+diagram+in+the+design+of+phase+I+combination+chemotherapy+trials.&rft.au=Korn%2C+E+L%3BSimon%2C+R&rft.aulast=Korn&rft.aufirst=E&rft.date=1993-04-01&rft.volume=11&rft.issue=4&rft.spage=794&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Oncology&rft.issn=0732183X&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Safety of rapid-rate transcranial magnetic stimulation in normal volunteers. AN - 85239836; pmid-7683602 AB - In 9 normal volunteers, we studied the safety of rapid-rate transcranial magnetic stimulation (rTMS) applied to different scalp positions at various frequencies and intensities. Pure tone threshold audiometry showed temporary threshold shifts in 3 subjects. In the subject stimulated at the highest intensity, rTMS induced a focal, secondarily generalized seizure despite the absence of definite risk factors for seizures. Rapid-rate TMS did not result in any important changes in the neurological examination findings, cognitive performance, electroencephalogram, electrocardiogram, and hormone levels (prolactin, adrenocorticotropic hormone, thyroid-stimulating hormone, luteinizing hormone, and follicle-stimulating hormone). In 10 additional subjects, the electromyographic activity in several contralateral muscles showed that trains of rTMS applied to the motor cortex induced a spread of cortical excitability. The spread of excitability depended on the intensity and frequency of the stimuli and probably constituted an early epileptogenic effect of rTMS. Guidelines for preventing the undesirable side effects of rTMS are offered. JF - Electroencephalography and Clinical Neurophysiology AU - Pascual-Leone, A AU - Houser, C M AU - Reese, K AU - Shotland, L I AU - Grafman, J AU - Sato, S AU - Valls-Solé J AU - Brasil-Neto, J P AU - Wassermann, E M AU - Cohen, L G AD - Human Cortical Physiology Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. PY - 1993 SP - 120 EP - 130 VL - 89 IS - 2 SN - 0013-4694, 0013-4694 KW - Reference Values KW - Magnetics KW - Audiometry KW - Human KW - Safety KW - Electroencephalography KW - Muscles KW - Brain KW - Electromyography KW - Mental Recall KW - Memory KW - Adult KW - Middle Age KW - Gonadotropins, Pituitary KW - Neuropsychological Tests KW - Neuropeptides KW - Male KW - Female KW - Reaction Time UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85239836?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Electroencephalography+and+Clinical+Neurophysiology&rft.atitle=Safety+of+rapid-rate+transcranial+magnetic+stimulation+in+normal+volunteers.&rft.au=Pascual-Leone%2C+A%3BHouser%2C+C+M%3BReese%2C+K%3BShotland%2C+L+I%3BGrafman%2C+J%3BSato%2C+S%3BValls-Sol%C3%A9+J%3BBrasil-Neto%2C+J+P%3BWassermann%2C+E+M%3BCohen%2C+L+G&rft.aulast=Pascual-Leone&rft.aufirst=A&rft.date=1993-04-01&rft.volume=89&rft.issue=2&rft.spage=120&rft.isbn=&rft.btitle=&rft.title=Electroencephalography+and+Clinical+Neurophysiology&rft.issn=00134694&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Court-ordered reimbursement for unproven medical technology. Circumventing technology assessment. AN - 85226122; pmid-8468767 AB - OBJECTIVE--Because we found examples where courts of law ruled against insurance carriers that had been sued for reimbursement for unproven medical procedures, we conducted a case study to determine the reasoning behind these decisions that run counter to accepted medical science. Such actions circumvent health technology assessment and could contribute to escalating health care costs and poorer quality health care. DATA SOURCES--A literature search identified 17 cases between 1980 and 1989 in which an insurance company was sued to reimburse a patient who had received an unproven or questionable health technology; 14 of these suits were decided in favor of the plaintiff, and the insurance company was ordered to pay. Discussed in this article are six of these cases, two involving Laetrile (amygdalin), two involving immunoaugmentative therapy, and two involving thermography, technologies that had previously been assessed as not safe, not effective, or inadequately evaluated. DATA SYNTHESIS AND CONCLUSIONS--The circumstances determining how the courts arrive at these "unscientific" decisions fall into three general categories: (1) for legal reasons, the insurance contract is interpreted in favor of the insured; (2) the reluctance and/or inability, legal or otherwise, of the courts to use published scientific literature; and (3) the use of adversarial "expert" witnesses with potential conflicts of interest. To address this situation, we first urge the legal and insurance industries to cooperate in improving the contract language and process in a way that would be both legally and scientifically appropriate. Second, we encourage the courts to use and foster the use of published peer-reviewed scientific material as evidence whenever possible. Third, we recommend that the courts choose their own unbiased expert witnesses to interpret scientific material. JF - JAMA AU - Ferguson, J H AU - Dubinsky, M AU - Kirsch, P J AD - Office of Medical Application of Research, National Institutes of Health, Bethesda, Md 20892. PY - 1993 SP - 2116 EP - 2121 VL - 269 IS - 16 SN - 0098-7484, 0098-7484 KW - United States KW - Contracts KW - Human KW - Immunotherapy KW - Wounds and Injuries KW - Reimbursement Mechanisms KW - Technology Assessment, Biomedical KW - Federal Government KW - Thermography KW - Neoplasms KW - Amygdalin KW - Male KW - Female KW - Complementary Therapies KW - Judicial Role UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85226122?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=JAMA&rft.atitle=Court-ordered+reimbursement+for+unproven+medical+technology.+Circumventing+technology+assessment.&rft.au=Ferguson%2C+J+H%3BDubinsky%2C+M%3BKirsch%2C+P+J&rft.aulast=Ferguson&rft.aufirst=J&rft.date=1993-04-01&rft.volume=269&rft.issue=16&rft.spage=2116&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - From the National Institute on Deafness and Other Communication Disorders. AN - 85203825; pmid-8483612 JF - Otolaryngology--Head and Neck Surgery AU - Snow, J B AD - National Institute on Deafness and other Communication Disorders, Bethesda, Maryland 20892, USA. PY - 1993 SP - 380 EP - 383 VL - 108 IS - 4 SN - 0194-5998, 0194-5998 KW - United States KW - Human KW - Deafness KW - National Institutes of Health (U.S.) KW - Communication Disorders UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85203825?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Otolaryngology--Head+and+Neck+Surgery&rft.atitle=From+the+National+Institute+on+Deafness+and+Other+Communication+Disorders.&rft.au=Snow%2C+J+B&rft.aulast=Snow&rft.aufirst=J&rft.date=1993-04-01&rft.volume=108&rft.issue=4&rft.spage=380&rft.isbn=&rft.btitle=&rft.title=Otolaryngology--Head+and+Neck+Surgery&rft.issn=01945998&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Speech production changes under fluency-evoking conditions in nonstuttering speakers. AN - 85157952; pmid-8487517 AB - Changes in airflow and intraoral pressure between baseline and four fluency-evoking conditions--choral reading (CR), metronome pacing (MET), delayed auditory feedback (DAF), and masking noise (NOISE)--were studied in 12 American English nonstuttering speakers. The duration, amplitude, and velocity of airflow and intraoral pressure development during the initial plosive and the duration and intensity of the following vowel were measured in eight target CVC words. Speech rate was computed for each sentence. Comparisons between baseline and the corresponding production in each condition revealed significant changes in peak flow, pressure rise time, peak instantaneous pressure velocity, speech rate, intensity, and vowel duration. Vowel duration increased under DAF, MET, and NOISE conditions. Peak pressure and pressure velocity decreased during CR and MET and increased during NOISE, but did not change during DAF. Subjects were consistent in the variables they modified across conditions. Changes in the aerodynamic variables were not related to intensity or rate changes. Thus, nonstuttering speakers modify intraoral pressure and flow under fluency-evoking conditions. JF - Journal of Speech and Hearing Research AU - Stager, S V AU - Ludlow, C L AD - Voice and Speech Section, VSLB, NIDCD, National Institutes of Health, Bethesda, MD 20892. PY - 1993 SP - 245 EP - 253 VL - 36 IS - 2 SN - 0022-4685, 0022-4685 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85157952?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Speech+and+Hearing+Research&rft.atitle=Speech+production+changes+under+fluency-evoking+conditions+in+nonstuttering+speakers.&rft.au=Stager%2C+S+V%3BLudlow%2C+C+L&rft.aulast=Stager&rft.aufirst=S&rft.date=1993-04-01&rft.volume=36&rft.issue=2&rft.spage=245&rft.isbn=&rft.btitle=&rft.title=Journal+of+Speech+and+Hearing+Research&rft.issn=00224685&rft_id=info:doi/ LA - English DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Potentiation of radiation effects in plateau phase human glioma cells by combination of metabolic inhibitors. AN - 75937416; 8359829 AB - Effects of glycolytic inhibitor 2-deoxy-D-glucose (2-DG) on radiation damage were studied in a human glioma cell line (BMG-1), grown to confluence in monolayer. After irradiation (60Co-gamma-rays, 2 Gy) and incubation with low concentrations of 2-DG (0.5, 1.25 mM; 2-DG/glucose = 0.1, 0.25; 2 hr), in the absence or presence of respiratory inhibitor KCN (0.5-2 mM), cells were trypsinized and plated to assay radiation induced cytogenetic damage (micronuclei formation). The observations made were: (1) 2-DG and/or KCN treatments did not induce damage in unirradiated cells. (2) Either of these treatments did not increase radiation induced micronuclei formation. (3) Presence of 2-DG along with KCN (1,2 mM) significantly enhanced the radiation induced micronuclei formation. (4) Preliminary experiments by macrocolony assay showed that radiation induced cell death was also significantly increased by the combined treatment. These observations suggest that presence of clinically feasible, low concentrations of 2-DG (2-DG/glucose < 0.5) for short intervals of time after radiation could increase radiation damage in non-cycling, hypoxic tumour cells with impaired oxidative and increased glycolytic energy metabolism. JF - Indian journal of experimental biology AU - Kalia, V K AD - Department of Biophysics, National Institute of Mental Health & Neurosciences, Bangalore, India. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 312 EP - 315 VL - 31 IS - 4 SN - 0019-5189, 0019-5189 KW - DNA, Neoplasm KW - 0 KW - Deoxyglucose KW - 9G2MP84A8W KW - Potassium Cyanide KW - MQD255M2ZO KW - Index Medicus KW - DNA, Neoplasm -- radiation effects KW - DNA, Neoplasm -- drug effects KW - Tumor Cells, Cultured KW - Cell Survival -- drug effects KW - Humans KW - Chemotherapy, Adjuvant KW - DNA Damage -- drug effects KW - Potassium Cyanide -- therapeutic use KW - Glioma -- drug therapy KW - Deoxyglucose -- therapeutic use KW - Brain Neoplasms -- drug therapy KW - Brain Neoplasms -- radiotherapy KW - Deoxyglucose -- pharmacology KW - Potassium Cyanide -- pharmacology KW - Glioma -- radiotherapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75937416?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Indian+journal+of+experimental+biology&rft.atitle=Potentiation+of+radiation+effects+in+plateau+phase+human+glioma+cells+by+combination+of+metabolic+inhibitors.&rft.au=Kalia%2C+V+K&rft.aulast=Kalia&rft.aufirst=V&rft.date=1993-04-01&rft.volume=31&rft.issue=4&rft.spage=312&rft.isbn=&rft.btitle=&rft.title=Indian+journal+of+experimental+biology&rft.issn=00195189&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-28 N1 - Date created - 1993-09-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Contamination and restoration of groundwater aquifers. AN - 75907815; 8354172 AB - Humans are exposed to chemicals in contaminated groundwaters that are used as sources of drinking water. Chemicals contaminate groundwater resources as a result of waste disposal methods for toxic chemicals, overuse of agricultural chemicals, and leakage of chemicals into the subsurface from buried tanks used to hold fluid chemicals and fuels. In the process, both the solid portions of the subsurface and the groundwaters that flow through these porous structures have become contaminated. Restoring these aquifers and minimizing human exposure to the parent chemicals and their degradation products will require the identification of suitable biomarkers of human exposure; better understandings of how exposure can be related to disease outcome; better understandings of mechanisms of transport of pollutants in the heterogeneous structures of the subsurface; and field testing and evaluation of methods proposed to restore and cleanup contaminated aquifers. In this review, progress in these many different but related activities is presented. JF - Environmental health perspectives AU - Piver, W T AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 237 EP - 247 VL - 100 SN - 0091-6765, 0091-6765 KW - Water Pollutants, Chemical KW - 0 KW - Index Medicus KW - Environmental Health KW - Humans KW - Porosity KW - Fresh Water -- chemistry KW - Water Pollutants, Chemical -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75907815?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Contamination+and+restoration+of+groundwater+aquifers.&rft.au=Piver%2C+W+T&rft.aulast=Piver&rft.aufirst=W&rft.date=1993-04-01&rft.volume=100&rft.issue=&rft.spage=237&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-22 N1 - Date created - 1993-09-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Int J Cancer. 1987 Feb 15;39(2):155-61 [3804490] Am J Ind Med. 1990;18(3):303-5 [2220835] Appl Environ Microbiol. 1987 Feb;53(2):254-60 [3105454] J Occup Med. 1979 Nov;21(11):741-4 [512718] Science. 1981 Jan 9;211(4478):132-8 [7444456] Br J Cancer. 1981 Feb;43(2):169-76 [7470379] Int J Cancer. 1982 Mar 15;29(3):239-47 [7040259] Am J Epidemiol. 1982 May;115(5):720-8 [7081203] J Natl Cancer Inst. 1983 Jul;71(1):31-7 [6575207] Am J Epidemiol. 1983 Jul;118(1):72-7 [6869365] Neurotoxicology. 1983 Spring;4(1):113-29 [6192367] J Natl Cancer Inst. 1984 Jun;72(6):1233-40 [6587145] Appl Environ Microbiol. 1985 Jan;49(1):242-3 [3919642] Appl Environ Microbiol. 1985 May;49(5):1080-3 [3923927] Am J Epidemiol. 1985 Feb;121(2):225-37 [4014117] Am J Epidemiol. 1985 Mar;121(3):391-402 [4014129] Environ Health Perspect. 1985 May;60:11-28 [4029096] J Occup Med. 1985 Aug;27(8):580-4 [3897488] Arch Environ Health. 1985 Jul-Aug;40(4):211-4 [4051575] J Natl Cancer Inst. 1986 Feb;76(2):229-34 [3456061] Br J Ind Med. 1986 Feb;43(2):75-83 [3753879] Scand J Work Environ Health. 1985 Dec;11(6):397-407 [3912986] JAMA. 1986 Sep 5;256(9):1141-7 [3801091] Carcinogenesis. 1986 Sep;7(9):1519-21 [3742724] Mayo Clin Proc. 1986 Sep;61(9):706-13 [3528698] J Natl Cancer Inst. 1987 May;78(5):899-910 [3471999] Neurology. 1987 Jul;37(7):1229-31 [3037439] Br J Cancer. 1988 Apr;57(4):443 [3390384] Br J Cancer. 1988 May;57(5):516-20 [3395559] Neurotoxicology. 1988 Summer;9(2):249-71 [2462700] Br J Ind Med. 1989 Feb;46(2):143-4 [2923826] Cancer Res. 1989 Sep 1;49(17):4682-9 [2547513] Br J Ind Med. 1989 Aug;46(8):516-20 [2775671] Br J Cancer. 1989 Sep;60(3):385-8 [2789947] Appl Environ Microbiol. 1989 Sep;55(9):2144-51 [2552919] Environ Health Perspect. 1989 Nov;83:117-43 [2695322] Environ Health Perspect. 1989 Nov;83:179-90 [2695324] J Am Coll Cardiol. 1990 Nov;16(5):1304-9 [2229779] Epidemiology. 1990 Sep;1(5):349-56 [2078610] Science. 1991 May 10;252(5007):830-3 [2028258] Appl Environ Microbiol. 1991 Mar;57(3):744-50 [1903914] Toxicol Lett. 1991 Jun;57(1):101-11 [2048155] Arch Microbiol. 1991;155(3):238-48 [1904702] Chem Res Toxicol. 1991 Jul-Aug;4(4):391-407 [1912325] Chem Res Toxicol. 1991 Jul-Aug;4(4):445-53 [1912332] Environ Health Perspect. 1991 Aug;94:135-41 [1954924] Environ Health Perspect. 1991 Aug;94:189-93 [1954930] Environ Health Perspect. 1989 Nov;83:191-203 [2533555] Environ Health Perspect. 1989 Nov;83:205-14 [2533556] Environ Health Perspect. 1989 Nov;83:5-24 [2559844] Int J Epidemiol. 1989 Dec;18(4):768-74 [2621012] J Natl Cancer Inst. 1990 Apr 4;82(7):575-82 [2313734] Carcinogenesis. 1990 May;11(5):755-60 [1692265] J Am Coll Cardiol. 1990 Jul;16(1):155-64 [2358589] Cancer Res. 1990 Oct 15;50(20):6585-91 [2208120] Br J Cancer. 1987 Jan;55(1):81-4 [3814481] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Genetic toxicology: current status of methods of carcinogen identification. AN - 75903919; 8354178 AB - A critical aspect of the efforts to relate the results of short-term genetic toxicity tests with those from long-term rodent tests for carcinogens is the quality and consistency of the studies conducted by the National Toxicology Program. Analysis of the results in relationship to chemical structure has shown that mutagenic potential is a primary risk factor for carcinogen identification. Chemicals positive in the Salmonella assay-generally possess "structural alerts" for electrophilic interactions, are predominantly represented among chemicals producing trans-species carcinogenic effects in rodents, and among those identified as carcinogenic to humans. Current efforts are aimed at defining toxicological, structural, and mechanistic properties of nonmutagens that are carcinogenic in rodents. JF - Environmental health perspectives AU - Tennant, R W AU - Zeiger, E AD - Experimental Carcinogenesis and Mutagenesis Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 307 EP - 315 VL - 100 SN - 0091-6765, 0091-6765 KW - Carcinogens KW - 0 KW - Mutagens KW - Index Medicus KW - Animals KW - Reproducibility of Results KW - Cells, Cultured KW - Carcinogenicity Tests KW - Biological Assay KW - Disease Models, Animal KW - Mice KW - Mice, Transgenic KW - Carcinogens -- toxicity KW - Mutagens -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75903919?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Genetic+toxicology%3A+current+status+of+methods+of+carcinogen+identification.&rft.au=Tennant%2C+R+W%3BZeiger%2C+E&rft.aulast=Tennant&rft.aufirst=R&rft.date=1993-04-01&rft.volume=100&rft.issue=&rft.spage=307&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-22 N1 - Date created - 1993-09-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1973 Aug;70(8):2281-5 [4151811] Mutat Res. 1988 Jan;204(1):17-115 [3277047] Proc Natl Acad Sci U S A. 1981 Jun;78(6):3779-83 [7022455] Mutat Res. 1983 May;113(3-4):173-215 [6341825] Ann N Y Acad Sci. 1983;407:387-94 [6576681] Mutat Res. 1988 Jun;203(3):145-54 [3374512] Environ Mol Mutagen. 1988;12 Suppl 13:19-36 [3416839] Environ Mol Mutagen. 1988;12 Suppl 13:195-229 [3416840] Mutat Res. 1989 Jun;223(2):73-103 [2662004] Mutat Res. 1989 Sep;227(1):59-62 [2770777] Mutagenesis. 1990 Jan;5(1):3-14 [2184307] Mutat Res. 1990 May;241(1):95-108 [2110294] Fundam Appl Toxicol. 1990 Apr;14(3):513-22 [2111256] Cell. 1990 Jun 1;61(5):759-67 [2188735] Mutat Res. 1990 Jun-Aug;234(3-4):135-9 [2366781] Mutat Res. 1990 Jun-Aug;234(3-4):187-93 [2114536] Mutat Res. 1990 Jun-Aug;234(3-4):257-61 [2366790] Science. 1990 Aug 31;249(4972):970-1 [2136249] Mutagenesis. 1990 Jul;5(4):313-21 [2118975] Cell. 1991 Jan 25;64(2):235-48 [1988146] Mutat Res. 1991 May;257(3):209-27 [2014033] Mutat Res. 1991 May;257(3):229-306 [1707500] Environ Mol Mutagen. 1990;16 Suppl 18:1-14 [2091921] Environ Mol Mutagen. 1990;16 Suppl 18:15-31 [2091922] Cancer Res. 1991 Jun 1;51(11):2751-61 [2032214] Science. 1991 Nov 22;254(5035):1138-46 [1659741] Science. 1991 Nov 22;254(5035):1153-60 [1957167] Mol Carcinog. 1991;4(6):420-40 [1793481] Mutat Res. 1992 Feb;271(1):39-48 [1371828] Environ Health Perspect. 1991 Dec;96:47-51 [1820276] Environ Health Perspect. 1993 Apr;100:283-91 [8354176] Environ Mutagen. 1983;5(5):705-16 [6617600] Mutat Res. 1984 Feb;130(1):11-25 [6420694] Environ Mutagen. 1985;7(1):1-51 [3967632] Environ Mutagen. 1985;7(5):663-76 [3930236] Environ Mutagen. 1985;7 Suppl 5:1-248 [3905369] Environ Mutagen. 1986;8(2):183-204 [3698942] Mutat Res. 1986 Sep;168(2):69-240 [3528831] Science. 1987 May 22;236(4804):933-41 [3554512] Proc Natl Acad Sci U S A. 1980 Apr;77(4):1763-7 [6929519] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Aquatic toxicology: past, present, and prospects. AN - 75903875; 8354173 AB - Aquatic organisms have played important roles as early warning and monitoring systems for pollutant burdens in our environment. However, they have significant potential to do even more, just as they have in basic biology where preparations like the squid axon have been essential tools in establishing physiological and biochemical mechanisms. This review provides a brief summary of the history of aquatic toxicology, focusing on the nature of aquatic contaminants, the levels of contamination in our waters, and the origins of these agents. It considers the features of the aquatic environment that determine the availability of xenobiotics to aquatic life and the fate of foreign chemicals within the organism. Finally, toxic effects are considered with primary emphasis on the potential of aquatic models to facilitate identification of the underlying mechanisms of toxicity. JF - Environmental health perspectives AU - Pritchard, J B AD - Laboratory of Cellular and Molecular Pharmacology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 249 EP - 257 VL - 100 SN - 0091-6765, 0091-6765 KW - Carcinogens, Environmental KW - 0 KW - Water Pollutants, Chemical KW - Index Medicus KW - Animals KW - Carcinogens, Environmental -- adverse effects KW - Water Pollutants, Chemical -- adverse effects KW - Toxicology -- trends KW - Forecasting KW - Water Pollutants, Chemical -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75903875?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Aquatic+toxicology%3A+past%2C+present%2C+and+prospects.&rft.au=Pritchard%2C+J+B&rft.aulast=Pritchard&rft.aufirst=J&rft.date=1993-04-01&rft.volume=100&rft.issue=&rft.spage=249&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-22 N1 - Date created - 1993-09-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Environ Health Perspect. 1987 Apr;71:77-85 [3297667] Am J Physiol. 1991 Dec;261(6 Pt 2):R1329-40 [1750557] Environ Health Perspect. 1987 Apr;71:97-103 [3297669] Science. 1967 May 12;156(3776):821-4 [6022229] Fed Proc. 1967 Jul-Aug;26(4):1029-39 [6028768] Science. 1968 Oct 11;162(3850):271-3 [4877438] Nature. 1969 Aug 16;223(5207):753-4 [5802690] Sci Am. 1970 Apr;222(4):72-8 [4984790] Comp Biochem Physiol. 1968 Sep;26(3):853-64 [5758312] Comp Biochem Physiol A Comp Physiol. 1972 May 1;42(1):205-11 [4402709] Comp Gen Pharmacol. 1973 Sep;4(15):305-13 [4788472] Nature. 1976 Jan 15;259(5539):122-4 [128701] Annu Rev Pharmacol Toxicol. 1977;17:167-77 [326162] Ann N Y Acad Sci. 1978 Sep 29;298:389-408 [280189] Environ Health Perspect. 1979 Feb;28:81-8 [488052] Environ Health Perspect. 1980 Feb;34:159-62 [6993200] Am J Med. 1981 Jan;70(1):9-11 [7457493] Regul Toxicol Pharmacol. 1981 Jun;1(1):110-2 [7186150] Toxicol Appl Pharmacol. 1985 Feb;77(2):325-33 [3975903] J Appl Toxicol. 1985 Aug;5(4):261-4 [4045099] Annu Rev Physiol. 1986;48:377-88 [3010818] Cancer Res. 1986 Aug;46(8):3817-24 [3731058] Bull Environ Contam Toxicol. 1987 Jun;38(6):1037-43 [3580610] Environ Health Perspect. 1987 Apr;71:105-19 [3297653] Environ Health Perspect. 1987 Apr;71:129-37 [3297655] Environ Health Perspect. 1987 Apr;71:147-53 [3297657] Environ Health Perspect. 1987 Apr;71:155-70 [3297658] Environ Health Perspect. 1987 Apr;71:17-24 [3297659] Environ Health Perspect. 1987 Apr;71:171-86 [3297660] Environ Health Perspect. 1987 Apr;71:25-9 [2439326] Environ Health Perspect. 1987 Apr;71:31-46 [3297662] Environ Health Perspect. 1987 Apr;71:5-16 [3297664] Environ Health Perspect. 1987 Apr;71:59-68 [3297665] Am J Physiol. 1987 Dec;253(6 Pt 1):G816-22 [3425718] Carcinogenesis. 1988 Jun;9(6):1029-32 [3370748] Vet Hum Toxicol. 1986;28 Suppl 1:38-44 [3334693] Am J Physiol. 1989 Sep;257(3 Pt 2):R484-93 [2551193] Science. 1989 Oct 20;246(4928):352-8 [2678474] Environ Health Perspect. 1991 Jan;90:101-9 [2050047] Environ Health Perspect. 1991 Jan;90:111-6 [2050048] Environ Health Perspect. 1991 Jan;90:149-54 [2050053] Environ Health Perspect. 1991 Jan;90:27-33 [2050071] Environ Health Perspect. 1991 Jan;90:69-73 [1904811] Environ Health Perspect. 1991 Jan;90:7-15 [2050084] Environ Health Perspect. 1991 Jan;90:75-84 [1904812] Cancer Res. 1964 Aug;24:1194-201 [14216151] Environ Health Perspect. 1991 Jan;90:85-92 [2050085] Environ Health Perspect. 1991 Jan;90:93-100 [2050086] Annu Rev Pharmacol Toxicol. 1991;31:371-99 [2064380] Science. 1991 Aug 2;253(5019):512-3 [1857982] J Toxicol Environ Health. 1991 Aug;33(4):395-453 [1875429] Pharmacol Toxicol. 1991 Jun;68(6):424-9 [1653953] J Theor Biol. 1991 Aug 7;151(3):417-28 [1943151] Toxicol Appl Pharmacol. 1991 Sep 15;110(3):486-504 [1949016] Environ Health Perspect. 1987 Apr;71:87-95 [3297668] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Carcinogenicity of 1,3-butadiene. AN - 75903365; 8354171 AB - 1,3-Butadiene, a high-production volume chemical used largely in the manufacture of synthetic rubber, is a multiple organ carcinogen in rats and mice. In inhalation studies conducted in mice by the National Toxicology Program, high rates of early lethal lymphomas occurring at exposure levels of 625 ppm or higher reduced the development and expression of later developing tumors at other sites. Use of survival-adjusted tumor rates to account for competing risk factors provided a clearer indication of the dose responses for 1,3-butadiene-induced neoplasms. An increase in lung tumors in female mice was observed at exposure concentrations as low as 6.25 ppm, the lowest concentration ever used in a long-term carcinogenicity study of this gas. Human exposures to 1,3-butadiene by workers employed at facilities that produce this chemical and at facilities that produce styrene-butadiene rubber have been measured at levels higher than those that cause cancer in animals. Furthermore, epidemiology studies have consistently revealed associations between occupational exposure to 1,3-butadiene and excess mortality due to lymphatic and hematopoietic cancers. In response to the carcinogenicity findings for 1,3-butadiene in animals and in humans, the Occupational Safety and Health Administration has proposed lowering the occupational exposure standard for this chemical from 1000 ppm to 2 ppm. Future work is needed to understand the mechanisms of tumor induction by 1,3-butadiene; however, the pursuit of this research should not delay the reduction of human exposure to this chemical. JF - Environmental health perspectives AU - Melnick, R L AU - Shackelford, C C AU - Huff, J AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 227 EP - 236 VL - 100 SN - 0091-6765, 0091-6765 KW - Air Pollutants, Occupational KW - 0 KW - Butadienes KW - Carcinogens, Environmental KW - 1,3-butadiene KW - JSD5FGP5VD KW - Index Medicus KW - Rats KW - Animals KW - Dose-Response Relationship, Drug KW - Risk Factors KW - Humans KW - Mice KW - Female KW - Carcinogens, Environmental -- adverse effects KW - Butadienes -- toxicity KW - Air Pollutants, Occupational -- adverse effects KW - Butadienes -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75903365?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Carcinogenicity+of+1%2C3-butadiene.&rft.au=Melnick%2C+R+L%3BShackelford%2C+C+C%3BHuff%2C+J&rft.aulast=Melnick&rft.aufirst=R&rft.date=1993-04-01&rft.volume=100&rft.issue=&rft.spage=227&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-22 N1 - Date created - 1993-09-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Natl Cancer Inst. 1966 Dec;37(6):825-38 [5955045] J Occup Med. 1987 Aug;29(8):675-80 [3655951] Mutat Res. 1979 Apr;66(4):367-71 [379632] Toxicol Lett. 1980 Aug;6(3):125-30 [6996220] Xenobiotica. 1982 Feb;12(2):137-44 [7090423] Scand J Work Environ Health. 1982 Dec;8(4):250-9 [7170621] J Cancer Res Clin Oncol. 1983;106(2):112-6 [6630281] Am J Ind Med. 1987;12(3):311-29 [3674024] Virology. 1987 Dec;161(2):457-62 [2825417] Arch Toxicol. 1987;61(1):7-11 [3439877] Biometrics. 1988 Jun;44(2):417-31 [3390507] Fundam Appl Toxicol. 1989 May;12(4):731-7 [2744275] Arch Toxicol Suppl. 1989;13:246-9 [2774939] Toxicol Appl Pharmacol. 1989 Oct;101(1):170-6 [2552616] Cancer Res. 1990 Aug 1;50(15):4818-23 [2196119] Environ Health Perspect. 1990 Jun;86:107-17 [2401250] Environ Health Perspect. 1990 Jun;86:11-8 [2401251] Environ Health Perspect. 1990 Jun;86:119-28 [2401252] Environ Health Perspect. 1990 Jun;86:129-34 [2401253] Environ Health Perspect. 1990 Jun;86:135-41 [2205483] Environ Health Perspect. 1990 Jun;86:49-55 [2169411] Environ Health Perspect. 1990 Jun;86:9-10 [2401277] Cancer Res. 1990 Oct 15;50(20):6592-9 [2208121] Rev Environ Contam Toxicol. 1992;124:111-44 [1732994] J Natl Cancer Inst. 1963 Jul;31:41-55 [14043038] Science. 1985 Feb 1;227(4686):548-9 [3966163] Arch Toxicol. 1984 Oct;55(4):213-8 [6517696] Arch Toxicol. 1984 Oct;55(4):219-23 [6517697] Toxicol Lett. 1986 Feb;30(2):131-6 [3705101] Arch Toxicol. 1986 Apr;58(4):235-8 [3718226] Cancer Res. 1986 Sep;46(9):4372-8 [3731095] Am Ind Hyg Assoc J. 1987 May;48(5):407-13 [3591659] Science. 1987 Sep 11;237(4820):1309-16 [3629242] Biochem Biophys Res Commun. 1978 Jan 30;80(2):298-305 [341894] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Advances in mechanisms of activation and deactivation of environmental chemicals. AN - 75902992; 8354165 AB - Environmental chemicals are both activated and detoxified by phase I and phase II enzymes. The principal enzymes involved in phase I reactions are the cytochrome P-450s. The phase II enzymes include hydrolase and the conjugative enzymes such as glucuronyltransferases, glutathione transferases, N-acetyltransferase, and sulfotransferase. Although other phase I and phase II enzymes exist, the present review is limited to these enzymes. Once thought to be a single enzyme, multiple cytochrome P-450 enzymes have been purified and characterized from many different species across the evolutionary tree. The application of molecular biology techniques to this field has identified more than 150 cytochrome P-450 genes to date. At least 20-30 cytochrome P-450 enzymes appear to exist in each mammalian species, and many polymorphisms in these enzymes are being identified. The cytochrome P-450 enzymes can now be expressed in recombinant form using cDNA expression systems. The phase II conjugative enzymes add a hydrophilic moiety such as sulfate, glucuronide, or acetate to compounds, which increases their water solubility and facilitates their excretion. However, conjugates of a number of compounds also result in more reactive electrophilic species, which appear to be the ultimate carcinogens. Many of these phase II enzymes also represent families of enzymes, and polymorphisms can affect the ability of these enzymes to metabolize chemicals. Whenever possible, we have reviewed knowledge of the human enzymes involved in particular pathways. JF - Environmental health perspectives AU - Goldstein, J A AU - Faletto, M B AD - Laboratory of Environmental Risk Analysis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 169 EP - 176 VL - 100 SN - 0091-6765, 0091-6765 KW - Environmental Pollutants KW - 0 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Molecular Structure KW - Cell Membrane -- enzymology KW - Humans KW - Cytosol -- enzymology KW - Cytochrome P-450 Enzyme System -- metabolism KW - Environmental Pollutants -- metabolism KW - Inactivation, Metabolic KW - Environmental Pollutants -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75902992?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Advances+in+mechanisms+of+activation+and+deactivation+of+environmental+chemicals.&rft.au=Goldstein%2C+J+A%3BFaletto%2C+M+B&rft.aulast=Goldstein&rft.aufirst=J&rft.date=1993-04-01&rft.volume=100&rft.issue=&rft.spage=169&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-22 N1 - Date created - 1993-09-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Pharmacol Rev. 1979 Dec;31(4):277-95 [399809] Science. 1965 Jan 22;147(3656):400-2 [14221486] Lancet. 1982 Oct 16;2(8303):842-5 [6126711] Nature. 1984 Nov 8-14;312(5990):169-70 [6504125] Carcinogenesis. 1985 Feb;6(2):199-201 [3971485] Carcinogenesis. 1985 Feb;6(2):219-23 [3971488] Cancer Res. 1987 Mar 1;47(5):1466-9 [3815349] Xenobiotica. 1988 Jan;18(1):29-39 [3354230] Cancer Res. 1988 Aug 15;48(16):4695-700 [3135117] Pharmacol Rev. 1988 Dec;40(4):243-88 [3072575] Cancer Res. 1989 Jun 15;49(12):3218-28 [2655891] Nature. 1989 Jun 22;339(6226):632-4 [2733794] Proc Natl Acad Sci U S A. 1989 Oct;86(20):7696-700 [2813353] Carcinogenesis. 1990 Jan;11(1):33-6 [2295125] Br J Clin Pharmacol. 1990 Jan;29(1):101-9 [2153391] Pharmacol Ther. 1990;45(2):153-239 [2405436] Cancer Res. 1990 Jun 1;50(11):3367-76 [2334931] Am J Hum Genet. 1990 Dec;47(6):994-1001 [1978565] DNA Cell Biol. 1991 Jan-Feb;10(1):1-14 [1991046] Mol Pharmacol. 1991 Feb;39(2):184-91 [1996083] Chem Res Toxicol. 1991 Jul-Aug;4(4):391-407 [1912325] Carcinogenesis. 1991 Oct;12(10):1839-45 [1934265] Pharmacol Rev. 1966 Mar;18(1):805-38 [5325210] Biochem Biophys Res Commun. 1966 Sep 8;24(5):668-74 [5970499] Pharmacol Rev. 1967 Sep;19(3):317-66 [4383307] J Biol Chem. 1968 Mar 25;243(6):1331-2 [4385007] Cancer Res. 1976 Sep;36(9 pt.1):3358-66 [788899] Chem Res Toxicol. 1991 Mar-Apr;4(2):168-79 [1664256] Arch Biochem Biophys. 1958 Jun;75(2):376-86 [13534720] Nature. 1959 Aug 1;184(Suppl 6):363-4 [13811548] J Biol Chem. 1962 Apr;237:1375-6 [14482007] Biochem Z. 1963;338:741-55 [14087340] J Biol Chem. 1964 Jul;239:2370-8 [14209971] J Biol Chem. 1964 Jul;239:2379-85 [14209972] Cancer. 1981 May 15;47(10):2327-45 [7272889] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Chemical agents and the immune response. AN - 75900085; 8354170 AB - Our desire to understand the potential adverse human health effects of environmental chemical exposure has coincided with an increased understanding of the immune system and an appreciation of its complex regulatory network. This has spawned a broad interest in the area of immunotoxicology within the scientific community as well as certain concerns in the public sector regarding chemical-induced hypersensitivity and immunosuppression. The incidence of alleged human sensitization to chemicals has increased, in part, due to the fact that chemical companies are moving to larger and/or different markets. It has been estimated that 35 million Americans suffer from allergic disease, of which 2-5% are from occupational exposure. Although there is not yet a clear understanding of dose-response relationships or disease predisposition, there are many well-defined examples (isocyanates, anhydrides) of chemical sensitizers in humans and experimental animals. Evidence that chemicals suppress immune responses in humans is considerably less well established, although there is a public perception that chemicals generally cause immunosuppression. This perception has been fueled by highly publicized legal cases and scientific controversies within the academic and industrial communities. As a consequence of these public and scientific concerns, many of the regulatory agencies are developing immunotoxicity testing guidelines. At the present, however, there are limitations on adequate human methodology and data that allow the extrapolation of animal data to assess human risk. The potential for human immunosuppression remains of concern, however, because of a large database generated from animal studies that demonstrates immunosuppression as well as reports of immunosuppression in humans inadvertently (e.g., halogenated aromatic hydrocarbons) or occupationally (asbestos, benzene) exposed to xenobiotics.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Environmental health perspectives AU - Luster, M I AU - Rosenthal, G J AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 219 EP - 226 VL - 100 SN - 0091-6765, 0091-6765 KW - Aerosols KW - 0 KW - Biological Factors KW - Environmental Pollutants KW - Index Medicus KW - AIDS/HIV KW - Humans KW - Autoimmunity -- drug effects KW - Acquired Immunodeficiency Syndrome -- drug therapy KW - Antibody Formation -- drug effects KW - Biological Factors -- adverse effects KW - Drug-Related Side Effects and Adverse Reactions KW - Immunity -- drug effects KW - Environmental Pollutants -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75900085?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Chemical+agents+and+the+immune+response.&rft.au=Luster%2C+M+I%3BRosenthal%2C+G+J&rft.aulast=Luster&rft.aufirst=M&rft.date=1993-04-01&rft.volume=100&rft.issue=&rft.spage=219&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-22 N1 - Date created - 1993-09-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Invest Dermatol. 1991 Jun;96(6):864-70 [1828476] J Invest Dermatol. 1959 Mar;32(3):445-50 [13641822] Cytokine. 1990 Jan;2(1):68-75 [2104215] Environ Res. 1978 Jul;16(1-3):92-100 [98327] J Immunol. 1982 May;128(5):2147-52 [6801132] Am J Clin Pathol. 1982 Apr;77(4):409-13 [7041618] Annu Rev Pharmacol Toxicol. 1986;26:547-65 [3521463] J Interferon Res. 1986 Apr;6(2):143-52 [2425014] Toxicol Ind Health. 1988 Sep;4(3):391-5 [3176044] Cell Immunol. 1988 Dec;117(2):289-302 [2973843] Int J Immunopharmacol. 1989;11(2):199-206 [2495254] Radiology. 1989 Jul;172(1):259-65 [2544923] Toxicol Appl Pharmacol. 1989 Nov;101(2):328-39 [2554533] Immunopharmacol Immunotoxicol. 1989;11(2-3):421-43 [2621324] Med Clin North Am. 1990 Mar;74(2):425-40 [2181213] Regul Toxicol Pharmacol. 1990 Feb;11(1):81-9 [2184468] Drugs. 1990 May;39(5):741-56 [2191850] Fundam Appl Toxicol. 1990 May;14(4):666-75 [2361570] J Natl Cancer Inst. 1990 Sep 5;82(17):1392-6 [2201784] J Neurol. 1990 Jul;237(4):247-50 [2391547] Toxicol Appl Pharmacol. 1990 Sep 15;105(3):492-502 [2237921] Lancet. 1991 Jan 26;337(8735):211-4 [1670850] Toxicol Appl Pharmacol. 1991 Mar 1;107(3):555-61 [2000641] Fundam Appl Toxicol. 1991 Jul;17(1):159-76 [1655546] J Immunol. 1991 Oct 1;147(7):2116-21 [1833452] Immunopharmacol Immunotoxicol. 1991;13(3):237-50 [1719060] Arch Environ Health. 1991 Sep-Oct;46(5):262-70 [1953033] J Invest Dermatol. 1991 Sep;97(3):478-82 [1678766] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Fertility, reproduction, and genetic disease: studies on the mutagenic effects of environmental agents on mammalian germ cells. AN - 75899917; 8354176 AB - Because genetically based diseases have a major impact on human health, the National Institute of Environmental Health Sciences (NIEHS) has conducted a research and testing program for more than a decade to address chemical induction of heritable genetic damage in the germ cells of mammals. Although most genetic disease results from preexisting mutations, a portion is due to the occurrence of new mutations. The supposition that exposure to mutagenic chemicals contributes to the occurrence of new mutations in the human population is strongly supported by the results from animal models. Such studies clearly demonstrate the potential of environmental chemicals to induce mutations in both somatic and reproductive cells of mammals. This NIEHS program has become a leader in the identification of genetic hazards in the environment and in the acquisition of animal model data used by regulatory agencies in assessing genetic risks to human health. JF - Environmental health perspectives AU - Shelby, M D AU - Bishop, J B AU - Mason, J M AU - Tindall, K R AD - Environmental Carcinogenesis and Mutagenesis Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 283 EP - 291 VL - 100 SN - 0091-6765, 0091-6765 KW - Environmental Pollutants KW - 0 KW - Mutagens KW - Index Medicus KW - Animals KW - Mammals KW - Humans KW - Mice KW - Forecasting KW - Reproduction -- drug effects KW - Germ Cells -- drug effects KW - Genetic Diseases, Inborn -- chemically induced KW - Environmental Pollutants -- adverse effects KW - Fertility -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75899917?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Fertility%2C+reproduction%2C+and+genetic+disease%3A+studies+on+the+mutagenic+effects+of+environmental+agents+on+mammalian+germ+cells.&rft.au=Shelby%2C+M+D%3BBishop%2C+J+B%3BMason%2C+J+M%3BTindall%2C+K+R&rft.aulast=Shelby&rft.aufirst=M&rft.date=1993-04-01&rft.volume=100&rft.issue=&rft.spage=283&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-22 N1 - Date created - 1993-09-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1989 Oct;86(20):7971-5 [2530578] Mutat Res. 1992 Jul;282(3):151-8 [1378547] Biochim Biophys Acta. 1990 Jun 1;1032(1):1-17 [2194566] Ann Hum Genet. 1967 Aug;31(1):1-20 [6056557] Mutat Res. 1975 Dec;33(2-3):239-50 [175269] Am J Med Genet. 1978;1(4):417-36 [665727] Science. 1981 May 22;212(4497):888-93 [7233180] J Med Genet. 1981 Apr;18(2):99-100 [7241541] Mutat Res. 1983 Apr;114(3):389-423 [6220220] Mutat Res. 1983 Aug;115(3):255-91 [6346080] Cell. 1983 Oct;34(3):1043-52 [6313205] Mutat Res. 1984 Nov;129(2):235-41 [6504062] Mutat Res. 1984 Dec;129(3):381-8 [6513965] Mutat Res. 1985 May-Jun;143(1-2):51-3 [2987686] Am J Med Genet. 1985 Jun;21(2):231-42 [4014310] Am J Med Genet. 1985 Jun;21(2):243-55 [4014311] Environ Mutagen. 1986;8(1):1-7 [3943495] Mutat Res. 1986 Jun;170(3):161-6 [3713725] J Biol Chem. 1986 Sep 15;261(26):12368-74 [3017971] Environ Mutagen. 1986;8(6):867-72 [3780618] Mutat Res. 1987 Jan;176(1):47-52 [3796658] Mutat Res. 1987 Feb;176(2):269-74 [3807937] Environ Mutagen. 1987;9(4):363-8 [3582296] Mutat Res. 1987 Aug;188(4):335-42 [3614250] Hum Genet. 1987 Nov;77(3):241-5 [3479387] Proc Natl Acad Sci U S A. 1988 Mar;85(6):1962-6 [3126501] Am J Hum Genet. 1988 May;42(5):677-93 [3358420] Mutat Res. 1988 May;199(1):175-81 [3362157] N Engl J Med. 1988 Jul 28;319(4):189-94 [3393170] Nature. 1988 Sep 29;335(6189):414-7 [3419517] Mutat Res. 1988 Nov;196(3):259-92 [3059177] N Engl J Med. 1989 Jan 5;320(1):19-23 [2909875] Mutat Res. 1989 Feb;210(2):313-22 [2911257] Mutat Res. 1989 Feb;210(2):337-44 [2911260] Mutat Res. 1989 May;226(1):61-4 [2716770] Proc Natl Acad Sci U S A. 1989 May;86(10):3704-8 [2726748] Mutat Res. 1989 Jun;212(2):241-52 [2499779] Mutat Res. 1990 Jun;230(2):205-17 [2374557] Environ Mol Mutagen. 1990;16(2):126-31 [2209562] Mutat Res. 1991 Jan;246(1):31-43 [1986266] Mutat Res. 1991 Feb;262(2):101-7 [2000095] Proc Natl Acad Sci U S A. 1991 Sep 15;88(18):7958-62 [1832771] Mutat Res. 1991 Sep-Oct;250(1-2):431-7 [1944356] Mutat Res. 1991 Sep-Oct;250(1-2):439-46 [1944357] Environ Mol Mutagen. 1991;18(4):303-6 [1748095] Fundam Appl Toxicol. 1992 Feb;18(2):189-92 [1601219] Mutat Res. 1992 Jun;282(2):127-33 [1377351] Mutat Res. 1990 Apr;229(2):161-72 [2320028] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Asbestos-induced lung disease. AN - 75899856; 8354168 AB - This review attempts to deal with two major questions concerning asbestos-induced lung disease: How does inhaled asbestos cause cell proliferation and fibrosis? and Will there continue to be risk from exposure to asbestos in schools and public buildings? The first is a scientific question that has spawned many interesting new experiments over the past 10 years, and there appear to be two hypothetical schemes which could explain, at least in part, the fibroproliferative effects of asbestos fibers. One supports the view that toxic oxygen radicals generated on fiber surfaces and/or intracellularly are the central mediators of disease. The second hypothesis is not mutually exclusive of the first, but, in my opinion, may be integral to it, i.e., the cellular injury induced by oxygen radicals stimulates the elaboration of multiple varieties of growth factors and cytokines that mediate the pathogenesis of asbestosis. There is increasing evidence that molecules such as platelet-derived growth factor and transforming growth factor beta, both synthesized and secreted by activated lung macrophages, are responsible, respectively, for the increased interstitial cell populations and extracellular matrix proteins that are the hallmarks of asbestos-induced fibrosis. The challenge today is to establish which combinations of the many factors released actually are playing a role in disease pathogenesis. The issue of continued risk currently is more a question of policy and perception than science because a sufficient database has not yet been established to allow full knowledge of the circumstances under which asbestos in buildings constitutes an ongoing health hazard. The litigious nature of this question does not help its resolution. In as much as public policy statements and risk assessment are not within my purview, I have focused on the state-of-the-art of asbestos as a complete carcinogen. It appears to be generally nongenotoxic, but all asbestos fiber types can induce chromosomal mutations and aneuploidy, perhaps through their ability to disrupt normal chromosome segregation. JF - Environmental health perspectives AU - Brody, A R AD - Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 21 EP - 30 VL - 100 SN - 0091-6765, 0091-6765 KW - Asbestos KW - 1332-21-4 KW - Index Medicus KW - Schools KW - Risk Factors KW - Humans KW - Cell Division -- physiology KW - Lung Diseases -- etiology KW - Pulmonary Fibrosis -- etiology KW - Environmental Exposure KW - Asbestos -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75899856?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Asbestos-induced+lung+disease.&rft.au=Brody%2C+A+R&rft.aulast=Brody&rft.aufirst=A&rft.date=1993-04-01&rft.volume=100&rft.issue=&rft.spage=21&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-22 N1 - Date created - 1993-09-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Res. 1991 Sep 15;51(18):4942-7 [1893384] Environ Res. 1992 Jun;58(1):97-116 [1317793] Am Rev Respir Dis. 1989 May;139(5):1265-73 [2540689] J Biol Chem. 1989 May 25;264(15):8771-8 [2542288] Am J Ind Med. 1989;15(5):511-6 [2741957] Br J Cancer. 1974 Mar;29(3):252-69 [4364384] Br J Exp Pathol. 1976 Oct;57(5):505-14 [1036714] Am Rev Respir Dis. 1981 Jun;123(6):670-9 [6267971] N Engl J Med. 1982 Jun 17;306(24):1446-55 [7043267] N Engl J Med. 1982 Jun 17;306(24):1480-2 [7078593] Am J Pathol. 1982 Oct;109(1):107-14 [7124904] Arch Pathol Lab Med. 1982 Oct 8;106(11):544-96 [6897166] Am J Pathol. 1983 Sep;112(3):326-37 [6311019] Lab Invest. 1983 Oct;49(4):468-75 [6312192] Am Rev Respir Dis. 1983 Oct;128(4):724-9 [6625350] Arch Biochem Biophys. 1984 Jan;228(1):373-6 [6320737] Cancer Res. 1984 May;44(5):2170-80 [6324999] Cancer Res. 1984 Nov;44(11):5017-22 [6091868] Exp Lung Res. 1984;7(2):133-47 [6098439] Carcinogenesis. 1985 Mar;6(3):473-5 [3978760] Proc Natl Acad Sci U S A. 1985 Jun;82(11):3884-8 [2987952] Inflammation. 1985 Jun;9(2):139-47 [2989174] Lab Invest. 1985 Sep;53(3):320-7 [3928965] Ann Occup Hyg. 1985;29(3):357-63 [4073703] Cell. 1985 Nov;43(1):277-86 [2416458] Cancer Genet Cytogenet. 1986 Feb 15;20(3-4):191-201 [3943062] Lab Invest. 1986 Feb;54(2):204-12 [3945053] Mutat Res. 1986 Mar;169(3):141-8 [3005853] Cancer Genet Cytogenet. 1986 Jul;22(3):225-37 [3708554] Cell. 1986 Jul 18;46(2):155-69 [3013421] Am Rev Respir Dis. 1986 Jul;134(1):128-33 [3729150] Cancer Res. 1986 Nov;46(11):5795-802 [3756923] J Clin Invest. 1987 Feb;79(2):319-26 [3543052] Cancer Res. 1987 Mar 15;47(6):1681-6 [3028612] Hereditas. 1986;105(2):233-9 [3818338] Am Rev Respir Dis. 1987 Jun;135(6):1345-52 [3592407] FASEB J. 1988 Apr;2(7):2272-7 [3280379] Am J Pathol. 1988 Apr;131(1):156-70 [2833103] Science. 1988 Jun 10;240(4858):1529-31 [2836952] J Cell Physiol. 1988 Oct;137(1):45-54 [2844836] J Clin Invest. 1988 Nov;82(5):1685-93 [3183063] Am J Pathol. 1989 Jan;134(1):133-40 [2913821] Am J Ind Med. 1988;14(6):635-41 [3232683] Environ Health Perspect. 1989 May;81:81-9 [2667990] Toxicol Appl Pharmacol. 1989 Aug;100(1):132-44 [2548304] Am Rev Respir Dis. 1989 Oct;140(4):1075-81 [2529800] Biochem J. 1989 Oct 15;263(2):539-45 [2556998] Science. 1990 Jan 19;247(4940):294-301 [2153315] Am J Respir Cell Mol Biol. 1989 Sep;1(3):231-5 [2624762] Am Rev Respir Dis. 1990 Mar;141(3):765-88 [2155556] Am J Pathol. 1990 Mar;136(3):695-705 [2156434] Am Rev Respir Dis. 1990 May;141(5 Pt 1):1266-71 [2160214] Eur J Cell Biol. 1990 Apr;51(2):327-34 [2190835] Science. 1990 Aug 31;249(4972):1007-11 [2204108] Am J Respir Cell Mol Biol. 1991 Dec;5(6):539-47 [1958381] Exp Lung Res. 1991 Nov-Dec;17(6):1011-24 [1663030] J Clin Invest. 1990 Oct;86(4):1055-64 [2170444] Proc Natl Acad Sci U S A. 1990 Oct;87(19):7385-9 [2170975] Chest. 1991 Jan;99(1):191-8 [1984952] CMAJ. 1991 Mar 1;144(5):554-6 [1998901] In Vitro Cell Dev Biol. 1990 Dec;26(12):1135-43 [1706697] Am J Respir Cell Mol Biol. 1991 May;4(5):397-407 [1850605] Toxicol Ind Health. 1990 Dec;6(6):629-36 [2097821] Environ Res. 1991 Jun;55(1):97-106 [1855494] Comment In: Environ Health Perspect. 1993 Dec;101(7):564-5 [8143579] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Mechanisms of multistep carcinogenesis and carcinogen risk assessment. AN - 75899078; 8354184 AB - Many different types of chemical exposures can increase the incidence of tumors in animals and humans, but usually a long period of time is required before the carcinogenic risk of an exposure is manifested. Both of these observations can be explained by a multistep/multigene model of carcinogenesis. In this model, a normal cell evolves into a cancer cell as the result of heritable changes in multiple, independent genes. The two-stage model of initiation and promotion for chemical carcinogenesis has provided a paradigm by which chemicals can act by qualitatively different mechanisms, but the process of carcinogenesis is now recognized as more complex than simply initiation and promotion. Even a three-stage model of initiation, promotion, and progression, which can be operationally defined, is not adequate to describe the carcinogenic process. The number of genes altered in a cancer cell compared to a normal cell is not known; recent evidence suggests that 3-10 genetic events are involved in common adult malignancies in humans. Two distinct classes of genes, protooncogenes and tumor-suppressor genes, are involved in the cancer process. Multiple oncogenes may be activated in a tumor, while multiple tumor-suppressor genes may be inactivated. Identification of the genes involved in carcinogenesis and elucidation of the mechanisms of their activation or inactivation allows a better understanding of how chemical carcinogens influence the process of neoplastic evolution. The findings of multiple genetic changes (including point mutations, chromosomal translocations, deletions, gene amplification, and numerical chromosome changes) in activated protooncogenes and inactivated tumor-suppressor genes provide experimental support for Boveri's somatic mutation theory of carcinogenesis. In addition to mutagenic mechanisms, chemicals may heritably alter cells by epigenetic mechanisms and enhance the clonal expansion of altered cells. Most chemical carcinogens operate via a combination of mechanisms, and even their primary mechanism of action may vary depending on the target tissues. The classification of chemicals by mechanism of action or by nongenotoxic or genotoxic activity has certain inherent difficulties because no classification of chemicals is exhaustive or definitive. JF - Environmental health perspectives AU - Barrett, J C AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 9 EP - 20 VL - 100 SN - 0091-6765, 0091-6765 KW - Estrogens KW - 0 KW - Asbestos KW - 1332-21-4 KW - Index Medicus KW - Animals KW - Risk Factors KW - Humans KW - Cell Division -- drug effects KW - Asbestos -- adverse effects KW - Estrogens -- adverse effects KW - Mutagenesis KW - Neoplasms -- chemically induced KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75899078?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Mechanisms+of+multistep+carcinogenesis+and+carcinogen+risk+assessment.&rft.au=Barrett%2C+J+C&rft.aulast=Barrett&rft.aufirst=J&rft.date=1993-04-01&rft.volume=100&rft.issue=&rft.spage=9&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-22 N1 - Date created - 1993-09-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Science. 1989 Apr 14;244(4901):207-11 [2565047] Carcinogenesis. 1989 May;10(5):847-50 [2565171] IARC Sci Publ. 1989;(90):54-73 [2663719] Environ Health Perspect. 1989 May;81:81-9 [2667990] Environ Health Perspect. 1989 May;81:91-4 [2667992] Cancer Res. 1989 Oct 15;49(20):5489-96 [2676144] Environ Health Perspect. 1989 Jul;82:125-63 [2676495] J Natl Cancer Inst. 1989 Dec 6;81(23):1780-6 [2685334] Science. 1990 Feb 9;247(4943):707-10 [2300822] Pharmacol Ther. 1990;46(3):469-86 [2188272] Cell. 1990 Jun 1;61(5):759-67 [2188735] Mutat Res. 1990 Jun-Aug;234(3-4):257-61 [2366790] Cancer Res. 1990 Dec 1;50(23):7415-21 [2174724] Ren Fail. 1991;13(4):211-25 [1780490] Am J Ind Med. 1992;21(2):253-73 [1536158] Regul Toxicol Pharmacol. 1992 Oct;16(2):111-25 [1279759] Cancer Res. 1950 Nov;10(11):713-7 [14783769] Arch Environ Health. 1963 Dec;7:668-74 [14077213] Science. 1989 May 12;244(4905):707-12 [2470152] Cancer Res. 1989 Jul 15;49(14):3713-21 [2660980] Mutat Res. 1989 Jun;223(2):73-103 [2662004] Proc Natl Acad Sci U S A. 1989 Jul;86(13):5099-103 [2567993] Cancer Res. 1984 May;44(5):2170-80 [6324999] Science. 1984 Jun 8;224(4653):1121-4 [6719137] Environ Res. 1984 Aug;34(2):227-41 [6086305] CRC Crit Rev Toxicol. 1974 Jan;2(4):419-43 [4822436] N Engl J Med. 1975 Feb 13;292(7):334-9 [1117962] Natl Cancer Inst Monogr. 1979 May;(51):239-50 [384263] Natl Cancer Inst Monogr. 1979 May;(51):41-56 [384264] J Natl Cancer Inst. 1980 Sep;65(3):627-30 [6774154] IARC Sci Publ. 1980;(27):243-55 [6449480] Science. 1981 Jun 19;212(4501):1402-4 [6262919] Science. 1981 Oct 23;214(4519):401-7 [7291981] J Supramol Struct Cell Biochem. 1981;17(2):133-46 [7033553] Carcinogenesis. 1981;2(12):1375-9 [7326837] Cancer Res. 1982 Aug;42(8):3040-5 [6284354] Carcinogenesis. 1982;3(8):895-8 [6812976] Cancer Res. 1983 May;43(5):2034-41 [6403231] J Natl Cancer Inst. 1983 Mar;70(3):455-63 [6572736] Mol Pharmacol. 1983 Mar;23(2):278-81 [6682170] Cancer Res. 1983 Aug;43(8):3814-21 [6861146] Nature. 1983 Jul 7-13;304(5921):67-9 [6866091] Environ Health Perspect. 1983 Apr;50:309-20 [6873021] Cancer Lett. 1983 Dec;21(2):141-7 [6652618] Cancer Res. 1984 Jan;44(1):184-9 [6317168] Proc Natl Acad Sci U S A. 1984 Aug;81(15):4940-4 [6589638] Mutat Res. 1984 Aug;140(4):205-7 [6472331] Pharmacol Rev. 1984 Jun;36(2 Suppl):53S-70S [6473503] Cancer Res. 1984 Nov;44(11):5017-22 [6091868] Gan. 1984 Dec;75(12):1046-8 [6526218] Carcinogenesis. 1985 Mar;6(3):473-5 [3978760] Nature. 1985 May 30-Jun 5;315(6018):382-5 [3923365] Carcinogenesis. 1985 Jun;6(6):865-71 [4006072] Carcinogenesis. 1985 Oct;6(10):1421-6 [3840060] Carcinog Compr Surv. 1985;9:123-37 [4053069] Carcinogenesis. 1985 Nov;6(11):1607-10 [2414025] Science. 1985 Nov 15;230(4727):770-6 [2997917] Environ Mutagen. 1986;8(1):129-59 [3510860] Cancer Res. 1986 Apr;46(4 Pt 2):2088-95 [3948182] Cancer Lett. 1986 Mar;30(3):269-74 [2870794] Cancer Res. 1986 Jun;46(6):2863-5 [3084079] Cancer Genet Cytogenet. 1986 Jul;22(3):225-37 [3708554] Nature. 1986 Jul 3-9;322(6074):78-80 [3014349] Proc Natl Acad Sci U S A. 1986 Aug;83(16):5825-9 [3016723] Carcinogenesis. 1986 Nov;7(11):1845-8 [3769132] Science. 1987 Jan 9;235(4785):177-82 [3798106] Science. 1987 Jan 16;235(4786):305-11 [3541204] Proc Natl Acad Sci U S A. 1987 Apr;84(7):2029-32 [3104907] Science. 1987 Sep 11;237(4820):1309-16 [3629242] Mutat Res. 1988 Jan;204(1):3-15 [3277048] Environ Health Perspect. 1987 Dec;76:65-70 [3447905] Science. 1988 Jul 1;241(4861):79-81 [3388020] N Engl J Med. 1988 Sep 1;319(9):525-32 [2841597] Proc Natl Acad Sci U S A. 1988 Sep;85(17):6389-93 [2457913] Carcinogenesis. 1988 Nov;9(11):2045-52 [3052903] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Chemicals and cancer in humans: first evidence in experimental animals. AN - 75898455; 8354167 AB - Certain human diseases have been traced to exposure to environmental and occupational chemicals. In many instances the first evidence of potential adverse effects came from experimental studies and were subsequently discovered in humans. Associations of human cancers, as a diverse group of diseases, and chemicals have been made since the middle 1700s. Since then, nearly 100 chemicals, mixtures of chemicals, or exposure circumstances are now recognized as being or strongly implicated as being carcinogenic to humans. Of the less than 1000 agents evaluated adequately for carcinogenicity in laboratory animals, a varying spectrum of data from studies on humans are available for only about 20-25%. So far, more than 60 agents are linked unequivocally as causing cancer in humans, and another 50 or so are strongly suspected of being carcinogenic to humans. Not all of these have been or can be evaluated in animals because some are industrial processes or "occupations," some are environmental and cultural risk factors, and some are mixtures of agents. For those that can be studied experimentally, the qualitative concordance between humans and animals approaches unity, and in every case there is at least one common organ site of cancer in both species. The evidence of carcinogenicity in experimental animals preceded that observed in humans for nearly 30 agents and is the subject of this paper. JF - Environmental health perspectives AU - Huff, J AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 201 EP - 210 VL - 100 SN - 0091-6765, 0091-6765 KW - Carcinogens, Environmental KW - 0 KW - Index Medicus KW - Animals KW - Environmental Health KW - Humans KW - Disease Models, Animal KW - Occupational Diseases -- chemically induced KW - Carcinogens, Environmental -- adverse effects KW - Neoplasms, Experimental -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75898455?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Chemicals+and+cancer+in+humans%3A+first+evidence+in+experimental+animals.&rft.au=Huff%2C+J&rft.aulast=Huff&rft.aufirst=J&rft.date=1993-04-01&rft.volume=100&rft.issue=&rft.spage=201&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-22 N1 - Date created - 1993-09-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Scand J Work Environ Health. 1992;18 Suppl 1:83-9 [1411384] Environ Health Perspect. 1993 Apr;100:189-200 [8394802] Environ Health Perspect. 1993 Apr;100:227-36 [8354171] Environ Health Perspect. 1993 Apr;100:39-44 [8354180] Environ Health Perspect. 1993 Apr;100:9-20 [8354184] Environ Health Perspect. 1990 Jun;86:107-17 [2401250] Environ Health Perspect. 1990 Jun;86:119-28 [2401252] Epidemiology. 1990 Sep;1(5):349-56 [2078610] Am J Public Health. 1991 Jun;81(6):791-800 [2029056] Scand J Work Environ Health. 1991 Feb;17(1):7-19 [2047810] Environ Health Perspect. 1991 Jan;90:127-32 [2050050] Cell Biol Toxicol. 1991 Jan;7(1):67-94 [2054688] Annu Rev Pharmacol Toxicol. 1991;31:621-52 [2064387] Scand J Work Environ Health. 1991 Aug;17(4):231-9 [1925434] Prog Histochem Cytochem. 1991;23(1-4):45-60 [1947167] Rev Environ Contam Toxicol. 1992;124:111-44 [1732994] Environ Health Perspect. 1991 Jun;93:247-70 [1773796] Cancer Res. 1992 Apr 15;52(8):2357-61 [1559239] Br J Ind Med. 1955 Apr;12(2):81-6 [14363586] Environ Health Perspect. 1990 Jun;86:27-36 [2401263] Cancer Res. 1990 Oct 15;50(20):6441-8 [2208102] Cancer Res. 1990 Oct 15;50(20):6592-9 [2208121] Prog Exp Tumor Res. 1969;11:222-34 [4888943] Cancer Res. 1971 May;31(5):516-22 [5582114] J Occup Med. 1974 Mar;16(3):150-1 [4856325] Med Lav. 1974 Nov-Dec;65(11-12):421-44 [4477887] Cancer Res. 1978 Apr;38(4):877-85 [346205] Environ Health Perspect. 1978 Feb;22:163-5 [648484] Annu Rev Pharmacol Toxicol. 1979;19:511-30 [378109] Environ Health Perspect. 1979 Oct;32:297-300 [120250] Ann N Y Acad Sci. 1981;363:139-44 [6942719] Environ Health Perspect. 1981 Oct;41:59-62 [6277614] J Occup Med. 1982 Oct;24(10):767-9 [7143123] Cancer Res. 1984 May;44(5):2244-50 [6370426] Ann Occup Hyg. 1984;28(3):291-305 [6508080] Int Arch Occup Environ Health. 1984;54(4):317-24 [6511101] Science. 1985 Feb 1;227(4686):548-9 [3966163] Int J Epidemiol. 1985 Mar;14(1):22-31 [3988437] Carcinogenesis. 1985 Nov;6(11):1653-65 [3902269] J Occup Med. 1985 Nov;27(11):835-40 [4067690] JAMA. 1986 Mar 28;255(12):1575-8 [3951093] JAMA. 1986 Sep 5;256(9):1141-7 [3801091] J Urol. 1986 Oct;136(4):834-6 [3020259] Carcinogenesis. 1986 Nov;7(11):1853-63 [3769134] J Natl Cancer Inst. 1987 Jan;78(1):191-3 [3467126] J Natl Cancer Inst. 1987 Feb;78(2):247-52 [3468288] Am J Ind Med. 1987;11(2):157-63 [3826078] J Occup Med. 1987 Mar;29(3):217-28 [3559766] Cancer Res. 1987 Jun 1;47(11):3012-31 [3105872] JAMA. 1987 May 1;257(17):2290 [3573228] Annu Rev Public Health. 1987;8:355-85 [3555527] Lancet. 1987 Nov 14;2(8568):1153 [2890054] J Natl Cancer Inst. 1987 Nov;79(5):911-21 [3479642] Fundam Appl Toxicol. 1987 Oct;9(3):367-79 [3319745] J Natl Cancer Inst. 1987 Dec;79(6):1269-79 [3480378] Int J Cancer. 1988 Feb 15;41(2):184-97 [3338870] Scand J Work Environ Health. 1987 Dec;13(6):493-504 [3433051] Int Arch Occup Environ Health. 1988;60(1):21-4 [3350600] Am J Public Health. 1988 May;78(5):570-1 [3354743] Ann N Y Acad Sci. 1988;534:31-8 [3291709] Ann N Y Acad Sci. 1988;534:78-83 [3291727] J Occup Med. 1988 Jun;30(6):475-6, 478, 480-1 [3392613] Cancer Metastasis Rev. 1988 Apr;7(1):5-18 [3293832] Risk Anal. 1988 Jun;8(2):205-14 [3045903] Acta Oncol. 1988;27(5):465-72 [3060154] Lancet. 1989 Apr 22;1(8643):911 [2565003] Toxicol Ind Health. 1989 Oct;5(5):699-730 [2815102] Jpn J Cancer Res. 1989 Sep;80(9):795-807 [2513295] Klin Wochenschr. 1989 Dec 4;67(23):1169-73 [2691755] Pharmacol Ther. 1990;46(3):469-86 [2188272] Am J Ind Med. 1990;17(6):683-99 [2343874] Exp Pathol. 1989;37(1-4):128-32 [2637142] Science. 1990 Aug 31;249(4972):970-1 [2136249] Scand J Work Environ Health. 1991 Aug;17(4):248-54 [1925436] J Natl Cancer Inst. 1992 May 20;84(10):764-71 [1573662] Environ Health Perspect. 1991 Dec;96:23-31 [1820269] Scand J Work Environ Health. 1992;18 Suppl 1:31-7 [1411375] Scand J Work Environ Health. 1992;18 Suppl 1:74-82 [1411383] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Developmental toxicology: status of the field and contribution of the National Toxicology Program. AN - 75880379; 8354175 AB - The NTP has conducted developmental toxicity studies on more than 50 chemicals, often in multiple species. Several chemicals caused developmental toxicity in the absence of any toxicity to the mother. Although hazard to humans is determined by the level of exposure to the chemical and its inherent toxicity, those agents that selectively disturb the development of the conceptus are of particular concern because other manifestations of toxicity would not warn the mother of overexposure. Whether the LOAEL (lowest-observed adverse effect level) for maternal toxicity was high or low did not correlate with the potential of chemicals to cause developmental toxicity. The form of developmental toxicity that determined the LOAEL most frequently was decreased body weight in mice and rats, but not rabbits, where the LOAEL was determined more often by an increase in resorptions. Several in vitro and short-term tests appear promising as screens to predict the outcome of developmental toxicity studies in mammals. However, the only screens that have undergone formal validation studies are those evaluated by the NTP. Improvements in our ability to predict risk to humans have been limited by our knowledge of the mechanisms by which agents cause developmental toxicity. Thus, future growth is dependent on a better understanding of the biological processes that regulate normal development, therein providing the necessary framework for understanding mechanisms of abnormal development. JF - Environmental health perspectives AU - Schwetz, B A AU - Harris, M W AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 269 EP - 282 VL - 100 SN - 0091-6765, 0091-6765 KW - Index Medicus KW - United States KW - Maternal-Fetal Exchange KW - Animals KW - Humans KW - Data Interpretation, Statistical KW - Forecasting KW - Abnormalities, Drug-Induced -- etiology KW - Female KW - Pregnancy KW - Embryonic and Fetal Development -- drug effects KW - Toxicology -- trends UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75880379?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Developmental+toxicology%3A+status+of+the+field+and+contribution+of+the+National+Toxicology+Program.&rft.au=Schwetz%2C+B+A%3BHarris%2C+M+W&rft.aulast=Schwetz&rft.aufirst=B&rft.date=1993-04-01&rft.volume=100&rft.issue=&rft.spage=269&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-22 N1 - Date created - 1993-09-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Toxicol Appl Pharmacol. 1985 Oct;81(1):113-27 [4049413] Neurotoxicology. 1990 Summer;11(2):189-98 [2234540] Fundam Appl Toxicol. 1987 Jan;8(1):115-26 [3556817] Fundam Appl Toxicol. 1987 May;8(4):571-82 [3609543] Fundam Appl Toxicol. 1987 Jul;9(1):173-81 [3622959] Toxicol Appl Pharmacol. 1987 Sep 15;90(2):206-16 [3629596] Rev Environ Contam Toxicol. 1988;102:1-78 [3275996] Fundam Appl Toxicol. 1988 Apr;10(3):395-412 [3371580] Teratology. 1988 Jun;37(6):539-52 [3400069] Fundam Appl Toxicol. 1991 Apr;16(3):401-13 [1855614] Fundam Appl Toxicol. 1991 May;16(4):742-8 [1884913] Environ Health Perspect. 1991 Aug;94:265-8 [1683285] Teratology. 1992 Apr;45(4):337-9 [1350114] Fundam Appl Toxicol. 1992 Feb;18(2):266-77 [1601227] Fundam Appl Toxicol. 1992 Jul;19(1):15-25 [1397797] Fundam Appl Toxicol. 1988 Nov;11(4):673-84 [3229591] Fundam Appl Toxicol. 1989 Apr;12(3):442-8 [2731659] Fundam Appl Toxicol. 1989 Nov;13(4):641-51 [2620788] Fundam Appl Toxicol. 1990 Jan;14(1):167-78 [2155147] Fundam Appl Toxicol. 1990 Apr;14(3):502-12 [2340980] Environ Health Perspect. 1990 Jun;86:79-84 [2205495] Teratology. 1990 Aug;42(2):131-6 [2171152] Fundam Appl Toxicol. 1990 Aug;15(2):350-6 [2227160] Fundam Appl Toxicol. 1986 Oct;7(3):434-43 [3781133] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - IL-1 receptor antagonist (IL-1ra) augments IL-2-induced pulmonary vascular leak. AN - 75844585; 8331927 AB - Interleukin-2 (IL-2) therapy is dose limited by a severe vascular leak with resulting systemic and pulmonary toxicity. Although recognized as a mediator of septic shock and vascular leak, the relative role of IL-1 in IL-2 toxicity is unclear. We evaluated the effect of IL-1 receptor antagonist (IL-1ra) on IL-2 lethality, pulmonary vascular leak, and treatment of pulmonary metastases in a murine model. In vivo induction of mRNA for IL-1 alpha was evaluated in liver by Northern blots after 0, 5, 8, and 11 doses of IL-2 in C3H/HEN mice. The expression index for the IL-1 alpha gene increased from 0.16 to 0.74 after 5 doses of IL-2, and further increased to 1.04 after 11 doses of IL-2. C3H/HEN mice (n = 56) were randomized to receive phosphate-buffered saline (PBS), IL-1ra high dose (HD), or IL-1ra low dose (LD) by continuous subcutaneous infusion via Alzet mini-pumps. The biologic effectiveness of the dose and administration of IL-1ra was determined by the ability to block IL-1-induced IL-6 production in vivo. Mean serum IL-6 levels 3 hr after intraperitoneal IL-1 alpha (10 micrograms/kg) were: PBS, 3730 +/- 526 (mean +/- SEM pg/ml); IL-1ra (LD), 1156 +/- 398; and IL-1ra (HD), 594 +/- 30 (P < 0.01, IL-1ra HD or LD vs PBS). Pulmonary vascular leak was measured by iv I125 albumin after 8 doses of IL-2 (100,000 U ip q 8 hr).(ABSTRACT TRUNCATED AT 250 WORDS) JF - The Journal of surgical research AU - Thom, A K AU - Fraker, D L AU - Norton, J A AD - Surgical Metabolism Section, National Cancer Institutes, National Institutes of Health, Bethesda, Maryland 20894. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 336 EP - 341 VL - 54 IS - 4 SN - 0022-4804, 0022-4804 KW - Interleukin-1 KW - 0 KW - Interleukin-2 KW - Interleukin-6 KW - RNA, Messenger KW - Receptors, Interleukin-1 KW - Index Medicus KW - Animals KW - Lung Neoplasms -- prevention & control KW - RNA, Messenger -- metabolism KW - Lung Neoplasms -- secondary KW - Interleukin-6 -- metabolism KW - Mice, Inbred C57BL KW - Mice, Inbred C3H KW - Gene Expression KW - Mice KW - Interleukin-1 -- genetics KW - Drug Synergism KW - Female KW - Interleukin-2 -- pharmacology KW - Pulmonary Circulation -- drug effects KW - Receptors, Interleukin-1 -- antagonists & inhibitors KW - Capillary Permeability -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75844585?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+surgical+research&rft.atitle=IL-1+receptor+antagonist+%28IL-1ra%29+augments+IL-2-induced+pulmonary+vascular+leak.&rft.au=Thom%2C+A+K%3BFraker%2C+D+L%3BNorton%2C+J+A&rft.aulast=Thom&rft.aufirst=A&rft.date=1993-04-01&rft.volume=54&rft.issue=4&rft.spage=336&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+surgical+research&rft.issn=00224804&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-16 N1 - Date created - 1993-08-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Interleukin-1 receptor antibody (IL-1rab) protection and treatment against lethal endotoxemia in mice. AN - 75842433; 8331925 AB - Interleukin-1 (IL-1) is a mediator of endotoxin shock and IL-1 receptor blockade has been shown to have therapeutic efficacy against endotoxic shock and sepsis in laboratory models. The current studies were designed to characterize the efficacy of a murine monoclonal IL-1 receptor antibody (IL-1rab) against endotoxin (LPS) lethality and to investigate whether combined anticytokine therapy using the IL-1rab and a highly specific polyclonal rabbit anti-mouse TNF antibody (TNF Ab) could provide additive or synergistic efficacy against LPS lethality in C57B1/6 female mice. A single intraperitoneal (ip) dose of IL-1rab, 0.1 or 0.2 mg, significantly reduced lethality from LPS, 30 to 40 mg/kg ip, compared to nonimmune IgG, 0.1 or 0.2 mg, in control mice (P2 < 0.05). Treatment with IL-1rab was effective when administered from 6 hr before to 1 hr after LPS. After LPS, circulating levels of IL-6 were significantly lower in IL-1rab-treated mice [IL-6 (ng/ml) 2 h after LPS: IgG, 100 +/- 25, IL-1rab, 41 +/- 8; 4 h after LPS: IgG, 46 +/- 13, IL-1rab, 8 +/- 1; P2 < 0.05 and 0.03, respectively]. Northern blot analysis showed that IL-1rab markedly lowered IL-6 gene expression after LPS. Combined treatment with IL-1rab and TNF Ab did not result in any improvement in survival after LPS compared to either agent alone. These results indicate that an IL-1 receptor antibody has therapeutic efficacy against LPS and significantly decreases IL-6 production.(ABSTRACT TRUNCATED AT 250 WORDS) JF - The Journal of surgical research AU - McNamara, M J AU - Norton, J A AU - Nauta, R J AU - Alexander, H R AD - Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 316 EP - 321 VL - 54 IS - 4 SN - 0022-4804, 0022-4804 KW - Antibodies KW - 0 KW - Cytokines KW - Endotoxins KW - Receptors, Interleukin-1 KW - Tumor Necrosis Factor-alpha KW - Index Medicus KW - Cytokines -- blood KW - Animals KW - Escherichia coli Infections -- therapy KW - Tumor Necrosis Factor-alpha -- immunology KW - Mice, Inbred C57BL KW - Escherichia coli Infections -- mortality KW - Mice KW - Escherichia coli Infections -- blood KW - Drug Synergism KW - Female KW - Receptors, Interleukin-1 -- immunology KW - Antibodies -- therapeutic use KW - Escherichia coli KW - Endotoxins -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75842433?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+surgical+research&rft.atitle=Interleukin-1+receptor+antibody+%28IL-1rab%29+protection+and+treatment+against+lethal+endotoxemia+in+mice.&rft.au=McNamara%2C+M+J%3BNorton%2C+J+A%3BNauta%2C+R+J%3BAlexander%2C+H+R&rft.aulast=McNamara&rft.aufirst=M&rft.date=1993-04-01&rft.volume=54&rft.issue=4&rft.spage=316&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+surgical+research&rft.issn=00224804&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-16 N1 - Date created - 1993-08-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Toxicokinetics of pentachloroanisole in F344 rats and B6C3F1 mice. AN - 75840563; 8337901 AB - 1. Toxicokinetics of pentachloroanisole (PCA) were studied in F344 rat and B6C3F1 mouse of both sexes by gavage at doses of 10, 20 and 40 mg/kg and by i.v. at 10 mg/kg. 2. PCA was rapidly demethylated to pentachlorophenol (PCP) in both rat and mouse and the resulting PCP plasma concentrations were much higher than that of parent PCA due to the much smaller apparent volume of distribution of PCP. 3. Peak plasma concentrations of PCA and PCP increased with dose in both rat and mouse. 4. Bioavailability of PCA was low in both rat and mouse and was sex independent. 5. The high plasma concentrations and relatively long biological half-life of PCP in both species after both i.v. and oral dosing with PCA indicate possible bioaccumulation of PCP upon multiple oral administrations of PCA. JF - Xenobiotica; the fate of foreign compounds in biological systems AU - Yuan, J H AU - Goehl, T J AU - Murrill, E AU - Moore, R AU - Clark, J AU - Hong, L AU - Irwin, R AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 427 EP - 438 VL - 23 IS - 4 SN - 0049-8254, 0049-8254 KW - Anisoles KW - 0 KW - pentachloroanisole KW - 14D125MH3W KW - Pentachlorophenol KW - D9BSU0SE4T KW - Index Medicus KW - Animals KW - Pentachlorophenol -- pharmacokinetics KW - Injections, Intravenous KW - Sex Characteristics KW - Intubation, Gastrointestinal KW - Mice KW - Pentachlorophenol -- blood KW - Biological Availability KW - Rats KW - Mice, Inbred Strains KW - Rats, Inbred F344 KW - Half-Life KW - Female KW - Male KW - Anisoles -- pharmacokinetics KW - Anisoles -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75840563?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Xenobiotica%3B+the+fate+of+foreign+compounds+in+biological+systems&rft.atitle=Toxicokinetics+of+pentachloroanisole+in+F344+rats+and+B6C3F1+mice.&rft.au=Yuan%2C+J+H%3BGoehl%2C+T+J%3BMurrill%2C+E%3BMoore%2C+R%3BClark%2C+J%3BHong%2C+L%3BIrwin%2C+R&rft.aulast=Yuan&rft.aufirst=J&rft.date=1993-04-01&rft.volume=23&rft.issue=4&rft.spage=427&rft.isbn=&rft.btitle=&rft.title=Xenobiotica%3B+the+fate+of+foreign+compounds+in+biological+systems&rft.issn=00498254&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-26 N1 - Date created - 1993-08-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Chlorisondamine, a non-competitive ganglionic blocker, antagonizes the cardiovascular effects of cocaine in conscious squirrel monkeys. AN - 75825502; 8100996 AB - Cocaine (0.3 mg/kg i.v.) produced prolonged pressor and tachycardiac responses in conscious squirrel monkeys. Peak pressor and tachycardiac responses following cocaine were 32.7 +/- 3.3 mm Hg and 78.8 +/- 7.4 beats/min, respectively. Pretreatment with 1 mg/kg chlorisondamine, a noncompetitive ganglionic blocker, attenuated the pressor (18.3 +/- 3.8 mm Hg) and tachycardiac (63.7 +/- 10 beats/min) effects of cocaine, while 5 mg/kg chlorisondamine completely prevented these effects of cocaine. This finding supports the conclusion that the cardiovascular effects of cocaine are centrally mediated. JF - Pharmacological research AU - Tella, S R AU - Schindler, C W AU - Goldberg, S R AD - Behavioral Pharmacology and Genetics Section, National Institute on Drug Abuse Addiction Research Center, Baltimore, MD 21224. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 233 EP - 239 VL - 27 IS - 3 SN - 1043-6618, 1043-6618 KW - Ganglionic Blockers KW - 0 KW - Hexamethonium Compounds KW - Hexamethonium KW - 3C9PSP36Z2 KW - Cocaine KW - I5Y540LHVR KW - Chlorisondamine KW - JD3M24F66I KW - Index Medicus KW - Animals KW - Heart Rate -- drug effects KW - Drug Interactions KW - Consciousness KW - Injections, Intravenous KW - Ganglionic Blockers -- pharmacology KW - Blood Pressure -- drug effects KW - Hexamethonium Compounds -- pharmacology KW - Chlorisondamine -- pharmacology KW - Saimiri -- physiology KW - Cardiovascular System -- drug effects KW - Cocaine -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75825502?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacological+research&rft.atitle=Chlorisondamine%2C+a+non-competitive+ganglionic+blocker%2C+antagonizes+the+cardiovascular+effects+of+cocaine+in+conscious+squirrel+monkeys.&rft.au=Tella%2C+S+R%3BSchindler%2C+C+W%3BGoldberg%2C+S+R&rft.aulast=Tella&rft.aufirst=S&rft.date=1993-04-01&rft.volume=27&rft.issue=3&rft.spage=233&rft.isbn=&rft.btitle=&rft.title=Pharmacological+research&rft.issn=10436618&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-12 N1 - Date created - 1993-08-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Crevice-forming mutants in the rigid core of bovine pancreatic trypsin inhibitor: crystal structures of F22A, Y23A, N43G, and F45A. AN - 75798606; 8518731 AB - Crystal structures of four mutants of bovine pancreatic trypsin inhibitor (F22A, Y23A, N43G, and F45A), engineered to alter their stability properties, have been determined. The mutated residues, which are highly conserved among Kunitz-type inhibitors, are located in the rigid core of the molecule. Replacement of the partially buried bulky residues of the wild-type protein with smaller residues resulted in crevices open to the exterior of the molecule. The overall three-dimensional structure of these mutants is very similar to that of the wild-type protein and only small rearrangements are observed among the atoms lining the crevices. JF - Protein science : a publication of the Protein Society AU - Danishefsky, A T AU - Housset, D AU - Kim, K S AU - Tao, F AU - Fuchs, J AU - Woodward, C AU - Wlodawer, A AD - Macromolecular Structure Laboratory, NCI-Frederick Cancer Research and Development Center, ABL, Basic Research Program, Maryland 21702. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 577 EP - 587 VL - 2 IS - 4 SN - 0961-8368, 0961-8368 KW - Trypsin Inhibitors KW - 0 KW - Water KW - 059QF0KO0R KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Animals KW - Protein Structure, Secondary KW - Cattle KW - X-Ray Diffraction KW - Models, Molecular KW - Pancreas KW - Water -- chemistry KW - Hydrogen Bonding KW - Trypsin Inhibitors -- chemistry KW - Trypsin Inhibitors -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75798606?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Protein+science+%3A+a+publication+of+the+Protein+Society&rft.atitle=Crevice-forming+mutants+in+the+rigid+core+of+bovine+pancreatic+trypsin+inhibitor%3A+crystal+structures+of+F22A%2C+Y23A%2C+N43G%2C+and+F45A.&rft.au=Danishefsky%2C+A+T%3BHousset%2C+D%3BKim%2C+K+S%3BTao%2C+F%3BFuchs%2C+J%3BWoodward%2C+C%3BWlodawer%2C+A&rft.aulast=Danishefsky&rft.aufirst=A&rft.date=1993-04-01&rft.volume=2&rft.issue=4&rft.spage=577&rft.isbn=&rft.btitle=&rft.title=Protein+science+%3A+a+publication+of+the+Protein+Society&rft.issn=09618368&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-23 N1 - Date created - 1993-07-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Biochemistry. 1972 Aug 1;11(16):2967-77 [5041905] Protein Sci. 1993 Apr;2(4):588-96 [7686069] Eur J Biochem. 1978 Jul 17;88(1):87-95 [27364] J Mol Biol. 1982 Sep 15;160(2):343-61 [6184480] J Mol Biol. 1984 Dec 5;180(2):301-29 [6210373] J Mol Biol. 1985 Sep 20;185(2):405-19 [2414451] Methods Enzymol. 1985;115:157-71 [3841179] Methods Enzymol. 1985;115:252-70 [3841182] J Mol Biol. 1986 Aug 20;190(4):593-604 [3097327] J Mol Biol. 1987 Jan 5;193(1):145-56 [2438420] Biochemistry. 1987 Aug 11;26(16):5163-72 [2444253] J Mol Biol. 1987 Dec 5;198(3):469-80 [2448484] Nature. 1988 Feb 11;331(6156):525-7 [2893289] Nature. 1988 Feb 11;331(6156):528-30 [2893290] Nature. 1988 Feb 11;331(6156):530-2 [2893291] J Biol Chem. 1988 May 5;263(13):6001-4 [2452157] Cold Spring Harb Symp Quant Biol. 1987;52:511-9 [2456884] Nature. 1989 Mar 9;338(6211):127-32 [2465497] J Mol Biol. 1991 Aug 5;220(3):757-70 [1714504] J Mol Biol. 1991 Sep 20;221(2):669-91 [1920440] Science. 1991 Nov 15;254(5034):974-80 [1948083] Science. 1992 Jan 10;255(5041):178-83 [1553543] J Mol Biol. 1992 Apr 5;224(3):671-83 [1373774] Proc Natl Acad Sci U S A. 1992 Jun 1;89(11):5083-7 [1594616] J Mol Biol. 1992 Oct 5;227(3):757-75 [1383552] J Mol Biol. 1973 Jul 5;77(3):417-36 [4737866] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Role of the herbicide atrazine in the development of non-Hodgkin's lymphoma. AN - 75797933; 8316777 AB - Atrazine is the most commonly used herbicide in the United States and is a wide-spread groundwater contaminant in the Midwest. The role of atrazine in the development of human non-Hodgkin's lymphoma (NHL) was investigated in three case-referent studies conducted in four midwestern states in the United States. A total of 993 white men with NHL and 2918 population-based referents were interviewed concerning their agricultural practices. When the results of the three studies were combined, atrazine use was associated with an odds ratio of 1.4 [95% confidence interval (95% CI) 1.1-1.8, 130 cases, 249 referents) for NHL. However, adjustments for the use of 2,4-dichlorophenoxyacetic acid and organophosphate insecticides reduced the apparent association between NHL and atrazine in all but one state and reduced the associations for the long-term and frequent users in Nebraska. Detailed analyses suggested that there was little or no increase in the risk of NHL attributable to the agricultural use of atrazine. JF - Scandinavian journal of work, environment & health AU - Hoar Zahm, S AU - Weisenburger, D D AU - Cantor, K P AU - Holmes, F F AU - Blair, A AD - Environmental Epidemiology Branch, National Cancer Institute, Rockville, Maryland 20892. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 108 EP - 114 VL - 19 IS - 2 SN - 0355-3140, 0355-3140 KW - Atrazine KW - QJA9M5H4IM KW - Index Medicus KW - Risk Factors KW - Humans KW - Adult KW - Aged KW - Midwestern United States KW - Middle Aged KW - Male KW - Female KW - Agricultural Workers' Diseases -- chemically induced KW - Occupational Exposure -- adverse effects KW - Lymphoma, Non-Hodgkin -- chemically induced KW - Atrazine -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75797933?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Scandinavian+journal+of+work%2C+environment+%26+health&rft.atitle=Role+of+the+herbicide+atrazine+in+the+development+of+non-Hodgkin%27s+lymphoma.&rft.au=Hoar+Zahm%2C+S%3BWeisenburger%2C+D+D%3BCantor%2C+K+P%3BHolmes%2C+F+F%3BBlair%2C+A&rft.aulast=Hoar+Zahm&rft.aufirst=S&rft.date=1993-04-01&rft.volume=19&rft.issue=2&rft.spage=108&rft.isbn=&rft.btitle=&rft.title=Scandinavian+journal+of+work%2C+environment+%26+health&rft.issn=03553140&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-28 N1 - Date created - 1993-07-28 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Scand J Work Environ Health. 1994 Jun;20(3):223-6 [7973496] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Leukocyte CD18 monoclonal antibody worsens endotoxemia and cardiovascular injury in canines with septic shock. AN - 75795917; 8099906 AB - We investigated the effects of a murine monoclonal antibody directed against the canine leukocyte CD11/18 adhesion complex (MAb R15.7) in a canine model of septic shock. Awake 2-yr-old purpose-bred beagles were studied 7 days before and 1, 2, 4, and 10 days after intraperitoneal placement of an Escherichia coli-infected fibrin clot. Starting 12 h before clot placement, animals received 0.5-1 mg/kg iv every 12 h (4 doses total) of either MAb R15.7 (MAb group, n = 8) or, as controls, murine serum protein (n = 8). After infected clot placement, all animals received antibiotic (ceftriaxne, 100 mg.kg-1.day-1 for 4 days). Two of eight control animals and four of eight MAb animals died (P = 0.4). During the first 8 h after clot placement, MAb animals, compared with control animals, had greater (P < 0.06) increases in serum endotoxin levels and higher (P < 0.05) neutrophil counts. Day 1 after clot placement, MAb animals, compared with control animals, had decreased (P < 0.05) central venous pressure and arterial pH and increased (P < 0.05) arterial lactate. Day 2 after clot placement, MAb animals, compared with control animals, had decreased (P < 0.05) cardiac index and mean arterial pressure. In summary, MAb R15.7, although associated with increased neutrophil counts, worsened serum endotoxemia, acidosis, and cardiovascular function in this canine model of septic shock. These data suggest that in septic shock, antibody directed against this leukocyte membrane protein complex may be harmful, possibly via impairment of normal leukocyte function. JF - Journal of applied physiology (Bethesda, Md. : 1985) AU - Eichacker, P Q AU - Hoffman, W D AU - Farese, A AU - Danner, R L AU - Suffredini, A F AU - Waisman, Y AU - Banks, S M AU - Mouginis, T AU - Wilson, L AU - Rothlein, R AD - Critical Care Medicine Department, National Institutes of Health, Bethesda 20892. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 1885 EP - 1892 VL - 74 IS - 4 SN - 8750-7587, 8750-7587 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, CD KW - Antigens, CD11 KW - Antigens, CD18 KW - Endotoxins KW - Receptors, Leukocyte-Adhesion KW - Index Medicus KW - Animals KW - Acid-Base Equilibrium KW - Neutrophils KW - Antibodies, Monoclonal -- blood KW - Dogs KW - Endotoxins -- toxicity KW - Receptors, Leukocyte-Adhesion -- immunology KW - Leukocyte Count KW - Antibodies, Monoclonal -- administration & dosage KW - Toxemia -- blood KW - Shock, Septic -- complications KW - Cardiovascular System -- injuries KW - Shock, Septic -- immunology KW - Cardiovascular System -- immunology KW - Toxemia -- immunology KW - Toxemia -- complications KW - Shock, Septic -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75795917?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+applied+physiology+%28Bethesda%2C+Md.+%3A+1985%29&rft.atitle=Leukocyte+CD18+monoclonal+antibody+worsens+endotoxemia+and+cardiovascular+injury+in+canines+with+septic+shock.&rft.au=Eichacker%2C+P+Q%3BHoffman%2C+W+D%3BFarese%2C+A%3BDanner%2C+R+L%3BSuffredini%2C+A+F%3BWaisman%2C+Y%3BBanks%2C+S+M%3BMouginis%2C+T%3BWilson%2C+L%3BRothlein%2C+R&rft.aulast=Eichacker&rft.aufirst=P&rft.date=1993-04-01&rft.volume=74&rft.issue=4&rft.spage=1885&rft.isbn=&rft.btitle=&rft.title=Journal+of+applied+physiology+%28Bethesda%2C+Md.+%3A+1985%29&rft.issn=87507587&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-19 N1 - Date created - 1993-07-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Seasonal variation in behavioral responses to m-CPP in patients with seasonal affective disorder and controls. AN - 75782546; 8390305 AB - This paper reports the behavioral responses to m-chlorophenylpiperazine (m-CPP), a serotonin agonist, in patients with seasonal affective disorder (SAD) and controls during the summer. Results are compared with the responses of SAD patients and controls given m-CPP in the winter. Results of the winter study were reported earlier by our group. Baseline Hamilton depression ratings in SAD patients were significantly lower in the summer than in winter (p < 0.05). Additionally, in both SAD patients and controls, there were seasonal differences on the National Institute of Mental Health (NIMH) self-rating scale items: "depressed affect," "dysphoria," and "functional deficit" at baseline. The behavioral responses to m-CPP across seasons differentiated patients from normals only in the "activation/euphoria" item, on which a far greater response was seen in patients than in controls during the winter. This behavioral response may be a state marker for winter depression, as it was significantly reduced after light treatment of these patients in the winter, and in the summer. SAD patients responded differently from controls on "altered self-awareness" and "dysphoria" independently of seasons, and these responses may be considered as possible trait markers for this condition. These results provide further evidence of a possible deficiency in serotonergic transmission in seasonal affective disorder. JF - Biological psychiatry AU - Joseph-Vanderpool, J R AU - Jacobsen, F M AU - Murphy, D L AU - Hill, J L AU - Rosenthal, N E AD - Section on Environmental Psychiatry, NIMH, Bethesda, MD 20892. Y1 - 1993/04/01/ PY - 1993 DA - 1993 Apr 01 SP - 496 EP - 504 VL - 33 IS - 7 SN - 0006-3223, 0006-3223 KW - Piperazines KW - 0 KW - Receptors, Serotonin KW - Serotonin Receptor Agonists KW - Serotonin KW - 333DO1RDJY KW - 1-(3-chlorophenyl)piperazine KW - REY0CNO998 KW - Index Medicus KW - Receptors, Serotonin -- physiology KW - Euphoria -- drug effects KW - Receptors, Serotonin -- drug effects KW - Serotonin -- physiology KW - Infusions, Intravenous KW - Synaptic Transmission -- drug effects KW - Humans KW - Circadian Rhythm -- drug effects KW - Euphoria -- physiology KW - Personality Inventory KW - Synaptic Transmission -- physiology KW - Circadian Rhythm -- physiology KW - Adult KW - Middle Aged KW - Female KW - Male KW - Serotonin Receptor Agonists -- adverse effects KW - Seasonal Affective Disorder -- drug therapy KW - Seasonal Affective Disorder -- physiopathology KW - Piperazines -- therapeutic use KW - Seasons KW - Serotonin Receptor Agonists -- therapeutic use KW - Seasonal Affective Disorder -- psychology KW - Piperazines -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75782546?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biological+psychiatry&rft.atitle=Seasonal+variation+in+behavioral+responses+to+m-CPP+in+patients+with+seasonal+affective+disorder+and+controls.&rft.au=Joseph-Vanderpool%2C+J+R%3BJacobsen%2C+F+M%3BMurphy%2C+D+L%3BHill%2C+J+L%3BRosenthal%2C+N+E&rft.aulast=Joseph-Vanderpool&rft.aufirst=J&rft.date=1993-04-01&rft.volume=33&rft.issue=7&rft.spage=496&rft.isbn=&rft.btitle=&rft.title=Biological+psychiatry&rft.issn=00063223&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-20 N1 - Date created - 1993-07-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Molecular genetics in Saccharomyces kluyveri: the HIS3 homolog and its use as a selectable marker gene in S. kluyveri and Saccharomyces cerevisiae. AN - 75780179; 8511965 AB - We cloned the Saccharomyces kluyveri HIS3 homolog, k-HIS3, and made a partial deletion of the gene. The k-HIS3 gene complemented a HIS3 deletion in S. cerevisiae. The DNA sequences of the open reading frames (ORFs) of the HIS3 homologs are 70% identical at the DNA level and 83% identical at the deduced amino acid level. The ORF upstream of the k-HIS3 gene is related to the PET56 gene of S. cerevisiae found upstream of the HIS3 gene of S. cerevisiae. The ORF downstream from the k-HIS3 gene is not related to the DED1 gene found downstream of the HIS3 gene in S. cerevisiae. JF - Yeast (Chichester, England) AU - Weinstock, K G AU - Strathern, J N AD - Laboratory of Eukaryotic Gene Expression, ABL-Basic Research Program, NCI-Frederick Cancer Research and Development Center, MD 21702-1201. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 351 EP - 361 VL - 9 IS - 4 SN - 0749-503X, 0749-503X KW - HIS3 KW - PET56 KW - URA3 KW - Genetic Markers KW - 0 KW - Uracil KW - 56HH86ZVCT KW - Hydro-Lyases KW - EC 4.2.1.- KW - imidazoleglycerolphosphate dehydratase KW - EC 4.2.1.19 KW - Index Medicus KW - Saccharomyces cerevisiae -- genetics KW - Base Sequence KW - Uracil -- metabolism KW - Transformation, Genetic KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Sequence Analysis, DNA KW - Selection, Genetic KW - Chromosome Mapping KW - Mutagenesis KW - Cloning, Molecular KW - Genes, Fungal -- genetics KW - Saccharomyces -- genetics KW - Hydro-Lyases -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75780179?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Yeast+%28Chichester%2C+England%29&rft.atitle=Molecular+genetics+in+Saccharomyces+kluyveri%3A+the+HIS3+homolog+and+its+use+as+a+selectable+marker+gene+in+S.+kluyveri+and+Saccharomyces+cerevisiae.&rft.au=Weinstock%2C+K+G%3BStrathern%2C+J+N&rft.aulast=Weinstock&rft.aufirst=K&rft.date=1993-04-01&rft.volume=9&rft.issue=4&rft.spage=351&rft.isbn=&rft.btitle=&rft.title=Yeast+%28Chichester%2C+England%29&rft.issn=0749503X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-15 N1 - Date created - 1993-07-15 N1 - Date revised - 2017-01-13 N1 - Gene symbol - HIS3; PET56; URA3 N1 - Genetic sequence - Z14125; GENBANK N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Fast pre-potential generation in rat hippocampal CA1 pyramidal neurons. AN - 75777391; 8506028 AB - Small all-or-none pre-potentials have been shown under some conditions to underlie antidromic and orthodromic spike discharge in somatic recordings of hippocampal pyramidal neurons [Andersen P. and Lomo T. (1966) Expl Brain Res. 2, 247-260; Kandel E. R. et al. (1961) J. Neurophysiol. 24, 225-242; Schwartzkroin P. A. (1977) Brain Res. 128, 53-68; Spencer W. A. and Kandel E. R. (1961) J. Neurophysiol. 24, 272-285]. These potentials are taken to reflect spike discharge in distant regions of the cell (axonal or dendritic) [Andersen P. and Lomo T. (1966) Expl Brain Res. 2, 247-260; Kandel E. R. and Spencer W. A. (1961) Ann. N. Y. Acad. Sci. 94, 570-603; Schwartzkroin P. A. (1977) Brain Res. 128, 53-68] or electronic spike conduction across a gap junction between neighboring pyramidal cells [Dudek F. E. et al. (1983) In Basic Mechanisms of Neural Hyperexcitability, pp. 31-73]. The present study compared pre-potentials recorded at the somatic and dendritic levels and used restricted applications of tetrodotoxin to examine the relationship between pre-potentials and Na+ spike discharge. Intrasomatic and intradendritic recordings were obtained from CA1 pyramidal neurons of rat hippocampal slices maintained in vitro. Orthodromic and antidromic spike discharge was evoked by stimulation of afferent fibers in stratum radiatum and pyramidal cell axons in the alveus, respectively. Focal pressure application of tetrodotoxin in the immediate vicinity of somatic or dendritic recordings uncovered pre-potentials following blockade of antidromic spike discharge. Blockade of these pre-potentials required the diffusion of tetrodotoxin to a location remote from the recording site. Focal application of tetrodotoxin in the cell body layer reliably uncovered orthodromic pre-potentials at the soma only when stimulus intensity was raised beyond threshold for somatic spike discharge; e.g. to intensities shown to initiate spike discharge in apical dendritic locations [Turner R. W. et al. (1991) J. Neurosci. 11, 2270-2280]. These data provide evidence that propagation of a Na+ spike over the pyramidal cell axis is preceded by a depolarization in the form of a pre-potential. The uncovering of orthodromic somatic pre-potentials by tetrodotoxin during suprathreshold activation further supports the proposal [Spencer W. A. and Kandel E. R. (1961) J. Neurophysiol. 24, 272-285] that dendritic spike discharge [Turner R. W. et al. (1991) J. Neurosci. 11, 2270-2280] can underlie fast pre-potential generation in pyramidal cell somata. JF - Neuroscience AU - Turner, R W AU - Meyers, D E AU - Barker, J L AD - Laboratory of Neurophysiology, National Institutes of Health, NINCDS, Bethesda, MD. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 949 EP - 959 VL - 53 IS - 4 SN - 0306-4522, 0306-4522 KW - Tetrodotoxin KW - 4368-28-9 KW - Sodium KW - 9NEZ333N27 KW - Index Medicus KW - Animals KW - Sodium -- physiology KW - Membrane Potentials -- physiology KW - Electrophysiology KW - Electric Stimulation KW - Rats KW - Neural Conduction -- physiology KW - In Vitro Techniques KW - Rats, Wistar KW - Membrane Potentials -- drug effects KW - Tetrodotoxin -- pharmacology KW - Dendrites -- drug effects KW - Male KW - Pyramidal Tracts -- cytology KW - Hippocampus -- physiology KW - Hippocampus -- cytology KW - Neurons -- physiology KW - Pyramidal Tracts -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75777391?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroscience&rft.atitle=Fast+pre-potential+generation+in+rat+hippocampal+CA1+pyramidal+neurons.&rft.au=Turner%2C+R+W%3BMeyers%2C+D+E%3BBarker%2C+J+L&rft.aulast=Turner&rft.aufirst=R&rft.date=1993-04-01&rft.volume=53&rft.issue=4&rft.spage=949&rft.isbn=&rft.btitle=&rft.title=Neuroscience&rft.issn=03064522&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-08 N1 - Date created - 1993-07-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Taste intensity performance in patients irradiated to the head and neck. AN - 75776920; 8511171 AB - Decrements in taste-detection thresholds during radiotherapy and subsequent recovery in the months after therapy are well documented. However, few studies have explored suprathreshold taste intensity perception in radiation patients. This cross-sectional study compared taste function in 15 men postradiation with a group of 23 healthy, nonirradiated male volunteers. A direct-scaling procedure was used to assess taste intensity perception of the four basic taste qualities. Patients performed nearly as well as control subjects on objective measures of suprathreshold functioning. Postradiation intensity judgments of salty (sodium chloride), sweet (sucrose), and bitter (quinine sulfate) solutions were not significantly reduced. Subtle, age-related taste impairments were identified for sour perception (citric acid) postradiotherapy. Younger patients judged citric acid to be more intense than did age-appropriate control subjects, whereas older patients judged it to be less intense. Moreover, younger patients were likely to be midly dysgeusic, whereas older patients appeared to be hypogeusic for citric acid. This study provides evidence for near normal suprathreshold taste intensity perception in patients who have received head and neck irradiation. JF - Physiology & behavior AU - Schwartz, L K AU - Weiffenbach, J M AU - Valdez, I H AU - Fox, P C AD - Clinical Investigations and Patient Care Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 671 EP - 677 VL - 53 IS - 4 SN - 0031-9384, 0031-9384 KW - Index Medicus KW - Salivation -- radiation effects KW - Radiotherapy Dosage KW - Humans KW - Adult KW - Ageusia -- physiopathology KW - Aged KW - Middle Aged KW - Follow-Up Studies KW - Salivation -- physiology KW - Male KW - Female KW - Taste Threshold -- radiation effects KW - Hodgkin Disease -- radiotherapy KW - Lymphoma, Non-Hodgkin -- radiotherapy KW - Head and Neck Neoplasms -- radiotherapy KW - Taste Threshold -- physiology KW - Carcinoma, Squamous Cell -- radiotherapy KW - Radiation Injuries -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75776920?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Physiology+%26+behavior&rft.atitle=Taste+intensity+performance+in+patients+irradiated+to+the+head+and+neck.&rft.au=Schwartz%2C+L+K%3BWeiffenbach%2C+J+M%3BValdez%2C+I+H%3BFox%2C+P+C&rft.aulast=Schwartz&rft.aufirst=L&rft.date=1993-04-01&rft.volume=53&rft.issue=4&rft.spage=671&rft.isbn=&rft.btitle=&rft.title=Physiology+%26+behavior&rft.issn=00319384&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-12 N1 - Date created - 1993-07-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Styrene inhalation toxicity studies in mice. I. Hepatotoxicity in B6C3F1 mice. AN - 75769377; 8504906 AB - Studies were conducted to evaluate the toxic effects of short-term repeated styrene inhalation in B6C3F1 mice. Male and female mice were exposed to 0, 125, 250, or 500 ppm styrene, 6 hr/day, for up to 14 days. Styrene toxicity was characterized by severe centrilobular hepatic necrosis and deaths after one exposure to 500 ppm or two exposures to 250 ppm. Mortality and hepatotoxicity were not increased by additional exposures, and in surviving mice, regeneration and repair of initial hepatic injury occurred in spite of continued exposure for 14 days. A marked sex difference was observed, with male mice significantly more susceptible to styrene toxicity than females. A nonlinear dose response was observed where mortality in male and female mice was greater in the 250 ppm dose group than that in the 500 ppm dose group. Severe congestion and necrosis of the liver was present in moribund mice; hepatic congestion and serum alanine aminotransferase and sorbitol dehydrogenase were significantly greater in moribund animals. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Morgan, D L AU - Mahler, J F AU - O'Connor, R W AU - Price, H C AU - Adkins, B AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 325 EP - 335 VL - 20 IS - 3 SN - 0272-0590, 0272-0590 KW - Styrenes KW - 0 KW - Styrene KW - 44LJ2U959V KW - Index Medicus KW - Mice, Inbred Strains KW - Animals KW - Liver -- blood supply KW - Drug Administration Schedule KW - Liver -- drug effects KW - Dose-Response Relationship, Drug KW - Body Weight -- drug effects KW - Mice KW - Administration, Inhalation KW - Male KW - Female KW - Organ Size -- drug effects KW - Chemical and Drug Induced Liver Injury -- blood KW - Chemical and Drug Induced Liver Injury -- mortality KW - Chemical and Drug Induced Liver Injury -- pathology KW - Styrenes -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75769377?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.atitle=Styrene+inhalation+toxicity+studies+in+mice.+I.+Hepatotoxicity+in+B6C3F1+mice.&rft.au=Morgan%2C+D+L%3BMahler%2C+J+F%3BO%27Connor%2C+R+W%3BPrice%2C+H+C%3BAdkins%2C+B&rft.aulast=Morgan&rft.aufirst=D&rft.date=1993-04-01&rft.volume=20&rft.issue=3&rft.spage=325&rft.isbn=&rft.btitle=&rft.title=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.issn=02720590&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-08 N1 - Date created - 1993-07-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Inhalation toxicity of 1,6-hexanediamine dihydrochloride in F344/N rats and B6C3F1 mice. AN - 75765226; 8504909 AB - 1,6-Hexanediamine (HDA) is a high production volume chemical which is used as an intermediate in the synthesis of paints, resins, inks, and textiles and as a corrosion inhibitor in lubricants. Two- and 13-week studies of the toxicity of the dihydrochloride salt of HDA (HDDC) were conducted in male and female Fischer 344/N rats and B6C3F1 mice using whole-body inhalation exposure. Both species were evaluated for histopathologic and reproductive effects, and rats were examined for clinical chemistry and hematologic changes. In the 2-week inhalation studies, animals were exposed to 10-800 mg HDDC/m3, 6 hr per day. All rats, all female mice, and two of five male mice in the high-exposure group died before the end of the study. Surviving mice in this group had a dose-dependent depression in body weight gain. Clinical signs were primarily related to upper respiratory tract irritation and included dyspnea and nasal discharge in both species. Treatment-related histopathologic lesions included inflammation and necrosis of the laryngeal epithelium of both species and the tracheal epithelium of mice, as well as focal inflammation and ulceration of the respiratory and olfactory nasal mucosa. In the 13-week inhalation studies, animals were exposed to HDDC at concentrations of 1.6-160 mg/m3 for 6 hr per day, 5 days per week. In addition to the base study groups, a supplemental group of rats at each exposure level was included to assess the effect of HDDC on reproduction. No treatment-related changes in organ weights or organ-to-body-weight ratios occurred in rats, and no treatment-related clinical signs or gross lesions were seen in either species. Chemical-related microscopic lesions were limited to the upper respiratory tract (larynx and nasal passages) in the two highest exposure groups and were similar in both species. These lesions included minimal to mild focal erosion, ulceration, inflammation, and hyperplasia of the laryngeal epithelium, in addition to degeneration of the olfactory and respiratory nasal epithelium. HDDC caused no significant changes in sperm morphology or vaginal cytology and no significant adverse effects on reproduction in rats or mice. Hematologic and clinical chemistry changes in rats were minor and sporadic and were not accompanied by related histologic findings. HDDC did not increase the frequency of micronucleated erythrocytes in mice.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Hébert, C D AU - Elwell, M R AU - Travlos, G S AU - Zeiger, E AU - French, J E AU - Bucher, J R AD - Experimental Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 348 EP - 359 VL - 20 IS - 3 SN - 0272-0590, 0272-0590 KW - Diamines KW - 0 KW - 1,6-diaminohexane KW - ZRA5J5B2QW KW - Index Medicus KW - Vagina -- drug effects KW - Animals KW - Drug Administration Schedule KW - Reproduction -- drug effects KW - Dose-Response Relationship, Drug KW - Vagina -- pathology KW - Spermatozoa -- pathology KW - Mice KW - Rats KW - Mice, Inbred Strains KW - Rats, Inbred F344 KW - Micronucleus Tests KW - Spermatozoa -- drug effects KW - Body Weight -- drug effects KW - Administration, Inhalation KW - Female KW - Male KW - Organ Size -- drug effects KW - Diamines -- administration & dosage KW - Diamines -- blood KW - Diamines -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75765226?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.atitle=Inhalation+toxicity+of+1%2C6-hexanediamine+dihydrochloride+in+F344%2FN+rats+and+B6C3F1+mice.&rft.au=H%C3%A9bert%2C+C+D%3BElwell%2C+M+R%3BTravlos%2C+G+S%3BZeiger%2C+E%3BFrench%2C+J+E%3BBucher%2C+J+R&rft.aulast=H%C3%A9bert&rft.aufirst=C&rft.date=1993-04-01&rft.volume=20&rft.issue=3&rft.spage=348&rft.isbn=&rft.btitle=&rft.title=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.issn=02720590&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-08 N1 - Date created - 1993-07-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Pharmacological issues in the treatment of bipolar disorder: focus on mood-stabilizing compounds. AN - 75762492; 8500079 AB - The acute and chronic pharmacotherapy of bipolar disorder requires an understanding of the pharmacology of very dissimilar compounds--the mood stabilizers (lithium, carbamazepine and valproate) and several classes of antidepressants. No definitive data are available on the primary mode of action of mood stabilizers, and those used show no single pharmacological property. On the other hand, the pharmacokinetics and dynamics of these compounds are well studied. JF - Canadian journal of psychiatry. Revue canadienne de psychiatrie AU - Potter, W Z AU - Ketter, T A AD - Section on Clinical Pharmacology, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - S51 EP - S56 VL - 38 IS - 3 Suppl 2 SN - 0706-7437, 0706-7437 KW - Anticonvulsants KW - 0 KW - Antidepressive Agents KW - Carbamazepine KW - 33CM23913M KW - Valproic Acid KW - 614OI1Z5WI KW - Index Medicus KW - Drug Interactions KW - Carbamazepine -- adverse effects KW - Carbamazepine -- pharmacokinetics KW - Humans KW - Infant, Newborn KW - Carbamazepine -- therapeutic use KW - Female KW - Pregnancy KW - Anticonvulsants -- pharmacokinetics KW - Bipolar Disorder -- blood KW - Antidepressive Agents -- pharmacokinetics KW - Bipolar Disorder -- drug therapy KW - Anticonvulsants -- adverse effects KW - Bipolar Disorder -- psychology KW - Antidepressive Agents -- therapeutic use KW - Valproic Acid -- adverse effects KW - Antidepressive Agents -- adverse effects KW - Valproic Acid -- therapeutic use KW - Anticonvulsants -- therapeutic use KW - Valproic Acid -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75762492?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Canadian+journal+of+psychiatry.+Revue+canadienne+de+psychiatrie&rft.atitle=Pharmacological+issues+in+the+treatment+of+bipolar+disorder%3A+focus+on+mood-stabilizing+compounds.&rft.au=Potter%2C+W+Z%3BKetter%2C+T+A&rft.aulast=Potter&rft.aufirst=W&rft.date=1993-04-01&rft.volume=38&rft.issue=3+Suppl+2&rft.spage=S51&rft.isbn=&rft.btitle=&rft.title=Canadian+journal+of+psychiatry.+Revue+canadienne+de+psychiatrie&rft.issn=07067437&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-01 N1 - Date created - 1993-07-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Epidermal growth factor receptor ligands regulate keratin 8 expression in keratinocytes, and transforming growth factor alpha mediates the induction of keratin 8 by the v-rasHa oncogene. AN - 75748447; 7684248 AB - Cytokeratins 8 and 18 (Endo A and B) are among the earliest expressed embryonic genes and the major components of the cytoskeleton in simple epithelia of the adult. Recent data indicate that these cytokeratins are aberrantly expressed in several epithelial tumor types and that expression in cultured mouse keratinocytes is linked to activation of the rasHa oncogene. Furthermore, up-regulation of K8/K18 in keratinocytes is associated with reciprocal suppression of K1. We now show that the aberrant expression of K8 and K18 and suppression of K1 in cultured keratinocytes transduced with the v-rasHa gene are mediated by a factor secreted into the culture medium. Furthermore, transforming growth factor alpha (TGF-alpha) and epidermal growth factor elicit an identical pattern of K8/K18 expression and K1 suppression in normal keratinocytes. The factor in medium from v-rasHa keratinocytes is TGF-alpha, as a specific blocking antibody for rat and mouse TGF-alpha prevents the expression of K8 and restores expression of K1. The tyrosine kinase inhibitor genistein also prevents K8 induction in v-rasHa keratinocytes and in normal keratinocytes treated with TGF-alpha- or v-rasHa-conditioned medium. However, simply stimulating proliferation of keratinocytes by cholera toxin does not result in expression of K8 or suppression of K1. Finally, tumor grafts from neoplastic epidermal cells overexpressing TGF-alpha via retroviral transduction of human TGF-alpha complementary DNA in vitro show coordinate expression of K8 and human TGF-alpha. These studies indicate that K8 expression in keratinocytes, and derivative neoplastic cells, in vivo and in vitro is regulated by epidermal growth factor receptor ligands. Since the expression of cytokines and K8/K18 in early embryogenesis is often coincident, cytokines may be the physiological mediators of K8/K18 expression in embryonic cells. JF - Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research AU - Cheng, C AU - Tennenbaum, T AU - Dempsey, P J AU - Coffey, R J AU - Yuspa, S H AU - Dlugosz, A A AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 317 EP - 327 VL - 4 IS - 4 SN - 1044-9523, 1044-9523 KW - v-rasHa KW - Biological Factors KW - 0 KW - Culture Media, Conditioned KW - Transforming Growth Factor alpha KW - Transforming Growth Factor beta KW - Epidermal Growth Factor KW - 62229-50-9 KW - Keratins KW - 68238-35-7 KW - Index Medicus KW - Biological Factors -- isolation & purification KW - Animals KW - Transforming Growth Factor beta -- physiology KW - Cells, Cultured KW - Mice KW - Gene Expression Regulation KW - Mice, Inbred BALB C KW - Genes, ras KW - Transforming Growth Factor alpha -- physiology KW - Keratinocytes -- metabolism KW - Keratins -- biosynthesis KW - Epidermal Growth Factor -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75748447?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cell+growth+%26+differentiation+%3A+the+molecular+biology+journal+of+the+American+Association+for+Cancer+Research&rft.atitle=Epidermal+growth+factor+receptor+ligands+regulate+keratin+8+expression+in+keratinocytes%2C+and+transforming+growth+factor+alpha+mediates+the+induction+of+keratin+8+by+the+v-rasHa+oncogene.&rft.au=Cheng%2C+C%3BTennenbaum%2C+T%3BDempsey%2C+P+J%3BCoffey%2C+R+J%3BYuspa%2C+S+H%3BDlugosz%2C+A+A&rft.aulast=Cheng&rft.aufirst=C&rft.date=1993-04-01&rft.volume=4&rft.issue=4&rft.spage=317&rft.isbn=&rft.btitle=&rft.title=Cell+growth+%26+differentiation+%3A+the+molecular+biology+journal+of+the+American+Association+for+Cancer+Research&rft.issn=10449523&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-18 N1 - Date created - 1993-06-18 N1 - Date revised - 2017-01-13 N1 - Gene symbol - v-rasHa N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Residues in pockets B and F of HLA-B27 are critical in the presentation of an influenza A virus nucleoprotein peptide and influence the stability of peptide - MHC complexes. AN - 75742702; 8494822 AB - Six pockets, designated A through F, which extend from the peptide binding site of class I HLA molecules, have been postulated to play an important role in determining peptide binding specificity. HLA-B27 mutant molecules with single amino acid substitutions at residues 9his-->phe, 24thr-->ser, 45glu-->thr, and 67cys-->ala in pocket B; 114his-->asn in pocket D; and 116asp-->phe in pocket F have been generated and characterized for their capacity to present an influenza A nucleoprotein peptide (NP 383-391) for cytotoxic T lymphocyte recognition. We report here that substitutions in residues 45, 67, and 116 affect presentation of NP 383-391 when peptide is processed and loaded during viral infection. Using 125I-labeled NP peptide, we demonstrate that substitutions in residues 67 and 116 alter the stability of NP-HLA-B27 complexes. A substitution at position 9 of the NP peptide complements the mutation introduced at residue 116, suggesting that the NP peptide binds with its carboxy terminal amino acid in pocket F. These findings indicate that polymorphic residues within pockets B and F of HLA-B27 play a crucial role in peptide binding and stability of peptide-MHC class I complexes. Furthermore, our results suggest that substitutions at allele-specific residues within pockets B and F alter the stability of NP-HLA-B27 complexes resulting in the diminution or abrogation of NP presentation during viral infection. JF - International immunology AU - Carreno, B M AU - Winter, C C AU - Taurog, J D AU - Hansen, T H AU - Biddison, W E AD - Molecular Immunology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 353 EP - 360 VL - 5 IS - 4 SN - 0953-8178, 0953-8178 KW - HLA-B27 Antigen KW - 0 KW - Macromolecular Substances KW - NP protein, Influenza A virus KW - Nucleoproteins KW - RNA-Binding Proteins KW - Viral Core Proteins KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Drug Stability KW - Base Sequence KW - Humans KW - DNA -- genetics KW - Adult KW - Molecular Sequence Data KW - Influenza A virus -- immunology KW - Influenza A virus -- metabolism KW - Amino Acid Sequence KW - Protein Binding KW - Binding Sites KW - Viral Core Proteins -- immunology KW - Nucleoproteins -- metabolism KW - HLA-B27 Antigen -- metabolism KW - Viral Core Proteins -- metabolism KW - HLA-B27 Antigen -- genetics KW - HLA-B27 Antigen -- chemistry KW - Nucleoproteins -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75742702?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+immunology&rft.atitle=Residues+in+pockets+B+and+F+of+HLA-B27+are+critical+in+the+presentation+of+an+influenza+A+virus+nucleoprotein+peptide+and+influence+the+stability+of+peptide+-+MHC+complexes.&rft.au=Carreno%2C+B+M%3BWinter%2C+C+C%3BTaurog%2C+J+D%3BHansen%2C+T+H%3BBiddison%2C+W+E&rft.aulast=Carreno&rft.aufirst=B&rft.date=1993-04-01&rft.volume=5&rft.issue=4&rft.spage=353&rft.isbn=&rft.btitle=&rft.title=International+immunology&rft.issn=09538178&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-23 N1 - Date created - 1993-06-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Pregnant women at work: sociodemographic perspectives. AN - 75727114; 8338526 AB - The 1988 National Maternal and Infant Health Survey, a stratified random sample of 9,953 live births, shows that women who work during pregnancy are more likely to be non-Hispanic white, married, of higher income and education, to have medical insurance, and of lower parity than nonemployed pregnant women (p < .0001). They begin prenatal care earlier, are less likely to smoke, and are more likely to state that the birth was wanted (p < .0001). Similar trends are seen for full-time as compared to part-time workers. Women employed as precision production workers, operators/fabricators, or in service occupations are disadvantaged with regard to sociodemographic and behavioral risks for pregnancy outcomes relative to women in professional and managerial occupations. Black race, parity, body mass index, and smoking, but not employment, are associated with low birth weight when gestational age is controlled. The effects of stress and its buffers, paternal characteristics, physical activity, and toxic exposures, both in and out of the workplace, should be considered, as should the normative and social policy context. JF - American journal of industrial medicine AU - Moss, N AU - Carver, K AD - Demographic and Behavioral Sciences Branch, Center for Population Research, National Institute of Child Health and Human Development, Bethesda, MD 20892. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 541 EP - 557 VL - 23 IS - 4 SN - 0271-3586, 0271-3586 KW - Index Medicus KW - United States KW - Obstetric Labor, Premature -- epidemiology KW - Infant, Low Birth Weight KW - Humans KW - Infant, Newborn KW - Prenatal Care KW - Socioeconomic Factors KW - Logistic Models KW - Risk Factors KW - Adult KW - Health Surveys KW - Adolescent KW - Occupations KW - Female KW - Employment -- statistics & numerical data KW - Women, Working -- statistics & numerical data KW - Pregnancy -- ethnology KW - Pregnancy -- statistics & numerical data UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75727114?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+industrial+medicine&rft.atitle=Pregnant+women+at+work%3A+sociodemographic+perspectives.&rft.au=Moss%2C+N%3BCarver%2C+K&rft.aulast=Moss&rft.aufirst=N&rft.date=1993-04-01&rft.volume=23&rft.issue=4&rft.spage=541&rft.isbn=&rft.btitle=&rft.title=American+journal+of+industrial+medicine&rft.issn=02713586&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-27 N1 - Date created - 1993-05-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The absence of cumulative bone marrow toxicity in patients with recurrent adenocarcinoma of the ovary receiving dose-intense taxol and granulocyte colony stimulating factor. AN - 75726898; 7683933 AB - Forty-eight patients with recurrent adenocarcinoma of the ovary were treated with taxol and granulocyte colony stimulating factor (G-CSF), with a target taxol dose intensity of 250 mg/m2 every 3 weeks (83.3 mg/m2/week). We have assessed the patterns of granulocyte and platelet toxicity seen in this cohort. Individual patients received up to nine cycles of therapy. Criteria for entry onto protocol included good end organ function, good performance status and the absence of substantial co-morbid disease. Mean taxol dose intensity was 79.0 mg/m2/week for the whole cohort and did not diminish with increased duration of therapy. Granulocytopenia and thrombocytopenia were well controlled, with the average duration of platelet and neutropenic nadirs being less than 1 day for all cycles. There was no evidence of cumulative toxicity for granulocytes nor platelets, for up to eight cycles of therapy. We conclude that taxol, when given with G-CSF support, can be safely administered in a dose-intense fashion for multiple cycles of therapy, without cumulative bone marrow toxicity. JF - Anti-cancer drugs AU - Bicher, A AU - Kohn, E AU - Sarosy, G AU - Davis, P AU - Adamo, D O AU - Jacob, J AU - Christian, M AU - Reed, E AD - Medical Ovarian Cancer Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 141 EP - 148 VL - 4 IS - 2 SN - 0959-4973, 0959-4973 KW - Receptors, Granulocyte Colony-Stimulating Factor KW - 0 KW - Granulocyte Colony-Stimulating Factor KW - 143011-72-7 KW - Paclitaxel KW - P88XT4IS4D KW - Index Medicus KW - Humans KW - Blood Platelets -- drug effects KW - Adult KW - Granulocytes -- drug effects KW - Aged KW - Middle Aged KW - Recurrence KW - Female KW - Paclitaxel -- adverse effects KW - Adenocarcinoma -- complications KW - Granulocyte Colony-Stimulating Factor -- therapeutic use KW - Bone Marrow Diseases -- prevention & control KW - Bone Marrow Diseases -- chemically induced KW - Ovarian Neoplasms -- complications KW - Paclitaxel -- therapeutic use KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Adenocarcinoma -- drug therapy KW - Ovarian Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75726898?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Anti-cancer+drugs&rft.atitle=The+absence+of+cumulative+bone+marrow+toxicity+in+patients+with+recurrent+adenocarcinoma+of+the+ovary+receiving+dose-intense+taxol+and+granulocyte+colony+stimulating+factor.&rft.au=Bicher%2C+A%3BKohn%2C+E%3BSarosy%2C+G%3BDavis%2C+P%3BAdamo%2C+D+O%3BJacob%2C+J%3BChristian%2C+M%3BReed%2C+E&rft.aulast=Bicher&rft.aufirst=A&rft.date=1993-04-01&rft.volume=4&rft.issue=2&rft.spage=141&rft.isbn=&rft.btitle=&rft.title=Anti-cancer+drugs&rft.issn=09594973&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-16 N1 - Date created - 1993-06-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - DRD2 dopamine receptor genotype, linkage disequilibrium, and alcoholism in American Indians and other populations. AN - 75719519; 8488955 AB - We defined interpopulation differences in the frequency of the dopamine D2 receptor DRD2/Taq1 A1 allele, which has previously been associated with alcoholism. Frequencies of the A1 allele in unrelated subjects were 0.18 to 0.20 (se = 0.02 to 0.03) in several Caucasian populations previously assessed, 0.38 (+/- 0.05) in American Blacks (n = 44), 0.63 (+/- 0.07) in Jemez Pueblo Indians (n = 23), and 0.80 (+/- 0.04) in Cheyenne Indians (n = 52). The existence of large interpopulation differences in the frequency of the Taq1 alleles suggests that associations to disease status could readily be generated or masked if disease and control groups were uneven in ethnic composition. To address the possibility that the 4-fold higher frequency of the A1 allele in Cheyenne Indians was related to an increased vulnerability to alcoholism in that population, 47 Cheyenne Indians were psychiatrically interviewed and blind-rated. However, there was no significant difference between interviewed controls (0.73 +/- 0.06, n = 24), subjects with alcoholism and/or drug abuse (0.74 +/- 0.06, n = 23) and noninterviewed population controls (0.87 +/- 0.05, n = 20). Legitimate association of the DRD2/Taq1 allele to alcoholism would presumably require it to be in linkage disequilibrium (nonrandom association) with a functional mutation at DRD2 or elsewhere. The level of disequilibrium would vary between populations and could place an upper bound on the strength of an association.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Alcoholism, clinical and experimental research AU - Goldman, D AU - Brown, G L AU - Albaugh, B AU - Robin, R AU - Goodson, S AU - Trunzo, M AU - Akhtar, L AU - Lucas-Derse, S AU - Long, J AU - Linnoila, M AD - Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 199 EP - 204 VL - 17 IS - 2 SN - 0145-6008, 0145-6008 KW - Genetic Markers KW - 0 KW - Receptors, Dopamine D2 KW - Index Medicus KW - Genetic Markers -- genetics KW - Alleles KW - Gene Frequency KW - Models, Genetic KW - Humans KW - Adult KW - African Continental Ancestry Group KW - Genotype KW - Receptors, Dopamine D2 -- genetics KW - Alcoholism -- genetics KW - Linkage Disequilibrium KW - Indians, North American -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75719519?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcoholism%2C+clinical+and+experimental+research&rft.atitle=DRD2+dopamine+receptor+genotype%2C+linkage+disequilibrium%2C+and+alcoholism+in+American+Indians+and+other+populations.&rft.au=Goldman%2C+D%3BBrown%2C+G+L%3BAlbaugh%2C+B%3BRobin%2C+R%3BGoodson%2C+S%3BTrunzo%2C+M%3BAkhtar%2C+L%3BLucas-Derse%2C+S%3BLong%2C+J%3BLinnoila%2C+M&rft.aulast=Goldman&rft.aufirst=D&rft.date=1993-04-01&rft.volume=17&rft.issue=2&rft.spage=199&rft.isbn=&rft.btitle=&rft.title=Alcoholism%2C+clinical+and+experimental+research&rft.issn=01456008&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-08 N1 - Date created - 1993-06-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Environmental health science research and human risk assessment. AN - 75717620; 8484031 JF - Regulatory toxicology and pharmacology : RTP AU - Olden, K AD - Office of the Director, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709-2233. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 230 EP - 233 VL - 17 IS - 2 Pt 1 SN - 0273-2300, 0273-2300 KW - Hazardous Substances KW - 0 KW - Index Medicus KW - Risk Factors KW - Humans KW - Communication KW - Research KW - Environmental Health KW - Hazardous Substances -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75717620?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Regulatory+toxicology+and+pharmacology+%3A+RTP&rft.atitle=Environmental+health+science+research+and+human+risk+assessment.&rft.au=Olden%2C+K&rft.aulast=Olden&rft.aufirst=K&rft.date=1993-04-01&rft.volume=17&rft.issue=2+Pt+1&rft.spage=230&rft.isbn=&rft.btitle=&rft.title=Regulatory+toxicology+and+pharmacology+%3A+RTP&rft.issn=02732300&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-01 N1 - Date created - 1993-06-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Serum creatine phosphokinase elevations in patients with tardive dyskinesia. AN - 75707686; 8097656 AB - We describe a case of marked increases in serum creatine phosphokinase (CPK) associated with a dramatic exacerbation of tardive dyskinesia (TD). Chart review of eight additional patients with severe TD revealed three cases with mild CPK elevations. These cases suggest that TD, especially when accompanied by dystonia, may be associated with pathology of striated muscle. JF - The British journal of psychiatry : the journal of mental science AU - Egan, M F AU - Dargham, A A AU - Kirch, D G AU - Wyatt, R J AD - Neuropsychiatry Branch, NIMH Neuroscience Research Center, St Elizabeth's, Washington, DC 20032. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 551 EP - 553 VL - 162 SN - 0007-1250, 0007-1250 KW - Antipsychotic Agents KW - 0 KW - Creatine Kinase KW - EC 2.7.3.2 KW - Index Medicus KW - Humans KW - Adult KW - Neurologic Examination -- drug effects KW - Middle Aged KW - Adolescent KW - Male KW - Antipsychotic Agents -- administration & dosage KW - Schizophrenia -- enzymology KW - Creatine Kinase -- blood KW - Dyskinesia, Drug-Induced -- enzymology KW - Dyskinesia, Drug-Induced -- psychology KW - Dyskinesia, Drug-Induced -- diagnosis KW - Schizophrenic Psychology KW - Schizophrenia -- drug therapy KW - Antipsychotic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75707686?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+British+journal+of+psychiatry+%3A+the+journal+of+mental+science&rft.atitle=Serum+creatine+phosphokinase+elevations+in+patients+with+tardive+dyskinesia.&rft.au=Egan%2C+M+F%3BDargham%2C+A+A%3BKirch%2C+D+G%3BWyatt%2C+R+J&rft.aulast=Egan&rft.aufirst=M&rft.date=1993-04-01&rft.volume=162&rft.issue=&rft.spage=551&rft.isbn=&rft.btitle=&rft.title=The+British+journal+of+psychiatry+%3A+the+journal+of+mental+science&rft.issn=00071250&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-03 N1 - Date created - 1993-06-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Molecular alterations in the neostriatum of human cocaine addicts. AN - 75707425; 7683144 AB - Molecular changes in the neostriatum of human subjects who died with a history of cocaine abuse were revealed in discrete cell populations by means of the techniques of in situ hybridization histochemistry and in vitro receptor binding and autoradiography. Cocaine subjects had a history of repeated cocaine use and had cocaine and/or cocaine metabolites on board at the time of death. These subjects were compared to control subjects that had both a negative history and toxicology of cocaine use. Selective alterations in mRNA levels of striatal neuropeptides were detected in cocaine subjects compared to control subjects, especially for the opioid peptides. Marked reductions in the levels of enkephalin mRNA and mu opiate receptor binding were found in the caudate and putamen, concomitant with elevations in levels of dynorphin mRNA and kappa opiate receptor binding in the putamen and caudate, respectively. Dopamine uptake site binding was reduced in the caudate and putamen of cocaine subjects. The greater magnitude of changes in the dorsolateral striatum (caudate and putamen) as opposed to the ventromedial striatum (nucleus accumbens) suggests that cocaine abuse preferentially alters the biosynthetic activity of striatal systems associated with sensorimotor functioning. Additionally, an imbalance in the activity of the two major striatal output pathways in cocaine users is implicated because peptide mRNA levels were reduced in enkephalinergic striatopallidal neurons and increased in dynorphinergic striatonigral neurons. Another imbalance, that of reductions of transmitter mRNA and receptor expression associated with euphoria (enkephalin and mu opiate receptors), together with elevations in mRNAs of transmitter systems associated with dysphoria (dynorphin and kappa opiate receptors), suggests a model of dysphoria and craving in the human cocaine addict brain. JF - Synapse (New York, N.Y.) AU - Hurd, Y L AU - Herkenham, M AD - Section on Functional Neuroanatomy, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 357 EP - 369 VL - 13 IS - 4 SN - 0887-4476, 0887-4476 KW - Enkephalins KW - 0 KW - RNA, Messenger KW - Receptors, Dopamine KW - Receptors, Opioid, kappa KW - Receptors, Opioid, mu KW - Substance P KW - 33507-63-0 KW - Dynorphins KW - 74913-18-1 KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Receptors, Dopamine -- drug effects KW - Humans KW - Receptors, Opioid, kappa -- metabolism KW - Receptors, Opioid, kappa -- drug effects KW - Substance P -- biosynthesis KW - Receptors, Opioid, mu -- metabolism KW - Histocytochemistry KW - Autoradiography KW - RNA, Messenger -- biosynthesis KW - In Situ Hybridization KW - Enkephalins -- biosynthesis KW - Adult KW - Putamen -- metabolism KW - Nucleus Accumbens -- metabolism KW - Receptors, Opioid, mu -- drug effects KW - Middle Aged KW - Adolescent KW - Female KW - Male KW - Receptors, Dopamine -- metabolism KW - Dynorphins -- biosynthesis KW - Substance-Related Disorders -- pathology KW - Neostriatum -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75707425?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Synapse+%28New+York%2C+N.Y.%29&rft.atitle=Molecular+alterations+in+the+neostriatum+of+human+cocaine+addicts.&rft.au=Hurd%2C+Y+L%3BHerkenham%2C+M&rft.aulast=Hurd&rft.aufirst=Y&rft.date=1993-04-01&rft.volume=13&rft.issue=4&rft.spage=357&rft.isbn=&rft.btitle=&rft.title=Synapse+%28New+York%2C+N.Y.%29&rft.issn=08874476&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-25 N1 - Date created - 1993-05-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Measurement of heroin and its metabolites by isotope-dilution electron-impact mass spectrometry. AN - 75707287; 8472364 AB - A solid-phase extraction procedure was developed for the isolation of heroin, 6-acetylmorphine, and morphine from blood, plasma, saliva, and urine with subsequent assay by gas chromatography/mass spectrometry. Aprotic solvents, mild elution conditions, and an enzyme inhibitor were used to ensure maximum analyte stability. Samples were extracted and the extract was divided into two equal portions. One portion was assayed directly for heroin; detector response was linear over a concentration range of 1.0 to 250 micrograms/L. The second part of the extract was reacted with N-methyl-bis-trifluoroacetamide and assayed for the trifluoroacetyl derivatives of 6-acetylmorphine and morphine; detector response was linear over a concentration range of 1.0 to 500 micrograms/L. The limit of sensitivity was 1.0 microgram/L for each analyte. Hydrolysis of heroin to 6-acetylmorphine during extraction and analysis was < 5%. The method can be used to corroborate heroin use and to study the pharmacological effects of heroin and its metabolites. JF - Clinical chemistry AU - Goldberger, B A AU - Darwin, W D AU - Grant, T M AU - Allen, A C AU - Caplan, Y H AU - Cone, E J AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 670 EP - 675 VL - 39 IS - 4 SN - 0009-9147, 0009-9147 KW - Morphine Derivatives KW - 0 KW - Heroin KW - 70D95007SX KW - Morphine KW - 76I7G6D29C KW - 6-O-monoacetylmorphine KW - M5E47P1ZCH KW - Index Medicus KW - Saliva -- chemistry KW - Humans KW - Indicator Dilution Techniques KW - Substance-Related Disorders -- metabolism KW - Quality Control KW - Male KW - Heroin -- analysis KW - Morphine -- urine KW - Morphine -- blood KW - Morphine -- analysis KW - Gas Chromatography-Mass Spectrometry KW - Heroin -- blood KW - Heroin -- urine KW - Body Fluids -- chemistry KW - Morphine Derivatives -- urine KW - Morphine Derivatives -- blood KW - Morphine Derivatives -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75707287?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+chemistry&rft.atitle=Measurement+of+heroin+and+its+metabolites+by+isotope-dilution+electron-impact+mass+spectrometry.&rft.au=Goldberger%2C+B+A%3BDarwin%2C+W+D%3BGrant%2C+T+M%3BAllen%2C+A+C%3BCaplan%2C+Y+H%3BCone%2C+E+J&rft.aulast=Goldberger&rft.aufirst=B&rft.date=1993-04-01&rft.volume=39&rft.issue=4&rft.spage=670&rft.isbn=&rft.btitle=&rft.title=Clinical+chemistry&rft.issn=00099147&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-14 N1 - Date created - 1993-05-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Substrate-specific proteases (BLT-esterase) are localized predominantly in the natural killer cells of unprimed mice. AN - 75707194; 8482926 AB - In leukocytes isolated from unprimed mice, the levels of extractable N alpha-Cbz-Lys-thiobenzylesteresterase (BLT-esterase) closely correlated with the number of natural killer (NK) cells. The spleens of mice that exhibit severe combined immunodeficiency (SCID) contained much higher levels of this enzyme than other mouse strains. Treatments that resulted in a local accumulation of NK cells (as assessed by lytic activity) produced a concomitant increase in BLT-esterase activity. However, short-term in vitro treatment of spleen cells with interferon (IFN)-alpha/beta indicated that BLT-esterase levels correlated more closely with absolute numbers of NK cells than with their lytic capacity. There was a very good correlation between the numbers of cells bearing the NK phenotype (NK-1.1+) and BLT-esterase levels. Cells positively sorted using the NK-specific antibodies NK-1.1 and LGL-1 had high enzymatic activity. The BLT-esterase levels were high in both the NK-1.1+/LGL-1- and NK-1.1+/LGL-1+ subsets. Highly purified CD4+ and CD8+ T cells and sIg+ B cells demonstrated negligible enzyme, as did populations of cells highly enriched for macrophages or neutrophils. However, it should be stressed that the inbred mice used on this study have been maintained in a pathogen-free facility. It would be anticipated that mice maintained under less stringent conditions could exhibit appreciable levels of BLT-esterase activity in their T cells. Nonetheless, BLT-esterase is present at high levels in NK cells and cannot be regarded as a T cell-specific enzyme. JF - Journal of leukocyte biology AU - Sayers, T J AU - Mason, L H AU - Pilaro, A AU - Wiltrout, T A AU - Komschlies, K AU - Munger, W L AU - Wiltrout, R H AD - Biological Carcinogenesis Development Program, PRI/DynCorp, NCI-FCRDC, Frederick, Maryland 21702-1201. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 454 EP - 461 VL - 53 IS - 4 SN - 0741-5400, 0741-5400 KW - Interferon Inducers KW - 0 KW - Interferon Type I KW - Recombinant Proteins KW - Poly I-C KW - 24939-03-5 KW - Polylysine KW - 25104-18-1 KW - poly ICLC KW - 59789-29-6 KW - Interferon-gamma KW - 82115-62-6 KW - Granzymes KW - EC 3.4.21.- KW - Serine Endopeptidases KW - Carboxymethylcellulose Sodium KW - K679OBS311 KW - Index Medicus KW - Animals KW - Liver -- enzymology KW - Interferon-gamma -- pharmacology KW - Mice, Nude KW - Mice KW - Mice, Inbred BALB C KW - Carboxymethylcellulose Sodium -- pharmacology KW - Poly I-C -- pharmacology KW - Polylysine -- pharmacology KW - Interferon Inducers -- pharmacology KW - Interferon Type I -- pharmacology KW - Liver -- drug effects KW - Kinetics KW - Lymph Nodes -- enzymology KW - T-Lymphocyte Subsets -- immunology KW - Mice, Inbred C57BL KW - Spleen -- immunology KW - Flow Cytometry KW - Substrate Specificity KW - Mice, SCID KW - Lymph Nodes -- drug effects KW - Male KW - Serine Endopeptidases -- metabolism KW - Killer Cells, Natural -- immunology KW - Killer Cells, Natural -- enzymology KW - Killer Cells, Natural -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75707194?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+leukocyte+biology&rft.atitle=Substrate-specific+proteases+%28BLT-esterase%29+are+localized+predominantly+in+the+natural+killer+cells+of+unprimed+mice.&rft.au=Sayers%2C+T+J%3BMason%2C+L+H%3BPilaro%2C+A%3BWiltrout%2C+T+A%3BKomschlies%2C+K%3BMunger%2C+W+L%3BWiltrout%2C+R+H&rft.aulast=Sayers&rft.aufirst=T&rft.date=1993-04-01&rft.volume=53&rft.issue=4&rft.spage=454&rft.isbn=&rft.btitle=&rft.title=Journal+of+leukocyte+biology&rft.issn=07415400&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-03 N1 - Date created - 1993-06-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Maturational changes in dermal absorption of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in Fischer 344 rats. AN - 75705095; 8480330 AB - An earlier study indicated that percutaneous absorption of a 40-nmol dose of TCDD decreased with aging in rats, suggesting that the potential for systemic exposure following dermal contact would be decreased in older age groups. In this study, maturational changes in potential for systemic exposure to TCDD following dermal application of a low dose (200 pmol) of this chemical were examined in male Fischer 344 rats. Absorption, tissue distribution, and elimination of TCDD, measured as TCDD-derived radioactivity, were examined 72 hr after dermal application of 200 pmol [3H]TCDD (111 pmol/cm2 applied over 1.8 cm2) to the interscapular region of 3-, 5-, 8-, 10-, and 36-week-old rats. The dose was applied in 60 microliters acetone and the application site was covered with a perforated metal cap; animals were held in individual metabolism cages. Dermal absorption was greatest in 3-week-old rats (approximately 129 pmol; approximately 64% of the administered dose), decreasing to approximately 80 pmol (approximately 40%) in 5-, 8-, and 10-week-old rats and to 45 pmol (approximately 22%) in 36-week-old rats. In each age group, 70 to 80% of the radioactivity remaining at the application site 72 hr after dosing could be removed with acetone swabs. Major tissue depots of radioactivity were liver and fat; skin and muscle were minor depots. Changes in distribution of absorbed TCDD-derived radioactivity reflected changes in body mass of these depots; however, tissue concentration also varied. Whole body dissection was performed on rats to determine body mass of tissue depots. Adipose tissue content (Y) increased linearly with body weight (X), Y = 0.03X + 2.1 (r2 = 0.95). Elimination of absorbed TCDD-derived radioactivity was incomplete in all age groups with larger residues being recovered in the carcass. Results indicate that TCDD is absorbed to a greater degree through skin of very young animals and that a significant decrease in potential for systemic exposure may occur during maturation and again during aging. JF - Toxicology and applied pharmacology AU - Anderson, Y B AU - Jackson, J A AU - Birnbaum, L S AD - Experimental Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 214 EP - 220 VL - 119 IS - 2 SN - 0041-008X, 0041-008X KW - Polychlorinated Dibenzodioxins KW - 0 KW - Index Medicus KW - Rats KW - Aging -- physiology KW - Animals KW - Rats, Inbred F344 KW - Administration, Cutaneous KW - Tissue Distribution KW - Male KW - Polychlorinated Dibenzodioxins -- pharmacokinetics KW - Polychlorinated Dibenzodioxins -- administration & dosage KW - Polychlorinated Dibenzodioxins -- toxicity KW - Skin Absorption -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75705095?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+applied+pharmacology&rft.atitle=Maturational+changes+in+dermal+absorption+of+2%2C3%2C7%2C8-tetrachlorodibenzo-p-dioxin+%28TCDD%29+in+Fischer+344+rats.&rft.au=Anderson%2C+Y+B%3BJackson%2C+J+A%3BBirnbaum%2C+L+S&rft.aulast=Anderson&rft.aufirst=Y&rft.date=1993-04-01&rft.volume=119&rft.issue=2&rft.spage=214&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=0041008X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-25 N1 - Date created - 1993-05-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Electrophysiological characterization of rat striatal neurons in vitro following a unilateral lesion of dopamine cells. AN - 75702081; 8480280 AB - The effects of a unilateral 6 to 19-week lesion of dopamine cells on the excitability of rat striatal neurons were investigated in vitro using the intracellularly recorded membrane properties of neurons obtained ipsilateral and contralateral to 6-hydroxydopamine (6-OHDA) injection sites. Neurons ipsilateral to the lesion site and in striatal tissue depleted of dopamine exhibited resting membrane potentials and membrane resistances similar to those recorded in contralateral striatal neurons. Denervation appeared to have no appreciable effect on the proportion of neurons exhibiting various patterns of neuronal spiking (repetitive, bursting, or single spike) evoked by depolarizing current pulses. Current-voltage determinations revealed nominal rectification in the majority of neurons and marked nonlinearity consistent with inward rectification at potentials hyperpolarized and depolarized to rest in a large proportion of the remaining neurons. Neurons ipsilateral to 6-OHDA lesion sites exhibited these relationships in the same proportion as contralateral control cells. However, ipsilateral neurons with nominal rectification exhibited an average rate constant for the early onset of small hyperpolarizing membrane transients which was significantly smaller than that of controls. This finding suggests that intrinsic membrane parameters regulating the excitability of certain striatal neurons may be under the influence of dopamine or other factors closely associated with nigrostriatal nerve terminals. JF - Synapse (New York, N.Y.) AU - Twery, M J AU - Thompson, L A AU - Walters, J R AD - Cellular Physiology and Neurotransmission Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 322 EP - 332 VL - 13 IS - 4 SN - 0887-4476, 0887-4476 KW - Oxidopamine KW - 8HW4YBZ748 KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Rats KW - Animals KW - Rats, Sprague-Dawley KW - Oxidopamine -- toxicity KW - Membrane Potentials -- physiology KW - Electrophysiology KW - Cell Membrane -- physiology KW - Male KW - Corpus Striatum -- cytology KW - Corpus Striatum -- physiology KW - Neurons -- physiology KW - Dopamine -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75702081?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Synapse+%28New+York%2C+N.Y.%29&rft.atitle=Electrophysiological+characterization+of+rat+striatal+neurons+in+vitro+following+a+unilateral+lesion+of+dopamine+cells.&rft.au=Twery%2C+M+J%3BThompson%2C+L+A%3BWalters%2C+J+R&rft.aulast=Twery&rft.aufirst=M&rft.date=1993-04-01&rft.volume=13&rft.issue=4&rft.spage=322&rft.isbn=&rft.btitle=&rft.title=Synapse+%28New+York%2C+N.Y.%29&rft.issn=08874476&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-25 N1 - Date created - 1993-05-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Treatment of Parkinson's disease with the partial dopamine agonist EMD 49980. AN - 75699914; 8097280 AB - The motor effects of the partial dopamine agonist EMD 49980 were evaluated in parkinsonian patients under controlled conditions. EMD 49980 monotherapy resulted in a mild improvement in parkinsonian symptoms, but when co-administered with levodopa, had no significant effect on dyskinesias or on the antiparkinsonian effect of the dopamine precursor. These results suggest that EMD 49980 exerts a net weak dopamine agonist effect but fails to ameliorate levodopa-induced dyskinesias. JF - Movement disorders : official journal of the Movement Disorder Society AU - Bravi, D AU - Davis, T L AU - Mouradian, M M AU - Chase, T N AD - Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 195 EP - 197 VL - 8 IS - 2 SN - 0885-3185, 0885-3185 KW - Dopamine Agents KW - 0 KW - Indoles KW - Pyridines KW - Receptors, Dopamine KW - roxindole KW - 43227SMS0O KW - Levodopa KW - 46627O600J KW - Index Medicus KW - Brain -- physiopathology KW - Dyskinesia, Drug-Induced -- drug therapy KW - Double-Blind Method KW - Humans KW - Brain -- drug effects KW - Adult KW - Neurologic Examination -- drug effects KW - Levodopa -- therapeutic use KW - Middle Aged KW - Dyskinesia, Drug-Induced -- physiopathology KW - Levodopa -- adverse effects KW - Male KW - Female KW - Receptors, Dopamine -- drug effects KW - Dopamine Agents -- therapeutic use KW - Receptors, Dopamine -- physiology KW - Indoles -- therapeutic use KW - Pyridines -- therapeutic use KW - Parkinson Disease -- physiopathology KW - Parkinson Disease -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75699914?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Movement+disorders+%3A+official+journal+of+the+Movement+Disorder+Society&rft.atitle=Treatment+of+Parkinson%27s+disease+with+the+partial+dopamine+agonist+EMD+49980.&rft.au=Bravi%2C+D%3BDavis%2C+T+L%3BMouradian%2C+M+M%3BChase%2C+T+N&rft.aulast=Bravi&rft.aufirst=D&rft.date=1993-04-01&rft.volume=8&rft.issue=2&rft.spage=195&rft.isbn=&rft.btitle=&rft.title=Movement+disorders+%3A+official+journal+of+the+Movement+Disorder+Society&rft.issn=08853185&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-18 N1 - Date created - 1993-05-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Validity of exposure in one job as a surrogate for exposure in a cohort study. AN - 75699240; 8480771 AB - Frequently, information pertaining to only one job is available or used to evaluate risk estimates of disease in occupational epidemiologic research. The amount of misclassification that such a practice could create has not, however, been examined. We used data from a mortality study of workers employed in 10 formaldehyde-producing or -using plants to address how closely several parameters of exposure based on the first, longest, or last job held in a company compared with those based on the worker's entire employment history at the plant. The best predictor for cumulative formaldehyde exposure at the plant was the longest job at that plant, with a correlation coefficient (r) of 0.70. The correlation with average exposure over the worker's employment was 0.77 for the first job and 0.74 for the longest and last jobs. Peak exposures and highest exposure levels experienced in the plant were more closely related to the first job (r = 0.72 and r = 0.74). The highest correlation with any of the measures was never with the last job. Variation between plants for each of these comparisons, however, was wide. These findings indicate that the use of a single job as a surrogate for exposure received at a particular worksite can result in different degrees of misclassification for different exposure measures. Even though the correlations were generally high, the associated misclassification of exposure could lead to a substantial underestimation of the relative risks in some situations. In this report two hypothetical examples show what effect the misclassification rates could have on estimates of disease risks. JF - American journal of industrial medicine AU - Vetter, R AU - Stewart, P A AU - Dosemeci, M AU - Blair, A AD - Occupational Studies Section, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 641 EP - 651 VL - 23 IS - 4 SN - 0271-3586, 0271-3586 KW - Formaldehyde KW - 1HG84L3525 KW - Index Medicus KW - Humans KW - Cohort Studies KW - Employment KW - Time Factors KW - Formaldehyde -- analysis KW - Occupational Exposure -- statistics & numerical data KW - Occupational Exposure -- analysis KW - Environmental Monitoring -- methods KW - Chemical Industry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75699240?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+industrial+medicine&rft.atitle=Validity+of+exposure+in+one+job+as+a+surrogate+for+exposure+in+a+cohort+study.&rft.au=Vetter%2C+R%3BStewart%2C+P+A%3BDosemeci%2C+M%3BBlair%2C+A&rft.aulast=Vetter&rft.aufirst=R&rft.date=1993-04-01&rft.volume=23&rft.issue=4&rft.spage=641&rft.isbn=&rft.btitle=&rft.title=American+journal+of+industrial+medicine&rft.issn=02713586&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-27 N1 - Date created - 1993-05-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Effect of varying the onset of exposure to DDT on its modulation of AFB1-induced hepatocarcinogenesis in the rat. AN - 75693006; 8097137 AB - We have previously reported that p,p'-dichlorodiphenyl-trichloroethane (DDT) inhibited the hepatocarcinogenicity of aflatoxin B1 (AFB1) if given to rats 1 week prior to AFB1 but could enhance the carcinogenesis when given 1 week after the completion of AFB1 treatment. However, simultaneous administration of DDT with AFB1 resulted in a slight reduction in the incidence of liver tumours. In the present experiment in which the dose of AFB1 was reduced to about half of that used previously, we observed that DDT markedly inhibited the hepatocarcinogenesis if given to animals starting at the same time with AFB1. On the other hand, giving DDT to animals starting in the middle of AFB1 treatment resulted in a significant enhancement of hepatocarcinogenesis. DDT exhibited a maximal tumour promoting effect when given either 1 or 3 weeks after completion of AFB1 treatment. It enhanced the number of animals bearing liver carcinomas as well as the number of carcinomas per animal. Determination of gamma-glutamyltranspeptidase in the serum revealed that the activity increased only in animals bearing big and/or a number of carcinomas in the livers especially in those promoted by DDT. These results therefore demonstrated that DDT will act as an inhibitor of AFB1-induced hepatocarcinogenesis if it is given to animals starting either prior to or at the same time as carcinogen. On the other hand, it will act as a tumour promoter if given to animals starting either in the middle of or after the completion of AFB1 treatment. JF - Carcinogenesis AU - Rojanapo, W AU - Kupradinun, P AU - Tepsuwan, A AU - Tanyakaset, M AD - Biochemistry and Chemical Carcinogenesis Section, National Cancer Institute, Bangkok, Thailand. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 663 EP - 667 VL - 14 IS - 4 SN - 0143-3334, 0143-3334 KW - Aflatoxin B1 KW - 9N2N2Y55MH KW - DDT KW - CIW5S16655 KW - gamma-Glutamyltransferase KW - EC 2.3.2.2 KW - Dimethyl Sulfoxide KW - YOW8V9698H KW - Index Medicus KW - Rats KW - Animals KW - Drug Administration Schedule KW - Rats, Wistar KW - gamma-Glutamyltransferase -- blood KW - Male KW - Organ Size -- drug effects KW - Liver -- pathology KW - Liver -- enzymology KW - DDT -- administration & dosage KW - Cocarcinogenesis KW - Liver Neoplasms, Experimental -- pathology KW - Liver -- drug effects KW - Liver Neoplasms, Experimental -- enzymology KW - DDT -- toxicity KW - Aflatoxin B1 -- administration & dosage KW - Liver Neoplasms, Experimental -- chemically induced KW - Aflatoxin B1 -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75693006?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Effect+of+varying+the+onset+of+exposure+to+DDT+on+its+modulation+of+AFB1-induced+hepatocarcinogenesis+in+the+rat.&rft.au=Rojanapo%2C+W%3BKupradinun%2C+P%3BTepsuwan%2C+A%3BTanyakaset%2C+M&rft.aulast=Rojanapo&rft.aufirst=W&rft.date=1993-04-01&rft.volume=14&rft.issue=4&rft.spage=663&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-17 N1 - Date created - 1993-05-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The role of O6-alkylguanine-DNA alkyltransferase in protecting Rat4 cells against the mutagenic effects of O6-substituted guanine residues incorporated in codon 12 of the H-ras gene. AN - 75691116; 8472320 AB - The role of rat O6-alkylguanine-DNA alkyltransferase (AGT) in modulating mutagenesis by O6-substituted guanines in the rat H-ras gene was examined. Rat4 cells were transfected with vectors carrying O6-methyl-, O6-ethyl- or O6-benzylguanine residues in place of the normal guanines at either the first, second, or both the first and second positions in codon 12 (GGA) of the H-ras coding sequence. The percentage of transformed colonies was determined for cells grown in normal medium or in medium containing O6-benzylguanine to completely deplete AGT. In parallel experiments with O6-methylguanine-containing vectors, the percentage of cellular DNA harboring codon 12 mutations was determined for normal cells and cells lacking AGT. A reasonable correspondence was observed between the percentage of mutated DNA and the percentage of transformed colonies produced in both types of cells. The results indicate that the contribution of AGT to the repair of O6-substituted guanine damage decreases as the O6 substituent is changed from methyl > ethyl > benzyl. Additionally, cellular AGT appears to repair an O6-methylguanine more readily at the first position of codon 12 than the second position. However, other repair mechanisms in these mammalian cells appear to play a major role in correcting low levels of O6-substituted guanine damage including O6-methylguanine damage. JF - Carcinogenesis AU - Bishop, R E AU - Dunn, L L AU - Pauly, G T AU - Dolan, M E AU - Moschel, R C AD - Chemistry of Carcinogenesis Laboratory, ABL-Basic Research Program, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 593 EP - 598 VL - 14 IS - 4 SN - 0143-3334, 0143-3334 KW - H-ras KW - Codon KW - 0 KW - O(6)-benzylguanine KW - 01KC87F8FE KW - 6-ethylguanine KW - 51866-19-4 KW - Guanine KW - 5Z93L87A1R KW - O-(6)-methylguanine KW - 9B710FV2AE KW - Methyltransferases KW - EC 2.1.1.- KW - O(6)-Methylguanine-DNA Methyltransferase KW - EC 2.1.1.63 KW - Index Medicus KW - Base Sequence KW - Cell Transformation, Neoplastic -- pathology KW - Transfection KW - Plasmids -- genetics KW - DNA Damage KW - Cells, Cultured KW - Molecular Sequence Data KW - Cell Transformation, Neoplastic -- genetics KW - Genes, ras -- genetics KW - DNA Repair KW - Codon -- genetics KW - Codon -- chemistry KW - Methyltransferases -- physiology KW - Guanine -- analogs & derivatives KW - Mutagenesis -- genetics KW - Guanine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75691116?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=The+role+of+O6-alkylguanine-DNA+alkyltransferase+in+protecting+Rat4+cells+against+the+mutagenic+effects+of+O6-substituted+guanine+residues+incorporated+in+codon+12+of+the+H-ras+gene.&rft.au=Bishop%2C+R+E%3BDunn%2C+L+L%3BPauly%2C+G+T%3BDolan%2C+M+E%3BMoschel%2C+R+C&rft.aulast=Bishop&rft.aufirst=R&rft.date=1993-04-01&rft.volume=14&rft.issue=4&rft.spage=593&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-17 N1 - Date created - 1993-05-17 N1 - Date revised - 2017-01-13 N1 - Gene symbol - H-ras N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Role of protein kinase C and cytokines on the function and production of cytolytic granules in alpha CD3-activated killer-cell-mediated killing of tumor cells. AN - 75687234; 8473055 AB - The effects of PMA and staurosporine (PKC depletor/antagonist) and IL-2/IL4 were used to determine the role of PKC and cytokine on alpha CD3-induced activated killer cells (CD3-AK). The present study examines their effects on the production of BLT-esterase and on the effector function of CD3-AK cells as well as the cytolytic granules. The production of BLT-esterase generally correlated with the cytolytic activity of CD3-AK cells and was reduced by PKC depletor/inhibitor but increased by IL-4. In studying the effector function of CD3-AK cells, we found that adding PMA or SSP at the effector phase inhibited the PKC-dependent slow lysis. PMA, but not SSP, also reduced fast lysis, which was shown to be a PKC-independent event. Additional experiments were performed to determine the effect of PKC on the lytic granules and to ascertain whether PMA has other effects on the effector-to-target relationship unrelated to PKC. It was found that neither PMA nor SSP affects the function of cytolytic granules, as measured by hemolytic assay against anucleated target (SRBC). These findings indicate that PKC has no direct effect on the granules. During testing against the nucleated tumor target through a novel approach using non-cytolytic surrogate killers, the lytic activity of the granules was inhibited by PMA, suggesting that exocytosis or delivery of granules to nucleated target cells may require mobilization of intracellular Ca2+ in the killer cells, and this process is inhibited by PMA. Our findings indicate that PKC and cytokines regulate the production but not the lytic activity of cytolytic granules. Nonetheless, delivery of cytolytic granules from killer cells to the nucleated tumor target appears to be a Ca(2+)-dependent event unrelated to PKC. JF - International journal of cancer AU - Wu, J AU - Shiver, J AU - Hargrove, M E AU - Ting, C C AD - Office of the Director, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/04/01/ PY - 1993 DA - 1993 Apr 01 SP - 973 EP - 977 VL - 53 IS - 6 SN - 0020-7136, 0020-7136 KW - Alkaloids KW - 0 KW - Antibodies KW - Antigens, CD3 KW - Cytokines KW - Protein Kinase C KW - EC 2.7.11.13 KW - Granzymes KW - EC 3.4.21.- KW - Serine Endopeptidases KW - Staurosporine KW - H88EPA0A3N KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Mice KW - Cytotoxicity, Immunologic KW - Tumor Cells, Cultured KW - Serine Endopeptidases -- metabolism KW - Immunotherapy, Adoptive KW - Mice, Inbred C57BL KW - Alkaloids -- pharmacology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Female KW - Protein Kinase C -- antagonists & inhibitors KW - Neoplasms, Experimental -- therapy KW - Antigens, CD3 -- pharmacology KW - Cytoplasmic Granules -- physiology KW - Cytokines -- physiology KW - Protein Kinase C -- physiology KW - Cytoplasmic Granules -- drug effects KW - Antibody-Dependent Cell Cytotoxicity -- physiology KW - Killer Cells, Natural -- immunology KW - Killer Cells, Natural -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75687234?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+cancer&rft.atitle=Role+of+protein+kinase+C+and+cytokines+on+the+function+and+production+of+cytolytic+granules+in+alpha+CD3-activated+killer-cell-mediated+killing+of+tumor+cells.&rft.au=Wu%2C+J%3BShiver%2C+J%3BHargrove%2C+M+E%3BTing%2C+C+C&rft.aulast=Wu&rft.aufirst=J&rft.date=1993-04-01&rft.volume=53&rft.issue=6&rft.spage=973&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=00207136&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-14 N1 - Date created - 1993-05-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - 7-Alkyldeoxyguanosine adduct detection by two-step HPLC and the 32P-postlabeling assay. AN - 75686122; 8386066 AB - 7-Alkyldeoxyguanosine DNA adducts may be a marker for some N-nitroso compound exposures and subsequent human cancer risk. A sensitive and highly specific assay for the detection of 7-methyl-2'-deoxyguanosine-3'-monophosphate (7-methyldGp) and 7-ethyl-2'-deoxyguanosine-3'-monophosphate (7-ethyldGp) has been developed by combining two different HPLC purification steps with the 32P-postlabeling assay. We previously reported that ion-pair reverse-phase (IP) chromatography coupled with the 32P-postlabeling assay detects 7-methyldGp in human lung, but have found that other nucleotides and unknown adducts co-elute. Thus, weak anion exchange (AE) HPLC was added in tandem with IP HPLC prior to the 32P-postlabeling assay. 2'-Deoxyguanosine-3'-monophosphate (dGp) is incorporated into the assay as an internal standard for the assessment of enzyme labeling efficiency and adduct recovery. The methodology was validated using radiolabeled DNA and liquid scintillation counting, which accounts for adduct loss from enzymatic digestion to detection. Levels of 7-ethyldGp also were correlated with accelerator mass spectrometry. The overall adduct recovery with this method was 58% for 7-methyldGp and 98% for 7-ethyldGp. The detection limit for both assays using 100 micrograms of DNA was one adduct in 10(8) unmodified dGp. 7-MethyldGp and 7-ethyldGp levels were determined in ten human lung samples at levels of 1.4-5.4 and 0.6-3.1 adducts per 10(7) dGp respectively, and in five human lymphocyte samples at levels of 5.0-8.3 and 0.3-1.4 adducts per 10(7) dGp respectively. Combining the two HPLC purification steps and the 32P-postlabeling assay attains chemical specificity, retains sufficient quantitative sensitivity and should be useful in human biomonitoring studies. JF - Carcinogenesis AU - Kato, S AU - Petruzzelli, S AU - Bowman, E D AU - Turteltaub, K W AU - Blomeke, B AU - Weston, A AU - Shields, P G AD - Laboratory of Human Carcinogenesis, National Cancer Institute, NIH Bethesda, MD 20892. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 545 EP - 550 VL - 14 IS - 4 SN - 0143-3334, 0143-3334 KW - Deoxyguanine Nucleotides KW - 0 KW - Phosphorus Radioisotopes KW - 7-methyl-2'-deoxyguanosine 3'-monophosphate KW - 123497-14-3 KW - 7-ethyl-2'-deoxyguanosine-3'-monophosphate KW - 149206-55-3 KW - Methylnitrosourea KW - 684-93-5 KW - Guanosine Monophosphate KW - 85-32-5 KW - DNA KW - 9007-49-2 KW - Ethylnitrosourea KW - P8M1T4190R KW - Index Medicus KW - Animals KW - Cattle KW - Humans KW - Methylnitrosourea -- pharmacology KW - Ethylnitrosourea -- pharmacology KW - Deoxyguanine Nucleotides -- analysis KW - Guanosine Monophosphate -- analysis KW - Guanosine Monophosphate -- analogs & derivatives KW - DNA -- analysis KW - Chromatography, High Pressure Liquid -- methods KW - DNA -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75686122?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=7-Alkyldeoxyguanosine+adduct+detection+by+two-step+HPLC+and+the+32P-postlabeling+assay.&rft.au=Kato%2C+S%3BPetruzzelli%2C+S%3BBowman%2C+E+D%3BTurteltaub%2C+K+W%3BBlomeke%2C+B%3BWeston%2C+A%3BShields%2C+P+G&rft.aulast=Kato&rft.aufirst=S&rft.date=1993-04-01&rft.volume=14&rft.issue=4&rft.spage=545&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-17 N1 - Date created - 1993-05-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - 4-Chloro-3-hydroxyanthranilate, 6-chlorotryptophan and norharmane attenuate quinolinic acid formation by interferon-gamma-stimulated monocytes (THP-1 cells). AN - 75685230; 8471029 AB - Accumulation of quinolinic acid and L-kynurenine occurs in the brain and/or blood following immune activation, and may derive from L-tryptophan following induction of indoleamine 2,3-dioxygenase and other kynurenine-pathway enzymes. In the present study a survey of various cell lines derived from either brain or systemic tissues showed that, while all cells examined responded to interferon-gamma by increased conversion of L-[13C6]tryptophan into L-kynurenine (human: B-lymphocytes, neuroblastoma, glioblastoma, lung, liver, kidney; rat brain: microglia, astrocytes and oligodendrocytes), only macrophage-derived cells (peripheral-blood mononuclear cells; THP-1, U-937) and certain liver cells (SKHep1) synthesized [13C6]quinolinic acid. Tumour necrosis factor-alpha enhanced the effects of interferon-gamma in THP-1 cells. Norharmane, 6-chloro-DL-tryptophan and 4-chloro-3-hydroxyanthranilate attenuated quinolinic acid formation by THP-1 cells with IC50 values of 51 microM, 58 microM and 0.11 microM respectively. Norharmane and 6-chloro-DL-tryptophan attenuated L-kynurenine formation with IC50 values of 43 microM and 51 microM respectively, whereas 4-chloro-3-hydroxyanthranilate had no effect on L-kynurenine accumulation. The reductions in L-kynurenine and quinolinic acid formation are consistent with the reports that norharmane is an inhibitor of indoleamine 2,3-dioxygenase, 6-chloro-DL-tryptophan is metabolized through the kynurenine pathway, and 4-chloro-3-hydroxyanthranilate is an inhibitor of 3-hydroxyanthranilate 3,4-dioxygenase. These results suggest that many tissues may contribute to the production of L-kynurenine following indoleamine 2,3-dioxygenase induction and immune activation. Quinolinic acid may be directly synthesized from L-tryptophan in both macrophages and certain types of liver cells, although uptake of quinolinic acid precursors from blood may contribute to quinolinic acid synthesis in cells that cannot convert L-kynurenine into quinolinic acid. JF - The Biochemical journal AU - Saito, K AU - Chen, C Y AU - Masana, M AU - Crowley, J S AU - Markey, S P AU - Heyes, M P AD - Section on Analytical Biochemistry, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1993/04/01/ PY - 1993 DA - 1993 Apr 01 SP - 11 EP - 14 VL - 291 ( Pt 1) SN - 0264-6021, 0264-6021 KW - Carbolines KW - 0 KW - Tumor Necrosis Factor-alpha KW - 6-chlorotryptophan KW - 17808-35-4 KW - 3-Hydroxyanthranilic Acid KW - 1UQB1BT4OT KW - 4-chloro-3-hydroxyanthranilic acid KW - 23219-33-2 KW - Kynurenine KW - 343-65-7 KW - Harmine KW - 4FHH5G48T7 KW - Interferon-gamma KW - 82115-62-6 KW - Tryptophan KW - 8DUH1N11BX KW - norharman KW - 94HMA1I78O KW - Quinolinic Acid KW - F6F0HK1URN KW - Index Medicus KW - Rats KW - Animals KW - Tumor Cells, Cultured KW - Brain -- cytology KW - Humans KW - Brain -- drug effects KW - Tumor Necrosis Factor-alpha -- pharmacology KW - Kynurenine -- metabolism KW - Brain -- metabolism KW - Macrophages -- drug effects KW - Cell Line KW - Macrophages -- metabolism KW - Tryptophan -- pharmacology KW - Tryptophan -- analogs & derivatives KW - 3-Hydroxyanthranilic Acid -- pharmacology KW - Quinolinic Acid -- metabolism KW - Leukocytes, Mononuclear -- metabolism KW - Harmine -- analogs & derivatives KW - Interferon-gamma -- pharmacology KW - Tryptophan -- metabolism KW - Leukocytes, Mononuclear -- drug effects KW - 3-Hydroxyanthranilic Acid -- analogs & derivatives KW - Harmine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75685230?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Biochemical+journal&rft.atitle=4-Chloro-3-hydroxyanthranilate%2C+6-chlorotryptophan+and+norharmane+attenuate+quinolinic+acid+formation+by+interferon-gamma-stimulated+monocytes+%28THP-1+cells%29.&rft.au=Saito%2C+K%3BChen%2C+C+Y%3BMasana%2C+M%3BCrowley%2C+J+S%3BMarkey%2C+S+P%3BHeyes%2C+M+P&rft.aulast=Saito&rft.aufirst=K&rft.date=1993-04-01&rft.volume=291+%28+Pt+1%29&rft.issue=&rft.spage=11&rft.isbn=&rft.btitle=&rft.title=The+Biochemical+journal&rft.issn=02646021&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-12 N1 - Date created - 1993-05-12 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Cell Biol. 1980 Jun;85(3):890-902 [6248568] Neuroscience. 1992 Nov;51(1):25-39 [1465184] Mol Aspects Med. 1983;6(2):101-97 [6371429] Arch Biochem Biophys. 1984 Aug 1;232(2):602-9 [6431906] Neuroscience. 1985 Jul;15(3):597-617 [2866466] J Neuroimmunol. 1987 Jul-Aug;15(3):263-78 [3110208] J Neurochem. 1993 Jan;60(1):180-92 [8417138] Proc Natl Acad Sci U S A. 1988 Jun;85(11):4079-81 [2967497] Anal Biochem. 1988 Aug 1;172(2):518-25 [3189792] Biochim Biophys Acta. 1989 Jul 11;1012(2):140-7 [2500976] Biol Chem Hoppe Seyler. 1989 Sep;370(9):1063-9 [2482041] J Neurochem. 1990 Sep;55(3):738-44 [2384749] Ann Neurol. 1991 Feb;29(2):202-9 [1826418] Neurosci Lett. 1991 Jan 28;122(2):265-9 [1827518] Brain Res. 1991 Feb 1;540(1-2):353-6 [1647247] Brain Res. 1991 Apr 12;546(1):151-4 [1830237] J Comp Neurol. 1991 Dec 1;314(1):125-35 [1797868] Biochem J. 1992 May 1;283 ( Pt 3):633-5 [1534219] FASEB J. 1992 Aug;6(11):2977-89 [1322853] J Neuropsychiatry Clin Neurosci. 1992 Summer;4(3):270-9 [1386770] J Neuroimmunol. 1992 Sep;40(1):71-80 [1387655] Brain. 1992 Oct;115 ( Pt 5):1249-73 [1422788] Arch Biochem Biophys. 1980 Aug;203(1):161-6 [6893263] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Regulation of thymidylate synthase in human colon cancer cells treated with 5-fluorouracil and interferon-gamma. AN - 75683739; 8474431 AB - The effects of fluorouracil (5-FU) and interferon-gamma (IFN-gamma) on the regulation of thymidylate synthase (TS) gene expression were investigated in the human colon cancer H630 cell line. By Western immunoblot analysis, TS protein levels in H630 cells were increased 3-, 5.5-, 5-, and 2.5-fold after 8-, 16-, 24-, and 36-hr exposure to 1 microM 5-FU, respectively. When H630 cells were exposed to varying concentrations of 5-FU (0.3-10 microM) for 24 hr, increases in TS protein up to 5.5-fold were observed. A 24-hr exposure to 1 microM 5-FU resulted in a 4.5-fold increase in the level of TS protein, whereas in 5-FU/IFN-gamma-treated cells TS protein was increased by only 1.8-fold, compared with control cells. IFN-gamma treatment alone did not affect TS protein levels, relative to control. Northern blot analysis revealed no changes in TS mRNA levels when H630 cells were exposed either to 1 microM 5-FU for 8-36 hr, to varying concentrations of 5-FU (0.3-10 microM) for 24 hr, or to the combination of 5-FU and IFN-gamma. Pulse-labeling studies with [35S]methionine demonstrated a 3.5-fold increase in net synthesis of TS in cells treated with 1 microM 5-FU, whereas the level of newly synthesized TS increased only 1.5-fold in cells treated with 5-FU/IFN-gamma, compared with control cells. Pulse-chase studies revealed that the half-lives of TS protein in control and 5-FU-treated cells were equivalent. These findings demonstrate that the increase in TS protein after 5-FU exposure and the subsequent inhibitory effect of IFN-gamma on TS protein expression are both regulated at the post-transcriptional level. JF - Molecular pharmacology AU - Chu, E AU - Koeller, D M AU - Johnston, P G AU - Zinn, S AU - Allegra, C J AD - NCI-Navy Medical Oncology Branch, Bethesda, Maryland 20889. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 527 EP - 533 VL - 43 IS - 4 SN - 0026-895X, 0026-895X KW - RNA, Messenger KW - 0 KW - RNA, Neoplasm KW - Interferon-gamma KW - 82115-62-6 KW - Thymidylate Synthase KW - EC 2.1.1.45 KW - Fluorouracil KW - U3P01618RT KW - Index Medicus KW - Protein Biosynthesis -- drug effects KW - Tumor Cells, Cultured KW - Enzyme Induction -- drug effects KW - RNA, Neoplasm -- drug effects KW - Humans KW - RNA, Messenger -- drug effects KW - Enzyme Stability -- drug effects KW - Drug Synergism KW - Gene Expression Regulation, Neoplastic -- drug effects KW - Thymidylate Synthase -- genetics KW - Thymidylate Synthase -- drug effects KW - Interferon-gamma -- pharmacology KW - Fluorouracil -- pharmacology KW - Thymidylate Synthase -- biosynthesis KW - Colonic Neoplasms -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75683739?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+pharmacology&rft.atitle=Regulation+of+thymidylate+synthase+in+human+colon+cancer+cells+treated+with+5-fluorouracil+and+interferon-gamma.&rft.au=Chu%2C+E%3BKoeller%2C+D+M%3BJohnston%2C+P+G%3BZinn%2C+S%3BAllegra%2C+C+J&rft.aulast=Chu&rft.aufirst=E&rft.date=1993-04-01&rft.volume=43&rft.issue=4&rft.spage=527&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmacology&rft.issn=0026895X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-18 N1 - Date created - 1993-05-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Reexamination of the microsomal transformation of N-hydroxynorcocaine to norcocaine nitroxide. AN - 75682950; 8386313 AB - Cocaine is known to be associated with hepatotoxicity in laboratory animals, and there is recent evidence that it also induces liver damage in humans. In both cases an N-oxidative pathway is responsible. Cocaine (NCN) is first N-demethylated to norcocaine, followed by oxidation to N-hydroxynorcocaine (NCNOH) and norcocaine nitroxide (NCNO.). On the basis of ESR studies of NCNOH with rat liver microsomes, it has been proposed that NCNO. induces hepatotoxicity by futile redox cycling between NCNO. and NCNOH at the expense of NADPH. The reaction is reported to be accompanied by formation of superoxide and lipid peroxyl radicals. It has also been reported that the same toxic sequence occurs with rat brain microsomes, leading to the formation of reactive free radicals in the brain. We have reexamined the microsomal metabolism of NCNOH to investigate the mechanism more thoroughly. Spin traps [5,5-dimethyl-1-pyrroline N-oxide and alpha-(4-pyridyl-1-oxide)-N-tert-butylnitrone] were used to investigate the formation of reactive free radicals, including superoxide, in liver and brain microsomal incubations. In agreement with the literature, we detected a six-line spectrum of a radical adduct of alpha-(4-pyridyl-1-oxide)-N-tert-butylnitrone from liver microsome incubations. In contrast, our results showed that brain microsomes were completely inactive, contrary to the literature. In addition, we did not find any NCNO.- or NCNOH-dependent formation of superoxide with either brain or liver microsomes. JF - Molecular pharmacology AU - Lloyd, R V AU - Shuster, L AU - Mason, R P AD - Laboratory for Molecular Biophysics, National Institutes of Health Research Triangle Park, North Carolina 27709. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 645 EP - 648 VL - 43 IS - 4 SN - 0026-895X, 0026-895X KW - Lipid Peroxides KW - 0 KW - Superoxides KW - 11062-77-4 KW - 8-hydroxynorcocaine KW - 72182-43-5 KW - norcocaine nitroxide KW - 81652-42-8 KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Rats KW - Animals KW - Superoxides -- metabolism KW - Rats, Sprague-Dawley KW - Biotransformation KW - Microsomes, Liver -- metabolism KW - Electron Spin Resonance Spectroscopy KW - In Vitro Techniques KW - Lipid Peroxides -- metabolism KW - Male KW - Female KW - Cocaine -- analogs & derivatives KW - Microsomes -- metabolism KW - Brain -- metabolism KW - Cocaine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75682950?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+pharmacology&rft.atitle=Reexamination+of+the+microsomal+transformation+of+N-hydroxynorcocaine+to+norcocaine+nitroxide.&rft.au=Lloyd%2C+R+V%3BShuster%2C+L%3BMason%2C+R+P&rft.aulast=Lloyd&rft.aufirst=R&rft.date=1993-04-01&rft.volume=43&rft.issue=4&rft.spage=645&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmacology&rft.issn=0026895X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-18 N1 - Date created - 1993-05-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Granulocyte-macrophage colony-stimulating factor induces human melanoma-cell migration. AN - 75682503; 8473054 AB - Tumor metastasis is the primary cause of death for cancer patients. The metastatic cascade requires successful tumor cell invasion into and through vascular and parenchymal barriers. We have shown that autocrine motility factor (AMF, autotaxin) and the insulin-like growth factors (IGFs) induce tumor-cell migration. Since granulocyte-macrophage colony-stimulating factor (GM-CSF) has been shown to prime neutrophils for chemotaxis, we have therefore studied the influence of GM-CSF upon tumor cells and report that GM-CSF stimulates migration of these cells in a dose-dependent fashion. The ED50 for A2058 human melanoma cell line chemotaxis to GM-CSF is approx. 60 pM. The motile response to GM-CSF was additive to that of IGF-I and AMF, both of which are potent attractants for tumor cells. Pre-treatment of cells for 2 hr with non-toxic concentrations of pertussis toxin (PT) or amiloride resulted in a 50% inhibition of chemotaxis to GM-CSF. Therefore, GM-CSF, through PT- and amiloride-sensitive signal pathways, is a potent attractant for melanoma cells, the response to which is additive to that of other attractants. The presence of the GM-CSF receptor in A2058 melanoma cells was indicated by Northern-blot analysis which identified message transcripts of 2.1 and 3.0 kb. These data emphasize the versatility of the melanoma cell migration response to an array of cytokines, including GM-CSF. JF - International journal of cancer AU - Kohn, E C AU - Hollister, G H AU - DiPersio, J D AU - Wahl, S AU - Liotta, L A AU - Schiffmann, E AD - Medicine Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/04/01/ PY - 1993 DA - 1993 Apr 01 SP - 968 EP - 972 VL - 53 IS - 6 SN - 0020-7136, 0020-7136 KW - Chemotactic Factors KW - 0 KW - Receptors, Granulocyte-Macrophage Colony-Stimulating Factor KW - Recombinant Proteins KW - Granulocyte-Macrophage Colony-Stimulating Factor KW - 83869-56-1 KW - Index Medicus KW - Sensitivity and Specificity KW - Recombinant Proteins -- pharmacology KW - Tumor Cells, Cultured -- drug effects KW - Humans KW - Signal Transduction -- drug effects KW - Cell Movement -- drug effects KW - Receptors, Granulocyte-Macrophage Colony-Stimulating Factor -- analysis KW - Melanoma -- pathology KW - Melanoma -- secondary KW - Granulocyte-Macrophage Colony-Stimulating Factor -- pharmacology KW - Chemotactic Factors -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75682503?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+cancer&rft.atitle=Granulocyte-macrophage+colony-stimulating+factor+induces+human+melanoma-cell+migration.&rft.au=Kohn%2C+E+C%3BHollister%2C+G+H%3BDiPersio%2C+J+D%3BWahl%2C+S%3BLiotta%2C+L+A%3BSchiffmann%2C+E&rft.aulast=Kohn&rft.aufirst=E&rft.date=1993-04-01&rft.volume=53&rft.issue=6&rft.spage=968&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=00207136&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-14 N1 - Date created - 1993-05-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Evaluation of the stereoisomers of deprenyl for amphetamine-like discriminative stimulus effects in rats. AN - 75679714; 8473997 AB - The antiparkinsonian agent l-deprenyl, a selective monoamine oxidase (MAO)-B inhibitor, is a phenylalkylamine derivative which is metabolized in part to l-methamphetamine and l-amphetamine. As the clinical use of amphetamine-like psychostimulants is limited by their potential for abuse, we evaluated l-deprenyl for amphetamine-like discriminative stimulus effects over a range of experimental conditions. Male Fisher rats were trained under a 5-response, fixed-ratio schedule of stimulus-shock termination or a 10-response, fixed-ratio schedule of food-presentation to discriminate between d-amphetamine (1.0 mg/kg i.p.) and saline in a two-lever, operant conditioning procedure. Full generalization was obtained to l-amphetamine (1.0-2.0 mg/kg), d-deprenyl (10.0-17.0 mg/kg) and l-deprenyl (17.0 and 30.0 mg/kg) under both the food-presentation and stimulus-shock termination schedules, and increases in responding on the lever appropriate to d-amphetamine were dose-dependent. The dose-effect functions for l-amphetamine, l-deprenyl and d-deprenyl were shifted slightly to the left under the stimulus-shock termination schedule compared to the food-presentation schedule. When l-deprenyl (3.0 or 5.6 mg/kg i.p.) was given 30 min before d-amphetamine it produced a small shift to the left in the dose-effect function for d-amphetamine under the food-presentation schedule. l-Deprenyl produced clear generalization to the d-amphetamine stimulus only at very high doses of 17.0 to 30.0 mg/kg, doses about 10-fold higher than those that have a selective action on MAO-B vs. MAO-A and which start to have marked rate decreasing actions on food-reinforced responding.(ABSTRACT TRUNCATED AT 250 WORDS) JF - The Journal of pharmacology and experimental therapeutics AU - Yasar, S AU - Schindler, C W AU - Thorndike, E B AU - Szelenyi, I AU - Goldberg, S R AD - Behavioral Pharmacology and Genetics Section, National Institute on Drug Abuse Addiction Research Center, Baltimore, Maryland. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 1 EP - 6 VL - 265 IS - 1 SN - 0022-3565, 0022-3565 KW - Amphetamines KW - 0 KW - Selegiline KW - 2K1V7GP655 KW - Index Medicus KW - Rats KW - Eating KW - Animals KW - Stereoisomerism KW - Rats, Inbred F344 KW - Drug Interactions KW - Discrimination Learning KW - Dose-Response Relationship, Drug KW - Electric Stimulation KW - Male KW - Selegiline -- pharmacology KW - Amphetamines -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75679714?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.atitle=Evaluation+of+the+stereoisomers+of+deprenyl+for+amphetamine-like+discriminative+stimulus+effects+in+rats.&rft.au=Yasar%2C+S%3BSchindler%2C+C+W%3BThorndike%2C+E+B%3BSzelenyi%2C+I%3BGoldberg%2C+S+R&rft.aulast=Yasar&rft.aufirst=S&rft.date=1993-04-01&rft.volume=265&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.issn=00223565&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-18 N1 - Date created - 1993-05-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Species differences in the production and clearance of 1,3-butadiene metabolites: a mechanistic model indicates predominantly physiological, not biochemical, control. AN - 75678471; 8472325 AB - Inhaled 1,3-butadiene, a monomer used in the production of synthetic rubber and other resins, is metabolized to mutagenic and carcinogenic epoxide intermediates. A physiologically based pharmacokinetic model of the uptake, tissue distribution, and metabolism of butadiene was constructed to determine if the biochemical kinetic constants obtained from in vitro studies are consistent with the observed in vivo uptake and metabolism. The model includes compartments for lung, blood, fat, liver, other rapidly perfused tissues ('viscera') and slowly perfused tissues. Metabolism of butadiene was assumed to occur in viscera in addition to lung and liver. Enzymatic reaction rate equations for the formation of 1,2-epoxy-3-butene, for hydrolysis of this epoxide, and for its conjugation with glutathione were also included. Physiological and biochemical parameters for the mouse, rat and human were obtained from the literature; they were not adjusted to produce a fit to experimental data. The model was used to test the hypothesis that differences in uptake and clearance of butadiene by the three species are due to differences in the activities of the metabolizing enzymes. The model reproduces whole-body observations for the mouse and rat. It predicts that inhalation uptake of butadiene and formation and retention of epoxybutene are controlled to a much greater extent by physiological parameters than by biochemical parameters and that storage in the fat represents a significant fraction of the retained butadiene. Accumulation of epoxybutene in the blood is predicted to be higher in mice than in rats or humans, but accumulation of the epoxide intermediate in the liver is predicted to be highest in humans. The epoxide tissue concentrations predicted by the model do not, by themselves, correlate with tumor incidence in mice and rats, indicating that other factors are crucial for carcinogenesis induced by butadiene. JF - Carcinogenesis AU - Kohn, M C AU - Melnick, R L AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 619 EP - 628 VL - 14 IS - 4 SN - 0143-3334, 0143-3334 KW - Butadienes KW - 0 KW - Epoxy Compounds KW - Mutagens KW - 3,4-epoxy-1-butene KW - 478ERR5NKR KW - 1,3-butadiene KW - JSD5FGP5VD KW - Index Medicus KW - Rats KW - Animals KW - Epoxy Compounds -- blood KW - Humans KW - Body Burden KW - Adsorption KW - Mice KW - Time Factors KW - Species Specificity KW - Mutagens -- metabolism KW - Mutagens -- pharmacokinetics KW - Butadienes -- metabolism KW - Models, Biological KW - Butadienes -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75678471?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Species+differences+in+the+production+and+clearance+of+1%2C3-butadiene+metabolites%3A+a+mechanistic+model+indicates+predominantly+physiological%2C+not+biochemical%2C+control.&rft.au=Kohn%2C+M+C%3BMelnick%2C+R+L&rft.aulast=Kohn&rft.aufirst=M&rft.date=1993-04-01&rft.volume=14&rft.issue=4&rft.spage=619&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-17 N1 - Date created - 1993-05-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Oral gossypol in the treatment of metastatic adrenal cancer. AN - 75670844; 8473376 AB - Medical treatment of metastatic adrenal cancer is largely unsuccessful and has considerable toxicity. We previously demonstrated the activity of the plant toxin gossypol against human adrenal cancers in nude mice. We therefore examined the efficacy and toxicity of oral gossypol as a treatment for adrenal cancer in humans. Twenty-one patients with metastatic adrenal cancer received oral gossypol at doses of 30-70 mg/day. Patients were monitored for side effects of gossypol, changes in hormone secretion, and tumor response. Eighteen patients completed at least 6 weeks of gossypol treatment. Three of these patients, whose tumors were refractory to other chemotherapeutic agents, had partial tumor responses (> or = 50% decrease in tumor volume) that lasted from several months to over 1 yr. One patient had a minor response followed by resection of her remaining disease, 1 patient had stable disease, and 13 patients had disease progression. Three patients died of their disease without receiving sufficient gossypol to achieve detectable drug levels, and were eliminated from the final analysis. The side effects of gossypol were generally well tolerated; the only serious side effect was abdominal ileus that resolved when the drug was temporarily withheld and restarted at a lower dose. We conclude that oral gossypol can be used relatively safely on an outpatient basis for the treatment of metastatic adrenal cancer. The response rate is similar to the other agents currently available for adrenal cancer, and responses were seen in patients who had failed other chemotherapeutic regimens. This study provides the first indication that gossypol may have activity against cancer in humans, suggesting the need for further investigation of gossypol as an antitumor agent. JF - The Journal of clinical endocrinology and metabolism AU - Flack, M R AU - Pyle, R G AU - Mullen, N M AU - Lorenzo, B AU - Wu, Y W AU - Knazek, R A AU - Nisula, B C AU - Reidenberg, M M AD - Developmental Endocrinology Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 1019 EP - 1024 VL - 76 IS - 4 SN - 0021-972X, 0021-972X KW - Gossypol KW - KAV15B369O KW - Abridged Index Medicus KW - Index Medicus KW - Aged, 80 and over KW - Humans KW - Adult KW - Treatment Outcome KW - Tomography, X-Ray Computed KW - Aged KW - Middle Aged KW - Adolescent KW - Male KW - Female KW - Radiography, Thoracic KW - Adrenal Gland Neoplasms -- diagnostic imaging KW - Gossypol -- administration & dosage KW - Gossypol -- therapeutic use KW - Adrenal Gland Neoplasms -- secondary KW - Gossypol -- adverse effects KW - Adrenal Gland Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75670844?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+clinical+endocrinology+and+metabolism&rft.atitle=Oral+gossypol+in+the+treatment+of+metastatic+adrenal+cancer.&rft.au=Flack%2C+M+R%3BPyle%2C+R+G%3BMullen%2C+N+M%3BLorenzo%2C+B%3BWu%2C+Y+W%3BKnazek%2C+R+A%3BNisula%2C+B+C%3BReidenberg%2C+M+M&rft.aulast=Flack&rft.aufirst=M&rft.date=1993-04-01&rft.volume=76&rft.issue=4&rft.spage=1019&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+clinical+endocrinology+and+metabolism&rft.issn=0021972X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-18 N1 - Date created - 1993-05-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The assessment and clinical implications of haloperidol acute-dose, steady-state, and withdrawal pharmacokinetics. AN - 75668790; 8463444 AB - In order to evaluate comprehensively haloperidol pharmacokinetics under fixed-dose treatment conditions, psychiatric patients were studied after treatment with an acute dose, during maintenance therapy, and after withdrawal from haloperidol following steady-state conditions. After single doses, haloperidol appeared rapidly in serum, achieving peak concentration at a mean of 4.5 hours. The range of observed elimination half-life was broad, between 8.5 and 66.6 hours, with a mean of 19.5 hours. Under conditions of chronic dosing, serial measurements of steady-state serum concentration revealed intrapatient coefficients of variation between 2 and 72%. The mean for all patients was 26.4%. Body clearance decreased nonsignificantly, and elimination half-life increased significantly after chronic dosing compared with kinetic parameters determined after a single dose. The concentration of haloperidol in serum obtained at 8 hours after a single dose correlated most strongly (r = 0.73; p < 0.0001) with steady-state concentration resulting from chronic dosing. A value of 4 ng/ml or lower determined 8 hours after a single oral dose of 0.2 mg/kg identified patients who did not accumulate haloperidol during chronic dosing of 0.4 mg/kg per day above a presumed therapeutic range for haloperidol of 5 to 15 ng/ml. The implications of these data for the clinical use of haloperidol are discussed. JF - Journal of clinical psychopharmacology AU - Khot, V AU - DeVane, C L AU - Korpi, E R AU - Venable, D AU - Bigelow, L B AU - Wyatt, R J AU - Kirch, D G AD - Neuropsychiatry Branch, National Institute of Mental Health Neuroscience Center, Saint Elizabeths, Washington, DC. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 120 EP - 127 VL - 13 IS - 2 SN - 0271-0749, 0271-0749 KW - Haloperidol KW - J6292F8L3D KW - Index Medicus KW - Drug Administration Schedule KW - Psychiatric Status Rating Scales KW - Half-Life KW - Double-Blind Method KW - Dose-Response Relationship, Drug KW - Humans KW - Metabolic Clearance Rate -- physiology KW - Drug Monitoring KW - Adult KW - Male KW - Female KW - Haloperidol -- adverse effects KW - Schizophrenia -- blood KW - Haloperidol -- pharmacokinetics KW - Haloperidol -- administration & dosage KW - Schizophrenic Psychology KW - Schizophrenia -- drug therapy KW - Substance Withdrawal Syndrome -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75668790?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+psychopharmacology&rft.atitle=The+assessment+and+clinical+implications+of+haloperidol+acute-dose%2C+steady-state%2C+and+withdrawal+pharmacokinetics.&rft.au=Khot%2C+V%3BDeVane%2C+C+L%3BKorpi%2C+E+R%3BVenable%2C+D%3BBigelow%2C+L+B%3BWyatt%2C+R+J%3BKirch%2C+D+G&rft.aulast=Khot&rft.aufirst=V&rft.date=1993-04-01&rft.volume=13&rft.issue=2&rft.spage=120&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+psychopharmacology&rft.issn=02710749&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-06 N1 - Date created - 1993-05-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Surgical management of pulmonary infections in chronic granulomatous disease of childhood. AN - 75663963; 8466336 AB - Chronic granulomatous disease of childhood is an inheritable disorder of phagocytic cell respiratory burst resulting in recurrent, life-threatening, catalase-positive infections. The lung is the most common site of infection, and pulmonary disease is the primary cause of death in greater than 50% of children with chronic granulomatous disease. Still, the role of surgery in management of this disease remains undefined. Between 1974 and 1990, 19 patients with chronic granulomatous disease required 31 thoracic interventions at our institution. Patients ranged in age from 2.5 to 27 years (mean age, 15 years). Seventeen of 19 patients (89%) had had previous pulmonary infections. Patients presented as toxic (temperature > 38.5 degrees C, chest pain, and cough) in 22 instances before the 31 procedures. Aggressive surgical intervention for diagnosis and extirpation of localized infections was undertaken with lobectomy/pneumonectomy with or without other procedures (5), bisegmentectomy (2), segmentectomy with or without other procedures (5), or wedge with or without other procedures (13). In five instances, an empyema was drained; a chest tube for a sterile collection was placed in one instance. There was one intraoperative death, and 3 patients died 22 to 600 days postoperatively with overwhelming sepsis. The mean hospitalization was 101 days (range, 24 to 600 days). Wound complications occurred in 5 patients, requiring 17 separate anesthetic debridements. A change in therapy was dictated by the results of the procedure in 23 of 31 instances (74%). Thoracic surgeons must be aware of this rare cause of immunosuppression in these children and, due to the unusual nature of the pulmonary infections, should follow an aggressive approach in their diagnosis and management. JF - The Annals of thoracic surgery AU - Pogrebniak, H W AU - Gallin, J I AU - Malech, H L AU - Baker, A R AU - Moskaluk, C A AU - Travis, W D AU - Pass, H I AD - Thoracic Oncology Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 844 EP - 849 VL - 55 IS - 4 SN - 0003-4975, 0003-4975 KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Adult KW - Child KW - Adolescent KW - Male KW - Female KW - Child, Preschool KW - Aspergillosis -- microbiology KW - Lung Diseases, Fungal -- microbiology KW - Aspergillosis -- surgery KW - Bacterial Infections -- microbiology KW - Bacterial Infections -- surgery KW - Lung Diseases, Fungal -- surgery KW - Granulomatous Disease, Chronic -- complications KW - Lung Diseases -- microbiology KW - Lung Diseases -- surgery UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75663963?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Annals+of+thoracic+surgery&rft.atitle=Surgical+management+of+pulmonary+infections+in+chronic+granulomatous+disease+of+childhood.&rft.au=Pogrebniak%2C+H+W%3BGallin%2C+J+I%3BMalech%2C+H+L%3BBaker%2C+A+R%3BMoskaluk%2C+C+A%3BTravis%2C+W+D%3BPass%2C+H+I&rft.aulast=Pogrebniak&rft.aufirst=H&rft.date=1993-04-01&rft.volume=55&rft.issue=4&rft.spage=844&rft.isbn=&rft.btitle=&rft.title=The+Annals+of+thoracic+surgery&rft.issn=00034975&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-04 N1 - Date created - 1993-05-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Cloning of the cDNA encoding a myosin heavy chain B isoform of Xenopus nonmuscle myosin with an insert in the head region. AN - 75662845; 8464900 AB - The complete amino acid sequence of Xenopus laevis nonmuscle myosin heavy chain B (MHC-B) has been deduced from overlapping cDNA clones isolated from an XTC cell library. RNA blots of various developmental stages, adult tissues, and XTC cells detect a single transcript of 7.5 kb which is expressed at similar levels throughout development. MHC-B mRNA was detected in XTC cells, heart, lung, spleen, and brain, at lower levels in ovary, testis, pancreas, stomach, liver, and eye, but not in kidney and skeletal muscle. Protein expression in adult tissues, as detected by immunoblot analysis, correlates well with mRNA expression. In chickens and humans, a fraction of the mRNA encoding the MHC-B isoform was found previously to contain a 10-amino acid insert at amino acid 211 near the ATP-binding site. As reported elsewhere, in the chicken this insert-bearing isoform is nervous system-specific. The Xenopus sequence shows a 16-amino acid insertion at the same position; 7 of 16 residues are identical to those in the chicken and human insertion, and these identical residues include a consensus target sequence for cyclin-p34cdc2 kinase. In contrast to chicken, all frog tissues and embryonic stages tested contained the insert-bearing form, and no evidence for a non-insert-bearing MHC-B isoform was found in Xenopus. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Bhatia-Dey, N AU - Adelstein, R S AU - Dawid, I B AD - Laboratory of Molecular Genetics, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/04/01/ PY - 1993 DA - 1993 Apr 01 SP - 2856 EP - 2859 VL - 90 IS - 7 SN - 0027-8424, 0027-8424 KW - Oligodeoxyribonucleotides KW - 0 KW - RNA, Messenger KW - DNA KW - 9007-49-2 KW - Myosins KW - EC 3.6.4.1 KW - Index Medicus KW - Animals KW - Genetic Variation KW - Protein Structure, Secondary KW - Humans KW - Organ Specificity KW - Amino Acid Sequence KW - RNA, Messenger -- genetics KW - Cloning, Molecular KW - Aging -- physiology KW - Base Sequence KW - Chickens KW - Polymerase Chain Reaction -- methods KW - Molecular Sequence Data KW - Sequence Homology, Amino Acid KW - Muscles -- physiology KW - Gene Library KW - Xenopus laevis -- genetics KW - DNA -- genetics KW - Myosins -- chemistry KW - Myosins -- genetics KW - Mutagenesis, Insertional UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75662845?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Cloning+of+the+cDNA+encoding+a+myosin+heavy+chain+B+isoform+of+Xenopus+nonmuscle+myosin+with+an+insert+in+the+head+region.&rft.au=Bhatia-Dey%2C+N%3BAdelstein%2C+R+S%3BDawid%2C+I+B&rft.aulast=Bhatia-Dey&rft.aufirst=N&rft.date=1993-04-01&rft.volume=90&rft.issue=7&rft.spage=2856&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-04 N1 - Date created - 1993-05-04 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - L11231; GENBANK; L09740 N1 - SuppNotes - Cited By: J Cell Biol. 1977 Jul;74(1):251-63 [141455] J Biol Chem. 1992 Sep 5;267(25):17864-71 [1355479] Cell. 1985 Oct;42(3):769-77 [2414011] Science. 1985 Nov 15;230(4727):767-70 [2932797] Science. 1987 May 29;236(4805):1081-6 [3576221] Science. 1987 May 29;236(4805):1086-91 [3576222] EMBO J. 1987 Nov;6(11):3499-505 [3322809] Annu Rev Biophys Biophys Chem. 1988;17:23-45 [3293586] Proc Natl Acad Sci U S A. 1988 Nov;85(21):8086-90 [3186710] Dev Biol. 1989 Jun;133(2):562-8 [2731640] Proc Natl Acad Sci U S A. 1989 Oct;86(20):7726-30 [2813355] J Cell Biol. 1990 Feb;110(2):367-78 [2404992] Differentiation. 1990 Mar;43(1):1-9 [1694800] Proc Natl Acad Sci U S A. 1990 Nov;87(22):9028-32 [2247479] Proc Natl Acad Sci U S A. 1990 Dec;87(23):9088-92 [2174552] J Cell Biol. 1991 Mar;112(5):915-24 [1999462] Development. 1991 Jan;111(1):1-14 [1901784] Mol Cell Biol. 1991 May;11(5):2481-8 [1850097] Annu Rev Physiol. 1991;53:653-81 [2042976] Science. 1991 Jul 12;253(5016):194-6 [1677215] Curr Opin Cell Biol. 1991 Feb;3(1):98-104 [1854490] Circ Res. 1991 Aug;69(2):530-9 [1860190] Methods Enzymol. 1991;200:62-81 [1956339] Genes Dev. 1992 Mar;6(3):356-66 [1347750] Curr Opin Cell Biol. 1992 Feb;4(1):27-35 [1558751] Methods Cell Biol. 1991;36:19-34 [1811134] Nucleic Acids Res. 1984 Jan 11;12(1 Pt 1):387-95 [6546423] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Evaluation of ketamine-xylazine in Syrian hamsters. AN - 75661126; 8467701 AB - Few parenteral anesthetics are safe and effective in the Syrian hamster. This study evaluated the anesthetic efficacy and potential for tissue damage of ketamine-xylazine (KX). Two dosage levels were administered intraperitoneally. Ketamine at 50 mg/kg combined with 10 mg/kg xylazine did not produce a consistent, reliable level of immobilization or anesthesia. Ketamine at 150 mg/kg combined with 10 mg/kg xylazine administered IP produced an adequate level of anesthesia without tissue damage for most procedures, but supplementation with lidocaine was necessary for peritoneal incision. Careful positioning of male hamsters for IP injection is imperative to prevent inadvertent injection into the testes with subsequent tissue damage. JF - The Cornell veterinarian AU - Payton, A J AU - Forsythe, D B AU - Dixon, D AU - Myers, P H AU - Clark, J A AU - Snipe, J R AD - Comparative Medicine Branch, National Institute of Environmental Health Science, National Institutes of Health, Research Triangle Park, NC 27709. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 153 EP - 161 VL - 83 IS - 2 SN - 0010-8901, 0010-8901 KW - Drug Combinations KW - 0 KW - Xylazine KW - 2KFG9TP5V8 KW - Ketamine KW - 690G0D6V8H KW - Index Medicus KW - Specific Pathogen-Free Organisms KW - Injections, Intraperitoneal KW - Evaluation Studies as Topic KW - Animals KW - Muscle Relaxation -- drug effects KW - Male KW - Female KW - Cricetinae KW - Xylazine -- adverse effects KW - Ketamine -- adverse effects KW - Xylazine -- administration & dosage KW - Anesthesia -- veterinary KW - Anesthesia -- methods KW - Mesocricetus KW - Ketamine -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75661126?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Cornell+veterinarian&rft.atitle=Evaluation+of+ketamine-xylazine+in+Syrian+hamsters.&rft.au=Payton%2C+A+J%3BForsythe%2C+D+B%3BDixon%2C+D%3BMyers%2C+P+H%3BClark%2C+J+A%3BSnipe%2C+J+R&rft.aulast=Payton&rft.aufirst=A&rft.date=1993-04-01&rft.volume=83&rft.issue=2&rft.spage=153&rft.isbn=&rft.btitle=&rft.title=The+Cornell+veterinarian&rft.issn=00108901&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-11 N1 - Date created - 1993-05-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Long-term biphasic effects of lithium treatment on phospholipase C-coupled M3-muscarinic acetylcholine receptors in cultured cerebellar granule cells. AN - 75654122; 8384505 AB - We have studied the long-term effects of lithium on neuronal morphology and the functional expression of phospholipase C-coupled m3-muscarinic acetylcholine receptors (mAChRs) in cerebellar granule cells. There was a biphasic dose-dependent effect on cell morphology following treatment with lithium for 7 days. At low concentrations ( or = 3 days. The biphasic effect was also demonstrated by the binding of [3H]ouabain to Na+, K(+)-ATPase, which was shown to be a convenient method for quantifying viable neurons.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Neurochemistry international AU - Gao, X M AU - Fukamauchi, F AU - Chuang, D M AD - Section on Molecular Neurobiology, Biological Psychiatry Branch, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 395 EP - 403 VL - 22 IS - 4 SN - 0197-0186, 0197-0186 KW - Receptors, Muscarinic KW - 0 KW - Ouabain KW - 5ACL011P69 KW - Lithium KW - 9FN79X2M3F KW - Type C Phospholipases KW - EC 3.1.4.- KW - Sodium-Potassium-Exchanging ATPase KW - EC 3.6.3.9 KW - Index Medicus KW - Ouabain -- metabolism KW - Animals KW - Sodium-Potassium-Exchanging ATPase -- metabolism KW - Cells, Cultured KW - Binding Sites -- drug effects KW - Time Factors KW - Cerebellum -- cytology KW - Granulocytes -- metabolism KW - Cerebellum -- drug effects KW - Granulocytes -- drug effects KW - Type C Phospholipases -- metabolism KW - Receptors, Muscarinic -- metabolism KW - Lithium -- pharmacology KW - Cerebellum -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75654122?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurochemistry+international&rft.atitle=Long-term+biphasic+effects+of+lithium+treatment+on+phospholipase+C-coupled+M3-muscarinic+acetylcholine+receptors+in+cultured+cerebellar+granule+cells.&rft.au=Gao%2C+X+M%3BFukamauchi%2C+F%3BChuang%2C+D+M&rft.aulast=Gao&rft.aufirst=X&rft.date=1993-04-01&rft.volume=22&rft.issue=4&rft.spage=395&rft.isbn=&rft.btitle=&rft.title=Neurochemistry+international&rft.issn=01970186&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-23 N1 - Date created - 1993-04-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Cytotoxic activities of recombinant immunotoxins composed of Pseudomonas toxin or diphtheria toxin toward lymphocytes from patients with adult T-cell leukemia. AN - 75652828; 8464234 AB - We have previously shown that the recombinant single-chain immunotoxin anti-Tac(Fv)-PE40, composed of the variable domains of the anti-Tac monoclonal antibody in a single-chain form joined to a derivative of Pseudomonas exotoxin (PE), is cytotoxic toward malignant cells from adult T-cell leukemia (ATL) patients. Using this assay, we have now compared the activity of anti-Tac(Fv)-PE40 with that of an improved version, anti-Tac(Fv)-PE40KDEL which contains an altered carboxyl terminus, and also with two chimeric toxins made with diphtheria toxin (DT). One of these is a fusion of amino acids 1-388 of DT with anti-Tac(Fv) and is termed DT388-anti-Tac(Fv). The other, DT388-IL2, contains interleukin 2 (IL2) at the carboxyl terminus of the same DT derivative. We incubated these toxins with malignant ATL peripheral blood mononuclear cells (PBMCs) for 1-3 days and then measured [3H]leucine incorporation. We found that anti-Tac(Fv)-PE40KDEL was the most cytotoxic agent and was followed in decreasing order of activity by anti-Tac(Fv)-PE40, DT388-anti-Tac(Fv), and finally DT388-IL2. Trypan blue staining showed that inhibition of protein synthesis correlated with cell death. Time course studies showed that the recombinant toxins containing anti-Tac(Fv) were cytotoxic even if exposed to the cells for only one hour. After intravenous injection into mice, the half-life of anti-Tac(Fv)-PE40 or anti-Tac(Fv)-PE40KDEL was 30 minutes. Normal PBMCs were resistant to all four toxins. Recombinant immunotoxins made with anti-Tac merit further study as potential reagents in the treatment of ATL. JF - Leukemia AU - Kreitman, R J AU - Chaudhary, V K AU - Waldmann, T A AU - Hanchard, B AU - Cranston, B AU - FitzGerald, D J AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 553 EP - 562 VL - 7 IS - 4 SN - 0887-6924, 0887-6924 KW - Antibodies, Monoclonal KW - 0 KW - Diphtheria Toxin KW - Endotoxins KW - Immunotoxins KW - Interleukin-2 KW - Recombinant Fusion Proteins KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Drug Screening Assays, Antitumor KW - Humans KW - Mice KW - Mice, Inbred BALB C KW - Antibodies, Monoclonal -- therapeutic use KW - Cytotoxicity, Immunologic KW - Lymphocytes -- immunology KW - Tumor Cells, Cultured KW - Interleukin-2 -- therapeutic use KW - Adult KW - Time Factors KW - Recombinant Fusion Proteins -- therapeutic use KW - Female KW - Leukemia-Lymphoma, Adult T-Cell -- therapy KW - Immunotoxins -- therapeutic use KW - Diphtheria Toxin -- therapeutic use KW - Pseudomonas -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75652828?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Leukemia&rft.atitle=Cytotoxic+activities+of+recombinant+immunotoxins+composed+of+Pseudomonas+toxin+or+diphtheria+toxin+toward+lymphocytes+from+patients+with+adult+T-cell+leukemia.&rft.au=Kreitman%2C+R+J%3BChaudhary%2C+V+K%3BWaldmann%2C+T+A%3BHanchard%2C+B%3BCranston%2C+B%3BFitzGerald%2C+D+J%3BPastan%2C+I&rft.aulast=Kreitman&rft.aufirst=R&rft.date=1993-04-01&rft.volume=7&rft.issue=4&rft.spage=553&rft.isbn=&rft.btitle=&rft.title=Leukemia&rft.issn=08876924&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-06 N1 - Date created - 1993-05-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Pancreatitis in human immunodeficiency virus-infected children receiving dideoxyinosine. AN - 75651249; 7681940 AB - To define predictive or contributory risk factors for pancreatitis in human immunodeficiency virus-infected children receiving dideoxyinosine (ddI), the authors evaluated 95 children, 3 months to 18 years of age, who had received ddI at 60 to 540 mg/m2 per day for a mean of 56 weeks. Pancreatitis developed in 7 patients (7%) but resolved in all upon withdrawal of ddI. Neither age, sex, nor CD4 count at study entry was predictive of pancreatitis, but pancreatitis appeared more likely to develop in hemophiliacs than in other patients (4 of 23 vs 3 of 72). Pancreatitis developed only in patients who received ddI at the highest dose levels (7 of 60 patients who received ddI at a dose > or = 360 mg/m2 per day vs 0 of 35 patients who received < or = 270 mg/m2 per day). Patients in whom pancreatitis developed had received a higher mean daily dose of ddI than patients with normal amylase and lipase levels throughout the study (348 mg/m2 vs 282 mg/m2), but no relationship with the cumulative dose or the duration of ddI therapy was observed. Although a statistically significant relationship between ddI plasma concentration (area under the curve) and pancreatitis was not conclusively demonstrated, as the number of patients in whom pancreatitis actually developed was small, such a relationship may have been obscured.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Pediatrics AU - Butler, K M AU - Venzon, D AU - Henry, N AU - Husson, R N AU - Mueller, B U AU - Balis, F M AU - Jacobsen, F AU - Lewis, L L AU - Pizzo, P A AD - Pediatric Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 747 EP - 751 VL - 91 IS - 4 SN - 0031-4005, 0031-4005 KW - Aspartate Aminotransferases KW - EC 2.6.1.1 KW - Alanine Transaminase KW - EC 2.6.1.2 KW - Lipase KW - EC 3.1.1.3 KW - Amylases KW - EC 3.2.1.- KW - Didanosine KW - K3GDH6OH08 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Dose-Response Relationship, Drug KW - Humans KW - Child KW - Lipase -- blood KW - Child, Preschool KW - Infant KW - Aspartate Aminotransferases -- blood KW - Alanine Transaminase -- blood KW - Incidence KW - Amylases -- blood KW - Adolescent KW - Male KW - Female KW - Pancreatitis -- enzymology KW - Pancreatitis -- epidemiology KW - HIV Infections -- drug therapy KW - Didanosine -- administration & dosage KW - HIV Infections -- enzymology KW - Didanosine -- pharmacokinetics KW - Pancreatitis -- chemically induced KW - Didanosine -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75651249?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pediatrics&rft.atitle=Pancreatitis+in+human+immunodeficiency+virus-infected+children+receiving+dideoxyinosine.&rft.au=Butler%2C+K+M%3BVenzon%2C+D%3BHenry%2C+N%3BHusson%2C+R+N%3BMueller%2C+B+U%3BBalis%2C+F+M%3BJacobsen%2C+F%3BLewis%2C+L+L%3BPizzo%2C+P+A&rft.aulast=Butler&rft.aufirst=K&rft.date=1993-04-01&rft.volume=91&rft.issue=4&rft.spage=747&rft.isbn=&rft.btitle=&rft.title=Pediatrics&rft.issn=00314005&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-03 N1 - Date created - 1993-05-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Overexpression of the HIV-1 gag-pol polyprotein results in intracellular activation of HIV-1 protease and inhibition of assembly and budding of virus-like particles. AN - 75651148; 7681610 AB - Some retroviruses, including HIV-1, regulate the relative amounts of gag and pol gene products by a translational frameshift mechanism. The consequences of altering the ratios of the Gag and Pol proteins were tested using vaccinia virus expression vectors, in which the gag and pol genes were fused by placing them in the same open reading frame. Immunoblotting of cell lysates indicated that a protein of approximately 160 kDa, the expected translation product of the fused gag-pol gene, was the dominant species detected with HIV-specific antiserum during the first several hours of infection with this recombinant virus. Subsequently, the full-length polyprotein diminished in amount and a series of Gag-related intermediate size proteins appeared. Later in infection, p24 and myristoylated p17 Gag proteins predominated and larger amounts of intracellularly processed reverse transcriptase, integrase, and protease were detected compared to the amounts formed with the wild-type gag-pol gene. Large numbers of budding, immature, and mature retrovirus-like particles were visualized by electron microscopy when the wild-type gag-pol gene was expressed, whereas no particles were detected in cells that expressed the fused gag-pol gene. The block to virus assembly was partially overcome by (i) inhibition of the HIV-1 protease with a peptidomimetic inhibitor, (ii) mutagenesis of the active site of the protease, or (iii) shortening of the Gag-Pol polyprotein by deletion of most of the reverse transcriptase gene. Nevertheless, budding was inefficient and the structures appeared immature and frequently aberrant. These results indicated that overproduction of the full-length Gag-Pol polyprotein and increased intracellular protease activity were both detrimental to viral assembly. Further experiments indicated that intracellular processing of Gag and Gag-Pol polyproteins occurred in the absence of particle formation when myristoylation was prevented. JF - Virology AU - Karacostas, V AU - Wolffe, E J AU - Nagashima, K AU - Gonda, M A AU - Moss, B AD - Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, Maryland 20892. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 661 EP - 671 VL - 193 IS - 2 SN - 0042-6822, 0042-6822 KW - gag KW - pol KW - Fusion Proteins, gag-pol KW - 0 KW - Myristic Acids KW - Myristic Acid KW - 0I3V7S25AW KW - HIV Reverse Transcriptase KW - EC 2.7.7.49 KW - RNA-Directed DNA Polymerase KW - HIV Protease KW - EC 3.4.23.- KW - Index Medicus KW - AIDS/HIV KW - Vaccinia virus -- genetics KW - Animals KW - Enzyme Activation KW - HeLa Cells KW - Humans KW - RNA-Directed DNA Polymerase -- metabolism KW - Plasmids KW - Myristic Acids -- metabolism KW - Frameshift Mutation KW - Base Sequence KW - Restriction Mapping KW - Microscopy, Electron KW - Cell Line KW - Sequence Deletion KW - Fusion Proteins, gag-pol -- biosynthesis KW - HIV-1 -- genetics KW - Fusion Proteins, gag-pol -- genetics KW - HIV-1 -- physiology KW - HIV Protease -- metabolism KW - Genes, gag KW - Genes, pol KW - HIV-1 -- ultrastructure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75651148?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Virology&rft.atitle=Overexpression+of+the+HIV-1+gag-pol+polyprotein+results+in+intracellular+activation+of+HIV-1+protease+and+inhibition+of+assembly+and+budding+of+virus-like+particles.&rft.au=Karacostas%2C+V%3BWolffe%2C+E+J%3BNagashima%2C+K%3BGonda%2C+M+A%3BMoss%2C+B&rft.aulast=Karacostas&rft.aufirst=V&rft.date=1993-04-01&rft.volume=193&rft.issue=2&rft.spage=661&rft.isbn=&rft.btitle=&rft.title=Virology&rft.issn=00426822&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-23 N1 - Date created - 1993-04-23 N1 - Date revised - 2017-01-13 N1 - Gene symbol - gag; pol N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Intraoperative radiotherapy in retroperitoneal sarcomas. Final results of a prospective, randomized, clinical trial. AN - 75648667; 8457152 AB - Thirty-five patients with surgically resected sarcomas of the retroperitoneum were enrolled in a prospective, randomized, clinical trial comparing 20-Gy intraoperative radiotherapy in combination with postoperative low-dose (35- to 40-Gy) external-beam radiotherapy with postoperative high-dose (50- to 55-Gy) external-beam radiotherapy alone. Chemotherapy with doxorubicin hydrochloride, cyclophosphamide (anhydrous), and methotrexate sodium was used for a portion of the trial. Fifteen patients who received intraoperative radiotherapy and 20 control patients were followed up for a minimum of 5 years (median follow-up, 8 years). Median survival times were similar for the group that received intraoperative radiotherapy (45 months) and the control group (52 months). There were no indications of benefit from adjunctive chemotherapy. The number of locoregional recurrences was significantly lower among those who received intraoperative radiotherapy (six of 15) than control patients (16 of 20). Patients who received intraoperative radiotherapy had fewer complications of disabling radiation-related enteritis (two of 15) than control patients (10 of 20), but radiation-related peripheral neuropathy was more frequent among those who received intraoperative radiotherapy (nine of 15) than among control patients (one of 20). JF - Archives of surgery (Chicago, Ill. : 1960) AU - Sindelar, W F AU - Kinsella, T J AU - Chen, P W AU - DeLaney, T F AU - Tepper, J E AU - Rosenberg, S A AU - Glatstein, E AD - Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 402 EP - 410 VL - 128 IS - 4 SN - 0004-0010, 0004-0010 KW - Abridged Index Medicus KW - Index Medicus KW - Neoplasm Recurrence, Local -- epidemiology KW - Neoplasm Staging KW - Combined Modality Therapy KW - Humans KW - Surgical Wound Infection -- etiology KW - Postoperative Complications -- etiology KW - Prospective Studies KW - Survival Rate KW - Radiotherapy Dosage KW - Adult KW - Incidence KW - Follow-Up Studies KW - Intraoperative Period KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Chemotherapy, Adjuvant KW - Radiation Injuries -- etiology KW - Retroperitoneal Neoplasms -- radiotherapy KW - Sarcoma -- radiotherapy KW - Retroperitoneal Neoplasms -- mortality KW - Sarcoma -- mortality KW - Sarcoma -- surgery KW - Retroperitoneal Neoplasms -- pathology KW - Sarcoma -- pathology KW - Retroperitoneal Neoplasms -- surgery UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75648667?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+surgery+%28Chicago%2C+Ill.+%3A+1960%29&rft.atitle=Intraoperative+radiotherapy+in+retroperitoneal+sarcomas.+Final+results+of+a+prospective%2C+randomized%2C+clinical+trial.&rft.au=Sindelar%2C+W+F%3BKinsella%2C+T+J%3BChen%2C+P+W%3BDeLaney%2C+T+F%3BTepper%2C+J+E%3BRosenberg%2C+S+A%3BGlatstein%2C+E&rft.aulast=Sindelar&rft.aufirst=W&rft.date=1993-04-01&rft.volume=128&rft.issue=4&rft.spage=402&rft.isbn=&rft.btitle=&rft.title=Archives+of+surgery+%28Chicago%2C+Ill.+%3A+1960%29&rft.issn=00040010&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-22 N1 - Date created - 1993-04-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Calcium potentiates cyclic AMP stimulation of pineal arylalkylamine N-acetyltransferase. AN - 75640865; 7681102 AB - Pineal arylalkylamine N-acetyltransferase (N-acetyltransferase) controls large daily changes in melatonin production. It is generally thought that the activity of this enzyme is controlled by norepinephrine acting exclusively via elevation of cyclic AMP. However, norepinephrine also elevates pineal intracellular Ca2+ concentration ([Ca2+]i), and it is not known whether Ca2+ is involved in regulating N-acetyltransferase activity other than through its established role in cyclic AMP production. In this study, the issue of whether Ca2+ enhances the effects of cyclic AMP on N-acetyltransferase activity was investigated. The effects of cyclic AMP protagonists (isobutylmethylxanthine, N6,2'-O-dibutyryladenosine 3',5'-cyclic monophosphate, 8-bromoadenosine 3',5'-cyclic monophosphate, and adenosine 3',5'-cyclic monophosphothioate, Sp-diastereomer) were examined in combination with [Ca2+]i protagonists (A23187, ionomycin, and phenylephrine). All [Ca2+]i protagonists potentiated the effects of cyclic AMP protagonists. For example, ionomycin potentiated the effects of low concentrations of 8-bromoadenosine 3',5'-cyclic monophosphate, and A23187 potentiated the effects of isobutylmethylxanthine without altering cyclic AMP accumulation. These findings indicate that Ca2+ and cyclic AMP probably act physiologically in a coordinated manner to stimulate N-acetyltransferase activity; these second messengers could act directly at one or more sites or through indirect actions mediated by kinases. JF - Journal of neurochemistry AU - Yu, L AU - Schaad, N C AU - Klein, D C AD - Section on Neuroendocrinology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 1436 EP - 1443 VL - 60 IS - 4 SN - 0022-3042, 0022-3042 KW - Phenylephrine KW - 1WS297W6MV KW - Calcimycin KW - 37H9VM9WZL KW - Cobalt KW - 3G0H8C9362 KW - Bucladesine KW - 63X7MBT2LQ KW - Cyclic AMP KW - E0399OZS9N KW - Arylamine N-Acetyltransferase KW - EC 2.3.1.5 KW - cobaltous chloride KW - EVS87XF13W KW - Calcium KW - SY7Q814VUP KW - 1-Methyl-3-isobutylxanthine KW - TBT296U68M KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Rats KW - Animals KW - Rats, Sprague-Dawley KW - Norepinephrine -- pharmacology KW - Cells, Cultured KW - Cobalt -- pharmacology KW - Calcimycin -- pharmacology KW - Drug Synergism KW - Bucladesine -- pharmacology KW - 1-Methyl-3-isobutylxanthine -- pharmacology KW - Organ Culture Techniques KW - Female KW - Phenylephrine -- pharmacology KW - Cyclic AMP -- pharmacology KW - Cyclic AMP -- metabolism KW - Cyclic AMP -- analogs & derivatives KW - Pineal Gland -- enzymology KW - Calcium -- pharmacology KW - Arylamine N-Acetyltransferase -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75640865?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neurochemistry&rft.atitle=Calcium+potentiates+cyclic+AMP+stimulation+of+pineal+arylalkylamine+N-acetyltransferase.&rft.au=Yu%2C+L%3BSchaad%2C+N+C%3BKlein%2C+D+C&rft.aulast=Yu&rft.aufirst=L&rft.date=1993-04-01&rft.volume=60&rft.issue=4&rft.spage=1436&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurochemistry&rft.issn=00223042&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-19 N1 - Date created - 1993-04-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Interleukin-1 alpha and interleukin-6 act additively to inhibit growth of MCF-7 breast cancer cells in vitro. AN - 75636252; 8453620 AB - We studied the effects of interleukin-1 alpha (IL-1) and interleukin-6 (IL-6) on MCF-7 breast cancer cells to determine whether these cytokines act additively/synergistically to alter cell growth and metabolism. We found that IL-1 alone (1000 units/ml) inhibited cell growth to a greater degree (83.8%) than IL-6 alone (29.2%, P < 0.001). The combination of IL-1 + IL-6 caused greater inhibition of growth (92.9%, P < 0.02) than either cytokine alone. The additive effect was dose dependent for both IL-1 and IL-6. IL-1 and IL-6 also antagonized estradiol (10(-9) M) stimulated growth. Antagonism by the combination was greater than for either cytokine alone (P < 0.001). IL-1 or IL-6 alone each down-regulated the estrogen receptor (36.7%, P < 0.01, and 23.2%, P < 0.05, respectively), but the combination IL-1 + IL-6 did not cause a significantly greater effect than IL-1 alone. Neither IL-1 or IL-6 blocked estradiol stimulation of progesterone receptor (PR) synthesis; however, the combination IL-1 + IL-6 increased PR content by 28.4% (P < 0.01). IL-1, but not IL-6, increased secretion of transforming growth factor-beta (TGF-beta) by 2.45-fold over 72 h (P < 0.01). The increase was time dependent (detectable at 24 h) and dose dependent (maximum increase of 5.3-fold, 10,000 units/ml, P < 0.02). IL-1-induced TGF-beta secretion was blocked by estradiol (10(-9) M). Neither cytokine altered secretion of insulin-like growth factor-1. These findings indicate that IL-1 and IL-6 act additively to inhibit growth in the absence or presence of estradiol and modulate the estrogen receptor and progesterone receptor content of these cells. TGF-beta may mediate the effects of IL-1; however, other pathways appear to be required for the additive effects of these cytokines. JF - Cancer research AU - Danforth, D N AU - Sgagias, M K AD - Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/04/01/ PY - 1993 DA - 1993 Apr 01 SP - 1538 EP - 1545 VL - 53 IS - 7 SN - 0008-5472, 0008-5472 KW - Interleukin-1 KW - 0 KW - Interleukin-6 KW - Receptors, Estrogen KW - Receptors, Progesterone KW - Transforming Growth Factor beta KW - Estradiol KW - 4TI98Z838E KW - Insulin-Like Growth Factor I KW - 67763-96-6 KW - Index Medicus KW - Drug Interactions KW - Tumor Cells, Cultured KW - Dose-Response Relationship, Drug KW - Humans KW - Cell Division -- drug effects KW - Insulin-Like Growth Factor I -- metabolism KW - Interleukin-1 -- pharmacology KW - Receptors, Progesterone -- metabolism KW - Interleukin-6 -- secretion KW - Breast Neoplasms -- pathology KW - Estradiol -- pharmacology KW - Breast Neoplasms -- metabolism KW - Interleukin-6 -- pharmacology KW - Receptors, Estrogen -- metabolism KW - Transforming Growth Factor beta -- metabolism KW - Interleukin-1 -- secretion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75636252?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Interleukin-1+alpha+and+interleukin-6+act+additively+to+inhibit+growth+of+MCF-7+breast+cancer+cells+in+vitro.&rft.au=Danforth%2C+D+N%3BSgagias%2C+M+K&rft.aulast=Danforth&rft.aufirst=D&rft.date=1993-04-01&rft.volume=53&rft.issue=7&rft.spage=1538&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-21 N1 - Date created - 1993-04-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Recombinant immunotoxins containing the VH or VL domain of monoclonal antibody B3 fused to Pseudomonas exotoxin. AN - 75634224; 8454854 AB - We prepared recombinant immunotoxins in Escherichia coli in which the VH or VL domains of mAb B3 were fused to a truncated form of Pseudomonas exotoxin (PE) (PE38KDEL). mAb B3 binds to a carbohydrate Ag found on the surfaces of many types of cancers and only a few normal tissues. PE38KDEL is a 38-kDa form of PE (66 kDa) that is missing the cell-binding domain of PE and has the carboxyl end changed from REDLK to KDEL. We show that immunotoxins in which the H chain or the L chain V region is fused to PE38KDEL bind to and kill carcinoma cells containing the B3 Ag. B3 Ag-negative cells were not affected. The cytotoxicity of these molecules is between 20- and 100-fold less than B3(Fv)-immunotoxins, containing both the H and L chain V regions. The VL-containing toxin was more active than the VH-containing toxin, indicating that the L chain of mAb B3 probably contributes more to Ag-binding than the H chain. Refolding experiments show that B3(VL)-PE38KDEL aggregates less than the VH-derivative or than a single chain immunotoxin B3(Fv)-PE38KDEL, which contains both domains in a single chain form. Furthermore, in addition to monomers, active homodimers of B3(VH)- and B3(VL)-PE38KDEL were obtained from renaturation experiments. The VL-toxin dimers, which might have their binding regions arranged in a manner similar to Bence Jones proteins (L chain homodimers), were found to have almost the same cytotoxicity as the monomers, whereas the VH-toxin dimers had decreased cytotoxic activity. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Brinkmann, U AU - Lee, B K AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/04/01/ PY - 1993 DA - 1993 Apr 01 SP - 2774 EP - 2782 VL - 150 IS - 7 SN - 0022-1767, 0022-1767 KW - Amino Acids KW - 0 KW - Antibodies, Monoclonal KW - Bacterial Toxins KW - Exotoxins KW - Immunoglobulin Heavy Chains KW - Immunoglobulin Light Chains KW - Immunoglobulin Variable Region KW - Immunotoxins KW - Recombinant Fusion Proteins KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Abridged Index Medicus KW - Index Medicus KW - Antibody Specificity KW - Base Sequence KW - Antibodies, Monoclonal -- genetics KW - Amino Acids -- chemistry KW - Humans KW - Amino Acids -- genetics KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Antibodies, Monoclonal -- chemistry KW - Plasmids KW - Mutation KW - Immunoglobulin Variable Region -- genetics KW - Recombinant Fusion Proteins -- biosynthesis KW - Exotoxins -- genetics KW - Pseudomonas aeruginosa -- genetics KW - Immunotoxins -- biosynthesis KW - Recombinant Fusion Proteins -- isolation & purification KW - Immunoglobulin Variable Region -- biosynthesis KW - Exotoxins -- immunology KW - Immunoglobulin Variable Region -- isolation & purification KW - Immunoglobulin Heavy Chains -- biosynthesis KW - Immunoglobulin Heavy Chains -- genetics KW - Immunoglobulin Light Chains -- isolation & purification KW - Immunoglobulin Light Chains -- biosynthesis KW - Pseudomonas aeruginosa -- immunology KW - Pseudomonas aeruginosa -- chemistry KW - Recombinant Fusion Proteins -- pharmacology KW - Immunoglobulin Light Chains -- genetics KW - Immunotoxins -- isolation & purification KW - Immunotoxins -- pharmacology KW - Immunoglobulin Heavy Chains -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75634224?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=Recombinant+immunotoxins+containing+the+VH+or+VL+domain+of+monoclonal+antibody+B3+fused+to+Pseudomonas+exotoxin.&rft.au=Brinkmann%2C+U%3BLee%2C+B+K%3BPastan%2C+I&rft.aulast=Brinkmann&rft.aufirst=U&rft.date=1993-04-01&rft.volume=150&rft.issue=7&rft.spage=2774&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.issn=00221767&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-20 N1 - Date created - 1993-04-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Suppression of oncogene-induced transformation by a deletion mutant of c-jun. AN - 75632918; 8455942 AB - Jun and Fos proteins are DNA-binding proteins that are involved in the control of gene expression through transcriptional regulation. We have made a deletion mutant of the c-jun gene that lacks amino acids 3-122 of c-jun, and thus is missing the major transactivation domain of c-jun, but retains the DNA-binding and leucine zipper domains. Unlike c-Jun, the mutant protein is unable to stimulate the transcription of an AP-1 responsive gene, and unlike c-jun this mutant gene is unable to transform rat embryo cells in cooperation with an activated ras gene. However, this mutant protein blocks in vitro DNA binding of Jun-Jun homodimers and Jun-Fos heterodimers, transcriptional activation induced by c-jun or c-fos and transformation of rat embryo cells induced by an activated ras gene and a deregulated c-jun or c-fos gene. In addition, transformation of rat embryo cells induced by an activated ras gene in the presence of the tumor promoter 12-O-tetradecanoyl phorbol 13-acetate (TPA) or by ras plus SV40 large T antigen is also inhibited by this dominant-negative mutant, suggesting that a member of the jun or fos family is involved in the pathways leading to transformation in these systems as well. The possible molecular mechanisms by which this dominant-negative mutant of c-jun blocks the functions of wild-type jun and fos family members are discussed. JF - Oncogene AU - Brown, P H AU - Alani, R AU - Preis, L H AU - Szabo, E AU - Birrer, M J AD - Biomarkers and Prevention Research Branch, National Cancer Institute, Kensington, Maryland 20895. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 877 EP - 886 VL - 8 IS - 4 SN - 0950-9232, 0950-9232 KW - c-fos KW - c-jun KW - ras KW - DNA-Binding Proteins KW - 0 KW - Proto-Oncogene Proteins c-fos KW - Proto-Oncogene Proteins c-jun KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Proto-Oncogene Proteins c-fos -- metabolism KW - DNA Mutational Analysis KW - Humans KW - Rats KW - Genes, ras KW - Base Sequence KW - Genes, Dominant KW - Cells, Cultured KW - Binding, Competitive KW - In Vitro Techniques KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Genes, Suppressor KW - Sequence Deletion KW - DNA-Binding Proteins -- metabolism KW - Proto-Oncogene Proteins c-jun -- genetics KW - Cell Transformation, Neoplastic -- drug effects KW - Transcriptional Activation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75632918?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncogene&rft.atitle=Suppression+of+oncogene-induced+transformation+by+a+deletion+mutant+of+c-jun.&rft.au=Brown%2C+P+H%3BAlani%2C+R%3BPreis%2C+L+H%3BSzabo%2C+E%3BBirrer%2C+M+J&rft.aulast=Brown&rft.aufirst=P&rft.date=1993-04-01&rft.volume=8&rft.issue=4&rft.spage=877&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=09509232&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-20 N1 - Date created - 1993-04-20 N1 - Date revised - 2017-01-13 N1 - Gene symbol - c-fos; c-jun; ras N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Analysis of nonnucleoside drug-resistant variants of human immunodeficiency virus type 1 reverse transcriptase. AN - 75616237; 7680393 AB - A number of chemically distinct nonnucleoside inhibitors of human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) have been reported. Several lines of evidence, including the isolation of RT mutants that show cross resistance, suggest that, despite their structural diversity, many of these inhibitors bind to a common site on HIV-1 RT. We have recently reported that, on the basis of analyses of HIV-1/HIV-2 chimeras, the natural product calanolide A may interact with a different site or sites in HIV-1 RT. We have used BspMI cassette mutagenesis to prepare a collection of HIV-1 RT mutants that show resistance to the known members of the general class of nonnucleoside inhibitors. This collection of mutants can be used to determine whether a new drug will show cross resistance with known inhibitors and to define amino acid positions critical for the action of the drugs. The mutants were used to analyze calanolide A, 1H,3H-thiazolo[3,4-a]benzimidazole(4i), and the acyclic nucleoside analog 1-[(2-hydroxyethoxy)methyl]-6-(phenylthio)thymine. These analyses suggest that all three drugs interact with HIV-1 RT within the previously defined common binding site for nonnucleoside inhibitors. However, the drugs respond differently to the panel of drug-resistant HIV-1 RTs, indicating that while the binding sites of the drugs overlap they are not identical. JF - Journal of virology AU - Boyer, P L AU - Currens, M J AU - McMahon, J B AU - Boyd, M R AU - Hughes, S H AD - ABL-Basic Research Program, NCI-Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 2412 EP - 2420 VL - 67 IS - 4 SN - 0022-538X, 0022-538X KW - Antiviral Agents KW - 0 KW - Benzimidazoles KW - Coumarins KW - Pyranocoumarins KW - Reverse Transcriptase Inhibitors KW - Thiazoles KW - 1-((2-hydroxyethoxy)methyl)-6-(phenylthio)thymine KW - 123027-56-5 KW - 1H,3H-thiazolo(3,4-a)benzimidazole KW - 35766-04-2 KW - HIV Reverse Transcriptase KW - EC 2.7.7.49 KW - Thymine KW - QR26YLT7LT KW - calanolide A KW - S5A9TQN46W KW - Index Medicus KW - AIDS/HIV KW - Drug Resistance, Microbial KW - Amino Acid Sequence KW - Structure-Activity Relationship KW - Thymine -- pharmacology KW - Thiazoles -- pharmacology KW - HIV -- drug effects KW - Thymine -- analogs & derivatives KW - Coumarins -- pharmacology KW - Benzimidazoles -- pharmacology KW - Antiviral Agents -- chemistry KW - HIV -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75616237?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Analysis+of+nonnucleoside+drug-resistant+variants+of+human+immunodeficiency+virus+type+1+reverse+transcriptase.&rft.au=Boyer%2C+P+L%3BCurrens%2C+M+J%3BMcMahon%2C+J+B%3BBoyd%2C+M+R%3BHughes%2C+S+H&rft.aulast=Boyer&rft.aufirst=P&rft.date=1993-04-01&rft.volume=67&rft.issue=4&rft.spage=2412&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-08 N1 - Date created - 1993-04-08 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nature. 1990 Feb 1;343(6257):470-4 [1689015] Science. 1990 Dec 7;250(4986):1411-3 [1701568] Proc Natl Acad Sci U S A. 1991 Feb 15;88(4):1451-5 [1705038] Proc Natl Acad Sci U S A. 1991 Mar 15;88(6):2356-60 [1706522] J Infect Dis. 1991 May;163(5):966-70 [1708400] Proc Natl Acad Sci U S A. 1991 Aug 1;88(15):6863-7 [1713693] J Virol. 1991 Sep;65(9):4887-92 [1714522] J Virol. 1991 Oct;65(10):5232-6 [1716689] Science. 1991 Sep 27;253(5027):1557-9 [1716788] Proc Natl Acad Sci U S A. 1991 Oct 1;88(19):8806-10 [1717988] Proc Natl Acad Sci U S A. 1991 Nov 1;88(21):9878-82 [1719542] J Biol Chem. 1991 Dec 15;266(35):23529-36 [1721050] Proc Natl Acad Sci U S A. 1991 Dec 15;88(24):11241-5 [1722324] J Virol. 1992 Feb;66(2):1031-9 [1370546] Farmaco. 1991 Jun;46(6):817-23 [1685321] Farmaco. 1991 Jul-Aug;46(7-8):925-33 [1686551] AIDS Res Hum Retroviruses. 1992 Feb;8(2):119-34 [1371690] AIDS Res Hum Retroviruses. 1992 Feb;8(2):145-52 [1371691] Mol Pharmacol. 1992 Mar;41(3):446-51 [1372083] Virology. 1992 Jun;188(2):900-4 [1374986] Science. 1992 Jun 26;256(5065):1783-90 [1377403] J Med Chem. 1992 Jul 24;35(15):2735-43 [1379639] Antimicrob Agents Chemother. 1992 Jul;36(7):1441-6 [1380789] J Biol Chem. 1992 Sep 5;267(25):17526-30 [1381350] Virology. 1992 Sep;190(1):269-77 [1382341] J Virol. 1992 Dec;66(12):7533-7 [1279205] Proc Natl Acad Sci U S A. 1988 Feb;85(4):1218-22 [2448794] J Med Chem. 1989 Dec;32(12):2507-9 [2479745] Science. 1989 Dec 1;246(4934):1155-8 [2479983] Biochem Biophys Res Commun. 1989 Dec 29;165(3):1375-81 [2575380] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Expression of sulfated glycoprotein 2 is associated with carcinogenesis induced by N-nitroso-N-methylurea in rat prostate and seminal vesicle. AN - 75614184; 8453611 AB - To understand the molecular mechanism of carcinogenesis in androgen-dependent tumors, we have searched for new markers which are associated with this process. In normal rat prostate and seminal vesicle, sulfated glycoprotein 2 (SGP-2) messenger RNA is barely detectable. However, we have found high levels of SGP-2 expression in the epithelial component of carcinomas of the prostate and seminal vesicle after initiation with N-nitroso-N-methylurea and promotion with testosterone propionate. We have also observed induction of SGP-2 expression in epithelial cells at early stages in carcinogenesis when cytologically malignant cells first begin to appear. SGP-2 has been reported previously to be associated with a variety of models of programmed cell death (apoptosis), including the prostate following castration. Our present findings provide a novel marker for carcinogenesis in the rat prostate and seminal vesicle. JF - Cancer research AU - Kadomatsu, K AU - Anzano, M A AU - Slayter, M V AU - Winokur, T S AU - Smith, J M AU - Sporn, M B AD - Laboratory of Chemoprevention, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1993/04/01/ PY - 1993 DA - 1993 Apr 01 SP - 1480 EP - 1483 VL - 53 IS - 7 SN - 0008-5472, 0008-5472 KW - Biomarkers, Tumor KW - 0 KW - Clusterin KW - Glycoproteins KW - Molecular Chaperones KW - Methylnitrosourea KW - 684-93-5 KW - Index Medicus KW - Rats KW - Animals KW - Blotting, Northern KW - Epithelium -- metabolism KW - Male KW - Prostatic Neoplasms -- metabolism KW - Biomarkers, Tumor -- metabolism KW - Prostatic Neoplasms -- pathology KW - Seminal Vesicles -- metabolism KW - Glycoproteins -- metabolism KW - Prostatic Neoplasms -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75614184?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Expression+of+sulfated+glycoprotein+2+is+associated+with+carcinogenesis+induced+by+N-nitroso-N-methylurea+in+rat+prostate+and+seminal+vesicle.&rft.au=Kadomatsu%2C+K%3BAnzano%2C+M+A%3BSlayter%2C+M+V%3BWinokur%2C+T+S%3BSmith%2C+J+M%3BSporn%2C+M+B&rft.aulast=Kadomatsu&rft.aufirst=K&rft.date=1993-04-01&rft.volume=53&rft.issue=7&rft.spage=1480&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-21 N1 - Date created - 1993-04-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Physical and functional characterization of transcriptional control elements in the equine infectious anemia virus promoter. AN - 75610142; 8383228 AB - Equine infectious anemia virus (EIAV) is a lentivirus that causes a chronic disease of horses characterized by cyclic episodes of fever, anemia, and viremia. Although the genome and promoter of EIAV are much less complex than those of its relatives the primate immunodeficiency viruses, the cellular proteins that activate and regulate transcription of EIAV have not yet been identified. In this report, we show by electrophoretic mobility shift assays and DNase I footprinting that the EIAV promoter contains multiple binding sites for ubiquitous, cell type-specific, and inducible cellular proteins. Functional analysis by transient transfection of canine osteosarcoma (D17) and human epithelial carcinoma (HeLa) cells with EIAV promoters containing deletions or individually mutated DNA-binding sites demonstrated that these DNA-binding elements cooperatively regulate transcriptional activity. A methylated DNA-binding site (MDBP; also designated EF-C or EP) acts as either a positive or negative regulator of promoter activity, depending on the cell type or condition. Two PEA2 elements, an AP-1 site, and an ets/PEA3 motif confer a positive effect on promoter activity. The EIAV promoter is shown to be activated by treatment of HeLa cells with phorbol myristate acetate (PMA). DNA-binding activities were induced in PMA-treated HeLa cells and formed complexes on oligonucleotides that contain the EIAV AP-1 and ets/PEA3 elements. Functional analysis of mutated promoters indicated that the ets/PEA3 motif was the principal mediator of PMA activation. JF - Journal of virology AU - Carvalho, M AU - Derse, D AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1993/04// PY - 1993 DA - April 1993 SP - 2064 EP - 2074 VL - 67 IS - 4 SN - 0022-538X, 0022-538X KW - DNA-Binding Proteins KW - 0 KW - Oligodeoxyribonucleotides KW - Transcription Factors KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Transcription Factors -- metabolism KW - HeLa Cells KW - Humans KW - Horses KW - Transcription, Genetic KW - Binding Sites KW - Base Sequence KW - Cells, Cultured KW - Oligodeoxyribonucleotides -- chemistry KW - In Vitro Techniques KW - Dogs KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Methylation KW - Sequence Deletion KW - DNA-Binding Proteins -- metabolism KW - Promoter Regions, Genetic KW - Gene Expression Regulation, Viral KW - Enhancer Elements, Genetic KW - Infectious Anemia Virus, Equine -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75610142?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Physical+and+functional+characterization+of+transcriptional+control+elements+in+the+equine+infectious+anemia+virus+promoter.&rft.au=Carvalho%2C+M%3BDerse%2C+D&rft.aulast=Carvalho&rft.aufirst=M&rft.date=1993-04-01&rft.volume=67&rft.issue=4&rft.spage=2064&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-08 N1 - Date created - 1993-04-08 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Virol. 1982 May;42(2):502-9 [7086969] J Virol. 1989 Jul;63(7):3001-15 [2542608] Science. 1984 Dec 14;226(4680):1337-9 [6095453] Rev Infect Dis. 1985 Jan-Feb;7(1):83-8 [2984759] Mol Cell Biol. 1985 Apr;5(4):649-58 [2985964] Gene. 1985;33(2):181-9 [3922855] Proc Natl Acad Sci U S A. 1986 Nov;83(22):8550-4 [3022296] J Virol. 1987 Mar;61(3):743-7 [3027401] Nature. 1987 Jul 16-22;328(6127):254-6 [3037385] EMBO J. 1987 May;6(5):1331-7 [3038517] EMBO J. 1987 Dec 1;6(12):3761-70 [3428273] J Virol. 1988 Sep;62(9):3522-6 [2841502] Nucleic Acids Res. 1988 Aug 25;16(16):8029-44 [2901711] Cell. 1988 Dec 2;55(5):917-24 [3142692] EMBO J. 1988 Aug;7(8):2475-83 [3142763] Mol Cell Biol. 1989 Mar;9(3):1327-31 [2498646] Mol Cell Biol. 1989 Apr;9(4):1804-9 [2725524] Oncogene. 1989 May;4(5):629-36 [2498806] Proc Natl Acad Sci U S A. 1989 Aug;86(15):5974-8 [2762307] Mol Cell Biol. 1989 Jul;9(7):2787-97 [2550788] Nucleic Acids Res. 1990 Jan 11;18(1):23-34 [2106664] J Virol. 1990 Apr;64(4):1616-24 [2157047] Genes Dev. 1990 Mar;4(3):401-9 [2186967] Proc Natl Acad Sci U S A. 1990 May;87(10):3723-7 [2187191] Mol Cell Biol. 1990 Jul;10(7):3683-9 [2355919] EMBO J. 1990 Jul;9(7):2241-6 [2162765] Mol Cell Biol. 1990 Nov;10(11):5857-64 [2172787] Nucleic Acids Res. 1990 Nov 11;18(21):6253-60 [2173824] J Virol. 1991 Mar;65(3):1605-10 [1847479] Oncogene. 1991 Apr;6(4):533-42 [1827665] J Virol. 1991 Jul;65(7):3468-74 [1645778] J Virol. 1991 Oct;65(10):5391-400 [1654447] Genes Dev. 1992 Mar;6(3):481-96 [1547944] Cell. 1992 May 29;69(5):751-7 [1591775] Cell Growth Differ. 1992 May;3(5):327-34 [1633115] Nucleic Acids Res. 1989 Jan 25;17(2):499-516 [2536920] Nucleic Acids Res. 1989 Feb 25;17(4):1459-74 [2537959] Nucleic Acids Res. 1983 Mar 11;11(5):1475-89 [6828386] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Functional elements DE2A, DE2B, and DE1A and the TATA box are required for activity of the chicken alpha A-crystallin gene in transfected lens epithelial cells. AN - 75642986; 8454650 AB - alpha A-crystallin is an abundant soluble protein of the vertebrate eye lens. In addition to the TATA box, four positive cis-regulatory elements of the chicken alpha A-crystallin gene have been identified by linker scanning mutagenesis, DNase I footprinting, and gel mobility shift experiments. The regulatory elements described here have been named DE2A (at positions -144 to -134), DE2B (at positions -128 to -118), and DE1A (at positions -114 to -103). DE2A and DE2B form a dyad of symmetry between positions -141 and -118 (5'-AGACTGTCAT....AGGTCAGTCT-3'), consistent with the close similarity in the mobility of complexes formed with lens nuclear proteins by these two elements. Mutations in DE2A, DE2B, and DE1A leading to loss of promoter activity using the bacterial chloramphenicol acetyltransferase reporter gene transfected into primary embryonic chicken lens epithelial cells resulted in a corresponding loss in the ability to compete for complex formation with lens nuclear proteins in gel mobility shift assays. Mutation of the alpha A-CRYBP1-like site (-67/-57), necessary for function of the mouse alpha A-crystallin promoter, did not affect the activity of the chicken promoter. The DNase I footprinting and gel mobility shift experiments confirmed the previously noted binding of nuclear proteins to a dyad of symmetry at positions -153 to -140. In contrast to DE2A, DE2B, and DE1A, mutagenesis and gel mobility shift experiments failed to correlate function and protein binding for the -153/-140 dyad. DE2A, DE2B, and DE1A agree well with the regulatory elements alpha CE1 (-162/-134), alpha CE3 (-135/-121), and alpha CE2 (-119/-99) (Matsuo, I., and Yasuda, K. (1992) Nucleic Acids Res. 20, 3701-3712) for this gene. The present results suggest, however, that the lens enhancer activity of alpha CE1 is due to the sequence -141/-134, which forms the upper half of the DE2A/DE2B dyad of symmetry, rather than the -153/-140 dyad as previously suspected. JF - The Journal of biological chemistry AU - Klement, J F AU - Cvekl, A AU - Piatigorsky, J AD - Laboratory of Molecular and Developmental Biology, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892-0006. Y1 - 1993/03/25/ PY - 1993 DA - 1993 Mar 25 SP - 6777 EP - 6784 VL - 268 IS - 9 SN - 0021-9258, 0021-9258 KW - Crystallins KW - 0 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Animals KW - Base Sequence KW - Epithelial Cells KW - Transfection KW - Cells, Cultured KW - Chick Embryo KW - Molecular Sequence Data KW - Transcription, Genetic KW - Epithelium -- metabolism KW - Regulatory Sequences, Nucleic Acid KW - Lens, Crystalline -- metabolism KW - Lens, Crystalline -- cytology KW - Gene Expression Regulation KW - Crystallins -- genetics KW - TATA Box UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75642986?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Functional+elements+DE2A%2C+DE2B%2C+and+DE1A+and+the+TATA+box+are+required+for+activity+of+the+chicken+alpha+A-crystallin+gene+in+transfected+lens+epithelial+cells.&rft.au=Klement%2C+J+F%3BCvekl%2C+A%3BPiatigorsky%2C+J&rft.aulast=Klement&rft.aufirst=J&rft.date=1993-03-25&rft.volume=268&rft.issue=9&rft.spage=6777&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-22 N1 - Date created - 1993-04-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Interaction of ADP-ribosylation factor with Escherichia coli enterotoxin that contains an inactivating lysine 112 substitution. AN - 75641466; 8454609 AB - Cholera toxin and Escherichia coli heat-labile enterotoxin (LT) exert their effects on cells through ADP-ribosylation of guanine nucleotide-binding proteins. Both toxins consist of one A subunit, which is an ADP-ribosyltransferase, and five B (or binding) subunits. Their enzymatic activities are latent; activation requires reduction and proteolysis, resulting in a catalytically active A1 protein and a much smaller A2 protein. These ADP-ribosyltransferases are activated by GTP-dependent 20-kDa ADP-ribosylation factors or ARFs. To determine if proteolysis plus reduction is required for appearance of the ARF allosteric site as well as for catalytic activity, an inactive mutant of LT, LT(E112K), with replacement of glutamate by lysine at position 112 of its A subunit, was utilized as a competitor in cholera toxin ADP-ribosyltransferase assays containing limiting amounts of ARF. LT(E112K) required trypsinization and reduction to become a potent, concentration-dependent inhibitor. Inhibition was reversed by increasing concentrations of ARF. Reduction or trypsinization alone did not generate an inhibitory form of LT(E112K). These studies are consistent with the conclusion that the ARF site is not expressed in the latent toxin. Both trypsinization and reduction are required for expression of a functional ARF binding site as well as for catalytic activity. JF - The Journal of biological chemistry AU - Moss, J AU - Stanley, S J AU - Vaughan, M AU - Tsuji, T AD - Laboratory of Cellular Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/03/25/ PY - 1993 DA - 1993 Mar 25 SP - 6383 EP - 6387 VL - 268 IS - 9 SN - 0021-9258, 0021-9258 KW - Bacterial Toxins KW - 0 KW - Enterotoxins KW - Escherichia coli Proteins KW - heat-labile enterotoxin, E coli KW - Adenosine Diphosphate KW - 61D2G4IYVH KW - Ribose KW - 681HV46001 KW - Cholera Toxin KW - 9012-63-9 KW - Trypsin KW - EC 3.4.21.4 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - ADP-Ribosylation Factors KW - EC 3.6.5.2 KW - Lysine KW - K3Z4F929H6 KW - Dithiothreitol KW - T8ID5YZU6Y KW - Index Medicus KW - Oxidation-Reduction KW - Dithiothreitol -- pharmacology KW - Hydrolysis KW - Lysine -- metabolism KW - Cholera Toxin -- metabolism KW - Binding Sites KW - Escherichia coli -- metabolism KW - Enterotoxins -- chemistry KW - Bacterial Toxins -- metabolism KW - Enterotoxins -- metabolism KW - GTP-Binding Proteins -- metabolism KW - Ribose -- metabolism KW - Bacterial Toxins -- chemistry KW - Adenosine Diphosphate -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75641466?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Interaction+of+ADP-ribosylation+factor+with+Escherichia+coli+enterotoxin+that+contains+an+inactivating+lysine+112+substitution.&rft.au=Moss%2C+J%3BStanley%2C+S+J%3BVaughan%2C+M%3BTsuji%2C+T&rft.aulast=Moss&rft.aufirst=J&rft.date=1993-03-25&rft.volume=268&rft.issue=9&rft.spage=6383&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-22 N1 - Date created - 1993-04-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Overexpression of protein kinase C-delta and -epsilon in NIH 3T3 cells induces opposite effects on growth, morphology, anchorage dependence, and tumorigenicity. AN - 75633211; 8454583 AB - We have determined the patterns of mRNA and protein expression of 7 protein kinase C (PKC) isozymes in NIH 3T3 cells. Only PKC-alpha is expressed abundantly in NIH 3T3 cells; endogenous levels of the other 6 PKC isozymes are low or undetectable. We have overexpressed PKC-delta and -epsilon in these cells to observe activation/translocation of these two isozymes and the biological consequences of overexpression. Both PKC-delta and -epsilon, but not PKC-alpha, are partially associated with the insoluble fraction even in the absence of phorbol 12-myristate 13-acetate (PMA). Upon PMA stimulation, both PKC-delta and -epsilon translocate to the insoluble fraction of cell homogenates, as can be observed with the endogenous PKC-alpha. Overexpression of PKC-delta induces significant changes in morphology and causes the cells to grow more slowly and to a decreased cell density in confluent cultures. These changes are accentuated by treatment with PMA. Overexpression of PKC-epsilon does not lead to morphological changes, but causes increased growth rates and higher cell densities in monolayers. None of the PKC-delta overexpressers grow in soft agar with or without PMA, but all the cell lines that overexpress PKC-epsilon grow in soft agar in the absence of PMA, but not in its presence. NIH 3T3 cells that overexpress PKC-epsilon also form tumors in nude mice with 100% incidence. This indicates that high expression of PKC-epsilon contributes to neoplastic transformation. JF - The Journal of biological chemistry AU - Mischak, H AU - Goodnight, J A AU - Kolch, W AU - Martiny-Baron, G AU - Schaechtle, C AU - Kazanietz, M G AU - Blumberg, P M AU - Pierce, J H AU - Mushinski, J F AD - Laboratory of Genetics, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1993/03/25/ PY - 1993 DA - 1993 Mar 25 SP - 6090 EP - 6096 VL - 268 IS - 9 SN - 0021-9258, 0021-9258 KW - Indoles KW - 0 KW - Isoenzymes KW - Maleimides KW - Protein Kinase C KW - EC 2.7.11.13 KW - bisindolylmaleimide I KW - L79H6N0V6C KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - 3T3 Cells KW - Animals KW - Blotting, Northern KW - Neoplasms, Experimental -- etiology KW - Enzyme Activation KW - Biological Transport KW - Mice, Nude KW - Mice KW - Cloning, Molecular KW - Brain -- enzymology KW - Blotting, Western KW - Enzyme Stability KW - Kinetics KW - Mice, Inbred C57BL KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Indoles -- pharmacology KW - Maleimides -- pharmacology KW - Protein Kinase C -- metabolism KW - Protein Kinase C -- genetics KW - Cell Division -- drug effects KW - Cell Adhesion -- drug effects KW - Isoenzymes -- genetics KW - Isoenzymes -- metabolism KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75633211?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Overexpression+of+protein+kinase+C-delta+and+-epsilon+in+NIH+3T3+cells+induces+opposite+effects+on+growth%2C+morphology%2C+anchorage+dependence%2C+and+tumorigenicity.&rft.au=Mischak%2C+H%3BGoodnight%2C+J+A%3BKolch%2C+W%3BMartiny-Baron%2C+G%3BSchaechtle%2C+C%3BKazanietz%2C+M+G%3BBlumberg%2C+P+M%3BPierce%2C+J+H%3BMushinski%2C+J+F&rft.aulast=Mischak&rft.aufirst=H&rft.date=1993-03-25&rft.volume=268&rft.issue=9&rft.spage=6090&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-22 N1 - Date created - 1993-04-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Escherichia coli dinG gene encodes a putative DNA helicase related to a group of eukaryotic helicases including Rad3 protein. AN - 20199913; 8739488 JF - Nucleic Acids Research AU - Koonin, E V AD - National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, MD 20894. Y1 - 1993/03/25/ PY - 1993 DA - 1993 Mar 25 SP - 1497 PB - Oxford University Press, Oxford Journals, Great Clarendon Street VL - 21 IS - 6 SN - 0305-1048, 0305-1048 KW - Genetics Abstracts; Microbiology Abstracts B: Bacteriology; Biochemistry Abstracts 2: Nucleic Acids KW - Escherichia coli KW - DNA helicase KW - J 02310:Genetics & Taxonomy KW - N 14835:Protein-Nucleic Acids Association KW - G 07770:Bacteria UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/20199913?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+Acids+Research&rft.atitle=Escherichia+coli+dinG+gene+encodes+a+putative+DNA+helicase+related+to+a+group+of+eukaryotic+helicases+including+Rad3+protein.&rft.au=Koonin%2C+E+V&rft.aulast=Koonin&rft.aufirst=E&rft.date=1993-03-25&rft.volume=21&rft.issue=6&rft.spage=1497&rft.isbn=&rft.btitle=&rft.title=Nucleic+Acids+Research&rft.issn=03051048&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2008-12-01 N1 - Last updated - 2015-03-27 N1 - SubjectsTermNotLitGenreText - DNA helicase; Escherichia coli ER - TY - JOUR T1 - The effects of treatment with interleukin-1 alpha on platelet recovery after high-dose carboplatin. AN - 75585796; 8437596 AB - Thrombocytopenia is a frequent side effect of cancer chemotherapy and commonly limits attempts to escalate drug doses. To determine whether interleukin-1 alpha could ameliorate carboplatin-induced thrombocytopenia, we combined it with high-dose carboplatin in 43 patients with advanced neoplasms. High-dose carboplatin (800 mg per square meter of body-surface area) was administered alone to a control group. Subsequent patients were randomly assigned to receive the same dose of carboplatin with interleukin-1 alpha, administered either before or after carboplatin. Interleukin-1 alpha was given intravenously at a dose of 0.03, 0.1, or 0.3 microgram per kilogram of body weight per day for five days. Carboplatin alone consistently produced thrombocytopenia with a median nadir of 19,000 platelets per cubic millimeter and a median of 10 days with less than 100,000 platelets per cubic millimeter. All 15 patients receiving interleukin-1 alpha before carboplatin had similar findings. In contrast, 5 of the 15 patients given one of the two higher doses of interleukin-1 alpha after carboplatin had minimal thrombocytopenia (nadir, 91,000 to 332,000 platelets per cubic millimeter). In the 10 patients given 0.3 microgram of interleukin-1 alpha per kilogram after carboplatin treatment, the platelet count recovered to 100,000 per cubic millimeter significantly earlier than in either the control group (P = 0.002) or the patients who received interleukin-1 alpha before carboplatin (P = 0.003), with the median times to recovery in the three groups being 16, 21, and 23 days, respectively. At the highest dose of interleukin-1 alpha, toxicity was substantial (but reversible), requiring inpatient support for hypotension, supraventricular arrhythmias, and pulmonary-capillary leak. Interleukin-1 alpha can accelerate the recovery of platelets after high-dose carboplatin therapy and may be clinically useful in preventing or treating thrombocytopenia induced by chemotherapy. JF - The New England journal of medicine AU - Smith, J W AU - Longo, D L AU - Alvord, W G AU - Janik, J E AU - Sharfman, W H AU - Gause, B L AU - Curti, B D AU - Creekmore, S P AU - Holmlund, J T AU - Fenton, R G AD - Biological Response Modifiers Program, Frederick Cancer Research and Development Center, National Cancer Institute, Md. Y1 - 1993/03/18/ PY - 1993 DA - 1993 Mar 18 SP - 756 EP - 761 VL - 328 IS - 11 SN - 0028-4793, 0028-4793 KW - Interleukin-1 KW - 0 KW - Carboplatin KW - BG3F62OND5 KW - Abridged Index Medicus KW - Index Medicus KW - Drug Therapy, Combination KW - Neoplasms -- drug therapy KW - Humans KW - Adult KW - Aged KW - Pilot Projects KW - Middle Aged KW - Time Factors KW - Male KW - Female KW - Platelet Count KW - Thrombocytopenia -- therapy KW - Interleukin-1 -- administration & dosage KW - Interleukin-1 -- therapeutic use KW - Thrombocytopenia -- chemically induced KW - Carboplatin -- adverse effects KW - Carboplatin -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75585796?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+New+England+journal+of+medicine&rft.atitle=The+effects+of+treatment+with+interleukin-1+alpha+on+platelet+recovery+after+high-dose+carboplatin.&rft.au=Smith%2C+J+W%3BLongo%2C+D+L%3BAlvord%2C+W+G%3BJanik%2C+J+E%3BSharfman%2C+W+H%3BGause%2C+B+L%3BCurti%2C+B+D%3BCreekmore%2C+S+P%3BHolmlund%2C+J+T%3BFenton%2C+R+G&rft.aulast=Smith&rft.aufirst=J&rft.date=1993-03-18&rft.volume=328&rft.issue=11&rft.spage=756&rft.isbn=&rft.btitle=&rft.title=The+New+England+journal+of+medicine&rft.issn=00284793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-24 N1 - Date created - 1993-03-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Effects of recent research on recommendations for periconceptional folate supplement use. AN - 75745745; 8494256 JF - Annals of the New York Academy of Sciences AU - Mills, J L AU - Raymond, E AD - Epidemiology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/03/15/ PY - 1993 DA - 1993 Mar 15 SP - 137 EP - 145 VL - 678 SN - 0077-8923, 0077-8923 KW - Folic Acid KW - 935E97BOY8 KW - Index Medicus KW - Humans KW - Cost-Benefit Analysis KW - Female KW - Pregnancy KW - Folic Acid -- economics KW - Folic Acid -- therapeutic use KW - Neural Tube Defects -- prevention & control KW - Folic Acid -- adverse effects KW - Folic Acid -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75745745?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+the+New+York+Academy+of+Sciences&rft.atitle=Effects+of+recent+research+on+recommendations+for+periconceptional+folate+supplement+use.&rft.au=Mills%2C+J+L%3BRaymond%2C+E&rft.aulast=Mills&rft.aufirst=J&rft.date=1993-03-15&rft.volume=678&rft.issue=&rft.spage=137&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+New+York+Academy+of+Sciences&rft.issn=00778923&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-17 N1 - Date created - 1993-06-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - A platelet-activating factor antagonist, RP 55778, inhibits cytokine-dependent induction of human immunodeficiency virus expression in chronically infected promonocytic cells. AN - 75666377; 7681601 AB - A platelet-activating factor antagonist, RP 55778, potently suppressed the induction of human immunodeficiency virus (HIV) expression in chronically infected promonocytic U1 cells. RP 55778 inhibited the production of reverse transcriptase activity in U1 cells stimulated with the transcriptionally active inducers of virus production, tumor necrosis factor alpha and phorbol 12-myristate 13-acetate. This effect was correlated only in part with a reduction in the levels of HIV RNA, suggesting that this agent was also affecting posttranscriptional levels of virus production. In this regard, RP 55778 effectively blocked the induction of HIV expression in U1 cells stimulated with interleukin 6 and granulocyte-macrophage colony-stimulating factor, which act predominantly as posttranscriptional activators of HIV expression. Finally, RP 55778 inhibited the production of endogenous tumor necrosis factor alpha in phorbol 12-myristate 13-acetate-stimulated cells, thereby interfering with an autocrine pathway of virus expression. The suppressive effects of RP 55778 on HIV expression appeared to be independent of the platelet-activating factor cell surface receptor on U1 cells. RP 55778 inhibited acute HIV replication in primary T-cell blasts and the proliferative capacity of these cells. This study suggests that RP 55778 may represent potentially useful compounds in the treatment of HIV infection. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Weissman, D AU - Poli, G AU - Bousseau, A AU - Fauci, A S AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/03/15/ PY - 1993 DA - 1993 Mar 15 SP - 2537 EP - 2541 VL - 90 IS - 6 SN - 0027-8424, 0027-8424 KW - Cytokines KW - 0 KW - Interleukin-6 KW - Platelet Activating Factor KW - Pyridines KW - RNA, Messenger KW - RNA, Viral KW - Recombinant Proteins KW - Thiazoles KW - Tumor Necrosis Factor-alpha KW - Granulocyte-Macrophage Colony-Stimulating Factor KW - 83869-56-1 KW - 3-(3-pyridinyl)-1H,3H-pyrrolo(1,2-c)thiazole-7-carboxamide KW - 93363-11-2 KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - HIV Reverse Transcriptase KW - EC 2.7.7.49 KW - RNA-Directed DNA Polymerase KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - AIDS/HIV KW - RNA, Viral -- biosynthesis KW - Humans KW - Tumor Necrosis Factor-alpha -- biosynthesis KW - Interleukin-6 -- pharmacology KW - RNA-Directed DNA Polymerase -- metabolism KW - RNA, Viral -- isolation & purification KW - Chloramphenicol O-Acetyltransferase -- metabolism KW - Granulocyte-Macrophage Colony-Stimulating Factor -- pharmacology KW - RNA, Messenger -- genetics KW - RNA Processing, Post-Transcriptional KW - Chloramphenicol O-Acetyltransferase -- genetics KW - RNA, Messenger -- metabolism KW - Transfection KW - Recombinant Proteins -- metabolism KW - Kinetics KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Monocytes KW - Fluorescent Antibody Technique KW - Cell Line KW - Thiazoles -- pharmacology KW - Platelet Activating Factor -- antagonists & inhibitors KW - Platelet Activating Factor -- pharmacology KW - Transcription, Genetic -- drug effects KW - Cytokines -- pharmacology KW - HIV-1 -- enzymology KW - Cytokines -- antagonists & inhibitors KW - HIV-1 -- physiology KW - Pyridines -- pharmacology KW - HIV-1 -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75666377?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=A+platelet-activating+factor+antagonist%2C+RP+55778%2C+inhibits+cytokine-dependent+induction+of+human+immunodeficiency+virus+expression+in+chronically+infected+promonocytic+cells.&rft.au=Weissman%2C+D%3BPoli%2C+G%3BBousseau%2C+A%3BFauci%2C+A+S&rft.aulast=Weissman&rft.aufirst=D&rft.date=1993-03-15&rft.volume=90&rft.issue=6&rft.spage=2537&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-23 N1 - Date created - 1993-04-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Neuroimmunol. 1989 Jul;23(2):109-16 [2656753] AIDS Res Hum Retroviruses. 1992 Feb;8(2):191-7 [1540407] Science. 1989 Jul 21;245(4915):305-8 [2665081] J Clin Invest. 1989 Sep;84(3):738-43 [2503543] Proc Natl Acad Sci U S A. 1989 Aug;86(15):5974-8 [2762307] Prog Clin Biol Res. 1989;308:919-24 [2780739] N Engl J Med. 1989 Dec 14;321(24):1621-5 [2586564] N Engl J Med. 1989 Dec 14;321(24):1626-31 [2511447] J Immunol. 1990 Jan 15;144(2):480-4 [2295799] Proc Natl Acad Sci U S A. 1990 Jan;87(2):782-5 [2300561] AIDS. 1990 Jan;4(1):21-7 [1969279] Am J Pathol. 1990 Apr;136(4):949-56 [2327475] J Biol Chem. 1990 Jun 5;265(16):9140-5 [2160958] J Exp Med. 1990 Jul 1;172(1):151-8 [2193094] Immunology. 1983 Jan;48(1):141-9 [6848449] Annu Rev Biochem. 1986;55:483-509 [3017194] Nature. 1987 Apr 16-22;326(6114):711-3 [3031512] Annu Rev Pharmacol Toxicol. 1987;27:237-55 [3555317] Science. 1987 Nov 6;238(4828):800-2 [3313729] J Immunol. 1988 Feb 15;140(4):1117-22 [2449497] Am J Med. 1988 Sep;85(3):289-91 [3414726] J Cell Biol. 1988 Oct;107(4):1269-77 [3049617] Circ Res. 1990 Jul;67(1):68-77 [2114228] J Immunol. 1990 Nov 1;145(9):3062-70 [2212673] Science. 1990 Sep 28;249(4976):1533-44 [1699273] J Exp Med. 1991 Jan 1;173(1):1-5 [1985116] Ann Intern Med. 1991 Apr 15;114(8):678-93 [1672248] J Mol Neurosci. 1990;2(2):79-84 [2078479] Invest Ophthalmol Vis Sci. 1991 Jul;32(8):2393-9 [1649146] J Immunol. 1991 Jul 15;147(2):509-14 [2071893] J Immunol. 1991 Oct 1;147(7):2290-4 [1680914] J Lipid Mediat. 1989 Nov-Dec;1(6):349-60 [2519903] J Immunol. 1989 Aug 1;143(3):964-70 [2545780] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Mutual regulation of the transcriptional activator NF-kappa B and its inhibitor, I kappa B-alpha. AN - 75629703; 8460169 AB - The NK-kappa B transcription factor complex is sequestered in the cytoplasm by the inhibitory protein I kappa B-alpha (MAD-3). Various cellular stimuli relieve this inhibition by mechanisms largely unknown, leading to NF-kappa B nuclear localization and transactivation of its target genes. It is demonstrated here with human T lymphocytes and monocytes that different stimuli, including tumor necrosis factor alpha and phorbol 12-myristate 13-acetate, cause rapid degradation of I kappa B-alpha, with concomitant activation of NF-kappa B, followed by a dramatic increase in I kappa B-alpha mRNA and protein synthesis. Transfection studies reveal that the I kappa B-alpha mRNA and the encoded protein are potently induced by NF-kappa B and by homodimers of p65 and of c-Rel. We propose a model in which NF-kappa B and I kappa B-alpha mutually regulate each other in a cycle: saturating amounts of the inhibitory I kappa B-alpha protein are destroyed upon stimulation, allowing rapid activation of NF-kappa B. Subsequently, I kappa B-alpha mRNA and protein levels are quickly induced by the activated NF-kappa B. This resurgence of I kappa B-alpha protein acts to restore an equilibrium in which NF-kappa B is again inhibited. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Brown, K AU - Park, S AU - Kanno, T AU - Franzoso, G AU - Siebenlist, U AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/03/15/ PY - 1993 DA - 1993 Mar 15 SP - 2532 EP - 2536 VL - 90 IS - 6 SN - 0027-8424, 0027-8424 KW - DNA-Binding Proteins KW - 0 KW - I kappa B beta protein KW - I-kappa B Proteins KW - Macromolecular Substances KW - NF-kappa B KW - RNA, Messenger KW - Tumor Necrosis Factor-alpha KW - Ionomycin KW - 56092-81-0 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Blotting, Northern KW - RNA, Messenger -- metabolism KW - Transfection KW - Humans KW - Tumor Necrosis Factor-alpha -- pharmacology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Cell Nucleus -- physiology KW - Ionomycin -- pharmacology KW - Gene Expression Regulation -- drug effects KW - Cell Nucleus -- drug effects KW - Cell Line KW - Monocytes -- immunology KW - DNA-Binding Proteins -- genetics KW - T-Lymphocytes -- immunology KW - NF-kappa B -- metabolism KW - NF-kappa B -- antagonists & inhibitors KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75629703?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Mutual+regulation+of+the+transcriptional+activator+NF-kappa+B+and+its+inhibitor%2C+I+kappa+B-alpha.&rft.au=Brown%2C+K%3BPark%2C+S%3BKanno%2C+T%3BFranzoso%2C+G%3BSiebenlist%2C+U&rft.aulast=Brown&rft.aufirst=K&rft.date=1993-03-15&rft.volume=90&rft.issue=6&rft.spage=2532&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-23 N1 - Date created - 1993-04-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nucleic Acids Res. 1983 Mar 11;11(5):1475-89 [6828386] Int Rev Cytol. 1993;143:1-62 [8449662] J Virol. 1984 Oct;52(1):172-82 [6090694] Anal Biochem. 1987 Apr;162(1):156-9 [2440339] Science. 1987 Oct 30;238(4827):692-4 [3118464] Cell. 1988 Apr 22;53(2):211-7 [3129195] Science. 1988 Oct 28;242(4878):540-6 [3140380] Oncogene. 1989 Jul;4(7):935-42 [2666912] Genes Dev. 1989 Nov;3(11):1689-98 [2691328] J Virol. 1990 Feb;64(2):584-91 [2153225] Nature. 1990 Apr 12;344(6267):678-82 [2157987] Cell. 1990 Apr 20;61(2):255-65 [2184941] Cell. 1990 Sep 7;62(5):1007-18 [2203531] Cell. 1990 Sep 7;62(5):1019-29 [2203532] Nature. 1990 Nov 1;348(6296):76-80 [2234062] Proc Natl Acad Sci U S A. 1990 Dec;87(24):10028-32 [2263603] Mol Cell Biol. 1991 Jan;11(1):259-66 [1986224] Cell. 1991 Jan 11;64(1):1-3 [1986861] Genes Dev. 1990 Nov;4(11):1975-84 [2125960] Proc Natl Acad Sci U S A. 1991 Feb 1;88(3):966-70 [1992489] Cell. 1991 Mar 8;64(5):961-9 [2001591] Science. 1991 Mar 22;251(5000):1490-3 [2006423] Biochim Biophys Acta. 1991 Apr 16;1072(1):63-80 [2018779] EMBO J. 1991 Jul;10(7):1817-25 [2050119] Cell. 1991 Jun 28;65(7):1281-9 [1829648] Genes Dev. 1991 Aug;5(8):1464-76 [1907941] Nature. 1991 Aug 22;352(6337):733-6 [1876189] Science. 1991 Sep 13;253(5025):1268-71 [1891714] EMBO J. 1991 Dec;10(12):3805-17 [1935902] Cell. 1991 Dec 20;67(6):1075-87 [1760839] J Biol Chem. 1992 Jan 5;267(1):239-46 [1309735] Mol Cell Biol. 1992 Feb;12(2):674-84 [1732739] Mol Cell Biol. 1992 Feb;12(2):685-95 [1531086] Proc Natl Acad Sci U S A. 1992 Mar 1;89(5):1875-9 [1542686] Genes Dev. 1992 May;6(5):745-60 [1577270] Proc Natl Acad Sci U S A. 1992 May 15;89(10):4333-7 [1533932] Mol Cell Biol. 1992 Jun;12(6):2898-908 [1588976] Nucleic Acids Res. 1992 May 25;20(10):2453-8 [1598203] J Clin Invest. 1992 Jul;90(1):121-9 [1634604] DNA Cell Biol. 1992 Sep;11(7):523-37 [1388725] Genes Dev. 1992 Oct;6(10):1899-913 [1340770] Nature. 1992 Sep 24;359(6393):339-42 [1406939] EMBO J. 1993 Jan;12(1):201-11 [7679069] Proc Natl Acad Sci U S A. 1983 Oct;80(20):6229-33 [6312449] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Cell type- and stage-specific expression of the CD20/B1 antigen correlates with the activity of a diverged octamer DNA motif present in its promoter. AN - 75622243; 7680653 AB - The CD20(B1) gene encodes a B cell-specific protein involved in the regulation of human B cell proliferation and differentiation. Studies with 5' deletion CD20 promoter-CAT constructs have previously revealed two regions of the promoter between bases -186 and -280 and between bases -280 and -454 which contained positive regulatory elements. In this study we identified a sequence element present in the most proximal region located between bases -214 and -201, TTCTTCTAATTAA, which is important in the high constitutive expression of CD20 in mature B cells and the induction of CD20 in pre-B cells. This sequence element was referred to as the BAT box and its deletion significantly reduced the activity of a CD20 promoter-CAT construct in B cells. Mobility shift assays with various mutant probes and B cell nuclear extracts demonstrated that the core sequence TAAT was essential for binding to this site. Cross competition experiments with an octamer sequence from the Ig heavy chain promoter, the BAT box, and a TA-rich sequence present in the CD21 promoter revealed that all three sequences bound the same nuclear proteins suggesting that the BAT box binding proteins were Oct-1 and Oct-2. Southwestern blotting and UV cross-linking studies confirmed that the BAT box binding proteins were Oct-1 and Oct-2. The affinity of the BAT box binding proteins for the BAT box was approximately 25-fold less than for the octamer sequence and the BAT box binding proteins dissociated from the BAT box 10-fold more rapidly than from the octamer sequence. Despite this lower affinity, a trimer of the BAT box sequence was as efficiently transactivated by an Oct-2 expression vector as was a trimer of the octamer sequence in HeLa cells. The BAT box and Oct-2 were also implicated in the induction of CD20 in the pre-B cell line, PB-697, via phorbol esters. The induction of CD20 mRNA was temporally associated with induction of Oct-2 mRNA and a BAT box-deleted CD20-CAT construct, in contrast to the wild type, was poorly induced by phorbol esters. Together these results suggest that the BAT box binding proteins are important in the B cell specific expression of CD20 and perhaps CD21. JF - The Journal of biological chemistry AU - Thévenin, C AU - Lucas, B P AU - Kozlow, E J AU - Kehrl, J H AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/03/15/ PY - 1993 DA - 1993 Mar 15 SP - 5949 EP - 5956 VL - 268 IS - 8 SN - 0021-9258, 0021-9258 KW - CD20(B1) KW - Antigens, CD KW - 0 KW - Antigens, CD20 KW - Antigens, Differentiation, B-Lymphocyte KW - DNA-Binding Proteins KW - HCFC1 protein, human KW - Host Cell Factor C1 KW - Octamer Transcription Factor-1 KW - Octamer Transcription Factor-2 KW - POU2F1 protein, human KW - POU2F2 protein, human KW - Receptors, Complement 3d KW - Transcription Factors KW - DNA KW - 9007-49-2 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Transcription Factors -- metabolism KW - HeLa Cells KW - DNA -- metabolism KW - DNA Mutational Analysis KW - Humans KW - Transcriptional Activation KW - Binding Sites KW - Base Sequence KW - Receptors, Complement 3d -- genetics KW - Tumor Cells, Cultured KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Mutation KW - Cell Line KW - Sequence Deletion KW - Antigens, Differentiation, B-Lymphocyte -- metabolism KW - B-Lymphocytes -- drug effects KW - Promoter Regions, Genetic KW - Antigens, Differentiation, B-Lymphocyte -- genetics KW - DNA-Binding Proteins -- genetics KW - Antigens, CD -- metabolism KW - Antigens, CD -- genetics KW - B-Lymphocytes -- immunology KW - B-Lymphocytes -- metabolism KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75622243?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Cell+type-+and+stage-specific+expression+of+the+CD20%2FB1+antigen+correlates+with+the+activity+of+a+diverged+octamer+DNA+motif+present+in+its+promoter.&rft.au=Th%C3%A9venin%2C+C%3BLucas%2C+B+P%3BKozlow%2C+E+J%3BKehrl%2C+J+H&rft.aulast=Th%C3%A9venin&rft.aufirst=C&rft.date=1993-03-15&rft.volume=268&rft.issue=8&rft.spage=5949&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-15 N1 - Date created - 1993-04-15 N1 - Date revised - 2017-01-13 N1 - Gene symbol - CD20(B1) N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Sequence specificity in the interaction of the four stereoisomeric benzo[c]phenanthrene dihydrodiol epoxides with the supF gene. AN - 75607070; 8443807 AB - The shuttle vector pS189 was treated with each of the four configurational isomers of benzo[c]phenanthrene 3,4-dihydrodiol 1,2-epoxide, and the modified DNA was used as a template in a polymerase arrest assay examining the supF gene. Sites at which polymerase (Sequenase, version 2.0) progress along the template was blocked were presumed to be at or near sites of adduct formation. The polymerase arrest sites were compared with recently reported mutation hotspots induced by these agents in this gene (Bigger et al., Proc. Natl. Acad. Sci. USA, 89: 368-372, 1992). For 31 of 32 mutation hotspots, a polymerase arrest band was present at or 1 or 2 nucleotides 3'- to that site, indicating that adduct formation tended to be associated with mutation hotspots. However, the arrest bands near mutation hotspots were not particularly prominent in all cases, and there were many sites of substantial polymerase arrest that were not in the vicinity of mutation hotspots. Thus, factors in addition to chemical selectivity must play key roles in determining sites of mutation. JF - Cancer research AU - Ross, H AU - Bigger, C A AU - Yagi, H AU - Jerina, D M AU - Dipple, A AD - Chemistry of Carcinogenesis Laboratory, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland 21702. Y1 - 1993/03/15/ PY - 1993 DA - 1993 Mar 15 SP - 1273 EP - 1277 VL - 53 IS - 6 SN - 0008-5472, 0008-5472 KW - supF KW - Carcinogens KW - 0 KW - DNA, Bacterial KW - Phenanthrenes KW - RNA, Transfer, Tyr KW - 1,2-epoxy-3,4-dihydroxy-1,2,3,4-tetrahydrobenzo(c)phenanthrene KW - 111001-48-0 KW - DNA-Directed DNA Polymerase KW - EC 2.7.7.7 KW - Index Medicus KW - Stereoisomerism KW - Base Sequence KW - DNA Repair KW - Genetic Vectors KW - Molecular Sequence Data KW - Escherichia coli -- genetics KW - Mutation KW - DNA-Directed DNA Polymerase -- metabolism KW - Phenanthrenes -- metabolism KW - Genes, Bacterial KW - Carcinogens -- metabolism KW - RNA, Transfer, Tyr -- genetics KW - DNA, Bacterial -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75607070?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Sequence+specificity+in+the+interaction+of+the+four+stereoisomeric+benzo%5Bc%5Dphenanthrene+dihydrodiol+epoxides+with+the+supF+gene.&rft.au=Ross%2C+H%3BBigger%2C+C+A%3BYagi%2C+H%3BJerina%2C+D+M%3BDipple%2C+A&rft.aulast=Ross&rft.aufirst=H&rft.date=1993-03-15&rft.volume=53&rft.issue=6&rft.spage=1273&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-07 N1 - Date created - 1993-04-07 N1 - Date revised - 2017-01-13 N1 - Gene symbol - supF N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Prognostic factors observed in current clinical trials. AN - 75605855; 8443767 AB - Adjuvant therapy of breast cancer has evolved over the past 15 years from an interesting clinical experiment to the standard of care for many patients. The toxicities of different treatments vary from those with minimal side effects, such as tamoxifen, to those with potentially life-threatening side effects. Current clinical trials are evaluating increasingly higher risk treatments, such as high-dose chemotherapy autologous bone marrow rescue. Chemotherapy is being used in groups that have previously been treated only with hormonal interventions or who have received no adjuvant therapy. The delineation of risk, such that the risks of treatment can be closely tied to the risk of recurrence is thus a desirable goal for clinical-laboratory research. Prognostic factors identified in treated patients, however, may be measures of treatment resistance versus treatment sensitivity rather than some underlying biologic characteristic defining a tumor's malignant potential. JF - Cancer AU - Dorr, F A AD - Medicine Section, National Cancer Institute, Bethesda, Maryland. Y1 - 1993/03/15/ PY - 1993 DA - 1993 Mar 15 SP - 2163 EP - 2168 VL - 71 IS - 6 Suppl SN - 0008-543X, 0008-543X KW - Abridged Index Medicus KW - Index Medicus KW - Randomized Controlled Trials as Topic KW - Neoplasm Staging KW - Humans KW - Prognosis KW - Female KW - Breast Neoplasms -- pathology KW - Clinical Trials as Topic KW - Breast Neoplasms -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75605855?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=Prognostic+factors+observed+in+current+clinical+trials.&rft.au=Dorr%2C+F+A&rft.aulast=Dorr&rft.aufirst=F&rft.date=1993-03-15&rft.volume=71&rft.issue=6+Suppl&rft.spage=2163&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-05 N1 - Date created - 1993-04-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - G-protein effects on retrograde axonal transport. AN - 75713657; 8481780 AB - Movements of medium and large sized membranous organelles (0.5-1 microns in diameter) were visualized within segments of the crab walking leg nerve with Nomarski differential interference contrast optics and subjected to video contrast enhancement. Accessibility to the axoplasm was demonstrated by intra-axonal fluorescence following addition of rhodamine conjugated to 40 kDa dextran to the external medium. Perfusion of the axons with a 1 microM solution of the 20 kDa G-protein, cp20, but not control solutions, reduced the number of organelles moving in the retrograde direction per unit time, but not the number of organelles moving in the anterograde direction. Such alteration of organelle movement may contribute to memory-specific changes of neuronal morphology. JF - Brain research AU - Moshiach, S AU - Nelson, T J AU - Sanchez-Andres, J V AU - Sakakibara, M AU - Alkon, D L AD - Neural Systems Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/03/12/ PY - 1993 DA - 1993 Mar 12 SP - 298 EP - 304 VL - 605 IS - 2 SN - 0006-8993, 0006-8993 KW - Botulinum Toxins KW - EC 3.4.24.69 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Index Medicus KW - Animals KW - Video Recording KW - In Vitro Techniques KW - Botulinum Toxins -- pharmacology KW - Biological Transport -- drug effects KW - GTP-Binding Proteins -- antagonists & inhibitors KW - Brachyura -- physiology KW - Movement -- physiology KW - GTP-Binding Proteins -- physiology KW - Organelles -- physiology KW - Extremities -- innervation KW - Axons -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75713657?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research&rft.atitle=G-protein+effects+on+retrograde+axonal+transport.&rft.au=Moshiach%2C+S%3BNelson%2C+T+J%3BSanchez-Andres%2C+J+V%3BSakakibara%2C+M%3BAlkon%2C+D+L&rft.aulast=Moshiach&rft.aufirst=S&rft.date=1993-03-12&rft.volume=605&rft.issue=2&rft.spage=298&rft.isbn=&rft.btitle=&rft.title=Brain+research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-02 N1 - Date created - 1993-06-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Characterization of single-chain antibody (sFv)-toxin fusion proteins produced in vitro in rabbit reticulocyte lysate. AN - 75625629; 8444903 AB - Chimeric proteins consisting of a fusion between binding-deficient mutants of diphtheria toxin (DT) or Pseudomonas exotoxin A (PE) and a single-chain antibody (E6 sFv) against the human transferrin receptor (TfnR) were expressed in a rabbit reticulocyte lysate system. Molecules utilizing PE40 (the carboxyl terminus 40 kDa of PE, lacking the binding domain) exhibited significant E6 sFv-mediated, cell type-specific cytotoxicity (IC50 1 x 10(-10) M) against a human erythroleukemia-derived cell line, K562. In contrast, a fusion protein between the same sFv and a DT mutant, DTM1 (containing two amino acid substitutions in the binding domain [S(508)F, S(525)F]) was not significantly cytotoxic, despite being enzymatically active. A tripartite protein in the form NH2-DTM1-E6 sFv-PE40-COOH exhibited cytotoxicity comparable to that of the PE40-sFv fusion (IC50 1 x 10(-10) M), suggesting that the deficit in activity of DTM1-sFv is not a function of misfolding of the sFv moiety or of a reduced ability to bind TfnR. In contrast to DTM1-E6 sFv, a fusion protein between a second DT mutant, CRM 107 [S(525)F], and the E6 sFv was specifically cytotoxic (IC50 1 x 10(-9) M), and toxicity could be blocked by addition of excess E6 antibody. The cell-free in vitro expression system we describe is rapid and may be used to express functional toxin-sFv fusion proteins. No protein refolding procedures are required, and the technique may be used to express proteins which, due to restrictions imposed on manipulation of toxin-encoding genes in Escherichia coli, could not be produced by more conventional methods. JF - The Journal of biological chemistry AU - Nicholls, P J AU - Johnson, V G AU - Andrew, S M AU - Hoogenboom, H R AU - Raus, J C AU - Youle, R J AD - Biochemistry Section, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/03/05/ PY - 1993 DA - 1993 Mar 05 SP - 5302 EP - 5308 VL - 268 IS - 7 SN - 0021-9258, 0021-9258 KW - Bacterial Toxins KW - 0 KW - Diphtheria Toxin KW - Exotoxins KW - Immunoglobulin Fragments KW - Immunotoxins KW - Recombinant Fusion Proteins KW - Virulence Factors KW - DNA KW - 9007-49-2 KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - Recombinant Fusion Proteins -- metabolism KW - Animals KW - Base Sequence KW - Recombinant Fusion Proteins -- genetics KW - Molecular Sequence Data KW - Vero Cells KW - Rabbits KW - Plasmids KW - Cell Line KW - Cell Survival KW - Exotoxins -- genetics KW - Immunotoxins -- toxicity KW - Diphtheria Toxin -- metabolism KW - Immunoglobulin Fragments -- genetics KW - Diphtheria Toxin -- genetics KW - Bacterial Toxins -- genetics KW - Bacterial Toxins -- metabolism KW - Immunotoxins -- immunology KW - Reticulocytes -- metabolism KW - Exotoxins -- metabolism KW - Immunotoxins -- genetics KW - Immunoglobulin Fragments -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75625629?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Characterization+of+single-chain+antibody+%28sFv%29-toxin+fusion+proteins+produced+in+vitro+in+rabbit+reticulocyte+lysate.&rft.au=Nicholls%2C+P+J%3BJohnson%2C+V+G%3BAndrew%2C+S+M%3BHoogenboom%2C+H+R%3BRaus%2C+J+C%3BYoule%2C+R+J&rft.aulast=Nicholls&rft.aufirst=P&rft.date=1993-03-05&rft.volume=268&rft.issue=7&rft.spage=5302&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-06 N1 - Date created - 1993-04-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Cell adherence to fibronectin and the aggregation of the high affinity immunoglobulin E receptor synergistically regulate tyrosine phosphorylation of 105-115-kDa proteins. AN - 75625556; 8444898 AB - Adherence of cells to extracellular matrix components modulates cellular responses. Here we compared the array of tyrosine phosphorylated proteins induced by the aggregation of the high affinity receptor for IgE (Fc epsilon RI) in fibronectin-adherent and in nonadherent rat basophilic leukemia (RBL-2H3) cells. Adherence to fibronectin in the absence of Fc epsilon RI aggregation induced tyrosine phosphorylation of 105-115-kDa proteins. This phosphorylation was reversed by EDTA and by a synthetic peptide containing the sequence Arg-Gly-Asp, demonstrating a requirement for fibronectin-integrin interaction. Aggregation of Fc epsilon RI in fibronectin-adherent cells markedly enhanced the tyrosine phosphorylation of the same 105-115-kDa proteins. There were minimal differences in tyrosine phosphorylation of other proteins induced by the aggregation of Fc epsilon RI in nonadherent and in fibronectin-adherent cells. Direct activation of protein kinase C and/or increase in calcium influx induced the phosphorylation of the 105-115-kDa proteins only in fibronectin-adherent cells. The magnitude of the phosphorylation of the 105-115-kDa proteins induced by the aggregation of Fc epsilon RI in fibronectin-adherent cells was substantially greater than the sum of that due to adherence to fibronectin and the aggregation of Fc epsilon RI in nonadherent cells. Therefore, cell adherence and the aggregation of Fc epsilon RI synergistically regulate tyrosine phosphorylation of the 105-115 kDa proteins. JF - The Journal of biological chemistry AU - Hamawy, M M AU - Mergenhagen, S E AU - Siraganian, R P AD - Laboratory of Immunology, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/03/05/ PY - 1993 DA - 1993 Mar 05 SP - 5227 EP - 5233 VL - 268 IS - 7 SN - 0021-9258, 0021-9258 KW - Fibronectins KW - 0 KW - Proteins KW - Receptors, IgE KW - Calcimycin KW - 37H9VM9WZL KW - Tyrosine KW - 42HK56048U KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Rats KW - Animals KW - Blotting, Western KW - Tumor Cells, Cultured KW - Phosphorylation KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Amino Acid Sequence KW - Calcimycin -- pharmacology KW - Precipitin Tests KW - Molecular Weight KW - Receptors, IgE -- metabolism KW - Proteins -- chemistry KW - Fibronectins -- metabolism KW - Tyrosine -- metabolism KW - Receptor Aggregation KW - Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75625556?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Cell+adherence+to+fibronectin+and+the+aggregation+of+the+high+affinity+immunoglobulin+E+receptor+synergistically+regulate+tyrosine+phosphorylation+of+105-115-kDa+proteins.&rft.au=Hamawy%2C+M+M%3BMergenhagen%2C+S+E%3BSiraganian%2C+R+P&rft.aulast=Hamawy&rft.aufirst=M&rft.date=1993-03-05&rft.volume=268&rft.issue=7&rft.spage=5227&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-06 N1 - Date created - 1993-04-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Opposite effects of NMDA and AMPA receptor blockade on catalepsy induced by dopamine receptor antagonists. AN - 75664467; 8385618 AB - Excitatory amino acid antagonists have been proposed as novel therapeutic agents for Parkinson's disease due to their ability to reverse akinesia in animal models of this disorder. To further evaluate this therapeutic potential, we examined the effects of a N-methyl-D-aspartate (NMDA) and an alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor antagonist on catalepsy produced by dopamine D1 or D2 receptor antagonists in rats. Male Sprague-Dawley rats were injected with dizocilpine (MK-801 0.025, 0.05 or 0.1 mg/kg i.p.), 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(f)quinoxaline (NBQX 12.5 mg/kg i.p.) or saline prior to administration of either raclopride (2.5 mg/kg i.p.) or SCH 23390 (0.5 mg/kg i.p.). Catalepsy was evaluated with both grid and bar tests every 20 min for 2.7 h. MK-801 (0.1 mg/kg) reversed the catalepsy produced by either raclopride or SCH 23390 but did not stimulate locomotion when given alone at this dose. At 0.05 mg/kg, MK-801 markedly decreased SCH 23390-induced catalepsy, but did not affect the catalepsy produced by raclopride. In contrast, NBQX increased raclopride-induced catalepsy, but had no effect on catalepsy elicited by SCH 23390. These findings suggest that blockade of NMDA receptors, but not non-NMDA receptors, may reverse the catalepsy produced by dopamine receptor antagonists. JF - European journal of pharmacology AU - Papa, S M AU - Engber, T M AU - Boldry, R C AU - Chase, T N AD - Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD 20892. Y1 - 1993/03/02/ PY - 1993 DA - 1993 Mar 02 SP - 247 EP - 253 VL - 232 IS - 2-3 SN - 0014-2999, 0014-2999 KW - Benzazepines KW - 0 KW - Dopamine Antagonists KW - Dopamine D2 Receptor Antagonists KW - Excitatory Amino Acid Antagonists KW - Quinoxalines KW - Receptors, AMPA KW - Receptors, Dopamine D1 KW - Receptors, N-Methyl-D-Aspartate KW - Salicylamides KW - 2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline KW - 118876-58-7 KW - Raclopride KW - 430K3SOZ7G KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - Index Medicus KW - Animals KW - Benzazepines -- pharmacology KW - Dose-Response Relationship, Drug KW - Dizocilpine Maleate -- pharmacology KW - Rats KW - Rats, Sprague-Dawley KW - Receptors, Dopamine D1 -- antagonists & inhibitors KW - Salicylamides -- pharmacology KW - Motor Activity -- drug effects KW - Quinoxalines -- pharmacology KW - Male KW - Catalepsy -- chemically induced KW - Receptors, N-Methyl-D-Aspartate -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75664467?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+pharmacology&rft.atitle=Opposite+effects+of+NMDA+and+AMPA+receptor+blockade+on+catalepsy+induced+by+dopamine+receptor+antagonists.&rft.au=Papa%2C+S+M%3BEngber%2C+T+M%3BBoldry%2C+R+C%3BChase%2C+T+N&rft.aulast=Papa&rft.aufirst=S&rft.date=1993-03-02&rft.volume=232&rft.issue=2-3&rft.spage=247&rft.isbn=&rft.btitle=&rft.title=European+journal+of+pharmacology&rft.issn=00142999&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-10 N1 - Date created - 1993-05-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Platinum drug-DNA interactions in human tissues measured by cisplatin-DNA enzyme-linked immunosorbent assay and atomic absorbance spectroscopy. AN - 85259514; pmid-8319613 AB - Studies of platinum drug-DNA adduct formation in tissues of cancer patients have involved both atomic absorbance spectroscopy (AAS), which measures total DNA-bound platinum, and anti-cisplatin-DNA enzyme-linked immunosorbent assay (ELISA), which detects a fraction of the AAS-measurable adduct. These studies were designed to explore mechanisms of drug-DNA interactions, to make correlations with clinical outcome, and possibly to validate DNA adduct measurements for use in occupational and environmental biomonitoring. The results, determined by both ELISA and AAS, demonstrate that cisplatin and its analog carboplatin bind to DNA in many human organs, including kidney, brain, peripheral nerve, and bone marrow, which are sites for drug toxicity. Platinum was also observed bound to ovarian tumor DNA. The adducts were highly persistent, being measurable in tissues obtained at autopsy up to 15 months after the last administration of platinum chemotherapy. A comparison of blood cell DNA adduct levels, determined by ELISA, and the clinical response of 139 patients with ovarian, testicular, colon, or breast cancer demonstrated a strong correlation between failure to form DNA adducts and failure of therapy. Conversely, patients who formed high levels of DNA adduct were most likely to respond favorably. A similar correlation was not observed for adducts determined by AAS; that is, the average total DNA-bound platinum levels were the same for patients who did not respond to therapy and for patients who had any kind of response. Thus, in this study, human blood cell DNA adducts measured by ELISA correlate with tumor remission, while those measured by AAS do not. JF - Environmental Health Perspectives AU - Poirier, M C AU - Reed, E AU - Shamkhani, H AU - Tarone, R E AU - Gupta-Burt, S AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion Division of Cancer Etiology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 149 EP - 154 VL - 99 SN - 0091-6765, 0091-6765 KW - Human KW - Prognosis KW - Tissue Distribution KW - DNA, Neoplasm KW - Blood Cells KW - Neoplasms KW - Comparative Study KW - Cisplatin KW - DNA KW - Enzyme-Linked Immunosorbent Assay KW - Spectrophotometry, Atomic Absorption KW - Male KW - Female KW - DNA Damage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85259514?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Platinum+drug-DNA+interactions+in+human+tissues+measured+by+cisplatin-DNA+enzyme-linked+immunosorbent+assay+and+atomic+absorbance+spectroscopy.&rft.au=Poirier%2C+M+C%3BReed%2C+E%3BShamkhani%2C+H%3BTarone%2C+R+E%3BGupta-Burt%2C+S&rft.aulast=Poirier&rft.aufirst=M&rft.date=1993-03-01&rft.volume=99&rft.issue=&rft.spage=149&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Lack of evidence for Huntington's disease-like cognitive dysfunction in obsessive-compulsive disorder. AN - 85251843; pmid-8471692 AB - Cognitive deficits in patients with structural lesions of the basal ganglia (e.g., Huntington's disease) commonly include slowed processing, reduced verbal fluency, difficulty switching set, impaired egocentric spatial ability, poor recall, and impaired acquisition of motor skills. The goal of this study was to determine if patients with obsessive-compulsive disorder (OCD) would have a similar pattern of cognitive dysfunction. A battery of neuropsychological tests, including reaction time-based measures of cognitive processing speed and a test of procedural, motor-skill learning, was administered to 17 unmedicated OCD patients and 16 age-and education-matched normal controls. Eleven individuals with trichotillomania, matched with the OCD patients on age, education, age at symptom onset, depression, and anxiety were also tested. Contrary to expectation, neither the OCD nor trichotillomania patients were impaired on any of the measures in the battery. The essentially normal performance by these patients suggests that the brain regions responsible for cognitive dysfunction in patients with Huntington's disease may differ from those associated with OCD. JF - Biological Psychiatry AU - Martin, A AU - Pigott, T A AU - Lalonde, F M AU - Dalton, I AU - Dubbert, B AU - Murphy, D L AD - Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, MD 20892. PY - 1993 SP - 345 EP - 353 VL - 33 IS - 5 SN - 0006-3223, 0006-3223 KW - Learning KW - Diagnosis, Differential KW - Verbal Behavior KW - Human KW - Brain KW - Brain Diseases KW - Cognition Disorders KW - Basal Ganglia KW - Psychiatric Status Rating Scales KW - Comparative Study KW - Adolescent KW - Neuropsychological Tests KW - Male KW - Huntington Disease KW - Female KW - Obsessive-Compulsive Disorder UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85251843?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biological+Psychiatry&rft.atitle=Lack+of+evidence+for+Huntington%27s+disease-like+cognitive+dysfunction+in+obsessive-compulsive+disorder.&rft.au=Martin%2C+A%3BPigott%2C+T+A%3BLalonde%2C+F+M%3BDalton%2C+I%3BDubbert%2C+B%3BMurphy%2C+D+L&rft.aulast=Martin&rft.aufirst=A&rft.date=1993-03-01&rft.volume=33&rft.issue=5&rft.spage=345&rft.isbn=&rft.btitle=&rft.title=Biological+Psychiatry&rft.issn=00063223&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Leukocyte esterase activity in effusion fluid of patients with otitis media. AN - 85211067; pmid-8464637 AB - Fluid obtained during myringotomy and tube placement in 20 patients with middle ear effusions was assayed for leukocyte esterase activity using a quantitative spectrophotometric assay. This quantitative assay used the synthetic substrate, N-tosyl indoxyl alaninate. Seven of the 20 samples showed no measurable enzyme activity (8 U/ml or less). The remaining samples demonstrated activity ranging from 20 to 1600 units. Although enzyme activity did not correlate well with the physical appearance of the fluid, it did correlate with clinical history, suggesting the presence of a purulent exudate rather than serous effusion. Leukocyte esterase activity in the fluid appears to hold promise as an indicator for the presence of chronic middle ear infection. The enzyme can be assayed by a simple and fast diagnostic strip test, with results available almost immediately. JF - Otolaryngology--Head and Neck Surgery AU - Lebovics, R S AU - Murthy, V V AU - Karmen, A AD - National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD 20892. PY - 1993 SP - 248 EP - 250 VL - 108 IS - 3 SN - 0194-5998, 0194-5998 KW - Otitis Media with Effusion KW - Drainage KW - Human KW - Hearing Loss, Conductive KW - Child KW - Exudates and Transudates KW - Recurrence KW - Child, Preschool KW - Infant KW - Blood KW - Prospective Studies KW - Carboxylic Ester Hydrolases KW - Middle Ear Ventilation KW - Chronic Disease KW - Adolescent UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85211067?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Otolaryngology--Head+and+Neck+Surgery&rft.atitle=Leukocyte+esterase+activity+in+effusion+fluid+of+patients+with+otitis+media.&rft.au=Lebovics%2C+R+S%3BMurthy%2C+V+V%3BKarmen%2C+A&rft.aulast=Lebovics&rft.aufirst=R&rft.date=1993-03-01&rft.volume=108&rft.issue=3&rft.spage=248&rft.isbn=&rft.btitle=&rft.title=Otolaryngology--Head+and+Neck+Surgery&rft.issn=01945998&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Single-chain immunotoxin fusions between anti-Tac and Pseudomonas exotoxin: relative importance of the two toxin disulfide bonds. AN - 76317448; 7873642 AB - Anti-Tac(Fv)-PE40 is a recombinant single-chain immunotoxin in which the variable heavy and light domains of the anti-IL2 receptor antibody, anti-Tac, are connected to each other by a peptide linker and then fused to PE40, a truncated form of Pseudomonas exotoxin (PE). This fusion protein has four disulfide bonds: one in each of the two variables domains, one in domain II (Cys 265-287), and one in domain Ib (Cys 372-379) of PE. To study the importance of the disulfide bonds of the toxin to the activity of single-chain immunotoxins, we constructed mutants in which either the cysteines in the toxin were changed to alanines or the amino acids 365-380 of PE were deleted. We began this study with anti-Tac(Fv)-PE40 and a more active variant, anti-Tac(Fv)-PE40KDEL, in which the carbonyl terminus is changed from REDLK to KDEL. From these proteins we made anti-Tac(Fv)-PE40(4)A and anti-Tac(Fv)-PE40KDEL4A, respectively, by converting cysteins at amino acids 265, 287, 372, and 379 of PE to alanines. This change resulted in a 20-100-fold loss of activity toward human target cells, but no significant change in binding affinity to p55. To determine the importance of the second toxin disulfide bond, we removed amino acids 365-380 from anti-Tac(Fv)-PE40, anti-Tac(Fv)-PE40KDEL, and anti-Tac(Fv)-PE40KDEL4A, resulting in anti-Tac(Fv)-PE38, anti-Tac(Fv)-PE38KDEL, and anti-Tac(Fv)-PE38KDEL2A, respectively.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Bioconjugate chemistry AU - Kreitman, R J AU - Batra, J K AU - Seetharam, S AU - Chaudhary, V K AU - FitzGerald, D J AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. PY - 1993 SP - 112 EP - 120 VL - 4 IS - 2 SN - 1043-1802, 1043-1802 KW - Bacterial Toxins KW - 0 KW - Disulfides KW - Exotoxins KW - Immunotoxins KW - Receptors, Interleukin-2 KW - Recombinant Fusion Proteins KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - Animals KW - Recombinant Fusion Proteins -- pharmacokinetics KW - Humans KW - Escherichia coli -- genetics KW - Mice KW - Cell Death -- drug effects KW - Mice, Inbred BALB C KW - Structure-Activity Relationship KW - Recombinant Fusion Proteins -- chemistry KW - Base Sequence KW - Molecular Sequence Data KW - Recombinant Fusion Proteins -- pharmacology KW - Female KW - Immunotoxins -- chemistry KW - Exotoxins -- genetics KW - Disulfides -- chemistry KW - Immunotoxins -- genetics KW - Exotoxins -- chemistry KW - Immunotoxins -- pharmacology KW - Receptors, Interleukin-2 -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76317448?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bioconjugate+chemistry&rft.atitle=Single-chain+immunotoxin+fusions+between+anti-Tac+and+Pseudomonas+exotoxin%3A+relative+importance+of+the+two+toxin+disulfide+bonds.&rft.au=Kreitman%2C+R+J%3BBatra%2C+J+K%3BSeetharam%2C+S%3BChaudhary%2C+V+K%3BFitzGerald%2C+D+J%3BPastan%2C+I&rft.aulast=Kreitman&rft.aufirst=R&rft.date=1993-03-01&rft.volume=4&rft.issue=2&rft.spage=112&rft.isbn=&rft.btitle=&rft.title=Bioconjugate+chemistry&rft.issn=10431802&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1995-04-06 N1 - Date created - 1995-04-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Important aspects of the evidence for TCDD carcinogenicity in man. AN - 75814601; 8319655 AB - Most of the evidence for the carcinogenicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in humans has centered on whether TCDD causes soft-tissue sarcomas (STS) and malignant lymphomas (ML). Recently, reports from two of the largest occupational cohort studies have become available. A critical reappraisal of these and other recent reports indicates that it is unlikely that TCDD causes malignant lymphomas in humans. For STS, the evidence for an etiologic role for TCDD is not convincing. However, more data and further clarification are needed before a clear and objective evaluation can be made. Factors such as level of exposure, sex, and host susceptibility may be critical determinants of whether cancer occurs; there is evidence from both humans and animals that these factors play a role, and therefore these factors should be considered in future evaluations. There is a serious need to rule out the possibility that observed effects are due to other concomitant exposures. Consideration of the carcinogenic effects of TCDD in animals reveals consistency with the human data and points to other cancers such as those of the thyroid gland and lung, for example, which are more likely candidates for investigating the role of TCDD in their occurrence, while at the same time providing a basis for a better understanding and interpretation of the human data. There are now sufficient epidemiologic studies in place that will provide a better climate for a definitive evaluation in the near future. JF - Environmental health perspectives AU - Johnson, E S AD - Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 383 EP - 390 VL - 99 SN - 0091-6765, 0091-6765 KW - Carcinogens KW - 0 KW - Polychlorinated Dibenzodioxins KW - Index Medicus KW - Registries KW - Occupational Exposure KW - Animals KW - Neoplasms, Experimental -- chemically induced KW - Humans KW - Soft Tissue Neoplasms -- chemically induced KW - Case-Control Studies KW - Lymphoma -- chemically induced KW - Occupational Diseases -- chemically induced KW - Sarcoma -- chemically induced KW - Male KW - Female KW - Polychlorinated Dibenzodioxins -- adverse effects KW - Carcinogens -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75814601?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Important+aspects+of+the+evidence+for+TCDD+carcinogenicity+in+man.&rft.au=Johnson%2C+E+S&rft.aulast=Johnson&rft.aufirst=E&rft.date=1993-03-01&rft.volume=99&rft.issue=&rft.spage=383&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-05 N1 - Date created - 1993-08-05 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Natl Cancer Inst. 1969 Jun;42(6):1101-14 [5793189] Crit Rev Toxicol. 1991;21(6):451-63 [1801848] Lancet. 1974 Jun 29;1(7870):1316-8 [4134297] Environ Health Perspect. 1977 Aug;19:25-9 [908306] Bull Environ Contam Toxicol. 1977 Nov;18(5):552-7 [412534] J Occup Med. 1978 Jun;20(6):427-9 [566788] Toxicol Appl Pharmacol. 1978 Nov;46(2):279-303 [734660] Nature. 1979 Apr 5;278(5704):548-9 [431718] Br J Cancer. 1979 Jun;39(6):711-7 [444410] Br J Ind Med. 1981 Feb;38(1):27-33 [7470401] Scand J Work Environ Health. 1981 Jun;7(2):119-30 [7313616] JAMA. 1984 May 11;251(18):2372-80 [6231388] Br J Cancer. 1985 Aug;52(2):259-70 [4027168] JAMA. 1986 Sep 5;256(9):1141-7 [3801091] Scand J Work Environ Health. 1987 Feb;13(1):9-17 [3576149] Tumori. 1987 Apr 30;73(2):99-107 [3576718] Cancer. 1988 Aug 1;62(3):652-6 [3390800] Carcinogenesis. 1988 Sep;9(9):1677-9 [3409472] J Occup Med. 1989 Feb;31(2):121-3 [2709162] Am J Epidemiol. 1989 Jun;129(6):1187-200 [2729256] Am J Ind Med. 1989;16(2):135-46 [2773945] Br J Ind Med. 1989 Aug;46(8):516-20 [2775671] Scand J Work Environ Health. 1989 Jun;15(3):203-9 [2781250] Br J Ind Med. 1989 Nov;46(11):809-14 [2590647] J Natl Cancer Inst. 1990 Mar 21;82(6):486-90 [2313720] Fundam Appl Toxicol. 1990 Feb;14(2):219-34 [2180763] J Occup Med. 1990 May;32(5):423 [2140857] Cancer. 1990 Aug 15;66(4):806-11 [2386907] JAMA. 1990 Oct 10;264(14):1824-31 [2402041] JAMA. 1990 Oct 10;264(14):1832-6 [2402042] N Engl J Med. 1991 Jan 24;324(4):212-8 [1985242] N Engl J Med. 1991 Jan 24;324(4):260-2 [1823116] Am J Ind Med. 1990;18(6):665-73 [2264565] Science. 1991 Feb 8;251(4994):624-6 [1846976] Epidemiology. 1990 Sep;1(5):349-56 [2078610] Cell Biol Toxicol. 1991 Jan;7(1):67-94 [2054688] Lancet. 1991 Oct 19;338(8773):959-64 [1681339] Lancet. 1991 Oct 26;338(8774):1027-32 [1681353] Comment In: Environ Health Perspect. 1994 Oct;102(10):814-5 [9738205] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Association of PAH-DNA adducts in peripheral white blood cells with dietary exposure to polyaromatic hydrocarbons. AN - 75814463; 8319640 AB - Previous investigations suggest that dietary sources of polycyclic aromatic hydrocarbons (PAHs) contribute to the PAH-DNA adduct load in peripheral white blood cells (WBCs). In the current study, we measured PAH-DNA adducts by enzyme-linked immunosorbent assay in WBCs obtained from 47 California wildland (forest) firefighters at two time points (early and late) during an active forest fire season. PAH-DNA adduct levels were not associated with recent firefighting activity, but were positively associated with frequency of charbroiled food consumption in the previous 2 weeks. In addition, adduct levels declined with time since last ingestion of charbroiled food. These studies indicate that recent consumption of charbroiled food contributes to the PAH-DNA adduct load in peripheral WBCs. JF - Environmental health perspectives AU - Rothman, N AU - Poirier, M C AU - Haas, R A AU - Correa-Villasenor, A AU - Ford, P AU - Hansen, J A AU - O'Toole, T AU - Strickland, P T AD - Epidemiology and Biostatistics Program, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 265 EP - 267 VL - 99 SN - 0091-6765, 0091-6765 KW - Polycyclic Compounds KW - 0 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Occupational Exposure KW - Leukocytes -- metabolism KW - Hot Temperature KW - Fires KW - Humans KW - Adult KW - Food Contamination KW - Middle Aged KW - Adolescent KW - Male KW - Female KW - Leukocytes -- drug effects KW - Polycyclic Compounds -- blood KW - DNA -- blood KW - Polycyclic Compounds -- adverse effects KW - Diet -- adverse effects KW - DNA -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75814463?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Association+of+PAH-DNA+adducts+in+peripheral+white+blood+cells+with+dietary+exposure+to+polyaromatic+hydrocarbons.&rft.au=Rothman%2C+N%3BPoirier%2C+M+C%3BHaas%2C+R+A%3BCorrea-Villasenor%2C+A%3BFord%2C+P%3BHansen%2C+J+A%3BO%27Toole%2C+T%3BStrickland%2C+P+T&rft.aulast=Rothman&rft.aufirst=N&rft.date=1993-03-01&rft.volume=99&rft.issue=&rft.spage=265&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-05 N1 - Date created - 1993-08-05 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Res. 1980 Feb;40(2):412-6 [7356524] J Natl Cancer Inst. 1987 Sep;79(3):449-56 [3114532] Mutat Res. 1991 Mar-Apr;259(3-4):251-61 [2017211] Carcinogenesis. 1988 Jul;9(7):1265-9 [3133129] Carcinogenesis. 1990 Jul;11(7):1241-3 [2372884] Cancer Res. 1988 Apr 15;48(8):2288-91 [3127049] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Detection of polycyclic aromatic hydrocarbon-DNA adducts in human lung. AN - 75812928; 8319638 AB - Synchronous fluorescence spectroscopy has been combined with immunoaffinity chromatography (IAC) and HPLC to detect polycyclic aromatic hydrocarbon (PAH)-DNA adducts and measure r-7,t-8-dihydroxy-t-9,10-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (BPDE)-DNA adducts in human tissues and cells. A monoclonal antibody (8E11) that recognizes a range of PAH-DNA adducts, but not chemically unrelated adducts, was used to prepare IAC columns. Samples of DNA (25 from human lung and 8 positive and negative controls) were hydrolyzed enzymically and subjected to IAC. Adducts captured by the antibodies and eluted in NaOH (50 mM) were analyzed for fluorescent properties. The spectral fluorescence excitation-emission matrices suggested the presence of mixtures of PAH-DNA adducts in some of the eluates. The eluates were subsequently hydrolyzed with acid (HCl, 0.1 N, 3 hr) and reanalyzed by synchronous fluorescence spectroscopy using a wavelength differential of 34 nm. In 6 of the 25 human lung DNA samples, materials with HPLC retention times identical to benzo[a]pyrene-7,10/8,9-tetrahydrotetrol were found to have fluorescence characteristics indistinguishable from pyrene. Comparisons with appropriate standards indicated that BPDE-DNA adduct levels were between 1 and 40 adducts in 10(8) unmodified nucleotides. No correlation was observed between lung DNA-adduct levels and measures of recent smoking (serum cotinine), but tissue samples taken from different portions of the same lungs showed variation in the DNA adduct levels detected. This finding complicates interpretation of the data and has important implications for the design of future experiments. JF - Environmental health perspectives AU - Weston, A AU - Bowman, E D AU - Shields, P G AU - Trivers, G E AU - Poirier, M C AU - Santella, R M AU - Manchester, D K AD - Laboratory of Human Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 257 EP - 259 VL - 99 SN - 0091-6765, 0091-6765 KW - DNA Adducts KW - 0 KW - Polycyclic Compounds KW - benzo(a)pyrene-7,8-dihydrodiol-9,10-epoxide-DNA KW - 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide KW - 55097-80-8 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Chromatography, Affinity KW - Spectrometry, Fluorescence KW - DNA Damage KW - Humans KW - Adult KW - Middle Aged KW - Adolescent KW - Male KW - Female KW - Chromatography, High Pressure Liquid KW - 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide -- analysis KW - Polycyclic Compounds -- analysis KW - Lung -- chemistry KW - Lung -- drug effects KW - DNA -- analysis KW - Polycyclic Compounds -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75812928?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Detection+of+polycyclic+aromatic+hydrocarbon-DNA+adducts+in+human+lung.&rft.au=Weston%2C+A%3BBowman%2C+E+D%3BShields%2C+P+G%3BTrivers%2C+G+E%3BPoirier%2C+M+C%3BSantella%2C+R+M%3BManchester%2C+D+K&rft.aulast=Weston&rft.aufirst=A&rft.date=1993-03-01&rft.volume=99&rft.issue=&rft.spage=257&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-05 N1 - Date created - 1993-08-05 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Carcinogenesis. 1984 Mar;5(3):373-7 [6423306] Proc Natl Acad Sci U S A. 1988 Dec;85(23):9243-7 [3143115] Chem Res Toxicol. 1989 Mar-Apr;2(2):104-8 [2519708] Basic Life Sci. 1990;53:63-81 [2126432] Carcinogenesis. 1991 Aug;12(8):1445-9 [1860165] Proc Natl Acad Sci U S A. 1989 Jul;86(13):5099-103 [2567993] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Radiation-induced neoplastic transformation of human cells. AN - 75797981; 8316792 AB - Ionizing radiation can induce cancers in humans and animals and can cause in vitro neoplastic transformation of various rodent cell systems. However, numerous attempts to achieve neoplastic transformation of human cells by radiation have generally proven unsuccessful. Neoplastic transformation of immortalized human epidermal keratinocytes by X-ray irradiation has recently been reported. The carcinogenic effect of radiation on cultured human cells will be briefly reviewed. The current state-of-the-art in radiation-induced transformation of human cells in culture is presented. This will provide insight into the molecular and cellular mechanisms in the conversion of normal cells to a neoplastic state of growth. JF - Scanning microscopy AU - Rhim, J S AU - Thraves, P AU - Dritschilo, A AU - Kuettel, M R AU - Lee, M S AD - Laboratory of Cellular and Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 209 EP - 15; discussion 215-6 VL - 7 IS - 1 SN - 0891-7035, 0891-7035 KW - ras KW - Index Medicus KW - Genes, ras KW - Gamma Rays KW - Cells, Cultured KW - Humans KW - Neoplasms, Radiation-Induced -- pathology KW - Neoplasms, Radiation-Induced -- genetics KW - Cell Transformation, Neoplastic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75797981?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Scanning+microscopy&rft.atitle=Radiation-induced+neoplastic+transformation+of+human+cells.&rft.au=Rhim%2C+J+S%3BThraves%2C+P%3BDritschilo%2C+A%3BKuettel%2C+M+R%3BLee%2C+M+S&rft.aulast=Rhim&rft.aufirst=J&rft.date=1993-03-01&rft.volume=7&rft.issue=1&rft.spage=209&rft.isbn=&rft.btitle=&rft.title=Scanning+microscopy&rft.issn=08917035&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-28 N1 - Date created - 1993-07-28 N1 - Date revised - 2017-01-13 N1 - Gene symbol - ras N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Genomic imprinting: implications for behavioral genetics. AN - 75795853; 8512528 AB - In recent years it has become apparent that the parental origin of genetic material has an impact on gene expression and this effect has become known as genomic imprinting. The evidence for the influence of genomic imprinting on behavior and in the etiology of certain neurobehavioral disorders is discussed. The possibilities for a role for genomic imprinting in the inheritance of behaviors related to alcohol abuse and alcoholism and in the paternal alcohol syndrome are also explored. JF - Behavior genetics AU - Durcan, M J AU - Goldman, D AD - Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland 20892. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 137 EP - 143 VL - 23 IS - 2 SN - 0001-8244, 0001-8244 KW - Index Medicus KW - Genetic Variation KW - Risk Factors KW - Humans KW - DNA Mutational Analysis KW - Angelman Syndrome -- genetics KW - Prader-Willi Syndrome -- genetics KW - Male KW - Female KW - Phenotype KW - Gene Expression Regulation KW - Alcoholism -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75795853?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Behavior+genetics&rft.atitle=Genomic+imprinting%3A+implications+for+behavioral+genetics.&rft.au=Durcan%2C+M+J%3BGoldman%2C+D&rft.aulast=Durcan&rft.aufirst=M&rft.date=1993-03-01&rft.volume=23&rft.issue=2&rft.spage=137&rft.isbn=&rft.btitle=&rft.title=Behavior+genetics&rft.issn=00018244&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-15 N1 - Date created - 1993-07-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Statistical analysis of animal cancer chemoprevention experiments. AN - 75786668; 8513108 AB - We explore the use of a statistical model proposed by Kokoska (1987, Biometrics 43, 525-534) for the analysis of animal cancer chemoprevention experiments. We show, using an example, that the results derived from the method can be sensitive to the parametric forms of the distributions that are assumed, particularly to the distribution of the number of tumors per animal. We propose goodness-of-fit tests to aid in the choice of the distributions. JF - Biometrics AU - Freedman, L S AU - Midthune, D N AU - Brown, C C AU - Steele, V AU - Kelloff, G J AD - Biometry Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 259 EP - 268 VL - 49 IS - 1 SN - 0006-341X, 0006-341X KW - Carcinogens KW - 0 KW - Index Medicus KW - Rats KW - Mammary Neoplasms, Experimental -- chemically induced KW - Animals KW - Biometry KW - Adenocarcinoma -- chemically induced KW - Data Interpretation, Statistical KW - Adenocarcinoma -- prevention & control KW - Mammary Neoplasms, Experimental -- prevention & control KW - Time Factors KW - Female KW - Drug Screening Assays, Antitumor -- statistics & numerical data KW - Neoplasms, Experimental -- chemically induced KW - Models, Statistical KW - Neoplasms, Experimental -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75786668?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biometrics&rft.atitle=Statistical+analysis+of+animal+cancer+chemoprevention+experiments.&rft.au=Freedman%2C+L+S%3BMidthune%2C+D+N%3BBrown%2C+C+C%3BSteele%2C+V%3BKelloff%2C+G+J&rft.aulast=Freedman&rft.aufirst=L&rft.date=1993-03-01&rft.volume=49&rft.issue=1&rft.spage=259&rft.isbn=&rft.btitle=&rft.title=Biometrics&rft.issn=0006341X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-21 N1 - Date created - 1993-07-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Biometrics. 1996 Sep;52(3):1157 [8805772] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Prednisone and piroxicam for treatment of primary Sjögren's syndrome. AN - 75780558; 8508556 AB - Primary Sjögren's syndrome is a systemic autoimmune exocrinopathy characterized by a lymphoplasmacytic infiltrate and destruction of salivary and lacrimal glandular tissues. There is no widely accepted or effective systemic therapy for this disorder. The purpose of this 6-month randomized, double-blinded, placebo-controlled study was to examine the effects of prednisone (30 mg, alternate days), piroxicam (20 mg, daily), or placebo on the salivary, lacrimal and immunologic alterations of primary Sjögren's syndrome. Eight patients were enrolled in each group. Salivary and lacrimal function were assessed at entry and at the completion of treatment. Labial minor salivary gland tissue was obtained at these times and examined for intensity of infiltration (focus scores) and for the relative proportion of glandular elements. Serologic and subjective evaluations were done as well, and patients were monitored for therapy-related side effects. Neither active treatment led to significant improvement in salivary or lacrimal function, although prednisone improved salivary flow in selected patients and was associated with positive subjective responses. Prednisone also significantly decreased the serum total protein, IgG, IgA, and sedimentation rate and increased the white cell count. There were no significant alterations in either focus scores or the percentage of glandular component tissues of minor glands with either active treatment. This study demonstrated that 6 months of prednisone or piroxicam at the doses utilized failed to improve the histological or functional parameters of salivary and lacrimal glands in primary Sjögren's syndrome. JF - Clinical and experimental rheumatology AU - Fox, P C AU - Datiles, M AU - Atkinson, J C AU - Macynski, A A AU - Scott, J AU - Fletcher, D AU - Valdez, I H AU - Kurrasch, R H AU - Delapenha, R AU - Jackson, W AD - Clinical Investigations and Patient Care Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892. PY - 1993 SP - 149 EP - 156 VL - 11 IS - 2 SN - 0392-856X, 0392-856X KW - Immunoglobulin A KW - 0 KW - Immunoglobulin G KW - Piroxicam KW - 13T4O6VMAM KW - Prednisone KW - VB0R961HZT KW - Index Medicus KW - Salivation KW - Immunoglobulin G -- analysis KW - Lacrimal Apparatus -- pathology KW - Double-Blind Method KW - Dose-Response Relationship, Drug KW - Humans KW - Lacrimal Apparatus -- physiology KW - Tears KW - Aged KW - Adult KW - Salivary Glands -- pathology KW - Immunoglobulin A -- analysis KW - Salivary Glands -- physiology KW - Middle Aged KW - Time Factors KW - Female KW - Male KW - Sjogren's Syndrome -- drug therapy KW - Prednisone -- adverse effects KW - Prednisone -- therapeutic use KW - Sjogren's Syndrome -- immunology KW - Sjogren's Syndrome -- physiopathology KW - Piroxicam -- therapeutic use KW - Piroxicam -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75780558?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+and+experimental+rheumatology&rft.atitle=Prednisone+and+piroxicam+for+treatment+of+primary+Sj%C3%B6gren%27s+syndrome.&rft.au=Fox%2C+P+C%3BDatiles%2C+M%3BAtkinson%2C+J+C%3BMacynski%2C+A+A%3BScott%2C+J%3BFletcher%2C+D%3BValdez%2C+I+H%3BKurrasch%2C+R+H%3BDelapenha%2C+R%3BJackson%2C+W&rft.aulast=Fox&rft.aufirst=P&rft.date=1993-03-01&rft.volume=11&rft.issue=2&rft.spage=149&rft.isbn=&rft.btitle=&rft.title=Clinical+and+experimental+rheumatology&rft.issn=0392856X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-15 N1 - Date created - 1993-07-15 N1 - Date revised - 2017-01-24 N1 - Last updated - 2017-01-25 ER - TY - JOUR T1 - A centromeric microsatellite probe on chromosome 3: LIB 9-95ca (D3S1338). AN - 75761107; 8499930 JF - Human molecular genetics AU - Schmidt, L AU - Li, H AU - Duh, F M AU - Wei, M H AU - Lerman, M I AU - Zbar, B AU - Tory, K AD - Biological Carcinogenesis and Development Program, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 335 VL - 2 IS - 3 SN - 0964-6906, 0964-6906 KW - DNA Probes KW - 0 KW - DNA, Satellite KW - Oligodeoxyribonucleotides KW - Index Medicus KW - DNA, Satellite -- genetics KW - Polymerase Chain Reaction KW - Base Sequence KW - Humans KW - Molecular Sequence Data KW - Oligodeoxyribonucleotides -- genetics KW - Repetitive Sequences, Nucleic Acid KW - Chromosomes, Human, Pair 3 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75761107?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Human+molecular+genetics&rft.atitle=A+centromeric+microsatellite+probe+on+chromosome+3%3A+LIB+9-95ca+%28D3S1338%29.&rft.au=Schmidt%2C+L%3BLi%2C+H%3BDuh%2C+F+M%3BWei%2C+M+H%3BLerman%2C+M+I%3BZbar%2C+B%3BTory%2C+K&rft.aulast=Schmidt&rft.aufirst=L&rft.date=1993-03-01&rft.volume=2&rft.issue=3&rft.spage=335&rft.isbn=&rft.btitle=&rft.title=Human+molecular+genetics&rft.issn=09646906&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-29 N1 - Date created - 1993-06-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Identification of a rare cystic fibrosis mutation (S4X) in a Slovenian population. AN - 75755287; 7684643 JF - Human molecular genetics AU - Glavac, D AU - Ravnik-Glavac, M AU - Dean, M AD - Biological Carcinogenesis and Development Program, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702-1201. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 315 EP - 316 VL - 2 IS - 3 SN - 0964-6906, 0964-6906 KW - CFTR KW - CFTR protein, human KW - 0 KW - Membrane Proteins KW - Cystic Fibrosis Transmembrane Conductance Regulator KW - 126880-72-6 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Pedigree KW - Base Sequence KW - Alleles KW - Slovenia KW - Polymorphism, Genetic KW - Humans KW - DNA Mutational Analysis KW - DNA -- genetics KW - Molecular Sequence Data KW - Membrane Proteins -- genetics KW - Male KW - Female KW - Cystic Fibrosis -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75755287?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Human+molecular+genetics&rft.atitle=Identification+of+a+rare+cystic+fibrosis+mutation+%28S4X%29+in+a+Slovenian+population.&rft.au=Glavac%2C+D%3BRavnik-Glavac%2C+M%3BDean%2C+M&rft.aulast=Glavac&rft.aufirst=D&rft.date=1993-03-01&rft.volume=2&rft.issue=3&rft.spage=315&rft.isbn=&rft.btitle=&rft.title=Human+molecular+genetics&rft.issn=09646906&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-29 N1 - Date created - 1993-06-29 N1 - Date revised - 2017-01-13 N1 - Gene symbol - CFTR N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - In utero methamphetamine effects: I. Behavior and monoamine uptake sites in adult offspring. AN - 75748743; 8497809 AB - Chronic in utero methamphetamine treatment, throughout gestation in rats, resulted in alterations in both behavior and brain monoamine function in the adult offspring. The higher dose of methamphetamine (10 mg/kg/b.i.d.) caused a significant decrease in square crossing and rearing in an open field, as well as a regional increase of serotonin and dopamine uptake sites. In contrast, the lower dose of in utero methamphetamine (2 mg/kg/b.i.d.) resulted in a significant decrease in regional densities of serotonin and dopamine uptake sites, and only decreased rearing behavior. Across treatment groups, there were significant correlations between open-field square crossing activity and the number of uptake sites in specific brain areas. Other measured behaviors, such as the neonate righting reflex and the adult Morris water maze performance, were unaffected by either in utero drug regimen. These results are discussed in terms of the known neurotoxicity of amphetamines and the ability of the immature nervous system to compensate for fetal exposure to methamphetamine. JF - Synapse (New York, N.Y.) AU - Weissman, A D AU - Caldecott-Hazard, S AD - Neuroscience Branch, National Institute on Drug Abuse, Baltimore, Maryland 21224. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 241 EP - 250 VL - 13 IS - 3 SN - 0887-4476, 0887-4476 KW - Biogenic Monoamines KW - 0 KW - Piperazines KW - Paroxetine KW - 41VRH5220H KW - Methamphetamine KW - 44RAL3456C KW - 1-(2 (diphenylmethoxy)ethyl)-4-(3-phenylpropyl)piperazine KW - 9J9974WIBA KW - Mazindol KW - C56709M5NH KW - Index Medicus KW - Rats KW - Piperazines -- pharmacokinetics KW - Animals KW - Rats, Sprague-Dawley KW - Mazindol -- pharmacokinetics KW - Brain -- metabolism KW - Paroxetine -- pharmacokinetics KW - Male KW - Female KW - Pregnancy KW - Behavior, Animal -- drug effects KW - Methamphetamine -- pharmacology KW - Biogenic Monoamines -- metabolism KW - Prenatal Exposure Delayed Effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75748743?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Synapse+%28New+York%2C+N.Y.%29&rft.atitle=In+utero+methamphetamine+effects%3A+I.+Behavior+and+monoamine+uptake+sites+in+adult+offspring.&rft.au=Weissman%2C+A+D%3BCaldecott-Hazard%2C+S&rft.aulast=Weissman&rft.aufirst=A&rft.date=1993-03-01&rft.volume=13&rft.issue=3&rft.spage=241&rft.isbn=&rft.btitle=&rft.title=Synapse+%28New+York%2C+N.Y.%29&rft.issn=08874476&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-22 N1 - Date created - 1993-06-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Primary depressives with secondary alcoholism compared with alcoholics and depressives. AN - 75730856; 8485985 AB - While a subset of depressed patients are believed to "self-medicate" their depression with alcohol, there are no studies comparing the phenomenological and diagnostic characteristics of patients with primary depression and secondary alcoholism with those of patients with depression or alcoholism alone. In this study, we compared 11 patients from each of these three diagnostic groups in terms of past history and current clinical presentation. The patients were matched for age, sex, and level of function. Comorbid patients were most likely to meet criteria for sedative dependence and panic disorder, and had higher scores on the Hamilton Anxiety Scale. In addition, they scored higher on a hypomania scale and had more first-degree relatives with a history of drug abuse. JF - Comprehensive psychiatry AU - Leibenluft, E AU - Madden, P A AU - Dick, S E AU - Rosenthal, N E AD - Clinical Psychobiology Branch, National Institute of Mental Health, Bethesda, MD. PY - 1993 SP - 83 EP - 86 VL - 34 IS - 2 SN - 0010-440X, 0010-440X KW - Index Medicus KW - Psychiatric Status Rating Scales KW - Humans KW - Adult KW - Alcohol Drinking -- psychology KW - Personality Inventory KW - Middle Aged KW - Personality Assessment KW - Self-Help Groups KW - Male KW - Female KW - Comorbidity KW - Depressive Disorder -- epidemiology KW - Alcoholism -- rehabilitation KW - Alcoholism -- epidemiology KW - Depressive Disorder -- psychology KW - Alcoholism -- psychology KW - Depressive Disorder -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75730856?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Comprehensive+psychiatry&rft.atitle=Primary+depressives+with+secondary+alcoholism+compared+with+alcoholics+and+depressives.&rft.au=Leibenluft%2C+E%3BMadden%2C+P+A%3BDick%2C+S+E%3BRosenthal%2C+N+E&rft.aulast=Leibenluft&rft.aufirst=E&rft.date=1993-03-01&rft.volume=34&rft.issue=2&rft.spage=83&rft.isbn=&rft.btitle=&rft.title=Comprehensive+psychiatry&rft.issn=0010440X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-10 N1 - Date created - 1993-06-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Gender effects in diagnosing alcohol abuse and dependence. AN - 75730854; 8486813 AB - Using a national population sample of 43,809 adults, male and female responses were compared for 41 indicators of alcohol abuse and dependence. While men reported all indicators more often than did women, the male to female ratio of positive responses varied according to both the construct represented by the item and its underlying prevalence. Items that might be construed as signs of weakness-physical effects, psychological effects, and loss of control or powerlessness--had lower male/female ratios than other items. Excess male prevalence was greatest for the least prevalent indicators. The paper presents alternative interpretations of these findings and discusses their implications for diagnostic classification. JF - Journal of clinical psychology AU - Dawson, D A AU - Grant, B F AD - Division of Biometry and Epidemiology, NIAAA/DBE, Rockville, MD 20857. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 298 EP - 307 VL - 49 IS - 2 SN - 0021-9762, 0021-9762 KW - Index Medicus KW - Cross-Sectional Studies KW - Age Factors KW - Psychiatric Status Rating Scales KW - Sex Factors KW - Humans KW - Adult KW - Incidence KW - Aged KW - Middle Aged KW - Adolescent KW - United States -- epidemiology KW - Male KW - Female KW - Alcoholism -- epidemiology KW - Alcoholism -- diagnosis KW - Alcoholism -- classification KW - Alcohol Drinking -- psychology KW - Gender Identity KW - Alcohol Drinking -- epidemiology KW - Alcoholism -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75730854?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+psychology&rft.atitle=Gender+effects+in+diagnosing+alcohol+abuse+and+dependence.&rft.au=Dawson%2C+D+A%3BGrant%2C+B+F&rft.aulast=Dawson&rft.aufirst=D&rft.date=1993-03-01&rft.volume=49&rft.issue=2&rft.spage=298&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+psychology&rft.issn=00219762&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-10 N1 - Date created - 1993-06-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Detection and characterization of 9-anthron-10-yl radicals formed by antipsoriatic and tumor-promoting 9-anthrones in aqueous buffers. AN - 75714750; 8386561 AB - Certain 1,8-dihydroxy-9-anthrones have been used for the topical treatment of psoriasis for over seventy-five years. The therapeutic usefulness of these compounds is limited, however, by side effects including severe skin inflammation and staining. Antipsoriatic 9-anthrones are also tumor promoters in mouse skin. The chemical mechanisms underlying the biological properties of 9-anthrones are believed to involve the generation of free radical products such as 9-anthron-10-yl radicals or secondary oxygen radicals such as O2.- or OH.. However, the specific role that 9-anthron-10-yl radicals may play in mediating the biological effects of 9-anthrones is uncertain because these species have not been detected in biological systems. In the present study we have used the EPR spin trapping technique to demonstrate for the first time the formation of the 1,8-dihydroxy-9-anthron-10-yl radical in aqueous buffers. Additionally, in order to gain information concerning the role of 9-anthron-10-yl radicals in tumor promotion and antipsoriatic activities, we have used this technique to investigate the formation of these radical species by a series of 9-anthrones of known tumor-promoting and antipsoriatic activities. All of the 9-anthrones studied formed spin adducts with 3,5-dibromo-4-nitrosobenzenesulfonic acid in aqueous buffers. The formation of these adducts was pH-dependent, being favored at alkaline pH.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Chemical research in toxicology AU - Hayden, P J AU - Chignell, C F AD - Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. PY - 1993 SP - 231 EP - 237 VL - 6 IS - 2 SN - 0893-228X, 0893-228X KW - Anthracenes KW - 0 KW - Buffers KW - Carcinogens KW - Free Radicals KW - Anthralin KW - U8CJK0JH5M KW - Index Medicus KW - Oxidation-Reduction KW - Hydrogen-Ion Concentration KW - Electron Spin Resonance Spectroscopy KW - Temperature KW - Spectrophotometry, Ultraviolet KW - Anthralin -- analysis KW - Anthracenes -- chemistry KW - Carcinogens -- chemistry KW - Psoriasis -- drug therapy KW - Anthracenes -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75714750?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+research+in+toxicology&rft.atitle=Detection+and+characterization+of+9-anthron-10-yl+radicals+formed+by+antipsoriatic+and+tumor-promoting+9-anthrones+in+aqueous+buffers.&rft.au=Hayden%2C+P+J%3BChignell%2C+C+F&rft.aulast=Hayden&rft.aufirst=P&rft.date=1993-03-01&rft.volume=6&rft.issue=2&rft.spage=231&rft.isbn=&rft.btitle=&rft.title=Chemical+research+in+toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-24 N1 - Date created - 1993-05-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Regulation of transglutaminase type I expression in squamous differentiating rabbit tracheal epithelial cells and human epidermal keratinocytes: effects of retinoic acid and phorbol esters. AN - 75714450; 8097865 AB - In the present study we describe the full length cDNA sequence for rabbit transglutaminase type I as well as the sequence for a 2.9-kilobase (kb) promoter fragment of the gene. Transglutaminase type I mRNA expression was inhibited in squamous differentiating epithelia by retinoic acid (RA) in a dose-dependent (EC50 = 1-2 nM) and transcriptional manner. In human epidermal keratinocytes transglutaminase type I mRNA was induced by 12-O-tetradecanoylphorbol-13-acetate (TPA) treatment, and this induction could be inhibited by bryostatin 1. In contrast, TPA treatment inhibited the expression of c-myc mRNA. Bryostatin 1 but not RA could prevent this decrease in c-myc mRNA expression, indicating that transglutaminase type I mRNA expression was associated with differentiation and not growth arrest. An SP1 element was found within 50 base pairs 5' of the transcription initiation site. A TATA-like element (CATAAAC) was found but was not capable of activating transcription. In addition, putative response elements for C-MYC, Ker1/AP2, 2 AP1 sites, a CK-8-mer, and an AP2 site were present in the 2.9-kb fragment. Transfection of RbTE cells with the 2.9-kb fragment ligated to a promoterless luciferase vector resulted in 2.2-fold more luciferase expression in differentiated vs. undifferentiated cells. Furthermore, luciferase activity was induced 7.4-fold in human epidermal keratinocytes induced to differentiate with TPA. TPA-induced luciferase activity was inhibited by both bryostatin 1 and RA. No known RA response elements were identified in the promoter.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Molecular endocrinology (Baltimore, Md.) AU - Saunders, N A AU - Bernacki, S H AU - Vollberg, T M AU - Jetten, A M AD - Cell Biology Section, National Institute of Environmental Health Sciences, National Institutes of Health Research Triangle Park, North Carolina 27709. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 387 EP - 398 VL - 7 IS - 3 SN - 0888-8809, 0888-8809 KW - Antineoplastic Agents KW - 0 KW - Bryostatins KW - Lactones KW - Macrolides KW - RNA, Messenger KW - bryostatin 1 KW - 37O2X55Y9E KW - Tretinoin KW - 5688UTC01R KW - DNA KW - 9007-49-2 KW - Luciferases KW - EC 1.13.12.- KW - Transglutaminases KW - EC 2.3.2.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Transcription, Genetic -- drug effects KW - Dose-Response Relationship, Drug KW - Humans KW - RNA, Messenger -- chemistry KW - Cell Differentiation KW - Epithelium -- enzymology KW - Rabbits KW - Amino Acid Sequence KW - RNA, Messenger -- biosynthesis KW - Lactones -- pharmacology KW - Luciferases -- biosynthesis KW - Regulatory Sequences, Nucleic Acid KW - Base Sequence KW - Transfection KW - Cells, Cultured KW - Gene Expression Regulation, Enzymologic -- drug effects KW - Molecular Sequence Data KW - DNA -- chemistry KW - Promoter Regions, Genetic -- genetics KW - Antineoplastic Agents -- pharmacology KW - Tretinoin -- pharmacology KW - Transglutaminases -- genetics KW - Keratinocytes -- enzymology KW - Transglutaminases -- biosynthesis KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Trachea -- cytology KW - Trachea -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75714450?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.atitle=Regulation+of+transglutaminase+type+I+expression+in+squamous+differentiating+rabbit+tracheal+epithelial+cells+and+human+epidermal+keratinocytes%3A+effects+of+retinoic+acid+and+phorbol+esters.&rft.au=Saunders%2C+N+A%3BBernacki%2C+S+H%3BVollberg%2C+T+M%3BJetten%2C+A+M&rft.aulast=Saunders&rft.aufirst=N&rft.date=1993-03-01&rft.volume=7&rft.issue=3&rft.spage=387&rft.isbn=&rft.btitle=&rft.title=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.issn=08888809&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-28 N1 - Date created - 1993-05-28 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - L10714; GENBANK; L10715 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Are the known bladder cancer risk-factors associated with more advanced bladder cancer? AN - 75707552; 8481494 AB - Risk factors for superficial and invasive bladder cancer were examined in a case-control study of 470 cases identified in 1967-68 in the Brockton and Boston Standard Metropolitan Areas (MA, United States) and of 500 population-based controls. Histologic specimens were reviewed and classified as superficial or invasive, following a standardized protocol. The tobacco-associated risk for superficial bladder cancer was odds ratio (OR) = 2.6 (95 percent confidence interval [CI] = 1.7-4.1) and the risk for invasive bladder cancer was OR = 1.7 (CI = 1.1-2.5). For subjects less than 60 years of age, the risks were greater for invasive tumors (OR = 4.3, CI = 1.2-15) than for superficial tumors (OR = 2.0, CI = 0.9-4.2), but this pattern for tobacco use was not found in older subjects. A strong trend of increased risk with increased amount of cigarettes smoked was shown only for invasive bladder tumors. No clear pattern of excess risk for invasive bladder tumors was seen for age at first use and years since last use of tobacco. The risk associated with occupational exposure to aromatic amine bladder carcinogens was OR = 1.7 (CI = 0.8-3.3) for superficial and OR = 1.5 (CI = 0.8-3.0) for invasive bladder cancer. For subjects less than 60 years of age, the risks were greater for invasive (OR = 12.0, CI = 2.1-65) than for superficial tumors (OR = 4.3, CI = 0.8-24), but this pattern for occupational exposure was not found in older subjects.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Cancer causes & control : CCC AU - Hayes, R B AU - Friedell, G H AU - Zahm, S H AU - Cole, P AD - Environmental Epidemiology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 157 EP - 162 VL - 4 IS - 2 SN - 0957-5243, 0957-5243 KW - Amines KW - 0 KW - Index Medicus KW - Occupational Exposure KW - Risk KW - Neoplasm Invasiveness KW - Age Factors KW - Risk Factors KW - Humans KW - Case-Control Studies KW - Aged KW - Middle Aged KW - Urinary Bladder Neoplasms -- pathology KW - Urinary Bladder Neoplasms -- epidemiology KW - Smoking -- adverse effects KW - Amines -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75707552?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+causes+%26+control+%3A+CCC&rft.atitle=Are+the+known+bladder+cancer+risk-factors+associated+with+more+advanced+bladder+cancer%3F&rft.au=Hayes%2C+R+B%3BFriedell%2C+G+H%3BZahm%2C+S+H%3BCole%2C+P&rft.aulast=Hayes&rft.aufirst=R&rft.date=1993-03-01&rft.volume=4&rft.issue=2&rft.spage=157&rft.isbn=&rft.btitle=&rft.title=Cancer+causes+%26+control+%3A+CCC&rft.issn=09575243&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-02 N1 - Date created - 1993-06-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Risk factors for small intestine cancer. AN - 75701526; 8481495 AB - Small intestine cancer is relatively rare. Clinical reports have suggested that several medical conditions may predispose to increased occurrence of this cancer, but otherwise its etiology is unknown. In one of the first case-control studies of this cancer, we compared questionnaire responses provided by next-of-kin of 430 persons who died of small intestine cancer cf921 controls who died of other causes. Subjects were identified from decedents included in the 1986 United States National Mortality Followback Survey. The questionnaires sought information on demographic and lifestyle characteristics, including diet and use of tobacco and alcohol. Tobacco and alcohol consumption were unrelated to risk of small intestine cancer, but weekly or more frequent consumption of red meat and monthly or more frequent intake of salt-cured/smoked foods were associated with two- to three fold increases in risk. The findings suggest that dietary factors probably are involved in risk of small intestine cancer, but additional research in other settings is required to clarify the determinants of these rare cancers. JF - Cancer causes & control : CCC AU - Chow, W H AU - Linet, M S AU - McLaughlin, J K AU - Hsing, A W AU - Chien, H T AU - Blot, W J AD - Epidemiology and Biostatistics Program, US National Cancer Institute, Bethesda, MD 20852. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 163 EP - 169 VL - 4 IS - 2 SN - 0957-5243, 0957-5243 KW - Index Medicus KW - Tobacco Use Disorder KW - Risk Factors KW - Humans KW - Adult KW - Case-Control Studies KW - Alcohol Drinking -- adverse effects KW - Middle Aged KW - Diet KW - United States -- epidemiology KW - Male KW - Female KW - Intestinal Neoplasms -- epidemiology KW - Intestine, Small -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75701526?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+causes+%26+control+%3A+CCC&rft.atitle=Risk+factors+for+small+intestine+cancer.&rft.au=Chow%2C+W+H%3BLinet%2C+M+S%3BMcLaughlin%2C+J+K%3BHsing%2C+A+W%3BChien%2C+H+T%3BBlot%2C+W+J&rft.aulast=Chow&rft.aufirst=W&rft.date=1993-03-01&rft.volume=4&rft.issue=2&rft.spage=163&rft.isbn=&rft.btitle=&rft.title=Cancer+causes+%26+control+%3A+CCC&rft.issn=09575243&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-02 N1 - Date created - 1993-06-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Studies on the mechanism of aromatase and other cytochrome P450 mediated deformylation reactions. AN - 75696869; 8476750 AB - Aromatase is a microsomal cytochrome P450 that converts androgens to estrogens by three sequential oxidations. The isolation of the 19-hydroxy and 19-oxo androgens suggests that the first two oxidations occur at the C19 carbon. However, the mechanism of the third oxidation, which results in C10--C19 bond cleavage, has not been determined. Two proposed mechanisms which remain viable involve either initial 1 beta-hydrogen atom abstraction or addition of the ferric peroxy anion from aromatase to the C19 aldehyde. Semiempirical molecular orbital calculations (AM1) were used to study potential reaction mechanisms initiated by initial 1 beta-hydrogen atom abstraction. Initially, the energetics of carbon--carbon bond cleavage of the keto and enol forms of C1-radicals were studied and were found to be energetically similar. A mechanism was proposed in which the 19-oxo intermediate is subject to initial nucleophilic attack by the protein. The geometry of the A-ring in the androgens is between that for the 1-radicals and estrogen, suggesting that some transition state stabilization for the homolytic cleavage reaction can occur. More recently, studies on liver microsomal cytochrome P450 mediated deformylation of xenobiotic aldehydes supports mechanisms involving an alkyl peroxy intermediate formed by addition of the ferric peroxy anion from aromatase to the C19 aldehyde. Although this intermediate could proceed through several different concerted or non-concerted pathways, one non-concerted pathway involves the heterolytic cleavage of the dioxygen bond resulting in an active oxygenating species (iron-oxene) and a diol. The diol could then undergo hydrogen atom abstraction followed by homolytic carbon--carbon bond cleavage as in the mechanisms modeled previously. When this cleavage was modeled for seven aldehydes, a good correlation with reported experimental aldehyde turnover numbers was obtained. However, when dialkoxy derivatives of the aldehydes are subject to microsomal metabolism, the rates of carbon-carbon cleavage products do not approach the rates of deformylation of the aldehyde analog. JF - The Journal of steroid biochemistry and molecular biology AU - Korzekwa, K R AU - Trager, W F AU - Mancewicz, J AU - Osawa, Y AD - Laboratory of Molecular Carcinogenesis, NCI, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 367 EP - 373 VL - 44 IS - 4-6 SN - 0960-0760, 0960-0760 KW - Aldehydes KW - 0 KW - Xenobiotics KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Aromatase KW - EC 1.14.14.1 KW - Index Medicus KW - Placenta -- enzymology KW - Xenobiotics -- metabolism KW - Humans KW - Microsomes, Liver -- enzymology KW - Aldehydes -- metabolism KW - Substrate Specificity KW - Female KW - Pregnancy KW - Aromatase -- metabolism KW - Cytochrome P-450 Enzyme System -- metabolism KW - Microsomes -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75696869?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+steroid+biochemistry+and+molecular+biology&rft.atitle=Studies+on+the+mechanism+of+aromatase+and+other+cytochrome+P450+mediated+deformylation+reactions.&rft.au=Korzekwa%2C+K+R%3BTrager%2C+W+F%3BMancewicz%2C+J%3BOsawa%2C+Y&rft.aulast=Korzekwa&rft.aufirst=K&rft.date=1993-03-01&rft.volume=44&rft.issue=4-6&rft.spage=367&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+steroid+biochemistry+and+molecular+biology&rft.issn=09600760&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-26 N1 - Date created - 1993-05-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Hepatic cytochrome P450 2B-type induction by ethyl/phenyl-substituted congeners of phenobarbital in the rat. AN - 75691625; 8477009 AB - As part of an investigation of the structural requirements for the induction, by phenobarbital-type inducers, of a coordinate pleiotropic response consisting of increases in hepatic cytochrome P450 2B (P450 2B) activity, increases in other phase I and II enzyme activities, and liver hypertrophy, we have examined a series of analogues of phenobarbital in which the ethyl/phenyl substitution at the sp3 carbon of the parent molecule was kept constant while the heterocyclic portion of the molecule was modified. The induction of hepatic P450 2B protein and ethoxy-, pentoxy-, and (benzyloxy)resorufin O-dealkylation activities, and epoxide hydration activity and liver/body weight ratio increase were examined in male F344/NCr rats fed the various congeners for 14 days at doses equimolar to 500 ppm phenobarbital. Increases in the measured parameters were maximal in rats fed phenobarbital or 5-ethyl-5-phenylhydantoin. The responses to primidone or 2-ethyl-2-phenylsuccinimide were approximately 65% of maximal, while glutethimide yielded a response approximately 50% of maximal. Induction of this response in rats fed the ring-opened and decarboxylated analogues, (ethylphenylacetyl)urea and 2-ethyl-2-phenylmalonamide, were < 25% of maximal. 5-Ethyl-5-phenyloxazolidinedione caused minimal increases in the measured end points when administered at a dose equimolar to 500 ppm phenobarbital. The profound differences among the congeners in ability to induce P450 2B protein and associated catalytic activities were not due to differences in food consumption by the various groups of rats.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Chemical research in toxicology AU - Nims, R W AU - Syi, J L AU - Wink, D A AU - Nelson, V C AU - Thomas, P E AU - Jones, C R AU - Diwan, B A AU - Keefer, L K AU - Rice, J M AU - Lubet, R A AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick Cancer Research and Development Center, Maryland 21702. PY - 1993 SP - 180 EP - 187 VL - 6 IS - 2 SN - 0893-228X, 0893-228X KW - Epoxy Compounds KW - 0 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Oxidoreductases KW - EC 1.- KW - Steroid Hydroxylases KW - EC 1.14.- KW - Aryl Hydrocarbon Hydroxylases KW - EC 1.14.14.1 KW - Cytochrome P-450 CYP1A1 KW - testosterone 7-alpha-hydroxylase, hamster KW - Epoxide Hydrolases KW - EC 3.3.2.- KW - Phenobarbital KW - YQE403BP4D KW - Index Medicus KW - Eating -- drug effects KW - Animals KW - Epoxide Hydrolases -- metabolism KW - Organ Size -- physiology KW - Chemistry, Physical KW - Epoxy Compounds -- metabolism KW - Body Weight -- physiology KW - Steroid Hydroxylases -- metabolism KW - Rats KW - Rats, Inbred F344 KW - Enzyme Induction -- drug effects KW - Oxidoreductases -- metabolism KW - Chemical Phenomena KW - Male KW - Protein Conformation KW - Phenobarbital -- pharmacology KW - Liver -- enzymology KW - Phenobarbital -- analogs & derivatives KW - Cytochrome P-450 Enzyme System -- metabolism KW - Cytochrome P-450 Enzyme System -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75691625?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+research+in+toxicology&rft.atitle=Hepatic+cytochrome+P450+2B-type+induction+by+ethyl%2Fphenyl-substituted+congeners+of+phenobarbital+in+the+rat.&rft.au=Nims%2C+R+W%3BSyi%2C+J+L%3BWink%2C+D+A%3BNelson%2C+V+C%3BThomas%2C+P+E%3BJones%2C+C+R%3BDiwan%2C+B+A%3BKeefer%2C+L+K%3BRice%2C+J+M%3BLubet%2C+R+A&rft.aulast=Nims&rft.aufirst=R&rft.date=1993-03-01&rft.volume=6&rft.issue=2&rft.spage=180&rft.isbn=&rft.btitle=&rft.title=Chemical+research+in+toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-24 N1 - Date created - 1993-05-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Single dose blood toxicokinetics of methacrylonitrile in the F344 rat. AN - 75672601; 8470115 AB - Methacrylonitrile (MAN) is a widely used industrial chemical. Minimal information is available on its effects or toxicokinetics; therefore, current investigations were undertaken as part of an overall effort to characterize MAN toxicity in laboratory animals. Groups of male F344 rats were administered MAN intravenously (29, 58, or 116 mg/kg) or perorally (58 mg/kg). Blood samples were collected at various time points after dosing and serum MAN concentrations were measured. Concentration versus time profiles were characterized by two phases and a two-compartment model was selected to fit the data. Toxicokinetic parameters were determined using Simusolv. The 39-min terminal half-life shows that 99% of an i.v. dose is eliminated in less than 5 hr, suggesting that the potential for MAN bioaccumulation is minimal. The volume of distribution at steady-state (747 ml/kg) indicates little distribution of MAN into tissues. Clearance is higher at 29 mg/kg than at the two other doses, suggesting that MAN elimination is saturable at doses above 29 mg/kg. MAN disposition is route-dependent. Approximately 36% of the i.v. dose was exhaled as unchanged MAN, while only 18% was eliminated via this route following po administration. MAN disposition data also suggest that a significant first-pass metabolism may occur because a higher percentage of metabolites was produced following oral vs i.v. administration. Perorally, 39% of the dose was exhaled as CO2 and 22% was excreted into the urine as metabolites over the 24-hr dosing interval. In comparison, following i.v. delivery, 26% of the dose was exhaled as CO2 and 16% was excreted into the urine as metabolites. About equal amounts of acetone were excreted following administration by either route. This information may prove useful in designing long-term toxicity studies for MAN by the National Toxicology Program and in interpreting the results of such studies. JF - Toxicology and applied pharmacology AU - Demby, K B AU - Sanchez, I M AU - Ghanayem, B I AD - National Institute of Environmental Health Sciences/NIH, Research Triangle Park, North Carolina 27709. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 115 EP - 121 VL - 119 IS - 1 SN - 0041-008X, 0041-008X KW - Methacrylates KW - 0 KW - Nitriles KW - methacrylonitrile KW - 04S4K38612 KW - Acetone KW - 1364PS73AF KW - Carbon Dioxide KW - 142M471B3J KW - Index Medicus KW - Rats KW - Administration, Oral KW - Regression Analysis KW - Animals KW - Rats, Inbred F344 KW - Analysis of Variance KW - Injections, Intravenous KW - Kinetics KW - Acetone -- metabolism KW - Carbon Dioxide -- metabolism KW - Male KW - Chromatography, High Pressure Liquid KW - Nitriles -- blood KW - Nitriles -- pharmacokinetics KW - Methacrylates -- pharmacokinetics KW - Nitriles -- administration & dosage KW - Methacrylates -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75672601?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+applied+pharmacology&rft.atitle=Single+dose+blood+toxicokinetics+of+methacrylonitrile+in+the+F344+rat.&rft.au=Demby%2C+K+B%3BSanchez%2C+I+M%3BGhanayem%2C+B+I&rft.aulast=Demby&rft.aufirst=K&rft.date=1993-03-01&rft.volume=119&rft.issue=1&rft.spage=115&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=0041008X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-11 N1 - Date created - 1993-05-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Elevated serum levels of neopterin but not beta 2-microglobulin in HIV-1-seronegative injecting drug users. AN - 75672044; 8471199 AB - To determine whether injecting drug use is associated with cellular immune activation in the absence of HIV-1 infection. Serum levels of neopterin and beta 2-microglobulin (beta 2M) were measured cross-sectionally in injecting drug users (IDU) enrolled in a prospective study. Two hundred and nineteen HIV-1-seronegative, healthy heterosexual black male IDU aged 21-49 years were selected from the Baltimore-based AIDS Linked to Intravenous Experiences (ALIVE) study. The possibility of including subjects in the process of seroconverting to HIV-1 was minimized by restricting the study to individuals who remained seronegative 6 months after the specimens used for analysis were collected. Mean serum beta 2M levels were not statistically different among groups of IDU whose usual pattern of injection was at least once a day for up to 3 consecutive days (daily users; n = 65), less than once per day (less-than-daily users; n = 75), or not at all for at least 2 weeks (non-recent users; n = 79). In contrast, the mean neopterin level was significantly (P = 0.039) greater in daily users (6.17 nmol/l) than in the other two groups (5.07 and 5.19 nmol/l, respectively, which were not statistically different). These results were not affected, by the frequency of using borrowed non-sterile works or by other demographic and risk factor variables. Frequent injecting drug use may be independently associated with a small elevation of serum neopterin levels, but not beta 2M levels. Although the occurrence of a type I error in this sample cannot be completely excluded, serum neopterin may be more sensitive than serum beta 2M in detecting activation of immunocompetent cells associated with frequent injecting drug use in this population. JF - AIDS (London, England) AU - Strickler, H D AU - Blanchard, J F AU - Vlahov, D AU - Taylor, E AU - Muñoz, A AU - Nelson, K E AU - Margolick, J B AD - Viral Epidemiology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 361 EP - 367 VL - 7 IS - 3 SN - 0269-9370, 0269-9370 KW - beta 2-Microglobulin KW - 0 KW - Biopterin KW - 22150-76-1 KW - Neopterin KW - 670-65-5 KW - Index Medicus KW - AIDS/HIV KW - Sexual Behavior KW - Prospective Studies KW - Humans KW - Cohort Studies KW - Adult KW - Middle Aged KW - Male KW - Biopterin -- analysis KW - Biopterin -- analogs & derivatives KW - beta 2-Microglobulin -- analysis KW - HIV Seropositivity KW - Substance Abuse, Intravenous -- blood KW - Substance Abuse, Intravenous -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75672044?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS+%28London%2C+England%29&rft.atitle=Elevated+serum+levels+of+neopterin+but+not+beta+2-microglobulin+in+HIV-1-seronegative+injecting+drug+users.&rft.au=Strickler%2C+H+D%3BBlanchard%2C+J+F%3BVlahov%2C+D%3BTaylor%2C+E%3BMu%C3%B1oz%2C+A%3BNelson%2C+K+E%3BMargolick%2C+J+B&rft.aulast=Strickler&rft.aufirst=H&rft.date=1993-03-01&rft.volume=7&rft.issue=3&rft.spage=361&rft.isbn=&rft.btitle=&rft.title=AIDS+%28London%2C+England%29&rft.issn=02699370&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-17 N1 - Date created - 1993-05-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Modeling blood/plasma concentrations in dosed feed and dosed drinking water toxicology studies. AN - 75666858; 8470117 AB - A computer model for predicting blood/plasma concentrations of test chemicals in dosed feed and dosed drinking water toxicology studies was developed. The model was constructed based on linear theory. The animal's feeding and drinking habits and the linear disposition kinetics of the test chemical obtained after a bolus gavage dose were built into the model. Blood/plasma concentrations of oxazepam and pentachlorophenol in dosed feed and dosed drinking water studies were predicted and compared with the experimentally determined data. The model proved highly reliable in predicting the blood/plasma concentrations of test chemical in dosed feed and dosed drinking water studies. The results suggest that if the kinetics of test chemicals fit a one-compartment model then bioaccumulation of the test chemical will occur in dosed feed or in dosed drinking water studies when absorption half-lives are less than 1.38 hr and elimination half-lives are longer than 5 hr. The extent of accumulation is mainly dependent on the elimination half-lives. For chemicals with absorption half-lives less than 1.38 hr and elimination half-lives less than 2 hr, the extent of bioaccumulation will be minimal. Blood/plasma concentrations of test chemicals in rats and mice will fluctuate daily and a quasi-steady state will be achieved after ad libitum exposure to dosed feed or dosed drinking water for approximately 4 days. If a daily 12-hr light cycle is used with the light cycle starting at 7:00 AM, the expected peak and trough blood concentrations in dosed feed studies will occur approximately in the early morning (5:00 AM) and in the late afternoon (4:00 PM), respectively. Similar results were obtained for dosed drinking water studies. The model should be applicable to dosed feed and dosed drinking water studies using other species. JF - Toxicology and applied pharmacology AU - Yuan, J AD - National Toxicology Program, National Institutes of Health, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 131 EP - 141 VL - 119 IS - 1 SN - 0041-008X, 0041-008X KW - Water KW - 059QF0KO0R KW - Oxazepam KW - 6GOW6DWN2A KW - Pentachlorophenol KW - D9BSU0SE4T KW - Index Medicus KW - Rats KW - Eating KW - Body Weight KW - Animals KW - Rats, Inbred F344 KW - Half-Life KW - Water -- chemistry KW - Rats, Wistar KW - Mice KW - Male KW - Female KW - Pentachlorophenol -- pharmacokinetics KW - Computer Simulation KW - Oxazepam -- pharmacokinetics KW - Toxicology -- methods KW - Pentachlorophenol -- blood KW - Pentachlorophenol -- administration & dosage KW - Oxazepam -- blood KW - Oxazepam -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75666858?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+applied+pharmacology&rft.atitle=Modeling+blood%2Fplasma+concentrations+in+dosed+feed+and+dosed+drinking+water+toxicology+studies.&rft.au=Yuan%2C+J&rft.aulast=Yuan&rft.aufirst=J&rft.date=1993-03-01&rft.volume=119&rft.issue=1&rft.spage=131&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=0041008X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-11 N1 - Date created - 1993-05-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - ICD-10 harmful use of alcohol and the alcohol dependence syndrome: prevalence and implications. AN - 75660724; 8461858 AB - Data from a 1988 survey on United States drinking practices and related problems was used to derive the prevalence and population estimates of harmful use of alcohol and the alcohol dependence syndrome as defined in the ICD-10 Clinical Descriptions and Diagnostic Guidelines Version (ICD-10-CDDG). Corresponding estimates were also presented for ICD-10-CDDG diagnoses that incorporated the duration criterion of the ICD-10-Diagnostic Criteria for Research Version (ICD-10-DCR). The prevalence of ICD-10 harmful use and dependence combined, with and without the duration criterion, were 5.2% and 7.1%, respectively. Corresponding harmful use rates were negligible (0.27%). Implications of the extremely low prevalence of harmful use in the US population and the impact of the duration criterion on the rates are discussed in terms of the fundamental nature of alcohol use disorders as syndromes and the viability of the harmful use of alcohol category as originally conceptualized. JF - Addiction (Abingdon, England) AU - Grant, B F AD - National Institute on Alcohol Abuse and Alcoholism, Division of Biometry and Epidemiology, Rockville, MD 20857. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 413 EP - 420 VL - 88 IS - 3 SN - 0965-2140, 0965-2140 KW - Index Medicus KW - Cross-Sectional Studies KW - Humans KW - Adult KW - Incidence KW - Aged KW - Middle Aged KW - Adolescent KW - United States -- epidemiology KW - Psychometrics KW - Male KW - Female KW - Alcoholism -- epidemiology KW - Alcoholism -- diagnosis KW - Alcohol Drinking -- psychology KW - Alcohol Drinking -- adverse effects KW - Psychiatric Status Rating Scales -- statistics & numerical data KW - Alcohol Drinking -- epidemiology KW - Alcoholism -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75660724?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Addiction+%28Abingdon%2C+England%29&rft.atitle=ICD-10+harmful+use+of+alcohol+and+the+alcohol+dependence+syndrome%3A+prevalence+and+implications.&rft.au=Grant%2C+B+F&rft.aulast=Grant&rft.aufirst=B&rft.date=1993-03-01&rft.volume=88&rft.issue=3&rft.spage=413&rft.isbn=&rft.btitle=&rft.title=Addiction+%28Abingdon%2C+England%29&rft.issn=09652140&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-06 N1 - Date created - 1993-05-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Overview of pharmacologic treatment approaches for alcohol and other drug addiction. Intoxication, withdrawal, and relapse prevention. AN - 75658323; 8456040 AB - Medication plays an increasingly important role in the treatment of alcohol and other drug addictions, in part because many patients do not respond to existing psychosocial treatment alone. This article provides a conceptual overview of current pharmacologic treatment approaches, and covers all three aspects of drug abuse--intoxication, withdrawal, and relapse prevention. JF - The Psychiatric clinics of North America AU - Gorelick, D A AD - Treatment Branch, National Institute on Drug Abuse, Maryland. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 141 EP - 156 VL - 16 IS - 1 SN - 0193-953X, 0193-953X KW - Index Medicus KW - Substance Withdrawal Syndrome -- prevention & control KW - Humans KW - Alcoholic Intoxication -- drug therapy KW - Poisoning -- drug therapy KW - Recurrence KW - Substance-Related Disorders -- drug therapy KW - Substance-Related Disorders -- rehabilitation KW - Alcoholism -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75658323?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Psychiatric+clinics+of+North+America&rft.atitle=Overview+of+pharmacologic+treatment+approaches+for+alcohol+and+other+drug+addiction.+Intoxication%2C+withdrawal%2C+and+relapse+prevention.&rft.au=Gorelick%2C+D+A&rft.aulast=Gorelick&rft.aufirst=D&rft.date=1993-03-01&rft.volume=16&rft.issue=1&rft.spage=141&rft.isbn=&rft.btitle=&rft.title=The+Psychiatric+clinics+of+North+America&rft.issn=0193953X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-20 N1 - Date created - 1993-04-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Epidemiology, prognostic factors, and prevention of lung cancer. AN - 75649820; 8457617 AB - Lung cancer continues to be a leading cause of preventable death, with an estimated 123,000 of the 143,000 lung cancer deaths in the United States in 1991 directly attributable to tobacco smoking. Given that mortality from this disease has not changed appreciably in the past two decades and despite continuing advances in cancer treatment, a new emphasis is being placed on prevention and early detection research through the identification of high-risk individuals and the definition of useful biomarkers. This review summarizes the status of these efforts over the past year. JF - Current opinion in oncology AU - Szabo, E AU - Mulshine, J AD - National Cancer Institute, Bethesda, Maryland. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 302 EP - 309 VL - 5 IS - 2 SN - 1040-8746, 1040-8746 KW - Index Medicus KW - Humans KW - Prognosis KW - Smoking -- adverse effects KW - Environmental Exposure -- adverse effects KW - Diet -- adverse effects KW - Lung Neoplasms -- prevention & control KW - Lung Neoplasms -- epidemiology KW - Lung Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75649820?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+opinion+in+oncology&rft.atitle=Epidemiology%2C+prognostic+factors%2C+and+prevention+of+lung+cancer.&rft.au=Szabo%2C+E%3BMulshine%2C+J&rft.aulast=Szabo&rft.aufirst=E&rft.date=1993-03-01&rft.volume=5&rft.issue=2&rft.spage=302&rft.isbn=&rft.btitle=&rft.title=Current+opinion+in+oncology&rft.issn=10408746&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-27 N1 - Date created - 1993-04-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Insertion of constant region domains of human IgG1 into CD4-PE40 increases its plasma half-life. AN - 75649163; 8455638 AB - CD4-PE40 is a recombinant toxin containing the binding domain of CD4 and a mutant form of Pseudomonas exotoxin A from which the cell binding domain has been removed. To increase the serum half-life of CD4-PE40, we have inserted various portions of the constant domain of human IgG1 into CD4-PE40. The constructs made include CD4-CH2-PE40, CD4-CH3-PE40, CD4-CH1-CH2-PE40 and CD4-CH2-CH3-PE40. The fusion proteins were expressed and purified from E. coli. Insertion of various domains from the constant region of IgG1 did not alter the cytotoxic activity of CD4-PE40; all these molecules were equally cytotoxic to cells expressing gp120 on their surface. However, there was a marked increase in the serum mean residence time of CD4-CH2-PE40 which was 115 min as compared to 47 min for CD4-PE40. Insertion of other domains also increased the half-life of CD4-PE40, however, CD4-CH2-PE40 was found to have the longest mean residence time in the circulation. One possible explanation for the increase in plasma half-life is diminished susceptibility of proteins to proteolysis. It was found that CD4-CH2-PE40 was much more resistant to proteolysis by trypsin than CD4-PE40. We proposed that insertion of the CH2 domain into CD4-PE40 covers up the protease sensitive sites in the molecule, thereby making the molecule less susceptible to degradation. The increase in size and reduced sensitivity to proteases could both be responsible for the increased plasma half-life of CD4-CH2-PE40. JF - Molecular immunology AU - Batra, J K AU - Kasturi, S AU - Gallo, M G AU - Voorman, R L AU - Maio, S M AU - Chaudhary, V K AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 379 EP - 386 VL - 30 IS - 4 SN - 0161-5890, 0161-5890 KW - Bacterial Proteins KW - 0 KW - CD4-Pseudomonas toxin KW - Exotoxins KW - Immunoglobulin Constant Regions KW - Immunoglobulin G KW - Immunotoxins KW - Recombinant Proteins KW - Trypsin KW - EC 3.4.21.4 KW - Thrombin KW - EC 3.4.21.5 KW - Fibrinolysin KW - EC 3.4.21.7 KW - Index Medicus KW - Animals KW - Electrophoresis, Polyacrylamide Gel KW - Fibrinolysin -- pharmacology KW - Humans KW - Mice KW - Mice, Inbred BALB C KW - Rats KW - Rats, Sprague-Dawley KW - Base Sequence KW - Half-Life KW - Thrombin -- pharmacology KW - Genetic Vectors KW - Molecular Sequence Data KW - Cytotoxicity Tests, Immunologic KW - Trypsin -- pharmacology KW - Male KW - Immunotoxins -- toxicity KW - Bacterial Proteins -- metabolism KW - Immunoglobulin G -- pharmacology KW - Recombinant Proteins -- pharmacokinetics KW - Exotoxins -- chemistry KW - Immunotoxins -- metabolism KW - Exotoxins -- immunology KW - Exotoxins -- pharmacokinetics KW - Recombinant Proteins -- toxicity KW - Bacterial Proteins -- toxicity KW - Immunotoxins -- chemistry KW - Bacterial Proteins -- chemistry KW - Immunotoxins -- immunology KW - Bacterial Proteins -- immunology KW - Recombinant Proteins -- immunology KW - Exotoxins -- toxicity KW - Recombinant Proteins -- chemistry KW - Immunoglobulin Constant Regions -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75649163?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+immunology&rft.atitle=Insertion+of+constant+region+domains+of+human+IgG1+into+CD4-PE40+increases+its+plasma+half-life.&rft.au=Batra%2C+J+K%3BKasturi%2C+S%3BGallo%2C+M+G%3BVoorman%2C+R+L%3BMaio%2C+S+M%3BChaudhary%2C+V+K%3BPastan%2C+I&rft.aulast=Batra&rft.aufirst=J&rft.date=1993-03-01&rft.volume=30&rft.issue=4&rft.spage=379&rft.isbn=&rft.btitle=&rft.title=Molecular+immunology&rft.issn=01615890&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-22 N1 - Date created - 1993-04-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Substance use risk factors for HIV infection. AN - 75638909; 8456038 AB - The focus on reducing needle sharing by IVDUs as an HIV-control strategy is well supported by epidemiologic data. Because of this emphasis, however, the role of other HIV risk factors in drug use is sometimes overlooked. Although needle sharing by IVDUs undoubtedly will continue to be one of the greatest risk factor for HIV infection in drug users, other risk factors in HIV infection also are associated with drug use and may contribute significantly to the spread of HIV infection. It is clear that the role of drug use in AIDS is not limited to needle sharing by IVDUs. HIV infection can be transmitted by any type of needle use. Nonintravenous drugs (e.g., crack) and other risk factors (e.g., unprotected sex) also may play a role in the spread of HIV infection. Because of its dependence potential, crack may come to play a major role in HIV transmission, primarily because of its link to unprotected sexual behavior. JF - The Psychiatric clinics of North America AU - Pickens, R W AU - Battjes, R AU - Svikis, D S AU - Gupman, A E AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 119 EP - 125 VL - 16 IS - 1 SN - 0193-953X, 0193-953X KW - Index Medicus KW - AIDS/HIV KW - Sexual Behavior KW - Risk Factors KW - Humans KW - Substance Abuse, Intravenous -- complications KW - HIV Infections -- transmission KW - HIV Infections -- etiology KW - Substance-Related Disorders -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75638909?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Psychiatric+clinics+of+North+America&rft.atitle=Substance+use+risk+factors+for+HIV+infection.&rft.au=Pickens%2C+R+W%3BBattjes%2C+R%3BSvikis%2C+D+S%3BGupman%2C+A+E&rft.aulast=Pickens&rft.aufirst=R&rft.date=1993-03-01&rft.volume=16&rft.issue=1&rft.spage=119&rft.isbn=&rft.btitle=&rft.title=The+Psychiatric+clinics+of+North+America&rft.issn=0193953X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-20 N1 - Date created - 1993-04-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Substance abuse vulnerability and D2 receptor genes. AN - 75637971; 7681236 AB - Dopamine systems are key to the actions of several substances. Inter-individual differences in genes encoding proteins involved in dopaminergic neurotransmission could plausibly explain some of the genetic bases for inter-individual differences in vulnerability to substance abuse. The restriction fragment length polymorphism (RFLP) markers TaqIA1 and B1 at the dopamine D2 receptor (DRD2) gene locus in Caucasians are associated with substance abuse behaviors. In most, but not all, studies of alcoholics and polysubstance abusers, these TaqIA1 and B1 gene markers are present more often in substance abusers than in control individuals. No study has identified substance abusers or controls by sampling randomly from the general population; allelic association findings could thus conceivably be confounded by RFLP differences based on ethnicity or other factors. However, meta-analyses of the data from controlled studies available to date are consistent with the proposal that DRD2 gene variants contribute to inter-individual differences in vulnerability to alcoholism and polysubstance abuse. JF - Trends in neurosciences AU - Uhl, G AU - Blum, K AU - Noble, E AU - Smith, S AD - Laboratory of Molecular Neurobiology, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 83 EP - 88 VL - 16 IS - 3 SN - 0166-2236, 0166-2236 KW - Receptors, Dopamine D2 KW - 0 KW - Index Medicus KW - Animals KW - Humans KW - Receptors, Dopamine D2 -- genetics KW - Substance-Related Disorders -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75637971?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Trends+in+neurosciences&rft.atitle=Substance+abuse+vulnerability+and+D2+receptor+genes.&rft.au=Uhl%2C+G%3BBlum%2C+K%3BNoble%2C+E%3BSmith%2C+S&rft.aulast=Uhl&rft.aufirst=G&rft.date=1993-03-01&rft.volume=16&rft.issue=3&rft.spage=83&rft.isbn=&rft.btitle=&rft.title=Trends+in+neurosciences&rft.issn=01662236&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-20 N1 - Date created - 1993-04-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Trends Neurosci. 1994 Feb;17(2):50-1 [7512766] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Standardization of the 32P-postlabeling assay for polycyclic aromatic hydrocarbon-DNA adducts. AN - 75636329; 8464380 AB - A modified method for the 32P-postlabeling assay that permits standardized quantitation for specific polycyclic aromatic hydrocarbon (PAH)-DNA adducts is described. This method has been designed to test the components of the 32P-postlabeling assay for use in the chemically specific detection of individual adducts with the ultimate goal of testing the biological significance of PAH-DNA adducts in humans. The approach relies upon high performance liquid chromatography (HPLC), concomitant labeling of 2'-deoxyguanosine (dGp) as an internal standard and thin layer chromatography (TLC), which identifies unmodified nucleotides along with PAH-DNA adducts on the same TLC plate. This method assesses labeling efficiency, detects the presence of unknown inhibitors, assesses the adequacy of digestion (when combined with HPLC) and allows for the development of calibration curves for directly determined molar ratios (adduct:internal standard). Chemically synthesized adduct standards and quantitative 32P-postlabeling data have been corroborated by UV spectroscopy, fluorescence spectroscopy and liquid scintillation counting where radiolabeled materials were available. Labeling efficiencies of the PAH-DNA adducts were found to be up to 100-fold less than expected and depended upon both the adduct and adduct levels (lower levels being less efficiently detected). The presence of unmodified nucleotides resulted in a 1.5-fold lower labeling efficiency. Mixtures of selected PAH-DNA adducts did not affect the labeling efficiencies of each other. The data suggest that previous 32P-postlabeling assay studies for PAH-DNA adducts may have underestimated adduct levels due to variations in labeling efficiency. JF - Mutagenesis AU - Shields, P G AU - Harris, C C AU - Petruzzelli, S AU - Bowman, E D AU - Weston, A AD - Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 121 EP - 126 VL - 8 IS - 2 SN - 0267-8357, 0267-8357 KW - Mutagens KW - 0 KW - Phosphorus Radioisotopes KW - Polycyclic Compounds KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Spectrometry, Fluorescence KW - Mutagens -- metabolism KW - Isotope Labeling -- methods KW - Spectrophotometry, Ultraviolet KW - Chromatography, Thin Layer KW - Chromatography, High Pressure Liquid KW - Structure-Activity Relationship KW - DNA -- isolation & purification KW - DNA -- metabolism KW - Polycyclic Compounds -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75636329?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutagenesis&rft.atitle=Standardization+of+the+32P-postlabeling+assay+for+polycyclic+aromatic+hydrocarbon-DNA+adducts.&rft.au=Shields%2C+P+G%3BHarris%2C+C+C%3BPetruzzelli%2C+S%3BBowman%2C+E+D%3BWeston%2C+A&rft.aulast=Shields&rft.aufirst=P&rft.date=1993-03-01&rft.volume=8&rft.issue=2&rft.spage=121&rft.isbn=&rft.btitle=&rft.title=Mutagenesis&rft.issn=02678357&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-06 N1 - Date created - 1993-05-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Effect of carnosine homocarnosine and anserine on hydroxylation of the guanine moiety in 2'-deoxyguanosine, DNA and nucleohistone with hydrogen peroxide in the presence of nickel(II). AN - 75632945; 8384089 AB - The oxidation of 2'-deoxyguanosine (dG) to 8-hydroxy-2'-deoxyguanosine (8-OH-dG) in free dG and the dG residues of DNA and nucleohistone with H2O2 in the presence of Ni(II) and histidyl oligopeptides, carnosine, homocarnosine and anserine was studied at physiological pH. The oxidation of free dG with H2O2 was enhanced by the oligopeptides, but not by Ni(II) alone. Much greater enhancement was produced by equimolar mixtures of Ni(II) with any of the oligopeptides or with L-histidine. In contrast, the oxidation of dG residues in DNA and nucleohistone with H2O2 was not affected by the oligopeptides, but was enhanced by Ni(II). The latter enhancement remained practically unchanged when Ni(II) was accompanied by equimolar amounts of homocarnosine or anserine, whereas carnosine tended to attenuate that enhancement. The extent of formation of 8-OH-dG in free dG depended on time and concentration of H2O2 and was highest at pH 7.4. An electron spin resonance study of the reaction mixture containing H2O2, Ni(II), carnosine, homocarnosine and/or anserine provided evidence for the generation of .OH radical in the reaction media. Although it has previously been concluded that carnosine, anserine and homocarnosine might serve as anti-oxidants, the present study does not support that conclusion and shows that these compounds may even act as pro-oxidants, especially when they are complexed with Ni(II). The results suggest that carnosine, homocarnosine and anserine, by enhancing oxidation of the free dG pool, may potentiate the carcinogenic effects of Ni(II) since the resulting 8-OH-dG can be misincorporated into DNA and thus produce a mutagenic lesion. JF - Carcinogenesis AU - Datta, A K AU - Shi, X AU - Kasprzak, K S AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702-1201. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 417 EP - 422 VL - 14 IS - 3 SN - 0143-3334, 0143-3334 KW - Histones KW - 0 KW - homocarnosine KW - 3650-73-5 KW - Guanine KW - 5Z93L87A1R KW - Nickel KW - 7OV03QG267 KW - Carnosine KW - 8HO6PVN24W KW - DNA KW - 9007-49-2 KW - Hydrogen Peroxide KW - BBX060AN9V KW - Deoxyguanosine KW - G9481N71RO KW - Anserine KW - HDQ4N37UGV KW - Index Medicus KW - Oxidation-Reduction KW - Histones -- metabolism KW - Electron Spin Resonance Spectroscopy KW - DNA -- metabolism KW - Hydroxylation KW - Deoxyguanosine -- metabolism KW - Carnosine -- analogs & derivatives KW - Nickel -- pharmacology KW - Hydrogen Peroxide -- pharmacology KW - Carnosine -- pharmacology KW - Anserine -- pharmacology KW - Guanine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75632945?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Effect+of+carnosine+homocarnosine+and+anserine+on+hydroxylation+of+the+guanine+moiety+in+2%27-deoxyguanosine%2C+DNA+and+nucleohistone+with+hydrogen+peroxide+in+the+presence+of+nickel%28II%29.&rft.au=Datta%2C+A+K%3BShi%2C+X%3BKasprzak%2C+K+S&rft.aulast=Datta&rft.aufirst=A&rft.date=1993-03-01&rft.volume=14&rft.issue=3&rft.spage=417&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-22 N1 - Date created - 1993-04-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Effects of dietary retinoic acid on skin papilloma and carcinoma formation in female SENCAR mice. AN - 75626731; 8453733 AB - Previously we have shown that dietary retinoids are essential for papilloma formation induced by either an initiation-promotion or a complete skin carcinogenesis protocol. The present study was conducted to further determine the effect of dietary retinoic acid (RA) on papilloma formation and the conversion of papillomas to carcinomas. Skin tumors were induced in 3 week old female SENCAR mice by an initiation-promotion protocol with one application of 20 micrograms of 7,12-dimethylbenz[a]anthracene (DMBA), followed by 20 weekly applications of 2 micrograms of 12-O-tetradecanoylphorbol-13-acetate (TPA). Mice were fed RA at one of the three doses: 0.3 (nutritionally marginal dose), 3 (near physiological) and 30 (pharmacological) micrograms/g of diet. Mice fed 30 micrograms of RA/g of diet had the same survival rate as the other two groups despite a lower body weight and all three groups had similar papilloma incidence, which reached 100% at age 18 weeks. Mice fed 3 micrograms of RA/g of diet had the highest papilloma yield (approximately 14 papillomas/mouse) of all groups and it peaked between weeks 18 and 38 of age. These papillomas later regressed such that mice from all three groups had about the same papilloma yield at week 44 of age. Mice fed 30 micrograms of RA/g of diet failed to develop any visible carcinoma, while mice fed 0.3 or 3 micrograms/g showed 1.9% conversion of papillomas to carcinomas. Therefore, dietary RA at 30 micrograms/g of diet inhibited the conversion of papillomas to carcinomas without affecting papilloma incidence. In addition, dietary RA at 30 and 0.3 micrograms/g of diet lowered papilloma yield. JF - Carcinogenesis AU - De Luca, L M AU - Sly, L AU - Jones, C S AU - Chen, L C AD - Differentiation Control Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 539 EP - 542 VL - 14 IS - 3 SN - 0143-3334, 0143-3334 KW - Tretinoin KW - 5688UTC01R KW - 9,10-Dimethyl-1,2-benzanthracene KW - 57-97-6 KW - Index Medicus KW - Animals KW - 9,10-Dimethyl-1,2-benzanthracene -- toxicity KW - Mice KW - Diet KW - Female KW - Tretinoin -- pharmacology KW - Papilloma -- prevention & control KW - Skin Neoplasms -- chemically induced KW - Carcinoma -- prevention & control KW - Skin Neoplasms -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75626731?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Effects+of+dietary+retinoic+acid+on+skin+papilloma+and+carcinoma+formation+in+female+SENCAR+mice.&rft.au=De+Luca%2C+L+M%3BSly%2C+L%3BJones%2C+C+S%3BChen%2C+L+C&rft.aulast=De+Luca&rft.aufirst=L&rft.date=1993-03-01&rft.volume=14&rft.issue=3&rft.spage=539&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-22 N1 - Date created - 1993-04-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Reconstitution of hair follicle development in vivo: determination of follicle formation, hair growth, and hair quality by dermal cells. AN - 75622890; 8440892 AB - Combinations of cultured and uncultured epidermal and dermal cell preparations from newborn and perinatal mice were grafted onto the backs of athymic nude mouse hosts to elucidate the cellular requirements for skin appendage formation. All epidermal populations studied, including a total epidermal keratinocyte preparation from trypsin-split skin, developing hair follicle buds isolated from epidermis, and preformed hair follicles isolated from dermis, make haired skin when grafted with fresh dermal cells. Only pre-formed hair follicles produce haired skin on grafts without an additional dermal component. Hair follicle buds grafted alone or with cultured dermal cells will reconstitute skin but without appendage formation. Thus, cells or factors present in fresh, but not cultured, dermal cells are essential for supporting hair growth from budding follicles, whereas more developed (pre-formed) follicles appear to contain all the necessary components for hair formation. Dissociation of isolated hair follicles by trypsin/ethylenediaminetetraacetic acid prior to grafting is permissive for hair growth, suggesting that follicle cells can be re-induced or reassociate in vivo. Dermal papilla cells, microdissected from rat vibrissal follicles and cultured for up to 14 passages, stimulate hair growth from follicle buds and influence the quality of hair growth from pre-formed hair follicles. Thus, dermal papilla cells maintain inductive capacity in culture and contribute to the reconstituted skin. This reconstitution model should be useful for identifying cell populations within the hair follicle compartment necessary for hair growth and for examining the effects of specific gene products on hair follicle growth and development in vivo. JF - The Journal of investigative dermatology AU - Weinberg, W C AU - Goodman, L V AU - George, C AU - Morgan, D L AU - Ledbetter, S AU - Yuspa, S H AU - Lichti, U AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 229 EP - 236 VL - 100 IS - 3 SN - 0022-202X, 0022-202X KW - Alkaline Phosphatase KW - EC 3.1.3.1 KW - Index Medicus KW - Animals KW - 3T3 Cells KW - Alkaline Phosphatase -- analysis KW - Mice KW - Models, Biological KW - Hair -- transplantation KW - Skin -- enzymology KW - Hair -- growth & development KW - Skin -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75622890?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+investigative+dermatology&rft.atitle=Reconstitution+of+hair+follicle+development+in+vivo%3A+determination+of+follicle+formation%2C+hair+growth%2C+and+hair+quality+by+dermal+cells.&rft.au=Weinberg%2C+W+C%3BGoodman%2C+L+V%3BGeorge%2C+C%3BMorgan%2C+D+L%3BLedbetter%2C+S%3BYuspa%2C+S+H%3BLichti%2C+U&rft.aulast=Weinberg&rft.aufirst=W&rft.date=1993-03-01&rft.volume=100&rft.issue=3&rft.spage=229&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+investigative+dermatology&rft.issn=0022202X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-01 N1 - Date created - 1993-04-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Limited prognostic value of changes in antineutrophil cytoplasmic antibody titer in patients with Wegener's granulomatosis. AN - 75621453; 8452581 AB - To assess the correlation and prognostic value of antineutrophil cytoplasmic antibody (cANCA) titers with disease activity in patients with Wegener's granulomatosis (WG). One hundred six patients with WG had serum ANCA determinations; 72 had serial titers obtained routinely at 1-3-month intervals. One hundred twelve subjects (19 of whom were healthy donors) served as controls. All serum samples were tested for cANCA by an indirect immunofluorescence technique. A prospective analysis of disease activity and cANCA values was performed. Disease activity was assessed according to clinical, laboratory, radiographic, and histopathologic findings. Positivity for cANCA was a sensitive (88%) marker of active WG. However, changes in serial titers temporally correlated with a change in disease status in only 64% of patients. Furthermore, an increase in the cANCA titer preceded clinical exacerbation of disease in only 24% of patients who had been in remission or had low-grade, smoldering disease. A rise in cANCA titer alone should not be considered adequate evidence of an impending clinical exacerbation, and therefore does not justify initiating or increasing immunosuppressive therapy. JF - Arthritis and rheumatism AU - Kerr, G S AU - Fleisher, T A AU - Hallahan, C W AU - Leavitt, R Y AU - Fauci, A S AU - Hoffman, G S AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 365 EP - 371 VL - 36 IS - 3 SN - 0004-3591, 0004-3591 KW - Antibodies, Antineutrophil Cytoplasmic KW - 0 KW - Autoantibodies KW - Biomarkers KW - Immunoglobulin G KW - Cyclophosphamide KW - 8N3DW7272P KW - Prednisone KW - VB0R961HZT KW - Abridged Index Medicus KW - Index Medicus KW - Sensitivity and Specificity KW - Prospective Studies KW - Cyclophosphamide -- therapeutic use KW - Prednisone -- therapeutic use KW - Humans KW - Prognosis KW - Predictive Value of Tests KW - Follow-Up Studies KW - Fluorescent Antibody Technique KW - False Positive Reactions KW - Granulomatosis with Polyangiitis -- immunology KW - Immunoglobulin G -- analysis KW - Granulomatosis with Polyangiitis -- pathology KW - Autoantibodies -- analysis KW - Granulomatosis with Polyangiitis -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75621453?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Arthritis+and+rheumatism&rft.atitle=Limited+prognostic+value+of+changes+in+antineutrophil+cytoplasmic+antibody+titer+in+patients+with+Wegener%27s+granulomatosis.&rft.au=Kerr%2C+G+S%3BFleisher%2C+T+A%3BHallahan%2C+C+W%3BLeavitt%2C+R+Y%3BFauci%2C+A+S%3BHoffman%2C+G+S&rft.aulast=Kerr&rft.aufirst=G&rft.date=1993-03-01&rft.volume=36&rft.issue=3&rft.spage=365&rft.isbn=&rft.btitle=&rft.title=Arthritis+and+rheumatism&rft.issn=00043591&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-12 N1 - Date created - 1993-04-12 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Arthritis Rheum. 1994 Apr;37(4):596-7 [8147939] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Use of pilocarpine during head and neck radiation therapy to reduce xerostomia and salivary dysfunction. AN - 75615998; 8448748 AB - Salivary gland hypofunction commonly develops during radiation therapy to the head and neck region. This study evaluated whether the sialogogue pilocarpine given during radiation therapy may reduce the severity of xerostomia and salivary dysfunction. Nine patients requiring head, neck, or mantle radiation therapy participated in this double-blind, placebo-controlled trial. The patients took either 5 mg of pilocarpine or placebo four times daily for 3 months, beginning the day before radiation therapy. Subjective complaints and salivary functions were assessed. The pilocarpine-treated group had a lower frequency of oral symptoms during treatment than the placebo-treated group. Although salivary flow decreased in all patients, the pilocarpine-treated group had smaller reductions in flow. No drug effect was observed in glands that were irradiated completely. Thus, pilocarpine appeared to stimulate salivary tissues outside the radiation field. These results suggest that stimulation with pilocarpine may reduce the severity of salivary dysfunction and associated oral symptoms during radiation therapy. JF - Cancer AU - Valdez, I H AU - Wolff, A AU - Atkinson, J C AU - Macynski, A A AU - Fox, P C AD - Clinical Investigations and Patient Care Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/03/01/ PY - 1993 DA - 1993 Mar 01 SP - 1848 EP - 1851 VL - 71 IS - 5 SN - 0008-543X, 0008-543X KW - Pilocarpine KW - 01MI4Q9DI3 KW - Abridged Index Medicus KW - Index Medicus KW - Double-Blind Method KW - Humans KW - Adult KW - Middle Aged KW - Male KW - Female KW - Radiotherapy -- adverse effects KW - Xerostomia -- etiology KW - Salivary Glands -- radiation effects KW - Salivary Glands -- drug effects KW - Xerostomia -- prevention & control KW - Pilocarpine -- therapeutic use KW - Head and Neck Neoplasms -- radiotherapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75615998?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=Use+of+pilocarpine+during+head+and+neck+radiation+therapy+to+reduce+xerostomia+and+salivary+dysfunction.&rft.au=Valdez%2C+I+H%3BWolff%2C+A%3BAtkinson%2C+J+C%3BMacynski%2C+A+A%3BFox%2C+P+C&rft.aulast=Valdez&rft.aufirst=I&rft.date=1993-03-01&rft.volume=71&rft.issue=5&rft.spage=1848&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-09 N1 - Date created - 1993-04-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - COUP-TF acts as a competitive repressor for estrogen receptor-mediated activation of the mouse lactoferrin gene. AN - 75615062; 8441416 AB - We previously demonstrated that the estrogen response module (mERM) of the mouse lactoferrin gene, which contains an overlapping chicken ovalbumin upstream promoter transcription factor (COUP-TF)- and estrogen receptor-binding element, is responsible for estrogen induction. In this report we show that COUP-TF represses the mERM response to estrogen stimulation. Mutation and deletion of the COUP-TF-binding element or reduction of the endogenous COUP-TF increases mERM estrogen responsiveness. Likewise, overexpression of the COUP-TF expression vector blocked the estrogen-stimulated response of mERM in transfected cells. The molecular mechanism of this repression is due to the competition between COUP-TF and the estrogen receptor for binding at identical contact sites in the overlapping region of the mERM. Our results indicate that two members of the steroid-thyroid receptor superfamily work in concert to modulate lactoferrin gene expression. JF - Molecular and cellular biology AU - Liu, Y AU - Yang, N AU - Teng, C T AD - Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 1836 EP - 1846 VL - 13 IS - 3 SN - 0270-7306, 0270-7306 KW - COUP Transcription Factor I KW - 0 KW - DNA-Binding Proteins KW - Nr2f1 protein, mouse KW - Receptors, Estrogen KW - Recombinant Proteins KW - Repressor Proteins KW - Transcription Factors KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Lactoferrin KW - EC 3.4.21.- KW - Index Medicus KW - Animals KW - Recombinant Proteins -- biosynthesis KW - Dose-Response Relationship, Drug KW - Transcription, Genetic KW - Mice KW - Chromosome Mapping KW - Mutagenesis, Site-Directed KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Base Sequence KW - Binding, Competitive KW - Molecular Sequence Data KW - Chickens -- genetics KW - Sequence Deletion KW - Transcription Factors -- pharmacology KW - Regulatory Sequences, Nucleic Acid -- genetics KW - Lactoferrin -- genetics KW - Lactoferrin -- biosynthesis KW - Transcription Factors -- metabolism KW - Repressor Proteins -- metabolism KW - DNA-Binding Proteins -- pharmacology KW - Receptors, Estrogen -- metabolism KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75615062?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+cellular+biology&rft.atitle=COUP-TF+acts+as+a+competitive+repressor+for+estrogen+receptor-mediated+activation+of+the+mouse+lactoferrin+gene.&rft.au=Liu%2C+Y%3BYang%2C+N%3BTeng%2C+C+T&rft.aulast=Liu&rft.aufirst=Y&rft.date=1993-03-01&rft.volume=13&rft.issue=3&rft.spage=1836&rft.isbn=&rft.btitle=&rft.title=Molecular+and+cellular+biology&rft.issn=02707306&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-01 N1 - Date created - 1993-04-01 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nucleic Acids Res. 1988 Dec 9;16(23):11057-74 [2905047] EMBO J. 1991 Aug;10(8):2237-45 [1906001] Cell. 1989 Feb 10;56(3):335-44 [2644044] Proc Natl Acad Sci U S A. 1989 Feb;86(4):1218-22 [2919170] Mol Cell Biol. 1989 Jan;9(1):43-9 [2927397] Trends Genet. 1988 Nov;4(11):309-14 [2853466] Cell. 1989 May 5;57(3):433-42 [2720778] Nature. 1989 Jul 13;340(6229):163-6 [2739739] Nucleic Acids Res. 1989 Jul 11;17(13):4975-91 [2762116] Cell. 1989 Nov 17;59(4):697-708 [2555064] J Biol Chem. 1990 Apr 15;265(11):6098-103 [2108152] Mol Endocrinol. 1990 Mar;4(3):363-9 [2188115] Cell. 1990 Jun 29;61(7):1217-24 [2142019] J Biol Chem. 1991 Nov 15;266(32):21880-5 [1939212] Cell. 1992 Jan 24;68(2):377-95 [1310259] Trends Biochem Sci. 1991 Nov;16(11):423-6 [1776172] Proc Natl Acad Sci U S A. 1992 Feb 15;89(4):1448-52 [1311101] Mol Cell Biol. 1992 Apr;12(4):1708-18 [1312668] Science. 1992 Apr 3;256(5053):94-7 [1348871] Mol Endocrinol. 1992 Mar;6(3):355-64 [1584212] Gene Expr. 1991;1(3):207-16 [1820218] Mol Cell Biol. 1992 Sep;12(9):4153-63 [1324415] Mol Cell Biol. 1992 Oct;12(10):4666-76 [1328857] Cell. 1990 Sep 21;62(6):1205-15 [2169352] Nucleic Acids Res. 1990 Sep 11;18(17):5097-106 [2119495] Cell. 1990 Dec 21;63(6):1267-76 [2124518] J Biol Chem. 1991 Jan 5;266(1):551-8 [1985915] Science. 1991 Feb 1;251(4993):561-5 [1899293] Genes Dev. 1990 Dec;4(12B):2353-65 [2279702] Mol Endocrinol. 1990 Apr;4(4):604-10 [2280777] Mol Endocrinol. 1990 Aug;4(8):1226-34 [1963474] Nature. 1990 Jul 26;346(6282):329-31 [2142753] Science. 1990 Sep 14;249(4974):1266-72 [2119054] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Methods Enzymol. 1980;65(1):499-560 [6246368] Annu Rev Genet. 1985;19:209-52 [3909942] Nature. 1986 Mar 13-19;320(6058):134-9 [3754034] Cell. 1986 Aug 29;46(5):645-52 [3742595] Cell. 1986 Sep 26;46(7):1053-61 [3463433] Mol Cell Biol. 1986 Dec;6(12):4259-67 [3796602] Pediatr Res. 1987 Jun;21(6):563-7 [3496579] Cancer Res. 1987 Aug 1;47(15):4184-8 [3038309] J Biol Chem. 1987 Jul 25;262(21):10134-9 [3611056] Cell. 1987 Aug 28;50(5):701-9 [3040258] J Biol Chem. 1987 Nov 25;262(33):16080-6 [3680243] J Reprod Immunol. 1987 Oct;12(2):137-48 [2963123] Methods Enzymol. 1987;154:367-82 [3323813] Science. 1988 May 13;240(4854):889-95 [3283939] J Biol Chem. 1988 Jul 25;263(21):10180-5 [2839477] Cell. 1988 Jul 29;54(3):313-23 [3396073] Infect Immun. 1988 Oct;56(10):2552-7 [3417349] Cell. 1988 Oct 7;55(1):145-56 [3167974] Cell. 1990 Sep 21;62(6):1189-204 [2169351] Mol Endocrinol. 1990 Dec;4(12):1964-71 [2082192] J Biol Chem. 1991 May 5;266(13):8248-54 [1708774] Cancer Res. 1991 Jun 1;51(11):3037-43 [1674448] J Virol. 1991 Jun;65(6):2853-60 [2033658] Science. 1991 Jun 14;252(5012):1546-8 [2047861] Endocrinology. 1989 Feb;124(2):992-9 [2463910] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Phase I trial of subcutaneous interleukin-6 in patients with advanced malignancies. AN - 75614550; 7680375 AB - Based on preclinical evidence in murine models that interleukin-6 (IL-6) mediates regression of metastatic tumors, we performed a phase I study of recombinant human IL-6 in patients with refractory advanced malignancies to determine its pharmacokinetics, toxicities, and possible immunologic and antitumor effects. Recombinant IL-6 was administered as a single subcutaneous dose daily for 7 days, with 7 days off therapy followed by another 7 days of IL-6. Doses were escalated in cohorts of three patients starting at 3 micrograms/kg/d, provided that toxicity at the preceding dose level was not dose-limiting. Dose-limiting toxicity was defined as grade III or IV major organ toxicity that did not resolve to grade II or less in 24 hours after stopping IL-6, using the National Cancer Institute Common Toxicity Criteria. Patients were treated with 3, 10, and 30 micrograms/kg/d IL-6 subcutaneously. Three patients each were treated at the 3- and 10-micrograms dose levels. Two of five patients treated with 30 micrograms/kg/d IL-6 subcutaneously had grade III major organ toxicity that required IL-6 therapy to be discontinued. All patients experienced fever, chills, and minor fatigue. Significant increases in C-reactive protein (CRP), fibrinogen, platelet counts, and lymphocyte IL-2 receptor levels were seen in patients at the 10- and 30-micrograms/kg dose levels. Decreases in albumin and hemoglobin were observed, particularly at the 30-micrograms/kg dose level. The half-life (T1/2 beta) was 4.2 hours, with a peak IL-6 level at 5 hours. No antitumor responses were seen. A safely tolerated dose of daily subcutaneous IL-6 is 10 micrograms/kg, with hepatotoxicity and cardiac arrhythmia being the dose-limiting toxicities at 30 micrograms/kg. Phase II trials of IL-6 administered subcutaneously daily for at least 7 days for two cycles with an intervening week of rest are recommended for phase II trials. However, patients with extensive replacement of liver by tumor and abnormal liver functions should receive IL-6 therapy with caution. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Weber, J AU - Yang, J C AU - Topalian, S L AU - Parkinson, D R AU - Schwartzentruber, D S AU - Ettinghausen, S E AU - Gunn, H AU - Mixon, A AU - Kim, H AU - Cole, D AD - National Cancer Institute, Surgery Branch, Bethesda, MD 20892. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 499 EP - 506 VL - 11 IS - 3 SN - 0732-183X, 0732-183X KW - Acute-Phase Proteins KW - 0 KW - Interleukin-6 KW - Recombinant Proteins KW - Index Medicus KW - Recombinant Proteins -- pharmacology KW - Humans KW - Recombinant Proteins -- pharmacokinetics KW - Aged KW - B-Lymphocytes -- drug effects KW - Acute-Phase Proteins -- drug effects KW - Adult KW - Injections, Subcutaneous KW - Flow Cytometry KW - Middle Aged KW - Immunity -- drug effects KW - Recombinant Proteins -- therapeutic use KW - Blood Cell Count -- drug effects KW - Female KW - Male KW - Neoplasms -- drug therapy KW - Interleukin-6 -- pharmacokinetics KW - Interleukin-6 -- therapeutic use KW - Interleukin-6 -- pharmacology KW - Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75614550?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=Phase+I+trial+of+subcutaneous+interleukin-6+in+patients+with+advanced+malignancies.&rft.au=Weber%2C+J%3BYang%2C+J+C%3BTopalian%2C+S+L%3BParkinson%2C+D+R%3BSchwartzentruber%2C+D+S%3BEttinghausen%2C+S+E%3BGunn%2C+H%3BMixon%2C+A%3BKim%2C+H%3BCole%2C+D&rft.aulast=Weber&rft.aufirst=J&rft.date=1993-03-01&rft.volume=11&rft.issue=3&rft.spage=499&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=0732183X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-06 N1 - Date created - 1993-04-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Typhlitis resulting from treatment with taxol and doxorubicin in patients with metastatic breast cancer. AN - 75612948; 8095437 AB - Typhlitis is being recognized with increasing frequency as a serious complication of aggressive chemotherapy for hematologic and solid malignancies. In this report the authors describe two cases of typhlitis in patients with metastatic breast cancer treated with taxol and doxorubicin. Both cases occurred during the first cycle of treatment with taxol (180 mg/m2) and doxorubicin (75 mg/m2), being given simultaneously as 72-hour continuous intravenous infusions. Two cases of typhlitis have occurred after combined treatment with taxol and doxorubicin, while typhlitis has not been described after treatment with either drug alone. JF - Cancer AU - Pestalozzi, B C AU - Sotos, G A AU - Choyke, P L AU - Fisherman, J S AU - Cowan, K H AU - O'Shaughnessy, J A AD - Medicine Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/03/01/ PY - 1993 DA - 1993 Mar 01 SP - 1797 EP - 1800 VL - 71 IS - 5 SN - 0008-543X, 0008-543X KW - Doxorubicin KW - 80168379AG KW - Paclitaxel KW - P88XT4IS4D KW - Abridged Index Medicus KW - Index Medicus KW - Carcinoma, Intraductal, Noninfiltrating -- secretion KW - Lymphatic Metastasis KW - Humans KW - Carcinoma -- drug therapy KW - Inflammation -- chemically induced KW - Adult KW - Middle Aged KW - Carcinoma -- secretion KW - Female KW - Carcinoma, Intraductal, Noninfiltrating -- drug therapy KW - Paclitaxel -- administration & dosage KW - Breast Neoplasms -- drug therapy KW - Doxorubicin -- adverse effects KW - Paclitaxel -- adverse effects KW - Doxorubicin -- administration & dosage KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Cecal Diseases -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75612948?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=Typhlitis+resulting+from+treatment+with+taxol+and+doxorubicin+in+patients+with+metastatic+breast+cancer.&rft.au=Pestalozzi%2C+B+C%3BSotos%2C+G+A%3BChoyke%2C+P+L%3BFisherman%2C+J+S%3BCowan%2C+K+H%3BO%27Shaughnessy%2C+J+A&rft.aulast=Pestalozzi&rft.aufirst=B&rft.date=1993-03-01&rft.volume=71&rft.issue=5&rft.spage=1797&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-09 N1 - Date created - 1993-04-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Differential induction of apoptosis in undifferentiated and differentiated HL-60 cells by DNA topoisomerase I and II inhibitors. AN - 75610953; 8382972 AB - The effects of monocytic/macrophage and granulocytic differentiation induced by phorbol myristate acetate (TPA) and all-trans retinoic acid, respectively, were tested on the induction of apoptosis in human promyelocytic leukemia HL-60 cells treated with topoisomerase I and II inhibitors. Using a filter-binding assay, we observed a strong inhibition of DNA fragmentation induced by 3- and 24-hour continuous exposure to camptothecin, VP-16, VM-26, and m-AMSA in TPA-differentiated cells. The inhibition of the typical internucleosomal DNA fragmentation was confirmed by agarose gel electrophoresis. By contrast, drug-induced DNA fragmentation was not inhibited in retinoic acid-differentiated cells, and apoptosis occurred in these cells after 4 to 5 days in the absence of drug treatment. The TPA inhibitory effect was maximal after 24 hours of treatment and was correlated with differentiation, because phorbol dibutyrate ester was active, whereas 4-alpha-TPA, a nontumor promoter that does not induce differentiation, was not active. Using alkaline elution, we observed that TPA and retinoic acid differentiation were associated with changes in topoisomerase-mediated DNA breaks that were not correlated with their differential effects on drug-induced DNA fragmentation. Moreover, TPA also inhibited DNA fragmentation induced by vinblastine, cycloheximide, calphostin C, and x-rays. Using a cell-free system, we observed that DNA fragmentation was not inhibited in nuclei from TPA-differentiated cells. Rather, inhibition of apoptosis seemed to take place in the cytoplasm. We conclude that phenotypic changes associated with TPA-induced differentiation include inactivation of a cytoplasmic activity that can induce DNA fragmentation associated with apoptosis. JF - Blood AU - Solary, E AU - Bertrand, R AU - Kohn, K W AU - Pommier, Y AD - Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/03/01/ PY - 1993 DA - 1993 Mar 01 SP - 1359 EP - 1368 VL - 81 IS - 5 SN - 0006-4971, 0006-4971 KW - Topoisomerase I Inhibitors KW - 0 KW - Topoisomerase II Inhibitors KW - Amsacrine KW - 00DPD30SOY KW - Tretinoin KW - 5688UTC01R KW - Etoposide KW - 6PLQ3CP4P3 KW - DNA KW - 9007-49-2 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Camptothecin KW - XT3Z54Z28A KW - Abridged Index Medicus KW - Index Medicus KW - Etoposide -- pharmacology KW - Tretinoin -- pharmacology KW - Tumor Cells, Cultured KW - Camptothecin -- pharmacology KW - DNA Damage KW - Humans KW - DNA -- metabolism KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Cell Differentiation -- drug effects KW - Amsacrine -- pharmacology KW - DNA -- drug effects KW - Apoptosis -- drug effects KW - Leukemia, Promyelocytic, Acute -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75610953?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Blood&rft.atitle=Differential+induction+of+apoptosis+in+undifferentiated+and+differentiated+HL-60+cells+by+DNA+topoisomerase+I+and+II+inhibitors.&rft.au=Solary%2C+E%3BBertrand%2C+R%3BKohn%2C+K+W%3BPommier%2C+Y&rft.aulast=Solary&rft.aufirst=E&rft.date=1993-03-01&rft.volume=81&rft.issue=5&rft.spage=1359&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=00064971&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-06 N1 - Date created - 1993-04-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Tetralogy of Fallot, truncus arteriosus, abnormal myocardial architecture and anomalies of the aortic arch system induced by bis-diamine in rat fetuses. AN - 75610715; 8436760 AB - The aim of this study was to analyze the relation between anomalies of the heart and aortic arch arteries in near-term rat fetuses exposed to the chemical bis-diamine. Bis-diamine is known to induce cardiovascular anomalies. Bis-diamine was given orally to normal pregnant rats, and the 65 fetuses were examined under a dissecting microscope after formalin fixation. There were 26 rat fetuses (40%) with a ventricular septal defect in the perimembranous portion, of which 14 (22%) had tetralogy of Fallot, 4 (6%) had truncus arteriosus and 8 (12%) had a relatively small defect with no other major anomalies. In 44 fetuses (68%) the middle latitudinal muscle bundle of the ventricular septum was continuous with the right ventricular free wall. There were, isolated or in association, a double- or right aortic arch in 6 fetuses (9%), aberrant subclavian arteries in 9 (14%), right ductus arteriosus in 12 (18%) and agenetic ductus in 4 (6%). The cross-sectional area of the ductus, as corrected by that of the aortic isthmus, was abnormally small in 47 rats (72%). The rat fetuses with a septal defect or abnormal myocardial architecture, or both, usually had a small ductus; it was very small or absent in those fetuses with tetralogy of Fallot. Of the four fetuses with truncus arteriosus, two had a vestigial vasculature on the truncus root and three had a rudimentary infundibulum. The cardinal defect may be the anomalous and reduced development of the sixth arch arteries, which by imposing pressure overload on the fetal right ventricle, may have led to either or both the persistence of ventricular septal defect as a vent or the formation of myocardial architecture favorable for the generation of pressure in the right ventricle. JF - Journal of the American College of Cardiology AU - Kuribayashi, T AU - Roberts, W C AD - Pathology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 1993/03/01/ PY - 1993 DA - 1993 Mar 01 SP - 768 EP - 776 VL - 21 IS - 3 SN - 0735-1097, 0735-1097 KW - Diamines KW - 0 KW - bis(dichloroacetyl)diamine KW - Abridged Index Medicus KW - Index Medicus KW - Rats KW - Animals KW - Myocardium -- pathology KW - Rats, Wistar KW - Female KW - Pregnancy KW - Abnormalities, Drug-Induced -- pathology KW - Truncus Arteriosus, Persistent -- chemically induced KW - Tetralogy of Fallot -- chemically induced KW - Diamines -- adverse effects KW - Aorta, Thoracic -- abnormalities KW - Heart Defects, Congenital -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75610715?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+American+College+of+Cardiology&rft.atitle=Tetralogy+of+Fallot%2C+truncus+arteriosus%2C+abnormal+myocardial+architecture+and+anomalies+of+the+aortic+arch+system+induced+by+bis-diamine+in+rat+fetuses.&rft.au=Kuribayashi%2C+T%3BRoberts%2C+W+C&rft.aulast=Kuribayashi&rft.aufirst=T&rft.date=1993-03-01&rft.volume=21&rft.issue=3&rft.spage=768&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+American+College+of+Cardiology&rft.issn=07351097&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-22 N1 - Date created - 1993-03-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Calcium ions are required for cell fusion mediated by the CD4-human immunodeficiency virus type 1 envelope glycoprotein interaction. AN - 75607106; 8437234 AB - Calcium ions are required for fusion of a wide variety of artificial and biological membranes. To examine the role of calcium ions for cell fusion mediated by interactions between CD4 and the human immunodeficiency virus type 1 (HIV-1) envelope glycoprotein (gp120-gp41), we used two experimental systems: (i) cells expressing gp120-gp41 and its receptor CD4, both encoded by recombinant vaccinia viruses, and (ii) chronically infected cells producing low levels of HIV-1. Fusion was measured by counting the number of syncytia and by monitoring the redistribution of fluorescence dyes by video microscopy. Syncytia did not form in solutions without calcium ions. Addition of calcium ions partially restored the formation of syncytia. EDTA and EGTA [ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid] blocked syncytium formation in culture media containing calcium ions. Membrane fusion as monitored by fluorescence dye redistribution also required calcium ions. Cell fusion increased with an increase in calcium ion concentration from 100 microM to 10 mM but was not affected by magnesium ions in the concentration range from 0 to 30 mM. Fibrinogen and fibronectin did not promote fusion in the absence or presence of Ca2+. Binding of soluble CD4 to gp120-gp41-expressing cells was not affected by Ca2+ and Mg2+. We conclude that Ca2+ is involved in postbinding steps in cell fusion mediated by the CD4-HIV-1 envelope glycoprotein interaction. JF - Journal of virology AU - Dimitrov, D S AU - Broder, C C AU - Berger, E A AU - Blumenthal, R AD - Section on Membrane Structure and Function, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 1647 EP - 1652 VL - 67 IS - 3 SN - 0022-538X, 0022-538X KW - Antigens, CD4 KW - 0 KW - Azides KW - HIV Envelope Protein gp120 KW - HIV Envelope Protein gp41 KW - Viral Envelope Proteins KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Sodium Azide KW - 968JJ8C9DV KW - Cycloheximide KW - 98600C0908 KW - Magnesium KW - I38ZP9992A KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - AIDS/HIV KW - Membrane Fusion KW - Cycloheximide -- pharmacology KW - HIV Envelope Protein gp41 -- metabolism KW - Adenosine Triphosphate -- metabolism KW - Magnesium -- pharmacology KW - Azides -- pharmacology KW - HIV Envelope Protein gp120 -- metabolism KW - HIV-1 -- metabolism KW - Cell Fusion -- drug effects KW - Calcium -- pharmacology KW - Viral Envelope Proteins -- metabolism KW - Antigens, CD4 -- metabolism KW - Acquired Immunodeficiency Syndrome -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75607106?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Calcium+ions+are+required+for+cell+fusion+mediated+by+the+CD4-human+immunodeficiency+virus+type+1+envelope+glycoprotein+interaction.&rft.au=Dimitrov%2C+D+S%3BBroder%2C+C+C%3BBerger%2C+E+A%3BBlumenthal%2C+R&rft.aulast=Dimitrov&rft.aufirst=D&rft.date=1993-03-01&rft.volume=67&rft.issue=3&rft.spage=1647&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-23 N1 - Date created - 1993-03-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Biochim Biophys Acta. 1977 Mar 17;465(3):579-98 [13835] J Exp Med. 1991 Aug 1;174(2):407-15 [1713252] Science. 1984 May 4;224(4648):497-500 [6200935] Nature. 1984 Dec 20-1985 Jan 2;312(5996):767-8 [6083454] Proc Natl Acad Sci U S A. 1985 Feb;82(4):978-82 [2983337] Science. 1986 May 30;232(4754):1123-7 [3010463] Proc Natl Acad Sci U S A. 1991 Sep 15;88(18):8082-6 [1896455] AIDS Res Hum Retroviruses. 1991 Oct;7(10):799-805 [1742075] J Virol. 1992 Jan;66(1):132-8 [1727475] Virology. 1992 Feb;186(2):712-24 [1370739] AIDS. 1992 Mar;6(3):249-56 [1348943] AIDS Res Hum Retroviruses. 1992 Apr;8(4):513-20 [1599758] J Virol. 1992 Aug;66(8):4794-802 [1629956] Proc Natl Acad Sci U S A. 1992 Sep 1;89(17):8356-60 [1518869] J Virol. 1992 Oct;66(10):6208-12 [1527858] AIDS. 1992 Jun;6(6):533-9 [1388873] J Virol. 1993 Feb;67(2):913-26 [8419649] Nature. 1986 Jul 31-Aug 6;322(6078):470-4 [3016552] Cell. 1986 Nov 7;47(3):333-48 [3094962] Nature. 1986 Oct 23-29;323(6090):725-8 [3095663] J Immunol. 1990 Mar 15;144(6):2131-9 [1690235] J Virol. 1990 May;64(5):2149-56 [2109100] J Virol. 1990 May;64(5):2448-51 [2182912] J Bioenerg Biomembr. 1990 Apr;22(2):157-79 [2139437] AIDS. 1990 Jun;4(6):553-8 [1974767] Science. 1990 Nov 23;250(4984):1139-42 [2251501] J Virol. 1991 Jan;65(1):31-41 [1985202] Proc Natl Acad Sci U S A. 1991 Mar 15;88(6):2189-93 [2006155] J Immunol. 1991 Apr 15;146(8):2578-87 [1673142] J Virol. 1991 May;65(5):2402-7 [1850019] J Cell Biol. 1978 Aug;78(2):465-79 [211140] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Developmental appearance of pineal adrenergic-->guanosine 3',5'-monophosphate response is determined by a process down-stream from elevation of intracellular Ca2+: possible involvement of a diffusible factor. AN - 75605824; 8095011 AB - Adrenergic stimulation of the adult pineal gland increases cAMP and cGMP production by over 100-fold. beta-Adrenergic stimulation results in Gs alpha-mediated cyclase activation; alpha 1-adrenergic activation potentiates the beta-adrenergic effects through mechanisms mediated by the intracellular Ca2+ concentration ([Ca2+]i) and Ca(2+)-phospholipid-dependent protein kinase. Development analysis of these responses has indicated that the adrenergic stimulation of cAMP is present several days after birth, but the cGMP response develops only after the second week of life. In the study presented here, the adrenergic-->cGMP response was analyzed in pineal glands from 10- and 25-day-old rats, with the intention of determining the basis of the developmental appearance of this response. Organ culture and tissue homogenate studies indicated that guanylate cyclase activity, cGMP phosphodiesterase activity, and adrenergic elevation of phospholipase-A2 were similar in pineal glands from 10- and 25-day-old rats. Norepinephrine stimulated an increase in [Ca2+]i in dispersed pinealocytes from 10-day-old rats, as has been previously demonstrated in adult pinealocytes. In contrast, several treatments that elevate [Ca2+]i had no effect on cGMP accumulation in forskolin-treated or beta-adrenergically activated glands from 10-day-old rats, but were fully effective in similarly treated glands from 25-day-old rats. However, glands from 10-day-old animals showed a 33-fold accumulation of cGMP when they were cultured together with glands from 25-day-old rats. These studies indicate that whereas many elements in the system that mediate adrenergic regulation of pineal cGMP are fully developed at 10 days of age, the developmental appearance of the cGMP response is triggered by the development of a process down-stream of the alpha 1-adrenergic stimulation of [Ca2+]i, and this process may involve a diffusible factor. JF - Endocrinology AU - White, B H AU - Klein, D C AD - Section on Neuroendocrinology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 1026 EP - 1034 VL - 132 IS - 3 SN - 0013-7227, 0013-7227 KW - Colforsin KW - 1F7A44V6OU KW - Arachidonic Acid KW - 27YG812J1I KW - Cyclic AMP KW - E0399OZS9N KW - Protein Kinases KW - EC 2.7.- KW - Phospholipases A KW - EC 3.1.1.32 KW - Phospholipases A2 KW - EC 3.1.1.4 KW - 3',5'-Cyclic-GMP Phosphodiesterases KW - EC 3.1.4.35 KW - Guanylate Cyclase KW - EC 4.6.1.2 KW - Cyclic GMP KW - H2D2X058MU KW - Isoproterenol KW - L628TT009W KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Potassium KW - RWP5GA015D KW - Calcium KW - SY7Q814VUP KW - Norepinephrine KW - X4W3ENH1CV KW - Abridged Index Medicus KW - Index Medicus KW - Aging -- metabolism KW - Animals KW - Cell Membrane -- enzymology KW - Cytosol -- enzymology KW - 3',5'-Cyclic-GMP Phosphodiesterases -- metabolism KW - Mice KW - Arachidonic Acid -- metabolism KW - Isoproterenol -- pharmacology KW - Rats KW - Protein Kinases -- metabolism KW - Colforsin -- pharmacology KW - Cells, Cultured KW - Kinetics KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Potassium -- pharmacology KW - Organ Culture Techniques KW - Phospholipases A -- metabolism KW - Guanylate Cyclase -- metabolism KW - Calcium -- metabolism KW - Pineal Gland -- metabolism KW - Pineal Gland -- growth & development KW - Cyclic GMP -- metabolism KW - Norepinephrine -- pharmacology KW - Cyclic AMP -- metabolism KW - Adrenal Glands -- physiology KW - Pineal Gland -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75605824?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Endocrinology&rft.atitle=Developmental+appearance+of+pineal+adrenergic--%26gt%3Bguanosine+3%27%2C5%27-monophosphate+response+is+determined+by+a+process+down-stream+from+elevation+of+intracellular+Ca2%2B%3A+possible+involvement+of+a+diffusible+factor.&rft.au=White%2C+B+H%3BKlein%2C+D+C&rft.aulast=White&rft.aufirst=B&rft.date=1993-03-01&rft.volume=132&rft.issue=3&rft.spage=1026&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=00137227&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-01 N1 - Date created - 1993-04-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Development of lipophilic anticancer agents for the treatment of brain tumors by the esterification of water-soluble chlorambucil. AN - 75601336; 8444006 AB - The lipophilic derivatives of the anticancer alkylating agent chlorambucil, chlorambucil-methyl, -isopropyl and -tertiary butyl esters, were synthesized and administered i.v. to anesthetized rats. Plasma and brain concentrations of these agents and of their active metabolites, chlorambucil and phenylacetic mustard, then were determined by high-performance liquid chromatography between 5 and 60 min. Whereas large amounts of chlorambucil-tertiary butyl ester entered and were maintained in brain, lower amounts of chlorambucil-isopropyl ester and no chlorambucil-methyl ester were found in brain. The comparative brain/plasma concentration-time integral ratios of the total active agents generated from chlorambucil-tertiary butyl, -isopropyl and -methyl esters were 0.85, 0.12 and 0.06, respectively, compared to a ratio of 0.02 for chlorambucil. In vitro alkylating activity of each ester was compared to that of equimolar chlorambucil, by reaction with 4-(p-nitrobenzyl)pyridine. Each ester possessed high intrinsic alkylating activity, equal to 38.4, 57.0 and 69.9% of chlorambucil activity, for the -tertiary butyl, -isopropyl and -methyl esters, respectively. Therefore each is an active antineoplastic agent irrespective of whether or not chlorambucil is regenerated. The rates of ester hydrolysis of these derivatives to chlorambucil were measured in fresh rat blood and in liver and brain homogenates at 37 degrees C. Chlorambucil-methyl and -isopropyl esters were hydrolysed quickly within 30 s in blood and liver, whereas chlorambucil-tertiary butyl ester was more stable with half-lives of approximately 7 h and 2 h, respectively. All proved to be relatively stable in brain homogenate. Steric hindrance around the ester linkage of chlorambucil-tertiary butyl ester reduces its affinity to and rate of hydrolysis by plasma and liver esterases, and allows it to accumulate within the brain. Chlorambucil-tertiary butyl ester maintains high levels in brain despite rapidly declining plasma concentrations and, due to these favorable pharmacokinetics and to its intrinsic anticancer activity, it possess promising characteristics for the treatment of malignant brain tumors. JF - Clinical & experimental metastasis AU - Genka, S AU - Deutsch, J AU - Shetty, U H AU - Stahle, P L AU - John, V AU - Lieberburg, I M AU - Ali-Osman, F AU - Rapoport, S I AU - Greig, N H AD - Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 131 EP - 140 VL - 11 IS - 2 SN - 0262-0898, 0262-0898 KW - Alkylating Agents KW - 0 KW - Antineoplastic Agents KW - Esters KW - Nitrogen Mustard Compounds KW - phenacid KW - 10477-72-2 KW - Chlorambucil KW - 18D0SL7309 KW - Index Medicus KW - Animals KW - Drug Stability KW - Esters -- pharmacokinetics KW - Solubility KW - Injections, Intravenous KW - Blood-Brain Barrier -- physiology KW - Brain -- metabolism KW - Alkylating Agents -- pharmacokinetics KW - Esters -- metabolism KW - Rats KW - Esters -- chemical synthesis KW - Rats, Wistar KW - Nitrogen Mustard Compounds -- pharmacokinetics KW - Female KW - Brain Neoplasms -- drug therapy KW - Antineoplastic Agents -- pharmacokinetics KW - Brain Neoplasms -- metabolism KW - Chlorambucil -- pharmacology KW - Antineoplastic Agents -- chemical synthesis KW - Chlorambucil -- pharmacokinetics KW - Antineoplastic Agents -- pharmacology KW - Chlorambucil -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75601336?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+%26+experimental+metastasis&rft.atitle=Development+of+lipophilic+anticancer+agents+for+the+treatment+of+brain+tumors+by+the+esterification+of+water-soluble+chlorambucil.&rft.au=Genka%2C+S%3BDeutsch%2C+J%3BShetty%2C+U+H%3BStahle%2C+P+L%3BJohn%2C+V%3BLieberburg%2C+I+M%3BAli-Osman%2C+F%3BRapoport%2C+S+I%3BGreig%2C+N+H&rft.aulast=Genka&rft.aufirst=S&rft.date=1993-03-01&rft.volume=11&rft.issue=2&rft.spage=131&rft.isbn=&rft.btitle=&rft.title=Clinical+%26+experimental+metastasis&rft.issn=02620898&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-07 N1 - Date created - 1993-04-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Translation of equine infectious anemia virus bicistronic tat-rev mRNA requires leaky ribosome scanning of the tat CTG initiation codon. AN - 75598003; 8382305 AB - We have examined the translational regulation of the equine infectious anemia virus (EIAV) bicistronic tat-rev mRNA. Site-directed mutagenesis of the tat leader region followed by expression of the tat-rev cDNA both in vitro and in transiently transfected cells established that tat translation is initiated exclusively at a CTG codon. Increasing the efficiency of tat translation by altering the CTG initiator to ATG resulted in a dramatic decrease in translation of the downstream (rev) cistron, indicating that leaky scanning of the tat CTG initiation codon permitted translation of the downstream rev cistron. Since the tat leader sequences precede the major EIAV splice donor and are therefore present at the 5' termini of both spliced and unspliced viral mRNAs, the expression of all EIAV structural and regulatory proteins is dependent on leaky scanning of the tat initiator. JF - Journal of virology AU - Carroll, R AU - Derse, D AD - Laboratory of Viral Carcinogenesis, National Cancer Institute-Frederick Cancer Research Center, Maryland 21702-1201. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 1433 EP - 1440 VL - 67 IS - 3 SN - 0022-538X, 0022-538X KW - rev KW - tat KW - Codon KW - 0 KW - DNA, Recombinant KW - RNA, Messenger KW - RNA, Viral KW - Viral Structural Proteins KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Index Medicus KW - AIDS/HIV KW - Peptide Chain Initiation, Translational KW - Genes, rev -- genetics KW - Transcription, Genetic KW - Amino Acid Sequence KW - Precipitin Tests KW - Genes, tat -- genetics KW - Transcriptional Activation KW - Mutagenesis, Site-Directed KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Base Sequence KW - RNA, Messenger -- metabolism KW - Transfection KW - Genetic Vectors KW - Molecular Sequence Data KW - RNA, Viral -- metabolism KW - Cell-Free System KW - Protein Biosynthesis KW - Gene Expression Regulation, Viral KW - Genes, Viral -- genetics KW - Infectious Anemia Virus, Equine -- genetics KW - Viral Structural Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75598003?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Translation+of+equine+infectious+anemia+virus+bicistronic+tat-rev+mRNA+requires+leaky+ribosome+scanning+of+the+tat+CTG+initiation+codon.&rft.au=Carroll%2C+R%3BDerse%2C+D&rft.aulast=Carroll&rft.aufirst=R&rft.date=1993-03-01&rft.volume=67&rft.issue=3&rft.spage=1433&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-23 N1 - Date created - 1993-03-23 N1 - Date revised - 2017-01-13 N1 - Gene symbol - rev; tat N1 - SuppNotes - Cited By: Virology. 1973 Apr;52(2):456-67 [4705382] Rev Infect Dis. 1985 Jan-Feb;7(1):83-8 [2984759] Proc Natl Acad Sci U S A. 1985 Dec;82(23):7919-23 [2999784] Cell. 1986 Jan 31;44(2):283-92 [3943125] Science. 1986 Feb 7;231(4738):589-94 [3003905] J Virol. 1986 Nov;60(2):394-9 [3021974] Cell. 1986 Nov 21;47(4):481-3 [3779834] Mol Cell Biol. 1986 Jul;6(7):2695-703 [3023945] Mol Cell Biol. 1986 Jul;6(7):2704-11 [3023946] Virology. 1986 Dec;155(2):309-21 [2431539] Virology. 1987 Jun;158(2):300-12 [3035786] J Biol Chem. 1987 Aug 25;262(24):11847-51 [3040720] Mol Cell Biol. 1987 Oct;7(10):3438-45 [3683388] Mol Cell Biol. 1989 Nov;9(11):5073-80 [2601709] Nature. 1990 Feb 15;343(6259):662-5 [2406607] J Virol. 1990 Apr;64(4):1616-24 [2157047] J Virol. 1990 Apr;64(4):1839-43 [2157066] Virology. 1990 May;176(1):280-8 [2158694] J Virol. 1990 Jun;64(6):2519-29 [2335812] J Virol. 1990 Aug;64(8):3716-25 [2164593] J Biol Chem. 1990 Sep 25;265(27):16491-7 [2168892] Proc Natl Acad Sci U S A. 1990 Nov;87(21):8301-5 [2236042] J Virol. 1990 Dec;64(12):6319-24 [2173797] Genes Dev. 1990 Sep;4(9):1560-72 [2174810] J Biol Chem. 1990 Dec 15;265(35):21714-9 [2123874] Mol Cell Biol. 1991 Jan;11(1):573-7 [1986249] EMBO J. 1991 Mar;10(3):655-64 [1825810] Trends Biochem Sci. 1990 Dec;15(12):477-83 [2077688] J Virol. 1991 Jul;65(7):3460-7 [1645777] J Virol. 1991 Jul;65(7):3468-74 [1645778] Virology. 1991 Oct;184(2):521-30 [1653485] J Virol. 1991 Nov;65(11):5886-94 [1656077] J Virol. 1991 Nov;65(11):5895-901 [1656078] J Biol Chem. 1991 Oct 25;266(30):19867-70 [1939050] J Virol. 1991 Dec;65(12):7012-5 [1658392] J Cell Biol. 1991 Nov;115(4):887-903 [1955461] Mol Cell Biol. 1992 Jan;12(1):207-19 [1729599] J Virol. 1992 Mar;66(3):1765-8 [1310778] J Virol. 1992 Jun;66(6):3455-65 [1316461] Anal Biochem. 1987 Nov 1;166(2):368-79 [2449095] Cell. 1988 Jan 29;52(2):185-95 [3277717] EMBO J. 1988 Jan;7(1):245-51 [2834203] J Virol. 1988 Aug;62(8):2636-43 [2839690] Nature. 1988 Jul 28;334(6180):320-5 [2839775] J Virol. 1988 Sep;62(9):3522-6 [2841502] J Virol. 1988 Dec;62(12):4486-92 [2846865] J Cell Biol. 1989 Feb;108(2):229-41 [2645293] J Biol Chem. 1989 Mar 25;264(9):5031-5 [2538469] J Mol Biol. 1989 Jan 20;205(2):363-72 [2538626] Proc Natl Acad Sci U S A. 1989 Mar;86(6):1836-40 [2538817] Proc Natl Acad Sci U S A. 1989 Jun;86(11):3978-81 [2726761] Gene. 1989 Apr 15;77(1):51-9 [2744487] J Virol. 1990 Jan;64(1):86-95 [2152836] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The woodchuck hepatitis virus X gene is important for establishment of virus infection in woodchucks. AN - 75597746; 8437213 AB - All mammalian hepadnaviruses possess a gene, termed X, that encodes a protein capable of transactivating virus gene expression. The X gene overlaps the polymerase and precore genes as well as two newly identified open reading frames (ORFs) termed ORF5 and ORF6. In this investigation, we examined whether ORF5, ORF6, and the X gene were important for the replication of woodchuck hepatitis virus (WHV) in susceptible woodchucks. First, we investigated whether proteins were produced from ORF5 and ORF6 by in vitro translation of appropriate viral transcripts, searched for antibodies against the putative proteins in the sera of animals infected with wild-type virus, and looked for an antisense WHV transcript, necessary for expression of a protein from ORF6, in the livers of acutely or chronically infected woodchucks. All such experiments yielded negative results. Next, we used oligonucleotide-directed mutagenesis to introduce termination codons into ORF5 and ORF6 at two locations within each ORF. Adult woodchucks in groups of three were transfected with one of the four mutant genomes. All of these woodchucks developed WHV infections that were indistinguishable from those of animals transfected with the wild-type WHV recombinant. Polymerase chain reaction amplification and direct DNA sequencing confirmed that reversion of the mutants to a wild-type genotype did not occur. Taken together, these data indicate that ORF5 and ORF6 are not essential for virus replication and are unlikely to represent authentic genes. Finally, we generated five WHV X-gene mutants that either removed the initiation codon for protein synthesis or truncated the carboxyl terminus of the protein by 3, 16, 31, or 52 amino acids. Groups of three adult woodchucks were transfected with one of the five X-gene mutants. Only the mutant that possessed an X gene lacking 3 amino acids from the carboxyl terminus was capable of replication within the 6-month time frame of the experiment. In contrast, all seven woodchucks transfected with wild-type WHV DNA developed markers consistent with viral infection. Thus, it is likely (P < 0.01) that the WHV X gene is important for virus replication in the natural host. JF - Journal of virology AU - Chen, H S AU - Kaneko, S AU - Girones, R AU - Anderson, R W AU - Hornbuckle, W E AU - Tennant, B C AU - Cote, P J AU - Gerin, J L AU - Purcell, R H AU - Miller, R H AD - Hepatitis Viruses Section, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 1218 EP - 1226 VL - 67 IS - 3 SN - 0022-538X, 0022-538X KW - Antibodies, Viral KW - 0 KW - Biomarkers KW - RNA Precursors KW - RNA, Antisense KW - Viral Proteins KW - Index Medicus KW - Animals KW - Protein Biosynthesis KW - Transcription, Genetic KW - Amino Acid Sequence KW - Genome, Viral KW - RNA, Antisense -- analysis KW - Virulence KW - Antibodies, Viral -- blood KW - Mutagenesis, Site-Directed KW - Animals, Newborn KW - Transfection KW - Molecular Sequence Data KW - Time Factors KW - RNA Precursors -- genetics KW - Open Reading Frames -- genetics KW - Liver -- microbiology KW - Immunoassay KW - Viral Proteins -- genetics KW - Marmota -- microbiology KW - Hepatitis B virus -- pathogenicity KW - Hepatitis, Viral, Animal -- genetics KW - Genes, Viral -- genetics KW - Hepatitis B virus -- growth & development KW - Viral Proteins -- biosynthesis KW - Hepatitis B virus -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75597746?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=The+woodchuck+hepatitis+virus+X+gene+is+important+for+establishment+of+virus+infection+in+woodchucks.&rft.au=Chen%2C+H+S%3BKaneko%2C+S%3BGirones%2C+R%3BAnderson%2C+R+W%3BHornbuckle%2C+W+E%3BTennant%2C+B+C%3BCote%2C+P+J%3BGerin%2C+J+L%3BPurcell%2C+R+H%3BMiller%2C+R+H&rft.aulast=Chen&rft.aufirst=H&rft.date=1993-03-01&rft.volume=67&rft.issue=3&rft.spage=1218&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-23 N1 - Date created - 1993-03-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: EMBO J. 1985 Jun;4(6):1507-14 [4029122] J Virol. 1990 Jun;64(6):3082-6 [2335828] Proc Natl Acad Sci U S A. 1978 Sep;75(9):4533-7 [212758] Proc Natl Acad Sci U S A. 1980 May;77(5):2941-5 [6930677] J Virol. 1980 Dec;36(3):829-36 [7463557] J Clin Microbiol. 1982 Mar;15(3):484-90 [7076821] Cell. 1982 Jun;29(2):403-15 [6180831] Anal Biochem. 1983 Jul 1;132(1):6-13 [6312838] J Virol. 1984 Mar;49(3):701-8 [6199511] Virology. 1984 Sep;137(2):390-9 [6485254] Virology. 1984 Nov;139(1):64-72 [6495660] J Infect Dis. 1985 Jun;151(6):1081-92 [2987366] Virus Res. 1985 Jun;2(4):301-15 [4036315] Proc Natl Acad Sci U S A. 1986 Apr;83(7):2233-7 [3457384] Intervirology. 1986;25(1):14-29 [3516924] Proc Natl Acad Sci U S A. 1986 Apr;83(8):2531-5 [3458214] Hepatology. 1987 Jan-Feb;7(1 Suppl):64S-73S [3804216] Nucleic Acids Res. 1986 Dec 22;14(24):9679-98 [3027659] Proc Natl Acad Sci U S A. 1987 May;84(9):2678-82 [3033659] Annu Rev Biochem. 1987;56:651-93 [3039907] J Virol. 1987 Nov;61(11):3448-53 [2822953] J Virol. 1988 Feb;62(2):427-34 [2826805] Science. 1988 Mar 18;239(4846):1420-2 [3347840] Virology. 1988 May;164(1):147-55 [2452512] J Virol. 1988 Oct;62(10):3832-9 [3418788] J Virol. 1988 Nov;62(11):3979-84 [2459409] Hepatology. 1989 Feb;9(2):322-7 [2643549] EMBO J. 1990 Jun;9(6):1889-95 [2347309] Oncogene. 1988 Nov;3(5):545-52 [2856254] Virology. 1990 Jul;177(1):406-10 [2191500] Proc Natl Acad Sci U S A. 1990 Aug;87(15):5628-32 [2165598] Cell. 1990 Nov 16;63(4):687-95 [2225072] Gastroenterol Jpn. 1990 Sep;25 Suppl 2:1-5 [2227261] Gastroenterol Jpn. 1990 Sep;25 Suppl 2:20-2 [2227263] Proc Natl Acad Sci U S A. 1990 Dec;87(23):9329-32 [2251274] Jpn J Cancer Res. 1990 Dec;81(12):1191-4 [2125986] Virology. 1991 Jun;182(2):841-5 [2024502] Science. 1991 May 10;252(5007):842-4 [1827531] Hepatology. 1991 Jul;14(1):29-37 [1712339] Cancer Res. 1991 Sep 15;51(18):4971-7 [1654208] J Virol. 1992 Feb;66(2):1223-7 [1731101] Oncogene. 1992 Mar;7(3):397-403 [1549357] J Med Virol. 1992 Feb;36(2):101-17 [1583465] J Virol. 1992 Jul;66(7):4382-9 [1318408] JAMA. 1965 Feb 15;191:541-6 [14239025] J Virol. 1989 Mar;63(3):1360-70 [2915383] FEBS Lett. 1989 Jan 30;243(2):115-8 [2465182] Nucleic Acids Res. 1989 Feb 11;17(3):1266 [2922271] Proc Natl Acad Sci U S A. 1989 Mar;86(6):1846-9 [2928306] Proc Natl Acad Sci U S A. 1989 Mar;86(6):2046-50 [2538828] Virology. 1989 Apr;169(2):479-84 [2705309] J Virol. 1989 Sep;63(9):4019-26 [2788226] J Clin Microbiol. 1989 Sep;27(9):1930-3 [2778059] Virology. 1989 Dec;173(2):764-6 [2596037] Mol Biol Med. 1989 Apr;6(2):151-60 [2615644] Cancer Detect Prev. 1989;14(2):227-9 [2695243] EMBO J. 1990 Feb;9(2):497-504 [2303039] Nature. 1990 Mar 1;344(6261):72-4 [2154703] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Induction of micronuclei by HTLV-I Tax: a cellular assay for function. AN - 75597679; 8438579 AB - Cellular chromosomal damage is ubiquitously seen in HTLV-I-transformed lymphocytes. It is also characteristic of cells that have been exposed to mutagens. A sensitive measurement for mutagen-induced DNA damage is the formation of micronuclei in treated cells. Because current evidence suggests that HTLV-I Tax is etiologically linked to transformation, we tested for its activity in inducing micronuclei. We show here that transfection into cells of a Tax-producing plasmid rapidly induced the formation of micronuclei. This effect cooperated with that of a mutagen (mitomycin C) and was correlated with the inherent trans-activation capacity of Tax. These findings suggest that a commonly used mutagen assay could be a quick biological test for putatively oncogenic proteins. JF - Virology AU - Majone, F AU - Semmes, O J AU - Jeang, K T AD - Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 456 EP - 459 VL - 193 IS - 1 SN - 0042-6822, 0042-6822 KW - Gene Products, tax KW - 0 KW - Index Medicus KW - AIDS/HIV KW - Cell Transformation, Viral -- physiology KW - Cytopathogenic Effect, Viral KW - Lymphocytes -- ultrastructure KW - Lymphocytes -- microbiology KW - Cell Line KW - Human T-lymphotropic virus 1 -- physiology KW - Micronuclei, Chromosome-Defective -- microbiology KW - Gene Products, tax -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75597679?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Virology&rft.atitle=Induction+of+micronuclei+by+HTLV-I+Tax%3A+a+cellular+assay+for+function.&rft.au=Majone%2C+F%3BSemmes%2C+O+J%3BJeang%2C+K+T&rft.aulast=Majone&rft.aufirst=F&rft.date=1993-03-01&rft.volume=193&rft.issue=1&rft.spage=456&rft.isbn=&rft.btitle=&rft.title=Virology&rft.issn=00426822&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-23 N1 - Date created - 1993-03-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Strontium induces murine keratinocyte differentiation in vitro in the presence of serum and calcium. AN - 75592651; 7679679 AB - Primary mouse keratinocytes in culture are induced to terminally differentiate by increasing extracellular Ca2+ concentrations (Cao) from 0.05 mM to > or = 0.1 mM. The addition of Sr2+ (> or = 2.5 mM) to medium containing 0.05 mM Ca2+ induces focal stratification and terminal differentiation, which are similar to that found after increasing the Cao to 0.12 mM. Sr2+ in 0.05 mM Ca2+ medium induces the expression of the differentiation-specific keratins, keratin 1 (K1), keratin 10 (K10), and the granular cell marker, filaggrin, as determined by both immunoblotting and immunofluorescence. Sr2+ induces the expression of those differentiation markers in a dose dependent manner, with an optimal concentration of 5 mM. In the absence of Ca2+ in the medium, the Sr2+ effects are reduced, and Sr2+ is ineffective when both Ca2+ and serum are deleted from the medium. Sr2+ treatment increases the ratio of fluorescence intensity of the intracellular Ca2+ sensitive probe, fura-2, indicating an associated rise in the level of intracellular free Ca2+ and/or Sr2+. At doses sufficient to induce differentiation, Sr2+ also increases the level of inositol phosphates in primary keratinocytes within 30 min. The uptake curves of 85Sr2+ by primary keratinocytes are similar to those of 45Ca2+. At low concentrations, the initial uptake of both 45Ca2+ and 85Sr2+ reaches a plateau within 1 hr; at higher concentrations, the uptake of both 45Ca2+ and 85Sr2+ increases continuously for 12 hr. In keratinocytes pre-equilibrated with 45Ca2+ in 0.05 mM Ca2+ medium, Sr2+ causes an increase of 45Ca2+ uptake, which is dependent on the presence of serum. These results suggest that Sr2+ utilizes the same signalling pathway as Ca2+ to induce keratinocyte terminal differentiation and that Ca2+ may be required to exert these effects. JF - Journal of cellular physiology AU - Li, L AU - Kruszewski, F H AU - Punnonen, K AU - Tucker, R W AU - Yuspa, S H AU - Hennings, H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 643 EP - 653 VL - 154 IS - 3 SN - 0021-9541, 0021-9541 KW - Culture Media KW - 0 KW - Intermediate Filament Proteins KW - filaggrin KW - Keratins KW - 68238-35-7 KW - Calcium KW - SY7Q814VUP KW - Strontium KW - YZS2RPE8LE KW - Index Medicus KW - Blood KW - Animals KW - Intermediate Filament Proteins -- biosynthesis KW - Cells, Cultured KW - Second Messenger Systems -- drug effects KW - Cell Division -- drug effects KW - Mice KW - Cell Membrane -- metabolism KW - Cell Differentiation -- drug effects KW - Keratins -- biosynthesis KW - Keratinocytes -- drug effects KW - Keratinocytes -- cytology KW - Keratinocytes -- metabolism KW - Calcium -- pharmacology KW - Strontium -- metabolism KW - Strontium -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75592651?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+cellular+physiology&rft.atitle=Strontium+induces+murine+keratinocyte+differentiation+in+vitro+in+the+presence+of+serum+and+calcium.&rft.au=Li%2C+L%3BKruszewski%2C+F+H%3BPunnonen%2C+K%3BTucker%2C+R+W%3BYuspa%2C+S+H%3BHennings%2C+H&rft.aulast=Li&rft.aufirst=L&rft.date=1993-03-01&rft.volume=154&rft.issue=3&rft.spage=643&rft.isbn=&rft.btitle=&rft.title=Journal+of+cellular+physiology&rft.issn=00219541&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-23 N1 - Date created - 1993-03-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Mouse differentiation-specific keratins 1 and 10 require a preexisting keratin scaffold to form a filament network. AN - 75588684; 7679677 AB - Keratins 1 (K1) and 10 (K10) are the predominant cytoskeletal intermediate filaments of epidermal cells during transition from the proliferative to the terminal differentiation stage. In situ, formation of the K1/K10 intermediate filament network occurs in the cytoplasm of cells with a preexisting cytoskeleton composed of keratins 5 and 14. To define cytoskeletal interactions permissive for formation of the K1/K10 filamentous network, active copies of mouse K1 and K10 genes were introduced into fibroblasts (NIH 3T3) which do not normally express these proteins. Transient and stable transfectants, as well as heterokaryons produced by fusions with epithelial cells, were evaluated for expression of K1 and K10 proteins and filament formation using specific antibodies. In contrast to keratin pairs K5/K14 and K8/K18, the K1/K10 pair failed to form an extensive keratin filament network on its own, although small isolated dense K1/K10 filament bundles were observed throughout the cytoplasm by EM. K1 and K10 filaments integrated only into the preexisting K5/K14 network upon fusion of the NIH 3T3 (K1/K10) cells with epithelial cells expressing endogenous K5/K14 or with NIH 3T3 cells which were transfected with active copies of the K5 and K14 genes. When combinations of active recombinant gene constructs for keratins 1, 5, 10, and 14 were tested in transient NIH 3T3 transfections, the most intact cytokeratin network observed by immunofluorescence was formed by the K5/K14 pair. The K1/K14 pair was capable of forming a cytoskeletal network, but the network was poorly developed, and usually perinuclear. Transfection of K10 in combination with K5 or K1 resulted in cytoplasmic agglomerates, but not a cytoskeleton. These results suggest that the formation of the suprabasal cytoskeleton in epidermis is dependent on the preexisting basal cell intermediate filament network. Furthermore, restrictions on filament formation appear to be more stringent for K10 than for K1. JF - The Journal of cell biology AU - Kartasova, T AU - Roop, D R AU - Holbrook, K A AU - Yuspa, S H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 1251 EP - 1261 VL - 120 IS - 5 SN - 0021-9525, 0021-9525 KW - Keratins KW - 68238-35-7 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - 3T3 Cells KW - Blotting, Western KW - Cell Fusion KW - Transfection KW - In Vitro Techniques KW - DNA -- genetics KW - Gene Expression KW - Cell Differentiation KW - Microscopy, Electron KW - Mice KW - Fluorescent Antibody Technique KW - Epidermis -- ultrastructure KW - Keratins -- physiology KW - Keratinocytes -- ultrastructure KW - Keratins -- chemistry KW - Intermediate Filaments -- ultrastructure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75588684?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+cell+biology&rft.atitle=Mouse+differentiation-specific+keratins+1+and+10+require+a+preexisting+keratin+scaffold+to+form+a+filament+network.&rft.au=Kartasova%2C+T%3BRoop%2C+D+R%3BHolbrook%2C+K+A%3BYuspa%2C+S+H&rft.aulast=Kartasova&rft.aufirst=T&rft.date=1993-03-01&rft.volume=120&rft.issue=5&rft.spage=1251&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+cell+biology&rft.issn=00219525&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-23 N1 - Date created - 1993-03-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Exp Cell Res. 1988 Dec;179(2):352-61 [2461310] Annu Rev Biochem. 1988;57:593-625 [3052284] Mol Cell Biol. 1989 Mar;9(3):1376-80 [2725504] Mol Cell Biol. 1989 Apr;9(4):1553-65 [2471065] Mol Carcinog. 1988;1(2):134-43 [2475137] Mol Cell Biol. 1989 Sep;9(9):3685-97 [2476664] Exp Cell Res. 1990 Apr;187(2):234-42 [1690663] J Biol Chem. 1990 May 25;265(15):8766-74 [1692836] Cell. 1990 Aug 24;62(4):681-96 [1696851] J Cell Biol. 1990 Dec;111(6 Pt 2):3049-64 [1702787] Cell. 1991 Jan 25;64(2):365-80 [1703046] J Cell Biol. 1991 May;113(4):843-55 [1709167] J Invest Dermatol. 1991 Aug;97(2):354-63 [1712823] J Cell Biol. 1991 Dec;115(5):1293-307 [1720124] J Cell Biol. 1963 Apr;17:208-12 [13986422] Virology. 1973 Aug;54(2):536-9 [4737663] Annu Rev Genet. 1975;9:407-86 [1108769] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Nature. 1979 Jan 11;277(5692):108-14 [215915] Proc Natl Acad Sci U S A. 1978 Oct;75(10):5034-8 [368806] Cell. 1980 Jan;19(1):245-54 [6153576] Cell. 1980 Apr;19(4):1033-42 [6155214] Nature. 1981 Sep 3;293(5827):72-4 [6791032] Methods Cell Biol. 1982;24:399-419 [6178945] Cell. 1982 Sep;30(2):361-72 [6183000] Proc Natl Acad Sci U S A. 1983 Feb;80(3):716-20 [6187003] Cell. 1983 Apr;32(4):1125-37 [6188536] Nature. 1983 Apr 28;302(5911):794-800 [6188955] Curr Probl Dermatol. 1983;11:277-91 [6197247] Cell. 1984 Apr;36(4):813-25 [6200235] EMBO J. 1982;1(2):161-5 [6201355] J Cell Biol. 1984 Apr;98(4):1388-96 [6201491] J Biol Chem. 1984 Jul 10;259(13):8037-40 [6203901] Proc Natl Acad Sci U S A. 1985 Mar;82(6):1609-13 [2580298] J Biol Chem. 1985 Jun 10;260(11):7142-9 [2581964] Nucleic Acids Res. 1985 Mar 11;13(5):1431-42 [2987824] J Cell Biol. 1985 Nov;101(5 Pt 1):1826-41 [2414304] J Cell Biol. 1986 May;102(5):1767-77 [2422179] EMBO J. 1986 Jun;5(6):1367-71 [3015602] Cell. 1987 Feb 13;48(3):453-63 [2433047] J Cell Biol. 1987 Aug;105(2):791-806 [2442174] Cancer Res. 1988 Jun 1;48(11):3245-52 [2452688] J Cell Biol. 1989 Apr;108(4):1477-93 [2466849] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - c-Ets-1 protein is hyperphosphorylated during mitosis. AN - 75588209; 8437861 AB - The ets-1 and ets-2 proto-oncogene products can serve as transcription factors and become phosphorylated in response to Ca(2+)-mediated signals. We have examined expression of Ets proteins during the cell cycle in cells synchronized by centrifugal elutriation or nocodazole-induced mitotic block. Both methods revealed the presence of a hyperphosphorylated isoform of Ets-1 during the mitotic phase. This isoform showed a characteristic mobility shift and was observed during mitosis in each of four cell lines (three human T-cell lines and a human astrocytoma) that express ets-1. In elutriated cells, only a small portion of the Ets-1 in cells from the G2/M fractions was hyperphosphorylated, while in nocodazole-arrested cells more of the Ets-1 was shifted. When cells were released from nocodazole arrest, this isoform disappeared within 1-2 h as cells completed mitosis and entered G1. This suggests that hyperphosphorylated Ets-1 is present transiently during early mitosis, before or around the time of the metaphase-anaphase transition. Exposure of unsynchronized cells to okadaic acid resulted in a dramatic hyperphosphorylation of virtually all Ets-1, suggesting that changes in cellular phosphatase activity are important for cell cycle regulation of Ets-1. Hyperphosphorylated Ets-1 appears to arise from multiple phosphorylations on serine in the exon 7-encoded domain of the protein and did not appear to alter sequence-specific DNA-binding activity. Although enhanced phosphorylation of Ets-2 was detected in nocodazole-arrested cells, no Ets-2 hyperphosphorylation was seen. JF - Oncogene AU - Fleischman, L F AU - Pilaro, A M AU - Murakami, K AU - Kondoh, A AU - Fisher, R J AU - Papas, T S AD - Laboratory of Molecular Oncology, National Cancer Institute, Frederick, Maryland 21702-1201. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 771 EP - 780 VL - 8 IS - 3 SN - 0950-9232, 0950-9232 KW - DNA-Binding Proteins KW - 0 KW - ERF protein, human KW - ETS1 protein, human KW - ETS2 protein, human KW - Ethers, Cyclic KW - Proto-Oncogene Protein c-ets-1 KW - Proto-Oncogene Protein c-ets-2 KW - Proto-Oncogene Proteins KW - Proto-Oncogene Proteins c-ets KW - Repressor Proteins KW - Trans-Activators KW - Transcription Factors KW - Okadaic Acid KW - 1W21G5Q4N2 KW - DNA KW - 9007-49-2 KW - Nocodazole KW - SH1WY3R615 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - DNA -- metabolism KW - Humans KW - Amino Acid Sequence KW - Ethers, Cyclic -- pharmacology KW - Nocodazole -- pharmacology KW - Base Sequence KW - Phosphorylation KW - Calcium -- physiology KW - Molecular Sequence Data KW - Cell Line KW - Transcription Factors -- metabolism KW - Mitosis KW - Proto-Oncogene Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75588209?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncogene&rft.atitle=c-Ets-1+protein+is+hyperphosphorylated+during+mitosis.&rft.au=Fleischman%2C+L+F%3BPilaro%2C+A+M%3BMurakami%2C+K%3BKondoh%2C+A%3BFisher%2C+R+J%3BPapas%2C+T+S&rft.aulast=Fleischman&rft.aufirst=L&rft.date=1993-03-01&rft.volume=8&rft.issue=3&rft.spage=771&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=09509232&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-25 N1 - Date created - 1993-03-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Sustained depletion of cortical and hippocampal serotonin and norepinephrine but not striatal dopamine by 1-methyl-4-(2'-aminophenyl)-1,2,3,6-tetrahydropyridine (2'-NH2-MPTP): a comparative study with 2'-CH3-MPTP and MPTP. AN - 75585808; 8094744 AB - Unlike 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), which produces consistent decreases in levels of striatal dopamine (DA) with considerably smaller and more variable effects on mouse brain levels of serotonin (5-HT) and norepinephrine (NE), a novel amine-substituted MPTP analogue, 1-methyl-4-(2'-aminophenyl)-1,2,3,6-tetrahydropyridine (2'-NH2-MPTP), administered in a standard mouse dosing paradigm for MPTP (20 mg/kg x 4) did not affect striatal DA but led to marked reductions (60-70%) in levels of 5-HT, 5-hydroxyindoleacetic acid (5-HIAA), and NE measured in frontal cortex and hippocampus 1 week after treatment. Another 2'-substituted MPTP analogue, 1-methyl-4-(2'-methylphenyl)-1,2,3,6- tetrahydropyridine, affected cortical and hippocampal 5-HT, 5-HIAA, and NE only minimally, while markedly reducing the DA content in striatum (90%), thus indicating that the substituent (-NH2 versus -CH3) at the 2' position is important for the differential effects of these MPTP analogues. In a replication study with a 3-week end point, hippocampal and cortical 5-HT, 5-HIAA,, and NE levels remained depressed with no indication of recovery. These results suggest that 2'-NH2-MPTP may be a novel, regionally selective neurotoxin for serotonergic and noradrenergic nerve terminals. JF - Journal of neurochemistry AU - Andrews, A M AU - Murphy, D L AD - Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 1167 EP - 1170 VL - 60 IS - 3 SN - 0022-3042, 0022-3042 KW - Dopamine Agents KW - 0 KW - 1-methyl-4-(2'-methylphenyl)-1,2,3,6-tetrahydropyridine KW - 102417-86-7 KW - 1-methyl-4-(2'-aminophenyl)-1,2,3,6-tetrahydropyridine KW - 108114-93-8 KW - Serotonin KW - 333DO1RDJY KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Dopamine KW - VTD58H1Z2X KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Animals KW - Cerebral Cortex -- metabolism KW - Corpus Striatum -- metabolism KW - Hippocampus -- metabolism KW - Dopamine Agents -- pharmacology KW - Mice, Inbred C57BL KW - Mice KW - Tissue Distribution KW - Male KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- analogs & derivatives KW - Norepinephrine -- metabolism KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- pharmacology KW - Dopamine -- metabolism KW - Brain -- metabolism KW - Serotonin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75585808?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neurochemistry&rft.atitle=Sustained+depletion+of+cortical+and+hippocampal+serotonin+and+norepinephrine+but+not+striatal+dopamine+by+1-methyl-4-%282%27-aminophenyl%29-1%2C2%2C3%2C6-tetrahydropyridine+%282%27-NH2-MPTP%29%3A+a+comparative+study+with+2%27-CH3-MPTP+and+MPTP.&rft.au=Andrews%2C+A+M%3BMurphy%2C+D+L&rft.aulast=Andrews&rft.aufirst=A&rft.date=1993-03-01&rft.volume=60&rft.issue=3&rft.spage=1167&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurochemistry&rft.issn=00223042&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-24 N1 - Date created - 1993-03-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Stratification of rodent carcinogenicity bioassay results to reflect relative human hazard. AN - 75585367; 7678907 AB - Trans-species, multiple site (particularly common site between species), mutagenic rodent carcinogens are less affected by the influences of polymorphic genes than are chemicals inducing more limited carcinogenic effects. Trans-species carcinogens, therefore, should represent a first priority for attention for human health risk. JF - Mutation research AU - Tennant, R W AD - Experimental Carcinogenesis and Mutagenesis Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/03// PY - 1993 DA - March 1993 SP - 111 EP - 118 VL - 286 IS - 1 SN - 0027-5107, 0027-5107 KW - Carcinogens KW - 0 KW - Mutagens KW - Index Medicus KW - Rats KW - Animals KW - Mutagenicity Tests KW - Hybridization, Genetic KW - Polymorphism, Genetic KW - Neoplasms, Experimental -- chemically induced KW - Humans KW - Carcinogenicity Tests KW - Biological Assay KW - Mutagens -- toxicity KW - Predictive Value of Tests KW - Organ Specificity KW - Mice KW - Species Specificity KW - Carcinogens -- classification KW - Carcinogens -- toxicity KW - Rodentia UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75585367?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutation+research&rft.atitle=Stratification+of+rodent+carcinogenicity+bioassay+results+to+reflect+relative+human+hazard.&rft.au=Tennant%2C+R+W&rft.aulast=Tennant&rft.aufirst=R&rft.date=1993-03-01&rft.volume=286&rft.issue=1&rft.spage=111&rft.isbn=&rft.btitle=&rft.title=Mutation+research&rft.issn=00275107&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-26 N1 - Date created - 1993-02-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Abnormal in vitro proliferation and differentiation of T cell colony-forming cells in patients with tropical spastic paraparesis/human T lymphocyte virus type I (HTLV-I)-associated myeloencephalopathy and healthy HTLV-I carriers. AN - 75581635; 8094736 AB - T cell colonies were generated from the peripheral blood mononuclear cells (PBMC) of 10 patients with tropical spastic paraparesis/human T lymphocyte virus type I (HTLV-I)-associated myeloencephalopathy (TSP/HAM), two healthy HTLV-I carriers, and 17 healthy HTLV-I-seronegative subjects. PBMC were cultured in methylcellulose in the absence of added growth factors (spontaneous T cell colonies), or in the presence of phorbol myristate acetate and interleukin 2 (induced T cell colonies). PBMC T cell colony-forming cells (T-CFC) from all TSP/HAM patients and HTLV-I carriers were able to grow in the absence of added growth factors and/or mitogenic stimulation. Pooled spontaneous and induced colonies were composed of cells bearing CD3+, CD4+, CD8+, and CD1+ antigens. Colonies from normal HTLV-I-seronegative subjects displayed mature cells bearing the CD3+, CD4+, CD8+, and CD1- surface phenotype. In addition, spontaneous and induced T cell colonies expressed HTLV-I antigens in 18-38% of the cells from TSP/HAM patients and HTLV-I carriers. These results demonstrate that HTLV-I infection is associated with an abnormal proliferation and differentiation of T cell progenitors in vitro and that the T-CFC from HTLV-I-seropositive individuals are infected, suggesting that T-CFC abnormalities may play a predominant role in the pathophysiology of HTLV-I. JF - The Journal of experimental medicine AU - Lunardi-Iskandar, Y AU - Gessain, A AU - Lam, V H AU - Gallo, R C AD - Laboratory of Tumor Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/03/01/ PY - 1993 DA - 1993 Mar 01 SP - 741 EP - 750 VL - 177 IS - 3 SN - 0022-1007, 0022-1007 KW - Antigens, CD3 KW - 0 KW - Antigens, CD4 KW - Antigens, CD8 KW - Interleukin-2 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - AIDS/HIV KW - Interleukin-2 -- pharmacology KW - Humans KW - Antigens, CD8 -- analysis KW - CD4-Positive T-Lymphocytes -- pathology KW - Cell Division -- physiology KW - CD4-Positive T-Lymphocytes -- immunology KW - CD4-Positive T-Lymphocytes -- microbiology KW - Phenotype KW - Antigens, CD3 -- analysis KW - Antigens, CD4 -- analysis KW - Cell Differentiation -- physiology KW - Cells, Cultured KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Human T-lymphotropic virus 1 -- physiology KW - Stem Cells -- pathology KW - T-Lymphocytes -- physiology KW - HTLV-I Infections -- pathology KW - Stem Cells -- physiology KW - T-Lymphocytes -- pathology KW - Carrier State -- microbiology KW - HTLV-I Infections -- physiopathology KW - Stem Cells -- immunology KW - Paraparesis, Tropical Spastic -- physiopathology KW - Paraparesis, Tropical Spastic -- pathology KW - Human T-lymphotropic virus 1 -- isolation & purification KW - T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75581635?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+experimental+medicine&rft.atitle=Abnormal+in+vitro+proliferation+and+differentiation+of+T+cell+colony-forming+cells+in+patients+with+tropical+spastic+paraparesis%2Fhuman+T+lymphocyte+virus+type+I+%28HTLV-I%29-associated+myeloencephalopathy+and+healthy+HTLV-I+carriers.&rft.au=Lunardi-Iskandar%2C+Y%3BGessain%2C+A%3BLam%2C+V+H%3BGallo%2C+R+C&rft.aulast=Lunardi-Iskandar&rft.aufirst=Y&rft.date=1993-03-01&rft.volume=177&rft.issue=3&rft.spage=741&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+experimental+medicine&rft.issn=00221007&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-19 N1 - Date created - 1993-03-19 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Immunology. 1975 Dec;29(6):1041-55 [1081491] J Virol. 1991 Mar;65(3):1628-33 [1995955] Lancet. 1976 Nov 20;2(7995):1113-5 [62950] Blood. 1977 Sep;50(3):481-92 [301762] Clin Exp Immunol. 1977 Jun;28(3):526-34 [330061] J Immunol Methods. 1979 May 10;27(1):61-74 [313425] Arthritis Rheum. 1980 Apr;23(4):385-91 [6966151] Blood. 1981 Nov;58(5):911-5 [6975138] Nature. 1981 Nov 19;294(5838):268-71 [6272125] Proc Natl Acad Sci U S A. 1981 Oct;78(10):6476-80 [7031654] Proc Natl Acad Sci U S A. 1984 Apr;81(8):2534-7 [6326131] Blood. 1984 Jul;64(1):105-9 [6610444] J Immunol. 1985 Jan;134(1):151-6 [3871098] Leuk Res. 1984;8(6):1025-36 [6334790] Clin Exp Immunol. 1985 May;60(2):285-93 [3874021] Lancet. 1985 Aug 24;2(8452):407-10 [2863442] Lancet. 1985 Nov 30;2(8466):1247-8 [2866324] Blood. 1986 Apr;67(4):1063-9 [3485456] Lancet. 1986 May 3;1(8488):1031-2 [2871307] Br J Haematol. 1986 Sep;64(1):195-203 [3019380] Blood. 1987 Jan;69(1):12-7 [3024755] Ann Neurol. 1987 Feb;21(2):117-22 [2881513] Leuk Res. 1987;11(8):753-60 [3114567] Cancer Detect Prev Suppl. 1987;1:525-33 [3500783] Proc Natl Acad Sci U S A. 1987 Dec;84(24):9189-93 [2447586] Neurology. 1988 May;38(5):816-8 [2896315] Ann Neurol. 1988 Feb;23(2):196-9 [2454067] Neurology. 1988 Aug;38(8):1302-7 [2899862] J Clin Invest. 1989 Feb;83(2):610-5 [2563266] Blood. 1990 Jan 15;75(2):428-33 [1967218] N Engl J Med. 1990 Feb 8;322(6):383-8 [2300089] Proc Natl Acad Sci U S A. 1990 Jul;87(13):5218-22 [2367534] Nature. 1976 Jan 15;259(5539):127-9 [1246350] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - On the possible role of involution in the natural history of breast cancer AN - 1434031591; 18537492 AB - Although the importance of the relationship between age and cancer incidence rates is recognized universally, little attention seems to have been paid to the relationship between the physiologic aging process in the breast and breast cancer risk. The natural history of breast cancer was examined in the context of involution of the breast, and it was proposed that the rate and extent of involution might be important determinants of breast cancer risk. It was concluded that additional studies to characterize the process of involution better histopathologically and to examine the associations between the rate and extent of involution and breast cancer risk are warranted. JF - Cancer AU - Henson, Donald E AU - Tarone, Robert E AD - Biostatistics Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 1993/03// PY - 1993 DA - Mar 1993 SP - 2154 EP - 2156 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 71 IS - S6 SN - 0008-543X, 0008-543X KW - Risk Abstracts; Health & Safety Science Abstracts KW - Health risks KW - Historical account KW - Age KW - Aging KW - Breast cancer KW - H 11000:Diseases/Injuries/Trauma KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434031591?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=On+the+possible+role+of+involution+in+the+natural+history+of+breast+cancer&rft.au=Henson%2C+Donald+E%3BTarone%2C+Robert+E&rft.aulast=Henson&rft.aufirst=Donald&rft.date=1993-03-01&rft.volume=71&rft.issue=S6&rft.spage=2154&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/10.1002%2F1097-0142%2819930315%2971%3A6%2B3.0.CO%3B2+-%23 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-09-01 N1 - Last updated - 2013-10-21 N1 - SubjectsTermNotLitGenreText - Historical account; Health risks; Age; Aging; Breast cancer DO - http://dx.doi.org/10.1002/1097-0142(19930315)71:6+<2154::AID-CNCR2820711605>3.0.CO;2 ER - TY - JOUR T1 - Cultured hippocampal neurons from trisomy 16 mouse, a model for Down's syndrome, have an abnormal action potential due to a reduced inward sodium current. AN - 75650892; 8384514 AB - Mouse trisomy 16 is an animal model for Down's syndrome (human trisomy 21). The whole-cell patch-clamp technique was used to compare passive and active electrical properties of trisomy 16 and diploid mouse 16 fetal hippocampal neurons maintained in culture for 2-5 weeks. There was no significant difference in any mean passive property, including resting potential, membrane resistance, capacitance and time constant. However, in trisomic neurons, the action potential had a 20% significantly slower rising phase and a 20% significantly smaller inward sodium current and inward sodium conductance than did control neurons. The outward conductance was not altered. The ratio of maximum inward conductance to maximum outward conductance was 30% less in the trisomy 16 cells. These results indicate that trisomy 16 hippocampal neurons have abnormal active electrical properties, most likely reflecting reduced sodium channel membrane density. Such subtle differences may influence elaboration of the hippocampus during development. JF - Brain research AU - Galdzicki, Z AU - Coan, E AU - Rapoport, S I AD - Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/02/26/ PY - 1993 DA - 1993 Feb 26 SP - 69 EP - 78 VL - 604 IS - 1-2 SN - 0006-8993, 0006-8993 KW - Sodium Channels KW - 0 KW - Tetraethylammonium Compounds KW - Tetrodotoxin KW - 4368-28-9 KW - Tetraethylammonium KW - 66-40-0 KW - Index Medicus KW - Karyotyping KW - Animals KW - Fetus KW - Reference Values KW - Electric Conductivity KW - Chromosome Banding KW - Tetraethylammonium Compounds -- pharmacology KW - Disease Models, Animal KW - Trisomy KW - Action Potentials -- drug effects KW - Mice KW - Pregnancy KW - Cells, Cultured KW - Mice, Neurologic Mutants KW - Mice, Inbred C57BL KW - Membrane Potentials -- drug effects KW - Tetrodotoxin -- pharmacology KW - Female KW - Down Syndrome -- physiopathology KW - Hippocampus -- physiology KW - Neurons -- drug effects KW - Neurons -- physiology KW - Sodium Channels -- physiology KW - Hippocampus -- physiopathology KW - Down Syndrome -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75650892?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research&rft.atitle=Cultured+hippocampal+neurons+from+trisomy+16+mouse%2C+a+model+for+Down%27s+syndrome%2C+have+an+abnormal+action+potential+due+to+a+reduced+inward+sodium+current.&rft.au=Galdzicki%2C+Z%3BCoan%2C+E%3BRapoport%2C+S+I&rft.aulast=Galdzicki&rft.aufirst=Z&rft.date=1993-02-26&rft.volume=604&rft.issue=1-2&rft.spage=69&rft.isbn=&rft.btitle=&rft.title=Brain+research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-26 N1 - Date created - 1993-04-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Endothelins release 51Cr from cultured human cerebromicrovascular endothelium. AN - 75628008; 8447814 AB - The effects of vasoactive peptides endothelins (ET-1, ET-2, ET-3, S6b, S6c) on release of 51Cr, production of inositol triphosphate (IP3), and release of arachidonic acid (AA) were examined in cultured microvascular endothelium derived from human brain (HBEC). ET-1 induced dose-dependent release of 51CR (EC50 = 7 +/- 2 nM), transient increase of IP3 (EC50 = 0.67 +/- 0.09 nM), and sustained release of AA (EC50= 59 +/- 7 nM) from HBEC. Under the same experimental conditions, viability of the cells was preserved (> 97%) as assessed by exclusion of vital dye trypan blue and release of lactate dehydrogenase (LDH). Dexamethasone (1 microM) inhibited ET-1-induced AA release, whereas it was ineffective on 51Cr release. Protein kinase C (PKC) inhibitor H7 (200 nM), calcium channel blocker verapamil (10 microM), or IP3 receptor antagonist ryonidine (5 microM) reduced ET-1 (100 nM)-induced release of 51Cr. These findings indicate that endothelins can induce an increase of HBEC permeability by a receptor-specific activation of PKC and intracellular calcium mobilization. JF - Biochemical and biophysical research communications AU - Stanimirovic, D B AU - McCarron, R AU - Bertrand, N AU - Spatz, M AD - Stroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/02/26/ PY - 1993 DA - 1993 Feb 26 SP - 1 EP - 8 VL - 191 IS - 1 SN - 0006-291X, 0006-291X KW - Chromium Radioisotopes KW - 0 KW - Endothelins KW - Isoquinolines KW - Piperazines KW - Protein Kinase Inhibitors KW - Ryanodine KW - 15662-33-6 KW - Arachidonic Acid KW - 27YG812J1I KW - Dexamethasone KW - 7S5I7G3JQL KW - 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine KW - 84477-87-2 KW - Inositol 1,4,5-Trisphosphate KW - 85166-31-0 KW - Verapamil KW - CJ0O37KU29 KW - L-Lactate Dehydrogenase KW - EC 1.1.1.27 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Dose-Response Relationship, Drug KW - L-Lactate Dehydrogenase -- analysis KW - Dexamethasone -- pharmacology KW - Humans KW - Verapamil -- pharmacology KW - Piperazines -- pharmacology KW - Arachidonic Acid -- metabolism KW - Inositol 1,4,5-Trisphosphate -- metabolism KW - Isoquinolines -- pharmacology KW - Cell Survival -- drug effects KW - Cell Membrane Permeability -- drug effects KW - Cells, Cultured KW - Kinetics KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Ryanodine -- pharmacology KW - Microcirculation KW - Endothelins -- pharmacology KW - Endothelium, Vascular -- metabolism KW - Endothelium, Vascular -- drug effects KW - Endothelium, Vascular -- cytology KW - Cerebrovascular Circulation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75628008?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+and+biophysical+research+communications&rft.atitle=Endothelins+release+51Cr+from+cultured+human+cerebromicrovascular+endothelium.&rft.au=Stanimirovic%2C+D+B%3BMcCarron%2C+R%3BBertrand%2C+N%3BSpatz%2C+M&rft.aulast=Stanimirovic&rft.aufirst=D&rft.date=1993-02-26&rft.volume=191&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Biochemical+and+biophysical+research+communications&rft.issn=0006291X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-06 N1 - Date created - 1993-04-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Cibacron blue-induced enhancement of agonist binding to cholecystokinin (CCK) receptors in solubilized pancreatic membranes. AN - 75594870; 8443227 AB - The pancreatic receptor for cholecystokinin (CCK) typifies many G protein-coupled receptors in that its ability to bind agonist can be reduced by GTP or the solubilization of membranes. We found, however, that a dye, cibacron blue, caused up to a 6-fold increase in binding of the CCK receptor agonist, 125I-CCK-8, to rat pancreatic membranes solubilized with digitonin. Binding optimally enhanced in this manner was comparable to binding of 125I-CCK-8 to native membranes with respect to time-course, maximal amount bound, reversibility, and sensitivity to inhibition by various CCK receptor ligands. Increases in affinity of the CCK receptor for CCK-8 accounted fully for the enhancement of binding of 125I-CCK-8. Cibacron blue did not enhance binding of 125I-CCK-8 to native membranes, and also failed to enhance binding of the CCK receptor antagonist, [3H]L-364,718, to solubilized or native membranes. The ability of cibacron blue to enhance binding of agonist but not that of antagonist suggests that this dye may mimic or perhaps stimulate the effects of G protein on CCK receptors. Such a phenomenon may provide new insights into the mechanisms by which receptors distinguish agonists from antagonists. JF - Biochimica et biophysica acta AU - Yuan, D S AU - Wank, S A AU - Gardner, J D AD - Digestive Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD. Y1 - 1993/02/23/ PY - 1993 DA - 1993 Feb 23 SP - 52 EP - 58 VL - 1146 IS - 1 SN - 0006-3002, 0006-3002 KW - Benzodiazepinones KW - 0 KW - Coloring Agents KW - Iodine Radioisotopes KW - Phenylurea Compounds KW - Receptors, Cholecystokinin KW - Triazines KW - L 365260 KW - 370JHF4586 KW - Guanosine 5'-O-(3-Thiotriphosphate) KW - 37589-80-3 KW - Cibacron Blue F 3GA KW - 5DV0L8V99J KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Devazepide KW - JE6P7QY7NH KW - Digitonin KW - KOO5CM684H KW - Sincalide KW - M03GIQ7Z6P KW - Index Medicus KW - Animals KW - Benzodiazepinones -- antagonists & inhibitors KW - Coloring Agents -- pharmacology KW - Drug Interactions KW - Membranes -- metabolism KW - Rats KW - Rats, Sprague-Dawley KW - Sincalide -- metabolism KW - Sincalide -- antagonists & inhibitors KW - Benzodiazepinones -- pharmacology KW - Male KW - Chromatography, Affinity -- methods KW - Triazines -- pharmacology KW - Pancreas -- metabolism KW - GTP-Binding Proteins -- metabolism KW - Receptors, Cholecystokinin -- metabolism KW - Receptors, Cholecystokinin -- drug effects KW - Receptors, Cholecystokinin -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75594870?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochimica+et+biophysica+acta&rft.atitle=Cibacron+blue-induced+enhancement+of+agonist+binding+to+cholecystokinin+%28CCK%29+receptors+in+solubilized+pancreatic+membranes.&rft.au=Yuan%2C+D+S%3BWank%2C+S+A%3BGardner%2C+J+D&rft.aulast=Yuan&rft.aufirst=D&rft.date=1993-02-23&rft.volume=1146&rft.issue=1&rft.spage=52&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+biophysica+acta&rft.issn=00063002&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-06 N1 - Date created - 1993-04-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - HIV envelope protein-induced neuronal damage and retardation of behavioral development in rat neonates. AN - 75638524; 8461978 AB - Cognitive and motor impairment are common symptoms among patients infected with the human immunodeficiency virus (HIV), including children who suffer neurological deficits and are frequently developmentally impaired. The HIV envelope protein, gp120, which has been shown to be toxic to neurons in culture, is shed in abundance by infected cells, and thus may play a significant role in the neuropathology of AIDS. To test this possible mechanism, neonatal rats were injected systemically with purified gp120 and the following consequences were observed: (1) radiolabeled gp120 and toxic fragments thereof were recovered in brain homogenates; (2) dystrophic changes were produced in pyramidal neurons of cerebral cortex; (3) retardation was evident in developmental milestones associated with complex motor behaviors. In parallel studies, co-treatment with peptide T, a gp120-derived peptide having a pentapeptide sequence homologous with vasoactive intestinal peptide, prevented or attenuated the morphological damage and behavioral delays associated with gp120 treatment. These studies suggest that gp120 and gp120-derived toxic fragments may contribute to the neurological and neuropsychiatric impairment related to HIV infection, and that peptide T appears to be effective in preventing gp120-associated neurotoxicity in developing rodents. JF - Brain research AU - Hill, J M AU - Mervis, R F AU - Avidor, R AU - Moody, T W AU - Brenneman, D E AD - Unit on Neurochemistry, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/02/19/ PY - 1993 DA - 1993 Feb 19 SP - 222 EP - 233 VL - 603 IS - 2 SN - 0006-8993, 0006-8993 KW - Antibodies, Monoclonal KW - 0 KW - Gene Products, env KW - HIV Envelope Protein gp120 KW - HIV Envelope Protein gp160 KW - HIV Envelope Protein gp41 KW - Iodine Radioisotopes KW - Peptide Fragments KW - Protein Precursors KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Acquired Immunodeficiency Syndrome -- physiopathology KW - Gene Products, env -- analysis KW - Humans KW - Aging KW - HIV Envelope Protein gp41 -- immunology KW - Mice KW - Rats KW - Animals, Newborn KW - Rats, Sprague-Dawley KW - Blotting, Western KW - Protein Precursors -- immunology KW - Reflex -- drug effects KW - Dendrites -- ultrastructure KW - HIV Envelope Protein gp41 -- analysis KW - Gene Products, env -- immunology KW - Protein Precursors -- analysis KW - Dendrites -- drug effects KW - Peptide Fragments -- toxicity KW - Brain -- drug effects KW - Neurons -- drug effects KW - Peptide Fragments -- analysis KW - HIV Envelope Protein gp120 -- metabolism KW - HIV Envelope Protein gp120 -- analysis KW - Neurons -- pathology KW - Brain -- physiopathology KW - Behavior, Animal -- drug effects KW - Brain -- pathology KW - Neurons -- physiology KW - HIV Envelope Protein gp120 -- toxicity KW - Motor Activity -- drug effects KW - Peptide Fragments -- pharmacokinetics KW - HIV UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75638524?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research&rft.atitle=HIV+envelope+protein-induced+neuronal+damage+and+retardation+of+behavioral+development+in+rat+neonates.&rft.au=Hill%2C+J+M%3BMervis%2C+R+F%3BAvidor%2C+R%3BMoody%2C+T+W%3BBrenneman%2C+D+E&rft.aulast=Hill&rft.aufirst=J&rft.date=1993-02-19&rft.volume=603&rft.issue=2&rft.spage=222&rft.isbn=&rft.btitle=&rft.title=Brain+research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-03 N1 - Date created - 1993-05-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Desensitization of the NMDA receptor complex by glycinergic ligands in cerebellar granule cell cultures. AN - 75638406; 8096423 AB - Glutamate neurotoxicity was examined in cultured cerebellar granule neurons following both prolonged (20-24 h) and brief (45 min) exposure to compounds acting at strychnine-insensitive glycine receptors. Glutamate neurotoxicity was reduced in a concentration-dependent fashion by brief exposure to the glycine partial agonists 1-aminocyclopropanecarboxylic acid (ACPC) and (+-)-3-amino-1-hydroxy-2-pyrrolidone (HA-966) and the competitive antagonist, 7-chlorokynurenic acid (7-CK) with a rank order efficacy: 7-CK > HA-966 > ACPC. Neither D-cycloserine (D-CS) nor glycine affected neurotoxicity produced by maximum glutamate concentrations, while glycine but not D-CS augmented the effects of submaximum glutamate concentrations. Prolonged exposure of cultures to either full (glycine) or partial agonists (ACPC, D-CS, HA-966) abolished the neuroprotective effects of ACPC and significantly diminished the neuroprotective effects of HA-966. In contrast, the neuroprotective effects of 7-CK were only marginally reduced by prolonged exposure to glycinergic ligands, while the neuroprotection afforded by compounds acting at other loci on the NMDA receptor complex (e.g. 2-amino-5-phosphonopentanoate (APV) and dizocilpine (MK-801)) were unaltered. These effects may represent homologous desensitization of the NMDA receptor complex at its strychnine-insensitive glycine receptor induced by prolonged exposure to glycinergic agonists and partial agonists. Nonetheless, levels of the NMDA receptor subunit zeta 1 mRNA were unaffected by prolonged exposure to ACPC, indicating the apparent desensitization could involve a post-translational modification of the NMDA receptor complex. JF - Brain research AU - Boje, K M AU - Wong, G AU - Skolnick, P AD - Laboratory of Neuroscience, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/02/19/ PY - 1993 DA - 1993 Feb 19 SP - 207 EP - 214 VL - 603 IS - 2 SN - 0006-8993, 0006-8993 KW - Amino Acids KW - 0 KW - Amino Acids, Cyclic KW - Glutamates KW - Neurotoxins KW - Oligodeoxyribonucleotides KW - Pyrrolidinones KW - RNA, Messenger KW - Receptors, N-Methyl-D-Aspartate KW - 1-aminocyclopropane-1-carboxylic acid KW - 3K9EJ633GL KW - Glutamic Acid KW - 3KX376GY7L KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - 2-Amino-5-phosphonovalerate KW - 76726-92-6 KW - 1-hydroxy-3-amino-2-pyrrolidone KW - F2JLV9220T KW - Kynurenic Acid KW - H030S2S85J KW - Strychnine KW - H9Y79VD43J KW - 7-chlorokynurenic acid KW - S7936QON2K KW - Glycine KW - TE7660XO1C KW - Index Medicus KW - Animals KW - Analysis of Variance KW - Blotting, Northern KW - Neurotoxins -- pharmacology KW - RNA, Messenger -- genetics KW - Dizocilpine Maleate -- pharmacology KW - Rats KW - Molecular Sequence Data KW - Kynurenic Acid -- analogs & derivatives KW - Amino Acids -- pharmacology KW - Time Factors KW - Pyrrolidinones -- pharmacology KW - Glycine -- physiology KW - Dose-Response Relationship, Drug KW - Kynurenic Acid -- pharmacology KW - Base Sequence KW - Rats, Sprague-Dawley KW - 2-Amino-5-phosphonovalerate -- pharmacology KW - RNA, Messenger -- metabolism KW - Cells, Cultured KW - Kinetics KW - Polymerase Chain Reaction -- methods KW - Strychnine -- pharmacology KW - Receptors, N-Methyl-D-Aspartate -- physiology KW - Cerebellum -- cytology KW - Glutamates -- pharmacology KW - Neurons -- drug effects KW - Neurons -- cytology KW - Receptors, N-Methyl-D-Aspartate -- antagonists & inhibitors KW - Neurons -- physiology KW - Receptors, N-Methyl-D-Aspartate -- genetics KW - Cerebellum -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75638406?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research&rft.atitle=Desensitization+of+the+NMDA+receptor+complex+by+glycinergic+ligands+in+cerebellar+granule+cell+cultures.&rft.au=Boje%2C+K+M%3BWong%2C+G%3BSkolnick%2C+P&rft.aulast=Boje&rft.aufirst=K&rft.date=1993-02-19&rft.volume=603&rft.issue=2&rft.spage=207&rft.isbn=&rft.btitle=&rft.title=Brain+research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-03 N1 - Date created - 1993-05-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Phase I study of debulking surgery and photodynamic therapy for disseminated intraperitoneal tumors. AN - 75591016; 8436523 AB - Phase I study designed to determine the maximum tolerated dose of intraoperative photodynamic therapy (PDT) at laparotomy/debulking surgery in patients with refractory or recurrent, disseminated intraperitoneal tumors. Patients received dihematoporphyrin ethers (DHE) 1.5-2.5 mg/kg by i.v. injection prior to surgery. Patients resected to < or = 5 mm of residual disease underwent laser light delivery to all peritoneal surfaces. Fifty-four patients entered the study. Thirty-nine underwent resection and light delivery/PDT. PDT dose was escalated by increasing DHE from 1.5 to 2.5 mg/kg, shortening the interval between DHE injection and surgery from 72 to 48 hr, and increasing the light dose. Initially, 630 nm red light alone was used. In this group, PDT of 2.8-3.0 J/cm2 induced small bowel edema and resulted in 3 small bowel perforations after bowel resection or enterotomy. Further light dose escalation, however, was achieved by switching to less penetrating 514 nm green light to the bowel/mesentery. In later patients, whole peritoneal PDT was supplemented with boost doses of 10-15 J/cm2 red light or 5-7.5 J/cm2 green light to high risk areas. Small bowel complications were not seen after switching to less penetrating green light. Dose limiting toxicities occurred in 2 of 3 patients at the highest light dose of 5.0 J/cm2 green light with boost. These patients had pleural effusions that required thoracentesis and postoperative respiratory support for 7-9 days, while one had a gastric perforation. At potential follow-up times of 3.8-43.1 months (median 22.1 months), 30/39 patients are alive and 9/39 are free of disease. The maximum tolerated dose of intraoperative PDT following debulking surgery performed 48 hr after intravenous administration 2.5 mg/kg DHE is 3.75 J/cm2 of 514 nm green light to the entire peritoneal surface with boosts to 5.0-7.5 J/cm2 of 514 nm green light or 10-15 J/cm2 of 630 nm red light to sites of gross disease encountered at surgery. JF - International journal of radiation oncology, biology, physics AU - DeLaney, T F AU - Sindelar, W F AU - Tochner, Z AU - Smith, P D AU - Friauf, W S AU - Thomas, G AU - Dachowski, L AU - Cole, J W AU - Steinberg, S M AU - Glatstein, E AD - Radiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/02/15/ PY - 1993 DA - 1993 Feb 15 SP - 445 EP - 457 VL - 25 IS - 3 SN - 0360-3016, 0360-3016 KW - Dihematoporphyrin Ether KW - 97067-70-4 KW - Index Medicus KW - Survival Rate KW - Infusions, Intravenous KW - Combined Modality Therapy KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Male KW - Female KW - Carcinoma -- surgery KW - Photochemotherapy -- adverse effects KW - Dihematoporphyrin Ether -- administration & dosage KW - Peritoneal Neoplasms -- drug therapy KW - Sarcoma -- drug therapy KW - Ovarian Neoplasms -- therapy KW - Ovarian Neoplasms -- drug therapy KW - Carcinoma -- therapy KW - Carcinoma -- drug therapy KW - Sarcoma -- surgery KW - Peritoneal Neoplasms -- surgery KW - Ovarian Neoplasms -- surgery KW - Peritoneal Neoplasms -- therapy KW - Sarcoma -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75591016?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+radiation+oncology%2C+biology%2C+physics&rft.atitle=Phase+I+study+of+debulking+surgery+and+photodynamic+therapy+for+disseminated+intraperitoneal+tumors.&rft.au=DeLaney%2C+T+F%3BSindelar%2C+W+F%3BTochner%2C+Z%3BSmith%2C+P+D%3BFriauf%2C+W+S%3BThomas%2C+G%3BDachowski%2C+L%3BCole%2C+J+W%3BSteinberg%2C+S+M%3BGlatstein%2C+E&rft.aulast=DeLaney&rft.aufirst=T&rft.date=1993-02-15&rft.volume=25&rft.issue=3&rft.spage=445&rft.isbn=&rft.btitle=&rft.title=International+journal+of+radiation+oncology%2C+biology%2C+physics&rft.issn=03603016&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-25 N1 - Date created - 1993-03-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Residues 1-254 of anthrax toxin lethal factor are sufficient to cause cellular uptake of fused polypeptides. AN - 75589992; 8429009 AB - Anthrax lethal toxin is a complex of protective antigen (PA, 735 amino acids) and lethal factor (LF, 776 amino acids) that lyses certain eukaryotic cells. LF interacts with PA to gain access to the cytosol to assert its toxicity. The internalization of LF requires that PA bind to a specific membrane receptor and be cleaved by a cell-surface protease (probably furin), so as to expose a site on PA to which LF binds with high affinity. To localize LF functional domains, amino, carboxyl, and internal deletions of LF were made. Toxicity was eliminated by deletion of 40 and 47 residues from the amino and carboxyl termini, respectively. Similarly, deleting the first of the four imperfect repeats of 19 amino acids located at residues 308-383 made LF non-toxic, showing that this region is also essential for activity. To identify the minimum region of LF which is required for binding to PA, varying amino-terminal portions of LF were fused to the ADP-ribosylation domain of Pseudomonas exotoxin A. Fusion proteins containing residues 1-254 of LF were toxic when administered with PA, while those having only residues 1-198 of LF were inactive, showing that the PA-binding domain of LF lies within residues 1-254. JF - The Journal of biological chemistry AU - Arora, N AU - Leppla, S H AD - Laboratory of Microbial Ecology, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/02/15/ PY - 1993 DA - 1993 Feb 15 SP - 3334 EP - 3341 VL - 268 IS - 5 SN - 0021-9258, 0021-9258 KW - Antigens, Bacterial KW - 0 KW - Bacterial Toxins KW - Exotoxins KW - Peptide Fragments KW - Recombinant Fusion Proteins KW - Virulence Factors KW - anthrax toxin KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - Macrophages KW - Animals KW - Exotoxins -- genetics KW - Biological Transport KW - Escherichia coli -- genetics KW - Plasmids KW - Cloning, Molecular KW - Recombinant Fusion Proteins -- metabolism KW - Bacillus anthracis -- genetics KW - Cell Survival -- drug effects KW - Kinetics KW - Restriction Mapping KW - Polymerase Chain Reaction -- methods KW - Binding, Competitive KW - Exotoxins -- metabolism KW - Recombinant Fusion Proteins -- pharmacology KW - CHO Cells KW - Cell Membrane -- metabolism KW - Repetitive Sequences, Nucleic Acid KW - Cell Line KW - Sequence Deletion KW - Cricetinae KW - Peptide Fragments -- metabolism KW - Bacterial Toxins -- genetics KW - Bacterial Toxins -- metabolism KW - Peptide Fragments -- pharmacology KW - Bacterial Toxins -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75589992?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Residues+1-254+of+anthrax+toxin+lethal+factor+are+sufficient+to+cause+cellular+uptake+of+fused+polypeptides.&rft.au=Arora%2C+N%3BLeppla%2C+S+H&rft.aulast=Arora&rft.aufirst=N&rft.date=1993-02-15&rft.volume=268&rft.issue=5&rft.spage=3334&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-09 N1 - Date created - 1993-03-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Protein-DNA interactions in the epsilon-globin gene silencer. AN - 75583173; 8429019 AB - The developmental control of expression of the human epsilon-globin gene appears to be mediated, at least in part, by a transcriptional silencer in the DNA 5' to the cap site of this gene. We have used site-directed mutagenesis and DNA-protein binding assays to define the active motifs of this epsilon-globin silencer. DNase I foot-printing of the silencer region with K562 cell nuclear extracts defined a sequence, which we designate as the epsilon-globin silencer motif or epsilon GSM (epsilon -278 to -258 base pairs (bp)) containing a region (epsilon -270 to -258) with 90% homology to the yeast mating type silencer, ABF-1 (autonomous replicating sequence binding factor one) and which also overlaps at (epsilon -269 to -262) with the human YY1 consensus sequence, an element which mediates transcription repression and activation of viral, mouse, and human genes. The DNase I footprint extended 5' in the silencer region to include an inverted repeat of a six-nucleotide motif (epsilon -267 to -278 bp) which shares 5 of 6 bases with the GATA-1 consensus sequence. In gel mobility shift assays, two specific proteins (A and B) in nuclear extracts from erythroleukemia K562 cells bound to the DNase I-footprinted region. Protein B, associated with epsilon-globin silencer activity in vitro, required an intact epsilon GSM sequence for binding. Mutation of 5 bases within the epsilon GSM in an epsilon-globin promoter-containing fragment extending upstream to 1400 bp in transient transfection assays increased activity by 3.0-fold compared with the native sequence, suggesting that the silencer activity was mediated by the epsilon GSM sequence. We found that protein A could be displaced by a competitor containing the GATA-1 consensus sequence, suggesting that protein A is a GATA-like protein. The region from -267 to -271 within the epsilon GSM and GATA-1 homology region was important for binding of both proteins A and B. These data suggest that protein binding to the epsilon GSM and GATA motifs mediate the negative effect of the silencer on transcription, possibly via direct competition for binding to this DNA region. Recombinant yeast ABF-1 and human YY1 bound to the epsilon GSM. Mutating three bases (epsilon -259, -262, -264) in the epsilon GSM decreased the binding affinity of protein B and recombinant human YY1 but increased the binding affinity of recombinant yeast ABF-1. Furthermore, competitor containing the YY1 consensus sequence competed for protein B binding, whereas competitor containing a perfect yeast ABF-1 consensus sequence did not.(ABSTRACT TRUNCATED AT 400 WORDS) JF - The Journal of biological chemistry AU - Peters, B AU - Merezhinskaya, N AU - Diffley, J F AU - Noguchi, C T AD - Laboratory of Chemical Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/02/15/ PY - 1993 DA - 1993 Feb 15 SP - 3430 EP - 3437 VL - 268 IS - 5 SN - 0021-9258, 0021-9258 KW - DNA-Binding Proteins KW - 0 KW - Erythroid-Specific DNA-Binding Factors KW - GATA1 Transcription Factor KW - GATA1 protein, human KW - Oligodeoxyribonucleotides KW - Transcription Factors KW - YY1 Transcription Factor KW - YY1 protein, human KW - Globins KW - 9004-22-2 KW - DNA KW - 9007-49-2 KW - Deoxyribonuclease I KW - EC 3.1.21.1 KW - Index Medicus KW - Sequence Homology, Nucleic Acid KW - Cell Nucleus -- metabolism KW - HeLa Cells KW - Humans KW - Transcription, Genetic KW - Saccharomyces cerevisiae -- genetics KW - Mutagenesis, Site-Directed KW - Polymerase Chain Reaction KW - Base Sequence KW - Tumor Cells, Cultured KW - Leukemia, Myelogenous, Chronic, BCR-ABL Positive KW - Molecular Sequence Data KW - Transcription Factors -- metabolism KW - DNA -- metabolism KW - Globins -- genetics KW - DNA -- genetics KW - Genes, Regulator KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75583173?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Protein-DNA+interactions+in+the+epsilon-globin+gene+silencer.&rft.au=Peters%2C+B%3BMerezhinskaya%2C+N%3BDiffley%2C+J+F%3BNoguchi%2C+C+T&rft.aulast=Peters&rft.aufirst=B&rft.date=1993-02-15&rft.volume=268&rft.issue=5&rft.spage=3430&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-09 N1 - Date created - 1993-03-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Pseudomonas exotoxin-based immunotoxins containing the antibody LL2 or LL2-Fab' induce regression of subcutaneous human B-cell lymphoma in mice. AN - 75572209; 8428363 AB - We have produced immunotoxins using LL2, a monoclonal antibody which binds to human B-cell lymphomas and which, in a radioiodinated form, induced responses in lymphoma patients (D.M. Goldberg et al., J. Clin. Oncol., 9: 548-564, 1991). We have coupled LL2 to Lys-PE38KDEL, a derivative of Pseudomonas exotoxin (PE) which does not bind to the PE receptor. LL2-PE38KDEL was cytotoxic toward several Burkitt's lymphoma lines, with 50% inhibitory concentration values ranging from 2 to 6 ng/ml (10-30 pM). Another immunotoxin, LL2-Fab'-PE38KDEL, was produced by chemically coupling the Fab' fragment of LL2 to Lys-PE38KDEL. LL2-Fab'-PE38KDEL also was cytotoxic toward the Burkitt's cells, with a 50% inhibitory concentration of 1-2 ng/ml (13-24 PM). The antibody LL2 alone had no cytotoxicity toward the malignant cells, and excess LL2 prevented the cytotoxicity of LL2-PE38KDEL and LL2-Fab'-PE38KDEL. Control immunotoxins UPC-10-PE38KDEL and Mu-9-Fab'-PE38KDEL were not cytotoxic. LL2-PE38KDEL and LL2-Fab'-PE38KDEL bound to cells with 50% and 17% of the affinity of LL2, respectively. Both immunotoxins, but not UPC-10-PE38KDEL, prevented the development of CA-46 tumors in nude mice. LL2-PE38KDEL and LL2-Fab'-PE38KDEL, but not the control immunotoxins, led to complete regressions of measurable s.c. CA-46 tumors in nude mice, when given at 50% and 35% of the 50% lethal dose, respectively. LL2 alone significantly retarded the growth of CA-46 tumors but did not cause complete tumor regressions. Immunotoxins containing derivatives of Pseudomonas exotoxin can be targeted to human B-cell lymphoma and merit further study as potential therapeutic agents. JF - Cancer research AU - Kreitman, R J AU - Hansen, H J AU - Jones, A L AU - FitzGerald, D J AU - Goldenberg, D M AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1993/02/15/ PY - 1993 DA - 1993 Feb 15 SP - 819 EP - 825 VL - 53 IS - 4 SN - 0008-5472, 0008-5472 KW - Antibodies, Monoclonal KW - 0 KW - Bacterial Toxins KW - Exotoxins KW - Immunoglobulin Fab Fragments KW - Immunotoxins KW - Virulence Factors KW - bectumomab KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - Animals KW - Drug Administration Schedule KW - Whole-Body Irradiation KW - Tumor Cells, Cultured KW - Antibodies, Monoclonal -- metabolism KW - Humans KW - Body Weight -- drug effects KW - Mice, Nude KW - Mice KW - Female KW - Antibodies, Monoclonal -- therapeutic use KW - Immunoglobulin Fab Fragments -- therapeutic use KW - Lymphoma, B-Cell -- therapy KW - Lymphoma, B-Cell -- radiotherapy KW - Skin Neoplasms -- therapy KW - Immunotoxins -- metabolism KW - Skin Neoplasms -- metabolism KW - Lymphoma, B-Cell -- metabolism KW - Immunoglobulin Fab Fragments -- metabolism KW - Exotoxins -- metabolism KW - Skin Neoplasms -- radiotherapy KW - Immunotoxins -- therapeutic use KW - Exotoxins -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75572209?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Pseudomonas+exotoxin-based+immunotoxins+containing+the+antibody+LL2+or+LL2-Fab%27+induce+regression+of+subcutaneous+human+B-cell+lymphoma+in+mice.&rft.au=Kreitman%2C+R+J%3BHansen%2C+H+J%3BJones%2C+A+L%3BFitzGerald%2C+D+J%3BGoldenberg%2C+D+M%3BPastan%2C+I&rft.aulast=Kreitman&rft.aufirst=R&rft.date=1993-02-15&rft.volume=53&rft.issue=4&rft.spage=819&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-10 N1 - Date created - 1993-03-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Activation of c-myb is an early bone-marrow event in a murine model for acute promonocytic leukemia. AN - 75567185; 7679511 AB - Insertional mutagenesis of c-myb by Moloney murine leukemia virus occurs in 100% of promonocytic leukemias (MMLS) induced by the virus. These leukemias, which resemble acute monocytic leukemia-M5 in humans are induced only in mice undergoing a peritoneal chronic inflammatory response. We have found that two leukemia-specific gag-myb mRNAs in MML provide molecular markers for detection of preleukemic cells in hematopoietic tissue in vivo. The two aberrant RNAs result from splicing of gag to either exon 3 or 4 of c-myb, depending on the site of proviral integration. After reverse transcription-PCR with nested primers and hybridization with specific gag-myb junction probes, one cell, having aberrant c-myb message, could be detected in a minimum of 10(5) liver cells or 10(6) spleen or bone-marrow cells. This approach was used to examine hematopoietic tissues of mice after pristane injection to induce inflammation and virus inoculation. Cells with gag-myb mRNAs could be detected as early as 2 weeks after virus inoculation. In mice receiving both pristane and virus, there was evidence of preleukemic cells in 83% of the mice by 3 weeks after virus infection. Furthermore, 100% of the mice were positive for preleukemic cells by 8 weeks, even though only 50% of mice have been shown to succumb to MML (peak time for disease latency is 12-16 weeks). Cells with these aberrant c-myb messages were initially detected in the bone marrow, but during intermediate stages of disease development these cells disseminated to the spleen, liver, and granuloma. At preleukemic times, from 3 to 8 weeks after virus infection, a lower percentage of mice were positive in the group that did not receive pristane compared with mice in the group receiving pristane. However, at 18 weeks, 100% of the mice in the group receiving virus only had evidence of cells expressing gag-myb RNA in their spleens and/or bone marrow; it is of interest that mice inoculated with virus alone never develop MML. This approach for detecting preleukemic cells will now allow the study of mechanisms by which these preleukemic cells progress to a more transformed state and, perhaps, to a more differentiated state. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Nason-Burchenal, K AU - Wolff, L AD - Laboratory of Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/02/15/ PY - 1993 DA - 1993 Feb 15 SP - 1619 EP - 1623 VL - 90 IS - 4 SN - 0027-8424, 0027-8424 KW - c-myb KW - gag KW - Oligodeoxyribonucleotides KW - 0 KW - RNA KW - 63231-63-0 KW - Index Medicus KW - 3T3 Cells KW - Animals KW - Neoplasm Staging KW - Mice KW - Organ Specificity KW - Mice, Inbred BALB C KW - Base Sequence KW - Blotting, Southern KW - Polymerase Chain Reaction -- methods KW - RNA -- isolation & purification KW - Molecular Sequence Data KW - Genes, gag KW - Female KW - RNA -- genetics KW - Oncogenes KW - Bone Marrow -- physiology KW - Leukemia, Promyelocytic, Acute -- genetics KW - Moloney murine leukemia virus -- genetics KW - Leukemia, Promyelocytic, Acute -- pathology KW - Mutagenesis, Insertional KW - Leukemia, Experimental -- pathology KW - Leukemia, Experimental -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75567185?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Activation+of+c-myb+is+an+early+bone-marrow+event+in+a+murine+model+for+acute+promonocytic+leukemia.&rft.au=Nason-Burchenal%2C+K%3BWolff%2C+L&rft.aulast=Nason-Burchenal&rft.aufirst=K&rft.date=1993-02-15&rft.volume=90&rft.issue=4&rft.spage=1619&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-16 N1 - Date created - 1993-03-16 N1 - Date revised - 2017-01-13 N1 - Gene symbol - c-myb; gag N1 - SuppNotes - Cited By: Virology. 1970 Dec;42(4):1136-9 [4099080] Cancer Res. 1992 Oct 1;52(19):5317-22 [1394137] J Immunol. 1978 Aug;121(2):641-7 [308074] Nature. 1981 Oct 15-21;293(5833):543-8 [6169994] Recent Results Cancer Res. 1984;93:51-68 [6089279] Proc Natl Acad Sci U S A. 1986 May;83(10):3204-8 [3010282] J Virol. 1987 Feb;61(2):336-43 [3027365] Anal Biochem. 1987 Apr;162(1):156-9 [2440339] J Virol. 1987 Dec;61(12):3721-5 [2824810] J Immunol. 1988 Jul 15;141(2):681-9 [2838552] Proc Natl Acad Sci U S A. 1988 Aug;85(15):5698-702 [3165197] Nucleic Acids Res. 1989 Mar 11;17(5):2141 [2928127] J Virol. 1990 Jan;64(1):155-60 [2403439] Biochim Biophys Acta. 1990 Jun 1;1032(1):39-52 [2194567] Mol Cell Biol. 1990 Aug;10(8):4239-42 [2370865] Genes Dev. 1990 Dec;4(12B):2235-41 [2279697] J Virol. 1992 Jan;66(1):512-23 [1309260] Br J Haematol. 1976 Aug;33(4):451-8 [188440] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Expression of biologically active recombinant keratinocyte growth factor. Structure/function analysis of amino-terminal truncation mutants. AN - 75576801; 8428972 AB - Keratinocyte growth factor (KGF) is a newly identified member of the fibroblast growth factor (FGF) family (FGF-7). KGF is expressed by stromal fibroblasts and acts on epithelial cells in a paracrine mode. To facilitate structure/function studies, we utilized the T7 prokaryotic expression system to synthesize this growth factor. Recombinant KGF (rKGF) was mitogenic with a specific activity around 10-fold higher than native KGF. By in vitro mutagenesis, we generated a series of KGF mutants with sequential deletions of the amino-terminal domain, the most divergent region among different FGF members. Mutant proteins, produced in bacteria, were tested for their ability to bind heparin, bind and activate the KGF receptor, and induce DNA synthesis. Heparin binding properties were preserved with deletion of up to 28 amino-terminal residues of the mature KGF but lost by the deletion of an additional 10 residues. Biological activity of mutants with deletions of up to 10 residues was comparable to that of rKGF. However, deletion of 29 residues resulted in significantly reduced ability to stimulate KGF receptor tyrosine-kinase activity and DNA synthesis, although this mutant bound the receptor at high affinity. These characteristics of a partial agonist may be useful in the development of competitive antagonists of KGF action. JF - The Journal of biological chemistry AU - Ron, D AU - Bottaro, D P AU - Finch, P W AU - Morris, D AU - Rubin, J S AU - Aaronson, S A AD - Laboratory of Cellular and Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/02/05/ PY - 1993 DA - 1993 Feb 05 SP - 2984 EP - 2988 VL - 268 IS - 4 SN - 0021-9258, 0021-9258 KW - Fgf7 protein, mouse KW - 0 KW - Fibroblast Growth Factor 10 KW - Growth Substances KW - Oligodeoxyribonucleotides KW - RNA, Messenger KW - Recombinant Proteins KW - Fibroblast Growth Factor 7 KW - 126469-10-1 KW - Fibroblast Growth Factors KW - 62031-54-3 KW - Heparin KW - 9005-49-6 KW - Index Medicus KW - Animals KW - Cell Division -- drug effects KW - Gene Expression KW - Mice KW - Amino Acid Sequence KW - RNA, Messenger -- genetics KW - Structure-Activity Relationship KW - Cloning, Molecular KW - Base Sequence KW - Blotting, Western KW - Cells, Cultured KW - Oligodeoxyribonucleotides -- chemistry KW - Genetic Vectors KW - In Vitro Techniques KW - Molecular Sequence Data KW - Heparin -- metabolism KW - Sequence Deletion KW - Growth Substances -- genetics KW - Growth Substances -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75576801?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Expression+of+biologically+active+recombinant+keratinocyte+growth+factor.+Structure%2Ffunction+analysis+of+amino-terminal+truncation+mutants.&rft.au=Ron%2C+D%3BBottaro%2C+D+P%3BFinch%2C+P+W%3BMorris%2C+D%3BRubin%2C+J+S%3BAaronson%2C+S+A&rft.aulast=Ron&rft.aufirst=D&rft.date=1993-02-05&rft.volume=268&rft.issue=4&rft.spage=2984&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-08 N1 - Date created - 1993-03-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Gene-specific DNA repair of interstrand cross-links induced by chemotherapeutic agents can be preferential. AN - 75562988; 8428941 AB - The gene-specific formation and repair of interstrand cross-links (ICL) were measured in the dihydrofolate reductase (DHFR) gene in hamster cells. Cells were treated with two different chemotherapeutic agents, nitrogen mustard and cisplatin, and the frequency of cross-links was quantified in the active gene and in a downstream, inactive region. About 5% of total lesions induced by these agents were ICL. Whereas the frequencies of cross-links formed were similar in the gene and in the noncoding region after cisplatin treatment, there were more nitrogen mustard-induced cross-links in the inactive region than in the active gene. At low levels of cross-linking, we found preferential DNA repair in the active gene as compared to the inactive region. At higher levels of cross-linking, there was no difference in repair rates between the gene and the noncoding region due to an increase in the repair efficiency in the inactive DNA. Implications of fine structural organization of cross-link repair are discussed. JF - The Journal of biological chemistry AU - Larminat, F AU - Zhen, W AU - Bohr, V A AD - Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/02/05/ PY - 1993 DA - 1993 Feb 05 SP - 2649 EP - 2654 VL - 268 IS - 4 SN - 0021-9258, 0021-9258 KW - Cross-Linking Reagents KW - 0 KW - Mechlorethamine KW - 50D9XSG0VR KW - DNA KW - 9007-49-2 KW - Tetrahydrofolate Dehydrogenase KW - EC 1.5.1.3 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Animals KW - Genes KW - In Vitro Techniques KW - DNA -- chemistry KW - CHO Cells KW - Transcription, Genetic KW - DNA Replication KW - Tetrahydrofolate Dehydrogenase -- genetics KW - Cricetinae KW - Cross-Linking Reagents -- chemistry KW - Cisplatin -- chemistry KW - Mechlorethamine -- toxicity KW - DNA Repair KW - Mechlorethamine -- chemistry KW - DNA Damage KW - Cisplatin -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75562988?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Gene-specific+DNA+repair+of+interstrand+cross-links+induced+by+chemotherapeutic+agents+can+be+preferential.&rft.au=Larminat%2C+F%3BZhen%2C+W%3BBohr%2C+V+A&rft.aulast=Larminat&rft.aufirst=F&rft.date=1993-02-05&rft.volume=268&rft.issue=4&rft.spage=2649&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-08 N1 - Date created - 1993-03-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Role of tyrosine kinase activity in signal transduction by the insulin-like growth factor-I (IGF-I) receptor. Characterization of kinase-deficient IGF-I receptors and the action of an IGF-I-mimetic antibody (alpha IR-3). AN - 75561523; 7679099 AB - The insulin-like growth factor-I (IGF-I) receptor is a member of a large family of transmembrane signal transducing molecules. The defining characteristic of this class of receptors is the intrinsic tyrosine kinase activity of the cytoplasmic domain. While it has been demonstrated that this tyrosine kinase activity is necessary for the action of a number of transmembrane tyrosine kinase receptors, no evidence of this type has been adduced to date with respect to the signaling requirement of the IGF-I receptor. We have now shown that stably transfected NIH-3T3 cell lines overexpressing human IGF-I receptors display increased responses to IGF-I and an IGF-I-mimetic antibody, alpha IR-3, in terms of short, intermediate, and long term actions initiated by activation of the IGF-I receptor. These include receptor autophosphorylation, activation of phosphatidylinositol-3-kinase and 2-deoxyglucose uptake, induction of ornithine decarboxylase gene expression, and stimulation of thymidine incorporation. In short term responses, the kinetics seen with alpha IR-3 were slower than those seen with IGF-I. These effects were severely decreased in clones expressing human IGF-I receptors in which the lysine residue in the ATP-binding site of the tyrosine kinase domain had been mutated to alanine or arginine. This was true for both IGF-I and alpha IR-3. These results indicate that, for all parameters tested, the tyrosine kinase activity of the IGF-I receptor is necessary for activation of the IGF-I-stimulated signal transduction cascade. Additionally, the effects of alpha IR-3 also require tyrosine kinase activity. JF - The Journal of biological chemistry AU - Kato, H AU - Faria, T N AU - Stannard, B AU - Roberts, C T AU - LeRoith, D AD - Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/02/05/ PY - 1993 DA - 1993 Feb 05 SP - 2655 EP - 2661 VL - 268 IS - 4 SN - 0021-9258, 0021-9258 KW - Oligodeoxyribonucleotides KW - 0 KW - RNA, Messenger KW - Receptors, Somatomedin KW - Phosphotyrosine KW - 21820-51-9 KW - Tyrosine KW - 42HK56048U KW - Deoxyglucose KW - 9G2MP84A8W KW - Phosphotransferases KW - EC 2.7.- KW - Phosphatidylinositol 3-Kinases KW - EC 2.7.1.- KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Ornithine Decarboxylase KW - EC 4.1.1.17 KW - Index Medicus KW - Gene Expression -- drug effects KW - 3T3 Cells KW - Animals KW - Enzyme Activation KW - Mice KW - Immunologic Techniques KW - RNA, Messenger -- genetics KW - Phosphotransferases -- metabolism KW - Ornithine Decarboxylase -- metabolism KW - Mutagenesis, Site-Directed KW - Base Sequence KW - Oligodeoxyribonucleotides -- chemistry KW - Molecular Sequence Data KW - Tyrosine -- metabolism KW - Tyrosine -- analogs & derivatives KW - Cell Cycle KW - Signal Transduction KW - Deoxyglucose -- metabolism KW - Receptors, Somatomedin -- physiology KW - Protein-Tyrosine Kinases -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75561523?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Role+of+tyrosine+kinase+activity+in+signal+transduction+by+the+insulin-like+growth+factor-I+%28IGF-I%29+receptor.+Characterization+of+kinase-deficient+IGF-I+receptors+and+the+action+of+an+IGF-I-mimetic+antibody+%28alpha+IR-3%29.&rft.au=Kato%2C+H%3BFaria%2C+T+N%3BStannard%2C+B%3BRoberts%2C+C+T%3BLeRoith%2C+D&rft.aulast=Kato&rft.aufirst=H&rft.date=1993-02-05&rft.volume=268&rft.issue=4&rft.spage=2655&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-08 N1 - Date created - 1993-03-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Different isozymes of protein kinase C mediate feedback inhibition of phospholipase C and stimulatory signals for exocytosis in rat RBL-2H3 cells. AN - 75560948; 8381401 AB - Previous studies indicated that rat basophilic RBL-2H3 cells contained the Ca(2+)-dependent alpha and beta and the Ca(2+)-independent delta, epsilon, and zeta isoforms of protein kinase C (PKC); of these, PKC beta and delta were the most potent transducers of signals for exocytosis in antigen-stimulated permeabilized cells. Exocytosis, nevertheless, was still dependent on an elevated free Ca2+. (Ozawa, K., Szallasi, Z., Kazanietz, M. G., Blumberg, P. M., Mischak, H., Mushinski, J. F., and Beaven, M. A. (1993) J. Biol. Chem. 268, 1749-1756). We now demonstrate that PKC alpha and epsilon, exclusively, inhibit antigen-induced hydrolysis of inositol phospholipids in the same permeabilized RBL-2H3 cells. Unlike secretion, the inhibitory actions occurred at a basal concentration (0.1 microM) of free Ca2+. The inhibitory actions of the two isozymes were potentiated by 20 nM phorbol 12-myristate 13-acetate. As indicated by the effects of the phorbol ester, the probable mechanism was reduced tyrosine phosphorylation of phospholipase C gamma 1. The negative regulation of phospholipase C was apparent in intact cells, because the PKC inhibitor Ro31-7549 or down-regulation of PKC with phorbol ester enhanced antigen-induced hydrolysis of inositol phospholipids. The concentrations of the various isozymes of PKC in RBL-2H3 cells, as estimated by immunoblotting studies, were sufficient for promotion of exocytosis (i.e. beta and delta) and inhibition of phospholipid hydrolysis (i.e. alpha and epsilon). JF - The Journal of biological chemistry AU - Ozawa, K AU - Yamada, K AU - Kazanietz, M G AU - Blumberg, P M AU - Beaven, M A AD - Laboratory of Chemical Pharmacology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/02/05/ PY - 1993 DA - 1993 Feb 05 SP - 2280 EP - 2283 VL - 268 IS - 4 SN - 0021-9258, 0021-9258 KW - Antigens KW - 0 KW - Indoles KW - Inositol Phosphates KW - Isoenzymes KW - Maleimides KW - Phosphatidylinositols KW - Ro 31-7549 KW - 125313-65-7 KW - Immunoglobulin E KW - 37341-29-0 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Type C Phospholipases KW - EC 3.1.4.- KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Phosphatidylinositols -- metabolism KW - Inositol Phosphates -- metabolism KW - Exocytosis KW - Isoenzymes -- metabolism KW - Rats KW - Calcium -- metabolism KW - Tumor Cells, Cultured KW - Immunoglobulin E -- physiology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Feedback KW - Indoles -- pharmacology KW - Antigens -- administration & dosage KW - Leukemia, Experimental -- enzymology KW - Signal Transduction KW - Maleimides -- pharmacology KW - Protein Kinase C -- metabolism KW - Basophils -- enzymology KW - Type C Phospholipases -- antagonists & inhibitors KW - Type C Phospholipases -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75560948?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Different+isozymes+of+protein+kinase+C+mediate+feedback+inhibition+of+phospholipase+C+and+stimulatory+signals+for+exocytosis+in+rat+RBL-2H3+cells.&rft.au=Ozawa%2C+K%3BYamada%2C+K%3BKazanietz%2C+M+G%3BBlumberg%2C+P+M%3BBeaven%2C+M+A&rft.aulast=Ozawa&rft.aufirst=K&rft.date=1993-02-05&rft.volume=268&rft.issue=4&rft.spage=2280&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-08 N1 - Date created - 1993-03-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Moderate caffeine use and the risk of spontaneous abortion and intrauterine growth retardation. AN - 75560818; 8421363 AB - To examine the relationship between caffeine consumption during pregnancy and the occurrence of spontaneous abortion and intrauterine growth retardation. A cohort of 431 women, enrolled in a multicenter study within 21 days of conception, was monitored throughout pregnancy to determine (1) caffeine exposure, (2) exposure to other risk factors, (3) fetal growth as assessed by ultrasonography, and (4) pregnancy outcome. Spontaneous abortion, intrauterine growth, birth weight, and head circumference. The mean (+/- SD) first-trimester caffeine consumption was not significantly higher in women who aborted (125.9 +/- 123.1 mg) than in women who delivered liveborn infants (111.6 +/- 107.0 mg) (P = 34). The adjusted odds ratio (OR) for spontaneous abortion was 1.15 (95% confidence interval [CI], 0.89 to 1.49). Early fetal growth, assessed by crown-rump length on ultrasonographic examination, was not affected by caffeine. Although the group consuming the most caffeine (> 300 mg/d) had a significantly higher proportion of babies with birth weights and head circumferences below the 10th percentile in the crude analysis, the association with caffeine was no longer significant when other risk factors (notably smoking) were taken into account. The adjusted ORs were 1.11 (95% CI, 0.88 to 1.40) for decreased birth weight and 1.09 (95% CI, 0.86 to 1.37) for smaller head circumference. Close monitoring of a cohort identified very soon after conception enabled us to identify all abortions after 21 days postconception, monitor intrauterine growth prospectively, and track caffeine use. Despite this intensive surveillance, we found no evidence that moderate caffeine use increased the risk of spontaneous abortion, intrauterine growth retardation, or microcephaly after accounting for other risk factors. JF - JAMA AU - Mills, J L AU - Holmes, L B AU - Aarons, J H AU - Simpson, J L AU - Brown, Z A AU - Jovanovic-Peterson, L G AU - Conley, M R AU - Graubard, B I AU - Knopp, R H AU - Metzger, B E AD - Epidemiology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/02/03/ PY - 1993 DA - 1993 Feb 03 SP - 593 EP - 597 VL - 269 IS - 5 SN - 0098-7484, 0098-7484 KW - Caffeine KW - 3G6A5W338E KW - Abridged Index Medicus KW - Index Medicus KW - Regression Analysis KW - Prospective Studies KW - Ultrasonography, Prenatal KW - Embryonic and Fetal Development KW - Risk Factors KW - Humans KW - Cohort Studies KW - Adult KW - Female KW - Pregnancy KW - Abortion, Spontaneous -- etiology KW - Fetal Growth Retardation -- etiology KW - Pregnancy Outcome -- epidemiology KW - Fetal Growth Retardation -- epidemiology KW - Caffeine -- adverse effects KW - Abortion, Spontaneous -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75560818?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=JAMA&rft.atitle=Moderate+caffeine+use+and+the+risk+of+spontaneous+abortion+and+intrauterine+growth+retardation.&rft.au=Mills%2C+J+L%3BHolmes%2C+L+B%3BAarons%2C+J+H%3BSimpson%2C+J+L%3BBrown%2C+Z+A%3BJovanovic-Peterson%2C+L+G%3BConley%2C+M+R%3BGraubard%2C+B+I%3BKnopp%2C+R+H%3BMetzger%2C+B+E&rft.aulast=Mills&rft.aufirst=J&rft.date=1993-02-03&rft.volume=269&rft.issue=5&rft.spage=593&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-17 N1 - Date created - 1993-02-17 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: JAMA. 1993 Jul 7;270(1):47; author reply 47-8 [8510294] JAMA. 1993 Jul 7;270(1):46-7; author reply 47-8 [8357378] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Learning and memory in monozygotic twins discordant for schizophrenia. AN - 85260504; pmid-8475218 AB - Learning and memory were assessed in 24 monozygotic (MZ) pairs of individuals discordant for schizophrenia or delusional disorder and seven normal pairs of MZ twins. On declarative memory tasks, the affected group displayed a pattern that might best be characterized as dysmnesic in that they performed significantly worse than the discordant unaffected group on story recall, paired associated learning, and visual recall of designs, but they learned over time, had relatively preserved recognition memory, and did not show profoundly accelerated rates of forgetting. Effortful, volitional retrieval from the lexicon, measured by verbal fluency, was also compromised in the affected group. On the other hand, procedural learning of the motor skill in a pursuit rotor task was relatively intact in the affected group. Comparisons of the normal group and unaffected group indicated that the latter group had very mild impairments in some aspects of episodic memory, namely, immediate and delayed recall of stories and delayed recall of designs. It is highly unlikely that the impairments observed in the affected group can be attributed to differences in genome, family environment, socioeconomic circumstance, or educational opportunity, as all of these were controlled by the twin paradigm. Rather, the impairments appear to be related to the intercession of disease. The neuropsychological profile is consistent with frontal lobe and medial temporal lobe dysfunction, as noted in this sample as well as other samples of schizophrenic singletons. Significant correlations between many measures of memory and global level of social and vocational functioning within the discordant group were also found. Thus difficulties in rapidly acquiring new information and propitiously retrieving old information may burden patients with schizophrenia in many of the transactions of everyday life. JF - Psychological Medicine AU - Goldberg, T E AU - Torrey, E F AU - Gold, J M AU - Ragland, J D AU - Bigelow, L B AU - Weinberger, D R AD - Clinical Brain Disorders Branch, National Institute of Mental Health, Neuroscience Center at Saint Elizabeths, Washington, DC 20032. PY - 1993 SP - 71 EP - 85 VL - 23 IS - 1 SN - 0033-2917, 0033-2917 KW - Verbal Behavior KW - Human KW - Learning Disorders KW - Memory Disorders KW - Wechsler Scales KW - Frontal Lobe KW - Schizophrenia KW - Psychiatric Status Rating Scales KW - Twins, Monozygotic KW - Adult KW - Temporal Lobe KW - Adolescent KW - Male KW - Female UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85260504?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychological+Medicine&rft.atitle=Learning+and+memory+in+monozygotic+twins+discordant+for+schizophrenia.&rft.au=Goldberg%2C+T+E%3BTorrey%2C+E+F%3BGold%2C+J+M%3BRagland%2C+J+D%3BBigelow%2C+L+B%3BWeinberger%2C+D+R&rft.aulast=Goldberg&rft.aufirst=T&rft.date=1993-02-01&rft.volume=23&rft.issue=1&rft.spage=71&rft.isbn=&rft.btitle=&rft.title=Psychological+Medicine&rft.issn=00332917&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Fine needle aspiration cytology of submucosal nodules in patients with Zollinger-Ellison syndrome. AN - 85224239; pmid-8093826 AB - Submucosal nodules are often encountered during investigations of the upper gastrointestinal (GI) tract. This is particularly true in diseases resulting in chronic hypergastrinemia, such as Zollinger-Ellison syndrome (ZES), in which submucosal gastric and duodenal lesions can occur. Forceps biopsy of submucosal lesions often yields only normal mucosa; however, fine needle aspiration cytology (FNAC) has recently been described as having high diagnostic accuracy for submucosal tumors. Therefore, we prospectively studied the use of FNAC in 43 patients with ZES. Overall, 33% of patients with ZES had nodules. In patients with the sporadic form of ZES, submucosal nodules were found in 18%, whereas submucosal nodules were found in 80% of patients who had ZES in conjunction with multiple endocrine neoplasia type I (MEN-I). FNAC identified 11/12 (92%) of the neuroendocrine tumors, and identified another 8/9 as non-neuroendocrine. Jumbo forceps biopsy was performed on 18 nodules and diagnosed one neuroendocrine tumor. Subsequently, 11 of these nodules were found to possess neuroendocrine tumor; thus only 1/11 (9%) neuroendocrine tumors removed were accurately identified by jumbo forceps biopsy. Of the first 14 nodules, sufficient tissue was left after biopsy to permit snare polypectomy on 12 nodules. Four nodules were found to contain neuroendocrine tumor. Snare polypectomy resulted in a duodenal perforation that required surgery in one patient, and thus was not performed on the final seven nodules.(ABSTRACT TRUNCATED AT 250 WORDS) JF - The American Journal of Gastroenterology AU - Benya, R V AU - Metz, D C AU - Hijazi, Y J AU - Fishbeyn, V A AU - Pisegna, J R AU - Jensen, R T AD - Digestive Diseases Branch, National Institutes of Health, Bethesda, Maryland. PY - 1993 SP - 258 EP - 265 VL - 88 IS - 2 SN - 0002-9270, 0002-9270 KW - Prospective Studies KW - Comparative Study KW - Zollinger-Ellison Syndrome KW - Human KW - Gastric Mucosa KW - Middle Age KW - Biopsy KW - Multiple Endocrine Neoplasia KW - Endoscopy, Digestive System KW - Intestinal Mucosa KW - Male KW - Female KW - Biopsy, Needle UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85224239?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+Journal+of+Gastroenterology&rft.atitle=Fine+needle+aspiration+cytology+of+submucosal+nodules+in+patients+with+Zollinger-Ellison+syndrome.&rft.au=Benya%2C+R+V%3BMetz%2C+D+C%3BHijazi%2C+Y+J%3BFishbeyn%2C+V+A%3BPisegna%2C+J+R%3BJensen%2C+R+T&rft.aulast=Benya&rft.aufirst=R&rft.date=1993-02-01&rft.volume=88&rft.issue=2&rft.spage=258&rft.isbn=&rft.btitle=&rft.title=The+American+Journal+of+Gastroenterology&rft.issn=00029270&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Retrieval inhibition in anomia. AN - 85154272; pmid-8428314 AB - Reading latencies for anomic temporal lobe epileptics, nonanomic epileptic patient controls, and normal controls were measured in semantic priming paradigms. Both the epileptic controls and the normal controls showed typical semantic facilitation with faster response times following related than unrelated primes. The anomic subjects, on the other hand, were much slower to read targets following presentation of semantically related items than following unrelated primes. This inhibition effect was seen to increase as the number of related primes increased. These patterns were observed both when picture primes (Experiment 1) and word primes (Experiment 2) were used. These findings were interpreted as evidence for a category-specific retrieval inhibition in the anomic epileptic subjects. JF - Brain and Language AU - Blaxton, T A AU - Bookheimer, S Y AD - National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892. PY - 1993 SP - 221 EP - 237 VL - 44 IS - 2 SN - 0093-934X, 0093-934X UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85154272?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+and+Language&rft.atitle=Retrieval+inhibition+in+anomia.&rft.au=Blaxton%2C+T+A%3BBookheimer%2C+S+Y&rft.aulast=Blaxton&rft.aufirst=T&rft.date=1993-02-01&rft.volume=44&rft.issue=2&rft.spage=221&rft.isbn=&rft.btitle=&rft.title=Brain+and+Language&rft.issn=0093934X&rft_id=info:doi/ LA - English DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Long-term protection of macaques against high-dose type D retrovirus challenge after immunization with recombinant vaccinia virus expressing envelope glycoproteins. AN - 76007548; 8411111 AB - Recombinant vaccinia virus expressing the envelope proteins of type D retrovirus-Washington (SRV-2/W) was used to immunize macaques against SRV-2 infection. Four immunized macaques which had resisted a prior low-dose challenge were rechallenged with a high dose (10(6) infectious particles) of SRV-2 two years after being immunized. All four non-immunized control macaques became infected, but the four vaccinated animals resisted this intravenous challenge, as determined by the inability to detect SRV-2 in peripheral blood mononuclear cells and by the lack of seroconversion to new viral antigens. JF - Journal of medical primatology AU - Benveniste, R E AU - Kuller, L AU - Roodman, S T AU - Hu, S L AU - Morton, W R AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick Cancer Research and Development Center, MD. PY - 1993 SP - 74 EP - 79 VL - 22 IS - 2-3 SN - 0047-2565, 0047-2565 KW - DNA, Viral KW - 0 KW - Vaccines, Synthetic KW - Viral Envelope Proteins KW - Viral Vaccines KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Immunoblotting KW - Vaccinia virus -- immunology KW - Macaca nemestrina KW - Immunization KW - Vaccines, Synthetic -- pharmacology KW - Polymerase Chain Reaction KW - Viral Envelope Proteins -- immunology KW - Base Sequence KW - Molecular Sequence Data KW - DNA, Viral -- blood KW - Vaccines, Synthetic -- administration & dosage KW - DNA, Viral -- genetics KW - Time Factors KW - Simian Acquired Immunodeficiency Syndrome -- immunology KW - Viral Vaccines -- administration & dosage KW - Retroviruses, Simian -- isolation & purification KW - Retroviruses, Simian -- genetics KW - Simian Acquired Immunodeficiency Syndrome -- microbiology KW - Viral Vaccines -- pharmacology KW - Simian Acquired Immunodeficiency Syndrome -- prevention & control KW - Retroviruses, Simian -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76007548?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+medical+primatology&rft.atitle=Long-term+protection+of+macaques+against+high-dose+type+D+retrovirus+challenge+after+immunization+with+recombinant+vaccinia+virus+expressing+envelope+glycoproteins.&rft.au=Benveniste%2C+R+E%3BKuller%2C+L%3BRoodman%2C+S+T%3BHu%2C+S+L%3BMorton%2C+W+R&rft.aulast=Benveniste&rft.aufirst=R&rft.date=1993-02-01&rft.volume=22&rft.issue=2-3&rft.spage=74&rft.isbn=&rft.btitle=&rft.title=Journal+of+medical+primatology&rft.issn=00472565&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-23 N1 - Date created - 1993-11-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Detection of serum antibodies in Ethiopian baboons that cross-react with SIV, HTLV-I, and type D retroviral antigens. AN - 76000786; 8411104 AB - Baboons (Papio cynocephalus) imported from Ethiopia were screened for antibodies to various primate retroviruses by immunoblotting. Antibodies that cross-reacted with SIV/Mne or with type D viral antigens were detected in approximately one-third of these animals. In addition, 20% of these baboons had antibodies that cross-reacted with HTLV-I viral antigens. These data suggest that wild-caught baboons are infected with retroviruses only partially related to known primate viral isolates. JF - Journal of medical primatology AU - Benveniste, R E AU - Hill, R W AU - Knott, W B AU - Tsai, C C AU - Kuller, L AU - Morton, W R AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702-1201. PY - 1993 SP - 124 EP - 128 VL - 22 IS - 2-3 SN - 0047-2565, 0047-2565 KW - Antibodies, Viral KW - 0 KW - Antigens, Viral KW - Gene Products, gag KW - Index Medicus KW - AIDS/HIV KW - Immunoblotting KW - Animals KW - Ethiopia KW - Gene Products, gag -- immunology KW - Cross Reactions KW - Antibodies, Viral -- blood KW - Simian Immunodeficiency Virus -- immunology KW - Papio -- immunology KW - Human T-lymphotropic virus 1 -- immunology KW - Papio -- microbiology KW - Retroviruses, Simian -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76000786?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+medical+primatology&rft.atitle=Detection+of+serum+antibodies+in+Ethiopian+baboons+that+cross-react+with+SIV%2C+HTLV-I%2C+and+type+D+retroviral+antigens.&rft.au=Benveniste%2C+R+E%3BHill%2C+R+W%3BKnott%2C+W+B%3BTsai%2C+C+C%3BKuller%2C+L%3BMorton%2C+W+R&rft.aulast=Benveniste&rft.aufirst=R&rft.date=1993-02-01&rft.volume=22&rft.issue=2-3&rft.spage=124&rft.isbn=&rft.btitle=&rft.title=Journal+of+medical+primatology&rft.issn=00472565&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-23 N1 - Date created - 1993-11-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Is aggressive therapy effective for lupus? AN - 75908284; 8356258 AB - Intravenous cyclophosphamide is an effective form of aggressive therapy for the management of a wide range of serious manifestations of systemic lupus erythematosus. Although it has been best studied in patients with progressive lupus nephritis, recent evidence indicates an important role for this therapy for other clinical lupus indications, particularly acute neurologic diseases. The available comparative data suggest that intravenous cyclophosphamide is far more effective than intensive corticosteroid therapies, including conventional high-dose oral therapy as well as bolus intravenous therapy. Differences in efficacy compared with oral regimens of cyclophosphamide or azathioprine are less clear, although clinical experience would seem to suggest that intravenous cyclophosphamide has a more rapid onset of action clinically than low-dose oral therapies. Finally, the toxicity profile of intravenous cyclophosphamide compares favorably with other aggressive approaches to drug management and does not pose an unacceptable risk. The future impact of several current investigational therapies remains to be defined. JF - Rheumatic diseases clinics of North America AU - Klippel, J H AD - National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 249 EP - 261 VL - 19 IS - 1 SN - 0889-857X, 0889-857X KW - Biological Products KW - 0 KW - Carcinogens KW - Immunoglobulins, Intravenous KW - Cyclophosphamide KW - 8N3DW7272P KW - Index Medicus KW - Lymphoid Tissue -- radiation effects KW - Evaluation Studies as Topic KW - Biological Products -- therapeutic use KW - Nervous System Diseases -- drug therapy KW - Lupus Nephritis -- drug therapy KW - Injections, Intravenous KW - Nervous System Diseases -- etiology KW - Humans KW - Recombination, Genetic KW - Plasma Exchange KW - Lupus Erythematosus, Systemic -- complications KW - Cyclophosphamide -- therapeutic use KW - Lupus Erythematosus, Systemic -- therapy KW - Cyclophosphamide -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75908284?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Rheumatic+diseases+clinics+of+North+America&rft.atitle=Is+aggressive+therapy+effective+for+lupus%3F&rft.au=Klippel%2C+J+H&rft.aulast=Klippel&rft.aufirst=J&rft.date=1993-02-01&rft.volume=19&rft.issue=1&rft.spage=249&rft.isbn=&rft.btitle=&rft.title=Rheumatic+diseases+clinics+of+North+America&rft.issn=0889857X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-22 N1 - Date created - 1993-09-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Which patients with antiphospholipid antibody should be treated and how? AN - 75890042; 8356257 AB - The tests for antiphospholipid antibody are relatively crude but usable. Asymptomatic persons with incidentally discovered antiphospholipid antibody do not need treatment. Those with symptoms are best treated with anticoagulation, but data specifically supporting aspirin, heparin, or warfarin or combinations thereof remain to be generated. High-dose corticosteroid therapy has at best equivocal efficacy and much toxicity and should be used only for lupus activity and not for phenomena of the antiphospholipid antibody syndrome. The roles of low-dose corticosteroid therapy, immunosuppressive agents, and other treatments are unknown. JF - Rheumatic diseases clinics of North America AU - Lockshin, M D AD - National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 235 EP - 247 VL - 19 IS - 1 SN - 0889-857X, 0889-857X KW - Adrenal Cortex Hormones KW - 0 KW - Antibodies, Antiphospholipid KW - Anticoagulants KW - Index Medicus KW - Thrombosis -- therapy KW - Thrombosis -- immunology KW - Adrenal Cortex Hormones -- therapeutic use KW - Thrombocytopenia -- therapy KW - Thrombocytopenia -- immunology KW - Immunologic Tests KW - Anticoagulants -- therapeutic use KW - Nervous System Diseases -- therapy KW - Nervous System Diseases -- immunology KW - Humans KW - Pregnancy -- immunology KW - Female KW - Antibodies, Antiphospholipid -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75890042?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Rheumatic+diseases+clinics+of+North+America&rft.atitle=Which+patients+with+antiphospholipid+antibody+should+be+treated+and+how%3F&rft.au=Lockshin%2C+M+D&rft.aulast=Lockshin&rft.aufirst=M&rft.date=1993-02-01&rft.volume=19&rft.issue=1&rft.spage=235&rft.isbn=&rft.btitle=&rft.title=Rheumatic+diseases+clinics+of+North+America&rft.issn=0889857X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-22 N1 - Date created - 1993-09-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Phase I trial of dihydrolenperone in lung cancer patients: a novel compound with in vitro activity against lung cancer. AN - 75887309; 8349433 AB - Antitumor activity of the butyrophenone dihydrolenperone in non-small cell lung cancer was initially suggested by in vitro screening against tumor cells derived from fresh surgical samples using the human tumor colony-forming assay. We have completed a directed phase I trial in patients with lung cancer. Thirty-two patients with lung cancer have completed 25 courses of therapy at doses of 10 to 60 mg/square meter orally on a twice daily schedule. Twenty-three men and 9 women with a median age of 55 (range 24-69) were entered. Twenty-four were performance status 0 or 1 and 8 were 2. The maximum tolerated dose was 50 mg/square meter orally twice daily and the dose limiting toxicity was somnolence. Of the 32 patients, 18 developed symptomatic hypotension (grade 1 or 2). There was no significant hematologic, renal, or hepatic toxicity. In vitro drug testing using the MTT [3-(4,5- dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (thiazolyl blue)] assay confirmed 50% inhibition of non-small cell and small cell lung cancer cell line growth at 70-450 micromolar concentrations. Plasma dihydrolenperone levels were at least 75-fold less than levels at which in vitro activity was observed. We conclude: 1) the maximum tolerated dose in our study is 50 mg/square meter orally twice daily, 2) the dose-limiting side effect of dihydrolenperone is somnolence, and 3) the concentrations of dihydrolenperone observed in plasma are significantly lower than those associated with in vitro activity. JF - Investigational new drugs AU - Johnson, B E AU - Parker, R AU - Tsai, C M AU - Baltz, J AU - Miller, M J AU - Shoemaker, R AU - Phelps, R AU - Bastian, A AU - Stocker, J AU - Phares, J AD - National Cancer Institute-Navy Medical Oncology Branch, Bethesda, MD 20889-5105. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 29 EP - 37 VL - 11 IS - 1 SN - 0167-6997, 0167-6997 KW - Antineoplastic Agents KW - 0 KW - Butyrophenones KW - Drugs, Investigational KW - dihydrolenperone KW - 9RJ5N8VE7Z KW - Haloperidol KW - J6292F8L3D KW - Index Medicus KW - Tumor Cells, Cultured KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Male KW - Female KW - Chromatography, High Pressure Liquid KW - Drugs, Investigational -- therapeutic use KW - Haloperidol -- therapeutic use KW - Butyrophenones -- blood KW - Lung Neoplasms -- drug therapy KW - Butyrophenones -- therapeutic use KW - Drugs, Investigational -- adverse effects KW - Antineoplastic Agents -- blood KW - Antineoplastic Agents -- therapeutic use KW - Butyrophenones -- adverse effects KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75887309?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Investigational+new+drugs&rft.atitle=Phase+I+trial+of+dihydrolenperone+in+lung+cancer+patients%3A+a+novel+compound+with+in+vitro+activity+against+lung+cancer.&rft.au=Johnson%2C+B+E%3BParker%2C+R%3BTsai%2C+C+M%3BBaltz%2C+J%3BMiller%2C+M+J%3BShoemaker%2C+R%3BPhelps%2C+R%3BBastian%2C+A%3BStocker%2C+J%3BPhares%2C+J&rft.aulast=Johnson&rft.aufirst=B&rft.date=1993-02-01&rft.volume=11&rft.issue=1&rft.spage=29&rft.isbn=&rft.btitle=&rft.title=Investigational+new+drugs&rft.issn=01676997&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-15 N1 - Date created - 1993-09-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Phase II study of fazarabine (NSC 281272) in patients with metastatic colon cancer. AN - 75886841; 7688714 AB - Fazarabine (Arabinofuranosyl-5-azacytosine) is a synthetic pyrimidine nucleoside which combines the arabinose sugar of cytosine arabinoside with the triazine base of 5-azacytidine. It has demonstrated activity against a variety of human solid tumor xenografts including colon, lung and breast cancers. Eighteen patients with refractory metastatic colon cancer were enrolled in a phase II trial of fazarabine. The drug was administered as a 72 hr continuous infusion every 3-4 weeks; the starting dose was 2 mg/m2/hr as established in a previous phase I study. The major toxicity was neutropenia, as predicted from the phase I study. The median time to nadir for cycle 1 was 20 days, with a median granulocyte count of 437/microliters (range 36-1600/microliters); recovery was within 2-4 days, with only one incidence of fever and neutropenia in 42 cycles. Especially noted for their absence were thrombocytopenia, nausea, vomiting and stomatitis. No objective clinical responses were seen; one patient had stabilization of rapidly growing liver metastases for a period of 7 months. In view of fazarabine's narrow range of toxicities, future dose intensification trials utilizing fazarabine in combination with hematopoietic growth factors are worthy of consideration. JF - Investigational new drugs AU - Ben-Baruch, N AU - Denicoff, A M AU - Goldspiel, B R AU - O'Shaughnessy, J A AU - Cowan, K H AD - Medicine Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 71 EP - 74 VL - 11 IS - 1 SN - 0167-6997, 0167-6997 KW - Antineoplastic Agents KW - 0 KW - Drugs, Investigational KW - fazarabine KW - 5V71D8JOKK KW - Azacitidine KW - M801H13NRU KW - Index Medicus KW - Infusions, Intravenous KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Male KW - Female KW - Drugs, Investigational -- therapeutic use KW - Azacitidine -- therapeutic use KW - Azacitidine -- adverse effects KW - Colonic Neoplasms -- drug therapy KW - Drugs, Investigational -- adverse effects KW - Adenocarcinoma -- secondary KW - Antineoplastic Agents -- therapeutic use KW - Adenocarcinoma -- drug therapy KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75886841?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Investigational+new+drugs&rft.atitle=Phase+II+study+of+fazarabine+%28NSC+281272%29+in+patients+with+metastatic+colon+cancer.&rft.au=Ben-Baruch%2C+N%3BDenicoff%2C+A+M%3BGoldspiel%2C+B+R%3BO%27Shaughnessy%2C+J+A%3BCowan%2C+K+H&rft.aulast=Ben-Baruch&rft.aufirst=N&rft.date=1993-02-01&rft.volume=11&rft.issue=1&rft.spage=71&rft.isbn=&rft.btitle=&rft.title=Investigational+new+drugs&rft.issn=01676997&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-15 N1 - Date created - 1993-09-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Chloroquinoxaline sulfonamide: a sulfanilamide antitumor agent entering clinical trials. AN - 75882779; 8349430 AB - Chloroquinoxaline sulfonamide (CQS) has been developed to the clinical trial stage based on its activity in the Human Tumor Colony Forming Assay (HTCFA). In the HTCFA, CQS demonstrated inhibition of colony formation against breast, lung, melanoma and ovarian carcinomas. The mechanism of action of CQS is unknown. It does not appear to inhibit folate metabolism as does the structurally similar sulfaquinoxaline. Preclinical toxicology studies in dogs and rats have shown that CQS is toxic to lymphoid organs, bone marrow, gastrointestinal tract, pancreas, CNS, adrenal glands and testes. Toxicity was generally reversible with the exception of testicular atrophy in dogs and rats which occurred late and was not reversible within the study time frame. The pharmacokinetic data indicate that CQS binds to serum proteins in a dose and species specific manner. Terminal half-lives appear to vary between species from 60 hours in mice, 15 hours in rats, and 45-132 hours in dogs. Preliminary data indicate a longer terminal half-life in humans. Two phase I trials are ongoing using a 60 min infusion schedule once every 28 days. The starting dose for each trial was 18 mg/m2. JF - Investigational new drugs AU - Fisherman, J S AU - Osborn, B L AU - Chun, H G AU - Plowman, J AU - Smith, A C AU - Christian, M C AU - Zaharko, D S AU - Shoemaker, R H AD - Investigational Drug Branch, Cancer Therapy Evaluation Program, National Cancer Institute, Bethesda. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 1 EP - 9 VL - 11 IS - 1 SN - 0167-6997, 0167-6997 KW - Antineoplastic Agents KW - 0 KW - Drugs, Investigational KW - Quinoxalines KW - Sulfanilamides KW - 5-chloroquinoxaline-2-sulfanilamide KW - O0408QB48D KW - Index Medicus KW - Drug Screening Assays, Antitumor KW - Animals KW - Humans KW - Clinical Trials as Topic KW - Drugs, Investigational -- therapeutic use KW - Drugs, Investigational -- pharmacokinetics KW - Sulfanilamides -- therapeutic use KW - Quinoxalines -- therapeutic use KW - Sulfanilamides -- pharmacokinetics KW - Antineoplastic Agents -- pharmacokinetics KW - Quinoxalines -- pharmacokinetics KW - Antineoplastic Agents -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75882779?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Investigational+new+drugs&rft.atitle=Chloroquinoxaline+sulfonamide%3A+a+sulfanilamide+antitumor+agent+entering+clinical+trials.&rft.au=Fisherman%2C+J+S%3BOsborn%2C+B+L%3BChun%2C+H+G%3BPlowman%2C+J%3BSmith%2C+A+C%3BChristian%2C+M+C%3BZaharko%2C+D+S%3BShoemaker%2C+R+H&rft.aulast=Fisherman&rft.aufirst=J&rft.date=1993-02-01&rft.volume=11&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Investigational+new+drugs&rft.issn=01676997&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-15 N1 - Date created - 1993-09-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The metabolism of di(2-ethylhexyl)phthalate in the earthworm Lumbricus terrestris. AN - 75740303; 8098688 AB - 1. Earthworms can hydrolyze di-(2-ethylhexyl) phthalate (DEHP) to mono-2-ethylhexyl phthalate (MEHP) and phthalic acid (PA). 2. They apparently cannot produce the side-chain-oxidized derivatives of MEHP that constitute the major DEHP metabolites in higher animals. 3. With the assistance of intestinal bacterial Pseudomonas, the worm-derived PA is degraded through protocatechuic and beta-carboxymuconic acids to CO2. 4. There is an indication of a second pathway for degradation of PA leading through benzoic acid. JF - Comparative biochemistry and physiology. C, Comparative pharmacology and toxicology AU - Albro, P W AU - Corbett, J T AU - Schroeder, J L AD - Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 335 EP - 344 VL - 104 IS - 2 SN - 0742-8413, 0742-8413 KW - Anti-Bacterial Agents KW - 0 KW - Soil Pollutants KW - Diethylhexyl Phthalate KW - C42K0PH13C KW - Index Medicus KW - Animals KW - Chromatography, Liquid KW - Anti-Bacterial Agents -- pharmacology KW - Intestines -- microbiology KW - Diethylhexyl Phthalate -- metabolism KW - Oligochaeta -- metabolism KW - Soil Pollutants -- metabolism KW - Oligochaeta -- microbiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75740303?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Comparative+biochemistry+and+physiology.+C%2C+Comparative+pharmacology+and+toxicology&rft.atitle=The+metabolism+of+di%282-ethylhexyl%29phthalate+in+the+earthworm+Lumbricus+terrestris.&rft.au=Albro%2C+P+W%3BCorbett%2C+J+T%3BSchroeder%2C+J+L&rft.aulast=Albro&rft.aufirst=P&rft.date=1993-02-01&rft.volume=104&rft.issue=2&rft.spage=335&rft.isbn=&rft.btitle=&rft.title=Comparative+biochemistry+and+physiology.+C%2C+Comparative+pharmacology+and+toxicology&rft.issn=07428413&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-24 N1 - Date created - 1993-06-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Predicting the cytochrome P450 mediated metabolism of xenobiotics. AN - 75723497; 8485584 AB - The cytochrome P450s play a unique role in the metabolism of xenobiotics. Characteristics which allow a vast number of foreign compounds to be metabolized by a limited number of enzymes include broad substrate specificity and broad regioselectivity. Because of their importance in both the metabolism and toxicity of drugs and environmental contaminants, efforts are being made to use computational methods to predict these biotransformation pathways. This review describes the recent progress towards the prediction of the tertiary structures of the various P450s and the determination of the electronic characteristics of substrates which determine their tendency to be oxidized by the P450s. JF - Pharmacogenetics AU - Korzekwa, K R AU - Jones, J P AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 1 EP - 18 VL - 3 IS - 1 SN - 0960-314X, 0960-314X KW - CYP101 KW - CYP2 KW - Apoproteins KW - 0 KW - Xenobiotics KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Mixed Function Oxygenases KW - EC 1.- KW - Camphor 5-Monooxygenase KW - EC 1.14.15.1 KW - Index Medicus KW - Molecular Structure KW - Animals KW - Mixed Function Oxygenases -- chemistry KW - Mixed Function Oxygenases -- metabolism KW - Sequence Alignment KW - Models, Molecular KW - Humans KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Apoproteins -- metabolism KW - Mixed Function Oxygenases -- genetics KW - Cytochrome P-450 Enzyme System -- genetics KW - Xenobiotics -- metabolism KW - Cytochrome P-450 Enzyme System -- chemistry KW - Cytochrome P-450 Enzyme System -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75723497?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacogenetics&rft.atitle=Predicting+the+cytochrome+P450+mediated+metabolism+of+xenobiotics.&rft.au=Korzekwa%2C+K+R%3BJones%2C+J+P&rft.aulast=Korzekwa&rft.aufirst=K&rft.date=1993-02-01&rft.volume=3&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Pharmacogenetics&rft.issn=0960314X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-10 N1 - Date created - 1993-06-10 N1 - Date revised - 2017-01-13 N1 - Gene symbol - CYP101; CYP2 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Regulation of cytochrome P450 genes: molecular mechanisms. AN - 75721569; 8387380 JF - Pharmacogenetics AU - Gonzalez, F J AU - Liu, S Y AU - Yano, M AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 51 EP - 57 VL - 3 IS - 1 SN - 0960-314X, 0960-314X KW - CYP KW - CYP1A1 KW - CYP2C6 KW - CYP2E1 KW - CYP4A KW - Receptors, Aryl Hydrocarbon KW - 0 KW - Receptors, Cell Surface KW - Receptors, Cytoplasmic and Nuclear KW - Receptors, Drug KW - Transcription Factors KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Phenobarbital KW - YQE403BP4D KW - Index Medicus KW - Receptors, Drug -- genetics KW - Animals KW - Phenobarbital -- pharmacology KW - Gene Expression Regulation, Enzymologic KW - Enzyme Induction -- drug effects KW - Humans KW - Receptors, Cell Surface -- genetics KW - Male KW - Female KW - Cytochrome P-450 Enzyme System -- genetics KW - Cytochrome P-450 Enzyme System -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75721569?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacogenetics&rft.atitle=Regulation+of+cytochrome+P450+genes%3A+molecular+mechanisms.&rft.au=Gonzalez%2C+F+J%3BLiu%2C+S+Y%3BYano%2C+M&rft.aulast=Gonzalez&rft.aufirst=F&rft.date=1993-02-01&rft.volume=3&rft.issue=1&rft.spage=51&rft.isbn=&rft.btitle=&rft.title=Pharmacogenetics&rft.issn=0960314X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-10 N1 - Date created - 1993-06-10 N1 - Date revised - 2017-01-13 N1 - Gene symbol - CYP; CYP1A1; CYP2C6; CYP2E1; CYP4A N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Dopamine D2 receptor gene Taq I 'A' locus map including 'A4' variant: relevance for alcoholism and drug abuse. AN - 75663306; 8096458 AB - The D2 dopamine receptor gene (DRD2) displays Taq I restriction fragment length polymorphisms (RFLPs) at two different loci, termed A and B. One of the three different Taq I A 'alleles' described at this site, the A1 allele (size = 6.6 kb), has been found to be associated with alcoholism and with drug abuse in the majority of studies reported to date. A complete map of the Taq I A RFLP site has been constructed, through hybridization with different fragments of the 3' flanking region and polymerase chain reaction (PCR). When screening 432 unrelated individuals to establish possible A1 allelic association with drug abuse or dependence, we have encountered a novel Taq I A RFLP, which we have named 'A4' (size = 8.6 kb). This sequence variant displays a frequency of approximately 1% in our sample and shows a Mendelizing genetic pattern in an Italian nuclear family. Primers suitable for detecting A4 using PCR have been designed. The A4, but not the A3 'allele', displays substantial overlap with the A1. In particular, A2 and A3 share the presence of a Taq I restriction site, whose absence in A1 and A4 is apparently associated with substance abuse vulnerability. Therefore, in association studies it is proper to contrast individuals displaying A1 and A4 RFLP patterns, with individuals displaying A2 and A3 RFLPs. JF - Drug and alcohol dependence AU - Persico, A M AU - O'Hara, B F AU - Farmer, S AU - Gysin, R AU - Flanagan, S D AU - Uhl, G R AD - National Institute on Drug Abuse, Addiction Research Center, Johns Hopkins University School of Medicine, Baltimore, MD. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 229 EP - 234 VL - 31 IS - 3 SN - 0376-8716, 0376-8716 KW - DNA Probes KW - 0 KW - Psychotropic Drugs KW - Receptors, Dopamine D2 KW - Street Drugs KW - Taq Polymerase KW - EC 2.7.7.- KW - DNA-Directed DNA Polymerase KW - EC 2.7.7.7 KW - Index Medicus KW - Pedigree KW - Polymerase Chain Reaction KW - Polymorphism, Restriction Fragment Length KW - Risk Factors KW - Humans KW - Alleles KW - Receptors, Dopamine D2 -- genetics KW - Alcoholism -- genetics KW - Chromosome Mapping KW - Substance-Related Disorders -- genetics KW - DNA-Directed DNA Polymerase -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75663306?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Drug+and+alcohol+dependence&rft.atitle=Dopamine+D2+receptor+gene+Taq+I+%27A%27+locus+map+including+%27A4%27+variant%3A+relevance+for+alcoholism+and+drug+abuse.&rft.au=Persico%2C+A+M%3BO%27Hara%2C+B+F%3BFarmer%2C+S%3BGysin%2C+R%3BFlanagan%2C+S+D%3BUhl%2C+G+R&rft.aulast=Persico&rft.aufirst=A&rft.date=1993-02-01&rft.volume=31&rft.issue=3&rft.spage=229&rft.isbn=&rft.btitle=&rft.title=Drug+and+alcohol+dependence&rft.issn=03768716&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-30 N1 - Date created - 1993-04-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Cytochrome P-450: the Japanese connection. AN - 75641480; 8463126 JF - Japanese journal of cancer research : Gann AU - Gelboin, H V AD - Department of Health and Human Services, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/02// PY - 1993 DA - February 1993 VL - 84 IS - 2 SN - 0910-5050, 0910-5050 KW - Carcinogens KW - 0 KW - Pharmaceutical Preparations KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Animals KW - Biotransformation KW - Humans KW - Pharmaceutical Preparations -- metabolism KW - Carcinogens -- metabolism KW - Cytochrome P-450 Enzyme System -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75641480?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Japanese+journal+of+cancer+research+%3A+Gann&rft.atitle=Cytochrome+P-450%3A+the+Japanese+connection.&rft.au=Gelboin%2C+H+V&rft.aulast=Gelboin&rft.aufirst=H&rft.date=1993-02-01&rft.volume=84&rft.issue=2&rft.spage=inside+front+cover&rft.isbn=&rft.btitle=&rft.title=Japanese+journal+of+cancer+research+%3A+Gann&rft.issn=09105050&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-30 N1 - Date created - 1993-04-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Selective blockade of spinal reflexes by omega-conotoxin in the isolated spinal cord of the neonatal rat. AN - 75641136; 7680794 AB - High-voltage-activated calcium currents can be pharmacologically separated into two components: omega-conotoxin-sensitive, dihydropyridine resistant (N-type) and dihydropyridine sensitive, omega-conotoxin-resistant (L-type). In the present study, omega-conotoxin completely blocked spinal monosynaptic responses and long-latency electrically evoked polysynaptic reflexes were 93% blocked. Short-latency electrically evoked and capsaicin-evoked polysynaptic reflexes were partially blocked (39 and 37% block, respectively). Nifedipine, a dihydropyridine type antagonist, had no effect on any evoked responses and Bay K 8644, a dihydropyridine agonist, only increased spontaneous firing. Dynorphin A blocks N currents, but its depressant effects were not altered by irreversible blockade of omega-conotoxin-sensitive N channels. These results demonstrate that omega-conotoxin-sensitive N channels play a major role in the synaptic transmission that mediates monosynaptic and electrically evoked slow polysynaptic reflexes, and a lesser but significant role in fast and capsaicin-evoked polysynaptic spinal reflexes. L-type channels play a minor role. Furthermore, dynorphin A depresses synaptic transmission by blockade of high threshold calcium channels that are distinct from the omega-conotoxin-sensitive N channel, or by a mechanism that does not directly involve calcium channels. JF - Neuroscience AU - Bell, J A AD - Neuroimaging and Drug Action Section, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 711 EP - 716 VL - 52 IS - 3 SN - 0306-4522, 0306-4522 KW - Calcium Channel Blockers KW - 0 KW - Ion Channels KW - Peptides, Cyclic KW - omega-Conotoxins KW - Conus magus toxin KW - 107407-86-3 KW - 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester KW - 71145-03-4 KW - Dynorphins KW - 74913-18-1 KW - Nifedipine KW - I9ZF7L6G2L KW - Capsaicin KW - S07O44R1ZM KW - Index Medicus KW - Animals KW - Synapses -- drug effects KW - 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester -- pharmacology KW - Electric Stimulation KW - Capsaicin -- pharmacology KW - Nifedipine -- pharmacology KW - Rats KW - Animals, Newborn KW - Evoked Potentials -- drug effects KW - Synapses -- physiology KW - Rats, Sprague-Dawley KW - In Vitro Techniques KW - Membrane Potentials -- drug effects KW - Dynorphins -- pharmacology KW - Calcium Channel Blockers -- pharmacology KW - Reflex -- drug effects KW - Spinal Cord -- drug effects KW - Ion Channels -- drug effects KW - Spinal Cord -- physiology KW - Peptides, Cyclic -- pharmacology KW - Ion Channels -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75641136?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroscience&rft.atitle=Selective+blockade+of+spinal+reflexes+by+omega-conotoxin+in+the+isolated+spinal+cord+of+the+neonatal+rat.&rft.au=Bell%2C+J+A&rft.aulast=Bell&rft.aufirst=J&rft.date=1993-02-01&rft.volume=52&rft.issue=3&rft.spage=711&rft.isbn=&rft.btitle=&rft.title=Neuroscience&rft.issn=03064522&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-15 N1 - Date created - 1993-04-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Seasonal changes in rule infractions among prisoners: a preliminary test of the temperature-aggression hypothesis. AN - 75620537; 8451356 AB - To test the temperature-aggression hypothesis, seasonal changes in aggression as indexed by reported rule infractions were studied for prisoners located at the Patuxent Institution, Jessup, Maryland. 5383 reports of rule infractions occurred between July 1987 and March 1991. Rule infractions occurred more frequently during the hot summer months than the three other seasons of the year. This summer effect, though significant, is only a few percent above a theoretical chance level based on the number of days comprising the seasons. A much stronger monthly effect over 45 months was found, but the bases of erratic fluctuations are not known. JF - Psychological reports AU - Haertzen, C AU - Buxton, K AU - Covi, L AU - Richards, H AD - Department of Health and Human Services, National Institute on Drug Abuse, Addiction Research Center, Baltimore, MD 21224. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 195 EP - 200 VL - 72 IS - 1 SN - 0033-2941, 0033-2941 KW - Index Medicus KW - Opioid-Related Disorders -- psychology KW - Humans KW - Hot Temperature -- adverse effects KW - Maryland KW - Male KW - Aggression -- psychology KW - Seasons KW - Temperature KW - Prisoners -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75620537?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychological+reports&rft.atitle=Seasonal+changes+in+rule+infractions+among+prisoners%3A+a+preliminary+test+of+the+temperature-aggression+hypothesis.&rft.au=Haertzen%2C+C%3BBuxton%2C+K%3BCovi%2C+L%3BRichards%2C+H&rft.aulast=Haertzen&rft.aufirst=C&rft.date=1993-02-01&rft.volume=72&rft.issue=1&rft.spage=195&rft.isbn=&rft.btitle=&rft.title=Psychological+reports&rft.issn=00332941&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-12 N1 - Date created - 1993-04-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Modulation of voltage-activated Ca currents by pain-inducing agents in a dorsal root ganglion neuronal line, F-11. AN - 75615313; 8383774 AB - Whole cell currents evoked by pain-inducing agents--bradykinin (Bk), capsaicin (Cap), and reciniferatoxin (RTX), and their modulation of voltage-activated Ca currents were examined in F-11 cells using a patch electrode voltage clamp technique. Most F-11 cells generated action potentials under current clamp if their membrane potentials were held sufficiently negative. Average peak inward Na current (INa) was 100 microA/cm2 and the INa was abolished by 10(-6) M tetrodotoxin. At least two types of Ca currents could be clearly distinguished on the basis of voltage dependency and kinetics; a low threshold transient ICa(t) and a high threshold sustained ICa(l). In addition, another high threshold transient Ca current, presumably ICa(n), was observed. About 30% of the cells produced inward current for these pain-inducing agents, when activated at the membrane holding potential of -70 mV. In some F-11 cells, the amplitude of action potential was observed to increase during 10(-6) M Cap-induced depolarization. Both low and high threshold Ca currents were reduced by 10(-6) M Bk in the majority of the cells. Similarly, both 10(-6) M Cap and 10(-9) M RTX reduced these Ca currents. However, a considerable number of cells showed an initial enhancement followed by reduction in the amplitude of these Ca currents. With higher concentrations of these ligands, all Ca currents were suppressed. Such modulation of voltage-activated Ca currents by pain-inducing agents occurred in both the presence and absence of apparent receptor-activated current flows in the cells. In pertussis toxin (PTX)-treated cells, the inhibitory modulation of Ca currents by pain-inducing agents was suppressed. In contrast, in cholera toxin (CTX)-treated cells, this inhibitory modulation appeared to be enhanced. These data indicate that the inhibitory modulation of Ca channel currents by Cap and RTX, similarly to that of Bk, involves a PTX-sensitive inhibitory G protein (Gi). JF - Journal of neuroscience research AU - Kusano, K AU - Gainer, H AD - Laboratory of Neurochemistry, National Institute of Neurological Disease and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/02/01/ PY - 1993 DA - 1993 Feb 01 SP - 158 EP - 169 VL - 34 IS - 2 SN - 0360-4012, 0360-4012 KW - Calcium Channel Blockers KW - 0 KW - Calcium Channels KW - Diterpenes KW - Peptides, Cyclic KW - Receptors, Bradykinin KW - Receptors, Neurotransmitter KW - omega-Conotoxins KW - Conus magus toxin KW - 107407-86-3 KW - Tetrodotoxin KW - 4368-28-9 KW - resiniferatoxin KW - A5O6P1UL4I KW - Capsaicin KW - S07O44R1ZM KW - Bradykinin KW - S8TIM42R2W KW - Index Medicus KW - Diterpenes -- pharmacology KW - Animals KW - Receptors, Neurotransmitter -- drug effects KW - Action Potentials -- drug effects KW - Mice KW - Electrophysiology KW - Capsaicin -- pharmacology KW - Rats KW - Rats, Sprague-Dawley KW - Calcium Channel Blockers -- pharmacology KW - Bradykinin -- pharmacology KW - Tetrodotoxin -- pharmacology KW - Receptors, Neurotransmitter -- biosynthesis KW - Peptides, Cyclic -- pharmacology KW - Cell Line KW - Ganglia, Spinal -- cytology KW - Calcium Channels -- physiology KW - Pain -- physiopathology KW - Pain -- chemically induced KW - Ganglia, Spinal -- physiology KW - Neurons -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75615313?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neuroscience+research&rft.atitle=Modulation+of+voltage-activated+Ca+currents+by+pain-inducing+agents+in+a+dorsal+root+ganglion+neuronal+line%2C+F-11.&rft.au=Kusano%2C+K%3BGainer%2C+H&rft.aulast=Kusano&rft.aufirst=K&rft.date=1993-02-01&rft.volume=34&rft.issue=2&rft.spage=158&rft.isbn=&rft.btitle=&rft.title=Journal+of+neuroscience+research&rft.issn=03604012&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-14 N1 - Date created - 1993-04-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) effects on enkephalinergic neurons in various regions of mouse brain. AN - 75602830; 8439770 AB - In order to elucidate the effects of MPTP on enkephalinergic neurons, dopamine (DA), norepinephrine (NE), proenkephalin (PE) mRNA and met-enkephalin (ME) were measured in striatum, olfactory tubercle, and prefrontal cortex of C57/B16 mice 1 day-2 weeks following treatment with 96 mg/kg MPTP HCl (24 mg/kg i.p., twice/day for 2 days). DA and its metabolites were depleted 70% in striatum and 40% in olfactory tubercle within 1 day. In cortex, DA was unchanged, whereas homovanillic acid and NE were depleted 50 and 40% respectively by 3 days. ME increased in all three brain regions at different times whereas PE mRNA showed a different pattern in each region, with an increase in olfactory tubercle, a decrease in cortex, and in striatum, a decrease at 1 day followed by an increase at 3 days. Thus enkephalinergic neurons in each region respond differently to MPTP treatment. In striatum and olfactory tubercle. DA is depleted sufficiently to release its tonic inhibition on the enkephalinergic neurons, thereby leading to increased enkephalin synthesis. In cortex, the change in NE metabolism appears to cause a decrease of ME release and thereby a depression of PE synthesis. The possible relationship between these results and the changes observed in Parkinson's disease are discussed. JF - Neurochemistry international AU - Mitsuo, K AU - Cosi, C AU - Harvey-White, J D AU - Schwartz, J P AD - Clinical Neuroscience Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 175 EP - 182 VL - 22 IS - 2 SN - 0197-0186, 0197-0186 KW - Enkephalins KW - 0 KW - Protein Precursors KW - RNA, Messenger KW - proenkephalin KW - 3,4-Dihydroxyphenylacetic Acid KW - 102-32-9 KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Dopamine KW - VTD58H1Z2X KW - Norepinephrine KW - X4W3ENH1CV KW - Homovanillic Acid KW - X77S6GMS36 KW - Index Medicus KW - Animals KW - Frontal Lobe -- drug effects KW - Corpus Striatum -- metabolism KW - Protein Precursors -- genetics KW - Dopamine -- metabolism KW - Mice KW - Homovanillic Acid -- metabolism KW - RNA, Messenger -- metabolism KW - 3,4-Dihydroxyphenylacetic Acid -- metabolism KW - Norepinephrine -- metabolism KW - Kinetics KW - Frontal Lobe -- metabolism KW - Mice, Inbred C57BL KW - Corpus Striatum -- drug effects KW - Olfactory Pathways -- metabolism KW - Olfactory Pathways -- drug effects KW - Male KW - Enkephalins -- genetics KW - Neurons -- metabolism KW - Brain -- cytology KW - Neurons -- drug effects KW - Brain -- drug effects KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- pharmacology KW - Enkephalins -- metabolism KW - Brain -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75602830?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurochemistry+international&rft.atitle=1-Methyl-4-phenyl-1%2C2%2C3%2C6-tetrahydropyridine+%28MPTP%29+effects+on+enkephalinergic+neurons+in+various+regions+of+mouse+brain.&rft.au=Mitsuo%2C+K%3BCosi%2C+C%3BHarvey-White%2C+J+D%3BSchwartz%2C+J+P&rft.aulast=Mitsuo&rft.aufirst=K&rft.date=1993-02-01&rft.volume=22&rft.issue=2&rft.spage=175&rft.isbn=&rft.btitle=&rft.title=Neurochemistry+international&rft.issn=01970186&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-01 N1 - Date created - 1993-04-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Inhibition of tumor formation from grafted murine papilloma cells by treatment of grafts with staurosporine, an inducer of squamous differentiation. AN - 75593267; 8435862 AB - The microbial alkaloid staurosporine induces responses associated with protein kinase C activation, resulting in terminal differentiation in cultures of both normal and neoplastic mouse epidermal cells. As a cancer chemotherapy model, we treated grafts of mouse epidermal tumor cell lines 308 and SP-1 repeatedly with staurosporine. A dose-dependent inhibition of tumor formation, maximal at 0.025 nmol per treatment, was observed. Higher and lower doses were less effective, suggesting a specific target for staurosporine action. A single, low-dose treatment 2 weeks after grafting also markedly reduced tumor formation. Although in vitro evidence suggests that staurosporine-induced terminal squamous differentiation results from activation of protein kinase C, we found no inhibition of tumor growth in similar studies with the protein kinase C activator 12-O-tetradecanoylphorbol-13-acetate. These results indicate that staurosporine is an effective antitumor agent for eradicating squamous cell tumors in vivo. JF - Carcinogenesis AU - Strickland, J E AU - Dlugosz, A A AU - Hennings, H AU - Yuspa, S H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 205 EP - 209 VL - 14 IS - 2 SN - 0143-3334, 0143-3334 KW - Alkaloids KW - 0 KW - Antineoplastic Agents KW - Protein Kinase C KW - EC 2.7.11.13 KW - Staurosporine KW - H88EPA0A3N KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Neoplasm Transplantation KW - Animals KW - Protein Kinase C -- antagonists & inhibitors KW - Tumor Cells, Cultured -- drug effects KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Disease Models, Animal KW - Mice, Nude KW - Mice KW - Mice, Inbred BALB C KW - Cell Differentiation -- drug effects KW - Time Factors KW - Skin Neoplasms -- drug therapy KW - Papilloma -- pathology KW - Carcinoma, Squamous Cell -- pathology KW - Skin Neoplasms -- pathology KW - Alkaloids -- pharmacology KW - Papilloma -- drug therapy KW - Carcinoma, Squamous Cell -- drug therapy KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75593267?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Inhibition+of+tumor+formation+from+grafted+murine+papilloma+cells+by+treatment+of+grafts+with+staurosporine%2C+an+inducer+of+squamous+differentiation.&rft.au=Strickland%2C+J+E%3BDlugosz%2C+A+A%3BHennings%2C+H%3BYuspa%2C+S+H&rft.aulast=Strickland&rft.aufirst=J&rft.date=1993-02-01&rft.volume=14&rft.issue=2&rft.spage=205&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-24 N1 - Date created - 1993-03-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Interpersonal stressors, substance abuse, and suicide. AN - 75581708; 8426175 AB - In contrast to suicide in depression, suicide associated with alcoholism and substance dependence may be preceded more often by interpersonal loss and conflict 6 weeks prior to death. We used psychological autopsy methodology in an effort to clarify and extend these findings using a more comprehensive typology of interpersonal stressors. Subjects included 57 suicide victims with diagnoses of alcohol/substance dependence (A/SD; N = 30) and mood/anxiety disorders (M/AD; N = 27). Consistent with previous studies, a substantial majority of the A/SD suicide victims were confronted with interpersonal stressors in the 6 weeks prior to death. Our investigation extends previous findings by indicating that a) A/SD suicide victims are confronted with a broader range of interpersonal stressors than M/AD suicide completers and b) the types of interpersonal stressors experienced by A/SD subjects in the weeks prior to suicide involve conflicts/arguments and attachment disruptions. JF - The Journal of nervous and mental disease AU - Duberstein, P R AU - Conwell, Y AU - Caine, E D AD - University of Rochester-NIMH Clinical Research Center for the Study of Psychopathology of the Elderly, New York. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 80 EP - 85 VL - 181 IS - 2 SN - 0022-3018, 0022-3018 KW - Abridged Index Medicus KW - Index Medicus KW - Divorce KW - Death KW - Humans KW - Adult KW - Middle Aged KW - Male KW - Female KW - Life Change Events KW - Interpersonal Relations KW - Substance-Related Disorders -- complications KW - Substance-Related Disorders -- psychology KW - Suicide -- statistics & numerical data KW - Alcoholism -- psychology KW - Alcoholism -- complications KW - Suicide -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75581708?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+nervous+and+mental+disease&rft.atitle=Interpersonal+stressors%2C+substance+abuse%2C+and+suicide.&rft.au=Duberstein%2C+P+R%3BConwell%2C+Y%3BCaine%2C+E+D&rft.aulast=Duberstein&rft.aufirst=P&rft.date=1993-02-01&rft.volume=181&rft.issue=2&rft.spage=80&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+nervous+and+mental+disease&rft.issn=00223018&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-03 N1 - Date created - 1993-03-03 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: J Nerv Ment Dis. 1993 Sep;181(9):588-9 [8245931] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The de facto US mental and addictive disorders service system. Epidemiologic catchment area prospective 1-year prevalence rates of disorders and services. AN - 75577999; 8427558 AB - After initial interviews with 20,291 adults in the National Institute of Mental Health Epidemiologic Catchment Area Program, we estimated prospective 1-year prevalence and service use rates of mental and addictive disorders in the US population. An annual prevalence rate of 28.1% was found for these disorders, composed of a 1-month point prevalence of 15.7% (at wave 1) and a 1-year incidence of new or recurrent disorders identified in 12.3% of the population at wave 2. During the 1-year follow-up period, 6.6% of the total sample developed one or more new disorders after being assessed as having no previous lifetime diagnosis at wave 1. An additional 5.7% of the population, with a history of some previous disorder at wave 1, had an acute relapse or suffered from a new disorder in 1 year. Irrespective of diagnosis, 14.7% of the US population in 1 year reported use of services in one or more component sectors of the de facto US mental and addictive service system. With some overlap between sectors, specialists in mental and addictive disorders provided treatment to 5.9% of the US population, 6.4% sought such services from general medical physicians, 3.0% sought these services from other human service professionals, and 4.1% turned to the voluntary support sector for such care. Of those persons with any disorder, only 28.5% (8.0 per 100 population) sought mental health/addictive services. Persons with specific disorders varied in the proportion who used services, from a high of more than 60% for somatization, schizophrenia, and bipolar disorders to a low of less than 25% for addictive disorders and severe cognitive impairment. Applications of these descriptive data to US health care system reform options are considered in the context of other variables that will determine national health policy. JF - Archives of general psychiatry AU - Regier, D A AU - Narrow, W E AU - Rae, D S AU - Manderscheid, R W AU - Locke, B Z AU - Goodwin, F K AD - Division of Epidemiology and Services Research, National Institute of Mental Health, National Institutes of Health, Rockville, Md. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 85 EP - 94 VL - 50 IS - 2 SN - 0003-990X, 0003-990X KW - Abridged Index Medicus KW - Index Medicus KW - Delivery of Health Care -- statistics & numerical data KW - Age Factors KW - Self-Help Groups -- utilization KW - Humans KW - Aged KW - Health Policy KW - Recurrence KW - National Health Programs KW - Catchment Area (Health) KW - Ambulatory Care KW - Prospective Studies KW - Hospitalization KW - Patient Acceptance of Health Care KW - Adult KW - Incidence KW - Social Support KW - Middle Aged KW - Adolescent KW - United States -- epidemiology KW - Male KW - Female KW - Prevalence KW - Substance-Related Disorders -- therapy KW - Mental Disorders -- therapy KW - Mental Disorders -- epidemiology KW - Mental Health Services -- utilization KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75577999?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+general+psychiatry&rft.atitle=The+de+facto+US+mental+and+addictive+disorders+service+system.+Epidemiologic+catchment+area+prospective+1-year+prevalence+rates+of+disorders+and+services.&rft.au=Regier%2C+D+A%3BNarrow%2C+W+E%3BRae%2C+D+S%3BManderscheid%2C+R+W%3BLocke%2C+B+Z%3BGoodwin%2C+F+K&rft.aulast=Regier&rft.aufirst=D&rft.date=1993-02-01&rft.volume=50&rft.issue=2&rft.spage=85&rft.isbn=&rft.btitle=&rft.title=Archives+of+general+psychiatry&rft.issn=0003990X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-26 N1 - Date created - 1993-02-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Tumorigenic conversion of human mesothelial cells as a consequence of platelet-derived growth factor-A chain overexpression. AN - 75577714; 8427711 AB - Overexpression of platelet-derived growth factor (PDGF)-A as well as PDGF-B chain mRNA has previously been reported in human mesothelioma cell lines. In this report, it has been established that the A but not the B chain protein is expressed at detectable levels in cell lysates and conditioned medium from these cell lines. In order to investigate the effect of overexpression of PDGF-A chain in a human mesothelial cell model system, a retroviral vector containing a human PDGF-A chain cDNA insert under the control of the Moloney murine leukemia virus (MoMLV) promoter was inserted into the SV-40 T-antigen immortalized human mesothelial cell line MeT-5A. Selected cells showed overexpression of PDGF-A chain relative to MeT-5A and induced tumors in athymic nude mice. PDGF-A chain overexpression was also found in the tumor specimens excised from the mice. PDGF-A mRNA and protein were expressed at a higher level in the tumor explant cell lines, suggesting a correlation of tumorigenicity with A chain production. JF - American journal of respiratory cell and molecular biology AU - Van der Meeren, A AU - Seddon, M B AU - Betsholtz, C A AU - Lechner, J F AU - Gerwin, B I AD - Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 214 EP - 221 VL - 8 IS - 2 SN - 1044-1549, 1044-1549 KW - Isoenzymes KW - 0 KW - Platelet-Derived Growth Factor KW - RNA, Messenger KW - platelet-derived growth factor A KW - Index Medicus KW - Karyotyping KW - Animals KW - Neoplasms, Experimental -- etiology KW - Humans KW - Gene Expression KW - Epithelium -- enzymology KW - Mice KW - Mice, Nude KW - RNA, Messenger -- genetics KW - Precipitin Tests KW - Isoenzymes -- metabolism KW - Tumor Cells, Cultured KW - Epithelial Cells KW - Transfection KW - Cells, Cultured KW - Platelet-Derived Growth Factor -- genetics KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75577714?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+respiratory+cell+and+molecular+biology&rft.atitle=Tumorigenic+conversion+of+human+mesothelial+cells+as+a+consequence+of+platelet-derived+growth+factor-A+chain+overexpression.&rft.au=Van+der+Meeren%2C+A%3BSeddon%2C+M+B%3BBetsholtz%2C+C+A%3BLechner%2C+J+F%3BGerwin%2C+B+I&rft.aulast=Van+der+Meeren&rft.aufirst=A&rft.date=1993-02-01&rft.volume=8&rft.issue=2&rft.spage=214&rft.isbn=&rft.btitle=&rft.title=American+journal+of+respiratory+cell+and+molecular+biology&rft.issn=10441549&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-11 N1 - Date created - 1993-03-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Evaluation of risks for non-Hodgkin's lymphoma by occupation and industry exposures from a case-control study. AN - 75571552; 8427258 AB - The etiology of non-Hodgkin's lymphoma (NHL) is not well understood. To develop hypotheses on causes of this tumor, data from a population-based case-control interview study of 1,867 white men (622 cases and 1,245 controls) in Iowa and Minnesota conducted during 1980-1983 were examined. Subjects, or their next of kin, were interviewed to obtain information on agricultural exposures, work history, medical conditions, and family history. This analysis focuses on risks of NHL by occupation, by industry, and by selected exposures. Although many comparisons were made, few significant associations were observed. Small numbers and limitations in exposure assessment, however, would tend to reduce opportunities to detect associations. The strongest finding was with various occupations that work in metals and metal products. The analysis by exposure estimates also uncovered a significant association with metals, but risks did not increase with estimated intensity of exposure. Slightly elevated risks were also noted among persons employed as painters and construction workers, agricultural and forestry workers, printers and typesetters, funeral directors and embalmers, and dry cleaners. Although the overall risks for benzene and other solvents were small, they increased slightly with level of assigned exposure. Although some associations may be due to chance, several of these occupations and industries have been linked to lymphoma in other investigations and deserve further attention. JF - American journal of industrial medicine AU - Blair, A AU - Linos, A AU - Stewart, P A AU - Burmeister, L F AU - Gibson, R AU - Everett, G AU - Schuman, L AU - Cantor, K P AD - Environmental Epidemiology Branch, National Cancer Institute, Rockville, Maryland 20892. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 301 EP - 312 VL - 23 IS - 2 SN - 0271-3586, 0271-3586 KW - Index Medicus KW - Risk Factors KW - Humans KW - Adult KW - Case-Control Studies KW - Aged KW - Minnesota -- epidemiology KW - Male KW - Iowa -- epidemiology KW - Lymphoma, Non-Hodgkin -- epidemiology KW - Lymphoma, Non-Hodgkin -- etiology KW - Occupational Exposure -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75571552?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+industrial+medicine&rft.atitle=Evaluation+of+risks+for+non-Hodgkin%27s+lymphoma+by+occupation+and+industry+exposures+from+a+case-control+study.&rft.au=Blair%2C+A%3BLinos%2C+A%3BStewart%2C+P+A%3BBurmeister%2C+L+F%3BGibson%2C+R%3BEverett%2C+G%3BSchuman%2C+L%3BCantor%2C+K+P&rft.aulast=Blair&rft.aufirst=A&rft.date=1993-02-01&rft.volume=23&rft.issue=2&rft.spage=301&rft.isbn=&rft.btitle=&rft.title=American+journal+of+industrial+medicine&rft.issn=02713586&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-04 N1 - Date created - 1993-03-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Recombinant interferon-gamma reduces PDGF-induced lung fibroblast growth but stimulates PDGF production by alveolar macrophages in vitro. AN - 75568816; 8428532 JF - Chest AU - Brody, A R AU - Bonner, J C AU - Badgett, A AD - Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, Research Triangle Park, NC. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 121S EP - 122S VL - 103 IS - 2 Suppl SN - 0012-3692, 0012-3692 KW - Platelet-Derived Growth Factor KW - 0 KW - Recombinant Proteins KW - Interferon-gamma KW - 82115-62-6 KW - Abridged Index Medicus KW - Index Medicus KW - Rats KW - Fibroblasts -- secretion KW - Fibroblasts -- drug effects KW - Animals KW - Drug Interactions KW - Dose-Response Relationship, Drug KW - Cells, Cultured -- secretion KW - Cell Division -- drug effects KW - Cells, Cultured -- drug effects KW - Time Factors KW - Lung -- secretion KW - Platelet-Derived Growth Factor -- pharmacology KW - Platelet-Derived Growth Factor -- drug effects KW - Lung -- cytology KW - Lung -- drug effects KW - Platelet-Derived Growth Factor -- secretion KW - Interferon-gamma -- pharmacology KW - Macrophages, Alveolar -- drug effects KW - Macrophages, Alveolar -- secretion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75568816?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chest&rft.atitle=Recombinant+interferon-gamma+reduces+PDGF-induced+lung+fibroblast+growth+but+stimulates+PDGF+production+by+alveolar+macrophages+in+vitro.&rft.au=Brody%2C+A+R%3BBonner%2C+J+C%3BBadgett%2C+A&rft.aulast=Brody&rft.aufirst=A&rft.date=1993-02-01&rft.volume=103&rft.issue=2+Suppl&rft.spage=121S&rft.isbn=&rft.btitle=&rft.title=Chest&rft.issn=00123692&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-10 N1 - Date created - 1993-03-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Raf revertant cells resist transformation by non-nuclear oncogenes and are deficient in the induction of early response genes by TPA and serum. AN - 75568153; 8426742 AB - A revertant cell line was generated from v-raf transformed NIH/3T3 fibroblasts. These cells, termed CHP25, express a functional v-raf oncogene. However, they are non-tumorigenic, do not form colonies in soft agar and possess a flat morphology. CHP25 cells are resistant to re-transformation by sis, ras, tyrosine kinase- as well as serine/threonine kinase-encoding oncogenes suggesting that Raf functions downstream of most membrane associated signal transducers. In contrast to v-raf transformed cells, in which the endogenous Raf-1 protein kinase is constitutively activated, v-Raf in CHP25 cells does not activate endogenous Raf-1 kinase. Since mitogen regulation of Raf-1 kinase in CHP25 cells is intact, we conclude that CHP25 cells are blocked at the level of Raf-1 substrate phosphorylation. Consistent with this interpretation CHP25 cells show specific alterations of early gene induction. The serum induction of c-fos and junD as well as the serum and TPA (12-O-tetradecanoylphorbol-13-acetate) induction of junB and egr-1 are almost completely abolished. Only v-fos can transform CHP25, whereas c-fos, v-myc, c-jun and junB are ineffective. These data suggest that the lesion responsible for the revertant phenotype of CHP25 cells is the inability to activate the AP-1 complex. We conclude that Raf-1 signaling is essential for transformation of NIH/3T3 cells by peripheral oncogenes and for regulation of a subset of early response genes by TPA and serum growth factors. JF - Oncogene AU - Kolch, W AU - Heidecker, G AU - Troppmair, J AU - Yanagihara, K AU - Bassin, R H AU - Rapp, U R AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, National Institutes of Health, Frederick, Maryland 21702. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 361 EP - 370 VL - 8 IS - 2 SN - 0950-9232, 0950-9232 KW - Raf KW - Proto-Oncogene Proteins c-fos KW - 0 KW - Retroviridae Proteins, Oncogenic KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Oncogene Proteins v-raf KW - EC 2.7.11.1 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - 3T3 Cells KW - Proto-Oncogene Proteins c-fos -- metabolism KW - Phosphorylation KW - Gene Expression KW - Mice KW - Genes, fos KW - Retroviridae Proteins, Oncogenic -- genetics KW - Protein-Tyrosine Kinases -- genetics KW - Oncogenes KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Blood Physiological Phenomena KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75568153?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncogene&rft.atitle=Raf+revertant+cells+resist+transformation+by+non-nuclear+oncogenes+and+are+deficient+in+the+induction+of+early+response+genes+by+TPA+and+serum.&rft.au=Kolch%2C+W%3BHeidecker%2C+G%3BTroppmair%2C+J%3BYanagihara%2C+K%3BBassin%2C+R+H%3BRapp%2C+U+R&rft.aulast=Kolch&rft.aufirst=W&rft.date=1993-02-01&rft.volume=8&rft.issue=2&rft.spage=361&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=09509232&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-26 N1 - Date created - 1993-02-26 N1 - Date revised - 2017-01-13 N1 - Gene symbol - Raf N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Use of services by persons with mental and addictive disorders. Findings from the National Institute of Mental Health Epidemiologic Catchment Area Program. AN - 75566498; 8381266 AB - The use of ambulatory and inpatient mental health and addiction services in the United States was estimated by means of data from the National Institute of Mental Health Epidemiologic Catchment Area Program standardized to the 1980 US census for adults 18 years of age and older. In a 1-year period, 22.8 million people used ambulatory services for mental or addictive disorder treatment; 54% of them had a current Diagnostic Interview Schedule/DSM-III mental disorder and another 37.4% had a history of psychiatric disorder or significant psychiatric symptoms. A total of 325.9 million ambulatory visits were made, and the average number of visits per treated person per year was 14.3. There were 1.4 million persons admitted to at least one inpatient mental health or addiction setting during a 1-year period; 80% of them had a current DIS/DSM-III disorder, and the remainder had a history of psychiatric disorder or significant psychiatric symptoms. Results were determined for specific mental and substance use diagnoses and service settings. Among treated persons with any mental or addictive disorder, the majority of visits were to mental and addictive disorders specialty settings (40.5% of total visits) and to support networks composed of friends, relatives, and self-help groups (37.0% of total visits). Although a large number of persons with mental and substance use disorders were seen in the general medical sector for mental health or addiction problems, they were seen less frequently and therefore made fewer visits to this sector (10.9% of total visits). JF - Archives of general psychiatry AU - Narrow, W E AU - Regier, D A AU - Rae, D S AU - Manderscheid, R W AU - Locke, B Z AD - Epidemiology and Psychopathology Research Branch, National Institute of Mental Health, National Institutes of Health, Rockville, Md. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 95 EP - 107 VL - 50 IS - 2 SN - 0003-990X, 0003-990X KW - Abridged Index Medicus KW - Index Medicus KW - Psychiatric Status Rating Scales KW - Ambulatory Care -- statistics & numerical data KW - Self-Help Groups -- utilization KW - Humans KW - Social Support KW - Substance Abuse Treatment Centers -- utilization KW - Hospitalization -- statistics & numerical data KW - United States -- epidemiology KW - National Health Programs KW - Male KW - Female KW - Comorbidity KW - Ambulatory Care Facilities -- utilization KW - Substance-Related Disorders -- therapy KW - Mental Disorders -- therapy KW - Mental Disorders -- epidemiology KW - Mental Health Services -- utilization KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75566498?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+general+psychiatry&rft.atitle=Use+of+services+by+persons+with+mental+and+addictive+disorders.+Findings+from+the+National+Institute+of+Mental+Health+Epidemiologic+Catchment+Area+Program.&rft.au=Narrow%2C+W+E%3BRegier%2C+D+A%3BRae%2C+D+S%3BManderscheid%2C+R+W%3BLocke%2C+B+Z&rft.aulast=Narrow&rft.aufirst=W&rft.date=1993-02-01&rft.volume=50&rft.issue=2&rft.spage=95&rft.isbn=&rft.btitle=&rft.title=Archives+of+general+psychiatry&rft.issn=0003990X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-26 N1 - Date created - 1993-02-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Hematopoietic growth factors and glucocorticoids synergize to mimic the effects of IL-1 on granulocyte differentiation and IL-1 receptor induction on bone marrow cells in vivo. AN - 75562865; 7678814 AB - The mechanisms by which interleukin-1 (IL-1) stimulates hematopoiesis are not clear. We have previously shown that in vivo administration of IL-1 indirectly increases IL-1 receptor (IL-1R) expression on both immature and mature bone marrow (BM) cells, partly due to IL-1-induced hematopoietic growth factor (HGF) production. Because IL-1 also stimulates the hypothalamic pituitary-adrenal axis resulting in the production of glucocorticoids (GC), we assessed whether in vivo treatment with HGF and glucocorticoids upregulates IL-1R. Administration of IL-1 to adrenalectomized mice reduces by 53% IL-specific binding on light density bone marrow (LDBM) cells compared to sham-operated mice. The administration of dexamethasone (dex) alone induced only a slight increase in IL-1R expression but synergized with granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage CSF (GM-CSF), IL-3 and IL-6 to upregulate IL-1R expression. Flow cytometry analysis using the RB6-8C5 antibody, which is differentially expressed on myeloid cells, indicated that combined G-CSF and dex treatment acts to promote increased numbers of differentiated myeloid progenitors in the bone marrow. Autoradiographic analysis confirmed that while G-CSF and dex increased IL-1R expression on all myeloid cells, it was particularly pronounced for myelocytes, promyelocytes and metamyelocytes. These results suggest that the ability of IL-1 to enhance granulocyte differentiation in vivo is partly due to its ability to induce a cascade of cytokines and steroids which in turn regulate IL-1 receptor expression. JF - Experimental hematology AU - Dubois, C M AU - Neta, R AU - Keller, J R AU - Jacobsen, S E AU - Oppenheim, J J AU - Ruscetti, F AD - Laboratory of Immunoregulation, NCI-Frederick Cancer Research & Development Center, MD 21702-1201. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 303 EP - 310 VL - 21 IS - 2 SN - 0301-472X, 0301-472X KW - Adrenal Cortex Hormones KW - 0 KW - Glucocorticoids KW - Hematopoietic Cell Growth Factors KW - Interleukin-1 KW - Interleukin-3 KW - Interleukin-6 KW - Receptors, Interleukin-1 KW - Granulocyte Colony-Stimulating Factor KW - 143011-72-7 KW - Dexamethasone KW - 7S5I7G3JQL KW - Granulocyte-Macrophage Colony-Stimulating Factor KW - 83869-56-1 KW - Index Medicus KW - Animals KW - Interleukin-3 -- pharmacology KW - Dexamethasone -- pharmacology KW - Mice KW - Interleukin-6 -- pharmacology KW - Autoradiography KW - Granulocyte Colony-Stimulating Factor -- pharmacology KW - Granulocyte-Macrophage Colony-Stimulating Factor -- pharmacology KW - Cells, Cultured KW - Up-Regulation -- drug effects KW - Adrenal Cortex Hormones -- metabolism KW - Flow Cytometry KW - Bone Marrow -- ultrastructure KW - Cell Differentiation -- drug effects KW - Drug Synergism KW - Bone Marrow -- drug effects KW - Male KW - Bone Marrow Cells KW - Interleukin-1 -- pharmacology KW - Receptors, Interleukin-1 -- analysis KW - Hematopoietic Cell Growth Factors -- metabolism KW - Granulocytes -- metabolism KW - Granulocytes -- drug effects KW - Hematopoietic Cell Growth Factors -- pharmacology KW - Glucocorticoids -- pharmacology KW - Granulocytes -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75562865?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Experimental+hematology&rft.atitle=Hematopoietic+growth+factors+and+glucocorticoids+synergize+to+mimic+the+effects+of+IL-1+on+granulocyte+differentiation+and+IL-1+receptor+induction+on+bone+marrow+cells+in+vivo.&rft.au=Dubois%2C+C+M%3BNeta%2C+R%3BKeller%2C+J+R%3BJacobsen%2C+S+E%3BOppenheim%2C+J+J%3BRuscetti%2C+F&rft.aulast=Dubois&rft.aufirst=C&rft.date=1993-02-01&rft.volume=21&rft.issue=2&rft.spage=303&rft.isbn=&rft.btitle=&rft.title=Experimental+hematology&rft.issn=0301472X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-04 N1 - Date created - 1993-03-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Effect of phenylpropanolamine on energy expenditure and weight loss in overweight women. AN - 75562316; 8424378 AB - The effect of phenylpropanolamine (PPA), a noncatecholamine sympathomimetic weight-loss agent, on energy expenditure (EE) and substrate oxidation was measured in a respiratory chamber in 24 overweight women after 4 d of treatment (PPA or placebo) during weight maintenance and after 7 wk of treatment on a hypoenergetic diet (70% of measured baseline 24-h EE). Twelve women (37 +/- 2 y, 74 +/- 6 kg, 33 +/- 1% body fat) were randomly assigned to the PPA group [75 mg osmotic release oral system (OROS)-PPA/d] and 12 (mean +/- SEM: 38 +/- 2 y, 79 +/- 1 kg, 37 +/- 1% body fat) to the placebo group. Baseline measurements of 24-h EE (7849 +/- 226 vs 7834 +/- 142 kJ/d), basal metabolic rate (BMR) and 24-h respiratory quotient (RQ) were comparable between PPA and placebo groups. After 4 d of treatment, there was no significant effect of PPA on 24-h EE, BMR, and 24-h RQ compared with placebo. Over the 7-wk diet period, however, the PPA group (n = 8) had greater weight loss than the placebo group (n = 10): -5.0 +/- 0.5 vs -3.0 +/- 0.4 kg (P < 0.05). The changes in 24-h EE and 24-h RQ over the 7 wk were not different between the groups. We conclude that weight loss is enhanced by OROS-PPA, but this change was not explained by changes in 24-h EE or 24-h RQ. The small number of subjects may have hindered detection of subtle differences in energy metabolism. JF - The American journal of clinical nutrition AU - Alger, S AU - Larson, K AU - Boyce, V L AU - Seagle, H AU - Fontvieille, A M AU - Ferraro, R T AU - Rising, R AU - Ravussin, E AD - Clinical Diabetes and Nutrition Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Phoenix, AZ 85016. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 120 EP - 126 VL - 57 IS - 2 SN - 0002-9165, 0002-9165 KW - Catecholamines KW - 0 KW - Placebos KW - Phenylpropanolamine KW - 33RU150WUN KW - Nitrogen KW - N762921K75 KW - Abridged Index Medicus KW - Index Medicus KW - Basal Metabolism KW - Double-Blind Method KW - Humans KW - Adult KW - Catecholamines -- urine KW - Middle Aged KW - Body Composition KW - Blood Pressure -- drug effects KW - Adolescent KW - Nitrogen -- metabolism KW - Female KW - Phenylpropanolamine -- adverse effects KW - Energy Metabolism -- drug effects KW - Weight Loss -- drug effects KW - Phenylpropanolamine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75562316?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+journal+of+clinical+nutrition&rft.atitle=Effect+of+phenylpropanolamine+on+energy+expenditure+and+weight+loss+in+overweight+women.&rft.au=Alger%2C+S%3BLarson%2C+K%3BBoyce%2C+V+L%3BSeagle%2C+H%3BFontvieille%2C+A+M%3BFerraro%2C+R+T%3BRising%2C+R%3BRavussin%2C+E&rft.aulast=Alger&rft.aufirst=S&rft.date=1993-02-01&rft.volume=57&rft.issue=2&rft.spage=120&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+clinical+nutrition&rft.issn=00029165&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-25 N1 - Date created - 1993-02-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - CD4 molecules with a diversity of mutations encompassing the CDR3 region efficiently support human immunodeficiency virus type 1 envelope glycoprotein-mediated cell fusion. AN - 75558883; 8419649 AB - The third complementarity-determining region (CDR3) within domain 1 of the human CD4 molecule has been suggested to play a critical role in membrane fusion mediated by the interaction of CD4 with the human immunodeficiency virus type 1 (HIV-1) envelope glycoprotein. To analyze in detail the role of CDR3 and adjacent regions in the fusion process, we used cassette mutagenesis to construct a panel of 30 site-directed mutations between residues 79 and 96 of the full-length CD4 molecule. The mutant proteins were transiently expressed by using recombinant vaccinia virus vectors and were analyzed for cell surface expression, recombinant gp120-binding activity, and overall structural integrity as assessed by reactivity with a battery of anti-CD4 monoclonal antibodies. Cells expressing the CD4 mutants were assayed for their ability to form syncytia when mixed with cells expressing the HIV-1 envelope glycoprotein. Surprisingly in view of published data from others, most of the mutations had little effect on syncytium-forming activity. Normal fusion was observed in 21 mutants, including substitution of human residues 85 to 95 with the corresponding sequences from either chimpanzee, rhesus, or mouse CD4; a panel of Ser-Arg double insertions after each residue from 86 to 91; and a number of other charge, hydrophobic, and proline substitutions and insertions within this region. The nine mutants that showed impaired fusion all displayed defective gp120 binding and disruption of overall structural integrity. In further contrast with results of other workers, we observed that transformant human cell lines expressing native chimpanzee or rhesus CD4 efficiently formed syncytia when mixed with cells expressing the HIV-1 envelope glycoprotein. These data refute the conclusion that certain mutations in the CDR3 region of CD4 abolish cell fusion activity, and they suggest that a wide variety of sequences can be functionally tolerated in this region, including those from highly divergent mammalian species. Syncytium formation mediated by several of the CDR3 mutants was partially or completely resistant to inhibition by the CDR3-directed monoclonal antibody L71, suggesting that the corresponding epitope is not directly involved in the fusion process.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Journal of virology AU - Broder, C C AU - Berger, E A AD - Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 913 EP - 926 VL - 67 IS - 2 SN - 0022-538X, 0022-538X KW - Antibodies, Monoclonal KW - 0 KW - Antigens, CD4 KW - HIV Envelope Protein gp120 KW - Peptide Fragments KW - Recombinant Proteins KW - Viral Fusion Proteins KW - Index Medicus KW - AIDS/HIV KW - Vaccinia virus -- genetics KW - Animals KW - HeLa Cells KW - DNA Mutational Analysis KW - Humans KW - Primates -- genetics KW - Amino Acid Sequence KW - Recombinant Proteins -- genetics KW - Structure-Activity Relationship KW - Peptide Fragments -- chemical synthesis KW - Base Sequence KW - Recombinant Proteins -- metabolism KW - Transformation, Genetic KW - Peptide Fragments -- pharmacology KW - Molecular Sequence Data KW - Cell Line KW - Protein Conformation KW - HIV-1 -- metabolism KW - Cell Fusion -- drug effects KW - Cell Fusion -- physiology KW - Antigens, CD4 -- genetics KW - Viral Fusion Proteins -- metabolism KW - Antigens, CD4 -- pharmacology KW - HIV Envelope Protein gp120 -- metabolism KW - Antigens, CD4 -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75558883?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=CD4+molecules+with+a+diversity+of+mutations+encompassing+the+CDR3+region+efficiently+support+human+immunodeficiency+virus+type+1+envelope+glycoprotein-mediated+cell+fusion.&rft.au=Broder%2C+C+C%3BBerger%2C+E+A&rft.aulast=Broder&rft.aufirst=C&rft.date=1993-02-01&rft.volume=67&rft.issue=2&rft.spage=913&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-11 N1 - Date created - 1993-02-11 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nature. 1990 Nov 29;348(6300):419-26 [2247146] Nature. 1990 Nov 29;348(6300):411-8 [1701030] AIDS Res Hum Retroviruses. 1990 Oct;6(10):1209-12 [2252640] J Immunol. 1990 Dec 15;145(12):4072-8 [1701782] J Virol. 1991 Mar;65(3):1133-40 [1995942] J Virol. 1991 Mar;65(3):1543-50 [1995952] J Biol Chem. 1991 Mar 25;266(9):5942-8 [1706342] Proc Natl Acad Sci U S A. 1991 Mar 15;88(6):2189-93 [2006155] Science. 1991 Jun 21;252(5013):1643-51 [2047872] J Exp Med. 1991 Aug 1;174(2):407-15 [1713252] J Acquir Immune Defic Syndr. 1991;4(9):923-4 [1895215] Proc Natl Acad Sci U S A. 1991 Sep 15;88(18):8082-6 [1896455] Annu Rev Immunol. 1991;9:649-78 [1910691] AIDS Res Hum Retroviruses. 1991 Jun;7(6):521-7 [1931230] Curr Opin Immunol. 1991 Aug;3(4):552-8 [1721822] J Biol Chem. 1992 Apr 5;267(10):6664-71 [1551875] Immunol Today. 1992 Jun;13(6):201-6 [1627247] J Immunol. 1992 Sep 1;149(5):1809-16 [1354681] AIDS. 1991;5 Suppl 2:S21-33 [1845049] DNA. 1984 Aug;3(4):339-43 [6489095] Cell. 1985 Aug;42(1):93-104 [2990730] Proc Natl Acad Sci U S A. 1986 Nov;83(21):8122-6 [3095828] Cell. 1987 Jun 5;49(5):659-68 [3107838] Proc Natl Acad Sci U S A. 1988 Apr;85(7):2357-61 [2451247] EMBO J. 1988 Feb;7(2):513-8 [3259178] Science. 1988 Aug 5;241(4866):712-6 [2969619] Cell. 1988 Sep 9;54(6):865-74 [3261635] FEBS Lett. 1988 Oct 24;239(1):88-92 [2846352] Proc Natl Acad Sci U S A. 1988 Dec;85(23):9273-7 [2461565] J Biol Chem. 1989 Apr 5;264(10):5812-7 [2647726] Arch Virol. 1989;105(1-2):129-35 [2785788] Cell. 1989 May 5;57(3):469-81 [2541915] Proc Natl Acad Sci U S A. 1989 Sep;86(18):7139-43 [2789382] Cell. 1990 Mar 9;60(5):747-54 [2107024] J Immunol. 1990 Mar 15;144(6):2131-9 [1690235] J Virol. 1990 May;64(5):2149-56 [2109100] J Virol. 1990 May;64(5):2448-51 [2182912] Virology. 1990 Apr;175(2):556-61 [1691563] Cell Immunol. 1990 Jun;128(1):101-17 [1971526] Proc Natl Acad Sci U S A. 1990 Sep;87(18):7150-4 [2402498] Science. 1990 Nov 23;250(4984):1139-42 [2251501] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Cell specificity of molecular changes during memory storage. AN - 75556123; 8419542 AB - The aeolid nudibranch, Hermissenda crassicornis, exhibits Pavlovian conditioning to paired light and rotational stimuli and it has been suggested that protein kinase C(PKC) may play a critical role in the cellular mechanism for this conditioned behavioral response in the B-cell photoreceptor. The present study was designed to further examine learning-specific PKC involvement in identified cellular areas, particularly those in the visual-vestibular network, of the Hermissenda nervous system after Pavlovian conditioning. As used in previous vertebrate studies, the highly specific PKC radioligand, [3H]phorbol-12,13-dibutyrate ([3H]-PDBU), was used to determine the binding characteristics of the molluscan protein receptor considered to be PKC. The binding was specific, saturable, and could be displaced by a soluble diacylglycerol analogue. The binding activity was distributed evenly between the cytosol and the membrane. All of these analyses suggest that [3H]PDBU binds primarily to PKC in Hermissenda as it does in many other systems. Computerized grain image analysis was then used to determine the cellular localization of PKC as a function of Pavlovian conditioning. The medial and intermediate B photoreceptor and the optic ganglion showed significantly increased [3H]PDBU binding in conditioned animals. The present results provide the first report of an associative learning change of a key signal transduction component in identified neurons. JF - Journal of neurochemistry AU - McPhie, D L AU - Matzel, L D AU - Olds, J L AU - Lester, D S AU - Kuzirian, A M AU - Alkon, D L AD - Neural Systems Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 646 EP - 651 VL - 60 IS - 2 SN - 0022-3042, 0022-3042 KW - Diglycerides KW - 0 KW - Tritium KW - 10028-17-8 KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - 1-oleoyl-2-acetylglycerol KW - 86390-77-4 KW - Index Medicus KW - Animals KW - Photic Stimulation KW - Diglycerides -- pharmacology KW - Conditioning (Psychology) KW - Kinetics KW - Mollusca KW - Autoradiography KW - Visual Perception KW - Binding Sites KW - Phorbol 12,13-Dibutyrate -- metabolism KW - Nervous System -- drug effects KW - Nervous System -- metabolism KW - Memory -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75556123?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neurochemistry&rft.atitle=Cell+specificity+of+molecular+changes+during+memory+storage.&rft.au=McPhie%2C+D+L%3BMatzel%2C+L+D%3BOlds%2C+J+L%3BLester%2C+D+S%3BKuzirian%2C+A+M%3BAlkon%2C+D+L&rft.aulast=McPhie&rft.aufirst=D&rft.date=1993-02-01&rft.volume=60&rft.issue=2&rft.spage=646&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurochemistry&rft.issn=00223042&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-09 N1 - Date created - 1993-02-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Baculovirus expression and purification of a soluble, mutant G-protein alpha subunit. AN - 75554630; 8425110 AB - The cDNA for the alpha i1 protein that had undergone site-directed mutagenesis to change glycine-2 to alanine was ligated into a baculovirus transfer vector. A recombinant virus was obtained by transfecting Sf9 cells with both the wild-type baculovirus DNA and the transfer vector and screening for recombinant plaques. Infection with the recombinant virus led to a high level of expression of the mutated alpha i1 protein in the soluble fraction of the cell. The protein was purified by ammonium sulfate precipitation, gel filtration, and immobilized dye chromatography. The typical yield was 7.5 mg from two 800-ml cultures. The protein showed immunoreactivity to three different alpha i-specific antibodies. It bound guanosine 5'-(gamma-thio)triphosphate (GTP gamma S) with a stoichiometry of 0.63 to 0.91 mol/mol and with a rate constant (kGTP gamma S) of binding of 0.126 min-1. When GTP gamma S bound, the protein was protected from complete tryptic cleavage. The recombinant protein was able to undergo pertussis toxin-catalyzed ADP ribosylation and bind beta gamma subunits but with a reduced affinity compared to that of alpha transducin. Thus using a recombinant baculovirus, a nonmyristylated G protein alpha subunit was abundantly expressed in Sf9 cells and milligram quantities of a functional protein were easily purified. JF - Protein expression and purification AU - Jones, T L AU - Woodard, C AU - Spiegel, A M AD - Molecular Pathophysiology Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 64 EP - 71 VL - 4 IS - 1 SN - 1046-5928, 1046-5928 KW - Guanosine 5'-O-(3-Thiotriphosphate) KW - 37589-80-3 KW - DNA KW - 9007-49-2 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Index Medicus KW - Rats KW - Animals KW - Base Sequence KW - Electrophoresis, Polyacrylamide Gel KW - Cells, Cultured KW - Molecular Sequence Data KW - Guanosine 5'-O-(3-Thiotriphosphate) -- metabolism KW - Amino Acid Sequence KW - Insects KW - Cloning, Molecular KW - Baculoviridae -- genetics KW - GTP-Binding Proteins -- isolation & purification KW - Mutation KW - GTP-Binding Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75554630?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Protein+expression+and+purification&rft.atitle=Baculovirus+expression+and+purification+of+a+soluble%2C+mutant+G-protein+alpha+subunit.&rft.au=Jones%2C+T+L%3BWoodard%2C+C%3BSpiegel%2C+A+M&rft.aulast=Jones&rft.aufirst=T&rft.date=1993-02-01&rft.volume=4&rft.issue=1&rft.spage=64&rft.isbn=&rft.btitle=&rft.title=Protein+expression+and+purification&rft.issn=10465928&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-04 N1 - Date created - 1993-03-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Enhancer-dependent transcription of the epsilon-globin promoter requires promoter-bound GATA-1 and enhancer-bound AP-1/NF-E2. AN - 75553678; 8423810 AB - We analyzed epsilon-globin transcription in erythroid cells and in erythroid extracts to determine the requirements for enhancer-dependent expression of this gene. Mutations that abolished GATA-1 binding at a single position in the promoter prevented interaction with enhancers, whereas elimination of a second more distal promoter GATA-1 site had no effect. Deletion or mutation of the GATA-1 sites in either the human beta-globin locus control region DNase-hypersensitive site II enhancer or the chicken beta A/epsilon-globin enhancer did not diminish the ability of the enhancers to interact with the promoter. In contrast, mutation of the AP-1/NF-E2 sites in these enhancers resulted in elimination of enhancement. In vitro transcription of these constructs was promoter dependent and was not sensitive to abolition of GATA-1 binding in the promoter, consistent with the role of GATA-1 solely as a mediator of the enhancer effect. Thus, GATA-1 regulates the response of the epsilon-globin gene to enhancers through a specific site in the promoter and requires enhancer AP-1/NF-E2 binding to transduce the enhancer effect on transcription. JF - Molecular and cellular biology AU - Gong, Q AU - Dean, A AD - Laboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 911 EP - 917 VL - 13 IS - 2 SN - 0270-7306, 0270-7306 KW - DNA-Binding Proteins KW - 0 KW - Erythroid-Specific DNA-Binding Factors KW - GATA1 Transcription Factor KW - GATA1 protein, human KW - Proto-Oncogene Proteins c-jun KW - Transcription Factors KW - Globins KW - 9004-22-2 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Base Sequence KW - Humans KW - Molecular Sequence Data KW - Protein Binding KW - Cell Line KW - Mutagenesis KW - Promoter Regions, Genetic KW - Transcription Factors -- metabolism KW - Enhancer Elements, Genetic KW - Globins -- genetics KW - Transcription, Genetic KW - Proto-Oncogene Proteins c-jun -- metabolism KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75553678?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+cellular+biology&rft.atitle=Enhancer-dependent+transcription+of+the+epsilon-globin+promoter+requires+promoter-bound+GATA-1+and+enhancer-bound+AP-1%2FNF-E2.&rft.au=Gong%2C+Q%3BDean%2C+A&rft.aulast=Gong&rft.aufirst=Q&rft.date=1993-02-01&rft.volume=13&rft.issue=2&rft.spage=911&rft.isbn=&rft.btitle=&rft.title=Molecular+and+cellular+biology&rft.issn=02707306&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-24 N1 - Date created - 1993-02-24 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Genes Dev. 1992 May;6(5):730-44 [1577269] Biotechniques. 1990 Feb;8(2):178-83 [2180450] Nucleic Acids Res. 1992 Sep 11;20(17):4429-36 [1408744] Nucleic Acids Res. 1983 Mar 11;11(5):1475-89 [6828386] Nucleic Acids Res. 1985 May 24;13(10):3599-615 [3859838] Proc Natl Acad Sci U S A. 1985 Oct;82(19):6384-8 [3879975] Proc Natl Acad Sci U S A. 1986 Mar;83(5):1359-63 [3456593] Proc Natl Acad Sci U S A. 1987 Jul;84(14):4786-90 [3474625] Cell. 1987 Dec 24;51(6):975-85 [3690667] Proc Natl Acad Sci U S A. 1988 Aug;85(16):5976-80 [3413070] Proc Natl Acad Sci U S A. 1988 Sep;85(17):6267-71 [3166139] Nucleic Acids Res. 1989 Jan 11;17(1):37-54 [2911469] Nature. 1989 Mar 30;338(6214):435-8 [2467208] Cell. 1990 Apr 6;61(1):9-11 [2180585] Nucleic Acids Res. 1990 Mar 25;18(6):1339-50 [2326182] EMBO J. 1990 Jul;9(7):2169-77 [2357965] Genes Dev. 1990 Jun;4(6):993-1006 [2116990] Nucleic Acids Res. 1990 Sep 25;18(18):5465-72 [2216720] Cell. 1990 Nov 16;63(4):665-72 [2225071] Nucleic Acids Res. 1990 Oct 25;18(20):6011-7 [2235483] Proc Natl Acad Sci U S A. 1990 Nov;87(22):9000-4 [2123346] Science. 1990 Nov 23;250(4984):1147-9 [2251502] Nature. 1991 Jan 17;349(6306):257-60 [1987478] Annu Rev Cell Biol. 1990;6:95-124 [2275826] Mol Cell Biol. 1991 Feb;11(2):843-53 [1990287] Proc Natl Acad Sci U S A. 1991 Mar 1;88(5):1626-30 [2000371] Proc Natl Acad Sci U S A. 1991 Apr 15;88(8):3004-8 [2014222] Mol Cell Biol. 1991 May;11(5):2558-66 [2017165] Cell. 1991 May 3;65(3):493-505 [1850324] J Biol Chem. 1991 May 15;266(14):8907-15 [2026603] Genes Dev. 1991 Jun;5(6):919-31 [2044960] Proc Natl Acad Sci U S A. 1991 Oct 1;88(19):8676-80 [1924329] Proc Natl Acad Sci U S A. 1991 Nov 15;88(22):10188-92 [1946439] Nature. 1992 Jan 16;355(6357):219-24 [1731219] Mol Cell Biol. 1992 Apr;12(4):1561-7 [1549112] Genes Dev. 1992 Apr;6(4):521-32 [1559609] Mol Cell Biol. 1992 May;12(5):2057-66 [1373805] Mol Cell Biol. 1992 May;12(5):2135-42 [1569944] Proc Natl Acad Sci U S A. 1992 May 1;89(9):3899-903 [1570310] Proc Natl Acad Sci U S A. 1989 Apr;86(8):2554-8 [2704733] Proc Natl Acad Sci U S A. 1989 Sep;86(17):6548-52 [2771941] Cell. 1989 Sep 8;58(5):877-85 [2776214] Prog Clin Biol Res. 1989;316A:179-91 [2594805] Genes Dev. 1989 Dec;3(12A):1845-59 [2620825] Trends Genet. 1991 Nov-Dec;7(11-12):377-81 [1668190] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Depressive symptoms and the self-reported use of alcohol, caffeine, and carbohydrates in normal volunteers and four groups of psychiatric outpatients. AN - 75550780; 8422081 AB - The authors examined the relationship between depressive symptoms and the self-reported use of alcohol, carbohydrates, and caffeine in normal volunteers and four groups of psychiatric outpatients. Outpatients and normal volunteers were given a questionnaire asking about their use of each of the three substances in response to each of the 14 depressive symptoms on the Hamilton Rating Scale for Depression. They also rated how much each substance improved each symptom. Twenty-six normal volunteers, 35 patients with major depression, 117 patients with seasonal affective disorder, 16 patients with alcohol dependence, and 24 patients with comorbid primary depression and secondary alcohol dependence completed the questionnaire. Test-retest reliability was established. Analysis of variance and stepwise multivariate discriminant function analyses were used to determine if diagnostic groups differed in the reported use and effect of each of the three substances. The responses concerning use and effect of alcohol of patients with alcohol dependence with or without depression were indistinguishable from each other. The responses of the patient groups regarding caffeine and carbohydrate use did not differ from each other, but all differed significantly from the responses of normal volunteers. Discriminant function analysis distinguished alcoholics from nonalcoholics in the relationship between drinking and the symptoms of anger and anhedonia. The relationship between symptoms and substance use varied depending on the substance. Alcoholics without depression were as likely to report drinking in response to depressive symptoms as were those who had had depression. Patients of all diagnostic groups were more likely than normal volunteers to report using caffeine and carbohydrates in response to depressive symptoms. JF - The American journal of psychiatry AU - Leibenluft, E AU - Fiero, P L AU - Bartko, J J AU - Moul, D E AU - Rosenthal, N E AD - Clinical Psychobiology Branch, NIMH, Bethesda, MD 20892. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 294 EP - 301 VL - 150 IS - 2 SN - 0002-953X, 0002-953X KW - Coffee KW - 0 KW - Dietary Carbohydrates KW - Caffeine KW - 3G6A5W338E KW - Abridged Index Medicus KW - Index Medicus KW - Self Medication -- psychology KW - Depressive Disorder -- prevention & control KW - Analysis of Variance KW - Psychiatric Status Rating Scales KW - Diagnosis, Differential KW - Caffeine -- administration & dosage KW - Alcoholism -- diagnosis KW - Humans KW - Depressive Disorder -- diagnosis KW - Alcoholism -- psychology KW - Ambulatory Care KW - Mental Disorders -- diagnosis KW - Dietary Carbohydrates -- administration & dosage KW - Depression -- psychology KW - Mental Disorders -- psychology KW - Depression -- diagnosis KW - Alcohol Drinking KW - Depression -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75550780?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+journal+of+psychiatry&rft.atitle=Depressive+symptoms+and+the+self-reported+use+of+alcohol%2C+caffeine%2C+and+carbohydrates+in+normal+volunteers+and+four+groups+of+psychiatric+outpatients.&rft.au=Leibenluft%2C+E%3BFiero%2C+P+L%3BBartko%2C+J+J%3BMoul%2C+D+E%3BRosenthal%2C+N+E&rft.aulast=Leibenluft&rft.aufirst=E&rft.date=1993-02-01&rft.volume=150&rft.issue=2&rft.spage=294&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+psychiatry&rft.issn=0002953X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-17 N1 - Date created - 1993-02-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Prospective study of efficacy and safety of lansoprazole in Zollinger-Ellison syndrome. AN - 75550021; 8425437 AB - Lansoprazole, a new substituted benzimidazole H+,K(+)-ATPase inhibitor, profoundly inhibits gastric acid secretion and has potential use in the management of diseases such as Zollinger-Ellison syndrome (ZES). In the present study we evaluated the efficacy and safety of lansoprazole in controlling acid hypersecretion in 20 patients with ZES. The starting dose was 60 mg once daily. Control of acid hypersecretion was defined as the dose required to reduce acid secretion to < 10 meq/hr in the last hour before the next dose. Doses were adjusted upwards until effective control was achieved. Patients not controlled with 120 mg once daily were placed on twice daily lansoprazole. Most patients (90%) required lansoprazole once daily. During long-term follow-up (mean 18.5 months), 25% of patients required upward dose adjustments and 25% of patients required twice daily lansoprazole. Following cessation of therapy, the mean time for gastric acid output to reach half basal acid output was 39.1 hr. Lansoprazole was well-tolerated without side effects. Clinical chemistry and hematological studies were unchanged, and no gastric carcinoids developed. These results demonstrate that lansoprazole is a safe and effective inhibitor of gastric acid hypersecretion in patients with Zollinger-Ellison syndrome. Because it has a long duration of action, lansoprazole can be used to control gastric acid hypersecretion in most patients with Zollinger-Ellison syndrome using a once daily dosing schedule. JF - Digestive diseases and sciences AU - Metz, D C AU - Pisegna, J R AU - Ringham, G L AU - Feigenbaum, K AU - Koviack, P D AU - Maton, P N AU - Gardner, J D AU - Jensen, R T AD - Digestive Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 245 EP - 256 VL - 38 IS - 2 SN - 0163-2116, 0163-2116 KW - 2-Pyridinylmethylsulfinylbenzimidazoles KW - 0 KW - Anti-Ulcer Agents KW - Lansoprazole KW - 0K5C5T2QPG KW - Adenosine Triphosphatases KW - EC 3.6.1.- KW - Omeprazole KW - KG60484QX9 KW - Abridged Index Medicus KW - Index Medicus KW - Dose-Response Relationship, Drug KW - Humans KW - Aged KW - Gastric Acidity Determination KW - Prospective Studies KW - Adult KW - Gastric Mucosa -- drug effects KW - Middle Aged KW - Time Factors KW - Gastric Mucosa -- secretion KW - Female KW - Male KW - Anti-Ulcer Agents -- adverse effects KW - Zollinger-Ellison Syndrome -- drug therapy KW - Omeprazole -- adverse effects KW - Omeprazole -- therapeutic use KW - Omeprazole -- administration & dosage KW - Anti-Ulcer Agents -- therapeutic use KW - Omeprazole -- analogs & derivatives KW - Adenosine Triphosphatases -- antagonists & inhibitors KW - Zollinger-Ellison Syndrome -- physiopathology KW - Anti-Ulcer Agents -- administration & dosage KW - Zollinger-Ellison Syndrome -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75550021?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Digestive+diseases+and+sciences&rft.atitle=Prospective+study+of+efficacy+and+safety+of+lansoprazole+in+Zollinger-Ellison+syndrome.&rft.au=Metz%2C+D+C%3BPisegna%2C+J+R%3BRingham%2C+G+L%3BFeigenbaum%2C+K%3BKoviack%2C+P+D%3BMaton%2C+P+N%3BGardner%2C+J+D%3BJensen%2C+R+T&rft.aulast=Metz&rft.aufirst=D&rft.date=1993-02-01&rft.volume=38&rft.issue=2&rft.spage=245&rft.isbn=&rft.btitle=&rft.title=Digestive+diseases+and+sciences&rft.issn=01632116&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-03 N1 - Date created - 1993-03-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Fertility drugs and ovarian cancer: red alert or red herring? AN - 75549896; 8425620 JF - Fertility and sterility AU - Spirtas, R AU - Kaufman, S C AU - Alexander, N J AD - Center for Population Research, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 291 EP - 293 VL - 59 IS - 2 SN - 0015-0282, 0015-0282 KW - Fertility Agents KW - 0 KW - Index Medicus KW - Neoplasm Invasiveness KW - Humans KW - Research Design KW - Female KW - Ovarian Neoplasms -- chemically induced KW - Fertility Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75549896?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fertility+and+sterility&rft.atitle=Fertility+drugs+and+ovarian+cancer%3A+red+alert+or+red+herring%3F&rft.au=Spirtas%2C+R%3BKaufman%2C+S+C%3BAlexander%2C+N+J&rft.aulast=Spirtas&rft.aufirst=R&rft.date=1993-02-01&rft.volume=59&rft.issue=2&rft.spage=291&rft.isbn=&rft.btitle=&rft.title=Fertility+and+sterility&rft.issn=00150282&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-03 N1 - Date created - 1993-03-03 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Fertil Steril. 1993 Jul;60(1):199-201 [8513952] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Improved radioimmunotherapeutic efficacy of an anticarcinoma monoclonal antibody (131I-CC49) when given in combination with gamma-interferon. AN - 75547920; 8425194 AB - The moderately differentiated human colon tumor cell line, HT-29, constitutively expresses low levels of the high molecular weight mucin, tumor-associated glycoprotein 72 (TAG-72), and the M(r) 180,000 carcinoembryonic antigen (CEA) when grown as s.c. tumors in athymic mice. We report that the in vivo administration of gamma-interferon (IFN-gamma) resulted in a time- and dose-dependent increase in both TAG-72 and CEA expression in the HT-29 tumors. Immunohistochemical staining revealed a more homogeneous TAG-72-positive tumor cell population after IFN-gamma. Furthermore, both anti-TAG-72 and anti-CEA monoclonal antibodies (MAbs) showed enhanced localization to the HT-29 tumors in mice treated with IFN-gamma. Using that experimental model, subsequent studies presented evidence showing that the combination of IFN-gamma with 131I-CC49, an anti-TAG-72 MAb, resulted in a statistically significant improvement in therapeutic efficacy when compared with 131I-CC49 alone. For example, treatment with 300 microCi of 131I-CC49 initially suppressed HT-29 tumor growth; however, that reduction in tumor growth was transient as evidenced by the emergence of additional tumor growth at later time points. In contrast, an 8-day treatment with IFN-gamma in combination with 300 microCi 131I-CC49 resulted in sustained suppression of HT-29 tumor growth. Thus, IFN-gamma in vivo can substantially increase the TAG-72 expression in human colon tumor xenografts which leads to an increased tumor localization of anti-TAG-72 MAbs and seems to be responsible for the enhanced antitumor effects when IFN-gamma was combined with 131I-CC49. The results provide further evidence for including a biological response modifier, such as IFN-gamma, which can increase the expression of specific tumor antigens (i.e., TAG-72 and CEA) subsequently leading to a dramatic improvement in the antitumor efficacy of a radionuclide-conjugated MAb. JF - Cancer research AU - Greiner, J W AU - Ullmann, C D AU - Nieroda, C AU - Qi, C F AU - Eggensperger, D AU - Shimada, S AU - Steinberg, S M AU - Schlom, J AD - Laboratory of Tumor Immunology and Biology, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1993/02/01/ PY - 1993 DA - 1993 Feb 01 SP - 600 EP - 608 VL - 53 IS - 3 SN - 0008-5472, 0008-5472 KW - Antibodies, Monoclonal KW - 0 KW - Antibodies, Neoplasm KW - Antigens, Neoplasm KW - Carcinoembryonic Antigen KW - Immunotoxins KW - Iodine Radioisotopes KW - Recombinant Proteins KW - TAG 12 KW - Interferon-gamma KW - 82115-62-6 KW - Index Medicus KW - Animals KW - Carcinoembryonic Antigen -- physiology KW - Combined Modality Therapy KW - Dose-Response Relationship, Drug KW - Humans KW - Antibodies, Neoplasm -- immunology KW - Mice KW - Mice, Nude KW - Antibodies, Monoclonal -- therapeutic use KW - Transplantation, Heterologous KW - Antigens, Neoplasm -- immunology KW - Antigens, Neoplasm -- physiology KW - Iodine Radioisotopes -- therapeutic use KW - Radioimmunotherapy KW - Colonic Neoplasms -- therapy KW - Interferon-gamma -- pharmacology KW - Immunotoxins -- therapeutic use KW - Colonic Neoplasms -- metabolism KW - Immunotoxins -- metabolism KW - Colonic Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75547920?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Improved+radioimmunotherapeutic+efficacy+of+an+anticarcinoma+monoclonal+antibody+%28131I-CC49%29+when+given+in+combination+with+gamma-interferon.&rft.au=Greiner%2C+J+W%3BUllmann%2C+C+D%3BNieroda%2C+C%3BQi%2C+C+F%3BEggensperger%2C+D%3BShimada%2C+S%3BSteinberg%2C+S+M%3BSchlom%2C+J&rft.aulast=Greiner&rft.aufirst=J&rft.date=1993-02-01&rft.volume=53&rft.issue=3&rft.spage=600&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-02 N1 - Date created - 1993-03-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Estrogen replacement therapy and endometrial cancer risk: unresolved issues. The Endometrial Cancer Collaborative Group. AN - 75543528; 8380913 AB - To clarify several unresolved issues regarding the relationship of estrogens to endometrial cancer risk. We conducted a hospital-based case-control study involving 300 menopausal women newly diagnosed with epithelial endometrial cancer and 207 population controls matched to the cases for age, race, and residence. Estrogen use significantly increased endometrial cancer risk (adjusted relative risk [RR] 3.0, 95% confidence interval [CI] 1.7-5.1). Although both short- and long-term use appeared to elevate the risk of early-stage tumors, an effect of estrogens on late-stage tumors was observed only for long-term use (RR 2.1, 95% CI 0.7-6.4). A small proportion of women reported having used progestogens simultaneously with estrogens, which was associated with a lower risk (RR 1.8) than use of estrogens alone (RR 3.4). Although the highest risks were for recent users of estrogens, persistent excess risks were seen even for those who had discontinued use of 5 or more years. There were no striking relationships according to the type of estrogen or regimen used, and associations with dose were inconsistent, although women who used low-dose preparations exclusively had the lowest risk. Estrogen injections or creams, used by only 5.9 and 5.1% of the subjects, respectively, were not significant risk factors after adjustment for estrogen pill use. Women who were thin or who smoked cigarettes appeared to be most adversely affected by estrogen use. Estrogen users failed to experience the protective effect normally associated with oral contraceptive use. The effect of estrogens on endometrial cancer risk appears to vary both by usage patterns and by patient characteristics. JF - Obstetrics and gynecology AU - Brinton, L A AU - Hoover, R N AD - Environmental Epidemiology Branch, National Cancer Institute, Bethesda, Maryland. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 265 EP - 271 VL - 81 IS - 2 SN - 0029-7844, 0029-7844 KW - Contraceptives, Oral KW - 0 KW - Estrogens, Conjugated (USP) KW - Abridged Index Medicus KW - Index Medicus KW - Contraceptives, Oral -- adverse effects KW - Odds Ratio KW - Risk Factors KW - Humans KW - Case-Control Studies KW - Confidence Intervals KW - Middle Aged KW - United States -- epidemiology KW - Time Factors KW - Smoking -- epidemiology KW - Female KW - Estrogens, Conjugated (USP) -- adverse effects KW - Estrogen Replacement Therapy -- adverse effects KW - Endometrial Neoplasms -- epidemiology KW - Endometrial Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75543528?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Obstetrics+and+gynecology&rft.atitle=Estrogen+replacement+therapy+and+endometrial+cancer+risk%3A+unresolved+issues.+The+Endometrial+Cancer+Collaborative+Group.&rft.au=Brinton%2C+L+A%3BHoover%2C+R+N&rft.aulast=Brinton&rft.aufirst=L&rft.date=1993-02-01&rft.volume=81&rft.issue=2&rft.spage=265&rft.isbn=&rft.btitle=&rft.title=Obstetrics+and+gynecology&rft.issn=00297844&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-22 N1 - Date created - 1993-02-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Identification of a DNA-binding domain in the amino terminus of adeno-associated virus Rep proteins. AN - 75543034; 8380475 AB - The Rep78 and Rep68 proteins of adeno-associated virus (AAV) bind to the AAV terminal repeat hairpin DNA and are required for viral replication. We have expressed a series of mutant rep genes from the human immunodeficiency virus type 1 long terminal repeat promoter in human 293 cells and in an in vitro transcription-translation system. Mutant proteins were analyzed for AAV hairpin DNA binding and AAV terminal resolution functions. Deletion of amino acid residues 523 through 621 of Rep 78 had no effect on these functions. Amber mutant Rep proteins truncated at either amino acid 237 or amino acid 243 showed no detectable hairpin DNA binding or terminal resolution activity. A frameshift mutant Rep protein which contained Rep78 amino acids 1 through 241 lacked terminal resolution functions but bound specifically to the AAV hairpin DNA. The carboxyl-terminal missense sequence in this mutant appeared to have complemented an AAV-specific DNA-binding domain within the amino terminus of the Rep protein. mutant Rep protein in which methionine 225 of Rep78 was deleted (M225dl) was reduced threefold in AAV hairpin binding and had no terminal resolution functions. A mutant Rep protein in which a glycine was substituted at position 225 (M225G) was fully functional in these assays. When M225dl extract was mixed with wild-type Rep78 extract, AAV terminal resolution by Rep78 was inhibited. These results suggest that the amino-terminal portion of Rep78 and Rep68 contains a domain which can direct binding to AAV terminal hairpin DNA and that elements within the central region of the protein stabilize binding. JF - Journal of virology AU - Owens, R A AU - Weitzman, M D AU - Kyöstiö, S R AU - Carter, B J AD - Laboratory of Molecular and Cellular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 997 EP - 1005 VL - 67 IS - 2 SN - 0022-538X, 0022-538X KW - Antibodies, Viral KW - 0 KW - DNA-Binding Proteins KW - Recombinant Proteins KW - Viral Proteins KW - rep proteins, Adeno-associated virus 2 KW - 137750-19-7 KW - Index Medicus KW - AIDS/HIV KW - Blotting, Western KW - Base Sequence KW - Electrophoresis KW - Recombinant Proteins -- biosynthesis KW - Transfection KW - Humans KW - Molecular Sequence Data KW - Subcellular Fractions KW - Cell Nucleus KW - Cell Line, Transformed KW - Plasmids KW - Structure-Activity Relationship KW - Mutagenesis KW - Viral Proteins -- genetics KW - Dependovirus -- genetics KW - DNA-Binding Proteins -- genetics KW - DNA-Binding Proteins -- biosynthesis KW - Viral Proteins -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75543034?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Identification+of+a+DNA-binding+domain+in+the+amino+terminus+of+adeno-associated+virus+Rep+proteins.&rft.au=Owens%2C+R+A%3BWeitzman%2C+M+D%3BKy%C3%B6sti%C3%B6%2C+S+R%3BCarter%2C+B+J&rft.aulast=Owens&rft.aufirst=R&rft.date=1993-02-01&rft.volume=67&rft.issue=2&rft.spage=997&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-11 N1 - Date created - 1993-02-11 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Virol. 1984 Sep;51(3):611-9 [6088786] J Mol Biol. 1984 Oct 15;179(1):1-20 [6094825] Mol Cell Biol. 1985 Aug;5(8):2051-60 [3018548] J Virol. 1986 Dec;60(3):823-32 [3023672] Proc Natl Acad Sci U S A. 1986 Dec;83(24):9759-63 [2432602] Virology. 1987 Nov;161(1):18-28 [2823460] J Virol. 1988 Jan;62(1):68-74 [2824856] J Virol. 1988 Sep;62(9):3356-63 [2841488] J Virol. 1989 Jul;63(7):3034-9 [2542611] J Virol. 1989 Jul;63(7):3095-104 [2542617] Virology. 1989 Jul;171(1):239-47 [2545030] Virology. 1989 Nov;173(1):120-8 [2554565] Cell. 1990 Jan 12;60(1):105-13 [2153052] J Virol. 1990 Apr;64(4):1764-70 [2157057] Cell. 1990 May 4;61(3):447-57 [2159383] J Virol. 1990 Dec;64(12):6204-13 [2173787] J Virol. 1991 Jan;65(1):396-404 [1845899] J Mol Biol. 1991 Feb 20;217(4):721-9 [2005621] Virology. 1991 Apr;181(2):738-41 [1849683] Virology. 1991 Sep;184(1):14-22 [1651588] J Virol. 1992 Feb;66(2):1119-28 [1309894] J Virol. 1992 Feb;66(2):1236-40 [1309900] J Virol. 1992 Jul;66(7):4050-7 [1318396] Virology. 1973 Apr;52(2):456-67 [4705382] Proc Natl Acad Sci U S A. 1976 Mar;73(3):742-6 [1062784] Virology. 1977 May 15;78(2):488-99 [867815] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Virology. 1979 Jan 30;92(2):449-62 [218354] Methods Enzymol. 1980;65(1):499-560 [6246368] J Virol. 1983 Feb;45(2):555-64 [6300419] J Virol. 1984 Aug;51(2):329-39 [6086948] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Mutations in or near the fusion peptide of the influenza virus hemagglutinin affect an antigenic site in the globular region. AN - 75536475; 7678310 AB - We previously described a monoclonal antibody (Y8-10C2) that binds influenza virus hemagglutinin (HA) monomers but not native trimers. In this study, we demonstrated that Y8-10C2 binds to the globular domain of HA and found evidence that its epitope is located at the interface of adjacent subunits. We further showed that at elevated temperatures, the Y8-10C2 epitope is transiently exposed in trimers for antibody binding. Introduction of intrasubunit chemical cross-links into HA reversibly inhibited both Y8-10C2 binding to trimers at elevated temperatures and viral fusion activity, indicating that exposure of the epitope requires the normal conformational flexibility of the molecule. Prolonged incubation of Y8-10C2 with virus at an elevated temperature resulted in neutralization of viral infectivity, allowing selection of neutralization-resistant virus mutants. Mutants were divided into two classes based on a radioimmunoassay in which the virus is attached to polyvinyl: those with reduced affinity for Y8-10C2 or other monoclonal antibodies specific for the globular domain and those with no alteration in their interaction with Y8-10C2 or other antibodies. DNA sequencing of HA genes revealed that the first type of mutants possessed single amino acid substitutions in the Y8-10C2 epitope itself, while remarkably, the second type of mutants possessed single amino acid substitutions in or near the fusion peptide of the HA, which is located in the stem of the HA at a considerable distance from the Y8-10C2 epitope. These findings indicate that the conformational flexibility of the HA affects its antigenicity and that single amino acid substitutions in or near the fusion peptide influence the flexibility of the globular domains. JF - Journal of virology AU - Yewdell, J W AU - Taylor, A AU - Yellen, A AU - Caton, A AU - Gerhard, W AU - Bächi, T AD - Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 933 EP - 942 VL - 67 IS - 2 SN - 0022-538X, 0022-538X KW - Antibodies, Monoclonal KW - 0 KW - Antibodies, Viral KW - Antigens, Viral KW - Epitopes KW - Hemagglutinin Glycoproteins, Influenza Virus KW - Hemagglutinins, Viral KW - Viral Envelope Proteins KW - Viral Fusion Proteins KW - Index Medicus KW - Hot Temperature KW - Antigen-Antibody Reactions KW - Antibody Specificity KW - Epitopes -- genetics KW - Models, Molecular KW - Hydrogen-Ion Concentration KW - Protein Denaturation KW - Radioimmunoassay KW - Mutagenesis KW - Hemagglutinins, Viral -- genetics KW - Viral Fusion Proteins -- genetics KW - Antigens, Viral -- genetics KW - Orthomyxoviridae -- genetics KW - Viral Envelope Proteins -- genetics KW - Protein Conformation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75536475?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Mutations+in+or+near+the+fusion+peptide+of+the+influenza+virus+hemagglutinin+affect+an+antigenic+site+in+the+globular+region.&rft.au=Yewdell%2C+J+W%3BTaylor%2C+A%3BYellen%2C+A%3BCaton%2C+A%3BGerhard%2C+W%3BB%C3%A4chi%2C+T&rft.aulast=Yewdell&rft.aufirst=J&rft.date=1993-02-01&rft.volume=67&rft.issue=2&rft.spage=933&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-11 N1 - Date created - 1993-02-11 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nature. 1984 Oct 18-24;311(5987):678-80 [6207440] Cell. 1985 Feb;40(2):431-9 [3967299] EMBO J. 1984 Dec 20;3(13):3329-32 [6526017] Virology. 1985 Aug;145(1):72-83 [2409671] Biochim Biophys Acta. 1986 Jan 29;854(2):198-206 [3942725] J Virol. 1986 Feb;57(2):623-8 [2418215] Cell. 1986 Sep 12;46(6):939-50 [3757030] J Cell Biol. 1986 Oct;103(4):1179-91 [2429970] Virology. 1986 Dec;155(2):484-97 [3788061] Annu Rev Biochem. 1987;56:365-94 [3304138] J Cell Biol. 1987 Dec;105(6 Pt 2):2887-96 [2447101] Cell. 1988 Mar 25;52(6):843-52 [2450677] Annu Rev Biophys Biophys Chem. 1989;18:187-211 [2660823] EMBO J. 1990 Jan;9(1):17-24 [2295311] Cell. 1990 May 18;61(4):553-6 [1693095] Cell. 1992 Feb 21;68(4):635-45 [1739972] J Virol. 1992 Aug;66(8):4940-50 [1629960] Nature. 1970 Aug 15;227(5259):680-5 [5432063] J Exp Med. 1978 Aug 1;148(2):383-92 [359746] Nature. 1979 May 17;279(5710):246-8 [86955] Nature. 1981 Jan 29;289(5796):373-8 [6162101] FEBS Lett. 1980 Dec 29;122(2):283-7 [7202720] J Cell Biol. 1981 Dec;91(3 Pt 1):601-13 [7328111] Proc Natl Acad Sci U S A. 1982 Feb;79(4):968-72 [6951181] Cell. 1982 Dec;31(2 Pt 1):417-27 [6186384] Virology. 1983 Apr 30;126(2):587-99 [6190310] Nature. 1983 Jul 7-13;304(5921):76-8 [6191220] Vopr Virusol. 1983 Mar-Apr;(2):163-9 [6868554] J Gen Virol. 1983 Aug;64 (Pt 8):1657-62 [6192202] J Virol. 1983 Oct;48(1):239-48 [6193286] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Analysis of multiple mRNAs from pathogenic equine infectious anemia virus (EIAV) in an acutely infected horse reveals a novel protein, Ttm, derived from the carboxy terminus of the EIAV transmembrane protein. AN - 75531756; 8419648 AB - Transcription of pathogenic equine infectious anemia virus (EIAV) in an acutely infected horse was examined by using the polymerase chain reaction and nucleotide sequencing. Four spliced transcripts were identified in liver tissue, in contrast to the multiplicity of alternatively spliced messages reported for in vitro-propagated human immunodeficiency virus, simian immunodeficiency virus, and, to a lesser extent, EIAV. Nucleotide sequence analysis demonstrated that three of these mRNAs encode known viral proteins: the envelope precursor, the product of the S2 open reading frame, and the regulatory proteins Tat and Rev. The fourth transcript encodes a novel Tat-TM fusion protein, Ttm. Ttm is a 27-kDa protein translated from the putative tat CTG initiation codon and containing the carboxy-terminal portion of TM immediately downstream from the membrane-spanning domain. p27ttm is expressed in EIAV-infected canine cells and was recognized by peptide antisera against both Tat and TM. Cells transfected with ttm cDNA also expressed p27ttm, which appeared to be localized to the endoplasmic reticulum or Golgi apparatus by indirect immunofluorescence. The carboxy terminus of lentiviral TM proteins has previously been shown to influence viral infectivity, growth kinetics, and cytopathology, suggesting that Ttm plays an important role in the EIAV life cycle. JF - Journal of virology AU - Beisel, C E AU - Edwards, J F AU - Dunn, L L AU - Rice, N R AD - Laboratory of Molecular Virology and Carcinogenesis, NCI-Frederick Cancer Research and Development Center, Maryland 21702. Y1 - 1993/02// PY - 1993 DA - February 1993 SP - 832 EP - 842 VL - 67 IS - 2 SN - 0022-538X, 0022-538X KW - Gene Products, rev KW - 0 KW - Gene Products, tat KW - Membrane Proteins KW - RNA, Messenger KW - RNA, Viral KW - Ttm protein, Equine infectious anemia virus KW - Viral Envelope Proteins KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Sequence Homology, Nucleic Acid KW - Endoplasmic Reticulum KW - RNA Splicing KW - Horses KW - Transcription, Genetic KW - Amino Acid Sequence KW - Exons -- genetics KW - Polymerase Chain Reaction KW - Base Sequence KW - Cell Compartmentation KW - Molecular Sequence Data KW - Golgi Apparatus KW - Equine Infectious Anemia -- genetics KW - RNA, Viral -- genetics KW - RNA, Messenger -- genetics KW - Viral Envelope Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75531756?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Analysis+of+multiple+mRNAs+from+pathogenic+equine+infectious+anemia+virus+%28EIAV%29+in+an+acutely+infected+horse+reveals+a+novel+protein%2C+Ttm%2C+derived+from+the+carboxy+terminus+of+the+EIAV+transmembrane+protein.&rft.au=Beisel%2C+C+E%3BEdwards%2C+J+F%3BDunn%2C+L+L%3BRice%2C+N+R&rft.aulast=Beisel&rft.aufirst=C&rft.date=1993-02-01&rft.volume=67&rft.issue=2&rft.spage=832&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-11 N1 - Date created - 1993-02-11 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M61575; GENBANK; M11337; M14855; M93674; K03334 N1 - SuppNotes - Cited By: J Virol. 1988 Dec;62(12):4691-6 [2846880] J Virol. 1988 Dec;62(12):4813-8 [2846892] Virology. 1991 Jan;180(1):439-41 [1984664] Biotechniques. 1990 Dec;9(6):754-8, 760-1 [2271177] Virology. 1991 May;182(1):177-85 [2024463] J Virol. 1991 Jun;65(6):2987-92 [1674547] J Virol. 1991 Jul;65(7):3932-7 [1645801] Virology. 1991 Aug;183(2):786-92 [1649509] Virology. 1991 Oct;184(2):521-30 [1653485] Virology. 1991 Nov;185(1):217-28 [1926774] Virology. 1991 Nov;185(1):258-70 [1926777] Biotechniques. 1991 Aug;11(2):180, 182, 184 [1931014] AIDS Res Hum Retroviruses. 1991 Jun;7(6):511-9 [1657072] Cell. 1992 Feb 7;68(3):545-60 [1739967] J Biol Chem. 1992 Apr 5;267(10):7121-7 [1551918] Virology. 1992 May;188(1):391-5 [1566581] AIDS Res Hum Retroviruses. 1989 Feb;5(1):7-22 [2541749] J Virol. 1989 Jun;63(6):2492-6 [2470916] J Med Primatol. 1989;18(3-4):311-9 [2547965] AIDS Res Hum Retroviruses. 1989 Aug;5(4):441-9 [2788444] J Gen Virol. 1989 Aug;70 ( Pt 8):1995-2006 [2549179] J Virol. 1989 Oct;63(10):4395-403 [2778881] J Virol. 1989 Nov;63(11):4709-14 [2795718] Nature. 1989 Oct 19;341(6243):573-4 [2677749] J Virol. 1989 Dec;63(12):5194-200 [2555550] Mol Cell Biol. 1989 Oct;9(10):4459-66 [2586518] Proc Natl Acad Sci U S A. 1989 Dec;86(23):9544-8 [2687883] Annu Rev Cell Biol. 1989;5:1-23 [2688704] Mol Cell Biol. 1989 Nov;9(11):5073-80 [2601709] Nature. 1990 Mar 8;344(6262):113 [2308630] EMBO J. 1990 Mar;9(3):965-70 [2178928] J Virol. 1990 Apr;64(4):1616-24 [2157047] J Virol. 1990 Apr;64(4):1839-43 [2157066] Biopolymers. 1990 Jan;29(1):171-7 [2328285] Virology. 1990 May;176(1):280-8 [2158694] Gene. 1990 Jul 16;91(2):173-8 [2170233] J Cell Biol. 1990 Oct;111(4):1343-50 [2170420] Virology. 1990 Nov;179(1):347-64 [2171210] J Virol. 1992 Jun;66(6):3455-65 [1316461] Curr Top Microbiol Immunol. 1992;176:143-64 [1600751] J Virol. 1992 Jul;66(7):4085-97 [1318398] PCR Methods Appl. 1991 Aug;1(1):17-24 [1842916] Natl Inst Anim Health Q (Tokyo). 1967 Spring;7(1):1-7 [4293211] Natl Inst Anim Health Q (Tokyo). 1968 Winter;8(4):182-6 [4307837] Am J Vet Res. 1972 Jan;33(1):11-8 [4333633] Arch Gesamte Virusforsch. 1973;42(4):361-70 [4358259] Cell. 1978 Jul;14(3):725-31 [210957] J Am Vet Med Assoc. 1982 Feb 1;180(3):272-5 [6276353] Intervirology. 1981;16(4):225-32 [6177659] Anal Biochem. 1982 Sep 1;125(1):125-30 [6183990] J Virol. 1990 Jun;64(6):2505-18 [2186172] J Virol. 1990 Jun;64(6):2519-29 [2335812] J Virol. 1990 Jun;64(6):3100-3 [2186180] AIDS Res Hum Retroviruses. 1990 Mar;6(3):299-305 [2187499] J Virol. 1990 Jul;64(7):3391-8 [2191150] J Virol. 1990 Aug;64(8):3770-8 [2164597] J Virol. 1990 Sep;64(9):4093-8 [2384914] J Virol. 1990 Sep;64(9):4585-8 [2384924] Nucleic Acids Res. 1984 Jan 11;12(1 Pt 1):387-95 [6546423] J Biol Chem. 1984 Aug 25;259(16):10539-44 [6206055] J Biochem Biophys Methods. 1984 Dec;10(3-4):203-9 [6530509] Cell. 1986 Jan 31;44(2):283-92 [3943125] Virology. 1986 Mar;149(2):217-29 [3004027] Cell. 1987 Jul 17;50(2):311-7 [2954653] Biopolymers. 1987 Sep;26(9):1601-20 [3663875] J Virol. 1987 Dec;61(12):3783-9 [2446008] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - State-dependent radial elasticity of attached cross-bridges in single skinned fibres of rabbit psoas muscle AN - 1647021799; 21249209 AB - 1. In a single skinned fibre of rabbit psoas muscle, upon attachment of cross-bridges to actin in the presence of ADP or pyrophosphate (PPi), the separation between the contractile filaments, as determined by equatorial X-ray diffraction, is found to decrease, suggesting that force is generated in the radial direction. 2. The single muscle fibres were subjected to compression by 0-8% of dextran T500. The changes in lattice spacings by dextran compression were compared with changes induced by cross-bridge attachment to actin. Based on this comparison, the magnitude and the direction of the radial force generated by the attached cross-bridges were estimated. The radial cross-bridge force varied with filament separation, and the magnitude of the radial cross-bridge force reached as high as the maximal axial force produced during isometric contraction. 3. One key parameter of the radial elasticity, i.e. the equilibrium spacing where the radial force is zero, was found to depend on the ligand bound to the myosin head. In the presence of ADP, the equilibrium spacing was 36 nm. In the presence of MgPPi the equilibrium spacing shifted to 35 nm and Ca2+ had little effect on the equilibrium spacing. 4. The equilibrium spacing was independent of the fraction of cross-bridges attached to actin. The fraction of cross-bridges attached in rigor was modulated from 100% to close to 0% by adding up to 10 mM of ATP gamma S in the rigor solution. The lattice spacing remained at 38 nm, the equilibrium spacing for nucleotide-free cross-bridges at mu = 170 mM. 5. Radial force generated by cross-bridges in rigor at large lattice spacings (38 nm less than or equal to d10 less than or equal to 46 nm) appeared to vary linearly with lattice spacing. 6. The titration of ATP gamma S to fibres in rigor provided a correlation between the radial stiffness of the nucleotide-free cross-bridges and the equatorial intensities. The relation between the equatorial intensity ratio I11/I10 and radial stiffness appeared to be approximately linear. 7. The fibres under different conditions showed a wide range of radial stiffness, which was not proportional to the apparent axial stiffness of the fibre. If the apparent axial stiffness is a measure of the fraction of cross-bridges bound to actin, it follows that the radial elastic constant is state dependent; or vice versa. 8. Differences in equilibrium lattice spacing and in radial elastic constant, most probably reflect differences in the molecular structure of the acto-myosin complex and there is more than one single conformation of the various strongly bound cross-bridge states. 9. Determining equilibrium spacings of the radial elasticity appears to be an effective new approach in detecting structural differences among the attached cross-bridges, since this approach is independent of the fraction of cross-bridges attached, a factor that frequently encumbers the interpretation of structural studies of attached cross-bridge states. JF - Journal of Physiology (London) AU - Xu, Sengen AU - Brenner, Bernhard AU - Yu, Leepo C AD - National Institutes of Health, Bethesda, MD 20892, USA Y1 - 1993/02/01/ PY - 1993 DA - 1993 Feb 01 SP - 283 EP - 299 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 461 IS - 1 SN - 0022-3751, 0022-3751 KW - Physical Education Index KW - X-Ray KW - Animal subjects KW - Muscles KW - Isometrics KW - Balance KW - PE 090:Sports Medicine & Exercise Sport Science UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647021799?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Physiology+%28London%29&rft.atitle=State-dependent+radial+elasticity+of+attached+cross-bridges+in+single+skinned+fibres+of+rabbit+psoas+muscle&rft.au=Xu%2C+Sengen%3BBrenner%2C+Bernhard%3BYu%2C+Leepo+C&rft.aulast=Xu&rft.aufirst=Sengen&rft.date=1993-02-01&rft.volume=461&rft.issue=1&rft.spage=283&rft.isbn=&rft.btitle=&rft.title=Journal+of+Physiology+%28London%29&rft.issn=00223751&rft_id=info:doi/10.1113%2Fjphysiol.1993.sp019514 LA - English DB - Physical Education Index N1 - Date revised - 2015-01-01 N1 - Document feature - figure 0 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - X-Ray; Animal subjects; Muscles; Isometrics; Balance DO - http://dx.doi.org/10.1113/jphysiol.1993.sp019514 ER - TY - JOUR T1 - Expression of Drosophila Rrp1 protein in Escherichia coli. Enzymatic and physical characterization of the intact protein and a carboxyl-terminally deleted exonuclease-deficient mutant. AN - 75549808; 7678415 AB - Drosophila Rrp1 protein purified from embryos has four tightly associated enzymatic activities: DNA strand transfer, single-strand DNA renaturation, 3'-exonuclease, and apurinic endonuclease. Copurifying with these activities is a single polypeptide that has an apparent M(r) of 105,000 when estimated by SDS-polyacrylamide gel electrophoresis. To determine if this polypeptide is sufficient for these activities, it has been overexpressed in Escherichia coli. In crude extracts of E. coli cells, an ATP-independent Mg(2+)-dependent strand transfer activity is observed upon activation of the promoter that drives expression of Rrp1. Rrp1 protein purified from induced E. coli cells has electrophoretic, chromatographic, and enzymatic properties similar to those of Drosophila Rrp1 protein. The carboxyl-terminal region of Rrp1 (amino acids 428-679) is homologous to E. coli exonuclease III. Rrp1 deleted for this region cannot carry out DNA strand transfer, but can renature complementary single-strand DNA. The strand transfer activity of this truncated protein can be restored if DNA 3'-exonuclease is provided in trans by pretreating the double-strand DNA substrate with E. coli exonuclease III. This demonstrates a likely role of the exonuclease in the in vitro DNA strand transfer reaction carried out by Rrp1 protein. Such a role is also suggested by an analysis of the polarity of the strand transfer reaction. JF - The Journal of biological chemistry AU - Sander, M AU - Carter, M AU - Huang, S M AD - Laboratory of Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993/01/25/ PY - 1993 DA - 1993 Jan 25 SP - 2075 EP - 2082 VL - 268 IS - 3 SN - 0021-9258, 0021-9258 KW - DNA, Single-Stranded KW - 0 KW - DNA, Viral KW - Drosophila Proteins KW - Escherichia coli Proteins KW - Recombinant Proteins KW - DNA KW - 9007-49-2 KW - Nucleotidyltransferases KW - EC 2.7.7.- KW - Rrp1 protein, Drosophila KW - Endodeoxyribonucleases KW - EC 3.1.- KW - Exodeoxyribonucleases KW - Exonucleases KW - exodeoxyribonuclease III KW - EC 3.1.11.2 KW - Deoxyribonuclease IV (Phage T4-Induced) KW - EC 3.1.21.2 KW - endonuclease IV, E coli KW - DNA-(Apurinic or Apyrimidinic Site) Lyase KW - EC 4.2.99.18 KW - Index Medicus KW - DNA, Single-Stranded -- metabolism KW - Immunoblotting KW - Animals KW - Drosophila -- enzymology KW - DNA -- metabolism KW - Endodeoxyribonucleases -- metabolism KW - Plasmids KW - Exodeoxyribonucleases -- metabolism KW - Molecular Weight KW - Drosophila -- embryology KW - Mutagenesis KW - Recombinant Proteins -- isolation & purification KW - Recombinant Proteins -- metabolism KW - Nucleic Acid Renaturation KW - Sequence Homology, Amino Acid KW - DNA, Viral -- metabolism KW - Exodeoxyribonucleases -- chemistry KW - Exonucleases -- metabolism KW - Nucleotidyltransferases -- metabolism KW - Nucleotidyltransferases -- genetics KW - Nucleotidyltransferases -- chemistry KW - Gene Expression KW - Escherichia coli -- genetics KW - Escherichia coli -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75549808?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Expression+of+Drosophila+Rrp1+protein+in+Escherichia+coli.+Enzymatic+and+physical+characterization+of+the+intact+protein+and+a+carboxyl-terminally+deleted+exonuclease-deficient+mutant.&rft.au=Sander%2C+M%3BCarter%2C+M%3BHuang%2C+S+M&rft.aulast=Sander&rft.aufirst=M&rft.date=1993-01-25&rft.volume=268&rft.issue=3&rft.spage=2075&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-18 N1 - Date created - 1993-02-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Repair of individual DNA strands in the hamster dihydrofolate reductase gene after treatment with ultraviolet light, alkylating agents, and cisplatin. AN - 75547784; 8420940 AB - We have analyzed gene-specific and strand-specific DNA damage and repair in the dihydrofolate reductase gene in hamster cells. Cells were UV-irradiated or treated with two types of chemotherapeutics, alkylating agents or cisplatin. UV-induced pyrimidine dimers were detected using a previously published technique in which the T4 endonuclease V enzyme is used to create nicks at the lesion sites. 6-4 photoproducts were detected in a similar assay using ABC excinuclease after prior reversal of the pyrimidine dimers with photolyase. Adducts formed by the alkylating agents nitrogen mustard and dimethyl sulfate were quantitated by generating strand breaks at basic sites after neutral depurination. Cisplatin-induced intrastrand adducts were detected with ABC excinuclease, and cisplatin interstrand cross-links were detected using a denaturation-reannealing reaction before electrophoresis. In accord with previous reports by other investigators, we find distinct strand specificity of the repair of pyrimidine dimers after UV; the transcribed strand was much more efficiently repaired than the nontranscribed strand. In contrast, there was little or no strand bias in the repair of the 6-4 photoproducts. For alkylating agents, a slight bias toward repair in the transcribed strand was found after treatment with nitrogen mustard, but there appeared to be no bias in the repair after treatment with dimethyl sulfate. Cisplatin interstrand cross-links are repaired with equal efficiency from the two strands, but the more common cisplatin-induced lesion, the intrastrand adduct, is preferentially repaired from the transcribed strand. In conclusion, there is strand bias in the repair of pyrimidine dimers and cisplatin intrastrand adducts, but the strand specificity of repair may not be a general feature for all DNA lesions, as we found little or no strand bias in the repair of other lesions studied. JF - The Journal of biological chemistry AU - May, A AU - Nairn, R S AU - Okumoto, D S AU - Wassermann, K AU - Stevnsner, T AU - Jones, J C AU - Bohr, V A AD - Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/01/25/ PY - 1993 DA - 1993 Jan 25 SP - 1650 EP - 1657 VL - 268 IS - 3 SN - 0021-9258, 0021-9258 KW - Alkylating Agents KW - 0 KW - Pyrimidine Dimers KW - Sulfuric Acid Esters KW - Mechlorethamine KW - 50D9XSG0VR KW - DNA KW - 9007-49-2 KW - Tetrahydrofolate Dehydrogenase KW - EC 1.5.1.3 KW - dimethyl sulfate KW - JW5CW40Z50 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Photochemistry KW - Animals KW - Pyrimidine Dimers -- metabolism KW - Blotting, Southern KW - Sulfuric Acid Esters -- pharmacology KW - CHO Cells KW - Mechlorethamine -- pharmacology KW - DNA -- radiation effects KW - Cricetinae -- genetics KW - DNA -- drug effects KW - Ultraviolet Rays KW - DNA Repair KW - DNA Damage KW - Alkylating Agents -- pharmacology KW - Cisplatin -- pharmacology KW - Tetrahydrofolate Dehydrogenase -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75547784?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Repair+of+individual+DNA+strands+in+the+hamster+dihydrofolate+reductase+gene+after+treatment+with+ultraviolet+light%2C+alkylating+agents%2C+and+cisplatin.&rft.au=May%2C+A%3BNairn%2C+R+S%3BOkumoto%2C+D+S%3BWassermann%2C+K%3BStevnsner%2C+T%3BJones%2C+J+C%3BBohr%2C+V+A&rft.aulast=May&rft.aufirst=A&rft.date=1993-01-25&rft.volume=268&rft.issue=3&rft.spage=1650&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-18 N1 - Date created - 1993-02-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Ca(2+)-dependent and Ca(2+)-independent isozymes of protein kinase C mediate exocytosis in antigen-stimulated rat basophilic RBL-2H3 cells. Reconstitution of secretory responses with Ca2+ and purified isozymes in washed permeabilized cells. AN - 75535699; 8420951 AB - Rat basophilic RBL-2H3 cells, which exhibit Ca(2+)-dependent secretion of granules when stimulated with antigen, contained the Ca(2+)-dependent alpha and beta and the Ca(2+)-independent delta, epsilon, and zeta isoforms of protein kinase C. These isoforms associated, to variable extents (i.e. delta the most and zeta the least), with the membrane fraction upon antigen stimulation but without external Ca2+; only the Ca(2+)-independent isoforms did so. Both types of isozymes were probably necessary for optimal responses to antigen as indicated by the following observations. All Ca(2+)-dependent isozymes were degraded in cells treated with 20 nM phorbol 12-myristate 13-acetate for 6 h, whereas the Ca(2+)-independent isozymes were not degraded and were retained when the cells were subsequently permeabilized and washed. Cells so treated still exhibited antigen-induced secretion (25-33% of normal) which was suppressed by selective inhibitors of protein kinase C (Ro31-7549 and calphostin C) thereby indicating a possible contribution of the Ca(2+)-independent isozymes in secretion. Normally, washed permeabilized cells lost all isozymes of protein kinase C and failed to secrete in response to antigen. A full secretory response to antigen could be reconstituted by the subsequent addition of nanomolar concentrations of either beta or delta isozymes of protein kinase C (other isozymes were much less effective) but only in the presence of 1 microM free Ca2+ to indicate distinct roles for Ca2+ and protein kinase C in exocytosis. JF - The Journal of biological chemistry AU - Ozawa, K AU - Szallasi, Z AU - Kazanietz, M G AU - Blumberg, P M AU - Mischak, H AU - Mushinski, J F AU - Beaven, M A AD - Laboratory of Chemical Pharmacology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/01/25/ PY - 1993 DA - 1993 Jan 25 SP - 1749 EP - 1756 VL - 268 IS - 3 SN - 0021-9258, 0021-9258 KW - Antigens KW - 0 KW - Isoenzymes KW - Recombinant Proteins KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Rats KW - Baculoviridae -- enzymology KW - Immunoblotting KW - Brain -- enzymology KW - Animals KW - Recombinant Proteins -- metabolism KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Cytoplasmic Granules -- physiology KW - Cell Membrane Permeability KW - Antigens -- immunology KW - Cell Line KW - Protein Kinase C -- metabolism KW - Exocytosis -- physiology KW - Basophils -- enzymology KW - Protein Kinase C -- antagonists & inhibitors KW - Basophils -- ultrastructure KW - Calcium -- pharmacology KW - Isoenzymes -- metabolism KW - Basophils -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75535699?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Ca%282%2B%29-dependent+and+Ca%282%2B%29-independent+isozymes+of+protein+kinase+C+mediate+exocytosis+in+antigen-stimulated+rat+basophilic+RBL-2H3+cells.+Reconstitution+of+secretory+responses+with+Ca2%2B+and+purified+isozymes+in+washed+permeabilized+cells.&rft.au=Ozawa%2C+K%3BSzallasi%2C+Z%3BKazanietz%2C+M+G%3BBlumberg%2C+P+M%3BMischak%2C+H%3BMushinski%2C+J+F%3BBeaven%2C+M+A&rft.aulast=Ozawa&rft.aufirst=K&rft.date=1993-01-25&rft.volume=268&rft.issue=3&rft.spage=1749&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-18 N1 - Date created - 1993-02-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Induction of brain cytochrome P-450IIE1 by chronic ethanol treatment. AN - 75564158; 8431773 AB - Cytochrome P-450 mediated metabolism is potentially involved in the expression of the pharmacological and/or toxicological effects of a wide variety of drugs and environmental chemicals upon tissues which contain this metabolic system. In the present investigation, the presence of cytochrome P-450IIE1 and associated mono-oxygenase activities in brain and the effect of chronic ethanol treatment on brain cytochrome P-450 (P-450) were studied. Aniline hydroxylase, N-nitroso-dimethylamine N-demethylase and p-nitrophenol hydroxylase activities (known to be mediated by P-450IIE1) were detectable in brain microsomes from untreated rats and were about 5%, 125% and 8.3%, respectively, of the corresponding hepatic levels. Chronic ethanol treatment resulted in induction of the above enzyme activities in brain microsomes by 243%, 496% and 155%, respectively. Intake of ethanol for a prolonged period also resulted in the induction of total P-450 in the brain (150% of the control). Addition of the antisera raised against rat liver cytochrome P-450IIE1 markedly inhibited brain microsomal p-nitrophenol hydroxylase activity. Immunoblot analysis of rat brain microsomes using the above antisera also revealed the induction of brain cytochrome P-450IIE1 following chronic ethanol administration. Immunocytochemical localization of cytochrome P-450IIE1 using the above antisera, revealed the preferential localization of the enzyme in the neuronal cell bodies in the cortex, hippocampus, basal ganglia, hypothalamic nuclei and reticular nuclei in the brainstem of rats treated chronically with ethanol. Based upon these studies, it is conceivable that chronic alcohol ingestion could enhance the sensitivity of certain regions of the brain to environmental chemicals that are metabolized to more toxic derivatives by the P-450 system. JF - Brain research AU - Anandatheerthavarada, H K AU - Shankar, S K AU - Bhamre, S AU - Boyd, M R AU - Song, B J AU - Ravindranath, V AD - Department of Neurochemistry, National Institute of Mental Health and Neuro Sciences, Bangalore, India. Y1 - 1993/01/22/ PY - 1993 DA - 1993 Jan 22 SP - 279 EP - 285 VL - 601 IS - 1-2 SN - 0006-8993, 0006-8993 KW - Ethanol KW - 3K9958V90M KW - Carbon Monoxide KW - 7U1EE4V452 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Mixed Function Oxygenases KW - EC 1.- KW - Cytochrome P-450 CYP2E1 KW - EC 1.14.13.- KW - Oxidoreductases, N-Demethylating KW - EC 1.5.- KW - Index Medicus KW - Animals KW - Liver -- enzymology KW - Spectrophotometry, Ultraviolet KW - Microsomes -- enzymology KW - Rats KW - Blotting, Western KW - Mixed Function Oxygenases -- metabolism KW - Enzyme Induction -- drug effects KW - Microsomes, Liver -- enzymology KW - Rats, Wistar KW - Neurons -- enzymology KW - Immunohistochemistry KW - Male KW - Microsomes -- drug effects KW - Brain -- enzymology KW - Ethanol -- pharmacology KW - Brain -- drug effects KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Oxidoreductases, N-Demethylating -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75564158?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research&rft.atitle=Induction+of+brain+cytochrome+P-450IIE1+by+chronic+ethanol+treatment.&rft.au=Anandatheerthavarada%2C+H+K%3BShankar%2C+S+K%3BBhamre%2C+S%3BBoyd%2C+M+R%3BSong%2C+B+J%3BRavindranath%2C+V&rft.aulast=Anandatheerthavarada&rft.aufirst=H&rft.date=1993-01-22&rft.volume=601&rft.issue=1-2&rft.spage=279&rft.isbn=&rft.btitle=&rft.title=Brain+research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-17 N1 - Date created - 1993-03-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Synergistic interactions of etoposide and interleukin-1 alpha are not due to DNA damage in human melanoma cells. AN - 75555220; 8422427 AB - Several possible mechanisms of the synergistic interactions of IL-1 alpha and VP-16 against A375-C6 human melanoma cells were investigated. Studies indicate that IL-1 alpha did not increase topoisomerase II-dependent VP-16-mediated DNA damage, nor did IL-1 alpha inhibit the repair of VP-16-induced DNA damage in these cells. Furthermore, IL-1 alpha by itself or in combination with VP-16 did not cause significant fragmentation of cellular DNA into oligomers, indicating programmed cell death (apoptosis) was not involved in the mechanism of synergy. In contrast, an IL-1-specific receptor antagonist significantly decreased IL-1 alpha toxicity toward the melanoma cells and nearly eliminated the synergistic interactions of IL-1 alpha with VP-16. These results strongly indicate that synergism of IL-1 alpha with VP-16 was dependent upon an IL-1-receptor-mediated processes. DNA-strand breakage was unlikely to be a primary intracellular target for IL-1 alpha cytotoxicity and synergism with VP-16. JF - Biochimica et biophysica acta AU - Monti, E AU - Mimnaugh, E G AU - Sinha, B K AD - Biochemical and Molecular Pharmacology Section, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/01/22/ PY - 1993 DA - 1993 Jan 22 SP - 231 EP - 235 VL - 1180 IS - 3 SN - 0006-3002, 0006-3002 KW - Cytotoxins KW - 0 KW - Interleukin-1 KW - Receptors, Interleukin-1 KW - Etoposide KW - 6PLQ3CP4P3 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Cytotoxins -- metabolism KW - Tumor Cells, Cultured KW - Cytotoxins -- toxicity KW - Humans KW - Receptors, Interleukin-1 -- metabolism KW - Drug Synergism KW - DNA Repair -- drug effects KW - Melanoma KW - DNA -- drug effects KW - Interleukin-1 -- metabolism KW - DNA Damage KW - Interleukin-1 -- toxicity KW - Etoposide -- toxicity KW - Etoposide -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75555220?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochimica+et+biophysica+acta&rft.atitle=Synergistic+interactions+of+etoposide+and+interleukin-1+alpha+are+not+due+to+DNA+damage+in+human+melanoma+cells.&rft.au=Monti%2C+E%3BMimnaugh%2C+E+G%3BSinha%2C+B+K&rft.aulast=Monti&rft.aufirst=E&rft.date=1993-01-22&rft.volume=1180&rft.issue=3&rft.spage=231&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+biophysica+acta&rft.issn=00063002&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-25 N1 - Date created - 1993-02-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Potassium channel stimulation by natriuretic peptides through cGMP-dependent dephosphorylation. AN - 75568553; 7678699 AB - Natriuretic peptides inhibit the release and action of many hormones through cyclic guanosine monophosphate (cGMP), but the mechanism of cGMP action is unclear. In frog ventricular muscle and guinea-pig hippocampal neurons, cGMP inhibits voltage-activated Ca2+ currents by stimulating phosphodiesterase activity and reducing intracellular cyclic AMP; however, this mechanism is not involved in the action of cGMP on other channels or on Ca2+ channels in other cells. Natriuretic peptide receptors in the rat pituitary also stimulate guanylyl cyclase activity but inhibit secretion by increasing membrane conductance to potassium. In an electrophysiological study on rat pituitary tumour cells, we identified the large-conductance, calcium- and voltage-activated potassium channels (BK) as the primary target of another inhibitory neuropeptide, somatostatin. Here we report that atrial natriuretic peptide also stimulates BK channel activity in GH4C1 cells through protein dephosphorylation. Unlike somatostatin, however, the effect of atrial natriuretic peptide on BK channel activity is preceded by a rapid and potent stimulation of cGMP production and requires cGMP-dependent protein kinase activity. Protein phosphatase activation by cGMP-dependent kinase could explain the inhibitory effects of natriuretic peptides on electrical excitability and the antagonism of cGMP and cAMP in many systems. JF - Nature AU - White, R E AU - Lee, A B AU - Shcherbatko, A D AU - Lincoln, T M AU - Schonbrunn, A AU - Armstrong, D L AD - Laboratory of Cellular and Molecular Pharmacology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993/01/21/ PY - 1993 DA - 1993 Jan 21 SP - 263 EP - 266 VL - 361 IS - 6409 SN - 0028-0836, 0028-0836 KW - Ethers, Cyclic KW - 0 KW - Potassium Channels KW - Scorpion Venoms KW - Tetraethylammonium Compounds KW - Thionucleotides KW - Charybdotoxin KW - 115422-61-2 KW - Okadaic Acid KW - 1W21G5Q4N2 KW - 8-bromocyclic GMP KW - 31356-94-2 KW - 8-((4-chlorophenyl)thio)cyclic-3',5'-AMP KW - 41941-66-6 KW - Tetraethylammonium KW - 66-40-0 KW - Atrial Natriuretic Factor KW - 85637-73-6 KW - Cyclic AMP KW - E0399OZS9N KW - Protein Kinases KW - EC 2.7.- KW - Phosphoprotein Phosphatases KW - EC 3.1.3.16 KW - Cyclic GMP KW - H2D2X058MU KW - Index Medicus KW - Phosphoprotein Phosphatases -- antagonists & inhibitors KW - Animals KW - Scorpion Venoms -- pharmacology KW - Tetraethylammonium Compounds -- pharmacology KW - Cyclic AMP -- analogs & derivatives KW - Ethers, Cyclic -- pharmacology KW - Pituitary Neoplasms KW - Thionucleotides -- pharmacology KW - Protein Kinases -- metabolism KW - Tumor Cells, Cultured KW - Cyclic AMP -- pharmacology KW - Membrane Potentials -- drug effects KW - Cyclic GMP -- metabolism KW - Cyclic GMP -- pharmacology KW - Atrial Natriuretic Factor -- pharmacology KW - Potassium Channels -- physiology KW - Potassium Channels -- drug effects KW - Cyclic GMP -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75568553?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature&rft.atitle=Potassium+channel+stimulation+by+natriuretic+peptides+through+cGMP-dependent+dephosphorylation.&rft.au=White%2C+R+E%3BLee%2C+A+B%3BShcherbatko%2C+A+D%3BLincoln%2C+T+M%3BSchonbrunn%2C+A%3BArmstrong%2C+D+L&rft.aulast=White&rft.aufirst=R&rft.date=1993-01-21&rft.volume=361&rft.issue=6409&rft.spage=263&rft.isbn=&rft.btitle=&rft.title=Nature&rft.issn=00280836&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-19 N1 - Date created - 1993-02-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Effects of temperature on ADP-ribosylation factor stimulation of cholera toxin activity. AN - 75569530; 8422366 AB - The effects of cholera toxin, a secretory product of Vibrio cholerae, result from ADP-ribosylation of the stimulatory guanine nucleotide-binding (Gs) protein of the adenylyl cyclase system. Cholera toxin A subunit (CTA) also uses agmatine, a simple guanidino compound, several proteins unrelated to Gs, and CTA itself as alternative ADP-ribose acceptors. The effects of toxin occur in the jejunum presumably at body core temperature. With agmatine as a model substrate, the optimal temperature for CTA-catalyzed ADP-ribosylation was 25-30 degrees C, and that for CTA-catalyzed auto-ADP-ribosylation was 20-25 degrees C. Both activities were significantly less at 37 degrees C, reflecting lower initial velocities, not heat-inactivation of the toxin. All the transferase activities of CTA are enhanced by ADP-ribosylation factors (ARFs), approximately 20-kDa guanine nucleotide-binding proteins that are ubiquitous in mammalian cells. Phospholipids and a soluble brain ARF, in a GTP-dependent manner, activated toxin NAD:agmatine ADP-ribosyltransferase activity; their simultaneous effect was maximal at physiological temperatures (approximately 37 degrees C). At lower temperatures, the stimulation by ARF was much less. There were similar effects on other toxin-catalyzed reactions, notably, the ADP-ribosylation of Gs alpha and the hydrolysis of NAD. Thus, host factors, such as ARF and phospholipid, synergistically increase cholera toxin activity at 37 degrees C and may be important in toxin action in the mammalian gut. JF - Biochemistry AU - Murayama, T AU - Tsai, S C AU - Adamik, R AU - Moss, J AU - Vaughan, M AD - Laboratory of Cellular Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/01/19/ PY - 1993 DA - 1993 Jan 19 SP - 561 EP - 566 VL - 32 IS - 2 SN - 0006-2960, 0006-2960 KW - Cardiolipins KW - 0 KW - Detergents KW - Guanine Nucleotides KW - Phospholipids KW - Agmatine KW - 70J407ZL5Q KW - Cholera Toxin KW - 9012-63-9 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - ADP-Ribosylation Factors KW - EC 3.6.5.2 KW - Index Medicus KW - Animals KW - Cattle KW - Phospholipids -- pharmacology KW - Agmatine -- metabolism KW - Temperature KW - Guanine Nucleotides -- metabolism KW - Rabbits KW - Cardiolipins -- pharmacology KW - Allosteric Regulation KW - Substrate Specificity KW - Detergents -- pharmacology KW - GTP-Binding Proteins -- metabolism KW - Cholera Toxin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75569530?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemistry&rft.atitle=Effects+of+temperature+on+ADP-ribosylation+factor+stimulation+of+cholera+toxin+activity.&rft.au=Murayama%2C+T%3BTsai%2C+S+C%3BAdamik%2C+R%3BMoss%2C+J%3BVaughan%2C+M&rft.aulast=Murayama&rft.aufirst=T&rft.date=1993-01-19&rft.volume=32&rft.issue=2&rft.spage=561&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-23 N1 - Date created - 1993-02-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Genetic differences in the time course for the development and persistence of the anticonvulsant effects of carbamazepine against cocaine seizures. AN - 75606517; 8435746 AB - Initial studies of the effect of chronic carbamazepine (CBZ) against cocaine-induced seizures indicated that there were genetic differences in both the time course for the development of the anticonvulsant effects of CBZ against cocaine-induced seizures and the persistence of these effects. The present studies were initiated to investigate the time course for the development and persistence of the anticonvulsant effects of chronic CBZ against cocaine seizures in BALB/cByJ, C57Bl/6J and SJL/J mice. The anticonvulsant actions of CBZ were dependent on the duration of CBZ administration, requiring 4-7 days to achieve maximal efficacy. However, once the anticonvulsant effects of CBZ were manifest, the effect persisted for up to 5 days after stopping CBZ treatment depending on the genotype. The levels of CBZ and its active epoxide metabolite were determined in plasma and brain at various time points during and after chronic CBZ treatment. The levels of CBZ and CBZ-10,11-epoxide were substantially reduced over the course of treatment in all three strains, such that the levels of the two compounds in plasma and brain could not account for the decreased susceptibility to cocaine seizures observed following chronic CBZ. These results suggest that the effects of CBZ on cocaine seizures are mediated by relatively long-term changes in one or more biological systems associated with cocaine's convulsant effects. JF - Brain research AU - Marley, R J AU - Shimosato, K AU - Frieman, M AU - Goldberg, S R AD - National Institute on Drug Abuse, Addiction Research Center, Baltimore, MD 21224. Y1 - 1993/01/15/ PY - 1993 DA - 1993 Jan 15 SP - 193 EP - 200 VL - 600 IS - 2 SN - 0006-8993, 0006-8993 KW - Anticonvulsants KW - 0 KW - Carbamazepine KW - 33CM23913M KW - Cocaine KW - I5Y540LHVR KW - carbamazepine epoxide KW - QC9505F279 KW - Index Medicus KW - Mice, Inbred Strains KW - Animals KW - Mice, Inbred C57BL KW - Mice KW - Brain -- metabolism KW - Diet KW - Mice, Inbred BALB C KW - Time Factors KW - Species Specificity KW - Male KW - Seizures -- chemically induced KW - Anticonvulsants -- pharmacology KW - Carbamazepine -- pharmacokinetics KW - Anticonvulsants -- pharmacokinetics KW - Carbamazepine -- blood KW - Carbamazepine -- analogs & derivatives KW - Seizures -- genetics KW - Carbamazepine -- pharmacology KW - Seizures -- prevention & control KW - Carbamazepine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75606517?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research&rft.atitle=Genetic+differences+in+the+time+course+for+the+development+and+persistence+of+the+anticonvulsant+effects+of+carbamazepine+against+cocaine+seizures.&rft.au=Marley%2C+R+J%3BShimosato%2C+K%3BFrieman%2C+M%3BGoldberg%2C+S+R&rft.aulast=Marley&rft.aufirst=R&rft.date=1993-01-15&rft.volume=600&rft.issue=2&rft.spage=193&rft.isbn=&rft.btitle=&rft.title=Brain+research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-23 N1 - Date created - 1993-03-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Engineering mouse P450coh to a novel corticosterone 15 alpha-hydroxylase and modeling steroid-binding orientation in the substrate pocket. AN - 75567221; 8419350 AB - The F209L mutation alters specificity of P450coh from coumarin 7-hydroxylation to 15 alpha-hydroxylation of 11-deoxysteroids such as testosterone and 11-deoxycorticosterone. Neither the wild-type nor F209L exhibits activity toward 11 beta-hydroxysteroids including corticosterone. Mutation of Phe-209 to Asn, however, confers on mutant F209N a high corticosterone 15 alpha-hydroxylase activity. F209V also exhibits low corticosterone 15 alpha-hydroxylase activity; Km and Vmax are 10-fold higher and lower, respectively, than for F209N. The results are consistent with the hypothesis that direct interaction of Asn-209 with 11OH is responsible for high corticosterone 15 alpha-hydroxylase activity. To support this hypothesis, a possible steroid-binding orientation is modeled in the substrate pocket of P450cam. Our weighted homology and constrained alignments map residue 209 of P450coh to Met-184 and Met-191 of P450cam. Energy minimization of corticosterone in the substrate pocket results in the 11OH of the steroid directed toward Met-184 (7 A) and Met-191 (16 A), and in C15 located near the sixth axial position of the heme. The steroid-binding model suggests that the P450cam's substrate pocket may be conserved in the mammalian P450 and can accommodate a steroid molecule, and that residue 209 appears to be located at the critical site that determines the steroid-substrate specificity of a P450 depending on the type of group at the 11-position of steroid molecule. JF - The Journal of biological chemistry AU - Iwasaki, M AU - Darden, T A AU - Pedersen, L G AU - Davis, D G AU - Juvonen, R O AU - Sueyoshi, T AU - Negishi, M AD - Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. Y1 - 1993/01/15/ PY - 1993 DA - 1993 Jan 15 SP - 759 EP - 762 VL - 268 IS - 2 SN - 0021-9258, 0021-9258 KW - Desoxycorticosterone KW - 40GP35YQ49 KW - Phenylalanine KW - 47E5O17Y3R KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Steroid Hydroxylases KW - EC 1.14.- KW - Aryl Hydrocarbon Hydroxylases KW - EC 1.14.14.1 KW - Cyp2a4 protein, mouse KW - Cytochrome P450 Family 2 KW - steroid 15-alpha-hydroxylase KW - Index Medicus KW - Animals KW - Thermodynamics KW - Models, Molecular KW - Amino Acid Sequence KW - Mice KW - Desoxycorticosterone -- chemistry KW - Binding Sites KW - Magnetic Resonance Spectroscopy KW - Desoxycorticosterone -- metabolism KW - Protein Engineering KW - Substrate Specificity KW - Molecular Conformation KW - Sequence Homology, Amino Acid KW - Protein Conformation KW - Mutagenesis, Site-Directed KW - Cytochrome P-450 Enzyme System -- genetics KW - Steroid Hydroxylases -- metabolism KW - Cytochrome P-450 Enzyme System -- metabolism KW - Steroid Hydroxylases -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75567221?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Engineering+mouse+P450coh+to+a+novel+corticosterone+15+alpha-hydroxylase+and+modeling+steroid-binding+orientation+in+the+substrate+pocket.&rft.au=Iwasaki%2C+M%3BDarden%2C+T+A%3BPedersen%2C+L+G%3BDavis%2C+D+G%3BJuvonen%2C+R+O%3BSueyoshi%2C+T%3BNegishi%2C+M&rft.aulast=Iwasaki&rft.aufirst=M&rft.date=1993-01-15&rft.volume=268&rft.issue=2&rft.spage=759&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-05 N1 - Date created - 1993-02-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Correlations between developmental ornithine decarboxylase gene expression and enzyme activity in the rat brain. AN - 75563179; 8431999 AB - The rise and decline in cerebral ODC activity during specific stages of development has been attributed to cytoplasmic intermediates which regulate ornithine decarboxylase activity. Here we examine whether transcriptional regulation contributes to the production of the developmental profiles of ODC activity. Postnatal cerebellar and neocortical tissue were obtained from Long-Evans hooded rats at postnatal days (PND) 5, 10, 15, 20, 25, 30, 90 and probed for ODC and actin gene expression, by Northern analysis. Our results indicate that ODC gene expression in the cerebellum was elevated at PND 5 and 10 followed by a gradual drop to the adult low levels by PND 20. By contrast, high levels of ODC gene expression in the neocortex were seen at PND 5 with an abrupt decrease at day 10 to low adult levels. The expression of the ODC gene in the neocortex follows closely the pattern for the ODC enzyme activity; however, it tends to remain elevated longer in the cerebellum. The levels of actin gene expression exhibited a distinct developmental profile in the postnatally developing cerebellum. However, actin mRNA levels remained unchanged in the neocortex, consistent with the prenatal development of this region. Our findings suggest that ODC gene expression may play an important role in the production of the ontogenetic patterns of ODC activity. JF - Brain research. Developmental brain research AU - Zawia, N H AU - Harry, G J AD - Developmental and Reproductive Toxicology Group, Systems Toxicity Branch, NIEHS, Research Triangle Park, NC 27709. Y1 - 1993/01/15/ PY - 1993 DA - 1993 Jan 15 SP - 53 EP - 57 VL - 71 IS - 1 SN - 0165-3806, 0165-3806 KW - Actins KW - 0 KW - RNA, Messenger KW - Ornithine Decarboxylase KW - EC 4.1.1.17 KW - Index Medicus KW - Rats KW - Animals KW - Blotting, Northern KW - Actins -- genetics KW - Cerebral Cortex -- enzymology KW - Kinetics KW - Cerebellum -- enzymology KW - Actins -- biosynthesis KW - Ornithine Decarboxylase -- metabolism KW - Brain -- enzymology KW - Aging -- metabolism KW - Ornithine Decarboxylase -- genetics KW - Gene Expression Regulation, Enzymologic KW - RNA, Messenger -- metabolism KW - RNA, Messenger -- genetics KW - Brain -- growth & development UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75563179?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research.+Developmental+brain+research&rft.atitle=Correlations+between+developmental+ornithine+decarboxylase+gene+expression+and+enzyme+activity+in+the+rat+brain.&rft.au=Zawia%2C+N+H%3BHarry%2C+G+J&rft.aulast=Zawia&rft.aufirst=N&rft.date=1993-01-15&rft.volume=71&rft.issue=1&rft.spage=53&rft.isbn=&rft.btitle=&rft.title=Brain+research.+Developmental+brain+research&rft.issn=01653806&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-15 N1 - Date created - 1993-03-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Enhancement of tumorigenesis by N-nitrosodiethylamine, N-nitrosopyrrolidine and N6-(methylnitroso)-adenosine by ethanol. AN - 75554493; 8422650 AB - Inclusion of 10% ethanol with 6.8 ppm N-nitrosodiethylamine in the drinking water of strain A male mice resulted in a 4-fold enhancement of multiplicity of lung tumors and a 16-fold increase in incidence of fore-stomach tumors, compared with carcinogen alone. Given with 40 ppm N-nitrosopyrrolidine, ethanol caused a 5.5-fold increase in lung tumor multiplicity. The inclusion of 15% ethanol with N6-(methylnitroso)adenosine, given orally to Swiss female mice, led to reduced body weights and shortened survival time related to hemangiosarcoma occurrence or increased incidence of thymic lymphoma, depending on dose of carcinogen. The data provide additional support for the proposal that co-administered ethanol increases the tumorigenicity of nitrosamines by blocking hepatic first-pass clearance. JF - Cancer letters AU - Anderson, L M AU - Carter, J P AU - Driver, C L AU - Logsdon, D L AU - Kovatch, R M AU - Giner-Sorolla, A AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick, MD. Y1 - 1993/01/15/ PY - 1993 DA - 1993 Jan 15 SP - 61 EP - 66 VL - 68 IS - 1 SN - 0304-3835, 0304-3835 KW - Carcinogens KW - 0 KW - Nitrosamines KW - N(6)-(methylnitroso)adenosine KW - 21928-82-5 KW - Diethylnitrosamine KW - 3IQ78TTX1A KW - Ethanol KW - 3K9958V90M KW - N-Nitrosopyrrolidine KW - SZ4J5WK201 KW - Index Medicus KW - Nitrosamines -- pharmacology KW - Mice, Inbred A KW - Animals KW - Drug Interactions KW - Mice KW - Lung Neoplasms -- chemically induced KW - Diethylnitrosamine -- pharmacology KW - N-Nitrosopyrrolidine -- pharmacology KW - Male KW - Female KW - Carcinogens -- pharmacology KW - Ethanol -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75554493?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+letters&rft.atitle=Enhancement+of+tumorigenesis+by+N-nitrosodiethylamine%2C+N-nitrosopyrrolidine+and+N6-%28methylnitroso%29-adenosine+by+ethanol.&rft.au=Anderson%2C+L+M%3BCarter%2C+J+P%3BDriver%2C+C+L%3BLogsdon%2C+D+L%3BKovatch%2C+R+M%3BGiner-Sorolla%2C+A&rft.aulast=Anderson&rft.aufirst=L&rft.date=1993-01-15&rft.volume=68&rft.issue=1&rft.spage=61&rft.isbn=&rft.btitle=&rft.title=Cancer+letters&rft.issn=03043835&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-22 N1 - Date created - 1993-02-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Regulating the fate of mRNA: the control of cellular iron metabolism. AN - 75551639; 8380757 JF - Cell AU - Klausner, R D AU - Rouault, T A AU - Harford, J B AD - Cell Biology and Metabolism Branch National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/01/15/ PY - 1993 DA - 1993 Jan 15 SP - 19 EP - 28 VL - 72 IS - 1 SN - 0092-8674, 0092-8674 KW - Iron-Binding Proteins KW - 0 KW - Iron-Regulatory Proteins KW - RNA, Messenger KW - RNA-Binding Proteins KW - Receptors, Cell Surface KW - ferritin receptor KW - Ferritins KW - 9007-73-2 KW - Iron KW - E1UOL152H7 KW - Index Medicus KW - Receptors, Cell Surface -- metabolism KW - Animals KW - Base Sequence KW - RNA-Binding Proteins -- metabolism KW - RNA-Binding Proteins -- genetics KW - Ferritins -- metabolism KW - Humans KW - Ferritins -- genetics KW - Molecular Sequence Data KW - Receptors, Cell Surface -- genetics KW - Homeostasis KW - RNA, Messenger -- metabolism KW - Iron -- toxicity KW - Iron -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75551639?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cell&rft.atitle=Regulating+the+fate+of+mRNA%3A+the+control+of+cellular+iron+metabolism.&rft.au=Klausner%2C+R+D%3BRouault%2C+T+A%3BHarford%2C+J+B&rft.aulast=Klausner&rft.aufirst=R&rft.date=1993-01-15&rft.volume=72&rft.issue=1&rft.spage=19&rft.isbn=&rft.btitle=&rft.title=Cell&rft.issn=00928674&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-24 N1 - Date created - 1993-02-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Alzheimer disease amyloid beta protein forms calcium channels in bilayer membranes: blockade by tromethamine and aluminum. AN - 75550270; 8380642 AB - Amyloid beta protein (A beta P) is the 40- to 42-residue polypeptide implicated in the pathogenesis of Alzheimer disease. We have incorporated this peptide into phosphatidylserine liposomes and then fused the liposomes with a planar bilayer. When incorporated into bilayers the A beta P forms channels, which generate linear current-voltage relationships in symmetrical solutions. A permeability ratio, PK/PCl, of 11 for the open A beta P channel was estimated from the reversal potential of the channel current in asymmetrical KCl solutions. The permeability sequence for different cations, estimated from the reversal potential of the A beta P-channel current for each system of asymmetrical solutions, is Pcs > PLi > PCa > or = PK > PNa. A beta P-channel current (either CS+ or Ca2+ as charge carriers) is blocked reversibly by tromethamine (millimolar range) and irreversibly by Al3+ (micromolar range). The inhibition of the A beta P-channel current by these two substances depends on transmembrane potential, suggesting that the mechanism of blockade involves direct interaction between tromethamine (or Al3+) and sites within the A beta P channel. Hitherto, A beta P has been presumed to be neurotoxic. On the basis of the present data we suggest that the channel activity of the polypeptide may be responsible for some or all of its neurotoxic effects. We further propose that a useful strategy for drug discovery for treatment of Alzheimer disease may include screening compounds for their ability to block or otherwise modify A beta P channels. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Arispe, N AU - Rojas, E AU - Pollard, H B AD - Laboratory of Cell Biology and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/01/15/ PY - 1993 DA - 1993 Jan 15 SP - 567 EP - 571 VL - 90 IS - 2 SN - 0027-8424, 0027-8424 KW - Amyloid beta-Peptides KW - 0 KW - Calcium Channels KW - Cations KW - Lipid Bilayers KW - Phosphatidylserines KW - Tromethamine KW - 023C2WHX2V KW - Aluminum KW - CPD4NFA903 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Permeability KW - Electric Conductivity KW - Humans KW - Membrane Potentials -- physiology KW - Alzheimer Disease -- etiology KW - Cations -- metabolism KW - Calcium -- metabolism KW - Calcium Channels -- metabolism KW - Amyloid beta-Peptides -- metabolism KW - Calcium Channels -- drug effects KW - Aluminum -- pharmacology KW - Amyloid beta-Peptides -- drug effects KW - Tromethamine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75550270?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Alzheimer+disease+amyloid+beta+protein+forms+calcium+channels+in+bilayer+membranes%3A+blockade+by+tromethamine+and+aluminum.&rft.au=Arispe%2C+N%3BRojas%2C+E%3BPollard%2C+H+B&rft.aulast=Arispe&rft.aufirst=N&rft.date=1993-01-15&rft.volume=90&rft.issue=2&rft.spage=567&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-18 N1 - Date created - 1993-02-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Neuron. 1991 Apr;6(4):487-98 [1673054] Prog Brain Res. 1990;86:257-67 [2150887] Ann Neurol. 1991 Aug;30(2):156-65 [1910274] Brain Res. 1991 Nov 1;563(1-2):311-4 [1786545] J Neurosci. 1992 Feb;12(2):376-89 [1346802] Proc Natl Acad Sci U S A. 1992 Mar 1;89(5):1539-43 [1371876] Science. 1992 Apr 10;256(5054):184-5 [1566067] Science. 1992 May 8;256(5058):780-3 [1589757] Annu Rev Biophys Biophys Chem. 1987;16:265-90 [2439098] Brain Res. 1988 Nov 22;474(1):100-11 [3214703] Science. 1990 Oct 12;250(4978):279-82 [2218531] Nature. 1991 Feb 21;349(6311):704-6 [1671712] Brain Res. 1990 Nov 19;533(2):315-20 [2289145] FASEB J. 1991 Mar 1;5(3):278-86 [2001787] J Mol Biol. 1991 Mar 5;218(1):149-63 [2002499] J Physiol. 1991 Sep;441:575-91 [1667801] J Mol Biol. 1992 Jun 20;225(4):1075-93 [1613791] Pharmacol Rev. 1962 Sep;14:447-72 [13937207] Nature. 1966 Jan 1;209(5018):109-10 [5927229] Br J Psychiatry. 1968 Jul;114(512):797-811 [5662937] Ann Neurol. 1981 Aug;10(2):184-92 [7283403] Biochem Biophys Res Commun. 1984 May 16;120(3):885-90 [6375662] Proc Natl Acad Sci U S A. 1985 Jun;82(12):4245-9 [3159021] Science. 1987 Feb 20;235(4791):877-80 [3810169] Science. 1987 Feb 20;235(4791):880-4 [2949367] Nature. 1987 Feb 19-25;325(6106):733-6 [2881207] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Biphasic generation of diacylglycerol by angiotensin and phorbol ester in bovine adrenal chromaffin cells. AN - 75546392; 8380691 AB - Stimulation of angiotensin receptors in bovine adrenal medullary cells with Sar1-angiotensin II increased diacylglycerol levels in a biphasic fashion. An initial peak occurred at 3 min and an increase was observed again at 60 min and even at 18 hrs. Phorbol 12-myristate 13-acetate produced a similar pattern of increase in diacylglycerol levels. Both the angiotensin analog and the phorbol ester also increased the release of (3H)choline into the culture medium from prelabelled cells. The long-term diacylglycerol production could be derived from phosphatidylcholine rather than from the phosphoinositides. The latter may be the source of the angiotensin stimulated initial production of diacylglycerol and activation of PKC. Activated PKC then turns on the continuous production of DAG which maintains PKC in an active state for long periods of time in the presence of the peptide. JF - Biochemical and biophysical research communications AU - Tuominen, R K AU - Werner, M H AU - Ye, H AU - McMillian, M K AU - Hudson, P M AU - Hannun, Y A AU - Hong, J S AD - Laboratory of Molecular and Integrative Neuroscience, NIEHS, NIH, Research Triangle Park, NC 27709. Y1 - 1993/01/15/ PY - 1993 DA - 1993 Jan 15 SP - 181 EP - 185 VL - 190 IS - 1 SN - 0006-291X, 0006-291X KW - Diglycerides KW - 0 KW - Phosphatidylcholines KW - Phosphatidylinositols KW - Tritium KW - 10028-17-8 KW - Angiotensin II KW - 11128-99-7 KW - Choline KW - N91BDP6H0X KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Phosphatidylinositols -- metabolism KW - Animals KW - Cattle KW - Cells, Cultured KW - Kinetics KW - Choline -- metabolism KW - Phosphatidylcholines -- metabolism KW - Time Factors KW - Adrenal Medulla -- drug effects KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Adrenal Medulla -- metabolism KW - Angiotensin II -- pharmacology KW - Diglycerides -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75546392?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+and+biophysical+research+communications&rft.atitle=Biphasic+generation+of+diacylglycerol+by+angiotensin+and+phorbol+ester+in+bovine+adrenal+chromaffin+cells.&rft.au=Tuominen%2C+R+K%3BWerner%2C+M+H%3BYe%2C+H%3BMcMillian%2C+M+K%3BHudson%2C+P+M%3BHannun%2C+Y+A%3BHong%2C+J+S&rft.aulast=Tuominen&rft.aufirst=R&rft.date=1993-01-15&rft.volume=190&rft.issue=1&rft.spage=181&rft.isbn=&rft.btitle=&rft.title=Biochemical+and+biophysical+research+communications&rft.issn=0006291X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-17 N1 - Date created - 1993-02-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Age contrast in ovarian pathology. AN - 75544666; 8420674 AB - BACKGROUND. Ovarian cancer accounts for approximately 23% of all gynecologic tumors and is the most common fatal gynecologic malignancy. These tumors can occur in women of all ages, but there are differences in the histologic types during various decades of life. CONCLUSIONS. During infancy and childhood, the predominant type of neoplasms are those of germ cell origin, such as teratomas, dysgerminomas, and endodermal sinus tumors. In adults, epithelial neoplasms, or tumors that originate from the epithelium that covers the ovarian surface, are the most common, accounting for almost 85% of all neoplasms after the age of 50 years. The peak incidence of benign epithelial tumors occurs between the ages of 20 and 40 years. Young women (30 to 40 years of age) are frequently affected by the so-called "tumors of low malignant potential," which have excellent prognosis. Older women, on the other hand, usually have the most aggressive forms of ovarian cancer, present with advanced disease, and have a dismal prognosis. JF - Cancer AU - Merino, M J AU - Jaffe, G AD - Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/01/15/ PY - 1993 DA - 1993 Jan 15 SP - 537 EP - 544 VL - 71 IS - 2 Suppl SN - 0008-543X, 0008-543X KW - Abridged Index Medicus KW - Index Medicus KW - Risk Factors KW - Humans KW - Adult KW - Middle Aged KW - Female KW - Aging -- physiology KW - Ovarian Neoplasms -- pathology KW - Ovarian Neoplasms -- classification KW - Ovarian Neoplasms -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75544666?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=Age+contrast+in+ovarian+pathology.&rft.au=Merino%2C+M+J%3BJaffe%2C+G&rft.aulast=Merino&rft.aufirst=M&rft.date=1993-01-15&rft.volume=71&rft.issue=2+Suppl&rft.spage=537&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-16 N1 - Date created - 1993-02-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Age does not influence taxol dose intensity in recurrent carcinoma of the ovary. AN - 75532590; 7678382 AB - In the treatment of advanced-stage ovarian cancer, it is common practice to treat elderly patients in a less aggressive fashion than young patients. This approach is based on the notion that age is associated with poor patient tolerance to aggressive chemotherapy. Relatively little data exist to support this contention. The most exciting new chemotherapy agent to be developed in the last 10 years is taxol, a diterpeniod derivative of the Northwestern yew Taxus brevifolia. The ability to administer dose-intensive taxol to adult patients with recurrent ovarian cancer was assessed retrospectively, and the question was asked whether the administered dose intensity of taxol was unfavorably influenced by age. Forty-eight patients with recurrent ovarian carcinoma received taxol at an initial dose of 250 mg/m2 every 3 weeks. Age in this cohort ranged from 26 to 74 years, with a median of 55. Twenty-nine percent (14 of 48) of the patients treated were 61 years of age or greater. Criteria for administration of taxol included a creatinine clearance of > 45 ml/minute, minimal abnormalities in liver function tests, good performance status, and the absence of substantial comorbid disease. Elderly patients in this cohort (age > 60 years) did not differ from younger patients with respect to administered dose intensity, number of cycles of therapy administered, or the occurrence of serious or mild toxicities. JF - Cancer AU - Bicher, A AU - Sarosy, G AU - Kohn, E AU - Adamo, D O AU - Davis, P AU - Jacob, J AU - Chabner, B A AU - Reed, E AD - Medicine Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1993/01/15/ PY - 1993 DA - 1993 Jan 15 SP - 594 EP - 600 VL - 71 IS - 2 Suppl SN - 0008-543X, 0008-543X KW - Granulocyte Colony-Stimulating Factor KW - 143011-72-7 KW - Paclitaxel KW - P88XT4IS4D KW - Abridged Index Medicus KW - Index Medicus KW - Drug Administration Schedule KW - Granulocyte Colony-Stimulating Factor -- therapeutic use KW - Dose-Response Relationship, Drug KW - Humans KW - Cohort Studies KW - Adult KW - Aged KW - Middle Aged KW - Female KW - Aging -- physiology KW - Paclitaxel -- adverse effects KW - Neoplasm Recurrence, Local -- drug therapy KW - Paclitaxel -- therapeutic use KW - Ovarian Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75532590?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=Age+does+not+influence+taxol+dose+intensity+in+recurrent+carcinoma+of+the+ovary.&rft.au=Bicher%2C+A%3BSarosy%2C+G%3BKohn%2C+E%3BAdamo%2C+D+O%3BDavis%2C+P%3BJacob%2C+J%3BChabner%2C+B+A%3BReed%2C+E&rft.aulast=Bicher&rft.aufirst=A&rft.date=1993-01-15&rft.volume=71&rft.issue=2+Suppl&rft.spage=594&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-16 N1 - Date created - 1993-02-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The A/J mouse lung as a model for developing new chemointervention strategies. AN - 75531279; 8417832 AB - The use of the A/J mouse lung as a model for developing new chemo-intervention strategies was investigated by first inducing lung tumors with a single dose of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone. Lungs were then staged for tumor development and intervention therapy was initiated 42 weeks after carcinogen treatment. At this time point, an average of 7 pulmonary lesions were present on a standard histological section and the relative frequency of lesions was distributed as alveolar hyperplasias (38%), adenomas (40%), and adenocarcinomas (22%). Mice were treated for 4 or 8 weeks with cis-platinum alone or in combination with either indomethacin, an inhibitor of prostaglandin synthesis, metoclopramide, an inducer of poly(ADP) ribosylation, or nifedipine, a calcium channel blocker. The effect of indomethacin, metoclopramide, and nifedipine on tumor growth was also determined. The most dramatic effects were observed in lungs from mice treated for 8 weeks. cis-Platinum treatment caused a 37% reduction in the size of carcinomas, while tumor mass was reduced by 50 to 60% with cis-platinum in combination with metoclopramide and/or indomethacin. The inclusion of indomethacin therapy in conjunction with cis-platinum significantly enhanced the effectiveness of cis-platinum for inhibiting the growth of adenocarcinomas. In contrast, nifedipine appeared to ameliorate any of the inhibitory growth effects seen with cis-platinum treatment. Although none of the therapeutic combinations affected the size of adenomas, morphological differences were observed among treatment groups. A moderate to marked decrease in cytoplasm was observed in adenomas from mice treated with cis-platinum in combination with indomethacin or metoclopramide, cis-platinum plus metoclopramide and indomethacin, or metoclopramide plus indomethacin. Taken together, the results from these studies demonstrate that the A/J mouse lung can be used as a model to study the effectiveness of new intervention therapies for controlling malignant tumor growth. This model should also be applicable for studying the effectiveness of cancer prevention therapies on the progression of pulmonary hyperplasia. JF - Cancer research AU - Belinsky, S A AU - Stefanski, S A AU - Anderson, M W AD - Laboratory of Molecular Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993/01/15/ PY - 1993 DA - 1993 Jan 15 SP - 410 EP - 416 VL - 53 IS - 2 SN - 0008-5472, 0008-5472 KW - Carcinogens KW - 0 KW - Nitrosamines KW - 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone KW - 7S395EDO61 KW - Index Medicus KW - Nitrosamines -- toxicity KW - Animals KW - Neoplasms, Experimental -- chemically induced KW - Body Weight -- drug effects KW - Carcinogens -- toxicity KW - Disease Models, Animal KW - Mice KW - Neoplasms, Experimental -- drug therapy KW - Neoplasms, Experimental -- pathology KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Female KW - Adenocarcinoma -- chemically induced KW - Lung Neoplasms -- drug therapy KW - Lung Neoplasms -- chemically induced KW - Adenocarcinoma -- drug therapy KW - Mice, Inbred A -- physiology KW - Lung Neoplasms -- pathology KW - Adenocarcinoma -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75531279?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=The+A%2FJ+mouse+lung+as+a+model+for+developing+new+chemointervention+strategies.&rft.au=Belinsky%2C+S+A%3BStefanski%2C+S+A%3BAnderson%2C+M+W&rft.aulast=Belinsky&rft.aufirst=S&rft.date=1993-01-15&rft.volume=53&rft.issue=2&rft.spage=410&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-03 N1 - Date created - 1993-02-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Reversible neurologic toxicity in patients treated with standard-dose fludarabine phosphate for mycosis fungoides and chronic lymphocytic leukemia. AN - 73446479; 8416307 JF - Annals of internal medicine AU - Cohen, R B AU - Abdallah, J M AU - Gray, J R AU - Foss, F AD - NCI/Navy Medical Oncology Branch, National Naval Medical Center, Bethesda, MD 20889. Y1 - 1993/01/15/ PY - 1993 DA - 1993 Jan 15 SP - 114 EP - 116 VL - 118 IS - 2 SN - 0003-4819, 0003-4819 KW - Antineoplastic Agents KW - 0 KW - Vidarabine KW - FA2DM6879K KW - fludarabine KW - P2K93U8740 KW - Abridged Index Medicus KW - Index Medicus KW - Magnetic Resonance Imaging KW - Combined Modality Therapy KW - Humans KW - Middle Aged KW - Male KW - Female KW - Skin Neoplasms -- drug therapy KW - Vidarabine -- analogs & derivatives KW - Leukemia, Lymphocytic, Chronic, B-Cell -- drug therapy KW - Antineoplastic Agents -- administration & dosage KW - Brain Diseases -- chemically induced KW - Brain Diseases -- diagnosis KW - Vidarabine -- administration & dosage KW - Vidarabine -- adverse effects KW - Mycosis Fungoides -- drug therapy KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73446479?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+internal+medicine&rft.atitle=Reversible+neurologic+toxicity+in+patients+treated+with+standard-dose+fludarabine+phosphate+for+mycosis+fungoides+and+chronic+lymphocytic+leukemia.&rft.au=Cohen%2C+R+B%3BAbdallah%2C+J+M%3BGray%2C+J+R%3BFoss%2C+F&rft.aulast=Cohen&rft.aufirst=R&rft.date=1993-01-15&rft.volume=118&rft.issue=2&rft.spage=114&rft.isbn=&rft.btitle=&rft.title=Annals+of+internal+medicine&rft.issn=00034819&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-13 N1 - Date created - 1993-01-13 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Ann Intern Med. 1993 Sep 1;119(5):437 [7687837] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Augmentation by erythropoietin of the fetal-hemoglobin response to hydroxyurea in sickle cell disease. AN - 73505128; 7677965 AB - Hydroxyurea increases the production of fetal hemoglobin in patients with sickle cell anemia, inhibiting the polymerization of hemoglobin S and potentially improving vaso-occlusive manifestations and hemolysis. Recombinant erythropoietin increases the number of reticulocytes containing fetal hemoglobin in laboratory animals and in humans. We studied whether hydroxyurea and erythropoietin might have a potentiating effect on the production of fetal hemoglobin in patients with sickle cell disease. We treated four patients who were receiving hydroxyurea for sickle cell disease (three who were homozygous for sickle cell anemia and one with sickle beta zero-thalassemia) with escalating doses of intravenous erythropoietin for seven weeks, along with oral iron sulfate. Doses of hydroxyurea on four consecutive days were alternated with doses of erythropoietin on three consecutive days. There was a 28 percent increase in the number of reticulocytes containing fetal hemoglobin and a 48 percent increase in the percentage of fetal hemoglobin, as compared with the maximal values obtained with hydroxyurea alone. The percentage of erythrocytes containing fetal hemoglobin (F cells) increased from 64 to 78 percent. As compared with hydroxyurea alone, treatment with hydroxyurea and erythropoietin decreased the mean (+/- SD) serum indirect bilirubin level from 0.8 +/- 0.2 to 0.5 +/- 0.1 mg per deciliter (13.3 +/- 2.9 to 8.9 +/- 2.2 mumol per liter) (P = 0.02), suggesting a further decrease in hemolysis. Red-cell filterability improved. Intravenous recombinant erythropoietin with iron supplementation alternating with hydroxyurea elevates fetal-hemoglobin and F-cell levels more than hydroxyurea alone. Such increases decrease intracellular polymerization of hemoglobin S and improve the overall rheologic characteristics of erythrocytes. A reduced dosage of hydroxyurea alternating with erythropoietin may prove less myelotoxic than hydroxyurea given daily or in pulsed-dose regimens. It may also increase levels of fetal hemoglobin in patients with sickle cell disease who have not been helped by hydroxyurea alone. JF - The New England journal of medicine AU - Rodgers, G P AU - Dover, G J AU - Uyesaka, N AU - Noguchi, C T AU - Schechter, A N AU - Nienhuis, A W AD - Laboratory of Chemical Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Md 20892. Y1 - 1993/01/14/ PY - 1993 DA - 1993 Jan 14 SP - 73 EP - 80 VL - 328 IS - 2 SN - 0028-4793, 0028-4793 KW - Ferrous Compounds KW - 0 KW - Recombinant Proteins KW - Erythropoietin KW - 11096-26-7 KW - ferrous sulfate KW - 39R4TAN1VT KW - Fetal Hemoglobin KW - 9034-63-3 KW - Hydroxyurea KW - X6Q56QN5QC KW - Abridged Index Medicus KW - Index Medicus KW - Drug Therapy, Combination KW - Humans KW - Erythrocyte Count KW - Adult KW - Drug Synergism KW - Reticulocytes KW - Ferrous Compounds -- therapeutic use KW - Recombinant Proteins -- therapeutic use KW - Male KW - Erythrocyte Indices KW - beta-Thalassemia -- blood KW - Erythropoietin -- therapeutic use KW - Hydroxyurea -- therapeutic use KW - Fetal Hemoglobin -- biosynthesis KW - Anemia, Sickle Cell -- blood KW - Anemia, Sickle Cell -- drug therapy KW - beta-Thalassemia -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73505128?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+New+England+journal+of+medicine&rft.atitle=Augmentation+by+erythropoietin+of+the+fetal-hemoglobin+response+to+hydroxyurea+in+sickle+cell+disease.&rft.au=Rodgers%2C+G+P%3BDover%2C+G+J%3BUyesaka%2C+N%3BNoguchi%2C+C+T%3BSchechter%2C+A+N%3BNienhuis%2C+A+W&rft.aulast=Rodgers&rft.aufirst=G&rft.date=1993-01-14&rft.volume=328&rft.issue=2&rft.spage=73&rft.isbn=&rft.btitle=&rft.title=The+New+England+journal+of+medicine&rft.issn=00284793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-19 N1 - Date created - 1993-01-19 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: N Engl J Med. 1993 Jan 14;328(2):129-31 [7677964] N Engl J Med. 1993 May 20;328(20):1498-9 [8479480] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Regulation of heat shock factor trimer formation: role of a conserved leucine zipper. AN - 75543002; 8421783 AB - The human and Drosophila heat shock transcription factors (HSFs) are multi-zipper proteins with high-affinity binding to DNA that is regulated by heat shock-induced trimerization. Formation of HSF trimers is dependent on hydrophobic heptad repeats located in the amino-terminal region of the protein. Two subregions at the carboxyl-terminal end of human HSF1 were identified that maintain the monomeric form of the protein under normal conditions. One of these contains a leucine zipper motif that is conserved between vertebrate and insect HSFs. These results suggest that the carboxyl-terminal zipper may suppress formation of trimers by the amino-terminal HSF zipper elements by means of intramolecular coiled-coil interactions that are sensitive to heat shock. JF - Science (New York, N.Y.) AU - Rabindran, S K AU - Haroun, R I AU - Clos, J AU - Wisniewski, J AU - Wu, C AD - Laboratory of Biochemistry, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/01/08/ PY - 1993 DA - 1993 Jan 08 SP - 230 EP - 234 VL - 259 IS - 5092 SN - 0036-8075, 0036-8075 KW - Heat-Shock Proteins KW - 0 KW - Macromolecular Substances KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Hot Temperature KW - Drosophila -- chemistry KW - Animals KW - Transfection KW - Humans KW - DNA -- metabolism KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Cell Line KW - Structure-Activity Relationship KW - Mutagenesis KW - Binding Sites KW - Heat-Shock Proteins -- metabolism KW - Leucine Zippers KW - Heat-Shock Proteins -- genetics KW - Heat-Shock Proteins -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75543002?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science+%28New+York%2C+N.Y.%29&rft.atitle=Regulation+of+heat+shock+factor+trimer+formation%3A+role+of+a+conserved+leucine+zipper.&rft.au=Rabindran%2C+S+K%3BHaroun%2C+R+I%3BClos%2C+J%3BWisniewski%2C+J%3BWu%2C+C&rft.aulast=Rabindran&rft.aufirst=S&rft.date=1993-01-08&rft.volume=259&rft.issue=5092&rft.spage=230&rft.isbn=&rft.btitle=&rft.title=Science+%28New+York%2C+N.Y.%29&rft.issn=00368075&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-12 N1 - Date created - 1993-02-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Immunotoxin therapy for cancer. AN - 73497361; 8416411 JF - JAMA AU - Pai, L H AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Md 20892. Y1 - 1993/01/06/ PY - 1993 DA - 1993 Jan 06 SP - 78 EP - 81 VL - 269 IS - 1 SN - 0098-7484, 0098-7484 KW - Antibodies, Monoclonal KW - 0 KW - Bacterial Toxins KW - DNA, Recombinant KW - Exotoxins KW - Immunotoxins KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Forecasting KW - Pseudomonas aeruginosa KW - Drug Design KW - Bacterial Toxins -- genetics KW - Exotoxins -- genetics KW - Bacterial Toxins -- therapeutic use KW - Immunotoxins -- therapeutic use KW - Immunotoxins -- genetics KW - Neoplasms -- therapy KW - Exotoxins -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73497361?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=proceeding&rft.jtitle=JAMA&rft.atitle=Immunotoxin+therapy+for+cancer.&rft.au=Pai%2C+L+H%3BPastan%2C+I&rft.aulast=Pai&rft.aufirst=L&rft.date=1993-01-06&rft.volume=269&rft.issue=1&rft.spage=78&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-15 N1 - Date created - 1993-01-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Identification of control elements 3' to the human keratin 1 gene that regulate cell type and differentiation-specific expression. AN - 75531320; 7677999 AB - To define DNA regulatory elements that mediate the response of the keratin 1 (K1) gene to Ca(2+)-induced differentiation, regions spanning the 5'- and 3'-flanking sequences, coding regions, and introns from the human K1 gene were cloned into vectors containing the chloramphenicol acetyltransferase (CAT) reporter gene and transfected into cultured mouse keratinocytes. A 4.3-kilobase (kb) region located 3' to the K1 gene stimulated CAT activity in response to increasing Ca2+ concentrations from 0.05 mM (basal cells) to 1.2 mM (differentiated cells). The 4.3-kb fragment was also active in human epidermal cells but inactive in NIH 3T3 cells and primary mouse fibroblasts. Deletion analysis localized the activity to the terminal 1682 base pairs (bp) of the flanking sequence which retained Ca2+ sensitivity in epidermal cells but was not active in mesenchymal cells. Removal of a 207-base pair element created an enhancer which was active in both epidermal and mesenchymal cells but was still Ca(2+)-inducible. Further deletions identified two elements which functioned synergistically to give maximal Ca(2+)-sensitive activity. Stably transfected epidermal cell lines expressed CAT under the direction of these elements when grafted onto nude mice to reconstitute an intact epidermis. Previously reported keratin regulatory motifs were not contained in the 1682-bp fragment, but an AP-1 site was identified in one of the synergistic subunits. JF - The Journal of biological chemistry AU - Huff, C A AU - Yuspa, S H AU - Rosenthal, D AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/01/05/ PY - 1993 DA - 1993 Jan 05 SP - 377 EP - 384 VL - 268 IS - 1 SN - 0021-9258, 0021-9258 KW - K1 KW - Recombinant Fusion Proteins KW - 0 KW - Keratins KW - 68238-35-7 KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - 3T3 Cells KW - Animals KW - Humans KW - Keratinocytes -- drug effects KW - Mice KW - Plasmids KW - Chloramphenicol O-Acetyltransferase -- metabolism KW - Cloning, Molecular KW - Recombinant Fusion Proteins -- metabolism KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Base Sequence KW - Transfection KW - Cells, Cultured KW - Kinetics KW - Restriction Mapping KW - Molecular Sequence Data KW - Keratinocytes -- cytology KW - Keratinocytes -- metabolism KW - Sequence Deletion KW - Keratins -- genetics KW - Regulatory Sequences, Nucleic Acid -- drug effects KW - Cell Differentiation -- physiology KW - Gene Expression Regulation -- drug effects KW - Calcium -- pharmacology KW - Cell Differentiation -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75531320?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Identification+of+control+elements+3%27+to+the+human+keratin+1+gene+that+regulate+cell+type+and+differentiation-specific+expression.&rft.au=Huff%2C+C+A%3BYuspa%2C+S+H%3BRosenthal%2C+D&rft.aulast=Huff&rft.aufirst=C&rft.date=1993-01-05&rft.volume=268&rft.issue=1&rft.spage=377&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-28 N1 - Date created - 1993-01-28 N1 - Date revised - 2017-01-13 N1 - Gene symbol - K1 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Use of Magnetic Stimulation for Functional Analysis of Speech and Language Processing AN - 85565985; 9406534 AB - The use of magnetic stimulation of peripheral & cortical nerve cells as a tool for the study of cognitive processing is examined. Experimental studies (N = 1 normal adult for all studies) on the visual recognition & lexical access components of a naming task are presented. The S named tachistoscopically presented pictures of common objects, & magnetic stimulation was applied to various cortical regions at 100 msec following presentation. The stimulation produced varying degrees of interference with picture recognition, but did not interfere with lexical access. It is suggested that lexical access does not occur at 100 msecs. A subsequent test varied timing & location of magnetic stimulation. Results, though preliminary, suggest that lexical retrieval occurs between 100 & 200 msecs after presentation. In a third study, the S was asked to press a button to indicate whether the name of a picture rhymed with one of two previously presented pictures, while the supramarginal gyrus was magnetially stimulated for the period 250-350 msecs after presentation. Results accorded with the well-known lateralization of phonological processing to the left cerebral hemisphere, & it is suggested that the cognitive processing involved in this task required more time than the lexical retrieval processing required for the naming task. It is concluded that magnetic stimulation has potential as a viable methodology for the study of cognitive processing. 3 Tables, 1 Figure, 41 References. J. Easton JF - Annual Bulletin, Research Institute of Logopedics and Phoniatrics AU - Ludlow, C L AU - Cohen, L G AU - Hallett, M AD - Voice/Speech/Language Branch NIDCD, 9000 Rockville Pike Bethesda MD 20892 Y1 - 1993///0, PY - 1993 DA - 0, 1993 SP - 51 EP - 66 VL - 27 SN - 0564-7630, 0564-7630 KW - visual recognition, lexical access KW - magnetic stimulation KW - naming tasks KW - normal adult KW - Cognitive Processes (12950) KW - Visual Media (94550) KW - Interference (Learning) (37150) KW - Language Processing (43550) KW - article KW - 6210: hearing and speech physiology; hearing and speech physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85565985?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Allba&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annual+Bulletin%2C+Research+Institute+of+Logopedics+and+Phoniatrics&rft.atitle=Use+of+Magnetic+Stimulation+for+Functional+Analysis+of+Speech+and+Language+Processing&rft.au=Ludlow%2C+C+L%3BCohen%2C+L+G%3BHallett%2C+M&rft.aulast=Ludlow&rft.aufirst=C&rft.date=1993-01-01&rft.volume=27&rft.issue=&rft.spage=51&rft.isbn=&rft.btitle=&rft.title=Annual+Bulletin%2C+Research+Institute+of+Logopedics+and+Phoniatrics&rft.issn=05647630&rft_id=info:doi/ LA - English DB - Linguistics and Language Behavior Abstracts (LLBA) N1 - Date revised - 2003-10-01 N1 - Last updated - 2016-09-27 N1 - CODEN - ABLPB8 N1 - SubjectsTermNotLitGenreText - Cognitive Processes (12950); Language Processing (43550); Interference (Learning) (37150); Visual Media (94550) ER - TY - JOUR T1 - The functions of saliva. AN - 85162008; pmid-8359042 AB - Oral health is determined to a considerable extent by our ability to produce saliva. Not only must adequate amounts be produced, but a large number of specific proteins also must be secreted for the mouth to function properly. This brief review is directed at describing (1) how saliva is secreted, (2) the consequences of decreased salivary function, (3) the components necessary for oral homeostasis, and (4) the common causes of salivary hypofunction. JF - Dysphagia AU - Kaplan, M D AU - Baum, B J AD - Clinical Investigations and Patient Care Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland. PY - 1993 SP - 225 EP - 229 VL - 8 IS - 3 SN - 0179-051X, 0179-051X UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85162008?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Dysphagia&rft.atitle=The+functions+of+saliva.&rft.au=Kaplan%2C+M+D%3BBaum%2C+B+J&rft.aulast=Kaplan&rft.aufirst=M&rft.date=1993-01-01&rft.volume=8&rft.issue=3&rft.spage=225&rft.isbn=&rft.btitle=&rft.title=Dysphagia&rft.issn=0179051X&rft_id=info:doi/ LA - English DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Ethanol action on excitatory amino acid activated ion channels. AN - 76319702; 7538302 AB - The effects of ethanol on excitatory amino acid activated ion channels were investigated using patch-clamp recording methods. Intoxicating concentrations of ethanol (5-50 mM) inhibited ion current activated by the glutamate receptor agonist N-methyl-D-aspartate (NMDA) in a concentration-dependent manner (IC50 = 30 mM). The intoxicating potency of different alcohols was correlated with their potency for inhibiting NMDA-activated current, suggesting that alcohol-induced inhibition of NMDA channel function may contribute to the neural and cognitive impairments associated with intoxication. Analysis of mechanism suggests that ethanol inhibits NMDA-activated current by altering gating of the channel, rather than by affecting channel conductance, ion permeance or regulatory sites on the channel. Anesthetic concentrations of ethanol (> 50 mM) produced a concentration-dependent inhibition of kainate- and quisqualate-activated currents (IC50 = 220 mM), suggesting that this inhibition may contribute to the general anesthetic effects of ethanol. This hypothesis is supported by the observations that the general anesthetic agents, trichloroethanol (the active metabolite of chloral hydrate), pentobarbital and halothane, all inhibit kainate- and quisqualate-activated currents. JF - Alcohol and alcoholism (Oxford, Oxfordshire). Supplement AU - Weight, F F AU - Peoples, R W AU - Wright, J M AU - Lovinger, D M AU - White, G AD - Laboratory of Molecular and Cellular Neurobiology, National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD 20892, USA. Y1 - 1993 PY - 1993 DA - 1993 SP - 353 EP - 358 VL - 2 SN - 1358-6173, 1358-6173 KW - Excitatory Amino Acids KW - 0 KW - Ion Channels KW - Ethanol KW - 3K9958V90M KW - N-Methylaspartate KW - 6384-92-5 KW - Quisqualic Acid KW - 8OC22C1B99 KW - Kainic Acid KW - SIV03811UC KW - Index Medicus KW - Quisqualic Acid -- pharmacology KW - Animals KW - Kainic Acid -- pharmacology KW - Neurons -- metabolism KW - N-Methylaspartate -- pharmacology KW - Cells, Cultured KW - Neurons -- drug effects KW - Brain -- drug effects KW - Brain -- metabolism KW - Ion Channels -- antagonists & inhibitors KW - Ion Channels -- drug effects KW - Excitatory Amino Acids -- pharmacology KW - Ethanol -- toxicity KW - Ion Channels -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76319702?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcohol+and+alcoholism+%28Oxford%2C+Oxfordshire%29.+Supplement&rft.atitle=Ethanol+action+on+excitatory+amino+acid+activated+ion+channels.&rft.au=Weight%2C+F+F%3BPeoples%2C+R+W%3BWright%2C+J+M%3BLovinger%2C+D+M%3BWhite%2C+G&rft.aulast=Weight&rft.aufirst=F&rft.date=1993-01-01&rft.volume=2&rft.issue=&rft.spage=353&rft.isbn=&rft.btitle=&rft.title=Alcohol+and+alcoholism+%28Oxford%2C+Oxfordshire%29.+Supplement&rft.issn=13586173&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1995-06-22 N1 - Date created - 1995-06-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The DRD2 dopamine receptor and the candidate gene approach in alcoholism. AN - 76318458; 7748310 AB - The cloning of the DRD2 dopamine receptor gene and discovery of an associated polymorphism permitted genetic association and linkage studies to alcoholism. Extensive allele frequency differences between populations provide an alternative explanation for explaining a DRD2 association to alcoholism which has been observed in some studies, but more frequently has not been replicated. JF - Alcohol and alcoholism (Oxford, Oxfordshire). Supplement AU - Goldman, D AD - Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, DICBR, Bethesda, MD 20892, USA. Y1 - 1993 PY - 1993 DA - 1993 SP - 27 EP - 29 VL - 2 SN - 1358-6173, 1358-6173 KW - Receptors, Dopamine D2 KW - 0 KW - Index Medicus KW - Alleles KW - Gene Frequency KW - Polymorphism, Genetic KW - Humans KW - Linkage Disequilibrium KW - Receptors, Dopamine D2 -- genetics KW - Alcoholism -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76318458?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcohol+and+alcoholism+%28Oxford%2C+Oxfordshire%29.+Supplement&rft.atitle=The+DRD2+dopamine+receptor+and+the+candidate+gene+approach+in+alcoholism.&rft.au=Goldman%2C+D&rft.aulast=Goldman&rft.aufirst=D&rft.date=1993-01-01&rft.volume=2&rft.issue=&rft.spage=27&rft.isbn=&rft.btitle=&rft.title=Alcohol+and+alcoholism+%28Oxford%2C+Oxfordshire%29.+Supplement&rft.issn=13586173&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1995-06-22 N1 - Date created - 1995-06-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Memory improvement without toxicity during chronic, low dose intravenous arecoline in Alzheimer's disease. AN - 76313949; 7871052 AB - Arecoline, a cholinergic agonist, administered at low doses by continuous intravenous infusion for up to 2 weeks, significantly and replicably improved memory in five of nine subjects with mild-moderate Alzheimer's disease. During dose finding, performance on a verbal memory task improved with an inverted U-shaped relation to dose. Six of nine subjects were classified as responders. During blinded, placebo-controlled, individualized optimal dosing for 5 days, verbal memory again improved in five of six responders but not in any non-responder. No adverse drug effects occurred. Arecoline, and possibly other cholinergic agonists, can safely improve memory in Alzheimer's disease at doses much lower than previously studied. JF - Psychopharmacology AU - Soncrant, T T AU - Raffaele, K C AU - Asthana, S AU - Berardi, A AU - Morris, P P AU - Haxby, J V AD - Unit on Pharmacology and Pharmacokinetics, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 421 EP - 427 VL - 112 IS - 4 SN - 0033-3158, 0033-3158 KW - Arecoline KW - 4ALN5933BH KW - Index Medicus KW - Hemodynamics -- drug effects KW - Body Temperature -- drug effects KW - Infusions, Intravenous KW - Dose-Response Relationship, Drug KW - Humans KW - Aged KW - Memory, Short-Term -- drug effects KW - Infusion Pumps KW - Psychomotor Performance -- drug effects KW - Cognition -- drug effects KW - Aged, 80 and over KW - Middle Aged KW - Neuropsychological Tests KW - Female KW - Male KW - Arecoline -- therapeutic use KW - Alzheimer Disease -- complications KW - Alzheimer Disease -- drug therapy KW - Memory Disorders -- etiology KW - Alzheimer Disease -- psychology KW - Arecoline -- adverse effects KW - Memory Disorders -- drug therapy KW - Arecoline -- administration & dosage KW - Memory Disorders -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76313949?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychopharmacology&rft.atitle=Memory+improvement+without+toxicity+during+chronic%2C+low+dose+intravenous+arecoline+in+Alzheimer%27s+disease.&rft.au=Soncrant%2C+T+T%3BRaffaele%2C+K+C%3BAsthana%2C+S%3BBerardi%2C+A%3BMorris%2C+P+P%3BHaxby%2C+J+V&rft.aulast=Soncrant&rft.aufirst=T&rft.date=1993-01-01&rft.volume=112&rft.issue=4&rft.spage=421&rft.isbn=&rft.btitle=&rft.title=Psychopharmacology&rft.issn=00333158&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1995-03-29 N1 - Date created - 1995-03-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Attenuation of some signs of opioid withdrawal by inhibitors of nitric oxide synthase. AN - 76311358; 7532866 AB - Effects of nitric oxide synthase (NOS) inhibitors (L-NG-nitroarginine, L-NG-nitroarginine methyl ester) on precipitated opioid withdrawal were studied in morphine-dependent rats given naloxone, in order to assess the involvement of nitric oxide (NO) in opioid dependence. L-NG-Nitroarginine (7.5 mg/kg, IP, 1 h before naloxone or b.i.d. on days 4-7 of an 8-day morphine treatment) reduced wet dog shakes and weight loss; when given by osmotic pumps (15 mg/kg per day), the drug reduced wet dog shakes but not weight loss. L-NG-Nitroarginine methyl ester (60 mg/kg, 1 h before naloxone) also reduced wet dog shakes and weight loss. The results indicate that NOS inhibitors warrant further study as potential treatments of the opioid withdrawal syndrome. JF - Psychopharmacology AU - Kimes, A S AU - Vaupel, D B AU - London, E D AD - Neuroimaging and Drug Action Section, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD 21224. Y1 - 1993 PY - 1993 DA - 1993 SP - 521 EP - 524 VL - 112 IS - 4 SN - 0033-3158, 0033-3158 KW - omega-N-Methylarginine KW - 27JT06E6GR KW - Nitric Oxide KW - 31C4KY9ESH KW - Arginine KW - 94ZLA3W45F KW - Nitric Oxide Synthase KW - EC 1.14.13.39 KW - Amino Acid Oxidoreductases KW - EC 1.4.- KW - NG-Nitroarginine Methyl Ester KW - V55S2QJN2X KW - Index Medicus KW - Rats KW - Behavior, Animal -- drug effects KW - Animals KW - Rats, Inbred F344 KW - Dose-Response Relationship, Drug KW - Weight Loss -- drug effects KW - Morphine Dependence -- psychology KW - Male KW - Arginine -- therapeutic use KW - Nitric Oxide -- antagonists & inhibitors KW - Amino Acid Oxidoreductases -- antagonists & inhibitors KW - Substance Withdrawal Syndrome -- drug therapy KW - Substance Withdrawal Syndrome -- psychology KW - Arginine -- analogs & derivatives KW - Arginine -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76311358?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychopharmacology&rft.atitle=Attenuation+of+some+signs+of+opioid+withdrawal+by+inhibitors+of+nitric+oxide+synthase.&rft.au=Kimes%2C+A+S%3BVaupel%2C+D+B%3BLondon%2C+E+D&rft.aulast=Kimes&rft.aufirst=A&rft.date=1993-01-01&rft.volume=112&rft.issue=4&rft.spage=521&rft.isbn=&rft.btitle=&rft.title=Psychopharmacology&rft.issn=00333158&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1995-03-29 N1 - Date created - 1995-03-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Pharmacological specificity of enhanced sensitivity to naltrexone in rats. AN - 76311202; 7870900 AB - Rats treated weekly with cumulative doses (1-100 mg/kg, IP) of naltrexone develop an enhanced sensitivity to the operant response-rate decreasing effect of naltrexone. In the present experiment the pharmacological specificity of that enhanced sensitivity was determined by testing a variety of drugs for cross-sensitivity to naltrexone. Cross-sensitivity was evaluated with two procedures. In one, dose-effect functions were determined for each of the test compounds before and after the development of enhanced sensitivity to naltrexone in a single group of rats. In the second procedure, one group of rats was made sensitive to naltrexone, while a second was not. Test compounds were then evaluated in both groups. For both procedures, a shift to the left in the dose-effect functions similar to naltrexone was considered evidence of cross-sensitivity. Of the opioid antagonists tested, only naloxone showed clear cross-sensitivity to naltrexone, although MR 2266 and diprenorphine also showed evidence of cross-sensitivity. The opioid antagonist quadazocine did not show cross-sensitivity to naltrexone on the day of testing, although some evidence of cross-sensitivity was evident 24 h later. In addition, the dose-effect function for d-amphetamine was significantly changed following naltrexone treatment. No evidence of cross-sensitivity was observed for the optical isomer of naloxone, d-naloxone, or for naloxone's quaternary derivative, naloxone methiodide. None of the opioid agonists or agonist-antagonists tested showed cross-sensitivity to naltrexone (i.e. morphine, U-50, 488H, ethylketocyclazocine, N-allylnormetazocine and pentazocine). The non-opioid drugs chlordiazepoxide and phencyclidine also failed to show evidence of cross-sensitivity.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Psychopharmacology AU - Schindler, C W AU - Goldberg, S R AU - Katz, J L AD - Preclinical Pharmacology Laboratory, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1993 PY - 1993 DA - 1993 SP - 60 EP - 68 VL - 110 IS - 1-2 SN - 0033-3158, 0033-3158 KW - Narcotic Antagonists KW - 0 KW - Narcotics KW - Naltrexone KW - 5S6W795CQM KW - Chlordiazepoxide KW - 6RZ6XEZ3CR KW - Amphetamine KW - CK833KGX7E KW - Phencyclidine KW - J1DOI7UV76 KW - Index Medicus KW - Animals KW - Stereoisomerism KW - Chlordiazepoxide -- pharmacology KW - Drug Interactions KW - Reinforcement Schedule KW - Dose-Response Relationship, Drug KW - Food KW - Phencyclidine -- pharmacology KW - Narcotics -- pharmacology KW - Rats KW - Amphetamine -- pharmacology KW - Narcotic Antagonists -- pharmacology KW - Male KW - Conditioning, Operant -- drug effects KW - Naltrexone -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76311202?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychopharmacology&rft.atitle=Pharmacological+specificity+of+enhanced+sensitivity+to+naltrexone+in+rats.&rft.au=Schindler%2C+C+W%3BGoldberg%2C+S+R%3BKatz%2C+J+L&rft.aulast=Schindler&rft.aufirst=C&rft.date=1993-01-01&rft.volume=110&rft.issue=1-2&rft.spage=60&rft.isbn=&rft.btitle=&rft.title=Psychopharmacology&rft.issn=00333158&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1995-03-29 N1 - Date created - 1995-03-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - 1,3-Butadiene induces cancer in experimental animals at all concentrations from 6.25 to 8000 parts per million. AN - 76300704; 8070878 AB - 1,3-Butadiene, a chemical produced in large volumes, induces cancer in many organs in rats (at 1000 and 8000 ppm) and mice (at 6.25 to 1250 ppm); however, the sites of tumour induction (seven in rats and nine in mice) and the magnitudes of response differ between the two species. Particularly noteworthy in the studies of mice exposed by inhalation were the early, extensive induction of malignant lymphomas, the induction of uncommon haemangiosarcomas of the heart and the development of malignant lung tumours at 6.25 ppm, the lowest concentration ever used in a long-term carcinogenicity study of this gas. In order to account for the impact of early mortality on the expression of late development of tumours, survival-adjusted tumour rates were computed for mice exposed to butadiene at 6.25-625 ppm. The results provide a more accurate characterization of concentration-dependent responses for butadiene-induced cancers. Stop-exposure studies revealed that the atmospheric concentration of butadiene was a greater contributing factor to the development of lymphomas than was duration of exposure. The studies in mice show a good correspondence with the reported associations between occupational exposure to butadiene and excess mortality from lymphatic and haematopoietic cancers; mice are thus a better experimental surrogate for humans. Although further work is needed to improve our understanding of the mechanisms of tumour induction by butadiene, pursuit of that research must not delay reduction of human exposure to this carcinogenic chemical. JF - IARC scientific publications AU - Melnick, R L AU - Huff, J E AD - Environmental Carcinogenesis Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina. Y1 - 1993 PY - 1993 DA - 1993 SP - 309 EP - 322 IS - 127 SN - 0300-5038, 0300-5038 KW - Butadienes KW - 0 KW - Carcinogens KW - 1,3-butadiene KW - JSD5FGP5VD KW - Index Medicus KW - Rats KW - Mice, Inbred Strains KW - Animals KW - Rats, Sprague-Dawley KW - Mice KW - Male KW - Female KW - Butadienes -- toxicity KW - Neoplasms, Experimental -- chemically induced KW - Carcinogens -- toxicity KW - Butadienes -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76300704?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=IARC+scientific+publications&rft.atitle=1%2C3-Butadiene+induces+cancer+in+experimental+animals+at+all+concentrations+from+6.25+to+8000+parts+per+million.&rft.au=Melnick%2C+R+L%3BHuff%2C+J+E&rft.aulast=Melnick&rft.aufirst=R&rft.date=1993-01-01&rft.volume=&rft.issue=127&rft.spage=309&rft.isbn=&rft.btitle=&rft.title=IARC+scientific+publications&rft.issn=03005038&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-09-29 N1 - Date created - 1994-09-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - A c-fos/c-jun-like factor and the pituitary-specific factor Pit-1 are both necessary to mediate induction of the human thyrotropin beta promoter. AN - 76292587; 8036746 JF - Transactions of the Association of American Physicians AU - Kim, M K AU - McClaskey, J H AU - Bodenner, D L AU - Weintraub, B D AD - Molecular, Cellular and Endocrinology Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 62 EP - 68 VL - 106 SN - 0066-9458, 0066-9458 KW - TSH KW - DNA-Binding Proteins KW - 0 KW - POU1F1 protein, human KW - Proto-Oncogene Proteins c-jun KW - Transcription Factor Pit-1 KW - Transcription Factors KW - Colforsin KW - 1F7A44V6OU KW - Thyrotropin-Releasing Hormone KW - 5Y5F15120W KW - Thyrotropin KW - 9002-71-5 KW - DNA KW - 9007-49-2 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Thyrotropin-Releasing Hormone -- pharmacology KW - Colforsin -- pharmacology KW - Base Sequence KW - HeLa Cells KW - Humans KW - DNA -- genetics KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Gene Expression Regulation -- drug effects KW - Cell Line KW - Promoter Regions, Genetic KW - Thyrotropin -- genetics KW - DNA-Binding Proteins -- genetics KW - Proto-Oncogene Proteins c-jun -- genetics KW - Transcription Factors -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76292587?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Transactions+of+the+Association+of+American+Physicians&rft.atitle=A+c-fos%2Fc-jun-like+factor+and+the+pituitary-specific+factor+Pit-1+are+both+necessary+to+mediate+induction+of+the+human+thyrotropin+beta+promoter.&rft.au=Kim%2C+M+K%3BMcClaskey%2C+J+H%3BBodenner%2C+D+L%3BWeintraub%2C+B+D&rft.aulast=Kim&rft.aufirst=M&rft.date=1993-01-01&rft.volume=106&rft.issue=&rft.spage=62&rft.isbn=&rft.btitle=&rft.title=Transactions+of+the+Association+of+American+Physicians&rft.issn=00669458&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-08-17 N1 - Date created - 1994-08-17 N1 - Date revised - 2017-01-13 N1 - Gene symbol - TSH N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Phase I study of Taxol, doxorubicin, plus granulocyte-colony stimulating factor in patients with metastatic breast cancer. AN - 76291578; 7517154 AB - The objective of this phase I trial was to determine the maximal tolerated dose (MTD) of Taxol and doxorubicin administered as a simultaneous intravenous infusion over 72 hours every 21 days. Granulocyte-colony stimulating factor (G-CSF) 10 micrograms/kg, was administered on days 4-18 of each cycle. The treated population consisted of metastatic breast cancer patients previously untreated with chemotherapy for metastatic disease, who had not received doxorubicin in the adjuvant setting and who had bidimensionally measurable disease. The MTD was determined to be 75 mg/m2 of doxorubicin and 160 mg/m2 of Taxol. The dose-limiting toxicity of the combination was clinical typhlitis in three of three patients. Other significant toxicities included grade 3 diarrhea at the higher dose levels and grade 4 neutropenia in all patients. Eighteen patients were treated on this initial phase I study. The overall response rate was 62%, with 6% complete responses and 56% partial responses. The combination of doxorubicin and Taxol by 72-hour continuous infusion with G-CSF is an active regimen in patients with metastatic breast cancer. JF - Journal of the National Cancer Institute. Monographs AU - Fisherman, J S AU - McCabe, M AU - Noone, M AU - Ognibene, F P AU - Goldspiel, B AU - Venzon, D J AU - Cowan, K H AU - O'Shaughnessy, J A AD - Medicine Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 189 EP - 194 IS - 15 SN - 1052-6773, 1052-6773 KW - Granulocyte Colony-Stimulating Factor KW - 143011-72-7 KW - Doxorubicin KW - 80168379AG KW - Paclitaxel KW - P88XT4IS4D KW - Index Medicus KW - Humans KW - Neoplasm Metastasis KW - Heart -- drug effects KW - Female KW - Paclitaxel -- administration & dosage KW - Breast Neoplasms -- drug therapy KW - Paclitaxel -- adverse effects KW - Granulocyte Colony-Stimulating Factor -- administration & dosage KW - Doxorubicin -- administration & dosage KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76291578?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute.+Monographs&rft.atitle=Phase+I+study+of+Taxol%2C+doxorubicin%2C+plus+granulocyte-colony+stimulating+factor+in+patients+with+metastatic+breast+cancer.&rft.au=Fisherman%2C+J+S%3BMcCabe%2C+M%3BNoone%2C+M%3BOgnibene%2C+F+P%3BGoldspiel%2C+B%3BVenzon%2C+D+J%3BCowan%2C+K+H%3BO%27Shaughnessy%2C+J+A&rft.aulast=Fisherman&rft.aufirst=J&rft.date=1993-01-01&rft.volume=&rft.issue=15&rft.spage=189&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute.+Monographs&rft.issn=10526773&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-08-04 N1 - Date created - 1994-08-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Development of breast cancer chemopreventive drugs. AN - 76291335; 8007699 AB - Breast cancer is the second highest cause of cancer mortality (19%) estimated for U.S. women in 1993 and accounts for the highest proportion of new cancer cases (32%) in this population. The rate of documented cases increased during the early 1970s and again in 1980-87, probably due to early mammographic detection. Increased knowledge of personal risk may also have been a consideration; however, 60% of women diagnosed with breast cancer have no known risk factor(s), such as family history, early age at menarche, late age at menopause, nulliparity, late age at first live birth, socioeconomic status, contraceptive use, postmenopausal estrogen replacement, or high fat intake. To prevent cancer, one strategy undertaken by the NCI is cancer chemoprevention, or intervention with chemical agents at the precancer stage to halt or slow the carcinogenic process. An objective of the NCI, DCPC is to develop promising cancer chemopreventive chemical agents as drugs for human use. Briefly, the process begins with identification of potential agents (e.g., pharmaceuticals, natural products, minor dietary constituents) from surveillance and analysis of the literature and from in vitro prescreen assays. Data on both efficacy (i.e., biological activities that either directly or indirectly indicate inhibition of carcinogenesis) and toxicity are gathered these sources. Various criteria are used to select and prioritize agents for entry into the NCI, DCPC preclinical testing program. The program begins with battery of in vitro efficacy screens using both animal and human cells to select agents for further testing; agents positive in these assays are considered for further testing. In the assay used for breast cancer chemoprevention, 7,12-dimethylbenz(a)anthracene (DMBA)-induced mouse mammary organ culture, 64 chemicals have inhibited formation of hyperplastic alveolar-like nodules. A panel of organ-specific animal screening assays are then used to assess efficacy in vivo. Two assays relevant for breast cancer chemoprevention are inhibition of N-methyl-N-nitrosourea- and DMBA-induced rat mammary gland carcinogenesis. Of 89 agents tested, 29 have inhibited cancer incidence, multiplicity, or both in at least one of the mammary assays; 21 agents are currently on test. Highly promising agents are then placed in traditional preclinical toxicity tests performed in two species. Finally, the most promising and least toxic agents enter clinical trials. Phase I clinical trials are designed to investigate human dose-related safety and pharmacokinetics of the drug. Phase II trials are small scale, placebo-controlled studies designed to determine chemopreventive efficacy and optimal dosing regimens.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Journal of cellular biochemistry. Supplement AU - Kelloff, G J AU - Boone, C W AU - Steele, V E AU - Crowell, J A AU - Lubet, R AU - Doody, L A AU - Greenwald, P AD - Chemoprevention Investigational Studies Branch (CISB), National Cancer Institute (NCI), National Institutes of Health, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 2 EP - 13 VL - 17G SN - 0733-1959, 0733-1959 KW - Antineoplastic Agents KW - 0 KW - Biomarkers, Tumor KW - Index Medicus KW - United States KW - Animals KW - Clinical Trials, Phase II as Topic KW - Clinical Trials, Phase III as Topic KW - Humans KW - National Institutes of Health (U.S.) KW - Cohort Studies KW - Adult KW - Aged KW - Middle Aged KW - Drug Design KW - Female KW - Breast Neoplasms -- prevention & control KW - Antineoplastic Agents -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76291335?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+cellular+biochemistry.+Supplement&rft.atitle=Development+of+breast+cancer+chemopreventive+drugs.&rft.au=Kelloff%2C+G+J%3BBoone%2C+C+W%3BSteele%2C+V+E%3BCrowell%2C+J+A%3BLubet%2C+R%3BDoody%2C+L+A%3BGreenwald%2C+P&rft.aulast=Kelloff&rft.aufirst=G&rft.date=1993-01-01&rft.volume=17G&rft.issue=&rft.spage=2&rft.isbn=&rft.btitle=&rft.title=Journal+of+cellular+biochemistry.+Supplement&rft.issn=07331959&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-07-21 N1 - Date created - 1994-07-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Taxol: a history of pharmaceutical development and current pharmaceutical concerns. AN - 76290674; 7912520 AB - Taxol, a unique diterpene anticancer compound derived from the bark of the Taxus brevifolia (Pacific yew) tree, induces cytotoxicity by a novel mechanism of action. An antimicrotubule agent, Taxol promotes the formation and stabilization of the tubulin polymer unlike other anticancer agents that induce microtubule disassembly. Because of its poor aqueous solubility, Taxol is formulated as a solution in 50% Cremophor EL and 50% dehydrated alcohol, USP. The Cremophor EL and dehydrated alcohol vehicle used in the formulation of Taxol creates some interesting challenges for its preparation and administration. The pharmaceutical concerns associated with the preparation and administration of Taxol are discussed. JF - Journal of the National Cancer Institute. Monographs AU - Adams, J D AU - Flora, K P AU - Goldspiel, B R AU - Wilson, J W AU - Arbuck, S G AU - Finley, R AD - Drug Management and Authorization Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 141 EP - 147 IS - 15 SN - 1052-6773, 1052-6773 KW - Paclitaxel KW - P88XT4IS4D KW - Index Medicus KW - Drug Stability KW - Animals KW - Solubility KW - Chemistry, Pharmaceutical KW - Humans KW - Drug Incompatibility KW - Paclitaxel -- chemistry KW - Paclitaxel -- administration & dosage KW - Paclitaxel -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76290674?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute.+Monographs&rft.atitle=Taxol%3A+a+history+of+pharmaceutical+development+and+current+pharmaceutical+concerns.&rft.au=Adams%2C+J+D%3BFlora%2C+K+P%3BGoldspiel%2C+B+R%3BWilson%2C+J+W%3BArbuck%2C+S+G%3BFinley%2C+R&rft.aulast=Adams&rft.aufirst=J&rft.date=1993-01-01&rft.volume=&rft.issue=15&rft.spage=141&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute.+Monographs&rft.issn=10526773&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-08-04 N1 - Date created - 1994-08-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Intraepithelial and postinvasive neoplasia as a stochastic continuum of clonal evolution, and its relationship to mechanisms of chemopreventive drug action. AN - 76290036; 8007692 AB - The progression of intraepithelial and postinvasive neoplasia depends on the occurrence of clonal evolution, defined as the continuous development of mutations and selective clonal expansions in the neoplastic cell population. The two continuously repeating events of clonal evolution, mutation and clonal expansion, occur at unpredictable times and locations. Therefore the neoplastic process is best characterized as a stochastic, i.e., probabilistic, continuum. The rate of intraepithelial neoplastic progression is continuously driven by the dosage level of exposure to mutagens and mitogens. For example, in chronic smokers the length of time before development of lung cancer depends on the number of cigarettes smoked per day. A commonly held misconception is that human carcinogenesis develops after an initial short period of mutation followed by a long period of stimulated proliferation (the multistage model). This incorrect idea derives from the sequential nature of the consecutive two- or three-step operational protocols imposed on experimental animal models by the experimenter. In reality, human carcinogenesis develops as the result of simultaneous and continuous exposure to mutagens and mitogens over the entire period of tumor development. A recent example is the finding that the intraepithelial neoplasia of colorectal adenomas continuously progresses through serial waves of mutation and clonal expansion. The rational design of chemopreventive agents should be based on blocking the two parameters which continuously drive neoplasia: mutagenesis and mitogenesis. In addition to blocking exposure, chemopreventive agents may act at many points during activation and DNA adduction of mutagens, or during stimulation of the proliferation signal pathway by mitogens. Based on the chemopreventive strategy of blocking mutagenesis and mitogenesis, chemopreventive agents are classed as either antimutagenic or antimitogenic. A third class, the antioxidants, are both antimutagenic and antimitogenic, and operate by the common mechanism of breaking free radical chain reactions initiated by reactive oxygen species. In the program of the Chemoprevention Investigational Studies Branch, Division of Cancer Prevention and Control, National Cancer Institute, preclinical development of antimutagens, antimitogens, and antioxidants is well under way, and some of these agents are highlighted here. JF - Journal of cellular biochemistry. Supplement AU - Boone, C W AU - Kelloff, G J AU - Freedman, L S AD - Division of Cancer Prevention and Control, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 14 EP - 25 VL - 17G SN - 0733-1959, 0733-1959 KW - Antioxidants KW - 0 KW - Mitogens KW - Mutagens KW - Reactive Oxygen Species KW - Index Medicus KW - Clone Cells KW - Humans KW - Antioxidants -- therapeutic use KW - Mitogens -- antagonists & inhibitors KW - Carcinoma in Situ -- pathology KW - Precancerous Conditions -- genetics KW - Precancerous Conditions -- prevention & control KW - Carcinoma in Situ -- genetics KW - Carcinoma in Situ -- prevention & control KW - Precancerous Conditions -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76290036?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+cellular+biochemistry.+Supplement&rft.atitle=Intraepithelial+and+postinvasive+neoplasia+as+a+stochastic+continuum+of+clonal+evolution%2C+and+its+relationship+to+mechanisms+of+chemopreventive+drug+action.&rft.au=Boone%2C+C+W%3BKelloff%2C+G+J%3BFreedman%2C+L+S&rft.aulast=Boone&rft.aufirst=C&rft.date=1993-01-01&rft.volume=17G&rft.issue=&rft.spage=14&rft.isbn=&rft.btitle=&rft.title=Journal+of+cellular+biochemistry.+Supplement&rft.issn=07331959&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-07-21 N1 - Date created - 1994-07-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Clinical development of Taxol. AN - 76285841; 7912517 AB - Taxol is the first of a novel class of anticancer drugs, the taxanes. Taxol's unique effects include its ability to polymerize tubulin into stable microtubules in the absence of cofactors and to induce the formation of stable microtubule bundles. During its development, formidable challenges were overcome: a suitable formulation was developed, an adequate supply was ensured, severe hypersensitivity reactions were diminished in incidence and severity, and clinical efficacy was demonstrated. Phase II evaluation is still underway; to date, clinical efficacy has been demonstrated in ovarian, breast, non-small-cell lung, and head and neck cancer. Response rates were low in early studies in melanoma, prostate, colon, cervix, and renal cancer, but for these tumors, additional evaluation is ongoing with a higher Taxol dose or different schedule. In December 1992, Food and Drug Administration approval was granted for use of Taxol as second-line therapy in ovarian cancer patients. Nevertheless, important questions regarding optimal use of this important new drug remain. These include determination of optimal dose and schedule and development of suitable combination chemotherapy regimens. The clinical development of Taxol and current status of phase I, II, and III clinical trials are reviewed. JF - Journal of the National Cancer Institute. Monographs AU - Arbuck, S G AU - Christian, M C AU - Fisherman, J S AU - Cazenave, L A AU - Sarosy, G AU - Suffness, M AU - Adams, J AU - Canetta, R AU - Cole, K E AU - Friedman, M A AD - M. A. Friedman, Cancer Therapy Evaluation Program, Division of Cancer Treatment, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 11 EP - 24 IS - 15 SN - 1052-6773, 1052-6773 KW - Paclitaxel KW - P88XT4IS4D KW - Index Medicus KW - Animals KW - Humans KW - Clinical Trials as Topic KW - Neoplasms -- drug therapy KW - Paclitaxel -- adverse effects KW - Paclitaxel -- therapeutic use KW - Paclitaxel -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76285841?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute.+Monographs&rft.atitle=Clinical+development+of+Taxol.&rft.au=Arbuck%2C+S+G%3BChristian%2C+M+C%3BFisherman%2C+J+S%3BCazenave%2C+L+A%3BSarosy%2C+G%3BSuffness%2C+M%3BAdams%2C+J%3BCanetta%2C+R%3BCole%2C+K+E%3BFriedman%2C+M+A&rft.aulast=Arbuck&rft.aufirst=S&rft.date=1993-01-01&rft.volume=&rft.issue=15&rft.spage=11&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute.+Monographs&rft.issn=10526773&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-08-04 N1 - Date created - 1994-08-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Nursing management of the patient receiving Taxol therapy. AN - 76282397; 7912521 AB - Taxol is an important new antitumor agent with demonstrated efficacy in ovarian and breast cancer. Toxicities identified, including cardiac, hypersensitivity reactions, and neurologic, require careful nursing assessment for management, Additional toxicities may be identified as Taxol is combined with other chemotherapeutic agents. Studies to determine the most effective dose and schedule are ongoing. The current evaluation of this new drug presents an important opportunity for nurses to contribute to its development through both clinical and research endeavors. Such contributions will facilitate the optimal nursing care of patients treated with Taxol. JF - Journal of the National Cancer Institute. Monographs AU - Noone, M H AU - McCabe, M S AU - Denicoff, A M AU - Lepore, J M AD - Medicine Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 149 EP - 154 IS - 15 SN - 1052-6773, 1052-6773 KW - Paclitaxel KW - P88XT4IS4D KW - Index Medicus KW - Patient Education as Topic KW - Humans KW - Neoplasms -- drug therapy KW - Paclitaxel -- adverse effects KW - Nursing Assessment KW - Neoplasms -- nursing KW - Paclitaxel -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76282397?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute.+Monographs&rft.atitle=Nursing+management+of+the+patient+receiving+Taxol+therapy.&rft.au=Noone%2C+M+H%3BMcCabe%2C+M+S%3BDenicoff%2C+A+M%3BLepore%2C+J+M&rft.aulast=Noone&rft.aufirst=M&rft.date=1993-01-01&rft.volume=&rft.issue=15&rft.spage=149&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute.+Monographs&rft.issn=10526773&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-08-04 N1 - Date created - 1994-08-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Taxol effect on cisplatin sensitivity and cisplatin cellular accumulation in human ovarian cancer cells. AN - 76282367; 7912534 AB - Taxol and cisplatin are the two most effective agents discovered to date for treating advanced-stage cancer of the ovary. Learning how best to combine these agents is the focus of preclinical and clinical studies conducted at a number of institutions. Taxol's effect on cellular sensitivity to cisplatin was studied in paired cisplatin-sensitive A2780 and cisplatin-resistant A2780/CP70 human ovarian cancer cell lines. Cisplatin growth curves were generated under conditions of specific sequencing with Taxol, and IC50s (concentrations at which growth is inhibited to 50% of control) for cisplatin were obtained and compared. Taxol was used at an IC10 dose in all experiments. Taxol treatments were for 24 hours and cisplatin treatments were for 1 hour in all experiments. Dimethyl sulfoxide (DMSO) was the diluent for all Taxol stock solutions. Separately, the effects of Taxol and DMSO on cisplatin cellular accumulation were measured. End points reported include measures of cytotoxicity and Taxol effects on cisplatin cellular accumulation. Using a microculture tetrazolium assay, cisplatin growth curves were obtained under the influence of Taxol, at a Taxol dose of 3 nM for both cell lines. DMSO alone had no effect on tumor cell growth. In A2780 cells, the influence of Taxol on cisplatin cytotoxicity was modest, whereas cisplatin-induced cell kill was augmented 1.5-fold when cisplatin was given immediately after Taxol. In A2780/CP70 cells, Taxol augmented cisplatin-induced cell kill by 30-fold when cisplatin was given immediately after Taxol; 75-fold when cisplatin was given 24 hours after completion of Taxol; and 19-fold when cisplatin was given 48 hours after completion of Taxol.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Journal of the National Cancer Institute. Monographs AU - Parker, R J AU - Dabholkar, M D AU - Lee, K B AU - Bostick-Bruton, F AU - Reed, E AD - Medicine Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 83 EP - 88 IS - 15 SN - 1052-6773, 1052-6773 KW - Paclitaxel KW - P88XT4IS4D KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Drug Interactions KW - Tumor Cells, Cultured KW - DNA Damage KW - Humans KW - Female KW - Cisplatin -- pharmacokinetics KW - Ovarian Neoplasms -- metabolism KW - Ovarian Neoplasms -- pathology KW - Cisplatin -- pharmacology KW - Paclitaxel -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76282367?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute.+Monographs&rft.atitle=Taxol+effect+on+cisplatin+sensitivity+and+cisplatin+cellular+accumulation+in+human+ovarian+cancer+cells.&rft.au=Parker%2C+R+J%3BDabholkar%2C+M+D%3BLee%2C+K+B%3BBostick-Bruton%2C+F%3BReed%2C+E&rft.aulast=Parker&rft.aufirst=R&rft.date=1993-01-01&rft.volume=&rft.issue=15&rft.spage=83&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute.+Monographs&rft.issn=10526773&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-08-04 N1 - Date created - 1994-08-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - A reassessment of cardiac toxicity associated with Taxol. AN - 76281579; 7912518 AB - Cardiac toxicity was first noted in patients receiving Taxol during continuous cardiac monitoring, which was performed because of the high incidence of serious hypersensitivity reactions noted early in phase I trials. After cardiac events were documented, patients with cardiac disease and those on medications known to alter cardiac conduction were excluded from most trials. The cardiac events reported with Taxol from the initiation of NCI-sponsored clinical trials through August 1992 are summarized. Adverse cardiac events were reviewed in four clinical databases: 1) the Cancer Therapy Evaluation Program's Adverse Drug Reaction database following treatment of more than 3400 patients; 2) all cardiac toxicities in patients on GOG-111 who were randomized to cisplatin plus either Taxol or cyclophosphamide; 3) cardiac toxicity in 198 patients who received 618 courses of Taxol with or without cisplatin during continuous cardiac monitoring; and 4) cardiac toxicities reported for the first 696 patients on NCI TRC-9103 for ovarian cancer. Published reports of studies of taxine's cardiac effects, and of cardiac toxicity associated with yew poisoning, Cremophor EL, and H1 and H2 antagonists, are also reviewed. In patients without significant cardiac risk factors, asymptomatic sinus bradycardia is frequent (approximately 30%). Heart block and conduction abnormalities occur infrequently and are often asymptomatic. The casual relationship of Taxol to atrial and ventricular arrhythmias and cardiac ischemia is less clear because many patients had other conditions known to be associated with cardiac events. Nevertheless, the incidence of serious cardiac events was low. Routine cardiac monitoring is not required for patients without risk factors. There are, however, insufficient data to make treatment recommendations for patients with cardiac disease and those taking medications that alter cardiac conduction. To maximize patient safety and the clinical database, physicians who administer Taxol should continue to be alert to potential cardiac toxicities associated with Taxol. JF - Journal of the National Cancer Institute. Monographs AU - Arbuck, S G AU - Strauss, H AU - Rowinsky, E AU - Christian, M AU - Suffness, M AU - Adams, J AU - Oakes, M AU - McGuire, W AU - Reed, E AU - Gibbs, H AD - Investigational Drug Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 117 EP - 130 IS - 15 SN - 1052-6773, 1052-6773 KW - Polyethylene Glycols KW - 30IQX730WE KW - cremophor KW - 39279-69-1 KW - Paclitaxel KW - P88XT4IS4D KW - Index Medicus KW - Animals KW - Arrhythmias, Cardiac -- chemically induced KW - Myocardial Infarction -- chemically induced KW - Humans KW - Polyethylene Glycols -- administration & dosage KW - Ovarian Neoplasms -- drug therapy KW - Female KW - Paclitaxel -- administration & dosage KW - Paclitaxel -- adverse effects KW - Heart Diseases -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76281579?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute.+Monographs&rft.atitle=A+reassessment+of+cardiac+toxicity+associated+with+Taxol.&rft.au=Arbuck%2C+S+G%3BStrauss%2C+H%3BRowinsky%2C+E%3BChristian%2C+M%3BSuffness%2C+M%3BAdams%2C+J%3BOakes%2C+M%3BMcGuire%2C+W%3BReed%2C+E%3BGibbs%2C+H&rft.aulast=Arbuck&rft.aufirst=S&rft.date=1993-01-01&rft.volume=&rft.issue=15&rft.spage=117&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute.+Monographs&rft.issn=10526773&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-08-04 N1 - Date created - 1994-08-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Dose-dependent inhibition of aspartate carbamoyltransferase in peripheral blood mononuclear cells in patients receiving N-(phosphonacetyl)-L-aspartate. AN - 76266355; 8178710 AB - Forty-eight patients with adenocarcinoma of the gastrointestinal tract were treated on this trial. The MTD of 5-FU given as a 72 hour infusion with high-dose leucovorin was initially determined to be 2000 mg/m2/d. Patients were treated at PALA dose levels ranging from 250 to 2848 mg/m2. Biochemical assessment of target enzyme activity was performed at each PALA dose level. We conclude that compared to each patient's own baseline, PALA at 250 mg/m2 failed to appreciably inhibit ACTase activity at 24 hours in most patients. More consistent inhibition of ACTase activity was seen with PALA at or above 1266 mg/m2, but toxicity was prohibitive with 2848 mg/m2 PALA. Even with the highest PALA doses, ACTase activity was back to baseline by 96 hours in most patients. PALA at 1266 mg/m2 given 24 hours prior to the start of 72 hour infusional 5-FU plus high-dose leucovorin was associated with acceptable toxicity and did not appear to compromise 5-FU dose-intensity. Finally, because of interpatient variability in the degree of ACTase inhibition following PALA, biochemical monitoring of target enzyme activity may permit more rational adjustment of the PALA dose in individual patients. JF - Advances in experimental medicine and biology AU - Grem, J L AU - McAtee, N AU - Drake, J C AU - Steinberg, S AU - Allegra, C J AD - National Cancer Institute, National Naval Medical Center, Bethesda, MD 20889-5105. Y1 - 1993 PY - 1993 DA - 1993 SP - 119 EP - 123 VL - 339 SN - 0065-2598, 0065-2598 KW - Antineoplastic Agents KW - 0 KW - Aspartic Acid KW - 30KYC7MIAI KW - sparfosic acid KW - 78QVZ7RG8L KW - Aspartate Carbamoyltransferase KW - EC 2.1.3.2 KW - Phosphonoacetic Acid KW - N919E46723 KW - Index Medicus KW - Dose-Response Relationship, Drug KW - Humans KW - Leukocytes, Mononuclear -- enzymology KW - Aspartic Acid -- administration & dosage KW - Aspartic Acid -- analogs & derivatives KW - Antineoplastic Agents -- administration & dosage KW - Phosphonoacetic Acid -- analogs & derivatives KW - Phosphonoacetic Acid -- administration & dosage KW - Aspartate Carbamoyltransferase -- antagonists & inhibitors KW - Leukocytes, Mononuclear -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76266355?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advances+in+experimental+medicine+and+biology&rft.atitle=Dose-dependent+inhibition+of+aspartate+carbamoyltransferase+in+peripheral+blood+mononuclear+cells+in+patients+receiving+N-%28phosphonacetyl%29-L-aspartate.&rft.au=Grem%2C+J+L%3BMcAtee%2C+N%3BDrake%2C+J+C%3BSteinberg%2C+S%3BAllegra%2C+C+J&rft.aulast=Grem&rft.aufirst=J&rft.date=1993-01-01&rft.volume=339&rft.issue=&rft.spage=119&rft.isbn=&rft.btitle=&rft.title=Advances+in+experimental+medicine+and+biology&rft.issn=00652598&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-06-07 N1 - Date created - 1994-06-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Purine analogs in lymphoproliferative disorders. AN - 76256165; 7907252 JF - Leukemia & lymphoma AU - Cheson, B D AD - Medicine Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 153 EP - 159 VL - 11 Suppl 2 SN - 1042-8194, 1042-8194 KW - Antineoplastic Agents KW - 0 KW - Pentostatin KW - 395575MZO7 KW - Cladribine KW - 47M74X9YT5 KW - Vidarabine KW - FA2DM6879K KW - fludarabine KW - P2K93U8740 KW - Index Medicus KW - Lymphoma, Non-Hodgkin -- drug therapy KW - Leukemia -- drug therapy KW - Multiple Myeloma -- drug therapy KW - Humans KW - Vidarabine -- analogs & derivatives KW - Lymphoproliferative Disorders -- drug therapy KW - Cladribine -- adverse effects KW - Pentostatin -- adverse effects KW - Cladribine -- therapeutic use KW - Vidarabine -- therapeutic use KW - Antineoplastic Agents -- therapeutic use KW - Vidarabine -- adverse effects KW - Pentostatin -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76256165?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Leukemia+%26+lymphoma&rft.atitle=Purine+analogs+in+lymphoproliferative+disorders.&rft.au=Cheson%2C+B+D&rft.aulast=Cheson&rft.aufirst=B&rft.date=1993-01-01&rft.volume=11+Suppl+2&rft.issue=&rft.spage=153&rft.isbn=&rft.btitle=&rft.title=Leukemia+%26+lymphoma&rft.issn=10428194&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-04-13 N1 - Date created - 1994-04-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Do benzodiazepine ligands contribute to hepatic encephalopathy? AN - 76239920; 8116487 AB - 1. Levels of BZ receptor ligands are elevated in the brain of animal models of FHF and humans with FHF. Some of these ligands have agonist properties and some are known 1, 4-BZs which bind to the DS receptor. Much of the BZ receptor ligand activity in HE is unidentified and it is possible that some may bind to receptor subtypes other than the DS receptor. 2. Average levels of BZ receptor ligands in the brain in HE do not appear to be sufficient to augment GABAergic tone to a degree that would result in severe encephalopathy (i.e. coma). However, these ligands have a heterogeneous distribution in the brain and their neuroinhibitory effects may be potentiated by increased availability of GABA at GABAA receptors. Furthermore, that these ligands may contribute to HE is suggested by anecdotal reports of ameliorations of HE being induced in a majority of patients by the BZ receptor antagonist flumazenil. 3. The response of HE to flumazenil in humans is usually incomplete and in animal models may be modest. Potential explanations for these findings include pharmacokinetics, BZ receptor subtype specificity and higher levels of BZ receptor ligands in the brain in humans with HE than in animal models. 4. Certain BZ receptor ligands e.g. Ro 15-3505 and Ro 15-4513, that are structurally related to flumazenil, are more efficacious at ameliorating HE than flumazenil in animal models. These findings may be more dependent on differences in BZ receptor subtype specificity than differences in intrinsic activity. The properties of an ideal BZ receptor ligand for administration to a patient with HE would appear to be: (i) antagonist action at BZ receptors, (ii) no intrinsic activity apparent after a conventional pharmacologic dose, (iii) high specificity and affinity for BZ receptors, (iv) slow metabolism, and (v) absence of toxic effects. Promising ligands, such as Ro 15-3505, with weak partial inverse agonist actions and hence analeptic potential, require careful evaluation of their therapeutic index before clinical application. 5. BZ receptor ligands may be useful in the management of HE. Specifically, they may be given IV: (i) to reverse effects of exogenous BZs; (ii) to aid in the differential diagnosis of encephalopathy; (iii) to provide prognostic information; and (iv) to optimize brain function. They may also be given orally with the objective of reducing dietary protein intolerance in patients with chronic liver disease. JF - Advances in experimental medicine and biology AU - Jones, E A AU - Basile, A S AU - Yurdaydin, C AU - Skolnich, P AD - Liver Disease Section, NIDDK, National Institutes of Health, Bethesda, Maryland. Y1 - 1993 PY - 1993 DA - 1993 SP - 57 EP - 69 VL - 341 SN - 0065-2598, 0065-2598 KW - Azides KW - 0 KW - Benzodiazepinones KW - GABA-A Receptor Antagonists KW - Ligands KW - Receptors, GABA-A KW - Benzodiazepines KW - 12794-10-4 KW - Flumazenil KW - 40P7XK9392 KW - Ro 15-3505 KW - 78756-33-9 KW - Ro 15-4513 KW - 91917-65-6 KW - Index Medicus KW - Benzodiazepinones -- therapeutic use KW - Animals KW - Humans KW - Flumazenil -- therapeutic use KW - Disease Models, Animal KW - Azides -- therapeutic use KW - Hepatic Encephalopathy -- drug therapy KW - Benzodiazepines -- therapeutic use KW - Receptors, GABA-A -- physiology KW - Hepatic Encephalopathy -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76239920?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advances+in+experimental+medicine+and+biology&rft.atitle=Do+benzodiazepine+ligands+contribute+to+hepatic+encephalopathy%3F&rft.au=Jones%2C+E+A%3BBasile%2C+A+S%3BYurdaydin%2C+C%3BSkolnich%2C+P&rft.aulast=Jones&rft.aufirst=E&rft.date=1993-01-01&rft.volume=341&rft.issue=&rft.spage=57&rft.isbn=&rft.btitle=&rft.title=Advances+in+experimental+medicine+and+biology&rft.issn=00652598&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-03-31 N1 - Date created - 1994-03-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - 6-[18F]fluoro-L-dopa and cerebral blood flow in unilaterally MPTP-treated monkeys. AN - 76229957; 7509198 AB - Intravenous administration of 15O-labeled water and 6-[18F]-L-fluorodopa were used to assess abnormal striatal activity in monkeys after long-term recovery of unilateral lesions of the dopaminergic nigro-striatal system induced by the neurotoxin MPTP. PET data were examined in relation to behavioral and biological parameters. Cerebral blood flow and 6-[18F]-L-DOPA uptake were found to be significantly reduced in the lesioned striatum, compared to the unaffected side and to normal controls. There was no correlation between cerebral blood flow and any of the behavioral parameters. The uptake rate constant of 18F-DOPA from blood to striatum and the ratios of striatum to occipital areas were highly correlated to the concentrations of homovanillic acid in the cerebrospinal fluid of the same animals but not to the rotational behavior. This MPTP-induced model of striatal dopamine deficiency in primates presents similarities with idiopathic Parkinson's disease and may be used to evaluate the effects of dopaminergic lesions and transplants on brain function. JF - Journal of neural transplantation & plasticity AU - Doudet, D J AU - Wyatt, R J AU - Cannon-Spoor, E AU - Suddath, R AU - McLellan, C A AU - Cohen, R M AD - Clinical Brain Imaging Section, NIMH, Bethesda, MD 20892. PY - 1993 SP - 27 EP - 38 VL - 4 IS - 1 SN - 0792-8483, 0792-8483 KW - fluorodopa F 18 KW - 2C598205QX KW - Methoxyhydroxyphenylglycol KW - 534-82-7 KW - Hydroxyindoleacetic Acid KW - 54-16-0 KW - Dihydroxyphenylalanine KW - 63-84-3 KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Dopamine KW - VTD58H1Z2X KW - Homovanillic Acid KW - X77S6GMS36 KW - Index Medicus KW - Animals KW - Injections, Intra-Arterial KW - Dopamine -- metabolism KW - Hydroxyindoleacetic Acid -- cerebrospinal fluid KW - Basal Ganglia -- blood supply KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- administration & dosage KW - Behavior, Animal -- drug effects KW - Homovanillic Acid -- cerebrospinal fluid KW - Methoxyhydroxyphenylglycol -- cerebrospinal fluid KW - Occipital Lobe -- blood supply KW - Carotid Artery, Internal KW - Occipital Lobe -- metabolism KW - Tomography, Emission-Computed KW - Macaca mulatta KW - Male KW - Basal Ganglia -- metabolism KW - Parkinson Disease, Secondary -- physiopathology KW - Parkinson Disease, Secondary -- chemically induced KW - MPTP Poisoning KW - Corpus Striatum -- metabolism KW - Parkinson Disease, Secondary -- cerebrospinal fluid KW - Corpus Striatum -- blood supply KW - Cerebrovascular Circulation KW - Dihydroxyphenylalanine -- pharmacokinetics KW - Dihydroxyphenylalanine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76229957?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neural+transplantation+%26+plasticity&rft.atitle=6-%5B18F%5Dfluoro-L-dopa+and+cerebral+blood+flow+in+unilaterally+MPTP-treated+monkeys.&rft.au=Doudet%2C+D+J%3BWyatt%2C+R+J%3BCannon-Spoor%2C+E%3BSuddath%2C+R%3BMcLellan%2C+C+A%3BCohen%2C+R+M&rft.aulast=Doudet&rft.aufirst=D&rft.date=1993-01-01&rft.volume=4&rft.issue=1&rft.spage=27&rft.isbn=&rft.btitle=&rft.title=Journal+of+neural+transplantation+%26+plasticity&rft.issn=07928483&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-03-25 N1 - Date created - 1994-03-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The strength of binding of the weakly-binding crossbridge created by sulfhydryl modification has very low calcium sensitivity. AN - 76228013; 8109326 AB - The acto-subfragment-1.ATP state is an important intermediate in the Ca-activated acto-S1 ATPase reaction, suggesting that the myosin.ATP crossbridge seen in muscle fibers similarly may be an important intermediate in the contractile cycle. Treatment of muscle fibers with either para-phenylenedimaleimide (pPDM) or N-phenylmaleimide (NPM) alters the myosin crossbridges so that they bind to the actin filament with about the same affinity as the myosin.ATP crossbridge. Additionally, the treated crossbridges and the myosin.ATP crossbridge have virtually identical attachment and detachment rate constants. Thus the treated crossbridges appear to be reasonable analogues of the weakly-binding myosin.ATP crossbridges of relaxed fibers and studies of the treated fibers may shed some light on the behavior of the physiologically important myosin.ATP crossbridge. We have examined the influence of Ca2+ on the binding and rate constants of pPDM- and NPM-treated weakly-binding crossbridges. In agreement with earlier solution studies, we found almost no Ca-sensitivity of the binding of pPDM- or NPM-treated crossbridges. JF - Advances in experimental medicine and biology AU - Barnett, V A AU - Schoenberg, M AD - Laboratory of Physical Biology, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 133 EP - 8; discussion 138-40 VL - 332 SN - 0065-2598, 0065-2598 KW - Alkylating Agents KW - 0 KW - Maleimides KW - Myosin Subfragments KW - Sulfhydryl Compounds KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - N-phenylmaleimide KW - 9U9KT462VW KW - N,N'-4-phenylenedimaleimide KW - BEC7P1E6J1 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Protein Binding -- drug effects KW - Alkylating Agents -- pharmacology KW - Myosin Subfragments -- chemistry KW - Rabbits KW - Myosin Subfragments -- drug effects KW - Maleimides -- pharmacology KW - Adenosine Triphosphate -- chemistry KW - Calcium -- chemistry KW - Sulfhydryl Compounds -- chemistry KW - Psoas Muscles -- physiology KW - Psoas Muscles -- drug effects KW - Psoas Muscles -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76228013?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advances+in+experimental+medicine+and+biology&rft.atitle=The+strength+of+binding+of+the+weakly-binding+crossbridge+created+by+sulfhydryl+modification+has+very+low+calcium+sensitivity.&rft.au=Barnett%2C+V+A%3BSchoenberg%2C+M&rft.aulast=Barnett&rft.aufirst=V&rft.date=1993-01-01&rft.volume=332&rft.issue=&rft.spage=133&rft.isbn=&rft.btitle=&rft.title=Advances+in+experimental+medicine+and+biology&rft.issn=00652598&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-03-21 N1 - Date created - 1994-03-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Glutathione-related enzymes, glutathione and multidrug resistance. AN - 76225955; 7765324 AB - This review examines the hypothesis that glutathione and its associated enzymes contribute to the overall drug-resistance seen in multidrug resistant cell lines. Reports of 34 cell lines independently selected for resistance to MDR drugs are compared for evidence of consistent changes in activity of glutathione-related enzymes as well as for changes in glutathione content. The role of glutathione S-transferases in MDR is further analyzed by comparing changes in sensitivity to MDR drugs in cell lines selected for resistance to non-MDR drugs that have resulting increases in glutathione S-transferase activity. In addition, results of studies in which genes for glutathione S-transferase isozymes were transfected into drug-sensitive cells are reviewed. The role of the glutathione redox cycle is examined by comparing changes in elements of this cycle in MDR cell lines as well as by analyzing reports of the effects of glutathione depletion on MDR drug sensitivity. Overall, there is no consistent or compelling evidence that glutathione and its associated enzymes augment resistance in multidrug resistant cell lines. JF - Cytotechnology AU - Moscow, J A AU - Dixon, K H AD - Medicine Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 155 EP - 170 VL - 12 IS - 1-3 SN - 0920-9069, 0920-9069 KW - Antineoplastic Agents KW - 0 KW - Carrier Proteins KW - Membrane Glycoproteins KW - P-Glycoprotein KW - Glutathione Transferase KW - EC 2.5.1.18 KW - Glutathione KW - GAN16C9B8O KW - Biotechnology KW - Oxidation-Reduction KW - Animals KW - Tumor Cells, Cultured KW - Humans KW - Female KW - Cell Line KW - Drug Resistance -- physiology KW - Drug Resistance -- genetics KW - Membrane Glycoproteins -- biosynthesis KW - Carrier Proteins -- metabolism KW - Glutathione -- metabolism KW - Carrier Proteins -- genetics KW - Glutathione Transferase -- metabolism KW - Glutathione Transferase -- biosynthesis KW - Antineoplastic Agents -- toxicity KW - Carrier Proteins -- biosynthesis KW - Membrane Glycoproteins -- metabolism KW - Membrane Glycoproteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76225955?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nursing+Standard+%282014%2B%29&rft.atitle=Patient+safety&rft.au=Young%2C+Lorna&rft.aulast=Young&rft.aufirst=Lorna&rft.date=2014-02-19&rft.volume=28&rft.issue=25&rft.spage=54&rft.isbn=&rft.btitle=&rft.title=Nursing+Standard+%282014%2B%29&rft.issn=00296570&rft_id=info:doi/10.7748%2Fns2014.02.28.25.54.s47 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-03-31 N1 - Date created - 1994-03-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The relationship between ethanol intake and DSM-III-R alcohol dependence: results of a national survey. AN - 76224436; 8312731 AB - Data from a representative sample of U.S. adults were analyzed to determine the association between average daily ethanol consumption and DSM-III-R (American Psychiatric Association, 1987) alcohol dependence adjusting for heavier drinking (i.e., drinking 5+ drinks on any one occasion) and sociodemographic variables, including age of onset of drinking and family history of alcoholism. Male gender, early onset of drinking, and drinking 5+ drinks on any one occasion during the past year were all associated with an increased risk of dependence. Factors associated with a decreased risk of dependence were age, being currently married, total body water, and income. The risk of dependence varied among population subgroups and was increased by nonblack race and positive family histories of alcoholism in the respondent's relatives. JF - Journal of substance abuse AU - Grant, B F AD - Division of Biometry and Epidemiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20857. Y1 - 1993 PY - 1993 DA - 1993 SP - 257 EP - 267 VL - 5 IS - 3 SN - 0899-3289, 0899-3289 KW - Ethanol KW - 3K9958V90M KW - Index Medicus KW - Humans KW - Ethanol -- administration & dosage KW - Aged KW - Socioeconomic Factors KW - Cross-Sectional Studies KW - Risk Factors KW - Adult KW - Incidence KW - Middle Aged KW - Adolescent KW - United States -- epidemiology KW - Female KW - Male KW - Alcoholism -- epidemiology KW - Alcoholism -- diagnosis KW - Alcohol Drinking -- psychology KW - Alcohol Drinking -- adverse effects KW - Alcohol Drinking -- genetics KW - Psychiatric Status Rating Scales -- statistics & numerical data KW - Alcoholism -- genetics KW - Alcohol Drinking -- epidemiology KW - Alcoholism -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76224436?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+substance+abuse&rft.atitle=The+relationship+between+ethanol+intake+and+DSM-III-R+alcohol+dependence%3A+results+of+a+national+survey.&rft.au=Grant%2C+B+F&rft.aulast=Grant&rft.aufirst=B&rft.date=1993-01-01&rft.volume=5&rft.issue=3&rft.spage=257&rft.isbn=&rft.btitle=&rft.title=Journal+of+substance+abuse&rft.issn=08993289&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-03-23 N1 - Date created - 1994-03-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Cisplatin. AN - 76223157; 8312126 JF - Cancer chemotherapy and biological response modifiers AU - Dabholkar, M AU - Reed, E AD - Medicine Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD. Y1 - 1993 PY - 1993 DA - 1993 SP - 86 EP - 97 VL - 14 SN - 0921-4410, 0921-4410 KW - DNA-Binding Proteins KW - 0 KW - Platinum KW - 49DFR088MY KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Drug Resistance -- physiology KW - Platinum -- chemistry KW - Humans KW - DNA-Binding Proteins -- drug effects KW - Gene Expression Regulation, Neoplastic -- drug effects KW - Cisplatin -- therapeutic use KW - DNA Damage KW - Cisplatin -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76223157?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+chemotherapy+and+biological+response+modifiers&rft.atitle=Cisplatin.&rft.au=Dabholkar%2C+M%3BReed%2C+E&rft.aulast=Dabholkar&rft.aufirst=M&rft.date=1993-01-01&rft.volume=14&rft.issue=&rft.spage=86&rft.isbn=&rft.btitle=&rft.title=Cancer+chemotherapy+and+biological+response+modifiers&rft.issn=09214410&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-03-22 N1 - Date created - 1994-03-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Antimetabolites. AN - 76218441; 8312100 JF - Cancer chemotherapy and biological response modifiers AU - Chu, E AU - Johnston, P G AU - Takimoto, C H AU - Politi, P M AU - Grem, J L AU - Chabner, B A AU - Allegra, C J AD - NCI-Navy Medical Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD. Y1 - 1993 PY - 1993 DA - 1993 SP - 1 EP - 25 VL - 14 SN - 0921-4410, 0921-4410 KW - Antimetabolites, Antineoplastic KW - 0 KW - Purines KW - Floxuridine KW - 039LU44I5M KW - Cytarabine KW - 04079A1RDZ KW - Fluorouracil KW - U3P01618RT KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - Cytarabine -- pharmacology KW - Fluorouracil -- adverse effects KW - Drug Resistance -- physiology KW - Methotrexate -- pharmacology KW - Floxuridine -- pharmacology KW - Humans KW - Purines -- pharmacology KW - Fluorouracil -- pharmacology KW - Drug Design KW - Antimetabolites, Antineoplastic -- pharmacokinetics KW - Antimetabolites, Antineoplastic -- metabolism KW - Antimetabolites, Antineoplastic -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76218441?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+chemotherapy+and+biological+response+modifiers&rft.atitle=Antimetabolites.&rft.au=Chu%2C+E%3BJohnston%2C+P+G%3BTakimoto%2C+C+H%3BPoliti%2C+P+M%3BGrem%2C+J+L%3BChabner%2C+B+A%3BAllegra%2C+C+J&rft.aulast=Chu&rft.aufirst=E&rft.date=1993-01-01&rft.volume=14&rft.issue=&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Cancer+chemotherapy+and+biological+response+modifiers&rft.issn=09214410&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-03-22 N1 - Date created - 1994-03-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Histopathology of human intraepithelial neoplasia with implications for chemoprevention strategy. AN - 76217707; 8304941 JF - Basic life sciences AU - Boone, C W AU - Kelloff, G J AU - Steele, V E AD - Division of Cancer Prevention and Control, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 291 EP - 300 VL - 61 SN - 0090-5542, 0090-5542 KW - Anticarcinogenic Agents KW - 0 KW - 9,10-Dimethyl-1,2-benzanthracene KW - 57-97-6 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Uterine Cervical Neoplasms -- prevention & control KW - Tetradecanoylphorbol Acetate -- toxicity KW - Animals KW - Anticarcinogenic Agents -- therapeutic use KW - Aneuploidy KW - 9,10-Dimethyl-1,2-benzanthracene -- toxicity KW - Humans KW - Anticarcinogenic Agents -- pharmacology KW - Mice KW - Epithelium -- pathology KW - Uterine Cervical Neoplasms -- pathology KW - Female KW - Neoplasms -- pathology KW - Skin Neoplasms -- chemically induced KW - Skin Neoplasms -- pathology KW - Neoplasms -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76217707?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Basic+life+sciences&rft.atitle=Histopathology+of+human+intraepithelial+neoplasia+with+implications+for+chemoprevention+strategy.&rft.au=Boone%2C+C+W%3BKelloff%2C+G+J%3BSteele%2C+V+E&rft.aulast=Boone&rft.aufirst=C&rft.date=1993-01-01&rft.volume=61&rft.issue=&rft.spage=291&rft.isbn=&rft.btitle=&rft.title=Basic+life+sciences&rft.issn=00905542&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-03-07 N1 - Date created - 1994-03-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Tolerance of small bowel anastomoses in rabbits to photodynamic therapy with dihematoporphyrin ethers and 630 nm red light. AN - 76203390; 8295476 AB - Photodynamic therapy (PDT) is being evaluated in experimental clinical trials in patients with peritoneal malignancies. Some patients require partial small bowel resection with re-anastomosis prior to PDT because of bulky tumor or focal involvement of the small bowel by tumor. To assess the safety of PDT in this setting, the tolerance of small bowel anastomoses in New Zealand white rabbits to PDT with dihematoporphyrin ethers (DHE) and 630 nm light was studied. With conventional DHE doses of 1.5-2.5 mg/kg given 24 hours prior to surgery and light doses of 0-20 J/cm2 of 630 nm light, no adverse effects were seen on the healing of small bowel anastomoses. Higher photosensitizer doses of 10 mg/kg and 20 mg/kg in conjunction with 20 J/cm2, however, induced failure and breakdown of fresh anastomoses in 2/3 and 4/4 animals, respectively. JF - Lasers in surgery and medicine AU - DeLaney, T F AU - Sindelar, W F AU - Thomas, G F AU - DeLuca, A M AU - Taubenberger, J K AD - Radiation Oncology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 664 EP - 671 VL - 13 IS - 6 SN - 0196-8092, 0196-8092 KW - Dihematoporphyrin Ether KW - 97067-70-4 KW - Index Medicus KW - Animals KW - Anastomosis, Surgical KW - Random Allocation KW - Reoperation KW - Rabbits KW - Laser Therapy KW - Dihematoporphyrin Ether -- therapeutic use KW - Photochemotherapy -- adverse effects KW - Intestine, Small -- drug effects KW - Intestine, Small -- surgery KW - Intestine, Small -- pathology KW - Intestine, Small -- radiation effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76203390?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Lasers+in+surgery+and+medicine&rft.atitle=Tolerance+of+small+bowel+anastomoses+in+rabbits+to+photodynamic+therapy+with+dihematoporphyrin+ethers+and+630+nm+red+light.&rft.au=DeLaney%2C+T+F%3BSindelar%2C+W+F%3BThomas%2C+G+F%3BDeLuca%2C+A+M%3BTaubenberger%2C+J+K&rft.aulast=DeLaney&rft.aufirst=T&rft.date=1993-01-01&rft.volume=13&rft.issue=6&rft.spage=664&rft.isbn=&rft.btitle=&rft.title=Lasers+in+surgery+and+medicine&rft.issn=01968092&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-03-01 N1 - Date created - 1994-03-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Strategies for detecting subclinical monoamine depletions in humans. AN - 76178230; 8289914 AB - Given the reported increase in the recreational use of controlled substance analogs such as MDMA and related drugs, it is important to determine whether these drugs produce neurotoxic effects in humans. Several strategies available for detecting preclinical neurotoxicity to dopamine and serotonin neurons have been discussed, and their strengths and limitations have been listed. In addition, some promising strategies that are still in the development stage (e.g., PET) have been mentioned. None of the available methods for detecting neurotoxicity is conclusive; therefore, converging lines of evidence will be essential to provide convincing indication of subclinical neurotoxicity in humans. Such studies will help define the public health risk of recreationally used drugs. Furthermore, documentation and determination of drug-induced neurotoxic changes may shed light on the pathophysiology of idiopathic neurodegenerative diseases involving monoaminergic neurons in humans and could be useful in the development of new treatment strategies. Finally, detailed neuropsychiatric evaluation of individuals with confirmed subclinical serotonergic neurotoxicity may enhance knowledge regarding the functional role of brain serotonin neurons in health and disease. JF - NIDA research monograph AU - McCann, U D AU - Ricaurte, G A AD - Section of Anxiety and Affective Disorders, National Institutes of Mental Health, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 53 EP - 60; discussion 60-2 VL - 136 SN - 1046-9516, 1046-9516 KW - Serotonin KW - 333DO1RDJY KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Hypothalamo-Hypophyseal System -- physiology KW - Humans KW - Tomography, Emission-Computed KW - Pituitary-Adrenal System -- physiology KW - Serotonin -- analysis KW - Brain -- drug effects KW - Dopamine -- analysis KW - Brain -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76178230?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Strategies+for+detecting+subclinical+monoamine+depletions+in+humans.&rft.au=McCann%2C+U+D%3BRicaurte%2C+G+A&rft.aulast=McCann&rft.aufirst=U&rft.date=1993-01-01&rft.volume=136&rft.issue=&rft.spage=53&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-02-23 N1 - Date created - 1994-02-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Medications development at the National Institute on Drug Abuse: focus on cocaine. AN - 76178188; 8289904 AB - NIDA's MDD is faced with the formidable task of identifying, characterizing, and developing new chemical entities to combat substance abuse. The primary challenge is to find one or more medications that will be useful in treating cocaine addiction, withdrawal, and abstinence. In addition, a treatment for cocaine overdose is in progress. Methodological approaches include testing compounds that alter endogenous neurotransmitters and compounds that suppress conditioned cues and stimuli. Compounds that appear efficacious in these tasks and that have a satisfactory safety profile will be studied in humans. JF - NIDA research monograph AU - Johnson, D N AU - Vocci, F J AD - Medications Development Division, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1993 PY - 1993 DA - 1993 SP - 57 EP - 70 VL - 135 SN - 1046-9516, 1046-9516 KW - Bromocriptine KW - 3A64E3G5ZO KW - Cocaine KW - I5Y540LHVR KW - Desipramine KW - TG537D343B KW - Index Medicus KW - Desipramine -- therapeutic use KW - Humans KW - Bromocriptine -- therapeutic use KW - Substance Withdrawal Syndrome -- drug therapy KW - Substance-Related Disorders -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76178188?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Medications+development+at+the+National+Institute+on+Drug+Abuse%3A+focus+on+cocaine.&rft.au=Johnson%2C+D+N%3BVocci%2C+F+J&rft.aulast=Johnson&rft.aufirst=D&rft.date=1993-01-01&rft.volume=135&rft.issue=&rft.spage=57&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-02-23 N1 - Date created - 1994-02-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Treatment of cocaine abusers: issues and perspectives. AN - 76173420; 8289890 JF - NIDA research monograph AU - Tims, F M AU - Leukefeld, C G AD - Treatment Services Research Branch, National Institute on Drug Abuse, National Institutes of Health, Rockville, MD 20857. Y1 - 1993 PY - 1993 DA - 1993 SP - 1 EP - 14 VL - 135 SN - 1046-9516, 1046-9516 KW - Cocaine KW - I5Y540LHVR KW - Methadone KW - UC6VBE7V1Z KW - Index Medicus KW - Psychotherapy KW - Humans KW - Treatment Outcome KW - Substance-Related Disorders -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76173420?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Treatment+of+cocaine+abusers%3A+issues+and+perspectives.&rft.au=Tims%2C+F+M%3BLeukefeld%2C+C+G&rft.aulast=Tims&rft.aufirst=F&rft.date=1993-01-01&rft.volume=135&rft.issue=&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-02-23 N1 - Date created - 1994-02-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Therapeutic efficacy of a high-affinity anticarcinoembryonic antigen monoclonal antibody (COL-1). AN - 76170868; 8292968 AB - COL-1 is a murine IgG2a monoclonal antibody (MAb) with a high affinity (1.4 x 10(9) M-1) for carcinoembryonic antigen (CEA) and no detectable reactivity for CEA-related antigens, such as nonspecific cross-reacting antigen (NCA) and normal fecal antigen (NFA). 125I-labeled COL-1 IgG was shown to efficiently and specifically target the LS-174T human colon carcinoma xenograft in athymic mice. Dose titration studies in this same model with 131I-labeled COL-1 demonstrated reduction of tumor growth rate when 300 microCi of the immunoconjugate was used (0.005 > p > 0.001). Administration of higher levels as a single dose led to increased toxicity. Dose fractionation experiments with 131I-COL-1 demonstrated the ability to administer much higher levels of the immunoconjugate with little or no toxicity, which resulted in a greater therapeutic efficacy. For example, three fractions of 200 microCi of 131I-COL-1 given at weekly intervals (for a total of 600 microCi) resulted in the substantial reduction (p < 0.0005) of the growth of established tumors in 100% (7/7) of mice, and in no evidence of tumor growth in 71% (5/7) of mice, at the end of the 63-day observation period. These results thus demonstrate the potential therapeutic efficacy for radiolabeled COL-1 in clinical trials and demonstrate the principle of the advantage of dose fractionation protocols for this immunoconjugate. JF - Biotechnology therapeutics AU - Siler, K AU - Eggensperger, D AU - Hand, P H AU - Milenic, D E AU - Miller, L S AU - Houchens, D P AU - Hinkle, G AU - Schlom, J AD - Laboratory of Tumor Immunology and Biology, National Cancer Institute, Bethesda, Maryland. Y1 - 1993 PY - 1993 DA - 1993 SP - 163 EP - 181 VL - 4 IS - 3-4 SN - 0898-2848, 0898-2848 KW - Antibodies, Monoclonal KW - 0 KW - Carcinoembryonic Antigen KW - Immunotoxins KW - Iodine Radioisotopes KW - Index Medicus KW - Neoplasm Transplantation KW - Adenocarcinoma, Mucinous -- radiotherapy KW - Animals KW - Tumor Cells, Cultured KW - Humans KW - Transplantation, Heterologous KW - Mice, Nude KW - Mice KW - Adenocarcinoma, Mucinous -- pathology KW - Female KW - Iodine Radioisotopes -- therapeutic use KW - Radioimmunotherapy KW - Colonic Neoplasms -- radiotherapy KW - Carcinoembryonic Antigen -- immunology KW - Iodine Radioisotopes -- administration & dosage KW - Immunotoxins -- therapeutic use KW - Immunotoxins -- administration & dosage KW - Colonic Neoplasms -- pathology KW - Antibodies, Monoclonal -- administration & dosage KW - Antibodies, Monoclonal -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76170868?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biotechnology+therapeutics&rft.atitle=Therapeutic+efficacy+of+a+high-affinity+anticarcinoembryonic+antigen+monoclonal+antibody+%28COL-1%29.&rft.au=Siler%2C+K%3BEggensperger%2C+D%3BHand%2C+P+H%3BMilenic%2C+D+E%3BMiller%2C+L+S%3BHouchens%2C+D+P%3BHinkle%2C+G%3BSchlom%2C+J&rft.aulast=Siler&rft.aufirst=K&rft.date=1993-01-01&rft.volume=4&rft.issue=3-4&rft.spage=163&rft.isbn=&rft.btitle=&rft.title=Biotechnology+therapeutics&rft.issn=08982848&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-02-28 N1 - Date created - 1994-02-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Advancing the application of behavioral treatment approaches for drug dependence. AN - 76168565; 8289928 JF - NIDA research monograph AU - Schuster, C R AU - Silverman, K AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1993 PY - 1993 DA - 1993 SP - 5 EP - 17 VL - 137 SN - 1046-9516, 1046-9516 KW - Index Medicus KW - Humans KW - Research KW - Substance-Related Disorders -- therapy KW - Behavior Therapy -- education KW - Substance-Related Disorders -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76168565?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Advancing+the+application+of+behavioral+treatment+approaches+for+drug+dependence.&rft.au=Schuster%2C+C+R%3BSilverman%2C+K&rft.aulast=Schuster&rft.aufirst=C&rft.date=1993-01-01&rft.volume=137&rft.issue=&rft.spage=5&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-02-23 N1 - Date created - 1994-02-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Influence of dietary protein concentration on severity of nephropathy in Fischer-344 (F-344/N) rats. AN - 76168426; 8290866 AB - Nephropathy is an age-related spontaneous disease of most rat strains, and protein content of diet may affect the severity. The purpose of this study was to determine the effect of a 15% protein nonpurified diet on body weight and severity of nephropathy in comparison to a 23% protein NIH-07 diet. Groups of 25 male and 25 female Fischer-344 (F-344) rats, 6 wk of age, were fed the 23 or 15% protein diet ad libitum for 2 yr. Rats were weighed at 1-4-wk intervals, and mean body weights were determined. Water consumption measurements and urinalysis were done at approximately 3-mo intervals during the second year of the study. At the end of the 2-yr study, kidneys from all rats, including those that died or were euthanatized after the eightieth week of the study, were examined by light microscopy and graded for severity of nephropathy as grades 1-4 (minimal, mild, moderate, marked). Growth patterns and the maximum body weights attained by each sex fed the 23 or 15% protein diet were not significantly different. The severity of nephropathy in male rats was significantly higher when fed the 23% protein diet (2.8 moderate to marked) compared to the 15% protein diet (1.3 minimal to mild). The severity of nephropathy in female rats increased slightly when fed the 23% protein diet (1.5 minimal to mild) compared to the 15% protein diet (1.0 minimal).(ABSTRACT TRUNCATED AT 250 WORDS) JF - Toxicologic pathology AU - Rao, G N AU - Edmondson, J AU - Elwell, M R AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993 PY - 1993 DA - 1993 SP - 353 EP - 361 VL - 21 IS - 4 SN - 0192-6233, 0192-6233 KW - Dietary Proteins KW - 0 KW - Index Medicus KW - Severity of Illness Index KW - Rats KW - Eating -- drug effects KW - Animals KW - Rats, Inbred F344 KW - Sex Factors KW - Dose-Response Relationship, Drug KW - Food, Formulated KW - Body Weight -- drug effects KW - Male KW - Female KW - Dietary Proteins -- toxicity KW - Kidney Diseases -- etiology KW - Dietary Proteins -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76168426?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+pathology&rft.atitle=Influence+of+dietary+protein+concentration+on+severity+of+nephropathy+in+Fischer-344+%28F-344%2FN%29+rats.&rft.au=Rao%2C+G+N%3BEdmondson%2C+J%3BElwell%2C+M+R&rft.aulast=Rao&rft.aufirst=G&rft.date=1993-01-01&rft.volume=21&rft.issue=4&rft.spage=353&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=01926233&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-02-24 N1 - Date created - 1994-02-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Decreased expression of manganese superoxide dismutase mRNA and protein after immortalization and transformation of mouse liver cells. AN - 76136704; 8260749 AB - Altered levels of superoxide dismutase (SOD), the enzyme that scavenges toxic superoxide anion produced during normal metabolism or after oxidative insult, have been implicated in multistage carcinogenesis of both rodents and humans. Using a mouse liver cell model, we report here that after cellular immortalization, both copper- and zinc-containing superoxide dismutase (Cu,ZnSOD) and manganese superoxide dismutase (MnSOD) activities decreased dramatically and that cellular transformation further decreased MnSOD but not Cu,ZnSOD activity. Decreased enzyme activities seen in transformed cells (Tx) were due to decreased amounts of immunoreactive enzyme protein that results from decreased superoxide dismutase mRNA expression. This downregulation of gene expression may occur at the transcriptional level, as suggested by results with cycloheximide (Chx) and actinomycin D (AcD) treatments. JF - Oncology research AU - Sun, Y AU - Colburn, N H AU - Oberley, L W AD - Cell Biology Section, National Cancer Institute, Frederick Cancer Research and Development Center, MD. Y1 - 1993 PY - 1993 DA - 1993 SP - 127 EP - 132 VL - 5 IS - 3 SN - 0965-0407, 0965-0407 KW - RNA, Messenger KW - 0 KW - Superoxide Dismutase KW - EC 1.15.1.1 KW - Index Medicus KW - Animals KW - Base Sequence KW - Down-Regulation KW - Molecular Sequence Data KW - Mice KW - Cell Line, Transformed KW - Mice, Inbred BALB C KW - Superoxide Dismutase -- analysis KW - Liver -- pathology KW - Liver -- enzymology KW - Gene Expression Regulation, Enzymologic KW - Cell Transformation, Neoplastic -- metabolism KW - RNA, Messenger -- analysis KW - Superoxide Dismutase -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76136704?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncology+research&rft.atitle=Decreased+expression+of+manganese+superoxide+dismutase+mRNA+and+protein+after+immortalization+and+transformation+of+mouse+liver+cells.&rft.au=Sun%2C+Y%3BColburn%2C+N+H%3BOberley%2C+L+W&rft.aulast=Sun&rft.aufirst=Y&rft.date=1993-01-01&rft.volume=5&rft.issue=3&rft.spage=127&rft.isbn=&rft.btitle=&rft.title=Oncology+research&rft.issn=09650407&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-01-25 N1 - Date created - 1994-01-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Evaluation of 2-(methylaminosulfonyl)-1-(arylsulfonyl)-1-methylhydrazines as anticancer agents. AN - 76136330; 8272148 AB - Seven new 2-(methylaminosulfonyl)-1-(arylsulfonyl)-1-methylhydrazines were prepared. The anticancer activity of these compounds was assessed in murine Ehrlich ascites carcinoma (EAC) by in vivo screening. Moderate in vivo activity in EAC was exhibited by three compounds. All of them were screened in vitro against a battery of human tumor cell lines at the National Cancer Institute (NCI), USA. One of them, compound 3a has displayed highly significant specificity in the renal tumor cell line RXF 393. These three compounds were also assessed for in vitro anti-HIV activity at the NCI, however, they have not reached the criteria of significant activity. The alkylating activity of the compounds was determined by measuring the absorbance of the alkylated product of 4-(4-nitrobenzyl)pyridine. It has been found that they are capable of acting as chemical alkylating agents. JF - Neoplasma AU - Sanyal, U AU - De, R AU - Dutta, S AU - Das, H AU - Ghost, M AD - Department of Chemotherapy, Chittaranjan National Cancer Institute, Calcutta, India. Y1 - 1993 PY - 1993 DA - 1993 SP - 219 EP - 222 VL - 40 IS - 4 SN - 0028-2685, 0028-2685 KW - Antineoplastic Agents KW - 0 KW - Antiviral Agents KW - Methylhydrazines KW - Index Medicus KW - AIDS/HIV KW - HIV -- drug effects KW - Drug Screening Assays, Antitumor KW - Animals KW - Tumor Cells, Cultured KW - Kidney Neoplasms KW - Humans KW - Mice KW - Carcinoma, Ehrlich Tumor KW - Cell Line KW - Structure-Activity Relationship KW - Antineoplastic Agents -- toxicity KW - Antiviral Agents -- toxicity KW - Methylhydrazines -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76136330?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neoplasma&rft.atitle=Evaluation+of+2-%28methylaminosulfonyl%29-1-%28arylsulfonyl%29-1-methylhydrazines+as+anticancer+agents.&rft.au=Sanyal%2C+U%3BDe%2C+R%3BDutta%2C+S%3BDas%2C+H%3BGhost%2C+M&rft.aulast=Sanyal&rft.aufirst=U&rft.date=1993-01-01&rft.volume=40&rft.issue=4&rft.spage=219&rft.isbn=&rft.btitle=&rft.title=Neoplasma&rft.issn=00282685&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-02-03 N1 - Date created - 1994-02-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Infectious cerebral amyloidosis: clinical spectrum, risks and remedies. AN - 76133883; 8270120 AB - The clinical and pathological features of the NIH series of 209 transmitted cases of sporadic Creutzfeldt-Jakob disease (CJD) are compared with familial and iatrogenic forms of spongiform encephalopathy. Real or potential risk factors are noted, including animal sources such as scrapie and BSE, iatrogenic sources such as homografts and cadaveric tissue extracts, and genetic defects in the chromosome 20 amyloid precursor gene. The paper concludes with a discussion of the means by which such risks may be minimized. JF - Developments in biological standardization AU - Brown, P AD - Laboratory of CNS studies, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD. Y1 - 1993 PY - 1993 DA - 1993 SP - 91 EP - 101 VL - 80 SN - 0301-5149, 0301-5149 KW - Index Medicus KW - Pedigree KW - Animals KW - Drug Contamination KW - Gerstmann-Straussler-Scheinker Disease -- pathology KW - Iatrogenic Disease KW - Humans KW - Kuru -- pathology KW - Organ Specificity KW - Transplantation -- adverse effects KW - Zoonoses KW - Meat -- adverse effects KW - Risk Factors KW - Cohort Studies KW - Food Contamination KW - Prion Diseases -- prevention & control KW - Middle Aged KW - Female KW - Male KW - Creutzfeldt-Jakob Syndrome -- pathology KW - Creutzfeldt-Jakob Syndrome -- microbiology KW - Creutzfeldt-Jakob Syndrome -- genetics KW - Amyloidosis -- epidemiology KW - Creutzfeldt-Jakob Syndrome -- transmission KW - Creutzfeldt-Jakob Syndrome -- ethnology KW - Amyloidosis -- pathology KW - Amyloidosis -- genetics KW - Amyloidosis -- microbiology KW - Creutzfeldt-Jakob Syndrome -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76133883?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Developments+in+biological+standardization&rft.atitle=Infectious+cerebral+amyloidosis%3A+clinical+spectrum%2C+risks+and+remedies.&rft.au=Brown%2C+P&rft.aulast=Brown&rft.aufirst=P&rft.date=1993-01-01&rft.volume=80&rft.issue=&rft.spage=91&rft.isbn=&rft.btitle=&rft.title=Developments+in+biological+standardization&rft.issn=03015149&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-02-03 N1 - Date created - 1994-02-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Acute effects of 4-ipomeanol on experimental lung tumors with bronchiolar or alveolar cell features in Syrian hamsters or C3H/HeNCr mice. AN - 76125807; 8270607 AB - 4-Ipomenaol (IPO) has been shown to induce P-450-mediated necrosis of Clara cells in experimental animals, and clinical trials were initiated to treat people with bronchioloalveolar cancers with this novel drug. We therefore performed experiments to examine two different animal lung tumor models for acute IPO cytotoxicity: hamster Clara-cell-derived adenocarcinomas and mouse alveolar type II cell tumors. Clara cells serve as stem cells for airway cell renewal and, therefore, tumors derived from Clara cells may likewise differentiate into various bronchiolar cell types, or undergo squamous cell metaplasia. Bronchiolar cell tumors were induced in Syrian hamsters by a single weekly gavage with 6.8 mg N-nitrosomethyl-n-heptylamine (NMHA)/animal for 35 weeks. NMHA-induced bronchiolar tumors were classified as well-differentiated lepidic bronchioloalveolar carcinomas, acinar adenocarcinoma, adenosquamous carcinoma, and squamous-cell carcinoma. After 35 and 46 experimental weeks, control and carcinogen-treated hamsters were injected once with doses of 40-110 mg IPO/kg i.p. and necropsied 15-48 h later. Solid and papillary tumors with alveolar cell features were induced transplacentally in C3H/HeNCr mice, by treating pregnant animals on gestation day 16 with 0.5 mmol N-nitrosoethylurea/kg, i.p. Offspring of control and carcinogen-treated mice were injected at 2-3 months of age with 35 mg or 50 mg IPO/kg i.p. and necropsied either 24-48 h or 5 and 12 days after injection. Light microscopic studies were carried out to assess cytotoxic effects in various tissues in both hamsters and mice; in hamsters, additional ultrastructural studies were performed. When administered to hamsters, IPO induced moderate to severe cytotoxicity in normal and dysplastic bronchiolar lining cells, in most lepidic bronchioloalveolar carcinomas, and in some glandular areas of adenosquamous cell carcinomas. Susceptible cells included normal, anaplastic, and neoplastic nonciliated and some ciliated bronchiolar cells. Undifferentiated and squamous tumor cells were resistant to IPO, as were resident normal alveolar type II cells. However, some adenocarcinomas composed primarily of ciliated and mucous cells also showed no IPO-induced necrosis, indicating a deficiency in appropriate activating enzymes. In the mice, IPO induced bronchiolar cell necrosis and, at the high dose, also severe pulmonary edema. No cytotoxicity was observed in normal or hyperplastic alveolar epithelium, nor in either solid or papillary growth forms of mouse alveolar cell tumors.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Journal of cancer research and clinical oncology AU - Rehm, S AU - Devor, D E AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, NCI/FCRDC, Frederick, Maryland 21702-1201. Y1 - 1993 PY - 1993 DA - 1993 SP - 41 EP - 50 VL - 120 IS - 1-2 SN - 0171-5216, 0171-5216 KW - Antineoplastic Agents KW - 0 KW - Terpenes KW - 4-ipomeanol KW - 32954-58-8 KW - Index Medicus KW - Carcinoma, Adenosquamous -- drug therapy KW - Animals KW - Mice, Inbred C3H KW - Mesocricetus KW - Mice KW - Adenocarcinoma -- drug therapy KW - Male KW - Female KW - Cricetinae KW - Adenocarcinoma, Bronchiolo-Alveolar -- drug therapy KW - Adenocarcinoma, Bronchiolo-Alveolar -- pathology KW - Lung Neoplasms -- drug therapy KW - Terpenes -- pharmacology KW - Antineoplastic Agents -- pharmacology KW - Terpenes -- adverse effects KW - Lung Neoplasms -- pathology KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76125807?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+cancer+research+and+clinical+oncology&rft.atitle=Acute+effects+of+4-ipomeanol+on+experimental+lung+tumors+with+bronchiolar+or+alveolar+cell+features+in+Syrian+hamsters+or+C3H%2FHeNCr+mice.&rft.au=Rehm%2C+S%3BDevor%2C+D+E&rft.aulast=Rehm&rft.aufirst=S&rft.date=1993-01-01&rft.volume=120&rft.issue=1-2&rft.spage=41&rft.isbn=&rft.btitle=&rft.title=Journal+of+cancer+research+and+clinical+oncology&rft.issn=01715216&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-02-02 N1 - Date created - 1994-02-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Targetted phototherapy with sensitizer-monoclonal antibody conjugate and light. AN - 76108663; 8252191 AB - Photodynamic therapy (PDT) was performed in vitro and in vivo using monoclonal antibody conjugated to hematoporphyrin (HP). The antibody (45-2D9) recognized a cell surface glycoprotein on cells derived from NIH 3T3 cells which were transformed with the ras oncogene (45-342). Radionuclide imaging with either In111 or I125 chelated to 45-2D9 or the isotype identical (IgG1) antibody MOPPC-21 revealed selectivity of 45-2D9 for 45-342 flank tumours in nude mice, and minimal targetting for a 45-342 clone which did not express the cell surface glycoprotein. The 45-2D9-HP conjugate resulted in selective killing of the 45-342 line compared with the parent line in vitro. At HP concentrations of 76 micrograms ml-1, the 45-2D9-HP conjugate resulted in significantly more long-term cures of PDT treated flank tumours compared with free HP at the same concentration. 45-2D9 alone had no effect on tumour growth. The antibody-HP conjugate resulted in significantly less local toxicity compared with standard Photofrin II PDT, and also achieved a greater number of long-term cures. This 'photoimmunotherapy' demonstrates the ability to treat established tumours with greater efficacy and decreased morbidity, probably due to specific sensitizer targetting which allows normal surrounding tissue to be spared upon illumination. JF - Surgical oncology AU - Pogrebniak, H W AU - Matthews, W AU - Black, C AU - Russo, A AU - Mitchell, J B AU - Smith, P AU - Roth, J A AU - Pass, H I AD - Thoracic Oncology Section, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 31 EP - 42 VL - 2 IS - 1 SN - 0960-7404, 0960-7404 KW - Antibodies, Monoclonal KW - 0 KW - Hematoporphyrins KW - Dihematoporphyrin Ether KW - 97067-70-4 KW - Index Medicus KW - Skin -- chemistry KW - Animals KW - 3T3 Cells KW - Muscles -- chemistry KW - Hematoporphyrins -- analysis KW - Treatment Outcome KW - Mice, Nude KW - Mice KW - Mice, Inbred BALB C KW - Dihematoporphyrin Ether -- therapeutic use KW - Photochemotherapy KW - Neoplasms, Experimental -- chemistry KW - Dihematoporphyrin Ether -- toxicity KW - Neoplasms, Experimental -- drug therapy KW - Antibodies, Monoclonal -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76108663?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Surgical+oncology&rft.atitle=Targetted+phototherapy+with+sensitizer-monoclonal+antibody+conjugate+and+light.&rft.au=Pogrebniak%2C+H+W%3BMatthews%2C+W%3BBlack%2C+C%3BRusso%2C+A%3BMitchell%2C+J+B%3BSmith%2C+P%3BRoth%2C+J+A%3BPass%2C+H+I&rft.aulast=Pogrebniak&rft.aufirst=H&rft.date=1993-01-01&rft.volume=2&rft.issue=1&rft.spage=31&rft.isbn=&rft.btitle=&rft.title=Surgical+oncology&rft.issn=09607404&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-01-10 N1 - Date created - 1994-01-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - NIH epilepsy branch trials: budgetary and practical issues. AN - 76101928; 8251102 JF - Epilepsy research. Supplement AU - Jacobs, M P AD - Epilepsy Branch, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 239 EP - 244 VL - 10 SN - 0922-9833, 0922-9833 KW - Anticonvulsants KW - 0 KW - Index Medicus KW - United States KW - Contract Services -- economics KW - Humans KW - Financing, Government -- legislation & jurisprudence KW - Contract Services -- legislation & jurisprudence KW - Research Support as Topic -- economics KW - Financing, Government -- economics KW - Competitive Bidding -- economics KW - Liability, Legal KW - Competitive Bidding -- legislation & jurisprudence KW - Research Support as Topic -- legislation & jurisprudence KW - Epilepsy -- economics KW - Clinical Trials as Topic -- economics KW - Anticonvulsants -- economics KW - National Institutes of Health (U.S.) -- economics KW - Anticonvulsants -- adverse effects KW - Budgets -- legislation & jurisprudence KW - Epilepsy -- drug therapy KW - Anticonvulsants -- therapeutic use KW - Clinical Trials as Topic -- legislation & jurisprudence UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76101928?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Epilepsy+research.+Supplement&rft.atitle=NIH+epilepsy+branch+trials%3A+budgetary+and+practical+issues.&rft.au=Jacobs%2C+M+P&rft.aulast=Jacobs&rft.aufirst=M&rft.date=1993-01-01&rft.volume=10&rft.issue=&rft.spage=239&rft.isbn=&rft.btitle=&rft.title=Epilepsy+research.+Supplement&rft.issn=09229833&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-01-13 N1 - Date created - 1994-01-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Optimization of the single-strand conformation polymorphism (SSCP) technique for detection of point mutations. AN - 76093493; 8257994 AB - The efficiency of detection of single base substitutions by single-stranded conformation polymorphism (SSCP) analysis was tested on 86 randomly distributed point mutations in a 193-bp-long DNA fragment of the mouse beta-globin gene. Multiple parameters were varied, including electrophoresis temperature, buffer concentration, gel concentration, acrylamide-to-bis-acrylamide ratio, and/or addition of different compounds to the gel matrix. Gels with a higher concentration of acrylamide and lower crosslinking gave optimal separation, and all 86 mutations can be clearly distinguished from the wild type on a 5% or 7.5% (2.6% C) acrylamide gel at 4 degrees C. Most of the mutations are also resolvable from wild type on gels with 5% urea or formamide, or 10% dimethylsulfoxide or sucrose. The relative position of the purine and pyrimidine-rich single strands were followed by an asymmetric PCR-SSCP technique. We found that most of the informativity comes from the purine rich strand, which appears to be much more sensitive to changes in the gel. The position or type of mutation showed no correlation with its ability to be detected. However, the neighboring base sequence around the mutation appears to have an effect on mobility. For example, A-->G substitutions in GC-rich regions significantly increase the mobility shift of the purine-rich strand, while most G-->A changes decrease it. We conclude that SSCP is a very efficient method for the detection of point mutations, if the parameters that effect the separation are optimized for a particular DNA fragment. JF - Human mutation AU - Glavac, D AU - Dean, M AD - Biological Carcinogenesis and Development Program, Program Resources Inc./DynCorp, National Cancer Institute, Frederick, Maryland 21702. Y1 - 1993 PY - 1993 DA - 1993 SP - 404 EP - 414 VL - 2 IS - 5 SN - 1059-7794, 1059-7794 KW - DNA, Single-Stranded KW - 0 KW - Gels KW - Globins KW - 9004-22-2 KW - Glycerol KW - PDC6A3C0OX KW - Index Medicus KW - Polymerase Chain Reaction KW - Animals KW - Base Sequence KW - Base Composition KW - Electrophoresis, Polyacrylamide Gel KW - Globins -- genetics KW - Temperature KW - Molecular Sequence Data KW - Mice KW - Nucleic Acid Conformation KW - Point Mutation -- genetics KW - DNA, Single-Stranded -- genetics KW - Polymorphism, Genetic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76093493?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Human+mutation&rft.atitle=Optimization+of+the+single-strand+conformation+polymorphism+%28SSCP%29+technique+for+detection+of+point+mutations.&rft.au=Glavac%2C+D%3BDean%2C+M&rft.aulast=Glavac&rft.aufirst=D&rft.date=1993-01-01&rft.volume=2&rft.issue=5&rft.spage=404&rft.isbn=&rft.btitle=&rft.title=Human+mutation&rft.issn=10597794&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-01-19 N1 - Date created - 1994-01-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Preclinical testing. AN - 76085397; 8251096 JF - Epilepsy research. Supplement AU - Cereghino, J J AU - Kupferberg, H J AD - Epilepsy Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 19 EP - 30 VL - 10 SN - 0922-9833, 0922-9833 KW - Anticonvulsants KW - 0 KW - Index Medicus KW - Brain -- physiopathology KW - Animals KW - Epilepsy -- physiopathology KW - Synaptic Transmission -- drug effects KW - Drug Approval KW - Brain -- drug effects KW - Synaptic Transmission -- physiology KW - Drug Evaluation, Preclinical -- methods KW - Structure-Activity Relationship KW - Anticonvulsants -- chemistry KW - Anticonvulsants -- pharmacokinetics KW - Anticonvulsants -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76085397?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Epilepsy+research.+Supplement&rft.atitle=Preclinical+testing.&rft.au=Cereghino%2C+J+J%3BKupferberg%2C+H+J&rft.aulast=Cereghino&rft.aufirst=J&rft.date=1993-01-01&rft.volume=10&rft.issue=&rft.spage=19&rft.isbn=&rft.btitle=&rft.title=Epilepsy+research.+Supplement&rft.issn=09229833&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-01-13 N1 - Date created - 1994-01-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Clinical use of cyclosporine in ocular disease. AN - 76084797; 8258496 JF - International ophthalmology clinics AU - de Smet, M D AU - Nussenblatt, R B AD - Laboratory of Immunology, National Eye Institute, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 31 EP - 45 VL - 33 IS - 4 SN - 0020-8167, 0020-8167 KW - Ophthalmic Solutions KW - 0 KW - Cyclosporine KW - 83HN0GTJ6D KW - Index Medicus KW - Humans KW - Autoimmune Diseases -- drug therapy KW - Uveitis -- drug therapy KW - Eye Diseases -- drug therapy KW - Cyclosporine -- adverse effects KW - Cyclosporine -- therapeutic use KW - Cyclosporine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76084797?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+ophthalmology+clinics&rft.atitle=Clinical+use+of+cyclosporine+in+ocular+disease.&rft.au=de+Smet%2C+M+D%3BNussenblatt%2C+R+B&rft.aulast=de+Smet&rft.aufirst=M&rft.date=1993-01-01&rft.volume=33&rft.issue=4&rft.spage=31&rft.isbn=&rft.btitle=&rft.title=International+ophthalmology+clinics&rft.issn=00208167&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-01-19 N1 - Date created - 1994-01-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Development of an animal model for testing human breast implantation materials. AN - 76084317; 8248715 AB - Although breast implant materials have been tested in laboratory species since the early 1950s, a standardized evaluation system does not currently exist in which human-made polymers are exposed directly to the mammary milieu of female animals. The present study evaluated such a model as the basis for future experiments on long-term tissue effects. Polyesterurethane disks, 6 mm in diameter x 3 mm thick, were inserted bilaterally beneath the axillobrachial and inguinal mammary/fat pads of 50 9-wk-old female B6D2F1 mice (4 implants each). Implant sites were examined histologically at time points 24 hr to 47 wk after surgery. An acute inflammatory reaction at the implant edges began within 24 hr, and macrophages were found lining the smooth polyurethane fiber surfaces at the periphery by day 2. Multinucleated foreign body giant cells formed by day 4, and by week 4 giant cells contained polyurethane fragments within the cytoplasm, implying degradation of the material. Implant sites showed declining subacute inflammatory responses and increasing fibrosis by week 5. By 13 wk, the polyurethane disks appeared to be integrated into the growing adipose and mammary tissues. Although not apparent on gross inspection, microscopic examination showed that polyurethane fibers moved progressively into adjacent tissues and were always associated with chronic granulomatous inflammation. Histologic findings in the present study are strikingly similar to the human response to polyurethane-coated breast implants. These results suggest the applicability of this model to appropriately test mammaplasty materials in mammary tissues. JF - Toxicologic pathology AU - Devor, D E AU - Waalkes, M P AU - Goering, P AU - Rehm, S AD - Tumor Pathology Section, National Cancer Institute, Frederick Cancer Research and Development Center, Maryland 21702. Y1 - 1993 PY - 1993 DA - 1993 SP - 261 EP - 273 VL - 21 IS - 3 SN - 0192-6233, 0192-6233 KW - Polyurethanes KW - 0 KW - polyurethane foam KW - 9009-54-5 KW - Index Medicus KW - Animals KW - Mammary Glands, Animal -- pathology KW - Mice, Inbred C57BL KW - Edema -- pathology KW - Disease Models, Animal KW - Mice KW - Female KW - Mice, Inbred DBA KW - Mammaplasty KW - Prostheses and Implants -- adverse effects KW - Polyurethanes -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76084317?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+pathology&rft.atitle=Development+of+an+animal+model+for+testing+human+breast+implantation+materials.&rft.au=Devor%2C+D+E%3BWaalkes%2C+M+P%3BGoering%2C+P%3BRehm%2C+S&rft.aulast=Devor&rft.aufirst=D&rft.date=1993-01-01&rft.volume=21&rft.issue=3&rft.spage=261&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=01926233&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-28 N1 - Date created - 1993-12-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Reducing the desire to drink. Pharmacology and neurobiology. AN - 76074756; 8234930 AB - The past decade has witnessed major advances in understanding of neural functioning and neurobiological bases of alcohol consumption. Concurrent with this, a range of exciting investigations have been conducted on pharmacologic agents that may curb drinking behavior. Research is reviewed on several promising medications influencing neurotransmitter and endocrine systems with particular attention to the serotonergic and opioid systems. Following this overview, recommendations are offered regarding research methodology to support future pharmacotherapy trials. JF - Recent developments in alcoholism : an official publication of the American Medical Society on Alcoholism, the Research Society on Alcoholism, and the National Council on Alcoholism AU - Litten, R Z AU - Allen, J P AD - Treatment Research Branch, National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20857. Y1 - 1993 PY - 1993 DA - 1993 SP - 325 EP - 344 VL - 11 SN - 0738-422X, 0738-422X KW - Alcohol Deterrents KW - 0 KW - Receptors, Neurotransmitter KW - Index Medicus KW - Receptors, Neurotransmitter -- physiology KW - Brain -- physiopathology KW - Animals KW - Combined Modality Therapy KW - Behavior Therapy KW - Humans KW - Brain -- drug effects KW - Receptors, Neurotransmitter -- drug effects KW - Alcoholism -- rehabilitation KW - Alcohol Deterrents -- adverse effects KW - Alcohol Drinking -- physiopathology KW - Alcohol Drinking -- prevention & control KW - Alcoholism -- physiopathology KW - Alcohol Deterrents -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76074756?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Recent+developments+in+alcoholism+%3A+an+official+publication+of+the+American+Medical+Society+on+Alcoholism%2C+the+Research+Society+on+Alcoholism%2C+and+the+National+Council+on+Alcoholism&rft.atitle=Reducing+the+desire+to+drink.+Pharmacology+and+neurobiology.&rft.au=Litten%2C+R+Z%3BAllen%2C+J+P&rft.aulast=Litten&rft.aufirst=R&rft.date=1993-01-01&rft.volume=11&rft.issue=&rft.spage=325&rft.isbn=&rft.btitle=&rft.title=Recent+developments+in+alcoholism+%3A+an+official+publication+of+the+American+Medical+Society+on+Alcoholism%2C+the+Research+Society+on+Alcoholism%2C+and+the+National+Council+on+Alcoholism&rft.issn=0738422X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-06 N1 - Date created - 1993-12-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Clara cell antigen in normal and migratory dysplastic Clara cells, and bronchioloalveolar carcinoma of Syrian hamsters induced by N-nitrosomethyl-n-heptylamine. AN - 76071665; 8242177 AB - Histogenetic features of lung tumours were studied in Syrian hamsters that had been induced with 6.8 mg N-nitrosomethyl-n-heptylamine/animal by gavage once a week for 35 weeks. At intervals from experimental week 2 until week 46, pulmonary tissues from hamsters were examined by light and electron microscopy. This report describes early hyperplastic lesions associated with terminal bronchioles and the progression of these lesions to bronchioloalveolar tumours. Using immunohistochemical and ultrastructural colloidal gold labelling techniques, hamster Clara cell antigen was found to be localized in Clara cell granules and smooth endoplasmic reticulum of normal cells, in dysplastic Clara cells migrating through basement membrane defects or from the open end of terminal bronchioles, and in hyperplastic peribronchiolar cell foci. The latter progressed to bronchioloalveolar tumours growing out along alveolar basement membranes in a characteristic lace-like, lepidic pattern. Tumours were composed of secretory (Clara), ciliated, mucous, and undifferentiated cells, as well as trapped, non-neoplastic alveolar type II cells. Hyperplastic neuroendocrine cell foci lining airways were immunoreactive for chromogranin, but these cells did not participate in the pre-neoplastic or neoplastic process. It is suggested that bronchioloalveolar carcinomas in hamsters are derived from bronchiolar secretory (Clara) cells growing along alveolar walls, differentiating into other bronchiolar cell types and entrapping resident alveolar type II cells. Due to the migratory capacity of Clara cells, it is also possible for tumours composed of bronchiolar cells to develop at the lung periphery. JF - Virchows Archiv. B, Cell pathology including molecular pathology AU - Rehm, S AU - Lijinsky, W AU - Thomas, B J AU - Kasprzak, B H AD - Tumor Pathology and Pathogenesis Section, National Cancer Institute, Frederick, MD 21702-1201. Y1 - 1993 PY - 1993 DA - 1993 SP - 181 EP - 190 VL - 64 IS - 3 SN - 0340-6075, 0340-6075 KW - Antigens, Neoplasm KW - 0 KW - Carcinogens KW - Clara cell antigen KW - Neoplasm Proteins KW - Nitrosamines KW - nitrosomethyl-N-heptylamine KW - 16338-99-1 KW - Index Medicus KW - Animals KW - Cytoplasmic Granules -- ultrastructure KW - Cell Nucleus -- ultrastructure KW - Endoplasmic Reticulum -- ultrastructure KW - Mesocricetus KW - Cytoplasmic Granules -- immunology KW - Microscopy, Electron KW - Epithelium -- ultrastructure KW - Microscopy, Immunoelectron KW - Epithelium -- pathology KW - Immunohistochemistry KW - Male KW - Cricetinae KW - Endoplasmic Reticulum -- immunology KW - Adenocarcinoma, Bronchiolo-Alveolar -- chemically induced KW - Adenocarcinoma, Bronchiolo-Alveolar -- pathology KW - Lung Neoplasms -- immunology KW - Antigens, Neoplasm -- analysis KW - Lung Neoplasms -- chemically induced KW - Neoplasm Proteins -- analysis KW - Adenocarcinoma, Bronchiolo-Alveolar -- immunology KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76071665?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Virchows+Archiv.+B%2C+Cell+pathology+including+molecular+pathology&rft.atitle=Clara+cell+antigen+in+normal+and+migratory+dysplastic+Clara+cells%2C+and+bronchioloalveolar+carcinoma+of+Syrian+hamsters+induced+by+N-nitrosomethyl-n-heptylamine.&rft.au=Rehm%2C+S%3BLijinsky%2C+W%3BThomas%2C+B+J%3BKasprzak%2C+B+H&rft.aulast=Rehm&rft.aufirst=S&rft.date=1993-01-01&rft.volume=64&rft.issue=3&rft.spage=181&rft.isbn=&rft.btitle=&rft.title=Virchows+Archiv.+B%2C+Cell+pathology+including+molecular+pathology&rft.issn=03406075&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-23 N1 - Date created - 1993-12-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Recent developments in alcoholism:genetic transmission. AN - 76070094; 8234925 AB - This chapter is an overview of developments in the study of genetic factors in vulnerability in alcoholism. The focus is on recent developments, including heritability studies in twins and transmission studies in families, both of which have continued to reveal evidence for a substantial role for genetic factors but also for etiologic complexity and variation in vulnerability across generations and across cultures. Studies are discussed which utilized psychophysiological and neurochemical markers for alcoholism for analysis of genetic association, transmission, and linkage. These markers include the low P300 event-related potential, sensitivity to ethanol's intoxicating and euphoric effects, platelet adenylate cyclase, and neurotransmitter metabolite concentrations. Although it is highly likely that many alcoholism-associated physiologic phenotypes are secondary traits, these approaches have increased the specificity of genetic analyses and genetic analyses are clarifying their relationship to alcoholism. For example, early efforts to study, in families, the co-occurrence of the P300 marker and alcoholism have yielded results indicating that the P300 abnormality precedes significant exposure to alcohol and that relatives of alcoholics are more likely to have this trait. In the area of animal models, two nonhuman primate species, the vervet monkey and the rhesus macaque, were shown to willingly consume alcohol to intoxicating blood levels. Also, linkage studies using the quantitative trait locus (QTL) mapping strategy were attempted for phenotypes relevant for alcoholism. The QTL strategy is theoretically capable of identifying determinant genes which contribute only a small portion of the variance. In human linkage studies, a genetic association was found to the DRD2 dopamine receptor. The DRD2 finding generated controversy, as a number of other groups failed to replicate it, and also focused attention on the advantages and pitfalls of the population association approach for detecting genes influencing behavior. The relationship of the alcohol metabolic gene variants to alcoholism was clarified by the finding that functional variants of alcohol and aldehyde dehydrogenases can act additively to determine vulnerability to alcoholism. JF - Recent developments in alcoholism : an official publication of the American Medical Society on Alcoholism, the Research Society on Alcoholism, and the National Council on Alcoholism AU - Goldman, D AD - Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 231 EP - 248 VL - 11 SN - 0738-422X, 0738-422X KW - Genetic Markers KW - 0 KW - Isoenzymes KW - Receptors, Dopamine D2 KW - Aldehyde Dehydrogenase KW - EC 1.2.1.3 KW - Index Medicus KW - Aldehyde Dehydrogenase -- genetics KW - Humans KW - Chromosome Mapping KW - Isoenzymes -- genetics KW - Genetic Markers -- genetics KW - Genetic Linkage -- genetics KW - Risk Factors KW - Arousal -- genetics KW - Receptors, Dopamine D2 -- genetics KW - Diseases in Twins -- genetics KW - Gene Frequency -- genetics KW - Female KW - Male KW - Alcoholism -- genetics KW - Alcoholism -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76070094?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Recent+developments+in+alcoholism+%3A+an+official+publication+of+the+American+Medical+Society+on+Alcoholism%2C+the+Research+Society+on+Alcoholism%2C+and+the+National+Council+on+Alcoholism&rft.atitle=Recent+developments+in+alcoholism%3Agenetic+transmission.&rft.au=Goldman%2C+D&rft.aulast=Goldman&rft.aufirst=D&rft.date=1993-01-01&rft.volume=11&rft.issue=&rft.spage=231&rft.isbn=&rft.btitle=&rft.title=Recent+developments+in+alcoholism+%3A+an+official+publication+of+the+American+Medical+Society+on+Alcoholism%2C+the+Research+Society+on+Alcoholism%2C+and+the+National+Council+on+Alcoholism&rft.issn=0738422X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-06 N1 - Date created - 1993-12-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Recent developments in alcoholism:pharmacological treatment. AN - 76066429; 8234933 AB - Neurobiological research over the past decade has greatly expanded our knowledge of alcohol's interaction with the nervous system and promises significant improvement in pharmacological treatment for all phases of alcoholism. Although no new treatment has yet become standard clinical practice, over the next decade benzodiazepine receptor antagonists and inverse agonists should improve treatment of acute alcohol intoxication, adrenergic agents and anticonvulsants should improve treatment of acute alcohol withdrawal, and serotonin uptake blockers and mu opiate receptor antagonists should improve long-term treatment of alcohol dependence. Future clinical research should reduce the current lack of knowledge on pharmacological treatment of alcoholism in special populations such as women, the elderly, and those with concurrent psychiatric diagnoses. JF - Recent developments in alcoholism : an official publication of the American Medical Society on Alcoholism, the Research Society on Alcoholism, and the National Council on Alcoholism AU - Gorelick, D A AD - Treatment Branch, National Institute on Drug Abuse, Baltimore, Maryland 21224. Y1 - 1993 PY - 1993 DA - 1993 SP - 413 EP - 427 VL - 11 SN - 0738-422X, 0738-422X KW - Alcohol Deterrents KW - 0 KW - Receptors, Neurotransmitter KW - Ethanol KW - 3K9958V90M KW - Index Medicus KW - Ethanol -- adverse effects KW - Alcohol Withdrawal Delirium -- rehabilitation KW - Combined Modality Therapy KW - Humans KW - Brain -- drug effects KW - Adult KW - Receptors, Neurotransmitter -- drug effects KW - Aged KW - Middle Aged KW - Male KW - Female KW - Alcoholism -- rehabilitation KW - Alcohol Deterrents -- adverse effects KW - Alcohol Deterrents -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76066429?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Recent+developments+in+alcoholism+%3A+an+official+publication+of+the+American+Medical+Society+on+Alcoholism%2C+the+Research+Society+on+Alcoholism%2C+and+the+National+Council+on+Alcoholism&rft.atitle=Recent+developments+in+alcoholism%3Apharmacological+treatment.&rft.au=Gorelick%2C+D+A&rft.aulast=Gorelick&rft.aufirst=D&rft.date=1993-01-01&rft.volume=11&rft.issue=&rft.spage=413&rft.isbn=&rft.btitle=&rft.title=Recent+developments+in+alcoholism+%3A+an+official+publication+of+the+American+Medical+Society+on+Alcoholism%2C+the+Research+Society+on+Alcoholism%2C+and+the+National+Council+on+Alcoholism&rft.issn=0738422X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-06 N1 - Date created - 1993-12-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Combined micropreparative techniques with synchronous fluorescence spectroscopy or 32P-postlabelling assay for carcinogen-DNA adduct determination. AN - 76047741; 8225491 AB - Methods for the detection of carcinogen-DNA adducts require both sensitivity and specificity. The 32P-postlabelling assay is highly sensitive but lacks adduct specificity. The strategy reported herein combines micropreparative techniques including HPLC and immunoaffinity chromatography (IAC) to enhance chemical specificity. The resultant assays have retained sensitivity for human DNA analysis. Combined HPLC and 32P-postlabelling has detected 7-methyldeoxyguanosine in human lung samples, while combined IAC and 32P-postlabelling has detected O6-methyldeoxyguanosine adducts in stomach tissue. The limits of detection are one adduct in 10(7) and 10(8) unmodified deoxyguanosine (dG), respectively. IAC was combined with 32P-postlabelling to detect polycyclic aromatic hydrocarbon (PAH)-DNA adducts in human lung. The detection limit was one adduct in 10(7) dG. Our laboratory has also employed synchronous fluorescence spectroscopy (SFS) for the detection of adducts formed from benzo[a]pyrene in human lung. Complex fluorescence matrices suggest the presence of other PAH-DNA adducts. Both the SFS assay and the 32P-postlabelling assay were applied to a series of human samples and a high correlation was found for adduct levels. The development of such assays using synthetic standards, internal standards, determination of calibration curves and validation with corroborating methods is required for chemically specific and sensitive adduct detection. JF - IARC scientific publications AU - Shields, P G AU - Kato, S AU - Bowman, E D AU - Petruzzelli, S AU - Cooper, D P AU - Povey, A C AU - Weston, A AD - Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 243 EP - 254 IS - 124 SN - 0300-5038, 0300-5038 KW - Carcinogens KW - 0 KW - DNA Adducts KW - Phosphorus Radioisotopes KW - Polycyclic Compounds KW - benzo(a)pyrene-DNA adduct KW - Benzo(a)pyrene KW - 3417WMA06D KW - DNA KW - 9007-49-2 KW - O(6)-methyl-2'-deoxyguanosine KW - 964-21-6 KW - Deoxyguanosine KW - G9481N71RO KW - Index Medicus KW - Chromatography, Affinity KW - Spectrometry, Fluorescence KW - Polycyclic Compounds -- analysis KW - DNA Damage KW - Benzo(a)pyrene -- analysis KW - Methods KW - Humans KW - Reference Standards KW - Lung -- chemistry KW - In Vitro Techniques KW - Deoxyguanosine -- analysis KW - Polycyclic Compounds -- adverse effects KW - Deoxyguanosine -- analogs & derivatives KW - DNA -- analysis KW - Carcinogens -- toxicity KW - Carcinogens -- analysis KW - DNA -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76047741?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=IARC+scientific+publications&rft.atitle=Combined+micropreparative+techniques+with+synchronous+fluorescence+spectroscopy+or+32P-postlabelling+assay+for+carcinogen-DNA+adduct+determination.&rft.au=Shields%2C+P+G%3BKato%2C+S%3BBowman%2C+E+D%3BPetruzzelli%2C+S%3BCooper%2C+D+P%3BPovey%2C+A+C%3BWeston%2C+A&rft.aulast=Shields&rft.aufirst=P&rft.date=1993-01-01&rft.volume=&rft.issue=124&rft.spage=243&rft.isbn=&rft.btitle=&rft.title=IARC+scientific+publications&rft.issn=03005038&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-06 N1 - Date created - 1993-12-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The use of immunotoxins for cancer therapy. AN - 76036354; 8217369 JF - European journal of cancer (Oxford, England : 1990) AU - Pai, L H AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 1993 PY - 1993 DA - 1993 SP - 1606 EP - 1609 VL - 29A IS - 11 SN - 0959-8049, 0959-8049 KW - Immunotoxins KW - 0 KW - Recombinant Proteins KW - Index Medicus KW - Humans KW - Recombinant Proteins -- therapeutic use KW - Structure-Activity Relationship KW - Neoplasms -- drug therapy KW - Immunotoxins -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76036354?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+cancer+%28Oxford%2C+England+%3A+1990%29&rft.atitle=The+use+of+immunotoxins+for+cancer+therapy.&rft.au=Pai%2C+L+H%3BPastan%2C+I&rft.aulast=Pai&rft.aufirst=L&rft.date=1993-01-01&rft.volume=29A&rft.issue=11&rft.spage=1606&rft.isbn=&rft.btitle=&rft.title=European+journal+of+cancer+%28Oxford%2C+England+%3A+1990%29&rft.issn=09598049&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-09 N1 - Date created - 1993-12-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Two-dimensional gel electrophoresis of major cytosolic proteins derived from spleen mononuclear cells of normal and leukemic rats. AN - 76025911; 8218474 AB - Proteins from leukemic spleen cells derived from a F344 rat transplant model were investigated by 2D gel electrophoresis. The cell line was maintained in vivo by serial transplant of mononuclear spleen cells from leukemic donors into syngeneic recipients. Cytosolic proteins from mononuclear cells (MNC) were isolated from spleens of normal and leukemic rats and separated by electrophoresis. Replicate data from silver-stained gels for each preparation were compiled into Master Images using image analysis algorithms in order to characterize the normal and leukemic protein profiles. Comparative analysis showed a total of 458 proteins that were reproducibly detected in normal MNC, while almost twice the number of proteins (828) were found in leukemic MNC, suggestive of the more mitotically active tumor cells. Profile analysis showed that normal and leukemic preparations shared 228 common proteins, with 600 proteins observed only in leukemic MNC, and 230 proteins found only in normal MNC. Differences in protein patterns between normal and leukemic MNC in rats probably reflects a shift in spleen leukocyte populations and a relative induction of gene expression in leukemic MNC as compared to the normal MNC. JF - Applied and theoretical electrophoresis : the official journal of the International Electrophoresis Society AU - Merrick, B A AU - He, C AU - Dieter, M P AU - Selkirk, J K AD - Chemical Carcinogenesis Mechanisms Group, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993 PY - 1993 DA - 1993 SP - 203 EP - 211 VL - 3 IS - 5 SN - 0954-6642, 0954-6642 KW - Neoplasm Proteins KW - 0 KW - Proteins KW - Index Medicus KW - Rats KW - Neoplasm Transplantation KW - Animals KW - Reference Values KW - Rats, Inbred F344 KW - Electrophoresis, Gel, Two-Dimensional KW - Image Processing, Computer-Assisted KW - Male KW - Spleen -- ultrastructure KW - Spleen -- chemistry KW - Leukocytes, Mononuclear -- chemistry KW - Proteins -- analysis KW - Cytosol -- chemistry KW - Leukemia, Experimental -- metabolism KW - Neoplasm Proteins -- analysis KW - Leukemia, Experimental -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76025911?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Applied+and+theoretical+electrophoresis+%3A+the+official+journal+of+the+International+Electrophoresis+Society&rft.atitle=Two-dimensional+gel+electrophoresis+of+major+cytosolic+proteins+derived+from+spleen+mononuclear+cells+of+normal+and+leukemic+rats.&rft.au=Merrick%2C+B+A%3BHe%2C+C%3BDieter%2C+M+P%3BSelkirk%2C+J+K&rft.aulast=Merrick&rft.aufirst=B&rft.date=1993-01-01&rft.volume=3&rft.issue=5&rft.spage=203&rft.isbn=&rft.btitle=&rft.title=Applied+and+theoretical+electrophoresis+%3A+the+official+journal+of+the+International+Electrophoresis+Society&rft.issn=09546642&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-17 N1 - Date created - 1993-12-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Mercuric chloride-induced alterations of levels of noradrenaline, dopamine, serotonin and acetylcholine esterase activity in different regions of rat brain during postnatal development. AN - 76025247; 8215912 AB - Wistar rats were fed mercuric chloride, 4 mg/kg body weight per day chronically from postnatal day 2 to 60 by gastric intubation. Mercury consumption was then discontinued until 170 days to allow time for recovery. Since mercury caused reduction in body weight, an underweight group was also included besides the normal saline group. Levels of noradrenaline (NA), dopamine (DA), 5-hydroxytryptamine (5-HT) and the activity of acetylcholine esterase (AChE) were assayed in various brain regions in different age groups. By 60 days of age, the mercury group showed elevations of NA levels in olfactory bulb (OB), visual cortex (VC) and brain stem (BS) but not in striatum-accumbens (SA) and hippocampus (HI). DA levels were also increased in OB, HI, VC and BS but not in SA. AChE activity was decreased in the mercury group only in HI and VC at 20 days of age. The Mercury group showed no behavioural abnormality outwardly; however, operant conditioning revealed a deficiency in performance. Nevertheless, all these changes disappeared after discontinuation of mercury intake. Thus the changes occurring in the brain at this level of oral mercuric chloride intake seem to reflect adaptive neural mechanisms rather than pathological damage. JF - Archives of toxicology AU - Lakshmana, M K AU - Desiraju, T AU - Raju, T R AD - Department of Neurophysiology, National Institute of Mental Health and Neuro Sciences, Bangalore, India. Y1 - 1993 PY - 1993 DA - 1993 SP - 422 EP - 427 VL - 67 IS - 6 SN - 0340-5761, 0340-5761 KW - Serotonin KW - 333DO1RDJY KW - Mercuric Chloride KW - 53GH7MZT1R KW - Acetylcholinesterase KW - EC 3.1.1.7 KW - Dopamine KW - VTD58H1Z2X KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Rats KW - Behavior, Animal -- drug effects KW - Animals KW - Body Weight -- drug effects KW - Rats, Wistar KW - Male KW - Female KW - Organ Size -- drug effects KW - Norepinephrine -- metabolism KW - Brain -- drug effects KW - Acetylcholinesterase -- metabolism KW - Dopamine -- metabolism KW - Brain -- metabolism KW - Mercuric Chloride -- toxicity KW - Serotonin -- metabolism KW - Brain -- growth & development UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76025247?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+toxicology&rft.atitle=Mercuric+chloride-induced+alterations+of+levels+of+noradrenaline%2C+dopamine%2C+serotonin+and+acetylcholine+esterase+activity+in+different+regions+of+rat+brain+during+postnatal+development.&rft.au=Lakshmana%2C+M+K%3BDesiraju%2C+T%3BRaju%2C+T+R&rft.aulast=Lakshmana&rft.aufirst=M&rft.date=1993-01-01&rft.volume=67&rft.issue=6&rft.spage=422&rft.isbn=&rft.btitle=&rft.title=Archives+of+toxicology&rft.issn=03405761&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-09 N1 - Date created - 1993-11-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Deletion mutagenesis of rat PC12 tyrosine hydroxylase regulatory and catalytic domains. AN - 76025150; 8105857 AB - The functional organization of rat tyrosine hydroxylase was investigated by deletion mutagenesis of the regulatory and catalytic domains. A series of tyrosine hydroxylase cDNA deletion mutants were amplified by PCR, cloned into the pET3C prokaryotic expression vector, and the mutant proteins were partially purified from E. coli. The results show that the deletion of up to 157 N-terminal amino acids activated the enzyme, but further deletion to position 184 completely destroyed catalytic activity. On the carboxyl end, the removal of 43 amino acids decreased but did not eliminate activity, suggesting that this region may play a different role in the regulation of the enzyme. These findings place the amino end of the catalytic domain between residues 158 and 184 and the carboxyl end at or prior to position 455. Deletions within the first 157 amino acids in the N-terminus caused an increase in hydroxylating activity, a decrease in the apparent Km for tyrosine and phenylalanine substrates, and a substantial increase in the Ki for dopamine inhibition. The results define this region of the N-terminus as the regulatory domain of tyrosine hydroxylase, whose primary functions are to restrict the binding of amino acid substrates and to facilitate catecholamine inhibition. The results also suggest that the well-established role of the regulatory domain in restricting cofactor binding may be secondary to an increase in catecholamine binding, which in turn lowers the affinity for the cofactor. These findings provide new insight into the functional organization and mechanisms of regulation of tyrosine hydroxylase. JF - Journal of molecular neuroscience : MN AU - Ribeiro, P AU - Wang, Y AU - Citron, B A AU - Kaufman, S AD - Laboratory of Neurochemistry, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 125 EP - 139 VL - 4 IS - 2 SN - 0895-8696, 0895-8696 KW - DNA, Complementary KW - 0 KW - DNA, Neoplasm KW - Neoplasm Proteins KW - Recombinant Fusion Proteins KW - Tyrosine 3-Monooxygenase KW - EC 1.14.16.2 KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Animals KW - Dopamine -- pharmacology KW - DNA, Complementary -- genetics KW - Protein Processing, Post-Translational KW - Dopamine -- metabolism KW - Recombinant Fusion Proteins -- chemistry KW - Binding Sites KW - Rats KW - Polymerase Chain Reaction KW - Base Sequence KW - Phosphorylation KW - Molecular Sequence Data KW - DNA, Neoplasm -- genetics KW - Feedback KW - Protein Structure, Tertiary KW - Sequence Deletion KW - Tyrosine 3-Monooxygenase -- genetics KW - Neoplasm Proteins -- genetics KW - PC12 Cells -- enzymology KW - Neoplasm Proteins -- chemistry KW - Tyrosine 3-Monooxygenase -- chemistry KW - Mutagenesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76025150?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+molecular+neuroscience+%3A+MN&rft.atitle=Deletion+mutagenesis+of+rat+PC12+tyrosine+hydroxylase+regulatory+and+catalytic+domains.&rft.au=Ribeiro%2C+P%3BWang%2C+Y%3BCitron%2C+B+A%3BKaufman%2C+S&rft.aulast=Ribeiro&rft.aufirst=P&rft.date=1993-01-01&rft.volume=4&rft.issue=2&rft.spage=125&rft.isbn=&rft.btitle=&rft.title=Journal+of+molecular+neuroscience+%3A+MN&rft.issn=08958696&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-07 N1 - Date created - 1993-12-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Biological actions of oncogenes. AN - 76024715; 8415879 AB - Cancer, in many cases, results from multistep genetic mutation. Certain genes can have a predisposed susceptibility to mutations that lead to cancer because of chromosome location or their importance in the control of cell cycles. Mutations that deregulate the expression or activity of enzymes involved in the biochemical pathways of growth and differentiation or that suppress the expression of negative cell cycle control factors result in activation of oncogenesis. The study of oncogenes and tumor suppressor genes has greatly influenced our understanding of the molecular origins of cancer. We focus here on the normal biological action of proto-oncogenes compared with the transforming activities of oncogenes and tumor suppressor genes, and we discuss possible mechanisms of oncogenic transformation. JF - Pharmacology & therapeutics AU - Smith, M R AU - Matthews, N T AU - Jones, K A AU - Kung, H F AD - Biological Carcinogenesis and Development Program, Program Resources Inc., DynCorp, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702. Y1 - 1993 PY - 1993 DA - 1993 SP - 211 EP - 236 VL - 58 IS - 2 SN - 0163-7258, 0163-7258 KW - Index Medicus KW - Animals KW - Humans KW - Genes, Tumor Suppressor -- physiology KW - Neoplasms -- physiopathology KW - Oncogenes -- physiology KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76024715?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacology+%26+therapeutics&rft.atitle=Biological+actions+of+oncogenes.&rft.au=Smith%2C+M+R%3BMatthews%2C+N+T%3BJones%2C+K+A%3BKung%2C+H+F&rft.aulast=Smith&rft.aufirst=M&rft.date=1993-01-01&rft.volume=58&rft.issue=2&rft.spage=211&rft.isbn=&rft.btitle=&rft.title=Pharmacology+%26+therapeutics&rft.issn=01637258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-23 N1 - Date created - 1993-11-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Comparison of pulmonary O6-methylguanine DNA adduct levels and Ki-ras activation in lung tumors from resistant and susceptible mouse strains. AN - 76022132; 8216736 AB - The role of O6-methylguanine (O6MG) DNA adduct formation and persistence in the formation of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK)-induced lung tumors from resistant C57BL/6 and susceptible A/J mice was investigated. In addition, the frequencies of pulmonary tumor formation and Ki-ras activation were defined in C57BL/6 mice treated with NNK or vinyl carbamate (VC), and the role of the p53 gene in pulmonary carcinogenesis in these resistant mice was examined. One day after treatment with 100 mg/kg NNK, O6MG adduct concentrations were twofold to eightfold higher in Clara cells and type II cells than in small cells or whole lungs from both mouse strains. The concentrations of O6MG in isolated cells decreased at a similar rate in the two strains of mice. Lung tumors were detected by 27 mo of age in 18% of the C57BL/6 mice after a single 100 mg/kg dose of NNK and in 46% of these mice after a single 60 mg/kg dose of VC. In contrast, the tumor incidence in untreated C57BL/6 mice was 4%. Only one of 22 lung tumors from C57BL/6 mice treated with NNK contained an activated Ki-ras gene that was associated with an O6MG DNA adduct, whereas previous studies detected activated Ki-ras oncogenes in most of the NNK-induced lung tumors analyzed from susceptible A/J and resistant C3H mice. The small differences in formation and persistence of the O6MG adduct in whole lung or isolated lung cells from A/J and C57BL/6 strains do not account for the differences in either susceptibility for tumor formation or activation of the Ki-ras gene between these strains. In contrast to the low number of NNK-induced tumors with Ki-ras mutations in the resistant mice, 11 of 20 lung tumors from VC-treated mice contained activated Ki-ras genes. Neither p53 tumor suppressor gene mutations nor overexpression of the p53 protein were detected in spontaneous or chemically induced lung tumors in C57BL/6 mice. Thus, although Ki-ras activation was detected in some tumors, pathways independent of ras activation and p53 inactivation also appear to be involved in lung tumorigenesis in this resistant mouse strain. JF - Molecular carcinogenesis AU - Devereux, T R AU - Belinsky, S A AU - Maronpot, R R AU - White, C M AU - Hegi, M E AU - Patel, A C AU - Foley, J F AU - Greenwell, A AU - Anderson, M W AD - Laboratory of Molecular Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993 PY - 1993 DA - 1993 SP - 177 EP - 185 VL - 8 IS - 3 SN - 0899-1987, 0899-1987 KW - Guanine KW - 5Z93L87A1R KW - DNA KW - 9007-49-2 KW - O-(6)-methylguanine KW - 9B710FV2AE KW - Index Medicus KW - Polymerase Chain Reaction KW - Mice, Inbred A KW - Animals KW - Base Sequence KW - Genes, p53 KW - Molecular Sequence Data KW - Mice, Inbred C57BL KW - Gene Expression KW - Mice KW - Mutation KW - Genes, ras KW - DNA -- metabolism KW - Guanine -- analogs & derivatives KW - Guanine -- metabolism KW - Lung Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76022132?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+Journal+of+Nutrition&rft.atitle=Multiplatform+metabolomic+fingerprinting+as+a+tool+for+understanding+hypercholesterolemia+in+Wistar+rats&rft.au=Gonz%C3%A1lez-pe%C3%B1a%2C+Diana%3BDudzik%2C+Danuta%3BColina-coca%2C+Clara%3Bde+Ancos%2C+Bego%C3%B1a%3BGarc%C3%ADa%2C+Antonia%3BBarbas%2C+Coral%3BS%C3%A1nchez-moreno%2C+Concepci%C3%B3n&rft.aulast=Gonz%C3%A1lez-pe%C3%B1a&rft.aufirst=Diana&rft.date=2016-04-01&rft.volume=55&rft.issue=3&rft.spage=997&rft.isbn=&rft.btitle=&rft.title=European+Journal+of+Nutrition&rft.issn=14366207&rft_id=info:doi/10.1007%2Fs00394-015-0914-1 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-22 N1 - Date created - 1993-12-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Molecular biology studies of tubercidin resistance in Trypanosoma cruzi. AN - 76018611; 8415556 AB - Trypanosomatids are incapable of de novo purine synthesis; purines are obtained through the scavenging of exogenous nucleosides. To advance our understanding of purine utilization, we mutagenized a Trypanosoma cruzi stock and selected for resistance to high levels of tubercidin (7-deazaadenosine, TUB), a purine analog. The TUB-resistant stocks were > 100 times more resistant to TUB than was the parental stock. TUB and uridine transport in the TUB-resistant stocks decreased by 50%-90%, whereas thymidine and adenosine transport were unaffected. These data imply that TUB-resistant stocks have defects in the pathways involved in the transport of TUB and uridine but not in the thymidine and adenosine transport pathways. Karyotype analyses using specific probes showed that the deletion of a 950-kb chromosome-size DNA occurred in both of the TUB-resistant stocks. These data suggest that genes involved in nucleoside transport are located in this DNA region. This study will facilitate the identification and characterization of the specific genes involved in nucleoside transport and aid in the elucidation and development of new chemotherapeutics for Chagas' disease. JF - Parasitology research AU - Nozaki, T AU - Dvorak, J A AD - Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 451 EP - 455 VL - 79 IS - 6 SN - 0932-0113, 0932-0113 KW - DNA, Protozoan KW - 0 KW - Tubercidin KW - M351LCX45Y KW - Index Medicus KW - Animals KW - Drug Resistance -- genetics KW - Biological Transport -- genetics KW - Mutagenesis KW - Tubercidin -- metabolism KW - Trypanosoma cruzi -- metabolism KW - Trypanosoma cruzi -- drug effects KW - Trypanosoma cruzi -- genetics KW - DNA, Protozoan -- genetics KW - Tubercidin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76018611?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Parasitology+research&rft.atitle=Molecular+biology+studies+of+tubercidin+resistance+in+Trypanosoma+cruzi.&rft.au=Nozaki%2C+T%3BDvorak%2C+J+A&rft.aulast=Nozaki&rft.aufirst=T&rft.date=1993-01-01&rft.volume=79&rft.issue=6&rft.spage=451&rft.isbn=&rft.btitle=&rft.title=Parasitology+research&rft.issn=09320113&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-24 N1 - Date created - 1993-11-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Measuring tobacco use among adolescents. AN - 76015126; 8210270 JF - Public health reports (Washington, D.C. : 1974) AU - Marcus, S E AU - Giovino, G A AU - Pierce, J P AU - Harel, Y AD - Analytical Studies and Decision Systems Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD. Y1 - 1993 PY - 1993 DA - 1993 SP - 20 EP - 24 VL - 108 Suppl 1 SN - 0033-3549, 0033-3549 KW - Abridged Index Medicus KW - Index Medicus KW - Plants, Toxic KW - Humans KW - Smoking Cessation KW - Health Surveys KW - Adult KW - Adolescent KW - United States -- epidemiology KW - Male KW - Female KW - Tobacco, Smokeless KW - Adolescent Behavior KW - Smoking -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76015126?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Public+health+reports+%28Washington%2C+D.C.+%3A+1974%29&rft.atitle=Measuring+tobacco+use+among+adolescents.&rft.au=Marcus%2C+S+E%3BGiovino%2C+G+A%3BPierce%2C+J+P%3BHarel%2C+Y&rft.aulast=Marcus&rft.aufirst=S&rft.date=1993-01-01&rft.volume=108+Suppl+1&rft.issue=&rft.spage=20&rft.isbn=&rft.btitle=&rft.title=Public+health+reports+%28Washington%2C+D.C.+%3A+1974%29&rft.issn=00333549&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-27 N1 - Date created - 1993-10-27 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: N Engl J Med. 1991 Sep 26;325(13):968-9 [1881424] CA Cancer J Clin. 1991 May-Jun;41(3):133-6 [1902136] Milbank Q. 1992;70(1):81-125 [1588892] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Intraepithelial neoplasia, surrogate endpoint biomarkers, and cancer chemoprevention. AN - 76014838; 8412208 AB - Neoplasia is a progression of molecular, cellular, and tissue changes starting with a critical cell mutation and advancing by clonal evolution, involving further multiple mutations and expanding mutated clones. This process is characterized by five general stages: latency, focal growth of normal-appearing but disorganized cells, abnormal-appearing cells (dysplasia), microinvasion, and finally, metastasis. The two driving forces of neoplastic progression in an epithelium are mutagenesis and mitogenesis. These forces frequently occur concurrently, produced by exposure of the epithelium to environmental and endogenous mutagens and mitogens. The major strategy of chemoprevention is to block the effects of both mutagens and mitogens during the early stages of predysplasia and dysplasia. Surrogate endpoint biomarkers (SEBs) are tissue, cellular, and molecular changes that correlate with the later development of cancer. Because of the savings in cost, labor, and time, SEBs are urgently needed to replace the use of cancer incidence reduction as the endpoint for chemopreventive agent clinical trials. The advent of computer-assisted cytometry allows each of the seven basic criteria of dysplasia to be individually assayed as an SEB. Since the dysplastic changes that characterize intraepithelial neoplasia are embodied in the causal pathway to invasive neoplasia, they are already validated as predictors of cancer incidence. More attention should be paid to the quality control of SEB assays, including control of variation in cell composition of tissue samples, assay protocol, instrumentation used, and observer performance. The dose-response relationship between a known chemopreventive agent and the SEB should also be evaluated. The Division of Cancer Prevention and Control, National Cancer Institute, has begun a program to test chemopreventive agents in short-term Phase II clinical trials using dysplasia-based SEBs. The SEBs are assayed, when possible, by computerized cytometry. Trials are being conducted for oral leukoplakia, cutaneous actinic keratosis, superficial bladder cancer, pulmonary metaplasia/dysplasia, cervical dysplasia (CIN III), and adenomatous colonic polyps. JF - Journal of cellular biochemistry. Supplement AU - Boone, C W AU - Kelloff, G J AD - Division of Cancer Prevention and Control, National Cancer Institute, National Institutes of Health, Bethesda, MD 20982. Y1 - 1993 PY - 1993 DA - 1993 SP - 37 EP - 48 VL - 17F SN - 0733-1959, 0733-1959 KW - Biomarkers, Tumor KW - 0 KW - Index Medicus KW - Clone Cells KW - Animals KW - Neoplasm Staging KW - Humans KW - Diagnosis, Computer-Assisted KW - Mutation KW - Flow Cytometry -- methods KW - Cell Division KW - Neoplasms -- pathology KW - Neoplasms -- prevention & control KW - Epithelium KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76014838?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+cellular+biochemistry.+Supplement&rft.atitle=Intraepithelial+neoplasia%2C+surrogate+endpoint+biomarkers%2C+and+cancer+chemoprevention.&rft.au=Boone%2C+C+W%3BKelloff%2C+G+J&rft.aulast=Boone&rft.aufirst=C&rft.date=1993-01-01&rft.volume=17F&rft.issue=&rft.spage=37&rft.isbn=&rft.btitle=&rft.title=Journal+of+cellular+biochemistry.+Supplement&rft.issn=07331959&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-16 N1 - Date created - 1993-11-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Imaging and dosimetry determinations using radiolabeled antibodies. AN - 76013864; 8105853 AB - Numerous studies using radiolabeled antibodies for imaging and therapy of lymphoma have been reported (Table 4). The targeting of lymphoma associated antigens with MoAb appears to be more favorable than the targeting of antigens on epithelial tumor. Antigen abundance may not be the overriding factor in this favorable targeting, since the number of antigenic sites per cell are often in the same range or lower than those targeted in epithelial tumors. This improved targeting is likely related to the greater access of antibody to the target antigen in lymph nodes, bone marrow, circulation, and other sites. With certain antibodies, trafficking of the cells targeted with the radiolabeled antibody may also result in favorable localization [19]. While the most frequently used isotope for imaging and therapy has been 131I, certain limitations have been observed, including its high-energy gamma rays and resulting lower resolution, and the frequent occurrence of dehalogenation [21,25,98]. Many of the antigens expressed by lymphomas undergo antigenic modulation. Antigens that undergo modulation may be targeted successfully, but once modulation occurs the antibody is broken down and the iodine is rapidly excreted from the cells. While this rapid release from normal organs is an advantage, it is an undesirable event at the tumor site. In contrast to the case of 131I MoAb, modulation may be an advantage for targeting with 111In labeled antibodies, since the radioactive metals are retained for longer periods at the tumor sites; even if the antibody is broken down, the 111In is not easily excreted from the cells [52]. Among the most consistent and favorable targeting observed to date is that seen with 111In T101 in CTCL. These studies have shown concentration of 111In in tumor of 10-100 times that seen in other tumor systems using iodinated antibodies. Unfortunately no studies have followed this lead and performed the necessary comparisons between 111In and 131I MoAb to determine if this is a consistent finding. The use of 99mTc labeled MoAb for imaging lymphomas is in its infancy, although preliminary reports appear promising [71]. While in epithelial tumors preferential tumor targeting may take more than 48 hours in lymphomas, targeting is usually seen within the first 24 hours, which is within the window of imaging time for 99mTc. Therefore, further evaluation of 99mTc antibodies should be performed. Determination of the optimum dose of antibody for imaging has been attempted. Studies using various anti-lymphoma directed antibodies have shown widely varying biodistribution and variable dose-response curves.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Cancer treatment and research AU - Carrasquillo, J AD - Department of Health & Human Services, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 65 EP - 97 VL - 68 SN - 0927-3042, 0927-3042 KW - Antibodies, Anti-Idiotypic KW - 0 KW - Antibodies, Monoclonal KW - Index Medicus KW - Radiation Dosage KW - Animals KW - Humans KW - Antibodies, Anti-Idiotypic -- blood KW - Hodgkin Disease -- diagnostic imaging KW - Radioimmunodetection KW - Lymphoma -- diagnostic imaging KW - Leukemia -- diagnostic imaging KW - Antibodies, Monoclonal -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76013864?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+treatment+and+research&rft.atitle=Imaging+and+dosimetry+determinations+using+radiolabeled+antibodies.&rft.au=Carrasquillo%2C+J&rft.aulast=Carrasquillo&rft.aufirst=J&rft.date=1993-01-01&rft.volume=68&rft.issue=&rft.spage=65&rft.isbn=&rft.btitle=&rft.title=Cancer+treatment+and+research&rft.issn=09273042&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-12-22 N1 - Date created - 1993-12-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Substance abuse among subjects screened out from an alcoholism research program. AN - 76011296; 8213699 AB - Three hundred and eight subjects were screened over the phone for admission to an inpatient alcohol treatment research unit. Using a structured interview, the prospective patients were asked questions regarding demographics, drinking history, previous treatments, physical health, family history, and a detailed history of past and present substance use. Drug use was studied as regular use versus no use or brief experimental use of five drug categories: cannabinoids, stimulants, sedatives, opiates, and hallucinogens. Fifty-one percent of the men and 48% of the women reported regular use of one or more of the drugs in addition to alcohol. For women, the amount of alcohol intake was positively correlated with use of stimulants (r = .32, p = .001), cannabinoids (r = .24, p = .019), sedatives (r = .30, p = .003), and hallucinogens (r = .30, p = .003). For men, correlations between the amount of alcohol intake and drug use were weaker but significant for stimulants (r = .21, p = .002), opiates (r = .15, p = .028), and hallucinogens (r = .15, p = .029). Women with alcoholic mothers displayed higher alcohol intake than women with nonalcoholic mothers (p = .02) and also showed more frequent use of most drugs. Although men with alcoholic fathers also showed greater alcohol intake compared to men with nonalcoholic fathers, the two groups did not differ in drug use. Younger subjects of both sexes were more likely to use cannabinoids, stimulants, opiates, and hallucinogens. Alcohol and sedative use was relatively constant across all age groups. JF - The American journal of drug and alcohol abuse AU - Schmitz, J AU - DeJong, J AU - Roy, A AU - Garnett, D AU - Moore, V AU - Lamparski, D AU - Waxman, R AU - Linnoila, M AD - Laboratory of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 359 EP - 368 VL - 19 IS - 3 SN - 0095-2990, 0095-2990 KW - Psychotropic Drugs KW - 0 KW - Street Drugs KW - Index Medicus KW - Patient Admission KW - Humans KW - Comorbidity KW - Cross-Sectional Studies KW - Adult KW - Incidence KW - Middle Aged KW - Maryland KW - Personality Assessment KW - Female KW - Male KW - Alcoholism -- rehabilitation KW - Mass Screening KW - Alcoholism -- epidemiology KW - Substance-Related Disorders -- rehabilitation KW - Substance-Related Disorders -- psychology KW - Alcoholism -- psychology KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76011296?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+journal+of+drug+and+alcohol+abuse&rft.atitle=Substance+abuse+among+subjects+screened+out+from+an+alcoholism+research+program.&rft.au=Schmitz%2C+J%3BDeJong%2C+J%3BRoy%2C+A%3BGarnett%2C+D%3BMoore%2C+V%3BLamparski%2C+D%3BWaxman%2C+R%3BLinnoila%2C+M&rft.aulast=Schmitz&rft.aufirst=J&rft.date=1993-01-01&rft.volume=19&rft.issue=3&rft.spage=359&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+drug+and+alcohol+abuse&rft.issn=00952990&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-17 N1 - Date created - 1993-11-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Clinician assessment of psychiatric comorbidity and alcoholism severity in adult alcoholic inpatients. AN - 76011214; 8213701 AB - Although psychiatric comorbidity and alcoholism severity are risk factors for poor outcomes in treating alcoholism, little is known about whether clinicians assess these conditions accurately. In this study we evaluated four clinicians' assessments of two indicators of alcoholism severity and three psychiatric co-morbidities in 78 inpatients in their third to seventh day of hospitalization in alcohol treatment programs. Clinicians overestimated the number of days drinking in 28% of subjects, and the number of drinks per drinking day in 37% of subjects. Clinicians underestimated alcohol consumption for patients with higher incomes. Clinicians correctly diagnosed 67% of 18 subjects with antisocial personality disorder, 65% of 26 with major depression, and 89% of 28 with drug abuse. These preliminary results need to be replicated in larger samples of clinicians to determine whether interventions are needed to improve the recognition of important prognostic factors in the treatment of alcoholic patients. JF - The American journal of drug and alcohol abuse AU - Dawes, M A AU - Frank, S AU - Rost, K AD - NIMH Center for Rural Mental Health Care Research, Department of Psychiatry, University of Arkansas for Medical Sciences, Little Rock 72205. Y1 - 1993 PY - 1993 DA - 1993 SP - 377 EP - 386 VL - 19 IS - 3 SN - 0095-2990, 0095-2990 KW - Index Medicus KW - Depressive Disorder -- psychology KW - Humans KW - Antisocial Personality Disorder -- psychology KW - Arkansas -- epidemiology KW - Substance-Related Disorders -- rehabilitation KW - Substance-Related Disorders -- psychology KW - Comorbidity KW - Depressive Disorder -- epidemiology KW - Antisocial Personality Disorder -- epidemiology KW - Substance Abuse Treatment Centers KW - Adult KW - Middle Aged KW - Antisocial Personality Disorder -- rehabilitation KW - Female KW - Male KW - Substance-Related Disorders -- epidemiology KW - Depressive Disorder -- rehabilitation KW - Alcoholism -- rehabilitation KW - Mental Disorders -- rehabilitation KW - Hospitalization KW - Alcoholism -- epidemiology KW - Mental Disorders -- epidemiology KW - Mental Disorders -- psychology KW - Alcoholism -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76011214?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+journal+of+drug+and+alcohol+abuse&rft.atitle=Clinician+assessment+of+psychiatric+comorbidity+and+alcoholism+severity+in+adult+alcoholic+inpatients.&rft.au=Dawes%2C+M+A%3BFrank%2C+S%3BRost%2C+K&rft.aulast=Dawes&rft.aufirst=M&rft.date=1993-01-01&rft.volume=19&rft.issue=3&rft.spage=377&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+drug+and+alcohol+abuse&rft.issn=00952990&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-17 N1 - Date created - 1993-11-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The nonmedical use of prescription drugs in the United States. AN - 76010393; 8413521 JF - NIDA research monograph AU - Adams, E H AU - Kopstein, A N AD - Office of the Director, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1993 PY - 1993 DA - 1993 SP - 109 EP - 119 VL - 131 SN - 1046-9516, 1046-9516 KW - Index Medicus KW - United States KW - Humans KW - Drug Utilization KW - Drug Prescriptions KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76010393?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=The+nonmedical+use+of+prescription+drugs+in+the+United+States.&rft.au=Adams%2C+E+H%3BKopstein%2C+A+N&rft.aulast=Adams&rft.aufirst=E&rft.date=1993-01-01&rft.volume=131&rft.issue=&rft.spage=109&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-15 N1 - Date created - 1993-11-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Characterization of HLA-DMB polymorphism. AN - 76008674; 8406617 JF - Immunogenetics AU - Carrington, M AU - Yeager, M AU - Mann, D AD - Biological Carcinogenesis and Development Program, Inc./DynCorp, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702-1201. Y1 - 1993 PY - 1993 DA - 1993 SP - 446 EP - 449 VL - 38 IS - 6 SN - 0093-7711, 0093-7711 KW - HLA-D Antigens KW - 0 KW - Index Medicus KW - France KW - Exons -- genetics KW - Base Sequence KW - Alleles KW - Sequence Homology, Nucleic Acid KW - Biological Evolution KW - Humans KW - Government Agencies KW - Molecular Sequence Data KW - Polymorphism, Genetic KW - HLA-D Antigens -- genetics KW - Genes, MHC Class II -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76008674?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Immunogenetics&rft.atitle=Characterization+of+HLA-DMB+polymorphism.&rft.au=Carrington%2C+M%3BYeager%2C+M%3BMann%2C+D&rft.aulast=Carrington&rft.aufirst=M&rft.date=1993-01-01&rft.volume=38&rft.issue=6&rft.spage=446&rft.isbn=&rft.btitle=&rft.title=Immunogenetics&rft.issn=00937711&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-01 N1 - Date created - 1993-11-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Development of chemopreventive agents for lung and upper aerodigestive tract cancers. AN - 76003376; 8412195 AB - The lung and upper aerodigestive tract (oral cavity, larynx, pharynx, upper esophagus) will harbor the greatest proportion (approximately 20%) of estimated new cancer cases in 1992. The estimated mortality rate is even higher (32%), which is reflected in a 5-year survival rate of only 7% and 12% for esophageal and lung cancer, respectively. Tobacco use appears to remain the major cause of aerodigestive cancers despite efforts at primary prevention--cessation of exposure. Another strategy to decrease this public health problem is secondary prevention or chemoprevention. Cancer chemoprevention is defined as intervention with chemical agents before invasion to halt or slow the carcinogenic process; potential agents may include minor dietary constituents and pharmaceuticals. The main objective of the Division of Cancer Prevention and Control (DCPC), National Cancer Institute, is to develop promising chemopreventive drugs for use in humans. The testing of cancer chemopreventives for efficacy in the clinic differs from that of cancer treatment drugs. Chemopreventive drug trials involve healthy target populations, and the endpoints are reduced cancer incidence or mortality, or increased latency, with no to minimal toxicity. The lung and upper aerodigestive tract represent a unique opportunity for intervention in this setting. Even with cessation of tobacco exposure, the risk of cancer in the entire epithelium remains high for years due to the "field cancerization" effect. Some of the first chemopreventive trials made use of this system due to the availability of a study population with a tissue at demonstrably high risk for malignant progression. Much of the evidence for chemopreventive efficacy is in the oral cavity because of the well-defined epithelial neoplastic progression, the existence of well-established preclinical models, and relative ease of tissue monitoring and sampling. In one of the first randomized trials, Hong and co-workers demonstrated that 13-cis-retinoic acid prevents the appearance of second primary tumors in patients previously treated for squamous cell carcinomas of the oral cavity and upper respiratory tract. Even using a high risk population, chemoprevention trials involve large sample sizes, lengthy duration and follow-up, and high cost. To circumvent these problems, the use of intermediate biomarkers as surrogate endpoints is being explored. Intermediate biomarkers are defined as biological alterations in tissue (histological, genetic, biochemical, proliferative, differentiation-related) occurring prior to cancer development. In the oral cavity, studies using modulation of a histological intermediate biomarker, dysplastic leukoplakia, as the endpoint have demonstrated response to a retinoid.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Journal of cellular biochemistry. Supplement AU - Kelloff, G J AU - Boone, C W AU - Steele, V K AU - Perloff, M AU - Crowell, J AU - Doody, L A AD - Division of Cancer Prevention and Control, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 2 EP - 17 VL - 17F SN - 0733-1959, 0733-1959 KW - Anticarcinogenic Agents KW - 0 KW - Biomarkers, Tumor KW - Index Medicus KW - Drug Evaluation KW - Animals KW - Humans KW - Clinical Trials as Topic KW - Drug Evaluation, Preclinical KW - Lung Neoplasms -- prevention & control KW - Digestive System Neoplasms -- prevention & control KW - Anticarcinogenic Agents -- therapeutic use KW - Digestive System Neoplasms -- mortality KW - Respiratory Tract Neoplasms -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76003376?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+cellular+biochemistry.+Supplement&rft.atitle=Development+of+chemopreventive+agents+for+lung+and+upper+aerodigestive+tract+cancers.&rft.au=Kelloff%2C+G+J%3BBoone%2C+C+W%3BSteele%2C+V+K%3BPerloff%2C+M%3BCrowell%2C+J%3BDoody%2C+L+A&rft.aulast=Kelloff&rft.aufirst=G&rft.date=1993-01-01&rft.volume=17F&rft.issue=&rft.spage=2&rft.isbn=&rft.btitle=&rft.title=Journal+of+cellular+biochemistry.+Supplement&rft.issn=07331959&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-16 N1 - Date created - 1993-11-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Current gaps and new directions for studying drug use and abuse behavior in minority youth. AN - 76001134; 8413515 JF - NIDA research monograph AU - de la Rosa, M R AU - Recio Adrados, J L AU - Kennedy, N J AU - Milburn, N AD - Epidemiologic Research Branch, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1993 PY - 1993 DA - 1993 SP - 321 EP - 340 VL - 130 SN - 1046-9516, 1046-9516 KW - Index Medicus KW - United States KW - Data Collection -- methods KW - Humans KW - Adolescent KW - Adolescent Behavior KW - Minority Groups -- psychology KW - Substance-Related Disorders -- ethnology KW - Substance-Related Disorders -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/76001134?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Current+gaps+and+new+directions+for+studying+drug+use+and+abuse+behavior+in+minority+youth.&rft.au=de+la+Rosa%2C+M+R%3BRecio+Adrados%2C+J+L%3BKennedy%2C+N+J%3BMilburn%2C+N&rft.aulast=de+la+Rosa&rft.aufirst=M&rft.date=1993-01-01&rft.volume=130&rft.issue=&rft.spage=321&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-15 N1 - Date created - 1993-11-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Mutational analysis of muscarinic acetylcholine receptors: structural basis of ligand/receptor/G protein interactions. AN - 75992328; 8412508 AB - Molecular cloning studies have revealed the existence of five molecularly distinct muscarinic acetylcholine receptors (m1-m5), which differ in their tissue distribution, ligand binding properties, and functional profiles. Structurally (and functionally), the muscarinic receptors are members of the superfamily of G protein-coupled receptors. A variety of different mutagenesis techniques have been used to study the molecular basis of muscarinic receptor function. This approach has led to the identification of distinct receptor domains (or individual amino acids) predicted to play key roles in ligand binding, agonist-dependent receptor activation, and G protein coupling. Since all G protein-linked receptors share a similar molecular architecture, the information gained from the mutational analysis of muscarinic receptors should help delineate functionally important regions of other members of this receptor family. JF - Life sciences AU - Wess, J AD - Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 1447 EP - 1463 VL - 53 IS - 19 SN - 0024-3205, 0024-3205 KW - Receptors, Muscarinic KW - 0 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Acetylcholine KW - N9YNS0M02X KW - Index Medicus KW - Animals KW - Humans KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Mutation KW - Structure-Activity Relationship KW - Binding Sites KW - Receptors, Muscarinic -- genetics KW - Acetylcholine -- metabolism KW - GTP-Binding Proteins -- metabolism KW - Receptors, Muscarinic -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75992328?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Life+sciences&rft.atitle=Mutational+analysis+of+muscarinic+acetylcholine+receptors%3A+structural+basis+of+ligand%2Freceptor%2FG+protein+interactions.&rft.au=Wess%2C+J&rft.aulast=Wess&rft.aufirst=J&rft.date=1993-01-01&rft.volume=53&rft.issue=19&rft.spage=1447&rft.isbn=&rft.btitle=&rft.title=Life+sciences&rft.issn=00243205&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-24 N1 - Date created - 1993-11-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Recombinant immunotoxins: new therapeutic agents for cancer treatment. AN - 75992212; 8402714 AB - We have developed new agents for the treatment of cancer by genetically modifying Pseudomonas exotoxin. We have deleted the cell-binding region of Pseudomonas exotoxin and replaced it with various growth factors or the combining regions of antibodies in a single chain form. These new recombinant molecules are called recombinant toxins. Several different types of recombinant toxins have been produced. B3(Fv)-PE38KDEL is a recombinant toxin that kills many different adenocarcinomas and epidermoid carcinomas. The molecule is now undergoing preclinical development. JF - Cancer detection and prevention AU - Pastan, I H AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 289 EP - 293 VL - 17 IS - 2 SN - 0361-090X, 0361-090X KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - Immunotoxins KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - Animals KW - Mice KW - Translocation, Genetic KW - Bacterial Toxins -- genetics KW - Exotoxins -- genetics KW - Neoplasms, Experimental -- genetics KW - Bacterial Toxins -- therapeutic use KW - Immunotoxins -- therapeutic use KW - Immunotoxins -- genetics KW - Neoplasms, Experimental -- drug therapy KW - Exotoxins -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75992212?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+detection+and+prevention&rft.atitle=Recombinant+immunotoxins%3A+new+therapeutic+agents+for+cancer+treatment.&rft.au=Pastan%2C+I+H&rft.aulast=Pastan&rft.aufirst=I&rft.date=1993-01-01&rft.volume=17&rft.issue=2&rft.spage=289&rft.isbn=&rft.btitle=&rft.title=Cancer+detection+and+prevention&rft.issn=0361090X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-09 N1 - Date created - 1993-11-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - In vitro approaches in developmental toxicology. AN - 75985358; 8400631 AB - While the usefulness of in vitro screens in developmental toxicology seemed obvious a decade or more ago, integration of in vitro or short-term screens for developmental toxicity into the toxicology armamentarium of tests has been very slow. The large number and complexity of critical events in normal development in vivo limit the usefulness of in vitro systems that measure a very narrow range of developmental events, even though such systems are very useful for mechanistic research. Better understanding of the regulatory mechanisms involved in normal development that is evolving from molecular and developmental biology laboratories should help to identify critical events and processes in development that could serve as functional screens for abnormal development in the future. JF - Reproductive toxicology (Elmsford, N.Y.) AU - Schwetz, B A AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993 PY - 1993 DA - 1993 SP - 125 EP - 127 VL - 7 Suppl 1 SN - 0890-6238, 0890-6238 KW - Index Medicus KW - Animals KW - In Vitro Techniques KW - Embryonic and Fetal Development -- drug effects KW - Toxicology -- methods KW - Abnormalities, Drug-Induced -- etiology KW - Drug Evaluation, Preclinical -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75985358?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Reproductive+toxicology+%28Elmsford%2C+N.Y.%29&rft.atitle=In+vitro+approaches+in+developmental+toxicology.&rft.au=Schwetz%2C+B+A&rft.aulast=Schwetz&rft.aufirst=B&rft.date=1993-01-01&rft.volume=7+Suppl+1&rft.issue=&rft.spage=125&rft.isbn=&rft.btitle=&rft.title=Reproductive+toxicology+%28Elmsford%2C+N.Y.%29&rft.issn=08906238&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-23 N1 - Date created - 1993-11-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Preferential incorporation of 3'-azido-2',3'-dideoxythymidine into telomeric DNA and Z-DNA-containing regions of Chinese hamster ovary cells. AN - 75978384; 8397798 AB - 3'-Azido-2',3'-dideoxythymidine (azidothymidine; AZT) induces bone marrow toxicity in patients chronically given therapeutic doses of drug and is tumorigenic in rodents, inducing squamous cell tumors in vaginal tissues of mice and rats. In the study reported here, we explored the incorporation of AZT into specific regions of mammalian chromosomal DNA. CHO cells were exposed to AZT for 4 h, allowed to complete at least one cell cycle, and then arrested in metaphase with colchicine. Regions of concentrated AZT incorporation were identified in individual metaphase chromosomes by immunohistochemistry using antiserum specific for AZT and a secondary antiserum with a streptavidin--Texas red end point. These studies demonstrated that most of the intensely staining regions were chromosomal ends or telomeres. When 18 metaphases were examined, all telomeres but one (39 of 40) were positive at least once. Using an anti-Z-DNA antibody, chromosomal regions containing DNA in Z conformation were also localized by immunohistochemistry using a rhodamine-conjugated secondary antibody. When metaphase chromosome spreads were stained for either AZT or Z-DNA, ideograms showing localization of AZT (18 metaphases) and DNA in Z configuration (26 metaphases) were drawn for every chromosome of each metaphase examined. These ideograms demonstrated that 60% of the regions that stained positive for AZT were also positive for Z-DNA. Furthermore, slides incubated with both antibodies, using streptavidin--Texas red to identify AZT and fluorescein to identify Z-DNA, confirmed colocalization of the two markers. Additional experiments exploring the induction of chromatin bridges in AZT-treated cells suggest that the analogue may be able to bind to and disrupt the normal functioning of telomeric DNA. JF - Molecular carcinogenesis AU - Olivero, O A AU - Poirier, M C AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, NIH, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 81 EP - 88 VL - 8 IS - 2 SN - 0899-1987, 0899-1987 KW - Chromatin KW - 0 KW - Zidovudine KW - 4B9XT59T7S KW - DNA KW - 9007-49-2 KW - Index Medicus KW - AIDS/HIV KW - Microscopy, Fluorescence KW - Animals KW - Chromatin -- chemistry KW - CHO Cells KW - Metaphase KW - Chromosome Mapping KW - Female KW - Cricetinae KW - Telomere -- metabolism KW - Zidovudine -- metabolism KW - DNA -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75978384?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+carcinogenesis&rft.atitle=Preferential+incorporation+of+3%27-azido-2%27%2C3%27-dideoxythymidine+into+telomeric+DNA+and+Z-DNA-containing+regions+of+Chinese+hamster+ovary+cells.&rft.au=Olivero%2C+O+A%3BPoirier%2C+M+C&rft.aulast=Olivero&rft.aufirst=O&rft.date=1993-01-01&rft.volume=8&rft.issue=2&rft.spage=81&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-19 N1 - Date created - 1993-11-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Combination chemoimmunotherapy for metastatic colorectal cancer using 5-fluorouracil, leucovorin and interleukin-2. AN - 75977405; 8398334 AB - 25 patients with metastatic colorectal cancer were entered into a phase II trial of combination chemoimmunotherapy using a sequential regimen of 5-fluorouracil (5-FU) and leucovorin and high-dose recombinant human interleukin-2 (rIL-2). Patients initially received three cycles of chemotherapy consisting of 500 mg/m2 of intravenous leucovorin followed by 375 mg/m2 of bolus 5-FU both given daily on days 1-5 of a 21 day cycle. Ten days after the last dose of chemotherapy in cycle 3, patients began high-dose rIL-2 at 720,000 IU/kg intravenously every 8 h to the maximum tolerated number of doses. After 7-10 days of recovery, this rIL-2 treatment was repeated to complete one full course of chemoimmunotherapy. There was no grade IV toxicity associated with 183 cycles of chemotherapy. Other than slight increases in the frequency of diarrhoea, stomatitis and hyperbilirubinaemia, rIL-2 toxicity was similar to that seen in patients given rIL-2 without chemotherapy. Of 23 evaluable patients, the overall response rate (partial + complete response) was 46% with 2 complete responses. Only 3 patients showed major tumour regression during the rIL-2 phase of therapy, but these 3 patients included both complete responders and the 3 most durable responses (15, 16 and 24 months). We conclude that sequential 5-FU/leucovorin and rIL-2 can be given safely without major increases in toxicity over either therapy alone, and although nearly all responses seen are largely attributable to chemotherapy, a contribution of immunotherapy to the minority of patients achieving complete or durable responses cannot be ruled out. JF - European journal of cancer (Oxford, England : 1990) AU - Yang, J C AU - Shlasko, E AU - Ritchey, J L AU - Landry, J G AU - White, D E AU - Rosenberg, S A AD - Surgery Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 355 EP - 359 VL - 29A IS - 3 SN - 0959-8049, 0959-8049 KW - Interleukin-2 KW - 0 KW - Recombinant Proteins KW - Leucovorin KW - Q573I9DVLP KW - Fluorouracil KW - U3P01618RT KW - Index Medicus KW - Interleukin-2 -- administration & dosage KW - Humans KW - Leucovorin -- administration & dosage KW - Lung Neoplasms -- secondary KW - Lung Neoplasms -- drug therapy KW - Liver Neoplasms -- secondary KW - Fluorouracil -- administration & dosage KW - Liver Neoplasms -- drug therapy KW - Adult KW - Middle Aged KW - Recombinant Proteins -- administration & dosage KW - Female KW - Male KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Colorectal Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75977405?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+cancer+%28Oxford%2C+England+%3A+1990%29&rft.atitle=Combination+chemoimmunotherapy+for+metastatic+colorectal+cancer+using+5-fluorouracil%2C+leucovorin+and+interleukin-2.&rft.au=Yang%2C+J+C%3BShlasko%2C+E%3BRitchey%2C+J+L%3BLandry%2C+J+G%3BWhite%2C+D+E%3BRosenberg%2C+S+A&rft.aulast=Yang&rft.aufirst=J&rft.date=1993-01-01&rft.volume=29A&rft.issue=3&rft.spage=355&rft.isbn=&rft.btitle=&rft.title=European+journal+of+cancer+%28Oxford%2C+England+%3A+1990%29&rft.issn=09598049&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-01 N1 - Date created - 1993-11-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Phospholipase C isozymes and modulation by cAMP-dependent protein kinase. AN - 75968276; 8398418 JF - Advances in second messenger and phosphoprotein research AU - Rhee, S G AU - Lee, C W AU - Jhon, D Y AD - Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 57 EP - 64 VL - 28 SN - 1040-7952, 1040-7952 KW - Isoenzymes KW - 0 KW - Colforsin KW - 1F7A44V6OU KW - Cyclic AMP KW - E0399OZS9N KW - Cyclic AMP-Dependent Protein Kinases KW - EC 2.7.11.11 KW - Type C Phospholipases KW - EC 3.1.4.- KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Second Messenger Systems KW - Colforsin -- pharmacology KW - Dose-Response Relationship, Drug KW - Humans KW - Cyclic AMP -- pharmacology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - T-Lymphocytes -- enzymology KW - Cell Line KW - Cyclic AMP-Dependent Protein Kinases -- metabolism KW - Type C Phospholipases -- antagonists & inhibitors KW - Isoenzymes -- metabolism KW - Type C Phospholipases -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75968276?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advances+in+second+messenger+and+phosphoprotein+research&rft.atitle=Phospholipase+C+isozymes+and+modulation+by+cAMP-dependent+protein+kinase.&rft.au=Rhee%2C+S+G%3BLee%2C+C+W%3BJhon%2C+D+Y&rft.aulast=Rhee&rft.aufirst=S&rft.date=1993-01-01&rft.volume=28&rft.issue=&rft.spage=57&rft.isbn=&rft.btitle=&rft.title=Advances+in+second+messenger+and+phosphoprotein+research&rft.issn=10407952&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-16 N1 - Date created - 1993-11-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Angiofollicular lymphoid hyperplasia (Castleman's disease) in two mice treated with polyoma virus or urethane. AN - 75964209; 8397437 AB - Localized angiofollicular hyperplasia, otherwise known as Castleman's disease, is described in the lymph nodes of 2 mice of different strains, one inoculated with polyoma virus at birth and the other given urethane within 24 hr of birth. A plasma cell component in the lesion, suggestive of bone marrow stem cell involvement, was present in the mouse treated with polyoma virus but absent in the mouse given intraperitoneal urethane. Dysregulated interleukin 6 has recently been reported to produce the systemic variety of angiofollicular hyperplasia in mice, but the role of this cytokine in the localized variety described in this report is not known. This lesion appears to be rare in mice, but when present it could easily be missed or overlooked because the typical layering of follicle cells and the relatively large germinal centers seen in humans do not appear prominent in mice. Although there is, obviously, no proof of a causal relationship between the lesion and polyoma virus or urethane, it is suggested that this lesion be searched for in order to estimate its frequency and possible etiologic associations. JF - Toxicologic pathology AU - Williams, A O AU - Banks, P M AU - Liebelt, A G AU - Stewart, H L AU - Saffiotti, U AD - Laboratory of Experimental Pathology, National Cancer Institutes, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 26 EP - 34 VL - 21 IS - 1 SN - 0192-6233, 0192-6233 KW - Urethane KW - 3IN71E75Z5 KW - Index Medicus KW - Animals KW - Mice, Inbred C57BL KW - Lymph Nodes -- pathology KW - Mice KW - Female KW - Giant Lymph Node Hyperplasia -- chemically induced KW - Tumor Virus Infections KW - Polyomavirus KW - Giant Lymph Node Hyperplasia -- pathology KW - Urethane -- toxicity KW - Giant Lymph Node Hyperplasia -- microbiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75964209?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+pathology&rft.atitle=Angiofollicular+lymphoid+hyperplasia+%28Castleman%27s+disease%29+in+two+mice+treated+with+polyoma+virus+or+urethane.&rft.au=Williams%2C+A+O%3BBanks%2C+P+M%3BLiebelt%2C+A+G%3BStewart%2C+H+L%3BSaffiotti%2C+U&rft.aulast=Williams&rft.aufirst=A&rft.date=1993-01-01&rft.volume=21&rft.issue=1&rft.spage=26&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=01926233&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-21 N1 - Date created - 1993-10-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Pathology of preneoplastic and neoplastic renal tubular lesions induced in F-344 rats by sodium barbital, a nongenotoxic renal carcinogen and nephrotoxin. AN - 75963531; 8378705 AB - Sodium barbital (NaBB), a long-duration sedative/hypnotic barbiturate, is a nongenotoxic nephrotoxin and induces chronic persistent increases in rates of cell proliferation in renal cortical tubules of male F-344/NCr rats. In 5 of our 2-stage carcinogenesis experiments with NaBB at doses of 500, 1,000, or 4,000 ppm for periods of up to 106 wk of age, renal tubular cell tumors were found in incidences of up to 25% in rats receiving only NaBB while fewer than 1% of controls had renal epithelial tumors. We reviewed renal tubular proliferative lesions found in these studies and classified the lesions based on morphology, histogenesis, and immunohistochemical findings. Renal dysplastic tubules (DTs; atypical hyperplasia), putative preneoplastic lesions rarely seen in controls, were found in the renal cortex of more than 50% of the NaBB-exposed rats. DTs were classified into grades 1-3, based on lesion size and growth patterns. All renal adenomas were usually of the basophilic phenotype, and 70% of basophilic adenomas displayed solid patterns, while tumors with papillary, cystic, or tubular patterns were seen less commonly. By serial or step sectioning of the DTs and tumors, evidence was found indicating that the high grades (grade 2 or 3) of DTs, some of which arose in the P1 or P2 segment of the proximal tubules, were sometimes connected to the adenomas. Vimentin expression was demonstrated immunohistochemically in NaBB-induced renal tubular adenomas but not in normal tubules. Tumors were usually not immunoreactive for glutathione S-transferase, placental form, but heterogeneous immunoreactivity was also seen in some tumors. Lysozyme was absent in preneoplastic and neoplastic lesions induced by NaBB, while some intact normal proximal convoluted tubules were immunoreactive. The common tumor phenotype induced by NaBB, the basophilic solid adenoma, was similar to the most common type of spontaneous renal tumor found in untreated aging F-344 rats. NaBB may promote naturally occurring renal preneoplastic or neoplastic tubular lesions of this unique phenotype, but it is also possible that it may induce these lesions de novo. JF - Toxicologic pathology AU - Kurata, Y AU - Diwan, B A AU - Uno, H AU - Rice, J M AU - Ward, J M AD - Tumor Pathology and Pathogenesis Section, NCI-Frederick Cancer Research and Development Center, Frederick, Maryland 21702-1201. Y1 - 1993 PY - 1993 DA - 1993 SP - 35 EP - 45 VL - 21 IS - 1 SN - 0192-6233, 0192-6233 KW - Carcinogens KW - 0 KW - Barbital KW - 5WZ53ENE2P KW - Index Medicus KW - Rats KW - Hyperplasia -- pathology KW - Animals KW - Rats, Inbred F344 KW - Hyperplasia -- chemically induced KW - Kidney -- pathology KW - Immunohistochemistry KW - Male KW - Carcinoma, Renal Cell -- pathology KW - Kidney Neoplasms -- pathology KW - Kidney Tubules -- pathology KW - Carcinoma, Renal Cell -- chemically induced KW - Adenoma -- ultrastructure KW - Kidney Neoplasms -- chemically induced KW - Carcinoma, Renal Cell -- ultrastructure KW - Carcinogens -- toxicity KW - Barbital -- toxicity KW - Precancerous Conditions -- pathology KW - Kidney Neoplasms -- ultrastructure KW - Kidney Tubules -- drug effects KW - Precancerous Conditions -- chemically induced KW - Adenoma -- chemically induced KW - Adenoma -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75963531?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+pathology&rft.atitle=Pathology+of+preneoplastic+and+neoplastic+renal+tubular+lesions+induced+in+F-344+rats+by+sodium+barbital%2C+a+nongenotoxic+renal+carcinogen+and+nephrotoxin.&rft.au=Kurata%2C+Y%3BDiwan%2C+B+A%3BUno%2C+H%3BRice%2C+J+M%3BWard%2C+J+M&rft.aulast=Kurata&rft.aufirst=Y&rft.date=1993-01-01&rft.volume=21&rft.issue=1&rft.spage=35&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=01926233&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-21 N1 - Date created - 1993-10-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Genetically engineered monoclonal antibodies armed with radionuclides. AN - 75957030; 8103951 JF - The Year in immunology AU - Waldmann, T A AD - Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, Md. Y1 - 1993 PY - 1993 DA - 1993 SP - 205 EP - 212 VL - 7 SN - 0256-2308, 0256-2308 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, CD4 KW - Immunotoxins KW - Neoplasm Proteins KW - Radioisotopes KW - Yttrium Radioisotopes KW - Bismuth KW - U015TT5I8H KW - Index Medicus KW - AIDS/HIV KW - Yttrium Radioisotopes -- therapeutic use KW - Neoplasms -- drug therapy KW - Animals KW - Neoplasm Proteins -- biosynthesis KW - Humans KW - Leukemia-Lymphoma, Adult T-Cell -- metabolism KW - Mice KW - Gene Expression Regulation, Neoplastic KW - Radioimmunotherapy KW - Neoplasms -- radiotherapy KW - Autoimmune Diseases -- diagnostic imaging KW - Bismuth -- therapeutic use KW - Neoplasms -- diagnostic imaging KW - Leukemia-Lymphoma, Adult T-Cell -- radiotherapy KW - Autoimmune Diseases -- metabolism KW - Radioimmunodetection KW - Autoimmune Diseases -- radiotherapy KW - Radioisotopes -- therapeutic use KW - Immunotoxins -- therapeutic use KW - Neoplasms -- metabolism KW - Protein Engineering KW - Antigens, CD4 -- classification KW - Antigens, CD4 -- analysis KW - Antibodies, Monoclonal -- genetics KW - CD4-Positive T-Lymphocytes -- immunology KW - Antigens, CD4 -- biosynthesis KW - Antigens, CD4 -- immunology KW - Antibodies, Monoclonal -- therapeutic use KW - Antibodies, Monoclonal -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75957030?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Year+in+immunology&rft.atitle=Genetically+engineered+monoclonal+antibodies+armed+with+radionuclides.&rft.au=Waldmann%2C+T+A&rft.aulast=Waldmann&rft.aufirst=T&rft.date=1993-01-01&rft.volume=7&rft.issue=&rft.spage=205&rft.isbn=&rft.btitle=&rft.title=The+Year+in+immunology&rft.issn=02562308&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-14 N1 - Date created - 1993-10-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Estrogen replacement therapy and breast cancer risk. AN - 75950504; 8405213 AB - Assessment of the effects of menopausal estrogens on the risk of breast cancer is obviously complex, with proper evaluations requiring attention to the effects of selection, recall, and surveillance biases; confounding factors; detailed exposure relations; and subgroup variations. Although much discussion has ensued over the extent to which variations between studies might be due to a variety of methodological differences, it is likely that the limited statistical power of many studies may be largely responsible for the divergent effects observed, particularly with regard to assessing the effect of long-term usage. Thus, in case-control studies in which population controls have been used and for which there have been a sufficient number of women using estrogens for approximately 10 or more years, it appears as though such an exposure may be associated with some elevated risk, possibly on the order of 30-80 percent (16, 34, 36-38)--a magnitude of risk that is obviously extremely difficult to detect in most epidemiologic studies. Evaluation of risks associated with short-term use is even more difficult, which has led most investigators to conclude that usage of less than 5 years is associated with no detectable excess risk. Problems with statistical power also plague evaluations of more detailed measures of use, including dosage and type of preparations, although there is some indication that nonconjugated preparations may be associated with a higher risk than other types of estrogens (16, 20, 36, 44, 51). In addition, there is some evidence that recent use may be associated with a modest elevation in risk (32, 33, 53), although effects of surveillance bias are difficult to resolve. Interpretation of the effect is complicated by several studies which have found estrogens to be associated with an increased risk of breast cancer incidence but a decreased risk of death, with the mortality ratios ranging from approximately 0.5 to 0.8 (33, 92, 93). Although one of these studies hypothesized that the relation with mortality may reflect a tendency for women with clinically recognized breast cancers and those at high risk not to be prescribed estrogens for long periods of time, studies showing that estrogen users have more favorable tumor characteristics at diagnosis than nonusers (20, 36) suggest that screening biases may be involved. The numerous contradictions regarding effects of menopausal estrogens from observational studies have heightened interest in the results of several ongoing controlled clinical trials.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Epidemiologic reviews AU - Brinton, L A AU - Schairer, C AD - Environmental Epidemiology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 66 EP - 79 VL - 15 IS - 1 SN - 0193-936X, 0193-936X KW - Estrogens KW - 0 KW - Index Medicus KW - Risk Factors KW - Humans KW - Meta-Analysis as Topic KW - Female KW - Estrogens -- administration & dosage KW - Breast Neoplasms -- genetics KW - Estrogen Replacement Therapy -- adverse effects KW - Estrogen Replacement Therapy -- methods KW - Breast Neoplasms -- etiology KW - Breast Neoplasms -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75950504?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Epidemiologic+reviews&rft.atitle=Estrogen+replacement+therapy+and+breast+cancer+risk.&rft.au=Brinton%2C+L+A%3BSchairer%2C+C&rft.aulast=Brinton&rft.aufirst=L&rft.date=1993-01-01&rft.volume=15&rft.issue=1&rft.spage=66&rft.isbn=&rft.btitle=&rft.title=Epidemiologic+reviews&rft.issn=0193936X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-11-09 N1 - Date created - 1993-11-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Gangliosides as receptors for bacterial enterotoxins. AN - 75934159; 8396312 JF - Advances in lipid research AU - Fishman, P H AU - Pacuszka, T AU - Orlandi, P A AD - Membrane Biochemistry Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 165 EP - 187 VL - 25 SN - 0065-2849, 0065-2849 KW - Bacterial Toxins KW - 0 KW - Enterotoxins KW - Escherichia coli Proteins KW - Gangliosides KW - Lipoproteins KW - Receptors, Cell Surface KW - Receptors, Immunologic KW - Receptors, Peptide KW - choleragen receptor KW - heat-labile enterotoxin, E coli KW - G(M1) Ganglioside KW - 37758-47-7 KW - Cholera Toxin KW - 9012-63-9 KW - Guanylate Cyclase KW - EC 4.6.1.2 KW - Receptors, Guanylate Cyclase-Coupled KW - enterotoxin receptor KW - Index Medicus KW - Receptors, Cell Surface -- metabolism KW - Animals KW - Lipoproteins -- metabolism KW - Receptors, Immunologic -- metabolism KW - Humans KW - Molecular Sequence Data KW - Carbohydrate Sequence KW - Lipid Metabolism KW - Enterotoxins -- chemistry KW - Bacterial Toxins -- metabolism KW - Enterotoxins -- metabolism KW - Bacterial Toxins -- chemistry KW - Cholera Toxin -- chemistry KW - Gangliosides -- metabolism KW - Cholera Toxin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75934159?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advances+in+lipid+research&rft.atitle=Gangliosides+as+receptors+for+bacterial+enterotoxins.&rft.au=Fishman%2C+P+H%3BPacuszka%2C+T%3BOrlandi%2C+P+A&rft.aulast=Fishman&rft.aufirst=P&rft.date=1993-01-01&rft.volume=25&rft.issue=&rft.spage=165&rft.isbn=&rft.btitle=&rft.title=Advances+in+lipid+research&rft.issn=00652849&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-05 N1 - Date created - 1993-10-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Genetic and molecular basis for cellular senescence. AN - 75930171; 8368137 AB - Normal human and rodent cells in culture exhibit a finite life span at the end of which they exhibit morphological changes and cease proliferating, a process termed cellular senescence or cellular aging. Many cancer cells differ from normal cells in that they do not senesce and have an indefinite life span in culture, suggesting that alterations relating to cellular senescence are involved in the neoplastic evolution of tumor cells. Recent experimental results strongly support a genetic basis for cellular senescence. Defects in the senescence program in transformed cells can be corrected by introduction of a specific chromosome from normal cells into the abnormal cells. Using this approach, possible senescence genes have been mapped to specific chromosomes. Cell cycle control genes that regulate entry into the DNA synthetic phase of the cell cycle must be altered in senescent cells. Recent findings suggest that phosphorylation of the retinoblastoma gene is altered in senescent cells. It is possible, but not yet proven, that aging at the cellular level contributes to the aging of the individual. Therefore, an understanding of cellular senescence at the genetic and molecular levels may provide new insights into both the cancer and aging processes. JF - Advances in experimental medicine and biology AU - Barrett, J C AU - Annab, L A AU - Futreal, P A AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993 PY - 1993 DA - 1993 SP - 27 EP - 43 VL - 330 SN - 0065-2598, 0065-2598 KW - HPRT KW - RB KW - Genetic Markers KW - 0 KW - Retinoblastoma Protein KW - CDC2 Protein Kinase KW - EC 2.7.11.22 KW - Index Medicus KW - Animals KW - CDC2 Protein Kinase -- metabolism KW - Humans KW - Fibroblasts -- cytology KW - Chromosome Mapping KW - Models, Biological KW - Cricetulus -- physiology KW - Phosphorylation KW - Cell Transformation, Neoplastic -- genetics KW - Retinoblastoma Protein -- genetics KW - Rodentia -- physiology KW - Chromosome Deletion KW - Lung -- cytology KW - Protein Processing, Post-Translational KW - Interphase KW - Mice KW - Retinoblastoma Protein -- biosynthesis KW - Longevity KW - Cell Fusion KW - Genes, Retinoblastoma KW - Cells, Cultured KW - Cell Death -- genetics KW - Species Specificity KW - Cricetinae KW - Mesocricetus -- physiology KW - Chromosomes, Human, Pair 1 KW - Hybrid Cells -- cytology KW - Cell Aging -- genetics KW - Chromosomes, Human, Pair 11 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75930171?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advances+in+experimental+medicine+and+biology&rft.atitle=Genetic+and+molecular+basis+for+cellular+senescence.&rft.au=Barrett%2C+J+C%3BAnnab%2C+L+A%3BFutreal%2C+P+A&rft.aulast=Barrett&rft.aufirst=J&rft.date=1993-01-01&rft.volume=330&rft.issue=&rft.spage=27&rft.isbn=&rft.btitle=&rft.title=Advances+in+experimental+medicine+and+biology&rft.issn=00652598&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-04 N1 - Date created - 1993-10-04 N1 - Date revised - 2017-01-13 N1 - Gene symbol - HPRT; RB N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The role of the septohippocampal pathway in the mediation of colchicine-induced compensatory changes in the rat hippocampus. AN - 75913154; 8361677 AB - To study the involvement of the septohippocampal pathway in colchicine-induced changes in the hippocampus, colchicine was used to lesion the septum and/or hippocampus of male, Fischer-344 rats. Rats were killed 12 weeks post-lesion and histochemical and biochemical measurements were performed. [3H]-QNB binding, choline acetyltransferase (ChAT) activity and agonist-stimulated release of inositol phosphates (IPs) were measured in hippocampal slices. AChE histochemistry was also performed to visualize AChE positive fibers in the hippocampus. Increases in ChAT activity, AChE staining and carbachol-stimulated IP release observed in hippocampal-lesioned animals were attenuated in animals receiving both septal and hippocampal lesions. However, the decrease observed in [3H]-QNB binding sites after intradentate colchicine was not affected by septal lesions. Subsequent studies also found enhanced sensitivity to excitatory amino acid (EAA)-stimulated IP release in hippocampal-lesioned animals. Similar to the changes observed in carbachol-stimulated PI hydrolysis, this increase was also long-lasting. However, the hyperstimulation of EAA-induced IP release was not attenuated by the septal lesion. Thus, it appears that the neurochemical and morphological changes observed in the hippocampus following intradentate colchicine are dependent upon more than one afferent projection to the hippocampus. JF - Neurotoxicology AU - Tandon, P AU - Barone, S AU - Bonner, M J AU - Ali, S F AU - Tilson, H A AD - Laboratory of Molecular and Integrative Neuroscience, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993 PY - 1993 DA - 1993 SP - 41 EP - 50 VL - 14 IS - 1 SN - 0161-813X, 0161-813X KW - Inositol Phosphates KW - 0 KW - Receptors, Muscarinic KW - Choline O-Acetyltransferase KW - EC 2.3.1.6 KW - Colchicine KW - SML2Y3J35T KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Inositol Phosphates -- metabolism KW - Neural Pathways -- physiology KW - Histocytochemistry KW - Choline O-Acetyltransferase -- metabolism KW - Male KW - Receptors, Muscarinic -- metabolism KW - Septum Pellucidum -- physiology KW - Hippocampus -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75913154?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurotoxicology&rft.atitle=The+role+of+the+septohippocampal+pathway+in+the+mediation+of+colchicine-induced+compensatory+changes+in+the+rat+hippocampus.&rft.au=Tandon%2C+P%3BBarone%2C+S%3BBonner%2C+M+J%3BAli%2C+S+F%3BTilson%2C+H+A&rft.aulast=Tandon&rft.aufirst=P&rft.date=1993-01-01&rft.volume=14&rft.issue=1&rft.spage=41&rft.isbn=&rft.btitle=&rft.title=Neurotoxicology&rft.issn=0161813X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-27 N1 - Date created - 1993-09-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Genetic determinants in carcinogenesis. AN - 75912819; 8356312 JF - Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer AU - Barrett, J C AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709. Y1 - 1993 PY - 1993 DA - 1993 SP - 1 EP - 13 VL - 128 SN - 0080-0015, 0080-0015 KW - Retinoblastoma Protein KW - 0 KW - Index Medicus KW - Aging -- physiology KW - Animals KW - Tumor Cells, Cultured KW - Genes, Retinoblastoma KW - Risk Factors KW - Humans KW - Retinoblastoma Protein -- metabolism KW - Rodentia KW - Cell Cycle KW - Neoplasms -- pathology KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75912819?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Recent+results+in+cancer+research.+Fortschritte+der+Krebsforschung.+Progres+dans+les+recherches+sur+le+cancer&rft.atitle=Genetic+determinants+in+carcinogenesis.&rft.au=Barrett%2C+J+C&rft.aulast=Barrett&rft.aufirst=J&rft.date=1993-01-01&rft.volume=128&rft.issue=&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Recent+results+in+cancer+research.+Fortschritte+der+Krebsforschung.+Progres+dans+les+recherches+sur+le+cancer&rft.issn=00800015&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-23 N1 - Date created - 1993-09-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The in vitro analysis of biochemical changes relevant to skin carcinogenesis. AN - 75909720; 8356327 JF - Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer AU - Yuspa, S H AU - Punnonen, K AU - Lee, E AU - Hennings, H AU - Strickland, J AU - Cheng, C AU - Glick, A AU - Dlugosz, A AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 299 EP - 308 VL - 128 SN - 0080-0015, 0080-0015 KW - Protein Kinases KW - EC 2.7.- KW - Index Medicus KW - Phenotype KW - Protein Kinases -- metabolism KW - Animals KW - Reference Values KW - Tumor Cells, Cultured KW - Epidermis -- cytology KW - Cell Differentiation KW - Keratinocytes -- pathology KW - Cell Transformation, Neoplastic -- metabolism KW - Skin Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75909720?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Recent+results+in+cancer+research.+Fortschritte+der+Krebsforschung.+Progres+dans+les+recherches+sur+le+cancer&rft.atitle=The+in+vitro+analysis+of+biochemical+changes+relevant+to+skin+carcinogenesis.&rft.au=Yuspa%2C+S+H%3BPunnonen%2C+K%3BLee%2C+E%3BHennings%2C+H%3BStrickland%2C+J%3BCheng%2C+C%3BGlick%2C+A%3BDlugosz%2C+A&rft.aulast=Yuspa&rft.aufirst=S&rft.date=1993-01-01&rft.volume=128&rft.issue=&rft.spage=299&rft.isbn=&rft.btitle=&rft.title=Recent+results+in+cancer+research.+Fortschritte+der+Krebsforschung.+Progres+dans+les+recherches+sur+le+cancer&rft.issn=00800015&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-23 N1 - Date created - 1993-09-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Negative regulation of mitogen-stimulated, anchorage-independent cell growth by a tumor-suppressor gene function. AN - 75904163; 8394717 AB - Immortal, nontumorigenic cell lines of Syrian hamster embryo (SHE) cells with different tumor-suppressing activity were isolated. Subclones from the parental cells were isolated that either had retained (supB+) or lost (supB-) the ability to suppress tumorigenicity after hybridization with tumor cells. The growth properties of these cells were studied to determine how this tumor-suppressor gene function influences cell growth. When the cells were grown on plastic, their growth properties were similar, and neither cell type grew in soft agar containing 10% serum, which supported the growth of tumorigenic cells. However, in agar supplemented with growth factors and 10% serum, supB- cells formed colonies whereas supB+ cells did not. Efficient growth (colony-forming efficiencies greater than 20%) of supB- cells was obtained in agar supplemented with serum and a combination of epidermal growth factor (EGF), platelet-derived growth factor (PDGF), and insulin (EPI) or with serum and basic fibroblast growth factor (bFGF). The effect of EPI and bFGF together was additive. supB+ cells failed to grow under any of these conditions, suggesting that the suppressor gene function blocked the growth response of the cells to multiple growth factors when the cells were suspended in agar. In SupB- cells, transforming growth factor-beta 1 and retinoic acid inhibited anchorage-independent growth response to EPI but not the growth response to bFGF. These observations are consistent with the hypothesis that bFGF stimulates the growth of supB- cells by a signal transduction pathway that differs from the pathway stimulated by EGF or PDGF. Thus, this suppressor gene function may regulate anchorage-independent growth at some common point in signal transduction for multiple mitogens. JF - Molecular carcinogenesis AU - Afshari, C A AU - Barrett, J C AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. Y1 - 1993 PY - 1993 DA - 1993 SP - 249 EP - 256 VL - 7 IS - 4 SN - 0899-1987, 0899-1987 KW - supB KW - Growth Substances KW - 0 KW - Insulin KW - Platelet-Derived Growth Factor KW - Receptors, Cell Surface KW - Transforming Growth Factor beta KW - Tumor Necrosis Factor-alpha KW - Fibroblast Growth Factor 2 KW - 103107-01-3 KW - Epidermal Growth Factor KW - 62229-50-9 KW - Interferon-gamma KW - 82115-62-6 KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Receptor, Insulin KW - Receptors, Platelet-Derived Growth Factor KW - Index Medicus KW - Fibroblast Growth Factor 2 -- pharmacology KW - Transforming Growth Factor beta -- pharmacology KW - Receptors, Platelet-Derived Growth Factor -- metabolism KW - Animals KW - Fetus KW - Drug Interactions KW - Receptor, Epidermal Growth Factor -- metabolism KW - Tumor Necrosis Factor-alpha -- pharmacology KW - Platelet-Derived Growth Factor -- pharmacology KW - Interferon-gamma -- pharmacology KW - Insulin -- pharmacology KW - Epidermal Growth Factor -- pharmacology KW - Mesocricetus KW - Cell Adhesion -- drug effects KW - Cell Line KW - Receptor, Insulin -- metabolism KW - Cricetinae KW - Receptors, Cell Surface -- metabolism KW - Genes, Tumor Suppressor KW - Growth Substances -- pharmacology KW - Cell Division -- physiology KW - Cell Division -- drug effects KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75904163?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+carcinogenesis&rft.atitle=Negative+regulation+of+mitogen-stimulated%2C+anchorage-independent+cell+growth+by+a+tumor-suppressor+gene+function.&rft.au=Afshari%2C+C+A%3BBarrett%2C+J+C&rft.aulast=Afshari&rft.aufirst=C&rft.date=1993-01-01&rft.volume=7&rft.issue=4&rft.spage=249&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-23 N1 - Date created - 1993-09-23 N1 - Date revised - 2017-01-13 N1 - Gene symbol - supB N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Cellular and molecular alterations in human epithelial cells transformed by recombinant human papillomavirus DNA. AN - 75898526; 8394744 AB - Human papillomaviruses (HPVs) contribute to the development of benign and malignant cervical cancer; however, the exact role of papillomaviruses in the multistage carcinogenesis process is unclear. The development of HPV-immortalized cervical and foreskin cell lines represents a useful model for studying the role of HPVs in cervical cancer. Studies with these cells show that HPV genes regulate epithelial cell growth and differentiation. Transfection of HPV types associated with invasive cervical cancer results in immortalization of human epithelial cells, whereas HPVs not associated with cancer are ineffective. The combination of E6 and E7 genes, which are normally retained and expressed in cervical carcinomas, is sufficient for immortalization; however, the E7 gene alone induces immortality less efficiently. Although the immortalized cells actively express HPV oncoproteins observed in cervical cancer, after injection of immortal cells into nude mice, tumors are rare, having been reported only for HPV-18. Immortalized cells are resistant to terminal differentiation; in fact, HPVs may contribute to the carcinogenic process by uncoupling the processes of cell growth and differentiation. Host regulation of viral genes also is important in the malignant process. Endogenous cytokines modify HPV gene expression and influence the pathogenesis of HPV infection in the cervix. HPV gene expression is regulated by cellular transcriptional activators and repressors. This normal regulation is altered by viral integration. HPVs become integrated preferentially at chromosomal regions near fragile sites and protooncogenes. In fact, immortality is associated with induction of structural rearrangements frequently affecting HPV integration sites. Structural and numerical alterations nonrandomly involve chromosomes 1, 11, 19, and 20, with chromosome 1 alteration being the most predominant. Wild-type functions of Rb and p53 are necessary to control normal cell growth, and mutation or loss of these suppressor genes often contributes to cancer development. In HPV-containing carcinomas, pRb and p53 were wild type. However, in carcinomas lacking HPV, both suppressor genes were mutated. Functional inactivation of these tumor suppressor genes by HPV oncoproteins E6 and E7 may explain this difference. Treatment of HPV-immortalized cells with ras or a subfragment of herpes simplex virus (HSV) of HPV-immortalized cells resulted in locally invasive carcinomas when the cells were implanted subcutaneously in nude mice. These experiments indicate that HPV integration and expression are insufficient for malignancy but that HPVs do participate in the multistep development of cancer. JF - Critical reviews in oncogenesis AU - DiPaolo, J A AU - Popescu, N C AU - Alvarez, L AU - Woodworth, C D AD - Laboratory of Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 337 EP - 360 VL - 4 IS - 4 SN - 0893-9675, 0893-9675 KW - DNA, Recombinant KW - 0 KW - DNA, Viral KW - Index Medicus KW - Uterine Cervical Neoplasms -- etiology KW - Genes, ras KW - Animals KW - Gene Expression Regulation, Viral KW - Humans KW - Simplexvirus -- genetics KW - Cell Differentiation KW - Epithelium -- pathology KW - Female KW - Papillomaviridae -- genetics KW - DNA, Recombinant -- genetics KW - DNA, Viral -- genetics KW - Cell Transformation, Viral KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75898526?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Critical+reviews+in+oncogenesis&rft.atitle=Cellular+and+molecular+alterations+in+human+epithelial+cells+transformed+by+recombinant+human+papillomavirus+DNA.&rft.au=DiPaolo%2C+J+A%3BPopescu%2C+N+C%3BAlvarez%2C+L%3BWoodworth%2C+C+D&rft.aulast=DiPaolo&rft.aufirst=J&rft.date=1993-01-01&rft.volume=4&rft.issue=4&rft.spage=337&rft.isbn=&rft.btitle=&rft.title=Critical+reviews+in+oncogenesis&rft.issn=08939675&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-17 N1 - Date created - 1993-09-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Cancer prevention research trials. AN - 75895678; 8346716 JF - Advances in cancer research AU - Greenwald, P AU - Malone, W F AU - Cerny, M E AU - Stern, H R AD - Division of Cancer Prevention and Control, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 1 EP - 23 VL - 61 SN - 0065-230X, 0065-230X KW - Antineoplastic Agents KW - 0 KW - Index Medicus KW - United States KW - Animals KW - Humans KW - National Institutes of Health (U.S.) KW - Clinical Trials as Topic KW - Research KW - Drug Synergism KW - Drug Evaluation, Preclinical KW - Neoplasms -- epidemiology KW - Neoplasms -- prevention & control KW - Neoplasms -- diet therapy KW - Antineoplastic Agents -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75895678?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advances+in+cancer+research&rft.atitle=Cancer+prevention+research+trials.&rft.au=Greenwald%2C+P%3BMalone%2C+W+F%3BCerny%2C+M+E%3BStern%2C+H+R&rft.aulast=Greenwald&rft.aufirst=P&rft.date=1993-01-01&rft.volume=61&rft.issue=&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Advances+in+cancer+research&rft.issn=0065230X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-07 N1 - Date created - 1993-09-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - No point mutation of Ha-ras or p53 genes expressed in preneoplastic-to-neoplastic progression as modeled in mouse JB6 cell variants. AN - 75894280; 8352891 AB - Alterations of the p53 gene have been found in many human and animal tumors, and ras mutations have been seen somewhat less frequently. Loss of p53 tumor suppressor activity has been implicated in multistage tumor promotion/progression after initiation by Ha-ras or Ki-ras activation. Whether p53 or ras alterations occur during promotion of neoplastic transformation in JB6 cells has not been reported. Using a series of mouse JB6 variants representing different stages of progression toward the tumor-cell phenotype, we investigated whether mutational activation of Ha-ras and mutational inactivation and altered expression of the p53 gene occurred during progression. We report here that neither point mutations of the Ha-ras or p53 genes nor p53 structural alterations were involved in this process. Although there was no significant difference in steady-state levels of p53 mRNA, an elevated level of immunoprecipitable p53 protein was observed in a subset of transformed cells. We also report the detection of a second 2.2-kb p53-hybridizing transcript. This transcript was not translated into p53 protein and may be a nuclear precursor of the mature message. Both p53-hybridizing transcripts were downregulated by prolonged 12-O-tetradecanoylphorbol-13-acetate (TPA) treatment (24 h) regardless of the stage of progression. We conclude from this study that in JB6 variants (1) mutational activation of Ha-ras and inactivation of p53 are unlikely to be involved in preneoplastic progression; (2) increased amounts of p53 protein may be involved in a subset of transformed cells, possibly reflecting a longer half-life, as demonstrated in other systems; and (3) late downregulation of p53 mRNA but not protein expression may be a secondary response in the TPA-mediated signal transduction pathway. JF - Molecular carcinogenesis AU - Sun, Y AU - Nakamura, K AU - Hegamyer, G AU - Dong, Z AU - Colburn, N AD - Cell Biology Section, National Cancer Institute, Frederick, Maryland. Y1 - 1993 PY - 1993 DA - 1993 SP - 49 EP - 57 VL - 8 IS - 1 SN - 0899-1987, 0899-1987 KW - Ha-ras KW - p53 KW - Codon KW - 0 KW - DNA Probes KW - RNA, Messenger KW - Tumor Suppressor Protein p53 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Apoptosis -- physiology KW - Transcription, Genetic -- genetics KW - Disease Models, Animal KW - Mice KW - RNA, Messenger -- genetics KW - Base Sequence KW - Down-Regulation -- physiology KW - Cells, Cultured KW - Apoptosis -- drug effects KW - Molecular Sequence Data KW - Cell Line, Transformed KW - Tumor Suppressor Protein p53 -- genetics KW - Skin Neoplasms -- genetics KW - Point Mutation -- genetics KW - Precancerous Conditions -- genetics KW - Genes, ras -- genetics KW - Gene Expression -- genetics KW - Genes, p53 -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75894280?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+carcinogenesis&rft.atitle=No+point+mutation+of+Ha-ras+or+p53+genes+expressed+in+preneoplastic-to-neoplastic+progression+as+modeled+in+mouse+JB6+cell+variants.&rft.au=Sun%2C+Y%3BNakamura%2C+K%3BHegamyer%2C+G%3BDong%2C+Z%3BColburn%2C+N&rft.aulast=Sun&rft.aufirst=Y&rft.date=1993-01-01&rft.volume=8&rft.issue=1&rft.spage=49&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-21 N1 - Date created - 1993-09-21 N1 - Date revised - 2017-01-13 N1 - Gene symbol - Ha-ras; p53 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - ADP-ribosylation factors: protein activators of cholera toxin. AN - 75878793; 8341803 JF - Progress in nucleic acid research and molecular biology AU - Moss, J AU - Vaughan, M AD - Laboratory of Cellular Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 47 EP - 65 VL - 45 SN - 0079-6603, 0079-6603 KW - Adenosine Diphosphate Ribose KW - 20762-30-5 KW - Cholera Toxin KW - 9012-63-9 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - ADP-Ribosylation Factors KW - EC 3.6.5.2 KW - Index Medicus KW - Animals KW - Humans KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Adenosine Diphosphate Ribose -- metabolism KW - GTP-Binding Proteins -- metabolism KW - Cholera Toxin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75878793?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Progress+in+nucleic+acid+research+and+molecular+biology&rft.atitle=ADP-ribosylation+factors%3A+protein+activators+of+cholera+toxin.&rft.au=Moss%2C+J%3BVaughan%2C+M&rft.aulast=Moss&rft.aufirst=J&rft.date=1993-01-01&rft.volume=45&rft.issue=&rft.spage=47&rft.isbn=&rft.btitle=&rft.title=Progress+in+nucleic+acid+research+and+molecular+biology&rft.issn=00796603&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-27 N1 - Date created - 1993-08-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Neuropsychological and neurophysiological assessment of the central effects of interleukin-2 administration. AN - 75878053; 8343265 AB - Neuropsychiatric disturbances may occur following interleukin-2 (IL2) administration. We studied the effects of IL2 infusion on cerebral functions in 7 patients with neuropsychological tests and event-related evoked potentials (P300). We observed a failure in the cognitive performances, an increase in latency, and a decrease in amplitude of P300. These effects followed IL2 administration and were reversible. JF - European journal of cancer (Oxford, England : 1990) AU - Caraceni, A AU - Martini, C AU - Belli, F AU - Mascheroni, L AU - Rivoltini, L AU - Arienti, F AU - Cascinelli, N AD - Pain Therapy and Palliative Care Division, National Cancer Institute of Milan, Italy. Y1 - 1993 PY - 1993 DA - 1993 SP - 1266 EP - 1269 VL - 29A IS - 9 SN - 0959-8049, 0959-8049 KW - Interleukin-2 KW - 0 KW - Recombinant Proteins KW - Index Medicus KW - Reaction Time -- drug effects KW - Humans KW - Evoked Potentials, Auditory -- drug effects KW - Adult KW - Recombinant Proteins -- adverse effects KW - Middle Aged KW - Neuropsychological Tests KW - Male KW - Female KW - Lymphocytes, Tumor-Infiltrating KW - Interleukin-2 -- adverse effects KW - Melanoma -- secondary KW - Melanoma -- physiopathology KW - Cognition Disorders -- chemically induced KW - Melanoma -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75878053?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+cancer+%28Oxford%2C+England+%3A+1990%29&rft.atitle=Neuropsychological+and+neurophysiological+assessment+of+the+central+effects+of+interleukin-2+administration.&rft.au=Caraceni%2C+A%3BMartini%2C+C%3BBelli%2C+F%3BMascheroni%2C+L%3BRivoltini%2C+L%3BArienti%2C+F%3BCascinelli%2C+N&rft.aulast=Caraceni&rft.aufirst=A&rft.date=1993-01-01&rft.volume=29A&rft.issue=9&rft.spage=1266&rft.isbn=&rft.btitle=&rft.title=European+journal+of+cancer+%28Oxford%2C+England+%3A+1990%29&rft.issn=09598049&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-07 N1 - Date created - 1993-09-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Biological evaluation of compounds for their physical dependence potential and abuse liability. XVI. Drug Evaluation Committee of the College of Problems of Drug Dependence, Inc. (1992). AN - 75876908; 8101975 JF - NIDA research monograph AU - Jacobson, A E AD - Laboratory of Medicinal Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 437 EP - 458 VL - 132 SN - 1046-9516, 1046-9516 KW - Analgesics KW - 0 KW - Central Nervous System Depressants KW - Central Nervous System Stimulants KW - Index Medicus KW - Rats KW - Central Nervous System Depressants -- pharmacology KW - Animals KW - Central Nervous System Stimulants -- pharmacology KW - In Vitro Techniques KW - Analgesics -- pharmacology KW - Mice KW - Macaca mulatta KW - Drug Evaluation, Preclinical KW - Male KW - Structure-Activity Relationship KW - Substance-Related Disorders -- psychology KW - Societies, Medical UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75876908?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Biological+evaluation+of+compounds+for+their+physical+dependence+potential+and+abuse+liability.+XVI.+Drug+Evaluation+Committee+of+the+College+of+Problems+of+Drug+Dependence%2C+Inc.+%281992%29.&rft.au=Jacobson%2C+A+E&rft.aulast=Jacobson&rft.aufirst=A&rft.date=1993-01-01&rft.volume=132&rft.issue=&rft.spage=437&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-02 N1 - Date created - 1993-09-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Functional organization of the striatum: relevance to actions of psychostimulant drugs of abuse. AN - 75873978; 8101973 JF - NIDA research monograph AU - Gerfen, C R AD - National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 82 EP - 91 VL - 125 SN - 1046-9516, 1046-9516 KW - c-fos KW - Central Nervous System Stimulants KW - 0 KW - Index Medicus KW - Animals KW - Humans KW - Gene Expression Regulation -- drug effects KW - Substance-Related Disorders -- physiopathology KW - Corpus Striatum -- physiopathology KW - Corpus Striatum -- anatomy & histology KW - Substance-Related Disorders -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75873978?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Functional+organization+of+the+striatum%3A+relevance+to+actions+of+psychostimulant+drugs+of+abuse.&rft.au=Gerfen%2C+C+R&rft.aulast=Gerfen&rft.aufirst=C&rft.date=1993-01-01&rft.volume=125&rft.issue=&rft.spage=82&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-02 N1 - Date created - 1993-09-02 N1 - Date revised - 2017-01-13 N1 - Gene symbol - c-fos N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The National Institute on Drug Abuse 1992--focus on the future: a steadfast commitment to research. AN - 75872371; 8341375 JF - NIDA research monograph AU - Millstein, R A AD - National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1993 PY - 1993 DA - 1993 SP - 9 EP - 17 VL - 132 SN - 1046-9516, 1046-9516 KW - Index Medicus KW - United States KW - National Institutes of Health (U.S.) -- trends KW - Substance-Related Disorders KW - Research UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75872371?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=The+National+Institute+on+Drug+Abuse+1992--focus+on+the+future%3A+a+steadfast+commitment+to+research.&rft.au=Millstein%2C+R+A&rft.aulast=Millstein&rft.aufirst=R&rft.date=1993-01-01&rft.volume=132&rft.issue=&rft.spage=9&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-09-02 N1 - Date created - 1993-09-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Suramin inhibits DNA damage in human prostate cancer cells treated with topoisomerase inhibitors in vitro. AN - 75854180; 8393191 AB - Suramin, a highly sulfonated drug, has been reported to be effective against several human malignancies in vitro and in vivo, and currently is undergoing clinical trials against prostate tumors. The biochemical and molecular mechanisms for suramin's antiproliferative activity are not clear. In order to define the biochemical basis for its antitumor activity and to enhance suramin's chemotherapeutic potential while decreasing its toxicity, we have examined interactions of suramin with topoisomerase I and II and several clinically active anticancer drugs against the human prostate (PC3 and LNCaP) cancer cell line. While etoposide, m-AMSA, camptothecin, and SN-38 (the active metabolite of CPT-11) were active in killing prostate cells as single agents, combinations of suramin and these agents were antagonistic against these cells. We found that suramin inhibited activities of purified topoisomerase I and II in vitro as measured by relaxation and cleavage assays. Further studies indicated that suramin also inhibited the drug-induced DNA damage in vitro and in isolated nuclei. These findings indicate that combinations of suramin with topoisomerase inhibitors, for example, VP-16, m-AMSA, or CPT, may not be beneficial to patients receiving suramin-containing chemotherapy. JF - The Prostate AU - Yamazaki, H AU - Dilworth, A AU - Myers, C E AU - Sinha, B K AD - Biochemical & Molecular Pharmacology Section, National Cancer Institute, NIH, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 25 EP - 36 VL - 23 IS - 1 SN - 0270-4137, 0270-4137 KW - Topoisomerase I Inhibitors KW - 0 KW - Topoisomerase II Inhibitors KW - Amsacrine KW - 00DPD30SOY KW - Suramin KW - 6032D45BEM KW - Etoposide KW - 6PLQ3CP4P3 KW - Camptothecin KW - XT3Z54Z28A KW - Index Medicus KW - Etoposide -- pharmacology KW - Amsacrine -- toxicity KW - Drug Interactions KW - Camptothecin -- pharmacology KW - Dose-Response Relationship, Drug KW - Humans KW - Etoposide -- toxicity KW - Tumor Cells, Cultured KW - Cell Survival -- drug effects KW - Camptothecin -- toxicity KW - Chemical Precipitation KW - Amsacrine -- pharmacology KW - Male KW - Prostatic Neoplasms -- pathology KW - Suramin -- toxicity KW - Suramin -- pharmacology KW - DNA Damage -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75854180?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Prostate&rft.atitle=Suramin+inhibits+DNA+damage+in+human+prostate+cancer+cells+treated+with+topoisomerase+inhibitors+in+vitro.&rft.au=Yamazaki%2C+H%3BDilworth%2C+A%3BMyers%2C+C+E%3BSinha%2C+B+K&rft.aulast=Yamazaki&rft.aufirst=H&rft.date=1993-01-01&rft.volume=23&rft.issue=1&rft.spage=25&rft.isbn=&rft.btitle=&rft.title=The+Prostate&rft.issn=02704137&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-08-24 N1 - Date created - 1993-08-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Analysis of mutagenesis induced by expression of retroviral reverse transcriptase in Escherichia coli. AN - 75784548; 7684931 AB - We showed that expression of reverse transcriptase from HIV or MuLV resulted in exceptionally high levels of mutagenesis in E coli. We observed high rates of mutagenesis in plasmid genes when reverse transcriptase was expressed off that plasmid. Although very high rates were observed in cis, our experiments could not detect mutagenic events in markers in other replicons (ie in trans). These results suggest mutagenic events occur preferentially on the same replicon in which the reverse transcriptase is encoded. JF - Biochimie AU - Ennis, D G AU - Crouch, R J AD - Laboratory of Molecular Genetics, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 101 EP - 105 VL - 75 IS - 1-2 SN - 0300-9084, 0300-9084 KW - Recombinant Proteins KW - 0 KW - RNA-Directed DNA Polymerase KW - EC 2.7.7.49 KW - Index Medicus KW - AIDS/HIV KW - Recombinant Proteins -- biosynthesis KW - Plasmids -- genetics KW - RNA-Directed DNA Polymerase -- biosynthesis KW - Escherichia coli -- genetics KW - Escherichia coli -- enzymology KW - HIV -- enzymology KW - Leukemia Virus, Murine -- enzymology KW - Mutagenesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75784548?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochimie&rft.atitle=Analysis+of+mutagenesis+induced+by+expression+of+retroviral+reverse+transcriptase+in+Escherichia+coli.&rft.au=Ennis%2C+D+G%3BCrouch%2C+R+J&rft.aulast=Ennis&rft.aufirst=D&rft.date=1993-01-01&rft.volume=75&rft.issue=1-2&rft.spage=101&rft.isbn=&rft.btitle=&rft.title=Biochimie&rft.issn=03009084&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-07 N1 - Date created - 1993-07-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - In situ kinetics and ascorbic acid requirements. AN - 75779660; 8506699 JF - World review of nutrition and dietetics AU - Levine, M AU - Cantilena, C C AU - Dhariwal, K R AD - Laboratory of Cell Biology and Genetics, National Institute of Diabetes, National Institutes of Health, Bethesda, Md. Y1 - 1993 PY - 1993 DA - 1993 SP - 114 EP - 127 VL - 72 SN - 0084-2230, 0084-2230 KW - Ascorbic Acid KW - PQ6CK8PD0R KW - Index Medicus KW - Nutritional Requirements KW - Animals KW - Humans KW - Male KW - Female KW - Ascorbic Acid -- adverse effects KW - Ascorbic Acid -- pharmacokinetics KW - Ascorbic Acid -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75779660?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=World+review+of+nutrition+and+dietetics&rft.atitle=In+situ+kinetics+and+ascorbic+acid+requirements.&rft.au=Levine%2C+M%3BCantilena%2C+C+C%3BDhariwal%2C+K+R&rft.aulast=Levine&rft.aufirst=M&rft.date=1993-01-01&rft.volume=72&rft.issue=&rft.spage=114&rft.isbn=&rft.btitle=&rft.title=World+review+of+nutrition+and+dietetics&rft.issn=00842230&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-07 N1 - Date created - 1993-07-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Predictors of antidepressant response. AN - 75779480; 8508153 AB - The development of new pharmacological agents has dramatically improved the treatment of major depressive disorders. But the question of whether there are reliable predictors of response to a particular agent or class of agent remains to be answered completely. The author provides an overview of current understanding of antidepressant response prediction in terms of three sources of variance: clinical variables, biological variables, and pharmacological response. He also notes evidence of the effectiveness of two nonpharmacological treatments, sleep deprivation therapy and light therapy. JF - Bulletin of the Menninger Clinic AU - Goodwin, F K AD - National Institute of Mental Health, Rockville, MD 20857. Y1 - 1993 PY - 1993 DA - 1993 SP - 146 EP - 160 VL - 57 IS - 2 SN - 0025-9284, 0025-9284 KW - Antidepressive Agents KW - 0 KW - Index Medicus KW - Patient Compliance -- psychology KW - Humans KW - Prognosis KW - Personality Inventory KW - Depressive Disorder -- psychology KW - Depressive Disorder -- drug therapy KW - Antidepressive Agents -- therapeutic use KW - Antidepressive Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75779480?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bulletin+of+the+Menninger+Clinic&rft.atitle=Predictors+of+antidepressant+response.&rft.au=Goodwin%2C+F+K&rft.aulast=Goodwin&rft.aufirst=F&rft.date=1993-01-01&rft.volume=57&rft.issue=2&rft.spage=146&rft.isbn=&rft.btitle=&rft.title=Bulletin+of+the+Menninger+Clinic&rft.issn=00259284&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-15 N1 - Date created - 1993-07-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Prospective study of the long-term efficacy and safety of lansoprazole in patients with the Zollinger-Ellison syndrome. AN - 75753031; 8490079 AB - The long-term safety and efficacy of lansoprazole were studied in 21 patients with Zollinger-Ellison syndrome. The initial maintenance dose was determined by acid inhibition studies. In all patients lansoprazole controlled gastric acid hypersecretion and peptic symptoms in both the short and long term. Patients were treated for a mean of 31 months (range 1-43 months) with all but 4 patients followed for > 18 months. The mean initial dose was 60 mg/day, with 2 patients requiring a twice daily dose and the others a single daily dose. During long-term treatment 6 patients required an increased dosage, 5 within the first year. Long-term maintenance doses were reduced in 5 of the 6 patients in whom this was attempted. No changes in serum gastrin concentration, haematological parameters, liver function studies or other biochemical parameters occurred due to lansoprazole. No patient developed a gastric carcinoid tumour while being treated with lansoprazole. These results demonstrate that long-term treatment with lansoprazole is both safe and effective in patients with Zollinger-Ellison syndrome, and suggest that this drug will be useful in such patients. Furthermore, maintenance doses of lansoprazole, determined by the currently recommended method of acute acid titration studies in patients with Zollinger-Ellison syndrome, are too high. JF - Alimentary pharmacology & therapeutics AU - Jensen, R T AU - Metz, D C AU - Koviack, P D AU - Feigenbaum, K M AD - Digestive Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 41 EP - 50, discussion 61-6 VL - 7 Suppl 1 SN - 0269-2813, 0269-2813 KW - 2-Pyridinylmethylsulfinylbenzimidazoles KW - 0 KW - Anti-Ulcer Agents KW - Gastrins KW - Lansoprazole KW - 0K5C5T2QPG KW - Aspartate Aminotransferases KW - EC 2.6.1.1 KW - Alanine Transaminase KW - EC 2.6.1.2 KW - Omeprazole KW - KG60484QX9 KW - Index Medicus KW - Drug Administration Schedule KW - Alanine Transaminase -- metabolism KW - Humans KW - Gastrins -- blood KW - Aged KW - Fasting -- blood KW - Aspartate Aminotransferases -- metabolism KW - Prospective Studies KW - Adult KW - Middle Aged KW - Follow-Up Studies KW - Male KW - Female KW - Anti-Ulcer Agents -- adverse effects KW - Zollinger-Ellison Syndrome -- drug therapy KW - Omeprazole -- adverse effects KW - Zollinger-Ellison Syndrome -- enzymology KW - Omeprazole -- therapeutic use KW - Anti-Ulcer Agents -- therapeutic use KW - Omeprazole -- analogs & derivatives KW - Zollinger-Ellison Syndrome -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75753031?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alimentary+pharmacology+%26+therapeutics&rft.atitle=Prospective+study+of+the+long-term+efficacy+and+safety+of+lansoprazole+in+patients+with+the+Zollinger-Ellison+syndrome.&rft.au=Jensen%2C+R+T%3BMetz%2C+D+C%3BKoviack%2C+P+D%3BFeigenbaum%2C+K+M&rft.aulast=Jensen&rft.aufirst=R&rft.date=1993-01-01&rft.volume=7+Suppl+1&rft.issue=&rft.spage=41&rft.isbn=&rft.btitle=&rft.title=Alimentary+pharmacology+%26+therapeutics&rft.issn=02692813&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-17 N1 - Date created - 1993-06-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Species differences in carcinogenesis. AN - 75752687; 8504209 AB - There are differences in response of different species to many carcinogens. Different organs respond to particular carcinogens, there are differences in potency (including resistance of some species), and there are varying effects of other parameters. Although animal studies identify carcinogens, it is impossible to predict accurately the potency or the target organ in humans of any carcinogen. Inter-species differences in response to carcinogens can be due to differences in metabolism and activation. However, even in the case of directly acting carcinogens, such as alkylnitrosoureas, quantitative differences in alkylation of DNA are insufficient to explain the differences in response of particular organs. Yet unknown reactions or interactions of carcinogens must be key factors in inter-species differences. JF - In vivo (Athens, Greece) AU - Lijinsky, W AD - Division of Biometry and Risk Assessment, National Institute of Environmental Health Sciences Research Triangle Park, North Carolina 27709. PY - 1993 SP - 65 EP - 72 VL - 7 IS - 1 SN - 0258-851X, 0258-851X KW - Carcinogens KW - 0 KW - Nitrosamines KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Molecular Structure KW - Nitrosamines -- toxicity KW - Animals KW - Humans KW - Organ Specificity -- physiology KW - Species Specificity KW - DNA -- drug effects KW - Alkylation KW - Carcinogens -- metabolism KW - Carcinogens -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75752687?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=In+vivo+%28Athens%2C+Greece%29&rft.atitle=Species+differences+in+carcinogenesis.&rft.au=Lijinsky%2C+W&rft.aulast=Lijinsky&rft.aufirst=W&rft.date=1993-01-01&rft.volume=7&rft.issue=1&rft.spage=65&rft.isbn=&rft.btitle=&rft.title=In+vivo+%28Athens%2C+Greece%29&rft.issn=0258851X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-07-08 N1 - Date created - 1993-07-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Epidemiology of epilepsy in developing countries. AN - 75732988; 8490989 AB - Epilepsy is an important health problem in developing countries, where its prevalence can be up to 57 per 1000 population. This article reviews the epidemiology of epilepsy in developing countries in terms of its incidence, prevalence, seizure type, mortality data, and etiological factors. The prevalence of epilepsy is particularly high in Latin America and in several African countries, notably Liberia, Nigeria, and the United Republic of Tanzania. Parasitic infections, particularly neurocysticercosis, are important etiological factors for epilepsy in many of these countries. Other reasons for the high prevalence include intracranial infections of bacterial or viral origin, perinatal brain damage, head injuries, toxic agents, and hereditary factors. Many of these factors are, however, preventable or modifiable, and the introduction of appropriate measures to achieve this could lead to a substantial decrease in the incidence of epilepsy in developing countries. JF - Bulletin of the World Health Organization AU - Senanayake, N AU - Román, G C AD - Neuroepidemiology Branch, National Institute of Neurological Disorders and Stroke (NINDS), National Institutes of Health, Bethesda, MD. Y1 - 1993 PY - 1993 DA - 1993 SP - 247 EP - 258 VL - 71 IS - 2 SN - 0042-9686, 0042-9686 KW - Index Medicus KW - Virus Diseases -- complications KW - Humans KW - Child KW - Poisoning -- complications KW - Adult KW - Parasitic Diseases -- complications KW - Incidence KW - Bacterial Infections -- complications KW - Craniocerebral Trauma -- complications KW - Adolescent KW - Female KW - Male KW - Prevalence KW - Developing Countries KW - Epilepsy -- classification KW - Epilepsy -- etiology KW - Epilepsy -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75732988?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bulletin+of+the+World+Health+Organization&rft.atitle=Epidemiology+of+epilepsy+in+developing+countries.&rft.au=Senanayake%2C+N%3BRom%C3%A1n%2C+G+C&rft.aulast=Senanayake&rft.aufirst=N&rft.date=1993-01-01&rft.volume=71&rft.issue=2&rft.spage=247&rft.isbn=&rft.btitle=&rft.title=Bulletin+of+the+World+Health+Organization&rft.issn=00429686&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-17 N1 - Date created - 1993-06-17 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Epilepsia. 1987 May-Jun;28(3):272-9 [3582291] Ann Neurol. 1986 Mar;19(3):224-38 [3963767] Q J Med. 1987 May;63(241):449-60 [3659262] J Neurol Neurosurg Psychiatry. 1987 Oct;50(10):1298-301 [3119775] Rev Med Panama. 1988 Jan;13(1):40-5 [2831568] Epilepsia. 1988 Mar-Apr;29(2):111-5 [3258234] Epilepsia. 1988 Mar-Apr;29(2):116-22 [3258235] Am J Prev Med. 1987 Sep-Oct;3(5):293-9 [3330662] N Engl J Med. 1988 Sep 8;319(10):641-3 [2842678] Neurology. 1988 Sep;38(9):1407-10 [3412588] BMJ. 1988 Nov 12;297(6658):1267 [3145079] Ceylon Med J. 1987 Dec;32(4):181-99 [3506450] J Neurol Sci. 1989 Mar;90(1):67-76 [2723675] East Afr Med J. 1989 May;66(5):343-8 [2791933] Arch Intern Med. 1990 Feb;150(2):325-7 [2302008] Southeast Asian J Trop Med Public Health. 1989 Dec;20(4):599-603 [2561717] N Engl J Med. 1990 Dec 13;323(24):1651-7 [2233962] Epilepsia. 1990 Nov-Dec;31(6):718-23 [2245802] J R Army Med Corps. 1990 Oct;136(3):146-9 [2266527] Epilepsy Res. 1990 Dec;7(3):230-9 [2289482] Acta Leiden. 1989;57(2):191-6 [2488997] Arq Neuropsiquiatr. 1991 Mar;49(1):43-6 [1863240] Chin Med J. 1957 Nov;75(11):892-907 [13500465] N Engl J Med. 1961 May 18;264:1027-30 [13708322] Pediatrics. 1961 Nov;28:778-91 [14466652] Neurology. 1964 May;14:443-54 [14147159] Epilepsia. 1968 Jun;9(2):77-85 [5247004] J Neurol Sci. 1969 Jan-Feb;8(1):27-48 [5790371] Med J Aust. 1970 Nov 21;2(21):966-8 [5493342] Trop Geogr Med. 1970 Dec;22(4):439-42 [5497378] Afr J Med Sci. 1971 Apr;2(2):165-71 [4255776] Afr J Med Sci. 1970 Apr;1(2):207-12 [5521680] Am J Epidemiol. 1972 Mar;95(3):292-8 [5010822] Dev Med Child Neurol. 1972 Apr;14(2):230-2 [5063914] Dev Med Child Neurol. 1974 Oct;16(5):659-63 [4214455] Epilepsia. 1975 Mar;16(1):1-66 [804401] J Assoc Physicians India. 1977 Mar;25(3):215-22 [72061] Epilepsia. 1977 Dec;18(4):549-54 [412669] Neurology. 1978 Jan;28(1):90-4 [563543] Southeast Asian J Trop Med Public Health. 1977 Dec;8(4):494-7 [614710] Trop Geogr Med. 1978 Sep;30(3):275-8 [734751] J Trop Med Hyg. 1979 Feb;82(2):38-40 [458906] Epilepsia. 1979 Dec;20(6):613-22 [499114] Arq Neuropsiquiatr. 1981 Mar;39(1):32-41 [6789802] East Afr Med J. 1981 Jun;58(6):437-44 [7308100] Neurology. 1982 Feb;32(2):174-9 [7198743] Acta Neurol Scand. 1982 Aug;66(2):216-26 [7136486] Lancet. 1983 Feb 12;1(8320):358 [6130361] Arch Intern Med. 1985 Mar;145(3):442-5 [3977513] Epilepsia. 1985 Mar-Apr;26(2):131-6 [3921351] J Trop Med Hyg. 1985 Feb;88(1):25-9 [4020930] Ann Pediatr (Paris). 1985 May;32(5):477-80 [4026144] Neuroepidemiology. 1985;4(2):108-16 [3831782] Neuroepidemiology. 1985;4(2):65-70 [3831783] Epilepsia. 1987 May-Jun;28(3):280-5 [3582292] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Genetic toxicity of fluoride. AN - 75732336; 8491210 AB - F- is not mutagenic in standard bacterial systems, but produces chromosome aberrations and gene mutations in cultured mammalian cells. Although there is disagreement in the literature concerning the ability of F- to induce chromosome aberrations in cultured human and rodent cells, the weight of the evidence leads to the conclusion that F- exposure results in increased chromosome aberrations in these test systems. NaF induced primarily chromatid gaps and chromatid breaks, indicating that the rodent cells are responsive in the G2 stage of the cell cycle. In contrast, studies with synchronized human cells indicated that the S phase was the most sensitive. If F- does have a cell cycle-specific effect, it could be expected that differences in the cell treatment and harvest protocols could lead to conflicting results for the induction of chromosome aberrations. Gene mutations were produced in cultured rodent and human cells in the majority of the studies. Unfortunately, a number of the in vitro and in vivo cytogenetic studies are of questionable utility because of the protocols used, the quality of the responses reported, or the interpretations of the data. The conflicting results in the in vivo cytogenetic studies are difficult to reconcile. There are reports of increased chromosome aberrations in rat bone marrow and testes, but other studies, using similar protocols and dose ranges, have reported no induced chromosome damage. Although some of the studies were performed at toxic levels of F-, other studies, including those that showed positive results, were at F- concentrations (1-5 ppm) equivalent to human exposure levels. In the majority of studies that were reported to be positive, there were high background frequencies, or the investigators reported categories of nuclear or chromosome damage that are difficult to interpret. Interestingly, many of the positive results were obtained when anaphase cells were scored, whereas similar treatment protocols in other laboratories yielded negative results when metaphase cells were the only cell type examined. It is difficult, without additional data, to determine the reasons for finding chromosome breaks in anaphase, but not metaphase, cells. Other reports have presented insufficient information to allow adequate evaluations. Therefore, at this time, the question of whether F- produces chromosome damage in vivo should be considered unresolved. JF - Environmental and molecular mutagenesis AU - Zeiger, E AU - Shelby, M D AU - Witt, K L AD - Experimental Carcinogenesis and Mutagenesis Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993 PY - 1993 DA - 1993 SP - 309 EP - 318 VL - 21 IS - 4 SN - 0893-6692, 0893-6692 KW - Mutagens KW - 0 KW - Fluorides KW - Q80VPU408O KW - Index Medicus KW - Animals KW - Mutagenicity Tests KW - DNA Repair KW - Mammals KW - Sister Chromatid Exchange KW - DNA Damage KW - Humans KW - Germ Cells -- drug effects KW - Rodentia KW - Drosophila KW - Fluorides -- toxicity KW - Chromosome Aberrations KW - Mutagens -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75732336?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+and+molecular+mutagenesis&rft.atitle=Genetic+toxicity+of+fluoride.&rft.au=Zeiger%2C+E%3BShelby%2C+M+D%3BWitt%2C+K+L&rft.aulast=Zeiger&rft.aufirst=E&rft.date=1993-01-01&rft.volume=21&rft.issue=4&rft.spage=309&rft.isbn=&rft.btitle=&rft.title=Environmental+and+molecular+mutagenesis&rft.issn=08936692&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-16 N1 - Date created - 1993-06-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Suppression of tumorigenicity of A549 lung adenocarcinoma cells by human chromosomes 3 and 11 introduced via microcell-mediated chromosome transfer. AN - 75724834; 8098218 AB - To map tumor suppressor genes for lung adenocarcinomas, we introduced normal human chromosomes 3, 7, and 11 into the A549 tumor cell line by microcell-mediated chromosome transfer to test which chromosomes had the ability to suppress tumorigenicity. These human chromosomes, which contain the neomycin gene as a selectable marker, were transferred into A549 lung adenocarcinoma cells at frequencies of 0.3-1.8 x 10(-6). Two microcell hybrid clones with an introduced chromosome 3, two with an introduced chromosome 7, and six with an introduced chromosome 11 were isolated and examined for their growth properties and tumorigenicity in nude mice. Whereas parental A549 cells formed tumors with an average latency of 68 d, both microcell hybrids with an introduced chromosome 3 failed to form tumors for over 360 d. Similar tumorigenicity results were obtained when the clones were implanted into denuded tracheas, a more orthotopic transplantation site. The two clones with an introduced chromosome 7 were still tumorigenic; they formed tumors within 100-123 d after injection and grew progressively, although the tumors grew slightly slower than the parental cells did. Among the six clones with an introduced chromosome 11, one clone was still highly tumorigenic but did not contain an extra copy of an intact introduced chromosome 11. Three clones with a single intact copy of introduced chromosome 11 formed tumors with latency periods significantly longer than those of the parental cells. Two clones had two copies of the introduced chromosome 11, and both failed to form tumors within 1 yr of injection. These results indicate that chromosomes 3 and 11 can suppress the tumorigenicity of A549 lung adenocarcinoma cells. JF - Molecular carcinogenesis AU - Satoh, H AU - Lamb, P W AU - Dong, J T AU - Everitt, J AU - Boreiko, C AU - Oshimura, M AU - Barrett, J C AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. Y1 - 1993 PY - 1993 DA - 1993 SP - 157 EP - 164 VL - 7 IS - 3 SN - 0899-1987, 0899-1987 KW - DNA, Neoplasm KW - 0 KW - Index Medicus KW - Neoplasm Transplantation KW - Karyotyping KW - Animals KW - Transfection KW - Polymorphism, Restriction Fragment Length KW - Humans KW - DNA, Neoplasm -- genetics KW - Mice, Nude KW - Mice KW - Chromosomes, Human, Pair 3 KW - Genes, Tumor Suppressor KW - Lung Neoplasms -- genetics KW - Adenocarcinoma -- genetics KW - Chromosomes, Human, Pair 11 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75724834?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+carcinogenesis&rft.atitle=Suppression+of+tumorigenicity+of+A549+lung+adenocarcinoma+cells+by+human+chromosomes+3+and+11+introduced+via+microcell-mediated+chromosome+transfer.&rft.au=Satoh%2C+H%3BLamb%2C+P+W%3BDong%2C+J+T%3BEveritt%2C+J%3BBoreiko%2C+C%3BOshimura%2C+M%3BBarrett%2C+J+C&rft.aulast=Satoh&rft.aufirst=H&rft.date=1993-01-01&rft.volume=7&rft.issue=3&rft.spage=157&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-15 N1 - Date created - 1993-06-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Neoplastic transformation of human cells in vitro. AN - 75717715; 8485202 AB - Efforts to investigate the progression of events that lead normal human cells in culture to become neoplastic in response to carcinogenic agents have been aided by the development of the suitable in vitro model systems. For initial human cell transformation studies, a flat, nontumorigenic clonal line, originally derived from a human osteosarcoma (HOS), was used. When treated with chemical carcinogens such as N-methyl-N-nitro-N-nitrosoguanidine (MNNG) and 3-methyl-cholanthrene (3MC), the HOS cells underwent morphological alterations and acquired tumorigenic properties. These cell lines were very useful inasmuch as a non-ras cellular transforming gene, met, and an activated H-ras oncogene have been isolated from MNNG-transformed and 3MC-transformed HOS lines, respectively, by DNA transfection procedure. Alteration of p53 gene in chemically transformed HOS cell lines has recently been shown. Although carcinogens cause human cancer, normal human cells in culture have proven difficult to achieve. Neoplastic transformation of human cells in culture has recently been achieved by a stepwise fashion-immortalization and conversion of the immortalized cells to tumorigenic cells. One of the critical initial events in the progression of normal human cells to tumor cells is the escape from cellular senescence. With few exceptions, normal human cells require immortalization to provide a practical system for transformation studies. Thus, the role of carcinogenic agents in the development of human cancers is now being defined using a variety of human cells. The neoplastic transformation in human cell cultures is reviewed. In doing so, this author attempts to put into perspective the history of human cell transformation by carcinogenic agents, and to discuss the current state of the art in transformation of human cells in culture; thus providing insight into the molecular and cellular mechanisms involved in the conversion of normal cells to a neoplastic state of growth. JF - Critical reviews in oncogenesis AU - Rhim, J S AD - Laboratory of Cellular and Molecular Biology, NCI, NIH, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 313 EP - 335 VL - 4 IS - 3 SN - 0893-9675, 0893-9675 KW - Proto-Oncogene Proteins KW - 0 KW - Proto-Oncogene Proteins c-met KW - EC 2.7.10.1 KW - Hydrocortisone KW - WI4X0X7BPJ KW - Index Medicus KW - Humans KW - Oncogenic Viruses -- pathogenicity KW - Gene Expression Regulation, Neoplastic -- drug effects KW - Proto-Oncogene Proteins -- physiology KW - Fibroblasts -- pathology KW - Tumor Cells, Cultured KW - Cells, Cultured KW - Hydrocortisone -- toxicity KW - Genes, ras -- physiology KW - Genes, p53 -- genetics KW - Gene Expression Regulation, Neoplastic -- radiation effects KW - Keratinocytes -- pathology KW - Cell Line, Transformed KW - Mutation KW - Cell Transformation, Viral KW - Cell Transformation, Neoplastic -- radiation effects KW - Cell Transformation, Neoplastic -- drug effects KW - Cell Transformation, Neoplastic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75717715?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Critical+reviews+in+oncogenesis&rft.atitle=Neoplastic+transformation+of+human+cells+in+vitro.&rft.au=Rhim%2C+J+S&rft.aulast=Rhim&rft.aufirst=J&rft.date=1993-01-01&rft.volume=4&rft.issue=3&rft.spage=313&rft.isbn=&rft.btitle=&rft.title=Critical+reviews+in+oncogenesis&rft.issn=08939675&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-09 N1 - Date created - 1993-06-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Mechanistic modelling and risk assessment. AN - 75687281; 8474985 AB - Risk Assessment in the United States has been rapidly changing over the last few years. The historical methods and endpoints by which risk estimates were derived are gradually being replaced by newer methods and a broader spectrum of endpoints. For carcinogenic risk assessment, there is movement from the routinely used "linearized multistage model" for low dose risk estimation to methodology which is more deeply rooted in carcinogenic mechanisms and which allows the incorporation of additional data into the estimation of risks in a direct, quantitative fashion. There is also a determined effort under way to develop methods for assessing risks from exposure based on other endpoints such as effects on the immune system and the reproductive system. This paper briefly discusses some of the statistical and mathematical issues which will play important roles in determining the utility and precision of these new methods for estimating risks from environmental exposures. JF - Pharmacology & toxicology AU - Portier, C J AD - Risk Methodology Section, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993 PY - 1993 DA - 1993 SP - 28 EP - 32 VL - 72 Suppl 1 SN - 0901-9928, 0901-9928 KW - Index Medicus KW - United States KW - Animals KW - Humans KW - Carcinogenicity Tests KW - Risk KW - Neoplasms -- chemically induced KW - Models, Theoretical UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75687281?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacology+%26+toxicology&rft.atitle=Mechanistic+modelling+and+risk+assessment.&rft.au=Portier%2C+C+J&rft.aulast=Portier&rft.aufirst=C&rft.date=1993-01-01&rft.volume=72+Suppl+1&rft.issue=&rft.spage=28&rft.isbn=&rft.btitle=&rft.title=Pharmacology+%26+toxicology&rft.issn=09019928&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-19 N1 - Date created - 1993-05-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Cytotoxic ribonucleases and chimeras in cancer therapy. AN - 75673366; 8472310 AB - Ribonucleases serve as cytotoxic agents during host defense and physiological cell death pathways. In bacteria, higher plants, and mammals, ribonucleases appear to bind cells, enter the cytosol where they degrade RNA, and kill the target cell. This process functions in interstrain competition in bacteria, in the death of incompatible pollen in higher plants, and likely plays a role in the antiparasitic and anticancer activity of eosinophils in man. One can alter the target cell specificity of RNases by coupling them to new cell-binding domains. Chemically coupling RNases to new binding moieties or fusing RNase genes to antibody genes results in chimeric molecules with specified cell-type cytotoxicity. Thus, one can target one's own host defense cytotoxins to select cell populations. This allows the use of human proteins, instead of plant and bacterial toxins, in the construction of immunotoxins. RNases also can be engineered to kill cells by cytosolic expression or to kill viruses by packaging into viruses. Engineering RNases into cell-type-specific cytotoxins may result in a new class of therapeutic reagents. We review a number of interesting physiological cell cytotoxicity pathways utilizing RNases and then describe the recent results on engineering RNases for therapeutic use. JF - Critical reviews in therapeutic drug carrier systems AU - Youle, R J AU - Newton, D AU - Wu, Y N AU - Gadina, M AU - Rybak, S M AD - Biochemistry Section, NINDS, NIH, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 1 EP - 28 VL - 10 IS - 1 SN - 0743-4863, 0743-4863 KW - Antineoplastic Agents KW - 0 KW - Colicins KW - Immunotoxins KW - Recombinant Fusion Proteins KW - Ribonucleases KW - EC 3.1.- KW - Index Medicus KW - Colicins -- therapeutic use KW - Fungi -- enzymology KW - Animals KW - Protein Engineering KW - Sequence Alignment KW - Humans KW - Molecular Sequence Data KW - Immunotoxins -- therapeutic use KW - Amino Acid Sequence KW - Plants -- enzymology KW - Neoplasms -- drug therapy KW - Ribonucleases -- antagonists & inhibitors KW - Ribonucleases -- pharmacology KW - Ribonucleases -- therapeutic use KW - Recombinant Fusion Proteins -- pharmacology KW - Antineoplastic Agents -- therapeutic use KW - Ribonucleases -- metabolism KW - Recombinant Fusion Proteins -- therapeutic use KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75673366?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Critical+reviews+in+therapeutic+drug+carrier+systems&rft.atitle=Cytotoxic+ribonucleases+and+chimeras+in+cancer+therapy.&rft.au=Youle%2C+R+J%3BNewton%2C+D%3BWu%2C+Y+N%3BGadina%2C+M%3BRybak%2C+S+M&rft.aulast=Youle&rft.aufirst=R&rft.date=1993-01-01&rft.volume=10&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Critical+reviews+in+therapeutic+drug+carrier+systems&rft.issn=07434863&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-20 N1 - Date created - 1993-05-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Introducing restriction sites into double-stranded plasmid DNA. AN - 75671205; 8386292 JF - Methods in enzymology AU - Kaslow, D C AU - Rawlings, D J AD - Molecular Vaccine Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 295 EP - 301 VL - 217 SN - 0076-6879, 0076-6879 KW - Indicators and Reagents KW - 0 KW - Oligodeoxyribonucleotides KW - DNA Restriction Enzymes KW - EC 3.1.21.- KW - Index Medicus KW - Base Sequence KW - DNA Restriction Enzymes -- metabolism KW - Genetic Vectors KW - Molecular Sequence Data KW - Escherichia coli -- genetics KW - Mutagenesis, Site-Directed KW - Restriction Mapping KW - Plasmids UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75671205?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Methods+in+enzymology&rft.atitle=Introducing+restriction+sites+into+double-stranded+plasmid+DNA.&rft.au=Kaslow%2C+D+C%3BRawlings%2C+D+J&rft.aulast=Kaslow&rft.aufirst=D&rft.date=1993-01-01&rft.volume=217&rft.issue=&rft.spage=295&rft.isbn=&rft.btitle=&rft.title=Methods+in+enzymology&rft.issn=00766879&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-18 N1 - Date created - 1993-05-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Issues and controversies surrounding qualitative strategies for identifying and forecasting cancer causing agents in the human environment. AN - 75665502; 8474975 AB - Certain chemicals, mixtures of chemicals, exposure circumstances, life-styles and personal or cultural habits, occupations, viruses, living conditions, and physical agents have been causally associated with cancers in humans. Most however are not considered potentially carcinogenic, and the proportion of 'agents' eventually identified to cause cancer is projected to be relatively low. Current methods to identify carcinogenic potential of chemicals rely largely on short-term in vitro and in vivo tests, mid- & long-term in vivo assays, molecular mechanisms, epidemiological investigations, and structural-activity-effect-relationships. Thus, the scientific and public health communities must continue to utilize available means and concomitantly strive to develop newer methods and tools to more easily, quickly, cheaply, and reliably identify carcinogens in the human milieu. Since adequate human studies are typically absent, the most useful method for identifying potential human carcinogens continues to be long-term carcinogenesis experiments. Agents identified as causing cancers in humans have been shown to cause cancer in animals, and this knowledge, together with similarities in mechanisms of carcinogenesis across species, led to the scientific logic and public health strategy that chemicals shown clearly to be carcinogenic in animals should be considered as being likely and anticipated to present cancer risks to humans. The quest of hazard identification efforts is cancer prevention, largely by reducing or eliminating exposures to chemicals that cause cancer and other diseases. JF - Pharmacology & toxicology AU - Huff, J AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993 PY - 1993 DA - 1993 SP - 12 EP - 27 VL - 72 Suppl 1 SN - 0901-9928, 0901-9928 KW - Carcinogens, Environmental KW - 0 KW - Index Medicus KW - Animals KW - Humans KW - Carcinogenicity Tests KW - Neoplasms -- chemically induced KW - Neoplasms -- physiopathology KW - Neoplasms -- epidemiology KW - Carcinogens, Environmental -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75665502?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacology+%26+toxicology&rft.atitle=Issues+and+controversies+surrounding+qualitative+strategies+for+identifying+and+forecasting+cancer+causing+agents+in+the+human+environment.&rft.au=Huff%2C+J&rft.aulast=Huff&rft.aufirst=J&rft.date=1993-01-01&rft.volume=72+Suppl+1&rft.issue=&rft.spage=12&rft.isbn=&rft.btitle=&rft.title=Pharmacology+%26+toxicology&rft.issn=09019928&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-19 N1 - Date created - 1993-05-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Consecutive silver staining and autoradiography of 35S and 32P-labeled cellular proteins: application for the analysis of signal transducing pathways. AN - 75664039; 8462506 AB - The methodology for the simultaneous analysis of protein synthesis concomitant with protein phosphorylation/dephosphorylation is described. The technique consists of metabolic labeling of rat liver epithelial (RLE) cells with [32P]orthophosphate and [35S]methionine, performing two-dimensional polyacrylamide gel electrophoresis (2-D PAGE) of the mixed samples, followed by silver staining and subsequent autoradiography of the dried silver stained 2-D PAGE electrophoretograms using two films placed back-to-back. The first film, which is positioned in direct contact with the dried silver-stained gel, visualized both exposure to 35S and 32P while the second film recorded exposure to only 32P due to the differential energy levels of the two isotopes. The juxta-positioning of the silver-stained images with the two autoradiographic film images permits the unambiguous mapping of the phosphorylated polypeptides back to their corresponding silver-stained and methionine-labeled counterparts. This strategy provides quantitative information utilizing both silver staining (measure of constitutive levels of protein expression) and metabolic labeling to measure rates of protein synthesis and/or degradation and phosphorylation and/or dephosphorylation using [35S]methionine and [32P]orthophosphate, respectively. We have utilized this methodology for the in vitro analysis of transforming growth factor type beta 1 (TGF-beta 1)-mediated signal transduction in RLE cells and have identified three nuclear polypeptides, 1 (pI 4.95/M(r) 97 kDa), 2 (5.00/85 kDa) and 3 (4.90/84 kDa) whose phosphorylation status is rapidly and transiently modulated by TGF-beta 1. The methodology described should have wide applications in studies where it is desirous to measure protein synthesis and/or degradation concomitant with signal transduction pathways involving protein phosphorylation. JF - Electrophoresis AU - Luo, L D AU - Wirth, P J AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. PY - 1993 SP - 127 EP - 136 VL - 14 IS - 1-2 SN - 0173-0835, 0173-0835 KW - Phosphoproteins KW - 0 KW - Phosphorus Radioisotopes KW - Sulfur Radioisotopes KW - Transforming Growth Factor beta KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Transforming Growth Factor beta -- physiology KW - Humans KW - Computers KW - Female KW - Phosphoproteins -- metabolism KW - Silver Staining KW - Autoradiography KW - Signal Transduction UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75664039?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Electrophoresis&rft.atitle=Consecutive+silver+staining+and+autoradiography+of+35S+and+32P-labeled+cellular+proteins%3A+application+for+the+analysis+of+signal+transducing+pathways.&rft.au=Luo%2C+L+D%3BWirth%2C+P+J&rft.aulast=Luo&rft.aufirst=L&rft.date=1993-01-01&rft.volume=14&rft.issue=1-2&rft.spage=127&rft.isbn=&rft.btitle=&rft.title=Electrophoresis&rft.issn=01730835&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-03 N1 - Date created - 1993-05-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Selective retention of polychlorinated biphenyl congeners in lung and liver after single-dose exposure of infant mice to Aroclor 1254. AN - 75658629; 8459365 AB - Infant male Swiss mice (8 days old) were given a single i.p. injection of 500 mg/kg of the polychlorinated biphenyl (PCB) mixture, Aroclor 1254, a treatment found in previous studies to result in promotion of nitrosamine-initiated lung and liver tumors. The amounts of the nine congeners that account for > 90% of the PCBs still present 1 day after treatment were quantified in liver, lung, and remainder of carcass 1, 7, 56, 84, and 112 days after treatment. Rates of decrease (half-times, dt1/2s) for total PCB concentration and for individual congeners were compared within and between compartments and with body weight doubling time. In carcass (adipose compartment) there was net loss beyond that expected from dilution due to growth, with the predicted lower dt1/2s for the more metabolizable congeners. By contrast, in lung, after a rapid loss during the 1st week, all congeners except for #153 (2,2'4,4'5,5'-hexachlorobiphenyl [HCB]) were retained and decreased in amount only as a function of dilution due to growth. One result was that congeners #105 (2,3,3',4,4'-pentachlorobiphenyl [PeCB]) and #138 (2,2',3,4,4',5'-HCB) constituted a higher proportion in lung than in carcass. A complex pattern was observed in liver: relative to carcass, there was retention of all congeners during the prepubertal growth phase, again with specific enrichment of #105, followed by more rapid depletion of certain congeners later. PCB-binding proteins and changes in lipid composition may contribute to these phenomena, which are of human relevance in that these congeners are commonly found in human serum and adipose samples. JF - Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer AU - Anderson, L M AU - Fox, S D AU - Riggs, C W AU - Issaq, H J AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702-1201. PY - 1993 SP - 3 EP - 16 VL - 12 IS - 1 SN - 0731-8898, 0731-8898 KW - Aroclors KW - 0 KW - Carcinogens KW - Chlorodiphenyl (54% Chlorine) KW - 11097-69-1 KW - Polychlorinated Biphenyls KW - DFC2HB4I0K KW - Index Medicus KW - Body Weight KW - Animals, Newborn KW - Animals KW - Mice KW - Time Factors KW - Male KW - Carcinogens -- toxicity KW - Polychlorinated Biphenyls -- metabolism KW - Liver -- metabolism KW - Aroclors -- toxicity KW - Lung -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75658629?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+environmental+pathology%2C+toxicology+and+oncology+%3A+official+organ+of+the+International+Society+for+Environmental+Toxicology+and+Cancer&rft.atitle=Selective+retention+of+polychlorinated+biphenyl+congeners+in+lung+and+liver+after+single-dose+exposure+of+infant+mice+to+Aroclor+1254.&rft.au=Anderson%2C+L+M%3BFox%2C+S+D%3BRiggs%2C+C+W%3BIssaq%2C+H+J&rft.aulast=ROY&rft.aufirst=TIRTHANKAR&rft.date=2016-06-01&rft.volume=59&rft.issue=2&rft.spage=393&rft.isbn=&rft.btitle=&rft.title=The+Historical+Journal&rft.issn=0018246X&rft_id=info:doi/10.1017%2FS0018246X15000370 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-26 N1 - Date created - 1993-04-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Quantitation of 2-amino-3-methylimidazo[4,5-f]quinoline and 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline DNA adducts in specific sequences using alkali or uvrABC excinuclease. AN - 75647876; 8457290 AB - 2-Amino-3-methylimidazo[4,5-f]quinoline (IQ) and 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MelQx) are carcinogens found in cooked meats that form DNA adducts upon metabolic activation. Purified DNA from Chinese hamster ovary (CHO) cells was reacted in vitro with the active metabolites N-acetoxy-IQ or N-acetoxy-MelQx, and the adduct levels in the 5' dihydrofolate reductase (DHFR) gene and downstream region were quantitated by Southern hybridization. Adducted and restricted DNA was treated with Escherichia coli uvrABC excinuclease or alkali (0.1 N NaOH, 37 degrees C, 60 min) to incise DNA at IQ and MelQx adduct sites. The DNA was then denatured with formamide, electrophoresed on a neutral agarose gel, transferred to a support membrane, and hybridized with sequence-specific DNA probes. Both uvrABC and alkali reduced the intensity of Southern hybridization in proportion to the number of IQ or MelQx adducts in DNA, indicating that these adducts are substrates for uvrABC and that they form alkali-labile lesions in DNA. IQ and MelQx adduct levels were the same in the 5' DHFR gene and in the downstream region. Southern hybridization analysis of pBR322 containing known levels of IQ or MelQx adducts showed that the efficiency of cutting IQ or MelQx adducts by uvrABC excinuclease and alkali was approximately 30% and 15%, respectively. 32P-postlabeling studies examining adduct level in bulk DNA further showed that the adduct profiles were identical in pBR322, CHO DNA, and cultured CHO cells exposed to the reactive metabolites of IQ or MelQx. The results indicate that IQ and MelQx adducts can be quantitated in specific genomic sequences and that this method should be directly applicable to studies of gene-specific repair of these adducts in cultured cells. JF - Molecular carcinogenesis AU - Nouso, K AU - Bohr, V A AU - Schut, H A AU - Snyderwine, E G AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 126 EP - 134 VL - 7 IS - 2 SN - 0899-1987, 0899-1987 KW - DHFR KW - Alkalies KW - 0 KW - DNA, Bacterial KW - Intercalating Agents KW - Mutagens KW - Phosphorus Radioisotopes KW - Quinolines KW - Quinoxalines KW - 2-amino-3,8-dimethylimidazo(4,5-f)quinoxaline KW - 77500-04-0 KW - DNA KW - 9007-49-2 KW - Tetrahydrofolate Dehydrogenase KW - EC 1.5.1.3 KW - Endodeoxyribonucleases KW - EC 3.1.- KW - 2-amino-3,4-dimethylimidazo(4,5-f)quinoline KW - G2Q7M1P33X KW - Index Medicus KW - Animals KW - Ultraviolet Rays KW - Electrophoresis KW - DNA Repair KW - Cricetulus KW - Endodeoxyribonucleases -- metabolism KW - Plasmids KW - Autoradiography KW - DNA, Bacterial -- analysis KW - DNA, Bacterial -- drug effects KW - Blotting, Southern KW - Cooking KW - Food Contamination KW - Escherichia coli KW - CHO Cells KW - DNA, Bacterial -- metabolism KW - Tetrahydrofolate Dehydrogenase -- genetics KW - Cricetinae KW - Quinolines -- toxicity KW - DNA Damage KW - Quinoxalines -- analysis KW - DNA -- metabolism KW - Quinoxalines -- toxicity KW - DNA -- analysis KW - Mutagens -- toxicity KW - Quinolines -- analysis KW - DNA -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75647876?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+carcinogenesis&rft.atitle=Quantitation+of+2-amino-3-methylimidazo%5B4%2C5-f%5Dquinoline+and+2-amino-3%2C8-dimethylimidazo%5B4%2C5-f%5Dquinoxaline+DNA+adducts+in+specific+sequences+using+alkali+or+uvrABC+excinuclease.&rft.au=Nouso%2C+K%3BBohr%2C+V+A%3BSchut%2C+H+A%3BSnyderwine%2C+E+G&rft.aulast=Nouso&rft.aufirst=K&rft.date=1993-01-01&rft.volume=7&rft.issue=2&rft.spage=126&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-26 N1 - Date created - 1993-04-26 N1 - Date revised - 2017-01-13 N1 - Gene symbol - DHFR N1 - Last updated - 2017-01-18 ER - TY - CONF T1 - Sixth Aspen Cancer Conference: molecular mechanisms of genetic deregulation in toxicity and carcinogenesis. AN - 75642616; 8096139 JF - Molecular carcinogenesis AU - Tennant, R W AU - Harris, C C AU - Kaufman, D G AU - Nesnow, S AU - Slaga, T J AU - Stevenson, D E AU - Trump, B F Y1 - 1993 PY - 1993 DA - 1993 SP - 67 EP - 72 VL - 7 IS - 2 KW - Anticarcinogenic Agents KW - 0 KW - Carcinogens KW - Reactive Oxygen Species KW - Index Medicus KW - Genes, Tumor Suppressor -- drug effects KW - Humans KW - Mitosis -- drug effects KW - Reactive Oxygen Species -- toxicity KW - Proto-Oncogenes KW - Mutation KW - Gene Expression Regulation, Neoplastic KW - Neoplasms -- chemically induced KW - Carcinogens -- toxicity KW - Neoplasms -- genetics KW - Neoplasms -- etiology KW - Cell Transformation, Neoplastic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75642616?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=Molecular+carcinogenesis&rft.atitle=Sixth+Aspen+Cancer+Conference%3A+molecular+mechanisms+of+genetic+deregulation+in+toxicity+and+carcinogenesis.&rft.au=Tennant%2C+R+W%3BHarris%2C+C+C%3BKaufman%2C+D+G%3BNesnow%2C+S%3BSlaga%2C+T+J%3BStevenson%2C+D+E%3BTrump%2C+B+F&rft.aulast=Tennant&rft.aufirst=R&rft.date=1993-01-01&rft.volume=7&rft.issue=2&rft.spage=67&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-26 N1 - Date created - 1993-04-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Neutral endopeptidase (EC 3.4.24.11) modulates the contractile effects of neuropeptides on muscle cells from the guinea-pig stomach. AN - 75635365; 8448012 AB - The objectives of this investigation were to characterize neuropeptide-degrading enzymes on the surface of gastric muscle cells and to determine their physiological function. Neutral endopeptidase (NEP, EC 3.4.24.11) activity was measured using the fluorogenic substrate glutaryl-Ala-Ala-Phe-4-methoxy-2-naphthylamine. The NEP inhibitors phosphoramidon and DL-thiorphan (1 microM) inhibited degradation of the substrate by gastric muscle membranes by 100% and by freshly dispersed gastric muscle cells by 55-60%. The phosphoramidon or DL-thiorphan-inhibitable activity, attributed to NEP, of membranes was 112 +/- 4.0 pmol h-1 (micrograms protein)-1 and of cells was 4.2 +/- 0.8 nmol h-1 (10(6) cells)-1. This activity was associated with membranes prepared from cells and was not detected in the cytoplasm or in the cell incubation solution. Gastric muscle membranes were fractionated by electrophoresis and analysed by Western blotting using two NEP antisera. Both antisera recognized a protein in membranes with an electrophoretic mobility identical to that of recombinant human NEP and an apparent molecular mass of approximately 95 kDa. Neuropeptides were degraded by membranes with specific activities in the order of [Leu5]enkephalin > [Met5]enkephalin > gastrin-releasing peptide-10 (GRP-10) > [D-Ala2][Leu5]enkephalin > somatostatin-14. Phosphoramidon and DL-thiorphan similarly inhibited the degradation of GRP-10 (mean of 35% inhibition), somatostatin-14 (57%) and the aminopeptidase-resistant analogue, [D-Ala2][Leu5]enkephalin (75%). When aminopeptidases were inhibited with amastatin (10 microM) phosphoramidon inhibited degradation of [Leu5]enkephalin (54%) and [Met5]enkephalin (100%). Phosphoramidon increased the potency of the contractile effects of neuropeptides on muscle cells by > 280-fold for somatostatin-14, 17-fold for GRP-10, 18-fold for [Met5]enkephalin and 14-fold for [Leu5]enkephalin. The results show that an NEP-like enzyme on the surface of gastric muscle cells degrades and inactivates enkephalins, GRP-10 and somatostatin-14 and acts in a manner analogous to that of acetylcholinesterase in the neuromuscular junction of skeletal muscle. JF - Experimental physiology AU - Gu, Z F AU - Menozzi, D AU - Okamoto, A AU - Maton, P N AU - Bunnett, N W AD - Digestive Diseases Branch, National Institutes of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 35 EP - 48 VL - 78 IS - 1 SN - 0958-0670, 0958-0670 KW - Neuropeptides KW - 0 KW - Oligopeptides KW - glutaryl-alanyl-alanyl-phenylalanyl-4-methoxy-2-naphthylamine KW - 2-Naphthylamine KW - CKR7XL41N4 KW - Neprilysin KW - EC 3.4.24.11 KW - Index Medicus KW - Animals KW - Guinea Pigs KW - Gastrointestinal Motility -- physiology KW - Humans KW - Muscle Contraction -- drug effects KW - In Vitro Techniques KW - Gastrointestinal Motility -- drug effects KW - Substrate Specificity KW - 2-Naphthylamine -- analogs & derivatives KW - Male KW - Neuropeptides -- metabolism KW - Neprilysin -- metabolism KW - Neuropeptides -- pharmacology KW - Stomach -- physiology KW - Muscles -- enzymology KW - Stomach -- enzymology KW - Stomach -- drug effects KW - Muscles -- physiology KW - Muscles -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75635365?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Experimental+physiology&rft.atitle=Neutral+endopeptidase+%28EC+3.4.24.11%29+modulates+the+contractile+effects+of+neuropeptides+on+muscle+cells+from+the+guinea-pig+stomach.&rft.au=Gu%2C+Z+F%3BMenozzi%2C+D%3BOkamoto%2C+A%3BMaton%2C+P+N%3BBunnett%2C+N+W&rft.aulast=Gu&rft.aufirst=Z&rft.date=1993-01-01&rft.volume=78&rft.issue=1&rft.spage=35&rft.isbn=&rft.btitle=&rft.title=Experimental+physiology&rft.issn=09580670&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-15 N1 - Date created - 1993-04-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - [3H]resiniferatoxin binding by the vanilloid receptor: species-related differences, effects of temperature and sulfhydryl reagents. AN - 75628084; 8446186 AB - Specific binding of [3H]resiniferatoxin (RTX) is thought to represent the vanilloid (capsaicin) receptor. In the present study, we have used this binding assay to elucidate the contribution of differential receptor expression to the capsaicin-resistance of hamsters and rabbits; binding parameters were compared to those of species (rats, mice) regarded as capsaicin-sensitive. Whereas the 5-fold lower affinity for [3H]RTX binding in the hamster (100 pM) as compared to the rat (20 pM) is unlikely to account for the 100-fold difference in the in vivo responses of RTX-induced inflammation and hypothermia, the lack of detectable specific [3H]RTX binding sites in the rabbit might represent the predominant mechanism of capsaicin-resistance in this species. Regulation of the vanilloid receptor was further characterized in the rat. In accord with the temperature dependence of both in vivo and in vitro capsaicin actions, we found a marked temperature dependence for association rates. Dissociation turned out to have complex kinetics dependent on time and receptor occupancy. Low pH (5.5-7.0) did not affect receptor binding. Preincubation with heavy metal cations and other sulfhydryl-reactive agents inhibited specific [3H]RTX binding indicating that the vanilloid receptor is a thiol-protein, and that free sulfhydryl groups play an essential role in agonist binding activity. Preliminary characterization suggested noncompetitive inhibition. JF - Naunyn-Schmiedeberg's archives of pharmacology AU - Szallasi, A AU - Blumberg, P M AD - Molecular Mechanisms of Tumor Promotion Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 84 EP - 91 VL - 347 IS - 1 SN - 0028-1298, 0028-1298 KW - Cations, Divalent KW - 0 KW - Diterpenes KW - Receptors, Drug KW - Sulfhydryl Reagents KW - resiniferatoxin KW - A5O6P1UL4I KW - Index Medicus KW - Space life sciences KW - Animals KW - Body Temperature -- drug effects KW - Hydrogen-Ion Concentration KW - Inflammation -- chemically induced KW - Temperature KW - Mice KW - Rabbits KW - Rats KW - Rats, Sprague-Dawley KW - Alligators and Crocodiles KW - In Vitro Techniques KW - Sulfhydryl Reagents -- pharmacology KW - Mesocricetus KW - Species Specificity KW - Female KW - Cations, Divalent -- pharmacology KW - Cricetinae KW - Diterpenes -- toxicity KW - Receptors, Drug -- metabolism KW - Receptors, Drug -- drug effects KW - Diterpenes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75628084?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Naunyn-Schmiedeberg%27s+archives+of+pharmacology&rft.atitle=%5B3H%5Dresiniferatoxin+binding+by+the+vanilloid+receptor%3A+species-related+differences%2C+effects+of+temperature+and+sulfhydryl+reagents.&rft.au=Szallasi%2C+A%3BBlumberg%2C+P+M&rft.aulast=Szallasi&rft.aufirst=A&rft.date=1993-01-01&rft.volume=347&rft.issue=1&rft.spage=84&rft.isbn=&rft.btitle=&rft.title=Naunyn-Schmiedeberg%27s+archives+of+pharmacology&rft.issn=00281298&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-07 N1 - Date created - 1993-04-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Toxicokinetics of [14C]-saligenin cyclic-o-tolyl phosphate in anesthetized male F-344 rats. AN - 75620989; 8448420 AB - Saligenin cyclic o-tolyl phosphate (SCOTP) has been proposed as the active metabolite of tri-o-cresyl phosphate (TOCP), a neurotoxic organophosphate. TOCP is also toxic to the testis and SCOTP mimics some of this toxicity. The stability of SCOTP in vivo and its uptake by selected tissues has been measured. Total radioactivity and SCOTP-associated radioactivity were determined in male F-344 rats treated i.v. with 1 mg of [14C]-SCOTP/kg. The half-life of SCOTP in blood was 8.0 +/- 1.1 min. Testes, brain, and muscle had lower concentrations of [14C]-SCOTP-derived radioactivity than blood. Liver and kidney had higher concentrations of radioactivity than blood. HPLC analysis of liver, kidney, testes, and blood extracts showed that 2.8, 48, 11, and 18%, respectively, of the radioactivity present at 5 min was SCOTP. The amount of SCOTP declined rapidly, and at 30 min SCOTP could be detected only in kidney. It appears that SCOTP, although reactive, has sufficient stability to be transported from organ to organ. There is no evidence, however, of active uptake of SCOTP from blood by the testes. Evidence was obtained that SCOTP may act as an alkylating agent. JF - Reproductive toxicology (Elmsford, N.Y.) AU - Burka, L T AU - Chapin, R E AD - National Toxicology Program, National Institute of Environmental Health Sciences Research, Triangle Park, North Carolina 27709. Y1 - 1993 PY - 1993 DA - 1993 SP - 81 EP - 86 VL - 7 IS - 1 SN - 0890-6238, 0890-6238 KW - Organophosphorus Compounds KW - 0 KW - Tritolyl Phosphates KW - 2-(2-cresyl)-4H-1-3-2-benzodioxaphosphorin-2-oxide KW - 1222-87-3 KW - Acetylcysteine KW - WYQ7N0BPYC KW - tri-o-cresyl phosphate KW - X8II18JD0A KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Testis -- metabolism KW - Half-Life KW - Spectrophotometry, Ultraviolet KW - Acetylcysteine -- metabolism KW - Tissue Distribution KW - Male KW - Chromatography, High Pressure Liquid KW - Tritolyl Phosphates -- pharmacokinetics KW - Tritolyl Phosphates -- toxicity KW - Organophosphorus Compounds -- toxicity KW - Organophosphorus Compounds -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75620989?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Reproductive+toxicology+%28Elmsford%2C+N.Y.%29&rft.atitle=Toxicokinetics+of+%5B14C%5D-saligenin+cyclic-o-tolyl+phosphate+in+anesthetized+male+F-344+rats.&rft.au=Burka%2C+L+T%3BChapin%2C+R+E&rft.aulast=Burka&rft.aufirst=L&rft.date=1993-01-01&rft.volume=7&rft.issue=1&rft.spage=81&rft.isbn=&rft.btitle=&rft.title=Reproductive+toxicology+%28Elmsford%2C+N.Y.%29&rft.issn=08906238&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-15 N1 - Date created - 1993-04-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Prevalence of volatile solvent inhalation among junior high school students in Japan and background life style of users. AN - 75618480; 8448518 AB - In order to estimate the prevalence of volatile solvent inhalation among junior high school students in Japan and to assess certain characteristics of the lifestyle of these users, the authors surveyed 5240 students 12-15 years of age. This was the first major survey of the prevalence of volatile solvent inhalation among junior high school students in Japan, from the point of view of the number of subjects and schools. 1.5% of subjects were students who had inhaled solvents. The regularity of life style rhythm was more significantly disturbed in Lifetime Users than in Non-Users. School life and family life were significantly less relaxed for Lifetime Users than for Non-Users. Drinking alcohol and smoking had a strong relationship with inhaling volatile solvents. The authors suggest that greatly increasing education on the harmful effects of volatile solvents inhalation and increasing the frequency with which the entire family eats dinner together will be an effective prevention strategy in Japan. JF - Addiction (Abingdon, England) AU - Wada, K AU - Fukui, S AD - Division of Drug Dependence and Psychotropic Drug Clinical Research, National Institute of Mental Health, NCNP, Chiba-ken, Japan. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 89 EP - 100 VL - 88 IS - 1 SN - 0965-2140, 0965-2140 KW - Solvents KW - 0 KW - Index Medicus KW - Japan -- epidemiology KW - Cross-Sectional Studies KW - Humans KW - Incidence KW - Child KW - Adolescent KW - Male KW - Female KW - Social Environment KW - Life Style KW - Cross-Cultural Comparison KW - Substance-Related Disorders -- prevention & control KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75618480?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Addiction+%28Abingdon%2C+England%29&rft.atitle=Prevalence+of+volatile+solvent+inhalation+among+junior+high+school+students+in+Japan+and+background+life+style+of+users.&rft.au=Wada%2C+K%3BFukui%2C+S&rft.aulast=Wada&rft.aufirst=K&rft.date=1993-01-01&rft.volume=88&rft.issue=1&rft.spage=89&rft.isbn=&rft.btitle=&rft.title=Addiction+%28Abingdon%2C+England%29&rft.issn=09652140&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-12 N1 - Date created - 1993-04-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Identification of thyroid-stimulating antibody-specific interaction sites in the N-terminal region of the thyrotropin receptor. AN - 75614689; 8095322 AB - Using mutants of the N-terminal region (residues 30-76) of the rat TSH receptor (TSHR), which substitute corresponding segments of rat gonadotropin receptors or hydrophilic (serine) and hydrophobic (alanine) amino acids as appropriate, we show that residues 30-33, 34-37, 42-45, 52-56, and 58-61, in addition to threonine-40, are determinants for the interaction of thyroid-stimulating autoantibodies (stimulating TSHRAbs) with the TSHR. The most important, residues 34-37, 42-45, and 52-56, whose mutants lose stimulating TSHRAb activity with at least 11 of 12 (> 90%) of the Graves' immunoglobulins G tested, are, like threonine-40, in regions of the TSHR that are nonhomologous with gonadotropin receptors. These data establish at least in part, therefore, the basis for the thyroid-specific effects of stimulating TSHRAbs. In no case do the same mutants lose their reactivity with TSH or blocking-type TSHR autoantibodies (blocking TSHRAbs) from hypothyroid patients with idiopathic myxedema. Since the latter have been shown to interact with high affinity TSH-binding sites on the C-terminal portion of the external domain of the TSHR, stimulating TSHRAbs and blocking TSHRAbs react with different receptor determinants, which can be presumed to have different roles in receptor function. This can explain the hyper- or hypothyroidism of different thyroid autoimmune diseases with receptor antibodies. Residues 30-33, 42-45, and threonine-40 appear to be related to the agonist action of TSH, since in each case mutation results in low affinity TSH binding, but normal TSH-increased cAMP activity, similar, for example, to a beta-adrenergic agonist. Using a receptor antibody to identify different receptor forms in the membrane, we can also identify determinants in this N-terminal region (residues 30-76) whose mutation results in a loss of all activities without apparently altering receptor synthesis, processing, or integration within the bilayer. These are residues 38 and 39, cysteine-41, residues 46-51, leucine-57, threonine-62, and, within residues 66-76, serine-69, alanine-71, phenylalanine-72, serine-74, leucine-75, and proline-76. We suggest that these residues are at the very least important in the conformational array of receptor determinants necessary for interactions with TSH and stimulating TSHRAbs. JF - Molecular endocrinology (Baltimore, Md.) AU - Kosugi, S AU - Ban, T AU - Kohn, L D AD - Laboratory of Biochemistry and Metabolism, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 114 EP - 130 VL - 7 IS - 1 SN - 0888-8809, 0888-8809 KW - Autoantibodies KW - 0 KW - Immunoglobulins, Thyroid-Stimulating KW - Receptors, Cell Surface KW - Receptors, Thyrotropin KW - Thyrotropin KW - 9002-71-5 KW - Cyclic AMP KW - E0399OZS9N KW - Index Medicus KW - Animals KW - Humans KW - Amino Acid Sequence KW - Binding Sites KW - Mutagenesis, Site-Directed KW - Rats KW - Thyrotropin -- pharmacology KW - Sequence Alignment KW - Second Messenger Systems -- drug effects KW - Cyclic AMP -- metabolism KW - Molecular Sequence Data KW - Receptors, Cell Surface -- genetics KW - Graves Disease -- immunology KW - Receptors, Thyrotropin -- metabolism KW - Autoantibodies -- metabolism KW - Receptors, Thyrotropin -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75614689?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.atitle=Identification+of+thyroid-stimulating+antibody-specific+interaction+sites+in+the+N-terminal+region+of+the+thyrotropin+receptor.&rft.au=Kosugi%2C+S%3BBan%2C+T%3BKohn%2C+L+D&rft.aulast=Kosugi&rft.aufirst=S&rft.date=1993-01-01&rft.volume=7&rft.issue=1&rft.spage=114&rft.isbn=&rft.btitle=&rft.title=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.issn=08888809&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-06 N1 - Date created - 1993-04-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Patterns of alcohol consumption: beverage effects on gender differences. AN - 75612973; 8448504 AB - This Data Note reports findings from 22,102 current drinkers who responded in the US National Interview Survey in 1988. Mean estimated alcohol intake of males exceeded that of females by a factor of two. Males drank more per occasion (ratio 1.45) and drank on more occasion (1.41). Mean ethanol content per drink was slightly less for males (ratio 0.95) attributable to a decreased proportion of drinks being wine and liquor. When beverage preferences were taken into account, the drinking patterns of males and females showed no meaningful differences among persons with similar levels of overall ethanol intake. The results do not support the view that the difference between ethanol consumption of males and females are due primarily to males drinking more per occasion. Apparent differences in drinking patterns are attributable to differences in preferred beverage. JF - Addiction (Abingdon, England) AU - Dawson, D A AD - National Institute on Alcohol Abuse and Alcoholism, Division of Biometry and Epidemiology, Rockville, MD 20857. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 133 EP - 138 VL - 88 IS - 1 SN - 0965-2140, 0965-2140 KW - Index Medicus KW - Cross-Sectional Studies KW - Sex Factors KW - Alcoholism -- epidemiology KW - Humans KW - Health Surveys KW - Incidence KW - United States -- epidemiology KW - Male KW - Female KW - Alcoholic Beverages -- statistics & numerical data KW - Alcohol Drinking -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75612973?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Addiction+%28Abingdon%2C+England%29&rft.atitle=Patterns+of+alcohol+consumption%3A+beverage+effects+on+gender+differences.&rft.au=Dawson%2C+D+A&rft.aulast=Dawson&rft.aufirst=D&rft.date=1993-01-01&rft.volume=88&rft.issue=1&rft.spage=133&rft.isbn=&rft.btitle=&rft.title=Addiction+%28Abingdon%2C+England%29&rft.issn=09652140&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-12 N1 - Date created - 1993-04-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Immunocytochemical and ultrastructural evidence of dendritic degeneration in motor neurons of aluminum-intoxicated rabbits. AN - 75597348; 8442404 AB - Using immunocytochemical and ultrastructural methods, we observed extensive and characteristic dendritic changes in motor neurons of rabbits inoculated intracisternally with aluminum phosphate. Anti-microtubule-associated protein 2 immunostaining revealed markedly reduced immunoreactivity in motor neuron dendrites and a reduced number of dendritic trees in aluminum phosphate-intoxicated rabbits. These dendritic changes were confirmed at the ultrastructural level; neurofilamentous accumulations, membranous inclusions and disrupted microtubules were common features of motor neuron axons. These observations suggest that dendrites are characteristically involved in aluminum intoxication in addition to the widely reported accumulation of phosphorylated neurofilament in perikarya and axons. JF - Acta neuropathologica AU - Wakayama, I AU - Nerurkar, V R AU - Garruto, R M AD - Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 122 EP - 128 VL - 85 IS - 2 SN - 0001-6322, 0001-6322 KW - Aluminum Compounds KW - 0 KW - Nerve Tissue Proteins KW - Phosphates KW - Aluminum KW - CPD4NFA903 KW - aluminum phosphate KW - F92V3S521O KW - Index Medicus KW - Nerve Tissue Proteins -- analysis KW - Animals KW - Rabbits KW - Microscopy, Electron KW - Immunoenzyme Techniques KW - Female KW - Nerve Degeneration -- drug effects KW - Phosphates -- toxicity KW - Dendrites -- ultrastructure KW - Dendrites -- chemistry KW - Aluminum -- toxicity KW - Motor Neurons -- ultrastructure KW - Motor Neurons -- drug effects KW - Motor Neurons -- chemistry KW - Dendrites -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75597348?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Acta+neuropathologica&rft.atitle=Immunocytochemical+and+ultrastructural+evidence+of+dendritic+degeneration+in+motor+neurons+of+aluminum-intoxicated+rabbits.&rft.au=Wakayama%2C+I%3BNerurkar%2C+V+R%3BGarruto%2C+R+M&rft.aulast=Wakayama&rft.aufirst=I&rft.date=1993-01-01&rft.volume=85&rft.issue=2&rft.spage=122&rft.isbn=&rft.btitle=&rft.title=Acta+neuropathologica&rft.issn=00016322&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-01 N1 - Date created - 1993-04-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Ligand/receptor binding for 2,3,7,8-TCDD: implications for risk assessment. AN - 75590858; 8381755 AB - There is renewed controversy regarding safe exposure levels for dioxin. At the heart of this controversy is the hypothesis that toxic effects of dioxin are receptor-mediated and therefore a "threshold" should exist below which no toxic effects can occur. Our research focuses on the ability of dioxin to alter protein levels in rodent livers. Established effects of exposure to dioxin are the induction of cytochrome P450-1A1 and P450-1A2 and a reduction in the maximal binding of the epidermal growth factor receptor in rat livers. An initiation-promotion protocol was used to study the effects of dioxin in female Sprague-Dawley rats. Animals were administered a single initiating dose of diethylnitrosamine followed by 16 biweekly gavage doses of 2,3,7,8-TCDD. Steady-state pharmacodynamic models were fit to these data assuming a combination of Hill kinetics and Michaelis-Menten kinetics. Two classes of models were developed which postulate two different mechanisms for the constitutive expression and TCDD-induced alterations in the levels of these proteins. The results are consistent with models which follow proportionate response in the low-dose region (no threshold) and with models which allow for a low-dose threshold. In all cases studied, the best fitting model exhibited no "threshold" for the effects of TCDD on the modulation of these proteins. The finding is consistent with the knowledge that for some receptor-mediated responses, there is a proportional relationship between receptor occupancy and biological response, even at low ligand concentrations.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Portier, C AU - Tritscher, A AU - Kohn, M AU - Sewall, C AU - Clark, G AU - Edler, L AU - Hoel, D AU - Lucier, G AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 48 EP - 56 VL - 20 IS - 1 SN - 0272-0590, 0272-0590 KW - Ligands KW - 0 KW - Polychlorinated Dibenzodioxins KW - Receptors, Aryl Hydrocarbon KW - Receptors, Drug KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Index Medicus KW - Animals KW - Receptor, Epidermal Growth Factor -- metabolism KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Liver -- metabolism KW - Liver -- chemistry KW - Models, Biological KW - Radioimmunoassay KW - Rats KW - Rats, Sprague-Dawley KW - Enzyme Induction -- drug effects KW - Risk Factors KW - Female KW - Receptors, Drug -- metabolism KW - Receptors, Drug -- drug effects KW - Polychlorinated Dibenzodioxins -- pharmacology KW - Polychlorinated Dibenzodioxins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75590858?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.atitle=Ligand%2Freceptor+binding+for+2%2C3%2C7%2C8-TCDD%3A+implications+for+risk+assessment.&rft.au=Portier%2C+C%3BTritscher%2C+A%3BKohn%2C+M%3BSewall%2C+C%3BClark%2C+G%3BEdler%2C+L%3BHoel%2C+D%3BLucier%2C+G&rft.aulast=Portier&rft.aufirst=C&rft.date=1993-01-01&rft.volume=20&rft.issue=1&rft.spage=48&rft.isbn=&rft.btitle=&rft.title=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.issn=02720590&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-15 N1 - Date created - 1993-03-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Effect of progesterone pretreatment on cadmium toxicity in the male Fischer (F344/NCr) rat. AN - 75590129; 8430418 AB - A previous report has indicated that progesterone pretreatment can markedly reduce cadmium toxicity in male NAW mice. Therefore we examined the effects of progesterone pretreatment on cadmium toxicity in male Fischer (F344/NCr) rats. A single sc injection of 20 mumol CdCl2/kg proved nonlethal over 24 hr but caused the typical spectrum of testicular lesions in these rats. However, when rats were pretreated with progesterone (100 mg/kg, sc, -48, -24, and 0 hr) and then given cadmium (20 mumol CdCl2/kg, 0 hr), this dose of cadmium proved very toxic, unexpectedly causing a 53% mortality. Progesterone pretreatment had no effect on cadmium-induced testicular lesions in surviving rats. Significant elevations in serum lactate dehydrogenase (LDH) activity, indicative of hepatotoxicity, were also observed in progesterone-pretreated rats given cadmium as compared to rats given cadmium alone. Progesterone pretreatment had no effect on the distribution of cadmium to liver, kidney, or testes. Progesterone pretreatment also had no effect on the cadmium-induced increases in hepatic or renal metallothionein (MT) or hepatic or testicular MT mRNA levels. In contrast, levels of the testicular cadmium-binding protein (TCBP) in progesterone-pretreated rats were doubled. These results indicate that, contrary to previously reported data for the mouse, progesterone pretreatment increased the lethality of cadmium in male Fischer (F344/NCr) rats and had no effect on cadmium-induced testicular toxicity. The mechanism by which progesterone enhanced cadmium toxicity, especially cadmium-induced hepatotoxicity, deserves further study. JF - Toxicology and applied pharmacology AU - Shiraishi, N AU - Barter, R A AU - Uno, H AU - Waalkes, M P AD - Inorganic Carcinogenesis Section, National Cancer Institute, Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 113 EP - 118 VL - 118 IS - 1 SN - 0041-008X, 0041-008X KW - cadmium-binding protein KW - 0 KW - Cadmium KW - 00BH33GNGH KW - Progesterone KW - 4G7DS2Q64Y KW - Metallothionein KW - 9038-94-2 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Metallothionein -- biosynthesis KW - Testis -- drug effects KW - Liver -- drug effects KW - Testis -- pathology KW - Male KW - Cadmium -- metabolism KW - Progesterone -- pharmacology KW - Cadmium -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75590129?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+applied+pharmacology&rft.atitle=Effect+of+progesterone+pretreatment+on+cadmium+toxicity+in+the+male+Fischer+%28F344%2FNCr%29+rat.&rft.au=Shiraishi%2C+N%3BBarter%2C+R+A%3BUno%2C+H%3BWaalkes%2C+M+P&rft.aulast=Shiraishi&rft.aufirst=N&rft.date=1993-01-01&rft.volume=118&rft.issue=1&rft.spage=113&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=0041008X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-08 N1 - Date created - 1993-03-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Progress in the treatment of tardive dyskinesia: theory and practice. AN - 75590041; 8094705 AB - About 20 percent of patients receiving long-term treatment with neuroleptic medications develop tardive dyskinesia. A 1988 review of treatment studies for the disorder found that 40 percent of patients showed at least 50 percent improvement in symptoms. This paper reviews studies published since 1984, including those not reviewed in 1988, to learn whether new or improved treatments for the disorder have been developed. Twenty-five open, blind, or double-blind studies (with a minimum of five patients) published between 1984 and May 1992 were examined. The studies involved neuroleptics, including clozapine, dopaminergic and dopamine-depleting agents, GABAergic drugs, vitamin E, calcium channel blockers, and adrenergic drugs. Overall, only 26 percent of patients who participated in the studies reviewed had a 50 percent or greater reduction in symptoms. The authors conclude that treatment of tardive dyskinesia remains a highly individual process and recommend that future studies be more carefully designed. JF - Hospital & community psychiatry AU - Feltner, D E AU - Hertzman, M AD - National Institute of Mental Health, St. Elizabeths Hospital, Washington, D.C. 20032. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 25 EP - 34 VL - 44 IS - 1 SN - 0022-1597, 0022-1597 KW - Antipsychotic Agents KW - 0 KW - Central Nervous System Agents KW - Index Medicus KW - Humans KW - Neurologic Examination -- drug effects KW - Dyskinesia, Drug-Induced -- drug therapy KW - Central Nervous System Agents -- adverse effects KW - Antipsychotic Agents -- therapeutic use KW - Schizophrenic Psychology KW - Central Nervous System Agents -- therapeutic use KW - Schizophrenia -- drug therapy KW - Dyskinesia, Drug-Induced -- etiology KW - Antipsychotic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75590041?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hospital+%26+community+psychiatry&rft.atitle=Progress+in+the+treatment+of+tardive+dyskinesia%3A+theory+and+practice.&rft.au=Feltner%2C+D+E%3BHertzman%2C+M&rft.aulast=Feltner&rft.aufirst=D&rft.date=1993-01-01&rft.volume=44&rft.issue=1&rft.spage=25&rft.isbn=&rft.btitle=&rft.title=Hospital+%26+community+psychiatry&rft.issn=00221597&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-25 N1 - Date created - 1993-03-25 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Hosp Community Psychiatry. 1993 Aug;44(8):795 [8104162] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Effects of chronic consumption of metanil yellow by developing and adult rats on brain regional levels of noradrenaline, dopamine and serotonin, on acetylcholine esterase activity and on operant conditioning. AN - 75589912; 8095244 AB - Metanil yellow is the principal non-permitted food colour used extensively in India. The effects of long-term consumption of metanil yellow on the developing and adult brain were studied using Wistar rats. Regional levels of noradrenaline, dopamine and serotonin, activity of acetylcholine esterase (AChE), and operant conditioning with food reward were assessed in rats fed, metanil yellow and in controls. In the treated rats the amine levels in the hypothalamus, striatum and brain stem were significantly affected, and the changes were not generally reversible even after withdrawal of metanil yellow in developing rats. The striatum showed an early reduction of AChE activity, whereas the hippocampus showed a delayed but persistent effect of reduced AChE activity. Treated rats also took more sessions to learn the operant conditioning behaviour. These effects on these major neurotransmitter systems and on learning, indicate that chronic consumption of metanil yellow can predispose both the developing and the adult central nervous system (CNS) of the rat to neurotoxicity. JF - Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association AU - Nagaraja, T N AU - Desiraju, T AD - Department of Neurophysiology, National Institute of Mental Health and Neuro Sciences, Bangalore, India. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 41 EP - 44 VL - 31 IS - 1 SN - 0278-6915, 0278-6915 KW - Azo Compounds KW - 0 KW - Food Coloring Agents KW - Neurotransmitter Agents KW - Serotonin KW - 333DO1RDJY KW - metanil yellow KW - 7SPF5O5BW8 KW - Acetylcholinesterase KW - EC 3.1.1.7 KW - Dopamine KW - VTD58H1Z2X KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Animals KW - Brain Stem -- metabolism KW - Hypothalamus -- drug effects KW - Corpus Striatum -- metabolism KW - Dopamine -- metabolism KW - Hypothalamus -- growth & development KW - Rats KW - Brain Stem -- drug effects KW - Brain Stem -- growth & development KW - Norepinephrine -- metabolism KW - Corpus Striatum -- growth & development KW - Hypothalamus -- metabolism KW - Rats, Wistar KW - Corpus Striatum -- drug effects KW - Serotonin -- metabolism KW - Male KW - Female KW - Conditioning, Operant -- drug effects KW - Azo Compounds -- administration & dosage KW - Neurotransmitter Agents -- metabolism KW - Food Coloring Agents -- toxicity KW - Brain -- drug effects KW - Acetylcholinesterase -- metabolism KW - Food Coloring Agents -- pharmacology KW - Food Coloring Agents -- administration & dosage KW - Azo Compounds -- toxicity KW - Azo Compounds -- pharmacology KW - Brain -- physiology KW - Brain -- growth & development UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75589912?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Food+and+chemical+toxicology+%3A+an+international+journal+published+for+the+British+Industrial+Biological+Research+Association&rft.atitle=Effects+of+chronic+consumption+of+metanil+yellow+by+developing+and+adult+rats+on+brain+regional+levels+of+noradrenaline%2C+dopamine+and+serotonin%2C+on+acetylcholine+esterase+activity+and+on+operant+conditioning.&rft.au=Nagaraja%2C+T+N%3BDesiraju%2C+T&rft.aulast=Nagaraja&rft.aufirst=T&rft.date=1993-01-01&rft.volume=31&rft.issue=1&rft.spage=41&rft.isbn=&rft.btitle=&rft.title=Food+and+chemical+toxicology+%3A+an+international+journal+published+for+the+British+Industrial+Biological+Research+Association&rft.issn=02786915&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-06 N1 - Date created - 1993-04-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Keratin 14 protein in cultured nonparenchymal rat hepatic epithelial cells: characterization of keratin 14 and keratin 19 as antigens for the commonly used mouse monoclonal antibody OV-6. AN - 75587211; 7679578 AB - We have recently reported that cell lines of nonparenchymal origin isolated from rat liver and pancreas, which have been suggested to be the progeny of a facultative stem cell compartment in vivo, express an unusual combination of keratins (K). These cell lines express K8 and K14 but not K18 and K5, their normal partners in filament formation (Bisgaard HC, Thorgeirsson SS, J Cell Physiol 147:333-343, 1991). However, upon spontaneous transformation and differentiation toward a hepatoblastlike progeny, K14 expression is abrogated and replaced by expression of K18 (Wirth et al., Electrophoresis 13:305-332, 1992). In the study presented here, we confirmed by protein sequence analysis that K14 was a major component of the intermediate filaments in a nonparenchymal cell line of hepatic origin. Immunocytochemical analysis of the cells in monolayer demonstrated that K8 as well as K14 were incorporated in the cellular cytoskeleton. Further analysis by immunoprecipitation showed that filament complexes were formed between K8 and K14 as atypical partners. Thus, we concluded that in some nonparenchymal cell lines isolated from rat liver, K8 and K14 form a major intermediate filament network. Finally, we showed that an antibody widely used in studies of the cell lineages of hepatic and pancreatic tissues and their neoplasms, the mouse monoclonal antibody OV-6, recognizes a common epitope in K14 and K19. JF - Molecular carcinogenesis AU - Bisgaard, H C AU - Parmelee, D C AU - Dunsford, H A AU - Sechi, S AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892-0037. Y1 - 1993 PY - 1993 DA - 1993 SP - 60 EP - 66 VL - 7 IS - 1 SN - 0899-1987, 0899-1987 KW - v-raf KW - Antibodies, Monoclonal KW - 0 KW - Antigens KW - Keratins KW - 68238-35-7 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Epithelial Cells KW - Cells, Cultured KW - Molecular Sequence Data KW - Mice KW - Epithelium -- immunology KW - Amino Acid Sequence KW - Male KW - Epithelium -- chemistry KW - Liver -- cytology KW - Liver -- immunology KW - Keratins -- immunology KW - Liver -- chemistry KW - Antigens -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75587211?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+carcinogenesis&rft.atitle=Keratin+14+protein+in+cultured+nonparenchymal+rat+hepatic+epithelial+cells%3A+characterization+of+keratin+14+and+keratin+19+as+antigens+for+the+commonly+used+mouse+monoclonal+antibody+OV-6.&rft.au=Bisgaard%2C+H+C%3BParmelee%2C+D+C%3BDunsford%2C+H+A%3BSechi%2C+S%3BThorgeirsson%2C+S+S&rft.aulast=Bisgaard&rft.aufirst=H&rft.date=1993-01-01&rft.volume=7&rft.issue=1&rft.spage=60&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-24 N1 - Date created - 1993-03-24 N1 - Date revised - 2017-01-13 N1 - Gene symbol - v-raf N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Application of microencapsulation for toxicology studies. III. Bioavailability of microencapsulated cinnamaldehyde. AN - 75584962; 8432430 AB - The bioavailability of microencapsulated cinnamaldehyde (CNMA) was investigated in male F344 rats. Rats were gavaged with CNMA in corn oil using either microencapsulated or the neat chemical at doses of 50, 250, and 500 mg/kg. No differences between the two formulations at any of the doses were found in either CNMA blood concentration profiles or in the rate of urinary hippuric acid excretion. Both formulations showed a low bioavailability (< 20%) at 250 and 500 mg/kg. Regardless of the formulation used, oral gavage of CNMA significantly increased the urinary excretion of hippuric acid. About 75% of the dose of CNMA was metabolized to hippuric acid and recovered in the urine. The total amount of hippuric acid recovered in a 50-hr urinary collection correlated well with the CNMA dose. The data suggest that there was complete release of CNMA from the microcapsules and that microencapsulation of CNMA does not affect its bioavailability or its metabolism. Since CNMA microcapsules are stable in rodent diet, the microencapsulation of CNMA, and perhaps other labile chemicals, will prevent degradation and facilitate the testing of such compounds in toxicology studies. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Yuan, J AU - Dieter, M P AU - Bucher, J R AU - Jameson, C W AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 83 EP - 87 VL - 20 IS - 1 SN - 0272-0590, 0272-0590 KW - Capsules KW - 0 KW - Hippurates KW - Acrolein KW - 7864XYD3JJ KW - cinnamic aldehyde KW - SR60A3XG0F KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Half-Life KW - Intubation, Gastrointestinal KW - Male KW - Chromatography, High Pressure Liquid KW - Hippurates -- urine KW - Biological Availability KW - Acrolein -- analogs & derivatives KW - Acrolein -- pharmacokinetics KW - Acrolein -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75584962?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.atitle=Application+of+microencapsulation+for+toxicology+studies.+III.+Bioavailability+of+microencapsulated+cinnamaldehyde.&rft.au=Yuan%2C+J%3BDieter%2C+M+P%3BBucher%2C+J+R%3BJameson%2C+C+W&rft.aulast=Yuan&rft.aufirst=J&rft.date=1993-01-01&rft.volume=20&rft.issue=1&rft.spage=83&rft.isbn=&rft.btitle=&rft.title=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.issn=02720590&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-15 N1 - Date created - 1993-03-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The effects of feed restriction on reproductive function in Sprague-Dawley rats. AN - 75584868; 8432425 AB - Although it is known that severe feed restriction (FR) and weight reduction (to 50-60% of control values) will sharply impair rat reproduction, few data exist on the effects of less severe body weight reduction. In the present studies, adult Sprague-Dawley rats were feed restricted and maintained at 90, 80, and 70% of control body weight (CBW) for up to 17 weeks. In females, this treatment had no effect on fertility or total number of implants per dam, but transiently increased the length of the estrous cycle and decreased by 20% the number of corpora lutea in the 70% CBW females. Ovary weight at necropsy was decreased only in the 70% CBW group. Liver and kidney weights varied with body weight. In males, fertility was not affected when they were mated to nonrestricted females. While prostate and seminal vesicles weight varied with body weight, testis and epididymis weights were unchanged by any degree of FR, as were the number of sperm in the cauda epididymis and the number of homogenization-resistant spermatids in the testis. The percentage motile sperm was slightly decreased at all levels of FR. These data show that the Sprague-Dawley rat is largely resistant to adverse reproductive changes caused by feed restriction to 70% CBW. These data should be of use in interpreting changes seen in toxicity studies that produce weight-reduce Sprague-Dawley rats. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Chapin, R E AU - Gulati, D K AU - Barnes, L H AU - Teague, J L AD - Developmental and Reproductive Toxicology Group, National Toxicology Program, NIEHS, Research Triangle Park, North Carolina 27709. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 23 EP - 29 VL - 20 IS - 1 SN - 0272-0590, 0272-0590 KW - Index Medicus KW - Rats KW - Eating -- physiology KW - Animals KW - Rats, Sprague-Dawley KW - Fertility KW - Organ Size -- physiology KW - Estrus -- physiology KW - Sperm Count KW - Body Weight -- physiology KW - Male KW - Female KW - Pregnancy KW - Reproduction -- physiology KW - Diet UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75584868?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.atitle=The+effects+of+feed+restriction+on+reproductive+function+in+Sprague-Dawley+rats.&rft.au=Chapin%2C+R+E%3BGulati%2C+D+K%3BBarnes%2C+L+H%3BTeague%2C+J+L&rft.aulast=Chapin&rft.aufirst=R&rft.date=1993-01-01&rft.volume=20&rft.issue=1&rft.spage=23&rft.isbn=&rft.btitle=&rft.title=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.issn=02720590&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-15 N1 - Date created - 1993-03-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Locomotor activity in mice during chronic treatment with caffeine and withdrawal. AN - 75583427; 7679219 AB - Chronic ingestion of caffeine by mice caused a marked reduction in locomotor exploratory activity. At least 4 days of withdrawal were required to restore activity to normal levels. Stimulatory effects of injected caffeine were lower in chronically treated mice and the biphasic dose-response (stimulatory followed by depressant) curve for injected caffeine was left shifted. Seven days of withdrawal were required before the dose-response curve to caffeine was identical to that of control mice. The depressant effects of a potent xanthine phosphodiesterase inhibitor, 1,3-dipropyl-7-methylxanthine, were blunted in caffeine-treated mice. The depressant effects of A1- and A2-selective adenosine analogs were enhanced after chronic caffeine. There was little or no effect of chronic caffeine on the stimulatory effects of dopaminergic agents (amphetamine, caffeine), while both depressant and stimulatory effects of cholinergic agents (nicotine, oxotremorine, scopolamine) were reduced. The results indicate that chronic caffeine affects functions of adenosine and cholinergic receptors related to regulation of locomotor exploratory activity. JF - Pharmacology, biochemistry, and behavior AU - Nikodijević, O AU - Jacobson, K A AU - Daly, J W AD - Laboratory of Bioorganic Chemistry, National Institutes of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 199 EP - 216 VL - 44 IS - 1 SN - 0091-3057, 0091-3057 KW - Dopamine Agents KW - 0 KW - Parasympathomimetics KW - Xanthines KW - 1,3-dipropyl-7-methylxanthine KW - 31542-63-9 KW - Caffeine KW - 3G6A5W338E KW - Adenosine KW - K72T3FS567 KW - 1-Methyl-3-isobutylxanthine KW - TBT296U68M KW - Index Medicus KW - Animals KW - Adenosine -- pharmacology KW - Parasympathomimetics -- pharmacology KW - Dose-Response Relationship, Drug KW - Dopamine Agents -- pharmacology KW - Mice KW - 1-Methyl-3-isobutylxanthine -- pharmacology KW - Xanthines -- pharmacology KW - Male KW - Substance Withdrawal Syndrome -- physiopathology KW - Caffeine -- pharmacology KW - Motor Activity -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75583427?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacology%2C+biochemistry%2C+and+behavior&rft.atitle=Locomotor+activity+in+mice+during+chronic+treatment+with+caffeine+and+withdrawal.&rft.au=Nikodijevi%C4%87%2C+O%3BJacobson%2C+K+A%3BDaly%2C+J+W&rft.aulast=Nikodijevi%C4%87&rft.aufirst=O&rft.date=1993-01-01&rft.volume=44&rft.issue=1&rft.spage=199&rft.isbn=&rft.btitle=&rft.title=Pharmacology%2C+biochemistry%2C+and+behavior&rft.issn=00913057&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-09 N1 - Date created - 1993-03-09 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Brain Res. 1984 Feb 27;294(1):186-9 [6697237] Pharmacol Biochem Behav. 1984 Mar;20(3):383-6 [6709673] Pharmacol Biochem Behav. 1984 Sep;21(3):375-9 [6494209] Life Sci. 1985 Jun 17;36(24):2347-58 [2989634] Psychopharmacology (Berl). 1985;87(4):421-4 [3936100] J Clin Invest. 1986 Jan;77(1):222-7 [3003150] Life Sci. 1986 Feb 17;38(7):577-88 [3003486] Pharmacol Biochem Behav. 1986 Feb;24(2):263-70 [2419924] Pharmacol Biochem Behav. 1986 Mar;24(3):761-4 [3703910] Br J Pharmacol. 1986 Jul;88(3):671-6 [3017491] J Med Chem. 1986 Jul;29(7):1305-8 [3806581] Prog Drug Res. 1987;31:273-313 [3326033] Brain Res. 1988 Feb 16;441(1-2):209-14 [3359231] Pharmacol Biochem Behav. 1988 Feb;29(2):411-8 [3362935] Biol Psychiatry. 1988 Apr 15;23(8):761-8 [2835113] Life Sci. 1988;43(5):387-98 [2456442] Brain Res Bull. 1988 Sep;21(3):479-82 [3214753] Epilepsia. 1989 Jan-Feb;30(1):26-33 [2912715] J Neural Transm Gen Sect. 1989;78(1):9-15 [2547026] Eur J Pharmacol. 1989 Oct 24;170(1-2):35-40 [2482186] FEBS Lett. 1990 Feb 12;261(1):67-70 [2307237] Pharmacol Biochem Behav. 1990 Feb;35(2):477-9 [2320659] J Biol Chem. 1990 Apr 25;265(12):6782-7 [2157711] Jpn J Pharmacol. 1990 Apr;52(4):533-9 [2342225] J Mol Recognit. 1989 Dec;2(4):170-8 [2561548] J Neurochem. 1990 Jul;55(1):31-8 [2355224] J Pharmacol Exp Ther. 1990 Jul;254(1):45-51 [2366189] Acta Physiol Scand. 1990 Oct;140(2):245-55 [2267953] J Pharmacol Exp Ther. 1991 Jan;256(1):62-8 [1846425] Proc Biol Sci. 1991 Apr 22;244(1309):57-62 [1677197] J Pharmacol Exp Ther. 1991 Oct;259(1):286-94 [1920121] Pharmacol Biochem Behav. 1991 May;39(1):97-103 [1924519] Psychopharmacologia. 1964 Mar 11;5:289-300 [14143341] Life Sci. 1974 Apr 16;14(8):1493-500 [4364279] Pharmacol Biochem Behav. 1977 Mar;6(3):359-61 [558624] Neuropharmacology. 1978 Jan;17(1):7-12 [652133] Proc Natl Acad Sci U S A. 1981 May;78(5):3260-4 [6265942] J Pharmacol Exp Ther. 1982 Sep;222(3):550-4 [6125581] Eur J Pharmacol. 1982 Aug 13;82(1-2):113-4 [6290230] Psychopharmacology (Berl). 1982;77(4):309-16 [6182575] Acta Physiol Scand. 1982 Jun;115(2):283-6 [6291335] Life Sci. 1983 Mar 7;32(10):1135-42 [6298543] Life Sci. 1983 Aug 22;33(8):779-87 [6888193] Brain Res. 1983 Aug 8;272(2):392-5 [6616215] J Pharmacol Exp Ther. 1983 Oct;227(1):167-73 [6194284] Erratum In: Pharmacol Biochem Behav 1993 Aug;45(4):1003 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Functional role of proline and tryptophan residues highly conserved among G protein-coupled receptors studied by mutational analysis of the m3 muscarinic receptor. AN - 75580737; 7679072 AB - Most G protein-coupled receptors contain a series of highly conserved proline and tryptophan residues within their hydrophobic transmembrane domains (TMD I-VII). To study their potential role in ligand binding and receptor function, the rat m3 muscarinic acetylcholine receptor was used as a model system. A series of mutant receptors in which the conserved proline and tryptophan residues were individually replaced with alanine and phenylalanine, respectively, was created and transiently expressed in COS-7 cells. [3H]N-methylscopolamine ([3H]NMS) saturation binding studies showed that three of the seven mutant receptors studied (Pro242-->Ala, TMD V; Pro505-->Ala, TMD VI; Pro540-->Ala, TMD VII) were expressed at 35-100 times lower levels than the wild-type receptor while displaying 'm3-like' antagonist binding affinities. Pro201-->Ala (TMD IV) showed drastically reduced binding affinities (up to 450-fold) for both muscarinic agonists and antagonists. Whereas most mutant receptors retained strong functional activity, Pro540-->Ala (TMD VII) was found to be severely impaired in its ability to stimulate carbachol-induced phosphatidyl inositol hydrolysis (Emax approximately 25% of wild type m3). Interestingly, this mutant receptor bound muscarinic agonists with 7- to 19-fold higher affinities than the wild type receptor. The Trp-->Phe substitutions (Trp192-->Phe, TMD IV; Trp503-->Phe, TMD VI; Trp530-->Phe, TMD VII) resulted in less pronounced changes (compared with the Pro-->Ala mutant receptors) in both ligand binding and receptor function. Our data indicate that the proline residues that are highly conserved across the entire superfamily of G protein-coupled receptors play key roles in receptor expression, ligand binding and receptor activation. JF - The EMBO journal AU - Wess, J AU - Nanavati, S AU - Vogel, Z AU - Maggio, R AD - National Institute of Neurological Disorders and Stroke, Laboratory of Molecular Biology, Bethesda, MD 20892. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 331 EP - 338 VL - 12 IS - 1 SN - 0261-4189, 0261-4189 KW - Codon KW - 0 KW - Parasympatholytics KW - Piperidines KW - Receptors, Muscarinic KW - Recombinant Proteins KW - Scopolamine Derivatives KW - RNA KW - 63231-63-0 KW - 4-diphenylacetoxy-1,1-dimethylpiperidinium KW - 81405-11-0 KW - Tryptophan KW - 8DUH1N11BX KW - Carbachol KW - 8Y164V895Y KW - Proline KW - 9DLQ4CIU6V KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Acetylcholine KW - N9YNS0M02X KW - N-Methylscopolamine KW - VDR09VTQ8U KW - Index Medicus KW - Animals KW - Codon -- genetics KW - Blotting, Northern KW - Scopolamine Derivatives -- metabolism KW - Parasympatholytics -- pharmacology KW - Parasympatholytics -- metabolism KW - Piperidines -- metabolism KW - Carbachol -- metabolism KW - Rats KW - Acetylcholine -- metabolism KW - Recombinant Proteins -- metabolism KW - Molecular Sequence Data KW - RNA -- isolation & purification KW - Protein Conformation KW - RNA -- genetics KW - Amino Acid Sequence KW - Acetylcholine -- pharmacology KW - Binding Sites KW - Piperidines -- pharmacology KW - Base Sequence KW - Transfection KW - Kinetics KW - Restriction Mapping KW - Carbachol -- pharmacology KW - Cell Line KW - Mutagenesis, Site-Directed KW - Receptors, Muscarinic -- genetics KW - GTP-Binding Proteins -- metabolism KW - Receptors, Muscarinic -- chemistry KW - Receptors, Muscarinic -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75580737?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+EMBO+journal&rft.atitle=Functional+role+of+proline+and+tryptophan+residues+highly+conserved+among+G+protein-coupled+receptors+studied+by+mutational+analysis+of+the+m3+muscarinic+receptor.&rft.au=Wess%2C+J%3BNanavati%2C+S%3BVogel%2C+Z%3BMaggio%2C+R&rft.aulast=Wess&rft.aufirst=J&rft.date=1993-01-01&rft.volume=12&rft.issue=1&rft.spage=331&rft.isbn=&rft.btitle=&rft.title=The+EMBO+journal&rft.issn=02614189&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-10 N1 - Date created - 1993-03-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 1988 Jul 25;263(21):10267-71 [2899076] FASEB J. 1992 Mar;6(6):2323-31 [1544542] J Biol Chem. 1988 Dec 5;263(34):18397-403 [2848036] J Biol Chem. 1989 Jan 5;264(1):489-95 [2909533] Nature. 1989 Mar 2;338(6210):67-70 [2493138] J Biol Chem. 1989 May 5;264(13):7564-9 [2540197] J Biol Chem. 1989 Jun 5;264(16):9266-70 [2542304] Mol Pharmacol. 1989 Dec;36(6):840-7 [2557534] Biochemistry. 1990 Mar 6;29(9):2335-42 [2159799] Annu Rev Pharmacol Toxicol. 1990;30:633-73 [2188581] J Mol Biol. 1990 Jun 20;213(4):899-929 [2359127] J Biol Chem. 1990 Aug 15;265(23):13702-8 [2380182] J Biol Chem. 1990 Sep 15;265(26):15762-9 [2144289] J Biol Chem. 1990 Dec 5;265(34):20887-92 [2249995] Mol Pharmacol. 1990 Dec;38(6):872-7 [2174507] J Pharmacol Exp Ther. 1991 Feb;256(2):727-33 [1994002] J Biol Chem. 1991 Mar 5;266(7):4269-75 [1999419] Eur J Biochem. 1991 Feb 26;196(1):1-10 [1848179] Trends Pharmacol Sci. 1990 Dec;11(12):492-9 [1964255] Biochem Soc Trans. 1991 Feb;19(1):133-8 [1903735] Mol Pharmacol. 1991 Jul;40(1):8-15 [1649965] Annu Rev Biochem. 1991;60:653-88 [1652922] Biochem Pharmacol. 1973 Dec 1;22(23):3099-108 [4202581] Anal Biochem. 1976 May 7;72:248-54 [942051] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Cell. 1980 May;20(1):95-105 [6893015] J Gen Physiol. 1981 Nov;78(5):521-45 [6796648] Biochem J. 1983 May 15;212(2):473-82 [6309146] Biochem J. 1986 Sep 15;238(3):625-42 [2948499] Proc Natl Acad Sci U S A. 1987 Jul;84(13):4384-8 [2885836] Science. 1987 Jul 31;237(4814):527-32 [3037705] Anal Biochem. 1987 Apr;162(1):156-9 [2440339] Mol Cell Biol. 1987 Aug;7(8):2745-52 [3670292] EMBO J. 1987 Nov;6(11):3269-75 [2828022] EMBO J. 1991 Dec;10(12):3729-34 [1657592] DNA Cell Biol. 1992 Jan-Feb;11(1):1-20 [1310857] Proc Natl Acad Sci U S A. 1988 Aug;85(15):5478-82 [2840663] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Inherited factors and environmental exposures in cancer risk. AN - 75571605; 8423501 AB - Carcinogenesis is a multistage process that results from the interaction of carcinogenic exposures, cellular macromolecules (eg, DNA), and endogenous mutational mechanisms. Involved in these processes are metabolic activation and detoxification of chemical carcinogens, genetic sequences of protooncogenes and tumor suppressor genes, and DNA repair, among others. Each of these vary widely among individuals and can be associated with increased cancer risk. Cytochrome P4501A1, P4502E1 and N-acetyl transferase 2 are examples of enzymes involved in the metabolic activation of potential environmental carcinogens such as polycyclic aromatic hydrocarbons, benzene, and aromatic amines, respectively. Germ-line mutations in these genes are common and associated with abnormal enzymatic function that are mechanistically related to quantitative changes in binding of carcinogens to DNA. Allelic frequencies for these mutations vary among different racial and ethnic populations and may explain, in part, differences in cancer rates. Risk assessments attempt to predict cancer rates in humans using mathematical models that are often based upon limited experimental data. They do not generally incorporate the numerous stages of carcinogenesis or interindividual variation. Thus, sensitive and resistant populations are not sufficiently considered. This limits the accuracy of currently applied risk assessment models. JF - Journal of occupational medicine. : official publication of the Industrial Medical Association AU - Shields, P G AD - Laboratory of Human Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 34 EP - 41 VL - 35 IS - 1 SN - 0096-1736, 0096-1736 KW - Carcinogens, Environmental KW - 0 KW - Polycyclic Compounds KW - Index Medicus KW - Risk KW - Acetylation KW - Carcinogens, Environmental -- adverse effects KW - Polymorphism, Genetic KW - Humans KW - Genes, p53 -- genetics KW - Polycyclic Compounds -- metabolism KW - Mutation KW - Cocarcinogenesis KW - Neoplasms -- chemically induced KW - Environmental Exposure KW - Neoplasms -- genetics KW - Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75571605?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+occupational+medicine.+%3A+official+publication+of+the+Industrial+Medical+Association&rft.atitle=Inherited+factors+and+environmental+exposures+in+cancer+risk.&rft.au=Shields%2C+P+G&rft.aulast=Shields&rft.aufirst=P&rft.date=1993-01-01&rft.volume=35&rft.issue=1&rft.spage=34&rft.isbn=&rft.btitle=&rft.title=Journal+of+occupational+medicine.+%3A+official+publication+of+the+Industrial+Medical+Association&rft.issn=00961736&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-23 N1 - Date created - 1993-02-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - CONF T1 - Molecular mechanisms of carcinogenesis in humans and rodents. AN - 75569245; 8094618 JF - Molecular carcinogenesis AU - Barrett, J C AU - Anderson, M Y1 - 1993 PY - 1993 DA - 1993 SP - 1 EP - 13 VL - 7 IS - 1 KW - Rb KW - nm23 KW - p53 KW - pp39 mos KW - ras KW - Carcinogens KW - 0 KW - Index Medicus KW - Animals KW - Genes, Tumor Suppressor KW - Humans KW - Carcinogens -- toxicity KW - Rodentia KW - Gene Amplification KW - Neoplasms -- genetics KW - Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75569245?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=Molecular+carcinogenesis&rft.atitle=Molecular+mechanisms+of+carcinogenesis+in+humans+and+rodents.&rft.au=Barrett%2C+J+C%3BAnderson%2C+M&rft.aulast=Barrett&rft.aufirst=J&rft.date=1993-01-01&rft.volume=7&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-24 N1 - Date created - 1993-03-24 N1 - Date revised - 2017-01-13 N1 - Gene symbol - Rb; nm23; p53; pp39 mos; ras N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Neoplastic progression of Syrian hamster embryo cells in culture. AN - 75566527; 8424093 JF - Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.) AU - Barrett, J C AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 30 EP - 36 VL - 202 IS - 1 SN - 0037-9727, 0037-9727 KW - Index Medicus KW - Animals KW - Cells, Cultured KW - Cell Aging KW - Humans KW - Cell Cycle -- physiology KW - Cell Death KW - Mesocricetus KW - Hybrid Cells -- cytology KW - Models, Biological KW - Cricetinae KW - Cell Division KW - Neoplasms -- pathology KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75566527?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+Society+for+Experimental+Biology+and+Medicine.+Society+for+Experimental+Biology+and+Medicine+%28New+York%2C+N.Y.%29&rft.atitle=Neoplastic+progression+of+Syrian+hamster+embryo+cells+in+culture.&rft.au=Barrett%2C+J+C&rft.aulast=Barrett&rft.aufirst=J&rft.date=1993-01-01&rft.volume=202&rft.issue=1&rft.spage=30&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+Society+for+Experimental+Biology+and+Medicine.+Society+for+Experimental+Biology+and+Medicine+%28New+York%2C+N.Y.%29&rft.issn=00379727&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-19 N1 - Date created - 1993-02-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Specific inhibition of FSH-stimulated cAMP accumulation by delta 9-tetrahydrocannabinol in cultured rat granulosa cells. AN - 75565811; 8381567 AB - delta 9-Tetrahydrocannabinol (THC), the major psychoactive component in marihuana has been shown to affect male and female reproduction in both humans and animals. THC has effects at the level at the pituitary-hypothalamic axis as well as a direct effect on the testis and ovary. A specific gonadal effect of THC is inhibition of steroidogenesis in cultured granulosa cells from immature, estrogen-treated rats that depends in part on a post-cyclic AMP site of action. The effect of THC on cAMP accumulation itself, however, has not yet been examined in this cell type. The aim of the present study was to examine the effect of THC on granulosa cell cAMP accumulation, a process that is important for several granulosa cell functions, including steroidogenesis. THC inhibited FSH-stimulated cAMP accumulation in a dose-dependent manner at concentrations which were not cytotoxic. This inhibition was evident by 2 hr and did not affect the dose of FSH which gave half-maximal stimulation, suggesting that THC does not compete with FSH for binding to its receptor. Detailed investigations regarding the mechanism of THC inhibition were conducted using forskolin and isoproterenol. In contrast to its effect on FSH stimulation, THC did not inhibit forskolin- or isoproterenol-stimulated cAMP accumulation, indicating a specific effect for the FSH receptor. In addition, inhibition of FSH-stimulated cAMP accumulation occurred in the presence of a phosphodiesterase inhibitor, indicating that THC does not decrease cAMP accumulation through an increase in the cAMP degradative pathway. These data indicate that a part of the reproductive toxicity seen with THC may be due to a specific alteration of the hormonal control of granulosa cell function via a specific inhibition of FSH-stimulated cAMP accumulation. JF - Toxicology and applied pharmacology AU - Treinen, K A AU - Sneeden, J L AU - Heindel, J J AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 53 EP - 57 VL - 118 IS - 1 SN - 0041-008X, 0041-008X KW - Dronabinol KW - 7J8897W37S KW - Follicle Stimulating Hormone KW - 9002-68-0 KW - Cyclic AMP KW - E0399OZS9N KW - Isoproterenol KW - L628TT009W KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Dose-Response Relationship, Drug KW - Cells, Cultured KW - Isoproterenol -- pharmacology KW - Female KW - Granulosa Cells -- drug effects KW - Dronabinol -- pharmacology KW - Cyclic AMP -- metabolism KW - Follicle Stimulating Hormone -- pharmacology KW - Granulosa Cells -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75565811?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+applied+pharmacology&rft.atitle=Specific+inhibition+of+FSH-stimulated+cAMP+accumulation+by+delta+9-tetrahydrocannabinol+in+cultured+rat+granulosa+cells.&rft.au=Treinen%2C+K+A%3BSneeden%2C+J+L%3BHeindel%2C+J+J&rft.aulast=Treinen&rft.aufirst=K&rft.date=1993-01-01&rft.volume=118&rft.issue=1&rft.spage=53&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=0041008X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-08 N1 - Date created - 1993-03-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Chemical effects in transgenic mice bearing oncogenes expressed in mammary tissue. AN - 75565684; 8093862 AB - Three transgenic mouse lines carrying v-Ha-ras (TG-SH), c-myc (TG-M) or c-neu (TG-NK) oncogenes under regulatory control of mouse mammary tumor virus (MMTV) long terminal repeat (LTR) sequences were evaluated for responses to two chemical carcinogens. p-Cresidine, a mutagenic urinary bladder carcinogen, increased the incidence of urinary bladder carcinomas in males and females in all three lines, and these tumors occurred at comparable incidences and grade in transgenic and non-transgenic mice. p-Cresidine did not affect the rates of mammary or salivary gland neoplasms in transgenic mice; these tumors did not occur in non-transgenic littermates. No other tumor types were observed in exposed or control animals. Reserpine, a non-mutagenic mammary gland carcinogen, was administered under the same protocol, but the high control rates of mammary gland adenocarcinomas in the TG-M and TG-NK strains made it difficult to detect any tumor-enhancing effect of reserpine. However, the incidences of multiple mammary gland tumors were significantly increased in dosed females from both lines. The incidence of mammary gland adenocarcinomas was significantly increased in TG-SH females receiving 5 p.p.m. reserpine. Reserpine did not induce any carcinogenic effects in non-transgenic mice. These results indicate that the transcriptional regulation of these three transgenes is a major determinant in the response to p-cresidine and reserpine. The use of transgenic models for the general detection of carcinogens may require lines in which appropriate genes are targeted for expression in many tissues, or lines in which critical genes have been inactivated. JF - Carcinogenesis AU - Tennant, R W AU - Rao, G N AU - Russfield, A AU - Seilkop, S AU - Braun, A G AD - National Institutes of Health, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 29 EP - 35 VL - 14 IS - 1 SN - 0143-3334, 0143-3334 KW - c-myc KW - c-neu KW - v-Ha-ras KW - Aniline Compounds KW - 0 KW - Carcinogens KW - Proto-Oncogene Proteins KW - cresidine KW - 4C11L78UR3 KW - Reserpine KW - 8B1QWR724A KW - Receptor, ErbB-2 KW - EC 2.7.10.1 KW - Index Medicus KW - Animals KW - Adenocarcinoma -- chemically induced KW - Genes, myc KW - Urinary Bladder Neoplasms -- genetics KW - Gene Expression KW - Mammary Tumor Virus, Mouse KW - Mammary Neoplasms, Experimental -- genetics KW - Adenocarcinoma -- genetics KW - Mice KW - Mice, Transgenic KW - Genes, ras KW - Mammary Neoplasms, Experimental -- chemically induced KW - Proto-Oncogene Proteins -- genetics KW - Female KW - Male KW - Urinary Bladder Neoplasms -- chemically induced KW - Survival Analysis KW - Oncogenes KW - Mammary Glands, Animal -- metabolism KW - Carcinogens -- toxicity KW - Aniline Compounds -- toxicity KW - Reserpine -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75565684?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Chemical+effects+in+transgenic+mice+bearing+oncogenes+expressed+in+mammary+tissue.&rft.au=Tennant%2C+R+W%3BRao%2C+G+N%3BRussfield%2C+A%3BSeilkop%2C+S%3BBraun%2C+A+G&rft.aulast=Tennant&rft.aufirst=R&rft.date=1993-01-01&rft.volume=14&rft.issue=1&rft.spage=29&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-04 N1 - Date created - 1993-03-04 N1 - Date revised - 2017-01-13 N1 - Gene symbol - c-myc; c-neu; v-Ha-ras N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The effects of feed restriction on reproductive function in Swiss CD-1 mice. AN - 75562089; 8432424 AB - Many test compounds used in toxicity studies produce a "systemic" toxicity manifested as reduced body weight gain. While it is known that reduced weight gain during juvenile growth reduces or delays reproductive competence, the effects of adult-onset feed restriction (FR) and inhibited weight gain on the reproductive system of mice are poorly known. To gain some information on the effects of graded body weight reduction, or reduced body weight gain, on commonly used reproductive endpoints, the studies reported below were conducted at two laboratories, using adult mice that were maintained at 90, 80, and 70% of concurrent control body weight (CBW) for up to 21 weeks. Estrous cyclicity and fertility in the females were significantly affected. While male fertility was variably affected, there was a significant decrease in the number of epididymal sperm and in the number of testicular spermatids in the 70% CBW groups. Testis weight was conserved in both studies; relative testis weight increased in all FR groups. These data can improve the interpretation of future studies by helping to separate chemically induced changes from those produced by reduced body weight gain. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Chapin, R E AU - Gulati, D K AU - Fail, P A AU - Hope, E AU - Russell, S R AU - Heindel, J J AU - George, J D AU - Grizzle, T B AU - Teague, J L AD - Developmental and Reproductive Toxicology Group, NIEHS, National Toxicology Program, Research Triangle Park, North Carolina 27709. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 15 EP - 22 VL - 20 IS - 1 SN - 0272-0590, 0272-0590 KW - Index Medicus KW - Animals KW - Mice, Inbred ICR KW - Fertility KW - Organ Size -- physiology KW - Estrus -- physiology KW - Sperm Count KW - Body Weight -- physiology KW - Mice KW - Male KW - Female KW - Pregnancy KW - Reproduction -- physiology KW - Diet UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75562089?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.atitle=The+effects+of+feed+restriction+on+reproductive+function+in+Swiss+CD-1+mice.&rft.au=Chapin%2C+R+E%3BGulati%2C+D+K%3BFail%2C+P+A%3BHope%2C+E%3BRussell%2C+S+R%3BHeindel%2C+J+J%3BGeorge%2C+J+D%3BGrizzle%2C+T+B%3BTeague%2C+J+L&rft.aulast=Chapin&rft.aufirst=R&rft.date=1993-01-01&rft.volume=20&rft.issue=1&rft.spage=15&rft.isbn=&rft.btitle=&rft.title=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.issn=02720590&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-15 N1 - Date created - 1993-03-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Critical aspects of initiation, promotion, and progression in multistage epidermal carcinogenesis. AN - 75561622; 8424089 AB - Carcinogenesis in mouse skin can be divided into three distinct stages: initiation, promotion, and progression (malignant conversion). Initiation, induced by a single exposure to a genotoxic carcinogen, can result from a mutation in a single critical gene (e.g., rasHa), apparently in only a few epidermal cells. The change is irreversible. Promotion, resulting in the development of numerous benign tumors (papillomas), is accomplished by the repeated application of a nonmutagenic tumor promoter. The effects of single applications of tumor promoters are reversible since papillomas do not develop after insufficient exposure of initiated skin to promoters or when the interval between individual promoter applications is increased sufficiently. The reversibility of promotion suggests an epigenetic mechanism. Promoter treatment provides an environment that allows the selective clonal expansion of foci of initiated cells. The conversion of squamous papillomas to carcinomas (termed progression or malignant conversion) occurs spontaneously at a low frequency. The rate of progression to malignancy can be significantly increased by treatment of papilloma-bearing mice with certain genotoxic agents. These progressor agents or converting agents are likely to act via a second genetic change in papillomas already bearing the initiating mutation. Progression in the skin is characterized by genetic changes that result in several distinct changes in the levels or activity of structural proteins, growth factors, and proteases. The mechanisms involved in progression are being studied in epidermal cell culture. In order to determine the in vivo phenotype of cultured cells, a grafting system was developed in which the cells were transferred from culture to a prepared skin bed in athymic mice. Introduction of an activated v-fos oncogene into initiated cells bearing an activated rasHa gene produced cells with a carcinoma phenotype, i.e., carcinomas formed when the cells were grafted as part of reconstituted skin. Grafted keratinocytes containing the rasHa gene alone produced papillomas; with v-fos alone, normal skin formed when grafted. The rasHa/fos carcinomas showed changes in differentiation markers characteristic of chemically induced carcinomas. A cell culture assay utilizing cells initiated by the introduction of an activated rasHa oncogene was developed to study progression. After exposure of initiated cells to progressor agents under conditions in which the proliferation of the rasHa-initiated cells was suppressed, proliferating foci developed, with a good correlation of activity in the assay with activity in the progression stage in vivo. The cell culture assay provides a quantitative model to study chemically induced neoplastic progression and may be useful to identify potential progressor agents. JF - Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.) AU - Hennings, H AU - Glick, A B AU - Greenhalgh, D A AU - Morgan, D L AU - Strickland, J E AU - Tennenbaum, T AU - Yuspa, S H AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 1 EP - 8 VL - 202 IS - 1 SN - 0037-9727, 0037-9727 KW - E1A KW - c-fos KW - fasHa KW - fos KW - myc KW - neoR KW - v-fos KW - v-rasHa KW - Carcinogens KW - 0 KW - Index Medicus KW - Genes, ras KW - Animals KW - Papilloma -- pathology KW - Mice KW - Keratinocytes -- pathology KW - Genes, fos KW - Gene Expression Regulation KW - Papilloma -- chemically induced KW - Cell Line KW - Mutagenesis KW - Oncogenes KW - Skin Neoplasms -- chemically induced KW - Skin Neoplasms -- pathology KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75561622?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+Society+for+Experimental+Biology+and+Medicine.+Society+for+Experimental+Biology+and+Medicine+%28New+York%2C+N.Y.%29&rft.atitle=Critical+aspects+of+initiation%2C+promotion%2C+and+progression+in+multistage+epidermal+carcinogenesis.&rft.au=Hennings%2C+H%3BGlick%2C+A+B%3BGreenhalgh%2C+D+A%3BMorgan%2C+D+L%3BStrickland%2C+J+E%3BTennenbaum%2C+T%3BYuspa%2C+S+H&rft.aulast=Hennings&rft.aufirst=H&rft.date=1993-01-01&rft.volume=202&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+Society+for+Experimental+Biology+and+Medicine.+Society+for+Experimental+Biology+and+Medicine+%28New+York%2C+N.Y.%29&rft.issn=00379727&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-19 N1 - Date created - 1993-02-19 N1 - Date revised - 2017-01-13 N1 - Gene symbol - E1A; c-fos; fasHa; fos; myc; neoR; v-fos; v-rasHa N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Transforming G protein-coupled receptors transduce potent mitogenic signals in NIH 3T3 cells independent on cAMP inhibition or conventional protein kinase C. AN - 75558818; 8380916 AB - We have used the expression of human acetylcholine muscarinic receptor (mAChR) genes in NIH 3T3 cells as a model for dissecting the molecular basis of cellular transformation induced by G protein-coupled receptors. Those mAChR subtypes efficiently coupled to PIP2 hydrolysis (m1, m3 and m5) induced agonist-dependent cell transformation whereas those inhibiting adenylyl cyclase (m2, m4) lack transforming activity. In the present study, we demonstrate that in cells expressing m1 but not m2 mAChRs the cholinergic agonist (carbachol) is alone as potent a stimulant for DNA synthesis as platelet-derived growth factor (PDGF) or serum. Furthermore, induction of DNA synthesis is shown to correlate with activation of PIP2 hydrolysis but not with inhibition of adenylyl cyclase. We also examined the role of protein kinase C (PKC) in mitogenic signalling through m1 mAChRs, and found that NIH 3T3 cells express PKC-alpha and PCK-zeta as the only conventional or Ca(2+)-independent PKC isozyme, respectively. Prolonged treatment with TPA depleted cells of PKC-alpha but not of PKC-zeta. In TPA-treated NIH 3T3 cells, the mitogenic response to a subsequent stimulation with TPA was absolutely abolished, but the response to PDGF or serum was not. Moreover, PKC depletion did not decrease DNA synthesis induced by carbachol. We conclude that carbachol potently induces reinitiation of DNA synthesis through the activation of transforming mAChR subtypes, independently of inhibition of adenylyl cyclase and conventional PKCs. JF - Oncogene AU - Stephens, E V AU - Kalinec, G AU - Brann, M R AU - Gutkind, J S AD - Laboratory of Cellular Development and Oncology, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 19 EP - 26 VL - 8 IS - 1 SN - 0950-9232, 0950-9232 KW - Adenylyl Cyclase Inhibitors KW - 0 KW - Isoenzymes KW - Phosphatidylinositols KW - Platelet-Derived Growth Factor KW - Receptors, Muscarinic KW - Carbachol KW - 8Y164V895Y KW - DNA KW - 9007-49-2 KW - Phosphotransferases KW - EC 2.7.- KW - Protein Kinase C KW - EC 2.7.11.13 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Phosphotransferases -- analysis KW - Phosphatidylinositols -- metabolism KW - Isoenzymes -- analysis KW - Animals KW - 3T3 Cells KW - Platelet-Derived Growth Factor -- pharmacology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Mice KW - Carbachol -- pharmacology KW - Protein Kinase C -- analysis KW - GTP-Binding Proteins -- physiology KW - Protein Kinase C -- physiology KW - Receptors, Muscarinic -- physiology KW - DNA -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75558818?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncogene&rft.atitle=Transforming+G+protein-coupled+receptors+transduce+potent+mitogenic+signals+in+NIH+3T3+cells+independent+on+cAMP+inhibition+or+conventional+protein+kinase+C.&rft.au=Stephens%2C+E+V%3BKalinec%2C+G%3BBrann%2C+M+R%3BGutkind%2C+J+S&rft.aulast=Stephens&rft.aufirst=E&rft.date=1993-01-01&rft.volume=8&rft.issue=1&rft.spage=19&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=09509232&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-22 N1 - Date created - 1993-02-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Pristane induces an indomethacin inhibitable inflammatory influx of CD4+ T cells and IFN-gamma production in plasmacytoma-susceptible BALB/cAnPt mice. AN - 75558600; 8425224 AB - In BALB/cAnPt (BALB/c) mice, the intraperitoneal injection of pristane induces the formation of chronic oil granulomatous tissue and a high incidence of plasmacytomas (PCT). DBA/2N (DBA) and (BALB/c x DBA)F1 hybrid (CDF1) mice develop oil granulomas but no PCT. Recent studies comparing pristane-injected conventionally housed BALB/c mice with specific pathogen-free BALB/c mice (SPF) demonstrated a significant reduction in both the incidence of PCT and the T cell infiltration of oil granulomatous tissue in SPF mice. In this study, FACS analysis was performed to determine the proportion of myeloid, T. and B cells present in pristane-induced peritoneal exudate (PE), and oil granulomas (OG) of BALB/c, DBA, and CDF1 mice. At all time points studied, the majority of cells recovered from the PE and OG of all three strains of mice were Mac-1+, presumably macrophages and neutrophils. Neither Ly-5(B220)+ B cells nor CD8+ T cells were significantly altered by pristane injection. BALB/c mice had a dramatic influx of CD4+ T lymphocytes (three- to fivefold) more than 50 days after the initial injection of pristane. The PCT-resistant DBA and CDF1 mice did not. This increase in CD4+ cells in BALB/c mice was not significantly affected by a second injection of pristane nor was it induced by a second injection in DBA mice. Indomethacin, which has been shown to prevent the development of PCT in BALB/c mice, prevented the infiltration of CD4+ T cells. In addition, pristane-induced levels of interferon-gamma greater than controls were found in the peritoneal lavages of BALB/c mice at all time points tested but not in DBA or indomethacin-treated BALB/c mice. In contrast, pristane injection increased levels of interleukin-5 in DBA but not BALB/c mice. JF - Cellular immunology AU - McDonald, A H AU - Degrassi, A AD - Laboratory of Genetics, National Cancer Institute/National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 157 EP - 170 VL - 146 IS - 1 SN - 0008-8749, 0008-8749 KW - Antigens, CD4 KW - 0 KW - Interleukin-5 KW - Terpenes KW - pristane KW - 26HZV48DT1 KW - Interferon-gamma KW - 82115-62-6 KW - Indomethacin KW - XXE1CET956 KW - Index Medicus KW - Animals KW - Interleukin-5 -- secretion KW - Plasmacytoma -- chemically induced KW - Mice KW - Mice, Inbred BALB C KW - Neoplasms, Experimental KW - Mice, Inbred DBA KW - Interferon-gamma -- secretion KW - Inflammation -- drug therapy KW - Terpenes -- pharmacology KW - T-Lymphocytes -- drug effects KW - T-Lymphocytes -- immunology KW - Antigens, CD4 -- immunology KW - Indomethacin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75558600?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cellular+immunology&rft.atitle=Pristane+induces+an+indomethacin+inhibitable+inflammatory+influx+of+CD4%2B+T+cells+and+IFN-gamma+production+in+plasmacytoma-susceptible+BALB%2FcAnPt+mice.&rft.au=McDonald%2C+A+H%3BDegrassi%2C+A&rft.aulast=McDonald&rft.aufirst=A&rft.date=1993-01-01&rft.volume=146&rft.issue=1&rft.spage=157&rft.isbn=&rft.btitle=&rft.title=Cellular+immunology&rft.issn=00088749&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-03 N1 - Date created - 1993-03-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Wegener granulomatosis in children and adolescents: clinical presentation and outcome. AN - 75558493; 8419611 AB - We prospectively studied and compared clinical features, treatment, course of illness, and long-term morbidity and mortality rates for Wegener granulomatosis in 23 childhood-onset patients with those of 135 adult-onset patients who were studied concurrently. Treatment was usually provided with glucocorticoids and cyclophosphamide. The mean follow-up period was 8.7 years for childhood-onset and 7.6 years for adult-onset Wegener granulomatosis. Most aspects of Wegener granulomatosis were similar in childhood-onset and adult-onset patients. Permanent morbidity from disease occurred in 86% of both groups. However, some features were significantly different. Wegener granulomatosis in childhood-onset patients was complicated five times more often by subglottic stenosis and twice as often by nasal deformity. Treatment-related permanent morbidity occurred in 22% of childhood-onset patients and 45% of adult-onset patients. After similar periods of cyclophosphamide therapy and follow-up, cyclophosphamide-related malignancies were less likely (0% vs 11%) to have developed in childhood-onset patients. Although 89% of patients treated with glucocorticoids and cyclophosphamide had remission, prolonged delay in achieving remission and relapses led in both patient groups to freedom from active disease for approximately 50% of the total patient-years. As a result, morbidity was substantial and has led to comparative studies of alternative therapies. JF - The Journal of pediatrics AU - Rottem, M AU - Fauci, A S AU - Hallahan, C W AU - Kerr, G S AU - Lebovics, R AU - Leavitt, R Y AU - Hoffman, G S AD - Laboratory of Clinical Investigation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 26 EP - 31 VL - 122 IS - 1 SN - 0022-3476, 0022-3476 KW - Cyclophosphamide KW - 8N3DW7272P KW - Prednisone KW - VB0R961HZT KW - Abridged Index Medicus KW - Index Medicus KW - Opportunistic Infections KW - Age Factors KW - Prednisone -- therapeutic use KW - Humans KW - Eye Diseases -- physiopathology KW - Lung Diseases -- physiopathology KW - Child KW - Laryngostenosis -- physiopathology KW - Cyclophosphamide -- adverse effects KW - Prospective Studies KW - Prednisone -- adverse effects KW - Cyclophosphamide -- therapeutic use KW - Survival Rate KW - Nose Diseases -- physiopathology KW - Adult KW - Treatment Outcome KW - Follow-Up Studies KW - Glomerulonephritis -- physiopathology KW - Adolescent KW - Male KW - Female KW - Remission Induction KW - Granulomatosis with Polyangiitis -- complications KW - Granulomatosis with Polyangiitis -- physiopathology KW - Granulomatosis with Polyangiitis -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75558493?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+pediatrics&rft.atitle=Wegener+granulomatosis+in+children+and+adolescents%3A+clinical+presentation+and+outcome.&rft.au=Rottem%2C+M%3BFauci%2C+A+S%3BHallahan%2C+C+W%3BKerr%2C+G+S%3BLebovics%2C+R%3BLeavitt%2C+R+Y%3BHoffman%2C+G+S&rft.aulast=Rottem&rft.aufirst=M&rft.date=1993-01-01&rft.volume=122&rft.issue=1&rft.spage=26&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pediatrics&rft.issn=00223476&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-08 N1 - Date created - 1993-02-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - non-Hodgkin's lymphoma and occupation in Sweden: a registry based analysis. AN - 75558203; 8431395 AB - Incidence of non-Hodgkin's lymphoma in different employment categories was evaluated from the Swedish Cancer-Environment Registry, which links cancer incidence during 1961 to 1979 with occupational information from the 1960 census. New associations were found for men employed in shoemaking and shoe repair, porcelain and earthenware industries, education, and other white collar occupations. Several findings supported associations found in other countries, including excesses among woodworkers, furniture makers, electric power plant workers, farmers, dairy workers, lorry drivers, and other land transport workers. Risks were not increased among chemists, chemical or rubber manufacturing workers, or petrochemical refinery workers. Caution must be used in drawing causal inferences from these linked registry data because information on exposure and duration of employment is not available. Nevertheless, this study has suggested new clues to possible occupational determinants of non-Hodgkin's lymphoma. JF - British journal of industrial medicine AU - Linet, M S AU - Malker, H S AU - McLaughlin, J K AU - Weiner, J A AU - Blot, W J AU - Ericsson, J L AU - Fraumeni, J F AD - Division of Cancer Etiology, National Cancer Institute, Rockville, Maryland. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 79 EP - 84 VL - 50 IS - 1 SN - 0007-1072, 0007-1072 KW - Index Medicus KW - Registries KW - Social Class KW - Risk Factors KW - Humans KW - Sweden -- epidemiology KW - Incidence KW - Occupations KW - Male KW - Occupational Exposure KW - Lymphoma, Non-Hodgkin -- epidemiology KW - Lymphoma, Non-Hodgkin -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75558203?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+industrial+medicine&rft.atitle=non-Hodgkin%27s+lymphoma+and+occupation+in+Sweden%3A+a+registry+based+analysis.&rft.au=Linet%2C+M+S%3BMalker%2C+H+S%3BMcLaughlin%2C+J+K%3BWeiner%2C+J+A%3BBlot%2C+W+J%3BEricsson%2C+J+L%3BFraumeni%2C+J+F&rft.aulast=Linet&rft.aufirst=M&rft.date=1993-01-01&rft.volume=50&rft.issue=1&rft.spage=79&rft.isbn=&rft.btitle=&rft.title=British+journal+of+industrial+medicine&rft.issn=00071072&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-18 N1 - Date created - 1993-03-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Am J Epidemiol. 1968 Mar;87(2):267-74 [4869663] Am J Ind Med. 1988;14(1):63-72 [3165602] J Natl Cancer Inst. 1969 Dec;43(6):1297-305 [5408805] Pathol Annu. 1977;12 Pt 2:411-25 [579657] Cancer Res. 1980 Aug;40(8 Pt 1):2645-52 [6992990] Environ Res. 1980 Jun;22(1):154-61 [7418674] Environ Res. 1980 Oct;23(1):181-90 [7428756] Scand J Work Environ Health. 1988 Aug;14(4):246-51 [3175557] Am J Ind Med. 1988;14(4):403-15 [3189356] Br J Ind Med. 1989 Jan;46(1):16-23 [2920139] Am J Ind Med. 1989;15(3):283-310 [2929617] Leuk Res. 1989;13(6):465-72 [2770331] Br J Ind Med. 1989 Aug;46(8):516-20 [2775671] Br J Cancer. 1989 Sep;60(3):385-8 [2789947] Environ Health Perspect. 1989 Jul;82:165-9 [2477239] Epidemiol Rev. 1989;11:59-78 [2680562] Am J Ind Med. 1989;16(6):631-43 [2556914] Nutr Cancer. 1989;12(4):333-41 [2608538] Am J Ind Med. 1990;18(3):303-5 [2220835] N Engl J Med. 1964 Oct 22;271:872-6 [14185112] Br J Cancer. 1981 Feb;43(2):169-76 [7470379] J Natl Cancer Inst. 1981 Mar;66(3):461-4 [6937703] Int J Cancer. 1982 Mar 15;29(3):239-47 [7040259] N Engl J Med. 1982 Jul 22;307(4):249 [7088076] J Occup Med. 1982 Jul;24(7):526-30 [6750057] Int J Epidemiol. 1982 Dec;11(4):345-55 [7152787] J Natl Cancer Inst. 1983 Jan;70(1):37-44 [6571919] J Natl Cancer Inst. 1983 Jul;71(1):1-4 [6575197] Am J Ind Med. 1983;4(4):523-32 [6869377] J Epidemiol Community Health. 1983 Dec;37(4):279-80 [6361201] Am J Ind Med. 1984;5(4):303-14 [6720693] J Natl Cancer Inst. 1984 Jun;72(6):1233-40 [6587145] Am J Ind Med. 1984;6(3):207-30 [6475966] J Occup Med. 1984 Nov;26(11):844-6 [6502289] Br J Ind Med. 1985 Mar;42(3):191-5 [3970885] Br J Ind Med. 1985 Mar;42(3):211-2 [3970890] Am J Ind Med. 1985;7(5-6):395-402 [4003402] Scand J Work Environ Health. 1985 Aug;11(4):249-55 [4059888] J Natl Cancer Inst. 1986 Feb;76(2):229-34 [3456061] Br J Ind Med. 1986 Mar;43(3):212-3 [3947586] Scand J Work Environ Health. 1985 Dec;11(6):397-407 [3912986] Br J Cancer. 1986 Feb;53(2):271-9 [3456788] J Occup Med. 1986 Apr;28(4):264-5 [3754574] Scand J Soc Med. 1986;14(3):151-60 [3489987] Cancer Res. 1987 Jan 1;47(1):287-91 [3791212] Int J Cancer. 1987 Feb 15;39(2):155-61 [3804490] J Natl Cancer Inst. 1987 May;78(5):899-910 [3471999] J Natl Cancer Inst. 1987 Jun;78(6):1137-44 [3473254] Br J Ind Med. 1987 Jun;44(6):382-95 [3606967] Am J Ind Med. 1987;12(5):615-23 [3687954] Br J Cancer. 1987 Oct;56(4):505-8 [3689667] Br J Ind Med. 1988 Jan;45(1):19-24 [3342183] Br J Ind Med. 1988 Jan;45(1):25-8 [3342184] Med Oncol Tumor Pharmacother. 1987;4(3-4):199-205 [3326982] Am J Ind Med. 1988;13(3):317-30 [3354583] Am J Ind Med. 1988;13(3):363-79 [3354585] Leuk Res. 1988;12(1):81-8 [3357350] Int J Epidemiol. 1988 Mar;17(1):27-32 [3384545] J Natl Cancer Inst. 1969 Jul;43(1):1-14 [5804605] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - The effect of cholesterol-lowering agents on hepatic and plasma cholesterol in Niemann-Pick disease type C. AN - 75557063; 8423912 AB - Niemann-Pick disease type C (NP-C) is a neurovisceral lipidosis characterized by defective intracellular trafficking of cholesterol and lysosomal accumulation of unesterified cholesterol, believed to be an offending metabolite. We studied the effect of cholesterol-lowering agents on hepatic and plasma cholesterol levels in NP-C by randomly assigning 25 patients with NP-C to one of five treatment regimens containing different combinations of cholestyramine, lovastatin, nicotinic acid, or dimethyl sulfoxide (DMSO). Unesterified cholesterol content was measured in liver biopsies before and after 4 months' treatment. All drug regimens except DMSO alone reduced hepatic and plasma cholesterol levels. Toxicity was limited and did not prevent any patient from completing the study. The combination of cholestyramine, lovastatin, and nicotinic acid lowered cholesterol levels in liver and blood with minimal side effects. A controlled clinical study will be necessary to determine if this regimen influences the rate of neurologic progression. JF - Neurology AU - Patterson, M C AU - Di Bisceglie, A M AU - Higgins, J J AU - Abel, R B AU - Schiffmann, R AU - Parker, C C AU - Argoff, C E AU - Grewal, R P AU - Yu, K AU - Pentchev, P G AD - Developmental and Metabolic Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 61 EP - 64 VL - 43 IS - 1 SN - 0028-3878, 0028-3878 KW - Anticholesteremic Agents KW - 0 KW - Cholestyramine Resin KW - 11041-12-6 KW - Niacin KW - 2679MF687A KW - Cholesterol KW - 97C5T2UQ7J KW - Lovastatin KW - 9LHU78OQFD KW - Dimethyl Sulfoxide KW - YOW8V9698H KW - Abridged Index Medicus KW - Index Medicus KW - Drug Therapy, Combination KW - Dimethyl Sulfoxide -- administration & dosage KW - Lovastatin -- administration & dosage KW - Humans KW - Adult KW - Cholestyramine Resin -- administration & dosage KW - Child KW - Niacin -- administration & dosage KW - Adolescent KW - Male KW - Child, Preschool KW - Liver -- pathology KW - Niemann-Pick Diseases -- drug therapy KW - Niemann-Pick Diseases -- diet therapy KW - Niemann-Pick Diseases -- blood KW - Cholesterol -- analysis KW - Anticholesteremic Agents -- therapeutic use KW - Anticholesteremic Agents -- adverse effects KW - Liver -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75557063?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurology&rft.atitle=The+effect+of+cholesterol-lowering+agents+on+hepatic+and+plasma+cholesterol+in+Niemann-Pick+disease+type+C.&rft.au=Patterson%2C+M+C%3BDi+Bisceglie%2C+A+M%3BHiggins%2C+J+J%3BAbel%2C+R+B%3BSchiffmann%2C+R%3BParker%2C+C+C%3BArgoff%2C+C+E%3BGrewal%2C+R+P%3BYu%2C+K%3BPentchev%2C+P+G&rft.aulast=Patterson&rft.aufirst=M&rft.date=1993-01-01&rft.volume=43&rft.issue=1&rft.spage=61&rft.isbn=&rft.btitle=&rft.title=Neurology&rft.issn=00283878&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-23 N1 - Date created - 1993-02-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Early dendrite development in spinal cord cell cultures: a quantitative study. AN - 75556654; 8423636 AB - Neurons in dissociated cell culture provide a favorable system for the quantitative analysis of structural changes and the examination of structure-function relationships during development. Fragment C of tetanus toxin was used to label neurons in murine spinal cord cell cultures and dendrite outgrowth was monitored by a number of measures. The dissociated neurons increased in morphologic complexity from approximate spheres to highly branched structures during the first week in culture. Much of the structural complexity of the dendrite arbor, as quantified by fractal dimension, was established within 48 hr after plating, i.e., prior to the development of interneuronal contacts. During the first few days in culture, dendrite branching complexity increased more rapidly than dendrite size, whereas after 4 days, fractal dimension remained relatively constant while dendrites continued to grow. Fractal analysis has provided data which suggest that the early development of dendrite branching complexity is determined intrinsically. Fractal dimension, as an effective index of morphologic complexity, should be a useful tool for the further study of extrinsic signals which might modify the generation or stabilization of dendrite form. JF - Journal of neuroscience research AU - Neale, E A AU - Bowers, L M AU - Smith, T G AD - Laboratory of Developmental Neurobiology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 54 EP - 66 VL - 34 IS - 1 SN - 0360-4012, 0360-4012 KW - Peptide Fragments KW - 0 KW - Tetanus Toxin KW - tetanus toxin fragment C KW - Index Medicus KW - Animals KW - Cells, Cultured KW - Cell Aging KW - Mice KW - Models, Neurological KW - Immunohistochemistry KW - Image Processing, Computer-Assisted KW - Spinal Cord -- metabolism KW - Fetus -- physiology KW - Dendrites -- physiology KW - Spinal Cord -- embryology KW - Spinal Cord -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75556654?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neuroscience+research&rft.atitle=Early+dendrite+development+in+spinal+cord+cell+cultures%3A+a+quantitative+study.&rft.au=Neale%2C+E+A%3BBowers%2C+L+M%3BSmith%2C+T+G&rft.aulast=Neale&rft.aufirst=E&rft.date=1993-01-01&rft.volume=34&rft.issue=1&rft.spage=54&rft.isbn=&rft.btitle=&rft.title=Journal+of+neuroscience+research&rft.issn=03604012&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-24 N1 - Date created - 1993-02-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Comparative analyses of heterochromatin in Microtus: sequence heterogeneity and localized expansion and contraction of satellite DNA arrays. AN - 75554947; 8428514 AB - Southern blotting, C-banding, base-specific fluorochrome staining, and fluorescence in situ hybridization were used to analyze the constitutive heterochromatin in eight species and subspecies of arvicolid rodents (genus Microtus). Autosomal centromeric regions portrayed considerable variability between species in the amount of C-band-positive material present; e.g., M. chrotorrhinus showed relatively little, whereas M. cabrerae exhibited extensive centromeric staining. Autosomal interstitial C-bands were noted in M. guentheri and two subspecies of M. ochrogaster. All Y chromosomes examined were predominately or completely heterochromatic, as were substantial portions of the giant X chromosomes in three species (M. agrestis, M. cabrerae, and M. chrotorrhinus). Hoechst 33258 staining (with its affinity for AT binding sites) showed bright fluorescence on the heterochromatin of the sex chromosomes of M. agrestis and moderate fluorescence on those of M. cabrerae and M. chrotorrhinus; however, only the heterochromatin of M. cabrerae and M. chrotorrhinus hybridized with an AT-rich satellite DNA probe (MSAT-160) isolated from M. chrotorrhinus. Hoechst 33258-bright autosomal centromeres of M. arvalis and M. cabrerae also hybridized to the probe, whereas the Hoechst 33258-bright Y chromosomes of M. arvalis and M. guentheri did not. Two pairs of autosomes in M. guentheri are comprised of six distinct regions, based upon C-banding, Hoechst 33258 staining, chromomycin A3/distamycin A staining, and in situ hybridization. The centromeric regions of acrocentric autosomes known to retain conserved G-banding patterns may exhibit variable hybridization intensity when different species or subspecies are compared. M. ochrogaster portrays considerable intersubspecific variability in the size and location of autosomal telomeric and interstitial C-bands that are also sites of hybridization. These latter two findings illustrate that dramatic differences in copy number of the tandem satellite array can exist at homologous chromosomal positions both within and between species. JF - Cytogenetics and cell genetics AU - Modi, W S AD - Biological Carcinogenesis and Development Program, Program Resources, Inc./DynCorp, National Cancer Institute, Frederick, MD 21702-1201. Y1 - 1993 PY - 1993 DA - 1993 SP - 142 EP - 148 VL - 62 IS - 2-3 SN - 0301-0171, 0301-0171 KW - DNA, Satellite KW - 0 KW - Fluorescent Dyes KW - Heterochromatin KW - Index Medicus KW - Phylogeny KW - Genetic Variation KW - Animals KW - X Chromosome KW - Chromosome Banding KW - Blotting, Southern KW - Y Chromosome KW - In Situ Hybridization, Fluorescence KW - Sequence Analysis, DNA KW - Repetitive Sequences, Nucleic Acid KW - Species Specificity KW - Male KW - Female KW - DNA, Satellite -- genetics KW - Heterochromatin -- chemistry KW - Arvicolinae -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75554947?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cytogenetics+and+cell+genetics&rft.atitle=Comparative+analyses+of+heterochromatin+in+Microtus%3A+sequence+heterogeneity+and+localized+expansion+and+contraction+of+satellite+DNA+arrays.&rft.au=Modi%2C+W+S&rft.aulast=Modi&rft.aufirst=W&rft.date=1993-01-01&rft.volume=62&rft.issue=2-3&rft.spage=142&rft.isbn=&rft.btitle=&rft.title=Cytogenetics+and+cell+genetics&rft.issn=03010171&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-08 N1 - Date created - 1993-03-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Cocaine tolerance and cross-tolerance. AN - 75554244; 8093724 AB - Pharmacological mechanisms by which tolerance develops to the behavioral effects of cocaine were assessed by examining cross-tolerance to specific drugs. Daily experimental sessions were conducted in which rats were trained to press a key under a fixed-ratio 30-response schedule of food reinforcement (each 30th response produced food). Each of the drugs studied decreased rates of responding before initiating daily (10 mg/kg, i.p.) treatment with cocaine. Treatment with cocaine produced a small, significant shift to the right in the cocaine dose-effect curve; the ED50 values changed from 13.3 to 21.7 mg/kg. Cross-tolerance was not conferred to the indirect agonist, d-amphetamine, the direct agonist apomorphine, the D1-selective agonists SKF 38393 or fenoldopam, or the D2-selective agonists quinpirole or (-)-NPA. Cross-tolerance was conferred to the close structural analog of cocaine, WIN 35,428, but not to another dopamine uptake inhibitor, GBR 12909. Tolerant rats showed no change in specific binding of [3H]SCH 23390 to D1 receptors, [3H]spiperone to D2 receptors, [3H]GBR 12935 to dopamine uptake sites in striatum, [3H]paroxetine to serotonin uptake sites or [3H]mazindol to norepinephrine uptake sites in cortex or hippocampus. In addition, there were no changes in transmitter levels indicative of neurotoxicity. Serum levels of cocaine were not appreciably different in groups of cocaine- and saline-treated rats. The present results suggest that the modest tolerance that can develop to the behavioral effects of cocaine does not confer significant functional or metabolic changes in the effects of drugs acting on dopaminergic systems. Importantly, the tolerance produced by repeated administration of cocaine does not produce a cross-tolerance to GBR 12909, suggesting differences in mechanism among different structural forms of dopamine uptake inhibitors. JF - The Journal of pharmacology and experimental therapeutics AU - Katz, J L AU - Griffiths, J W AU - Sharpe, L G AU - De Souza, E B AU - Witkin, J M AD - Psychobiology Laboratory, National Institute on Drug Abuse Addiction Research Center, Baltimore, Maryland. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 183 EP - 192 VL - 264 IS - 1 SN - 0022-3565, 0022-3565 KW - Benzazepines KW - 0 KW - Dopamine Agents KW - Neurotransmitter Uptake Inhibitors KW - Receptors, Dopamine D1 KW - Tritium KW - 10028-17-8 KW - Spiperone KW - 4X6E73CJ0Q KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Animals KW - Corpus Striatum -- metabolism KW - Dopamine Agents -- pharmacology KW - Spiperone -- metabolism KW - Benzazepines -- metabolism KW - Receptors, Dopamine D1 -- metabolism KW - Binding Sites KW - Rats KW - Drug Tolerance KW - Rats, Sprague-Dawley KW - Corpus Striatum -- ultrastructure KW - Neurotransmitter Uptake Inhibitors -- pharmacology KW - Male KW - Behavior, Animal -- drug effects KW - Cocaine -- pharmacology KW - Cocaine -- metabolism KW - Cocaine -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75554244?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.atitle=Cocaine+tolerance+and+cross-tolerance.&rft.au=Katz%2C+J+L%3BGriffiths%2C+J+W%3BSharpe%2C+L+G%3BDe+Souza%2C+E+B%3BWitkin%2C+J+M&rft.aulast=Katz&rft.aufirst=J&rft.date=1993-01-01&rft.volume=264&rft.issue=1&rft.spage=183&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.issn=00223565&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-23 N1 - Date created - 1993-02-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Activated murine neutrophils induce unscheduled DNA synthesis in B lymphocytes. AN - 75550521; 7678145 AB - Activated neutrophils induce DNA damage in neighboring cells by secreting reactive oxygen compounds into the extracellular milieu. Repair of this damage is required to prevent mutagenesis and neoplastic transformation. Conditions were established to detect the activation of excision-repair pathways (unscheduled DNA synthesis) by measuring stimulated thymidine uptake in target B lymphocytes exposed to activated neutrophils. Murine neutrophils were cocultured in serum-free medium with splenic B cells or with murine plasmacytoma cells for 2 h. Unscheduled DNA synthesis in the B cells was detected at neutrophil:target cell ratios of 1:1 to 4:1 when the neutrophils were activated with phorbol myristate acetate. Reagent H2O2 alone (> or = 6 microM) also induced UDS whereas HOCl (up to 4 mM) did not. No repair synthesis was observed within the neutrophils themselves. Control experiments indicated that the induction of UDS by neutrophils and H2O2 was not due to formation of a stable genotoxic compound from HU. On the contrary, scavenging of free H2O2 by HU probably lowered the levels of UDS that could be detected by these agents. Induction of unscheduled DNA synthesis by neutrophils and H2O2 occurred under conditions of less cytostasis than was found with other DNA-damaging agents such as 4-nitroquinoline 1-oxide or gamma-irradiation. This may reflect a heightened responsiveness of the cells to repair of damage from physiological oxidants. The results demonstrate that DNA damage induced by reactive oxygen intermediates can be repaired by nucleotide excision-repair pathways. JF - Mutation research AU - Janz, S AU - Shacter, E AD - Laboratory of Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 173 EP - 186 VL - 293 IS - 2 SN - 0027-5107, 0027-5107 KW - Oxidants KW - 0 KW - Reactive Oxygen Species KW - Terpenes KW - pristane KW - 26HZV48DT1 KW - Hydrogen Peroxide KW - BBX060AN9V KW - Index Medicus KW - Hydrogen Peroxide -- toxicity KW - Mice, Inbred Strains KW - Animals KW - Cells, Cultured KW - In Vitro Techniques KW - Oxidants -- toxicity KW - Mice KW - Terpenes -- pharmacology KW - Cell Separation -- methods KW - DNA Repair KW - Neutrophils -- physiology KW - Reactive Oxygen Species -- toxicity KW - B-Lymphocytes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75550521?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutation+research&rft.atitle=Activated+murine+neutrophils+induce+unscheduled+DNA+synthesis+in+B+lymphocytes.&rft.au=Janz%2C+S%3BShacter%2C+E&rft.aulast=Janz&rft.aufirst=S&rft.date=1993-01-01&rft.volume=293&rft.issue=2&rft.spage=173&rft.isbn=&rft.btitle=&rft.title=Mutation+research&rft.issn=00275107&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-01 N1 - Date created - 1993-02-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Mutagenic activation of IQ, PhIP and MeIQx by hepatic microsomes from rat, monkey and man: low mutagenic activation of MeIQx in cynomolgus monkeys in vitro reflects low DNA adduct levels in vivo. AN - 75550075; 8425272 AB - Cooked meat, poultry and fish contain a number of mutagenic and carcinogenic heterocyclic amines, including 2-amino-3-methylimidazo[4,5-f]quinoline (IQ), 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP). In the present study we examined the capacity of hepatic microsomes from Fischer 344 rats, cynomolgus monkeys and humans to metabolically activate IQ, MeIQx and PhIP in vitro using the Ames Salmonella mutagenicity assay. The mutagenic activation of IQ was similar among the three species; however, there were significant differences among the species in the activation of PhIP and MeIQx. Liver microsomes from humans showed the greatest capacity to activate PhIP and MeIQx, followed by rats, and then monkeys. The largest differences between the species were observed when MeIQx was used as the mutagen. MeIQx-DNA adducts formed in vivo were then compared among rats and monkeys given MeIQx by gavage (20 mg/kg/day, 10 doses). 32P-Postlabeling analysis, carried out under intensification conditions, was used to examine MeIQx-DNA adducts in the liver, kidney, heart, colon and white blood cells. MeIQx-DNA adducts were highest in all tissues examined from male rats, followed by female rats, and much lower in monkeys. In the liver, the total MeIQx-DNA adduct levels of monkeys were approximately 19 and approximately 10 times lower than in male and female rats respectively. In extrahepatic tissues, the differences in MeIQx-DNA adduct levels between monkeys and rats were even greater. The results suggest that the low level of MeIQx-DNA adducts found in vivo in cynomolgus monkeys reflects a low capacity to activate MeIQx via the hepatic cytochrome P450 monooxygenase system. JF - Carcinogenesis AU - Davis, C D AU - Schut, H A AU - Adamson, R H AU - Thorgeirsson, U P AU - Thorgeirsson, S S AU - Snyderwine, E G AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 61 EP - 65 VL - 14 IS - 1 SN - 0143-3334, 0143-3334 KW - Imidazoles KW - 0 KW - Mutagens KW - Quinolines KW - Quinoxalines KW - 2-amino-3-methylimidazo(4,5-f)quinoline KW - 30GL3D3T0G KW - 2-amino-3,8-dimethylimidazo(4,5-f)quinoxaline KW - 77500-04-0 KW - 2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine KW - 909C6UN66T KW - Index Medicus KW - Rats KW - Animals KW - Macaca fascicularis KW - Biotransformation KW - Humans KW - Tissue Distribution KW - Species Specificity KW - Salmonella typhimurium -- genetics KW - Male KW - Female KW - Quinolines -- toxicity KW - Imidazoles -- pharmacokinetics KW - Imidazoles -- toxicity KW - DNA Damage KW - Microsomes, Liver -- metabolism KW - Quinoxalines -- toxicity KW - Quinoxalines -- pharmacokinetics KW - Mutagens -- toxicity KW - Mutagens -- pharmacokinetics KW - Quinolines -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75550075?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Mutagenic+activation+of+IQ%2C+PhIP+and+MeIQx+by+hepatic+microsomes+from+rat%2C+monkey+and+man%3A+low+mutagenic+activation+of+MeIQx+in+cynomolgus+monkeys+in+vitro+reflects+low+DNA+adduct+levels+in+vivo.&rft.au=Davis%2C+C+D%3BSchut%2C+H+A%3BAdamson%2C+R+H%3BThorgeirsson%2C+U+P%3BThorgeirsson%2C+S+S%3BSnyderwine%2C+E+G&rft.aulast=Davis&rft.aufirst=C&rft.date=1993-01-01&rft.volume=14&rft.issue=1&rft.spage=61&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-04 N1 - Date created - 1993-03-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Effects of 3'-azido-3'-deoxythymidine metabolites on simian virus 40 origin-dependent replication and heteroduplex repair in HeLa cell extracts. AN - 75549676; 8380884 AB - Although the capacity of 3'-azido-3'-deoxythymidine (AZT) triphosphate, an active metabolite of the antiviral agent zidovudine (AZT), to inhibit polymerization by a variety of purified DNA polymerases has been described, it is important to understand its effect on replication by the more complex protein assemblies responsible for DNA replication in human cells. In the present study, we have determined the effects of AZT metabolites on the efficiency of simian virus 40 origin-dependent bidirectional replication of double-stranded DNA in extracts of human HeLa cells. Replication was inhibited by AZT diphosphate and AZT triphosphate, but only at concentrations exceeding those thought to be present in vivo. However, replication was inhibited by AZT monophosphate at concentrations previously reported to accumulate in human cells cultured in the presence of AZT, suggesting that AZT monophosphate may contribute to cytotoxicity by inhibiting chromosomal replication. In an attempt to determine whether AZT treatment could have longer term mutagenic effects on cells, we also determined the effects of these AZT derivatives on replication fidelity and on the efficiency of repair of DNA substrates containing single-base mismatches. Despite the ability of a normal deoxynucleoside monophosphate to reduce the fidelity of DNA replication, presumably by reducing exonucleolytic proofreading of errors, neither the mono-, di-, nor triphosphate form of AZT reduced base substitution fidelity when present in replication reactions. Similarly, the efficiency of repair of DNA substrates containing single-base mismatches was unaffected by these compounds. However, replication fidelity was affected by perturbations in relative and absolute concentrations of deoxynucleoside triphosphate substrates similar to those reported to occur in AZT-treated cells. Thus, AZT treatment could potentially be mutagenic in vivo via reduced replication fidelity resulting from alterations in deoxynucleoside triphosphate pools. JF - Molecular pharmacology AU - Bebenek, K AU - Thomas, D C AU - Roberts, J D AU - Eckstein, F AU - Kunkel, T A AD - Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 57 EP - 63 VL - 43 IS - 1 SN - 0026-895X, 0026-895X KW - Antiviral Agents KW - 0 KW - Dideoxynucleotides KW - Thymine Nucleotides KW - 3'-azido-3'-deoxythymidine 5'-diphosphate KW - 106060-89-3 KW - 3'-azido-3'-deoxythymidine 5'phosphate KW - 29706-85-2 KW - Zidovudine KW - 4B9XT59T7S KW - 3'-azido-3'-deoxythymidine 5'-triphosphate KW - 6RGF96R053 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - AIDS/HIV KW - HeLa Cells KW - Humans KW - Simian virus 40 -- drug effects KW - DNA -- biosynthesis KW - Simian virus 40 -- physiology KW - Zidovudine -- analogs & derivatives KW - Virus Replication -- drug effects KW - Antiviral Agents -- pharmacology KW - Zidovudine -- pharmacology KW - Thymine Nucleotides -- pharmacology KW - DNA Repair -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75549676?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+pharmacology&rft.atitle=Effects+of+3%27-azido-3%27-deoxythymidine+metabolites+on+simian+virus+40+origin-dependent+replication+and+heteroduplex+repair+in+HeLa+cell+extracts.&rft.au=Bebenek%2C+K%3BThomas%2C+D+C%3BRoberts%2C+J+D%3BEckstein%2C+F%3BKunkel%2C+T+A&rft.aulast=Bebenek&rft.aufirst=K&rft.date=1993-01-01&rft.volume=43&rft.issue=1&rft.spage=57&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmacology&rft.issn=0026895X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-23 N1 - Date created - 1993-02-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Risk factors for motor response complications in L-dopa-treated parkinsonian patients. AN - 75549141; 8420213 JF - Advances in neurology AU - Peppe, A AU - Dambrosia, J M AU - Chase, T N AD - Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 698 EP - 702 VL - 60 SN - 0091-3952, 0091-3952 KW - Antiparkinson Agents KW - 0 KW - Drug Combinations KW - carbidopa, levodopa drug combination KW - Levodopa KW - 46627O600J KW - Carbidopa KW - MNX7R8C5VO KW - Index Medicus KW - Age Factors KW - Risk Factors KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Long-Term Care KW - Follow-Up Studies KW - Dyskinesia, Drug-Induced -- etiology KW - Male KW - Female KW - Antiparkinson Agents -- adverse effects KW - Neurologic Examination -- drug effects KW - Carbidopa -- adverse effects KW - Levodopa -- therapeutic use KW - Antiparkinson Agents -- therapeutic use KW - Motor Activity -- drug effects KW - Carbidopa -- therapeutic use KW - Levodopa -- adverse effects KW - Parkinson Disease -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75549141?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advances+in+neurology&rft.atitle=Risk+factors+for+motor+response+complications+in+L-dopa-treated+parkinsonian+patients.&rft.au=Peppe%2C+A%3BDambrosia%2C+J+M%3BChase%2C+T+N&rft.aulast=Peppe&rft.aufirst=A&rft.date=1993-01-01&rft.volume=60&rft.issue=&rft.spage=698&rft.isbn=&rft.btitle=&rft.title=Advances+in+neurology&rft.issn=00913952&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-11 N1 - Date created - 1993-02-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Striatal dopaminoceptive system changes and motor response complications in L-dopa-treated patients with advanced Parkinson's disease. AN - 75548617; 8420133 JF - Advances in neurology AU - Chase, T N AU - Engber, T M AU - Mouradian, M M AD - Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 181 EP - 185 VL - 60 SN - 0091-3952, 0091-3952 KW - Receptors, Dopamine KW - 0 KW - Levodopa KW - 46627O600J KW - Index Medicus KW - Parkinson Disease, Secondary -- physiopathology KW - Parkinson Disease, Secondary -- chemically induced KW - Animals KW - Drug Administration Schedule KW - Chorea -- chemically induced KW - Dose-Response Relationship, Drug KW - Humans KW - Chorea -- physiopathology KW - Receptors, Dopamine -- drug effects KW - Receptors, Dopamine -- physiology KW - Motor Skills -- physiology KW - Corpus Striatum -- physiopathology KW - Motor Skills -- drug effects KW - Neurologic Examination -- drug effects KW - Levodopa -- therapeutic use KW - Corpus Striatum -- drug effects KW - Levodopa -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75548617?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advances+in+neurology&rft.atitle=Striatal+dopaminoceptive+system+changes+and+motor+response+complications+in+L-dopa-treated+patients+with+advanced+Parkinson%27s+disease.&rft.au=Chase%2C+T+N%3BEngber%2C+T+M%3BMouradian%2C+M+M&rft.aulast=Chase&rft.aufirst=T&rft.date=1993-01-01&rft.volume=60&rft.issue=&rft.spage=181&rft.isbn=&rft.btitle=&rft.title=Advances+in+neurology&rft.issn=00913952&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-11 N1 - Date created - 1993-02-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Analysis of activated protooncogenes in B6C3F1 mouse liver tumors induced by ciprofibrate, a potent peroxisome proliferator. AN - 75548315; 8425263 AB - Liver tumors from B6C3F1 mice induced by the potent peroxisome proliferator ciprofibrate, a hypolipidemic drug, were evaluated for the presence of transforming genes by the nude mouse tumorigenicity assay. As reported earlier, the tumors were not activated by a point mutation in codon 61 of H-ras. Two of the eight tumors examined contained a mutation in codon 13 or an H-ras gene mutated in codon 117. Screening of another 23 ciprofibrate-induced liver tumors by oligonucleotide hybridization analysis and direct DNA sequencing resulted in the identification of three tumor DNA samples with point mutations in codon 117 of the H-ras gene. In addition, another tumor sample contained a K-ras gene with a mutation in codon 61. Mutations in these codons have been seen only rarely in chemically induced liver tumors from this mouse strain. Of 15 spontaneous B6C3F1 liver tumors screened in the same manner, one exhibited a K-ras gene activated by a mutation in codon 13 and a second contained an H-ras gene activated by a mutation in codon 117. These ras gene mutations have not been reported previously from spontaneous liver tumors. The frequency and spectrum of ras oncogene mutations characterized in ciprofibrate-induced liver tumors differ significantly from the frequency and pattern identified in spontaneously occurring liver tumors. The results of this study with a limited number of samples suggest that ras protooncogene activation or activation of other protooncogenes that can be detected by the nude mouse tumorigenicity assay are not frequent events in the mechanism of carcinogenicity of the peroxisome proliferator ciprofibrate. However, the lower frequency and distinct pattern of H-ras mutations observed in these tumors disprove the assumption of promotion of spontaneous hepatocarcinogenesis by ciprofibrate. JF - Carcinogenesis AU - Hegi, M E AU - Fox, T R AU - Belinsky, S A AU - Devereux, T R AU - Anderson, M W AD - Laboratory of Molecular Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 145 EP - 149 VL - 14 IS - 1 SN - 0143-3334, 0143-3334 KW - H-ras KW - K-ras KW - N-ras KW - Carcinogens KW - 0 KW - Codon KW - DNA, Neoplasm KW - Fibric Acids KW - Clofibric Acid KW - 53PF01Q249 KW - ciprofibrate KW - F8252JGO9S KW - Index Medicus KW - Gene Expression -- drug effects KW - 3T3 Cells KW - Animals KW - Mice KW - Mice, Nude KW - Base Sequence KW - Transfection KW - Point Mutation KW - Molecular Sequence Data KW - Mice, Inbred C3H KW - Mice, Inbred C57BL KW - Male KW - Liver Neoplasms, Experimental -- genetics KW - Clofibric Acid -- toxicity KW - Genes, ras -- drug effects KW - Carcinogens -- toxicity KW - Liver Neoplasms, Experimental -- chemically induced KW - Clofibric Acid -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75548315?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Analysis+of+activated+protooncogenes+in+B6C3F1+mouse+liver+tumors+induced+by+ciprofibrate%2C+a+potent+peroxisome+proliferator.&rft.au=Hegi%2C+M+E%3BFox%2C+T+R%3BBelinsky%2C+S+A%3BDevereux%2C+T+R%3BAnderson%2C+M+W&rft.aulast=Hegi&rft.aufirst=M&rft.date=1993-01-01&rft.volume=14&rft.issue=1&rft.spage=145&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-04 N1 - Date created - 1993-03-04 N1 - Date revised - 2017-01-13 N1 - Gene symbol - H-ras; K-ras; N-ras N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Milacemide therapy for Parkinson's disease. AN - 75547739; 8380487 AB - The clinical effects of central glutamatergic stimulation by the glycine prodrug milacemide were studied in six patients with Parkinson's disease under double-blind, placebo-controlled conditions. When administered as monotherapy at a single oral dose of 1,200 mg, the drug increased overall parkinsonian severity transiently, mostly due to an effect on rigidity. Milacemide did not, however, alter levodopa-induced dyskinesias. These results support the view that drugs acting on the glutamatergic system can influence motor function in patients with extrapyramidal movement disorders and that pharmaceutical agents that selectively block certain subtypes of glutamate receptors may ameliorate parkinsonian symptoms. JF - Movement disorders : official journal of the Movement Disorder Society AU - Giuffra, M E AU - Sethy, V H AU - Davis, T L AU - Mouradian, M M AU - Chase, T N AD - Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 47 EP - 50 VL - 8 IS - 1 SN - 0885-3185, 0885-3185 KW - Acetamides KW - 0 KW - Monoamine Oxidase Inhibitors KW - Receptors, N-Methyl-D-Aspartate KW - milacemide KW - 0HXT24RECU KW - Levodopa KW - 46627O600J KW - Carbidopa KW - MNX7R8C5VO KW - Index Medicus KW - Double-Blind Method KW - Infusions, Intravenous KW - Dose-Response Relationship, Drug KW - Synaptic Transmission -- drug effects KW - Humans KW - Neurologic Examination KW - Carbidopa -- adverse effects KW - Aged KW - Drug Therapy, Combination KW - Single-Blind Method KW - Receptors, N-Methyl-D-Aspartate -- drug effects KW - Levodopa -- therapeutic use KW - Middle Aged KW - Carbidopa -- therapeutic use KW - Muscle Rigidity -- drug therapy KW - Levodopa -- adverse effects KW - Muscle Rigidity -- chemically induced KW - Female KW - Male KW - Monoamine Oxidase Inhibitors -- adverse effects KW - Acetamides -- therapeutic use KW - Parkinson Disease -- drug therapy KW - Monoamine Oxidase Inhibitors -- therapeutic use KW - Acetamides -- adverse effects KW - Parkinson Disease -- diagnosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75547739?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Movement+disorders+%3A+official+journal+of+the+Movement+Disorder+Society&rft.atitle=Milacemide+therapy+for+Parkinson%27s+disease.&rft.au=Giuffra%2C+M+E%3BSethy%2C+V+H%3BDavis%2C+T+L%3BMouradian%2C+M+M%3BChase%2C+T+N&rft.aulast=Giuffra&rft.aufirst=M&rft.date=1993-01-01&rft.volume=8&rft.issue=1&rft.spage=47&rft.isbn=&rft.btitle=&rft.title=Movement+disorders+%3A+official+journal+of+the+Movement+Disorder+Society&rft.issn=08853185&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-11 N1 - Date created - 1993-02-11 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Mov Disord. 1994 Sep;9(5):585-6 [7990857] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Coordinate changes in gene expression which mark the spinous to granular cell transition in epidermis are regulated by protein kinase C. AN - 75547329; 7678013 AB - The protective function of skin depends on successful completion of a tightly regulated multi-step differentiation program, during which the induction of markers for a specific stage in epidermal differentiation is coupled to repression of markers expressed at the preceding stage. We have explored the role of protein kinase C (PKC) in this process using an in vitro model system, in which cultures of primary mouse epidermal keratinocytes are induced to terminally differentiate by raising the Ca2+ concentration in the medium from 0.05 to 0.12 mM. At doses which activate PKC, 12-O-tetradecanoylphorbol-13-acetate (TPA) and 1-oleoyl-2-acetylglycerol block Ca(2+)-mediated induction of the spinous cell markers keratins K1 and K10 at both the protein and mRNA level. TPA and 1-oleoyl-2-acetylglycerol also rapidly repress K1 and K10 mRNA expression when added to differentiating keratinocyte cultures already expressing these markers. The inhibition of K1 mRNA expression by TPA is blocked in cells where PKC has been inactivated with bryostatin. TPA-mediated loss of K1 mRNA is also blocked in cells exposed to cycloheximide or actinomycin D implicating a PKC-induced protein factor in this process. The loss of K1 mRNA in TPA-treated cultures is the result of both a selective destabilization of K1 transcripts and a rapid inhibition of K1 gene transcription. In contrast to the dramatic repression of mRNAs typical for spinous cell differentiation, activation of PKC concurrently enhances expression of mRNAs and proteins for the granular cell markers loricrin and filaggrin. This response does not occur in cells pre-treated with bryostatin to inactivate PKC. Our results suggest that PKC is a fundamental regulator of the coordinate changes in keratinocyte gene expression that occur during the spinous to granular cell transition in epidermis. JF - The Journal of cell biology AU - Dlugosz, A A AU - Yuspa, S H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 217 EP - 225 VL - 120 IS - 1 SN - 0021-9525, 0021-9525 KW - Intermediate Filament Proteins KW - 0 KW - Membrane Proteins KW - RNA, Messenger KW - filaggrin KW - loricrin KW - Dactinomycin KW - 1CC1JFE158 KW - Keratins KW - 68238-35-7 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Gene Expression -- drug effects KW - Intermediate Filament Proteins -- genetics KW - Dactinomycin -- pharmacology KW - Animals KW - In Vitro Techniques KW - Enzyme Activation -- drug effects KW - Calcium -- physiology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Mice KW - Membrane Proteins -- genetics KW - RNA, Messenger -- genetics KW - Mice, Inbred BALB C KW - Cell Differentiation -- drug effects KW - Keratins -- genetics KW - Keratinocytes -- physiology KW - Epidermis -- physiology KW - Epidermis -- cytology KW - Protein Kinase C -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75547329?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+cell+biology&rft.atitle=Coordinate+changes+in+gene+expression+which+mark+the+spinous+to+granular+cell+transition+in+epidermis+are+regulated+by+protein+kinase+C.&rft.au=Dlugosz%2C+A+A%3BYuspa%2C+S+H&rft.aulast=Dlugosz&rft.aufirst=A&rft.date=1993-01-01&rft.volume=120&rft.issue=1&rft.spage=217&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+cell+biology&rft.issn=00219525&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-27 N1 - Date created - 1993-01-27 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Res. 1987 Sep 1;47(17):4674-80 [2441853] J Cell Biol. 1988 Aug;107(2):427-46 [2458356] Cell. 1987 Oct 23;51(2):251-60 [2822255] Cancer Res. 1988 Jan 1;48(1):74-81 [2891434] J Invest Dermatol. 1988 Jan;90(1):37-43 [2447194] Mol Cell Biol. 1989 Feb;9(2):769-75 [2523515] J Biol Chem. 1989 May 25;264(15):8992-9 [2498322] J Invest Dermatol. 1989 Jul;93(1):108-15 [2473132] J Cell Biol. 1989 Sep;109(3):1207-17 [2475508] J Cell Physiol. 1989 Nov;141(2):235-42 [2808535] Genes Dev. 1989 Oct;3(10):1507-17 [2482225] Cell. 1990 Jun 15;61(6):1103-12 [2190691] Mol Cell Biol. 1990 Aug;10(8):4243-55 [2115122] Cell. 1990 Aug 10;62(3):527-38 [2165866] Genes Dev. 1990 May;4(5):835-48 [1696235] Biol Reprod. 1990 Jul;43(1):73-9 [2168218] Mol Cell Biol. 1990 Nov;10(11):5983-90 [2233728] Arch Dermatol. 1991 Jan;127(1):57-63 [1986708] J Cell Biol. 1990 Dec;111(6 Pt 2):2807-14 [2269655] Genes Dev. 1990 Nov;4(11):1985-98 [1703506] Mol Pharmacol. 1991 Feb;39(2):124-9 [1847491] New Biol. 1989 Nov;1(2):121-6 [2518709] EMBO J. 1991 Sep;10(9):2497-505 [1868832] J Invest Dermatol. 1985 Jun;84(6):508-12 [3998499] Nature. 1984 Oct 4-10;311(5985):433-8 [6090941] Cancer Res. 1991 Sep 1;51(17):4677-84 [1678684] Nucleic Acids Res. 1985 Mar 11;13(5):1431-42 [2987824] Cancer Res. 1985 Nov;45(11 Pt 1):5540-6 [3863706] Cancer Res. 1985 Nov;45(11 Pt 2):5845-50 [2414001] J Cell Biol. 1986 Nov;103(5):1945-55 [2430980] J Cell Biol. 1986 Dec;103(6 Pt 1):2067-72 [3023396] EMBO J. 1986 Nov;5(11):2853-7 [2431900] Cell. 1987 Jun 19;49(6):835-44 [3555845] Differentiation. 1987;35(2):143-50 [2450799] Carcinogenesis. 1988 Apr;9(4):555-62 [2451575] J Biol Chem. 1991 Aug 25;266(24):15771-81 [1874734] Mol Cell Biol. 1991 Sep;11(9):4473-82 [1875933] Carcinogenesis. 1991 Sep;12(9):1651-8 [1893524] Development. 1991 Feb;111(2):253-8 [1909952] Proc Natl Acad Sci U S A. 1991 Sep 15;88(18):7948-52 [1716766] Proc Natl Acad Sci U S A. 1991 Sep 15;88(18):7988-92 [1832772] J Biol Chem. 1991 Sep 25;266(27):17809-14 [1917923] J Cell Biol. 1991 Nov;115(3):745-54 [1717491] Am J Physiol. 1991 Nov;261(5 Pt 1):C767-73 [1951667] Biochim Biophys Acta. 1991 Dec 10;1072(2-3):129-57 [1751545] Development. 1991 Sep;113(1):283-93 [1722450] Pharmacol Ther. 1991;51(1):71-95 [1771178] Cell. 1992 Mar 20;68(6):1021-9 [1547501] Mol Cell Biol. 1992 Jun;12(6):2793-803 [1588971] Mol Carcinog. 1992;5(4):286-92 [1379814] J Cell Biol. 1989 Nov;109(5):2295-312 [2478566] Biochemistry. 1979 Nov 27;18(24):5294-9 [518835] Cell. 1980 Jan;19(1):245-54 [6153576] Biochem Biophys Res Commun. 1980 Nov 28;97(2):700-8 [6110426] Cancer Res. 1982 Jun;42(6):2344-9 [6122503] Proc Natl Acad Sci U S A. 1983 Feb;80(3):716-20 [6187003] Nature. 1983 Jun 2-8;303(5916):401-6 [6304522] J Biol Chem. 1983 Sep 25;258(18):11063-73 [6193119] Carcinogenesis. 1984 Jun;5(6):735-40 [6327111] Carcinogenesis. 1984 Aug;5(8):1071-7 [6204790] Biochem Biophys Res Commun. 1984 Aug 16;122(3):1234-40 [6206852] Cancer Res. 1988 Jun 1;48(11):3245-52 [2452688] Carcinogenesis. 1988 Jun;9(6):1033-8 [2453303] Cancer Res. 1987 Oct 15;47(20):5445-50 [2888531] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Soluble CD4 enhances the efficacy of immunotoxins directed against gp41 of the human immunodeficiency virus. AN - 75546476; 8419938 AB - Monoclonal antibodies specific for the gp120 or gp41 portions of the human immunodeficiency virus (HIV) envelope protein gp160 were conjugated to ricin A chain, and their immunotoxic activities against HIV-infected cells were evaluated in the presence or absence of soluble CD4 (sCD4). Immunotoxin activity was measured in vitro as cytotoxicity and inhibition of secretion of infectious HIV. The efficacy of anti-gp41 immunotoxins was enhanced at least 30-fold in the presence of sCD4. This effect was specific for HIV-infected cells, but not for uninfected cells, and was seen at concentrations of sCD4 as low as 0.1 micrograms/ml. Anti-gp120 immunotoxins were marginally inhibited at higher concentrations of sCD4. Flow cytometry analyses showed that sCD4 increased the expression of gp41 on the surface of infected cells and increased internalization of gp120 and gp41. These data suggest that sCD4 alters the cellular trafficking of HIV envelope proteins. These findings also have important implications for the therapeutic use of anti-HIV immunotoxins and may be generalizable to other immunotoxins as well. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Pincus, S H AU - McClure, J AD - Laboratory of Microbial Structure and Function, National Institute of Allergy and Infectious Diseases, Rocky Mountain Laboratories, Hamilton, MT 59840. Y1 - 1993/01/01/ PY - 1993 DA - 1993 Jan 01 SP - 332 EP - 336 VL - 90 IS - 1 SN - 0027-8424, 0027-8424 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, CD4 KW - HIV Envelope Protein gp120 KW - HIV Envelope Protein gp41 KW - Immunotoxins KW - Ricin KW - 9009-86-3 KW - Index Medicus KW - AIDS/HIV KW - Antibody Specificity KW - Animals KW - Tumor Cells, Cultured KW - Dose-Response Relationship, Drug KW - Kinetics KW - Humans KW - Mice KW - Flow Cytometry KW - Cell Line KW - HIV -- drug effects KW - HIV Envelope Protein gp120 -- immunology KW - HIV -- immunology KW - Antigens, CD4 -- pharmacology KW - HIV Envelope Protein gp41 -- immunology KW - Immunotoxins -- pharmacology KW - Ricin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75546476?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Soluble+CD4+enhances+the+efficacy+of+immunotoxins+directed+against+gp41+of+the+human+immunodeficiency+virus.&rft.au=Pincus%2C+S+H%3BMcClure%2C+J&rft.aulast=Pincus&rft.aufirst=S&rft.date=1993-01-01&rft.volume=90&rft.issue=1&rft.spage=332&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-08 N1 - Date created - 1993-02-08 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Mol Immunol. 1982 Dec;19(12):1551-9 [6219282] J Clin Invest. 1986 Mar;77(3):977-84 [3081579] J Virol. 1986 Aug;59(2):284-91 [3016298] J Clin Invest. 1986 Sep;78(3):666-73 [3489008] Cell. 1986 Nov 7;47(3):333-48 [3094962] Science. 1987 Nov 20;238(4830):1098-104 [3317828] Proc Natl Acad Sci U S A. 1988 Apr;85(7):2357-61 [2451247] Nature. 1988 Sep 22;335(6188):369-72 [2843774] Science. 1988 Nov 25;242(4882):1166-8 [2847316] Nature. 1989 Feb 9;337(6207):525-31 [2536900] Proc Natl Acad Sci U S A. 1989 Mar;86(6):1987-91 [2538826] J Immunol. 1989 May 1;142(9):3070-5 [2540236] Proc Natl Acad Sci U S A. 1989 Dec;86(23):9539-43 [2480605] J Virol. 1990 Feb;64(2):936-40 [2296090] Nature. 1990 Apr 12;344(6267):667-70 [1970124] J Exp Med. 1990 Sep 1;172(3):745-57 [1696955] J Immunol. 1990 Oct 15;145(8):2527-32 [2120333] J Infect Dis. 1990 Dec;162(6):1233-8 [2230256] Science. 1990 Nov 23;250(4984):1139-42 [2251501] AIDS Res Hum Retroviruses. 1990 Oct;6(10):1209-12 [2252640] J Infect Dis. 1991 Jan;163(1):64-70 [1984477] J Immunol. 1991 Jun 15;146(12):4315-24 [1710247] Biotechniques. 1991 Mar;10(3):336-42 [2064772] J Exp Med. 1991 Aug 1;174(2):407-15 [1713252] Proc Natl Acad Sci U S A. 1991 Sep 15;88(18):8082-6 [1896455] J Virol. 1992 Jan;66(1):235-43 [1727487] Immunol Today. 1992 Jun;13(6):201-6 [1627247] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Patterns of pesticide use among farmers: implications for epidemiologic research. AN - 75539040; 8420582 AB - Epidemiologic studies of farmers have linked pesticides with certain cancers. Information on exposures from many of these studies was obtained by interview of farmers or their next-of-kin. The reliability and validity of data on pesticide use obtained by recall, often years after the event, have been questioned. Pesticide use, however, is an integral component in most agricultural operations, and the farmers' knowledge and recall of chemicals used may be better than for many other occupations. Contrary to general belief, many farmers typically use only a few pesticides during their lifetimes and make only a few applications per year. Data from U.S. Department of Agriculture surveys indicate that herbicides are applied to wheat, corn, soybeans, and cotton and that application of insecticides to corn averages two or fewer times per year. In epidemiologic studies at the National Cancer Institute, the proportion of farmers ever reporting lifetime use of five or more different chemicals was 7% for insecticides and 20% for herbicides. Surrogate respondents have often been used in epidemiologic studies of cancer; they are able to recall pesticide use with less detail than the farmers themselves. The pesticides reported by surrogates were the same as reported by subjects themselves, but with less frequency. Comparison of reporting by cases and controls provided no evidence of case-response (differential) bias; thus, inaccurate recall of pesticide use by subjects or surrogates would tend to diminish risk estimates and dilute exposure-response gradients. JF - Epidemiology (Cambridge, Mass.) AU - Blair, A AU - Zahm, S H AD - Occupational Studies Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 55 EP - 62 VL - 4 IS - 1 SN - 1044-3983, 1044-3983 KW - Herbicides KW - 0 KW - Index Medicus KW - Cross-Sectional Studies KW - Risk Factors KW - Humans KW - Case-Control Studies KW - Incidence KW - Midwestern United States -- epidemiology KW - Herbicides -- adverse effects KW - Agricultural Workers' Diseases -- epidemiology KW - Neoplasms -- chemically induced KW - Agricultural Workers' Diseases -- chemically induced KW - Neoplasms -- epidemiology KW - Occupational Exposure -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75539040?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Epidemiology+%28Cambridge%2C+Mass.%29&rft.atitle=Patterns+of+pesticide+use+among+farmers%3A+implications+for+epidemiologic+research.&rft.au=Blair%2C+A%3BZahm%2C+S+H&rft.aulast=Blair&rft.aufirst=A&rft.date=1993-01-01&rft.volume=4&rft.issue=1&rft.spage=55&rft.isbn=&rft.btitle=&rft.title=Epidemiology+%28Cambridge%2C+Mass.%29&rft.issn=10443983&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-17 N1 - Date created - 1993-02-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Mutagenicity of glyceryl trinitrate (nitroglycerin) in Salmonella typhimurium. AN - 75538442; 7678153 AB - The recent finding that the clinical nitrovasodilator, glyceryl trinitrate (GTN), is mutagenic in Salmonella typhimurium strain TA1535 has been examined in closer detail, with emphasis on its mechanism of action. GTN increased the number of His+ revertants to a maximum of 4 times over background at a GTN dose of 5 mumol/plate. Hamster liver S9 depressed the toxicity of high GTN doses and increased the maximum number of revertants to 5 times over background at 10 mumol/plate. GTN did not cause significant reversion in any of the six other S. typhimurium strains tested (TA1975, TA102, TA1538, TA100, TA100NR, YG1026), although signs of toxicity were observed. Therefore, the mutagenicity of GTN was manifest only in the repair-deficient (uvrB and lacking in pKM101) strain which is responsive to single base changes. Oligonucleotide probe hybridization of TA1535 revertants showed that virtually all of the GTN-induced mutants contained C-->T transitions in either the first or second base of the hisG46 (CCC) target codon, with a preference for the latter. A similar mutational spectrum was seen previously with a complex of spermine and nitric oxide (NO) which releases nitric oxide. This suggests that NO, which can be derived from GTN via metabolic reduction, may be responsible for GTN's mutagenic action. The known NO scavenger oxymyoglobin did not substantially alter the dose response of GTN, indicating that extracellular NO was not mediating reversion. The data are consistent with the hypothesis that intracellular nitric oxide is responsible for the observed mutations. JF - Mutation research AU - Maragos, C M AU - Andrews, A W AU - Keefer, L K AU - Elespuru, R K AD - Chemistry Section, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 187 EP - 195 VL - 298 IS - 3 SN - 0027-5107, 0027-5107 KW - hisG KW - Codon KW - 0 KW - Mutagens KW - Histidine KW - 4QD397987E KW - Nitroglycerin KW - G59M7S0WS3 KW - Index Medicus KW - Mutagenicity Tests KW - DNA Repair KW - Biotransformation KW - Histidine -- genetics KW - Species Specificity KW - Mutagenesis -- drug effects KW - Salmonella typhimurium -- drug effects KW - Nitroglycerin -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75538442?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutation+research&rft.atitle=Mutagenicity+of+glyceryl+trinitrate+%28nitroglycerin%29+in+Salmonella+typhimurium.&rft.au=Maragos%2C+C+M%3BAndrews%2C+A+W%3BKeefer%2C+L+K%3BElespuru%2C+R+K&rft.aulast=Maragos&rft.aufirst=C&rft.date=1993-01-01&rft.volume=298&rft.issue=3&rft.spage=187&rft.isbn=&rft.btitle=&rft.title=Mutation+research&rft.issn=00275107&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-01 N1 - Date created - 1993-02-01 N1 - Date revised - 2017-01-13 N1 - Gene symbol - hisG N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Pivotal role of amino acid at position 138 in the allosteric hinge reorientation of cAMP receptor protein. AN - 75536304; 8380500 AB - The cAMP receptor protein (CRP) of Escherichia coli needs cAMP for an allosteric change to regulate gene expression by binding to specific DNA sites. The hinge region connecting the DNA-binding domain to the cAMP-binding domain has been proposed to participate in the cAMP-induced allosteric change necessary to adjust C and D alpha-helices for movement of the DNA-binding F alpha-helix away from the protein surface. The role of the hinge region for a conformation change in CRP was tested by studying the effects of single amino acid substitutions at residue 138 located within the hinge. Physiological studies of wild-type and mutant cells and biochemical analysis of purified wild-type and mutant CRP revealed at least three groups of altered CRPs: (i) CRP that behaves like wild type (CRP+); (ii) CRP that binds cAMP but does not complete the structural changes required for specific DNA binding, proteolytic cleavage, and transcription activation (CRPallo); and (iii) CRP that shows some or all of these conformational changes without cAMP (CRP*). These results show a pivotal role of position 138 from which change emanates and provide further evidence that a hinge reorientation involving residue 138 is involved in the interhelical adjustments. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Ryu, S AU - Kim, J AU - Adhya, S AU - Garges, S AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/01/01/ PY - 1993 DA - 1993 Jan 01 SP - 75 EP - 79 VL - 90 IS - 1 SN - 0027-8424, 0027-8424 KW - Carrier Proteins KW - 0 KW - Cyclic AMP Receptor Protein KW - DNA-Binding Proteins KW - Receptors, Cyclic AMP KW - Recombinant Proteins KW - Cyclic AMP KW - E0399OZS9N KW - beta-Galactosidase KW - EC 3.2.1.23 KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Genes, Bacterial KW - beta-Galactosidase -- metabolism KW - Recombinant Proteins -- metabolism KW - Kinetics KW - Cyclic AMP -- metabolism KW - beta-Galactosidase -- genetics KW - Transcription, Genetic KW - Amino Acid Sequence KW - Recombinant Proteins -- chemistry KW - Allosteric Site KW - Receptors, Cyclic AMP -- genetics KW - Receptors, Cyclic AMP -- chemistry KW - Protein Structure, Secondary KW - Escherichia coli -- metabolism KW - Carrier Proteins -- metabolism KW - DNA-Binding Proteins -- chemistry KW - Carrier Proteins -- chemistry KW - Carrier Proteins -- genetics KW - Escherichia coli -- genetics KW - Receptors, Cyclic AMP -- metabolism KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75536304?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Pivotal+role+of+amino+acid+at+position+138+in+the+allosteric+hinge+reorientation+of+cAMP+receptor+protein.&rft.au=Ryu%2C+S%3BKim%2C+J%3BAdhya%2C+S%3BGarges%2C+S&rft.aulast=Ryu&rft.aufirst=S&rft.date=1993-01-01&rft.volume=90&rft.issue=1&rft.spage=75&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-08 N1 - Date created - 1993-02-08 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Mol Biol. 1985 Mar 5;182(1):91-107 [2987511] Proc Natl Acad Sci U S A. 1992 Oct 15;89(20):9700-4 [1409686] EMBO J. 1985 Dec 1;4(12):3329-32 [3004951] J Biol Chem. 1986 Dec 15;261(35):16332-9 [3023348] J Mol Biol. 1987 Nov 20;198(2):311-26 [2828639] J Bacteriol. 1988 Apr;170(4):1417-22 [2832360] Biochemistry. 1974 Jun 4;13(12):2567-72 [4364836] Biochemistry. 1974 Jun 4;13(12):2573-8 [4364837] J Mol Biol. 1977 Jul;114(1):47-60 [198551] Biochemistry. 1978 Jun 27;17(13):2469-73 [209817] FEBS Lett. 1980 Jan 1;109(1):121-4 [6243574] Methods Enzymol. 1980;65(1):856-77 [6246379] Biochemistry. 1981 Aug 4;20(16):4774-80 [6271171] Mol Gen Genet. 1981;182(3):480-9 [6272064] Biochemistry. 1989 Aug 22;28(17):6914-24 [2554959] Nucleic Acids Res. 1989 Dec 25;17(24):10295-305 [2557589] Biochemistry. 1990 Apr 10;29(14):3557-62 [2162197] Biochemistry. 1991 May 21;30(20):5076-80 [1645189] Science. 1991 Aug 30;253(5023):1001-7 [1653449] J Bacteriol. 1992 Feb;174(3):655-8 [1310089] Microbiol Rev. 1992 Mar;56(1):100-22 [1315922] Science. 1984 May 25;224(4651):831-8 [6372090] J Biol Chem. 1982 Aug 25;257(16):9518-24 [6286624] Cell. 1985 Jul;41(3):745-51 [2988785] N1 - Last updated - 2017-01-18 ER - TY - CONF T1 - Summary of the 27th United States-Japan Joint Conference on Cholera and Related Diarrheal Diseases. AN - 75535930; 8093361 JF - The Journal of infectious diseases AU - Spriggs, D R AU - Guerrant, R L Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 1 EP - 6 VL - 167 IS - 1 KW - Bacterial Toxins KW - 0 KW - Enterotoxins KW - Escherichia coli Proteins KW - Shiga Toxin 1 KW - heat stable toxin (E coli) KW - Cholera Toxin KW - 9012-63-9 KW - Abridged Index Medicus KW - Index Medicus KW - Virulence KW - Animals KW - Vibrio cholerae -- pathogenicity KW - Humans KW - Escherichia coli -- pathogenicity KW - Cholera Toxin -- toxicity KW - Bacterial Toxins -- toxicity KW - Enterotoxins -- toxicity KW - Disease Outbreaks KW - South America -- epidemiology KW - Shigella -- pathogenicity KW - Cholera -- microbiology KW - Cholera -- epidemiology KW - Diarrhea -- therapy KW - Diarrhea -- microbiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75535930?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=The+Journal+of+infectious+diseases&rft.atitle=Summary+of+the+27th+United+States-Japan+Joint+Conference+on+Cholera+and+Related+Diarrheal+Diseases.&rft.au=Spriggs%2C+D+R%3BGuerrant%2C+R+L&rft.aulast=Spriggs&rft.aufirst=D&rft.date=1993-01-01&rft.volume=167&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+infectious+diseases&rft.issn=00221899&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-02 N1 - Date created - 1993-02-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Role of dopamine autoxidation, hydroxyl radical generation, and calcium overload in underlying mechanisms involved in MPTP-induced parkinsonism. AN - 75535495; 8380519 JF - Advances in neurology AU - Chiueh, C C AU - Miyake, H AU - Peng, M T AD - National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 251 EP - 258 VL - 60 SN - 0091-3952, 0091-3952 KW - Calcium Channels KW - 0 KW - Free Radicals KW - Hydroxides KW - Potassium Channels KW - Hydroxyl Radical KW - 3352-57-6 KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Iron KW - E1UOL152H7 KW - Monoamine Oxidase KW - EC 1.4.3.4 KW - Potassium KW - RWP5GA015D KW - Calcium KW - SY7Q814VUP KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Potassium -- physiology KW - Neural Pathways -- physiopathology KW - Animals KW - Cell Death -- physiology KW - Nerve Degeneration -- drug effects KW - Calcium Channels -- physiology KW - Iron -- physiology KW - Potassium Channels -- physiology KW - Potassium Channels -- drug effects KW - Cell Death -- drug effects KW - Nerve Degeneration -- physiology KW - Monoamine Oxidase -- physiology KW - Neural Pathways -- drug effects KW - Rats KW - Oxidation-Reduction KW - Corpus Striatum -- physiopathology KW - Calcium Channels -- drug effects KW - Corpus Striatum -- drug effects KW - Parkinson Disease, Secondary -- physiopathology KW - Brain -- physiopathology KW - Parkinson Disease, Secondary -- chemically induced KW - Substantia Nigra -- physiopathology KW - Brain -- drug effects KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- pharmacology KW - Calcium -- physiology KW - Substantia Nigra -- drug effects KW - Dopamine -- metabolism KW - Hydroxides -- metabolism KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75535495?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advances+in+neurology&rft.atitle=Role+of+dopamine+autoxidation%2C+hydroxyl+radical+generation%2C+and+calcium+overload+in+underlying+mechanisms+involved+in+MPTP-induced+parkinsonism.&rft.au=Chiueh%2C+C+C%3BMiyake%2C+H%3BPeng%2C+M+T&rft.aulast=Chiueh&rft.aufirst=C&rft.date=1993-01-01&rft.volume=60&rft.issue=&rft.spage=251&rft.isbn=&rft.btitle=&rft.title=Advances+in+neurology&rft.issn=00913952&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-11 N1 - Date created - 1993-02-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Myelin injury and repair. AN - 75535201; 8420125 JF - Advances in neurology AU - Webster, H D AD - Laboratory of Experimental Neuropathology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 67 EP - 73 VL - 59 SN - 0091-3952, 0091-3952 KW - Index Medicus KW - Animals KW - Humans KW - Demyelinating Diseases -- therapy KW - Nerve Regeneration -- physiology KW - Demyelinating Diseases -- pathology KW - Demyelinating Diseases -- chemically induced KW - Demyelinating Diseases -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75535201?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advances+in+neurology&rft.atitle=Myelin+injury+and+repair.&rft.au=Webster%2C+H+D&rft.aulast=Webster&rft.aufirst=H&rft.date=1993-01-01&rft.volume=59&rft.issue=&rft.spage=67&rft.isbn=&rft.btitle=&rft.title=Advances+in+neurology&rft.issn=00913952&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-05 N1 - Date created - 1993-02-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Tissue implants in treatment of parkinsonian syndromes in animals and implications for use of tissue implants in humans. AN - 75534602; 8420215 JF - Advances in neurology AU - Kopin, I J AU - Bankiewicz, K S AU - Plunkett, R J AU - Jacobowitz, D M AU - Oldfield, E H AD - National Institute of Neurological Disorders, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993 PY - 1993 DA - 1993 SP - 707 EP - 714 VL - 60 SN - 0091-3952, 0091-3952 KW - Receptors, Dopamine KW - 0 KW - Oxidopamine KW - 8HW4YBZ748 KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Receptors, Dopamine -- drug effects KW - Animals KW - Basal Ganglia -- surgery KW - Humans KW - Dopamine -- physiology KW - Neurologic Examination KW - Adrenal Medulla -- transplantation KW - Haplorhini KW - Rats KW - Receptors, Dopamine -- physiology KW - Fetal Tissue Transplantation -- physiology KW - Basal Ganglia -- physiopathology KW - Parkinson Disease, Secondary -- physiopathology KW - Parkinson Disease, Secondary -- chemically induced KW - Parkinson Disease, Secondary -- surgery KW - Parkinson Disease -- physiopathology KW - Brain Tissue Transplantation -- physiology KW - Parkinson Disease -- surgery UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75534602?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advances+in+neurology&rft.atitle=Tissue+implants+in+treatment+of+parkinsonian+syndromes+in+animals+and+implications+for+use+of+tissue+implants+in+humans.&rft.au=Kopin%2C+I+J%3BBankiewicz%2C+K+S%3BPlunkett%2C+R+J%3BJacobowitz%2C+D+M%3BOldfield%2C+E+H&rft.aulast=Kopin&rft.aufirst=I&rft.date=1993-01-01&rft.volume=60&rft.issue=&rft.spage=707&rft.isbn=&rft.btitle=&rft.title=Advances+in+neurology&rft.issn=00913952&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-11 N1 - Date created - 1993-02-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Mutagenicity of the human carcinogen treosulphan, and its hydrolysis product, dl-1,2:3,4-diepoxybutane in mammalian cells. AN - 75533647; 8419160 AB - The cytotoxicity and mutagenicity of the human carcinogen, treosulphan, and its hydrolysis product, dl-1,2:3,4-diepoxybutane (DEB), were studied in Chinese hamster ovary, AS52, cells. Treosulphan (0.1-1.0 mM) is toxic and mutagenic at the gpt locus. A strong pH dependence was noted. DEB is cytotoxic and mutagenic at a much lower dose (0.025 mM), but these effects were not affected by pH. The results suggest that the toxic and mutagenic effects of treosulphan are mediated by its hydrolysis product DEB, and that the conversion of treosulphan to DEB is highly pH-dependent. JF - Environmental and molecular mutagenesis AU - Zhu, S AU - Zeiger, E AD - Experimental Carcinogenesis and Mutagenesis Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1993 PY - 1993 DA - 1993 SP - 95 EP - 99 VL - 21 IS - 1 SN - 0893-6692, 0893-6692 KW - Epoxy Compounds KW - 0 KW - Mutagens KW - erythritol anhydride KW - 60OB65YNAB KW - treosulfan KW - CO61ER3EPI KW - Busulfan KW - G1LN9045DK KW - Index Medicus KW - Animals KW - Mutagenicity Tests KW - Analysis of Variance KW - Cell Survival -- drug effects KW - Dose-Response Relationship, Drug KW - Hydrogen-Ion Concentration KW - CHO Cells KW - Colony-Forming Units Assay KW - Time Factors KW - Hydrolysis KW - Cricetinae KW - Busulfan -- analogs & derivatives KW - Busulfan -- metabolism KW - Cell Division -- drug effects KW - Mutagens -- toxicity KW - Epoxy Compounds -- toxicity KW - Busulfan -- toxicity KW - Mutagenesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75533647?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+and+molecular+mutagenesis&rft.atitle=Mutagenicity+of+the+human+carcinogen+treosulphan%2C+and+its+hydrolysis+product%2C+dl-1%2C2%3A3%2C4-diepoxybutane+in+mammalian+cells.&rft.au=Zhu%2C+S%3BZeiger%2C+E&rft.aulast=Zhu&rft.aufirst=S&rft.date=1993-01-01&rft.volume=21&rft.issue=1&rft.spage=95&rft.isbn=&rft.btitle=&rft.title=Environmental+and+molecular+mutagenesis&rft.issn=08936692&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-10 N1 - Date created - 1993-02-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Major salivary gland function in patients with radiation-induced xerostomia: flow rates and sialochemistry. AN - 75528650; 8416881 AB - Radiation therapy for cancer of the head and neck region often causes salivary gland dysfunction and xerostomia. Several reports suggest that the submandibular/sublingual (SM/SL) glands may be less radiosensitive than the parotid. The purpose of this study was to evaluate differential radiation effects on the major salivary glands. Fifty patients with radiation-induced xerostomia were evaluated (33 males, 17 females; mean age 52.7). The average total tumor dose was 6034 cGy. Major salivary gland function was compared with that of 50 non-irradiated controls. Salivary flow rates included unstimulated and stimulated flows of both the parotid and SM/SL glands. Sialochemical analyses included total protein, lysozyme, lactoferrin, sodium, chloride, and potassium. All four measures of salivary flow were significantly reduced in patients as compared to controls (p = .0001). Like the parotid, submandibular/sublingual gland dysfunction appears to be radiation dose- and field-dependent. Patients in the lowest radiation dose quartile ( or = 6800 cGy; p = .025). Glands that were partially irradiated were more likely to have some residual function than fully irradiated glands (p = .003). Lactoferrin content was increased in parotid saliva of radiation patients (p = .0001). Chloride content was significantly increased also (p = .0001). The SM/SL glands are clearly dysfunctional in post-irradiation xerostomia patients compared to controls, in terms of both flow rates and sialochemistry. JF - International journal of radiation oncology, biology, physics AU - Valdez, I H AU - Atkinson, J C AU - Ship, J A AU - Fox, P C AD - Clinical Investigations and Patient Care Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 41 EP - 47 VL - 25 IS - 1 SN - 0360-3016, 0360-3016 KW - Index Medicus KW - Aged, 80 and over KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Adolescent KW - Male KW - Female KW - Xerostomia -- etiology KW - Salivary Glands -- radiation effects KW - Salivary Glands -- physiopathology KW - Saliva -- chemistry KW - Head and Neck Neoplasms -- radiotherapy KW - Xerostomia -- physiopathology KW - Radiotherapy -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75528650?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+radiation+oncology%2C+biology%2C+physics&rft.atitle=Major+salivary+gland+function+in+patients+with+radiation-induced+xerostomia%3A+flow+rates+and+sialochemistry.&rft.au=Valdez%2C+I+H%3BAtkinson%2C+J+C%3BShip%2C+J+A%3BFox%2C+P+C&rft.aulast=Valdez&rft.aufirst=I&rft.date=1993-01-01&rft.volume=25&rft.issue=1&rft.spage=41&rft.isbn=&rft.btitle=&rft.title=International+journal+of+radiation+oncology%2C+biology%2C+physics&rft.issn=03603016&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-28 N1 - Date created - 1993-01-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - In situ retroviral-mediated gene transfer for the treatment of brain tumors in rats. AN - 75524623; 8380127 AB - Gene transfer with vectors derived from murine retroviruses is restricted to cells which are proliferating and synthesizing DNA at the time of infection. This suggests that retroviral-mediated gene transfer might permit targeting of gene integration into malignant cells in organs composed mainly of quiescent nonproliferating cells, such as in the brain. Accordingly, selective introduction of genes encoding for susceptibility to otherwise nontoxic drugs ("suicide" genes) into proliferating brain tumors may be used to treat this cancer. We investigated the efficacy and dynamics of in vivo transduction of growing brain tumors with the herpes simplex-thymidine kinase gene followed by administration of the antiviral drug ganciclovir. Ganciclovir is phosphorylated by thymidine kinase to toxic triphosphates that interfere with DNA synthesis, resulting in the preferential death of the transduced tumor cells. Rats inoculated with 4 x 10(4) 9L gliosarcoma cells into the frontal lobe were treated 7 days later with an intratumoral stereotaxic injection of murine fibroblasts (NIH 3T3 cells) that were producing a retroviral vector containing the herpes simplex-thymidine kinase gene. Controls received vector producer and nonproducer NIH 3T3 cell lines containing the Escherichia coli lacZ (beta-galactosidase) gene as well as nonproducer NIH 3T3 cells containing the thymidine kinase gene. The animals were rested for 7 days to allow time for in situ transduction of the proliferating tumor cells with the herpes-thymidine kinase retroviral vector. The animals were then treated with ganciclovir, 15 mg/kg i.p. twice a day for 14 days. Gliomas receiving an injection of 3-5 x 10(6) thymidine kinase producer cells regressed completely in 23 of 30 rats given ganciclovir therapy, while 25 of 26 control rats developed large tumors. Intratumoral injection of a lower concentration of thymidine kinase vector producer cells (1.8 x 10(6)) resulted in a lower frequency of tumor regression (5 of 13 rats). To estimate the efficiency of in vivo gene transfer, 9L brain tumors were given injections of 5 x 10(6) beta-galactosidase vector producer cells. 5-Bromo-4-chloro-3-indolyl-beta-D-galactopyranaside staining revealed maximal staining of beta-galactosidase within the tumor 7-14 days after injection of the vector producer cells. In vivo transduction rates in harvested tumors ranged from 10 to 70%. There was no evidence of transduction of the surrounding normal neural tissue. Occasional blood vessel endothelial cells within or adjacent to the tumor were observed to be 5-bromo-4- chloro-3-indolyl-beta-D-galactopyranaside positive.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Cancer research AU - Ram, Z AU - Culver, K W AU - Walbridge, S AU - Blaese, R M AU - Oldfield, E H AD - Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke Clinical Center, NIH, Bethesda, Maryland 20892. Y1 - 1993/01/01/ PY - 1993 DA - 1993 Jan 01 SP - 83 EP - 88 VL - 53 IS - 1 SN - 0008-5472, 0008-5472 KW - HStk KW - Thymidine Kinase KW - EC 2.7.1.21 KW - beta-Galactosidase KW - EC 3.2.1.23 KW - Ganciclovir KW - P9G3CKZ4P5 KW - Index Medicus KW - Animals KW - Drug Screening Assays, Antitumor KW - Combined Modality Therapy KW - Dose-Response Relationship, Drug KW - Genes, Viral -- genetics KW - Humans KW - Escherichia coli -- genetics KW - Genes, Bacterial -- genetics KW - Simplexvirus -- enzymology KW - Mice KW - Transduction, Genetic -- physiology KW - 3T3 Cells -- enzymology KW - Rats KW - Neoplasm Transplantation KW - Lac Operon -- genetics KW - Rats, Inbred F344 KW - Tumor Cells, Cultured KW - Transfection KW - 3T3 Cells -- physiology KW - Simplexvirus -- genetics KW - beta-Galactosidase -- genetics KW - Thymidine Kinase -- genetics KW - Ganciclovir -- pharmacology KW - Brain Neoplasms -- therapy KW - Glioma -- drug therapy KW - Brain Neoplasms -- drug therapy KW - Brain Neoplasms -- genetics KW - Glioma -- therapy KW - Genetic Therapy KW - Retroviridae -- genetics KW - Glioma -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75524623?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=In+situ+retroviral-mediated+gene+transfer+for+the+treatment+of+brain+tumors+in+rats.&rft.au=Ram%2C+Z%3BCulver%2C+K+W%3BWalbridge%2C+S%3BBlaese%2C+R+M%3BOldfield%2C+E+H&rft.aulast=Ram&rft.aufirst=Z&rft.date=1993-01-01&rft.volume=53&rft.issue=1&rft.spage=83&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-25 N1 - Date created - 1993-01-25 N1 - Date revised - 2017-01-13 N1 - Gene symbol - HStk N1 - SuppNotes - Comment In: Cancer Res. 1994 Jul 15;54(14):3947-8 [8033119] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Pseudomonas exotoxin conjugated to monoclonal antibody MRK16 specifically kills multidrug resistant cells in cultured renal carcinomas and in MDR-transgenic mice. AN - 75524390; 8417204 AB - Using renal carcinoma and prostate carcinoma cell lines, we investigated the concept of targeting and killing multidrug resistant cells in urogenital cancers. Renal carcinoma lines HTB44, 45, 46, and 47 expressed a relatively low, but detectable level of multidrug resistance (MDR)1 mRNA as indicated by Northern blot analysis, whereas prostate lines LNCaP and DU145 were found to be MDR1-negative. Anti-P-glycoprotein monoclonal antibody MRK16 was conjugated to Pseudomonas exotoxin (PE) by a stable thioether bond. Treatment with MRK16-PE resulted in a dose-dependent killing of multidrug resistant renal carcinoma cells, while non-MDR expressing prostate carcinoma cells were not affected. Addition of excess MRK16 blocked the effect of MRK16-PE. Furthermore, MOPC-PE, a non-MDR associated monoclonal antibody control conjugate, did not target and kill multidrug resistant renal carcinoma cells. Having established that MRK16-PE was active against and specific for multidrug resistant cells in culture, we also tested bioactivity in MDR-transgenic mice, whose bone marrow cells express the human MDR1 gene at a level approximately equal to that found in many human cancers. Again, MRK16-PE killed multidrug resistant bone marrow cells with high efficiency in an intact animal, and killing was blocked by unconjugated MRK16. JF - The Journal of urology AU - Mickisch, G H AU - Pai, L H AU - Siegsmund, M AU - Campain, J AU - Gottesman, M M AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 174 EP - 178 VL - 149 IS - 1 SN - 0022-5347, 0022-5347 KW - Antibodies, Monoclonal KW - 0 KW - Bacterial Toxins KW - Exotoxins KW - Immunotoxins KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Tumor Cells, Cultured -- drug effects KW - Humans KW - Drug Resistance KW - Mice KW - Mice, Transgenic KW - Male KW - Antibodies, Monoclonal -- therapeutic use KW - Carcinoma, Renal Cell -- pathology KW - Kidney Neoplasms -- drug therapy KW - Kidney Neoplasms -- pathology KW - Exotoxins -- pharmacology KW - Bacterial Toxins -- pharmacology KW - Carcinoma, Renal Cell -- drug therapy KW - Prostatic Neoplasms -- drug therapy KW - Prostatic Neoplasms -- pathology KW - Bacterial Toxins -- therapeutic use KW - Immunotoxins -- therapeutic use KW - Exotoxins -- therapeutic use KW - Immunotoxins -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75524390?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+urology&rft.atitle=Pseudomonas+exotoxin+conjugated+to+monoclonal+antibody+MRK16+specifically+kills+multidrug+resistant+cells+in+cultured+renal+carcinomas+and+in+MDR-transgenic+mice.&rft.au=Mickisch%2C+G+H%3BPai%2C+L+H%3BSiegsmund%2C+M%3BCampain%2C+J%3BGottesman%2C+M+M%3BPastan%2C+I&rft.aulast=Mickisch&rft.aufirst=G&rft.date=1993-01-01&rft.volume=149&rft.issue=1&rft.spage=174&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+urology&rft.issn=00225347&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-25 N1 - Date created - 1993-01-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Initiators and promoters of lung cancer. AN - 75521550; 8380133 AB - As we expand our knowledge of the initiators and promoters of lung cancer, early detection and intervention strategies show great potential in individuals at high risk, especially smokers and exsmokers. Documented mutations of dominant oncogenes and tumor suppressor genes in human lung cancer cells may represent important steps in the pathogenesis of invasive cancer. The precise molecular events and their sequence that lead to tumor promotion in lung cancer, however, are less well understood. Chemointervention with agents like the retinoids may halt proliferation of cancer cells prior to the development of metastatic competence. Use of anti-growth-factor therapy and peptide hormone antagonists may also have a role in intervention approaches. This paper reviews present understanding of the initiation and promotion of lung cancer, as well as preventive strategies currently proposed for patients at risk. JF - Chest AU - Mulshine, J L AU - Treston, A M AU - Brown, P H AU - Birrer, M J AU - Shaw, G L AD - Biomarkers and Prevention Research Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 4S EP - 11S VL - 103 IS - 1 Suppl SN - 0012-3692, 0012-3692 KW - Carcinogens KW - 0 KW - Gastrins KW - Peptides KW - Retinoids KW - Gastrin-Releasing Peptide KW - 80043-53-4 KW - Abridged Index Medicus KW - Index Medicus KW - Oncogenes -- genetics KW - Gastrins -- antagonists & inhibitors KW - Genes, ras -- genetics KW - Tumor Cells, Cultured KW - Retinoids -- therapeutic use KW - Protein Processing, Post-Translational -- genetics KW - Genes, Tumor Suppressor -- genetics KW - Humans KW - Smoking -- genetics KW - Peptides -- antagonists & inhibitors KW - Carcinoma, Non-Small-Cell Lung -- prevention & control KW - Lung Neoplasms -- prevention & control KW - Carcinoma, Non-Small-Cell Lung -- genetics KW - Lung Neoplasms -- genetics KW - Carcinoma, Small Cell -- prevention & control KW - Carcinoma, Small Cell -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75521550?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chest&rft.atitle=Initiators+and+promoters+of+lung+cancer.&rft.au=Mulshine%2C+J+L%3BTreston%2C+A+M%3BBrown%2C+P+H%3BBirrer%2C+M+J%3BShaw%2C+G+L&rft.aulast=Mulshine&rft.aufirst=J&rft.date=1993-01-01&rft.volume=103&rft.issue=1+Suppl&rft.spage=4S&rft.isbn=&rft.btitle=&rft.title=Chest&rft.issn=00123692&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-28 N1 - Date created - 1993-01-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Kainate-induced changes in opioid peptide genes and AP-1 protein expression in the rat hippocampus. AN - 75519895; 8417141 AB - In the rat hippocampus, jun, c-fos, and fos-related antigen immunoreactivity, AP-1 DNA binding, and opioid peptide gene expression were examined after kainate treatment to determine whether the induction and DNA binding of AP-1 transcription factors are correlated with the expression of the opioid peptide genes. One and one-half hours after kainate administration, fos-related antigen and jun immunoreactivity and AP-1 DNA binding were induced; maximal elevation was observed after 4.5 h. Transcription factor expression and DNA binding increased in a dose-dependent manner. Preprodynorphin and preproenkephalin mRNA induction was also dose dependent. The anticonvulsants, pentobarbital and diazepam, effectively blocked electroencephalographic seizure activity caused by kainate treatment, whereas valproic acid was approximately 50% effective. Opioid peptide gene expression, fos-related antigen and jun immunoreactivity, and AP-1 DNA binding all reflected similar reductions after anticonvulsant treatment. Therefore, expression and DNA binding activity of the AP-1 transcription factors are correlated with opioid peptide gene expression in the rat hippocampus. JF - Journal of neurochemistry AU - Pennypacker, K R AU - Walczak, D AU - Thai, L AU - Fannin, R AU - Mason, E AU - Douglass, J AU - Hong, J S AD - Laboratory of Molecular and Integrative Neuroscience, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 204 EP - 211 VL - 60 IS - 1 SN - 0022-3042, 0022-3042 KW - Anticonvulsants KW - 0 KW - Endorphins KW - Molecular Probes KW - Proto-Oncogene Proteins c-jun KW - Transcription Factors KW - DNA KW - 9007-49-2 KW - Kainic Acid KW - SIV03811UC KW - Index Medicus KW - Seizures -- chemically induced KW - Transcription Factors -- physiology KW - Animals KW - Transcription Factors -- metabolism KW - Seizures -- physiopathology KW - Dose-Response Relationship, Drug KW - DNA -- metabolism KW - Electroencephalography KW - Rats KW - Anticonvulsants -- pharmacology KW - Molecular Probes -- genetics KW - Base Sequence KW - Rats, Inbred F344 KW - Molecular Sequence Data KW - Gene Expression Regulation -- drug effects KW - Male KW - Kainic Acid -- pharmacology KW - Hippocampus -- physiology KW - Hippocampus -- metabolism KW - Genes -- drug effects KW - Endorphins -- genetics KW - Proto-Oncogene Proteins c-jun -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75519895?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neurochemistry&rft.atitle=Kainate-induced+changes+in+opioid+peptide+genes+and+AP-1+protein+expression+in+the+rat+hippocampus.&rft.au=Pennypacker%2C+K+R%3BWalczak%2C+D%3BThai%2C+L%3BFannin%2C+R%3BMason%2C+E%3BDouglass%2C+J%3BHong%2C+J+S&rft.aulast=Pennypacker&rft.aufirst=K&rft.date=1993-01-01&rft.volume=60&rft.issue=1&rft.spage=204&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurochemistry&rft.issn=00223042&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-25 N1 - Date created - 1993-01-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Immunohistochemistry and Morphology of Reactive Lesions in Lymph Nodes and Spleen from Rats and Mice AN - 755137347; 13645551 AB - The use of immunohistochemistry with anatomical and systematized classifications of nonneoplastic lesions in hematopoietic pathology of lymph nodes and spleens from rats and mice is described. Polyclonal antisera and monoclonal antibodies to leukocyte and other antigens can be used with frozen or fixed tissue sections to identify changes in cell populations in these tissues in response to tissue injury and aging. A classification for reactive lesions of lymph nodes and spleen is proposed that can be utilized for computerized pathology and toxicology data systems. These classifications are based on a systematized anatomic distribution of the lesions with the aid of immunohistochemistry. The association of some lesions with early leukemia or lymphoma of rats and mice is also discussed. JF - Toxicologic Pathology AU - Ward, Jerrold M AU - Uno, Hiroshi AU - Frith, Charles H AD - Veterinary and Tumor Pathology Section, Office of Laboratory Animal Science, National Cancer Institute, Frederick, Maryland 21702-1201 Y1 - 1993 PY - 1993 DA - 1993 SP - 199 EP - 205 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU UK VL - 21 IS - 2 SN - 0192-6233, 0192-6233 KW - Toxicology Abstracts UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/755137347?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+Pathology&rft.atitle=Immunohistochemistry+and+Morphology+of+Reactive+Lesions+in+Lymph+Nodes+and+Spleen+from+Rats+and+Mice&rft.au=Ward%2C+Jerrold+M%3BUno%2C+Hiroshi%3BFrith%2C+Charles+H&rft.aulast=Ward&rft.aufirst=Jerrold&rft.date=1993-01-01&rft.volume=21&rft.issue=2&rft.spage=199&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F019262339302100212 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2010-09-01 N1 - Last updated - 2011-12-14 DO - http://dx.doi.org/10.1177/019262339302100212 ER - TY - JOUR T1 - Retrovirus-Induced Lymphoproliferation as a Model for Developing Diagnostic Criteria for Malignant Lymphoma in Mice AN - 755135340; 13645553 AB - Several methods for evaluating lymphoproliferative lesions in mice were compared. The model systems included spontaneous lymphomas arising in CWD mice and NFS mice congenic for ecotropic murine leukemia virus (MuLV) induction loci and a series of transplants in mice with severe combined immunodeficiency disease mutation of cells derived from mice infected with LP-BM5 MuLV. Primary lymphomas and donor tissues and transplants were examined using histopathology, flow cytometry, and Southern blot analysis of DNA for rearrangements of immunoglobulin and T-cell receptor genes and for viral integrations. The use of flow cytometric analysis, to establish cell lineage and define population size, and DNA analysis, for cell lineage and clonality determination, allowed the identification of malignant lymphoproliferations. Histologic evaluation did not define clonal populations of particular lineage but did provide other indications of malignancy such as invasiveness and presence of a dominant morphologic cell type. Thus, the precision of diagnosis of mouse lymphomas can be considerably enhanced by augmenting histopathologic examination with antigenic and molecular characterizations that can define malignant populations. JF - Toxicologic Pathology AU - Fredrickson, Torgny N AU - Tang, Yao AU - Chattopadhyay, Sisir K AU - Morse, Herbert C AU - Hartley, Janet W AD - Registry of Experimental Cancers, National Cancer Institute, Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892 Y1 - 1993 PY - 1993 DA - 1993 SP - 219 EP - 228 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU UK VL - 21 IS - 2 SN - 0192-6233, 0192-6233 KW - Toxicology Abstracts; Immunology Abstracts; Virology & AIDS Abstracts KW - Cell lineage KW - T-cell receptor KW - Donors KW - Invasiveness KW - Animal models KW - Lymphocytes KW - Murine leukemia virus KW - Flow cytometry KW - Integration KW - Malignancy KW - DNA KW - Severe combined immunodeficiency KW - Lymphoma KW - Mutation KW - Immunoglobulins KW - F 06955:Immunomodulation & Immunopharmacology KW - V 22310:Genetics, Taxonomy & Structure KW - X 24300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/755135340?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+Pathology&rft.atitle=Retrovirus-Induced+Lymphoproliferation+as+a+Model+for+Developing+Diagnostic+Criteria+for+Malignant+Lymphoma+in+Mice&rft.au=Fredrickson%2C+Torgny+N%3BTang%2C+Yao%3BChattopadhyay%2C+Sisir+K%3BMorse%2C+Herbert+C%3BHartley%2C+Janet+W&rft.aulast=Fredrickson&rft.aufirst=Torgny&rft.date=1993-01-01&rft.volume=21&rft.issue=2&rft.spage=219&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F019262339302100214 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2010-09-01 N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - Cell lineage; Invasiveness; Donors; T-cell receptor; Animal models; Lymphocytes; Flow cytometry; Integration; Malignancy; DNA; Severe combined immunodeficiency; Mutation; Lymphoma; Immunoglobulins; Murine leukemia virus DO - http://dx.doi.org/10.1177/019262339302100214 ER - TY - JOUR T1 - Mutational analysis of the p50 subunit of NF-kappa B and inhibition of NF-kappa B activity by trans-dominant p50 mutants. AN - 73496765; 8416374 AB - The NF-kappa B family of DNA-binding proteins regulates the expression of many cellular and viral genes. Each of these proteins has an N-terminal region that is homologous to the c-Rel proto-oncogene product, and this Rel homology region defines both DNA binding and protein dimerization properties of the individual proteins. Most of the NF-kappa B family members have been shown to associate with themselves or with each other to form homodimers or heterodimers, and previous studies have shown that dimerization of NF-kappa B factors is necessary to provide a functional DNA binding domain. We have used site-directed mutagenesis to identify regions in the Rel homology domain of the p50/NF-kappa B protein that are important for DNA binding and protein dimerization. Our studies have identified mutations of p50 that interfere with DNA binding only and those that interfere with protein dimerization. Mutations of p50 which disrupt only DNA binding were still able to associate with other members of the NF-kappa B protein family. We demonstrate that such heterodimeric complexes inhibit transcriptional activation mediated in trans through a cis-acting kappa B motif; therefore, we have identified trans-dominant negative mutants of p50. JF - Journal of virology AU - Bressler, P AU - Brown, K AU - Timmer, W AU - Bours, V AU - Siebenlist, U AU - Fauci, A S AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 288 EP - 293 VL - 67 IS - 1 SN - 0022-538X, 0022-538X KW - Macromolecular Substances KW - 0 KW - NF-kappa B KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Oncogenes -- genetics KW - Cells, Cultured KW - DNA Mutational Analysis KW - Structure-Activity Relationship KW - Protein Conformation KW - Cloning, Molecular KW - Transcriptional Activation -- genetics KW - NF-kappa B -- genetics KW - NF-kappa B -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73496765?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Mutational+analysis+of+the+p50+subunit+of+NF-kappa+B+and+inhibition+of+NF-kappa+B+activity+by+trans-dominant+p50+mutants.&rft.au=Bressler%2C+P%3BBrown%2C+K%3BTimmer%2C+W%3BBours%2C+V%3BSiebenlist%2C+U%3BFauci%2C+A+S&rft.aulast=Bressler&rft.aufirst=P&rft.date=1993-01-01&rft.volume=67&rft.issue=1&rft.spage=288&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-15 N1 - Date created - 1993-01-15 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cell. 1991 Jan 25;64(2):439-46 [1988156] Science. 1988 Oct 28;242(4878):540-6 [3140380] Cell. 1991 Mar 8;64(5):961-9 [2001591] Science. 1991 Mar 22;251(5000):1490-3 [2006423] EMBO J. 1991 Jul;10(7):1817-25 [2050119] J Virol. 1984 Oct;52(1):172-82 [6090694] Mol Cell Biol. 1992 Feb;12(2):674-84 [1732739] Oncogene Res. 1989;4(1):1-8 [2654811] Nucleic Acids Res. 1989 Jun 26;17(12):4589-604 [2546123] Cell. 1989 Jul 28;58(2):227-9 [2665943] Nature. 1990 Apr 12;344(6267):678-82 [2157987] Cell. 1990 Apr 20;61(2):255-65 [2184941] Cell. 1990 Sep 7;62(5):1007-18 [2203531] Cell. 1990 Sep 7;62(5):1019-29 [2203532] Cell. 1990 Sep 7;62(5):841-3 [2203533] Mol Cell Biol. 1990 Oct;10(10):5473-85 [2204816] Cell. 1990 Nov 16;63(4):803-14 [2225078] Nature. 1990 Nov 1;348(6296):76-80 [2234062] EMBO J. 1991 Jul;10(7):1827-32 [1675604] Cell. 1991 Jun 28;65(7):1191-201 [1648449] Genes Dev. 1991 Aug;5(8):1464-76 [1907941] Nature. 1991 Aug 22;352(6337):733-6 [1876189] Science. 1991 Sep 13;253(5025):1268-71 [1891714] J Immunol. 1991 Oct 1;147(7):2290-4 [1680914] EMBO J. 1991 Dec;10(12):3805-17 [1935902] Cell. 1991 Dec 20;67(6):1075-87 [1760839] Mol Cell Biol. 1992 Feb;12(2):444-54 [1732726] Proc Natl Acad Sci U S A. 1991 Feb 1;88(3):966-70 [1992489] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Characterization of ribosomal frameshifting for expression of pol gene products of human T-cell leukemia virus type I. AN - 73494997; 8416368 AB - For study of the pol gene expression of human T-cell leukemia virus type I (HTLV-I), RNA was transcribed in vitro from proviral DNA and translated in rabbit reticulocyte lysates. This cell-free translation resulted in two major translation products representing the Gag and Gag-Pro polyproteins. By contrast, the Gag-Pro-Pol polyprotein could be readily observed only when translation was performed with mutant mRNA in which the protease (pro) reading frame was aligned to gag to eliminate the frameshifting event in the gag-pro overlap. The results indicated that two independent ribosomal frameshifting events are required for expression of the HTLV-I pol gene product. Studies with mutant DNAs facilitated the characterization of the primary structure of the HTLV-I mRNA responsible for the ribosomal frameshift in the pro-pol overlap and demonstrated that the frameshift occurs at the signal sequence UUUAAAC. Direct amino acid sequencing of the transframe protein localized the site of the frameshift to the asparagine codon AAC. JF - Journal of virology AU - Nam, S H AU - Copeland, T D AU - Hatanaka, M AU - Oroszlan, S AD - Laboratory of Molecular Virology and Carcinogenesis, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1993/01// PY - 1993 DA - January 1993 SP - 196 EP - 203 VL - 67 IS - 1 SN - 0022-538X, 0022-538X KW - gag KW - pol KW - pro KW - Gene Products, pol KW - 0 KW - RNA, Messenger KW - Recombinant Proteins KW - HIV Protease KW - EC 3.4.23.- KW - Index Medicus KW - AIDS/HIV KW - Ribosomes -- metabolism KW - HIV Protease -- genetics KW - Protein Biosynthesis KW - Recombinant Proteins -- biosynthesis KW - Amino Acid Sequence KW - Genes, gag -- genetics KW - Recombinant Proteins -- genetics KW - RNA, Messenger -- biosynthesis KW - Frameshift Mutation KW - Mutagenesis, Site-Directed KW - Base Sequence KW - Molecular Sequence Data KW - Cell-Free System KW - Human T-lymphotropic virus 1 -- genetics KW - Genes, pol -- genetics KW - Gene Products, pol -- biosynthesis KW - Transcription, Genetic KW - Gene Products, pol -- genetics KW - Open Reading Frames -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73494997?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Characterization+of+ribosomal+frameshifting+for+expression+of+pol+gene+products+of+human+T-cell+leukemia+virus+type+I.&rft.au=Nam%2C+S+H%3BCopeland%2C+T+D%3BHatanaka%2C+M%3BOroszlan%2C+S&rft.aulast=Nam&rft.aufirst=S&rft.date=1993-01-01&rft.volume=67&rft.issue=1&rft.spage=196&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-15 N1 - Date created - 1993-01-15 N1 - Date revised - 2017-01-13 N1 - Gene symbol - gag; pol; pro N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Nucleic Acids Res. 1979 Nov 24;7(6):1513-23 [388356] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256] Nature. 1981 Oct 15-21;293(5833):543-8 [6169994] Nature. 1981 Nov 19;294(5838):268-71 [6272125] Proc Natl Acad Sci U S A. 1981 Oct;78(10):6476-80 [7031654] Proc Natl Acad Sci U S A. 1982 Mar;79(6):2031-5 [6979048] Cell. 1983 Mar;32(3):853-69 [6299578] Proc Natl Acad Sci U S A. 1983 Jun;80(12):3618-22 [6304725] J Biol Chem. 1984 Feb 10;259(3):1695-702 [6319407] Nucleic Acids Res. 1984 Sep 25;12(18):7035-56 [6091052] Nucleic Acids Res. 1984 Sep 25;12(18):7057-70 [6207484] Nature. 1985 Jan 24-30;313(6000):277-84 [2578615] Proc Natl Acad Sci U S A. 1985 Feb;82(3):677-81 [2983308] Proc Natl Acad Sci U S A. 1985 Mar;82(6):1618-22 [3885215] Biochem Biophys Res Commun. 1985 Aug 30;131(1):347-54 [2994655] Virology. 1985 Apr 30;142(2):357-77 [2997990] Science. 1985 Dec 13;230(4731):1237-42 [2416054] Nucleic Acids Res. 1985 Dec 20;13(24):8765-85 [3001650] Science. 1986 Mar 28;231(4745):1567-72 [3006247] Cell. 1986 May 9;45(3):375-85 [2421920] Biochem Biophys Res Commun. 1986 Aug 29;139(1):129-35 [3021121] J Virol. 1987 Feb;61(2):480-90 [3027377] J Gen Virol. 1987 Feb;68 ( Pt 2):499-506 [3029287] Proc Natl Acad Sci U S A. 1987 Jun;84(12):4298-302 [3035577] Proc Natl Acad Sci U S A. 1987 Oct;84(20):7041-5 [2823251] Nature. 1988 Jan 21;331(6153):280-3 [2447506] EMBO J. 1987 Dec 1;6(12):3779-85 [3428275] J Virol. 1988 May;62(5):1808-9 [3357211] J Virol. 1988 Oct;62(10):3718-28 [2843670] Cell. 1988 Nov 4;55(3):447-58 [2846182] J Virol. 1989 May;63(5):2400-4 [2467996] Cell. 1989 May 19;57(4):537-47 [2720781] Virology. 1989 Dec;173(2):736-42 [2556852] Trends Biochem Sci. 1990 May;15(5):186-90 [2193436] Curr Top Microbiol Immunol. 1990;157:93-124 [2168307] Virus Genes. 1990 Jul;4(2):121-36 [2402881] Proc Natl Acad Sci U S A. 1992 Jan 15;89(2):713-7 [1309954] Adv Virus Res. 1992;41:193-239 [1575083] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - L'antico lago di Agordo TT - The ancient Agordo Lake AN - 51045338; 1998-026621 JF - Memorie di Scienze Geologiche AU - Friz, C AU - Villi, V Y1 - 1993 PY - 1993 DA - 1993 SP - 67 EP - 78 PB - Societa Cooperativa Tipografica, Padua VL - 45 SN - 0391-8602, 0391-8602 KW - clay KW - lacustrine features KW - isotopes KW - northern Italy KW - lakes KW - Europe KW - gravel KW - Holocene KW - Italy KW - Southern Europe KW - Cenozoic KW - bedding KW - radioactive isotopes KW - dates KW - carbon KW - sediments KW - absolute age KW - sedimentary structures KW - hydrology KW - sand KW - Quaternary KW - clastic sediments KW - landform evolution KW - sedimentation KW - silt KW - lithofacies KW - planar bedding structures KW - limnology KW - Agordo Lake KW - lacustrine environment KW - Agordo Italy KW - C-14 KW - Cordevole Valley KW - 24:Quaternary geology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/51045338?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ageorefmodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Memorie+di+Scienze+Geologiche&rft.atitle=L%27antico+lago+di+Agordo&rft.au=Friz%2C+C%3BVilli%2C+V&rft.aulast=Friz&rft.aufirst=C&rft.date=1993-01-01&rft.volume=45&rft.issue=&rft.spage=67&rft.isbn=&rft.btitle=&rft.title=Memorie+di+Scienze+Geologiche&rft.issn=03918602&rft_id=info:doi/ LA - Italian DB - GeoRef N1 - Copyright - GeoRef, Copyright 2012, American Geosciences Institute. N1 - Date revised - 1998-01-01 N1 - Number of references - 23 N1 - Document feature - illus. incl. sects., 2 tables, sketch map N1 - Last updated - 2012-06-07 N1 - SubjectsTermNotLitGenreText - absolute age; Agordo Italy; Agordo Lake; bedding; C-14; carbon; Cenozoic; clastic sediments; clay; Cordevole Valley; dates; Europe; gravel; Holocene; hydrology; isotopes; Italy; lacustrine environment; lacustrine features; lakes; landform evolution; limnology; lithofacies; northern Italy; planar bedding structures; Quaternary; radioactive isotopes; sand; sedimentary structures; sedimentation; sediments; silt; Southern Europe ER - TY - JOUR T1 - Biological studies on the carcinogenic mechanisms of quartz AN - 50147865; 1995-035689 JF - Reviews in Mineralogy AU - Saffiotti, Umberto AU - Daniel, Lambert N AU - Mao, Yan AU - Williams, A Olufemi AU - Kaighn, M Edward AU - Ahmed, Nadera AU - Knapton, Alan D A2 - Guthrie, George D., Jr. A2 - Mossman, Brooke T. Y1 - 1993 PY - 1993 DA - 1993 SP - 523 EP - 544 PB - Mineralogical Society of America, Washington, DC VL - 28 SN - 0275-0279, 0275-0279 KW - silicates KW - experimental studies KW - silica minerals KW - medical geology KW - pollutants KW - pollution KW - human ecology KW - carcinogens KW - laboratory studies KW - toxicity KW - quartz KW - framework silicates KW - minerals KW - 22:Environmental geology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/50147865?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ageorefmodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Reviews+in+Mineralogy&rft.atitle=Biological+studies+on+the+carcinogenic+mechanisms+of+quartz&rft.au=Saffiotti%2C+Umberto%3BDaniel%2C+Lambert+N%3BMao%2C+Yan%3BWilliams%2C+A+Olufemi%3BKaighn%2C+M+Edward%3BAhmed%2C+Nadera%3BKnapton%2C+Alan+D&rft.aulast=Saffiotti&rft.aufirst=Umberto&rft.date=1993-01-01&rft.volume=28&rft.issue=&rft.spage=523&rft.isbn=&rft.btitle=&rft.title=Reviews+in+Mineralogy&rft.issn=02750279&rft_id=info:doi/ LA - English DB - GeoRef N1 - Conference title - Short course ; Health effects of mineral dusts N1 - Copyright - GeoRef, Copyright 2012, American Geosciences Institute. N1 - Date revised - 1995-01-01 N1 - Number of references - 53 N1 - PubXState - DC N1 - Document feature - illus. incl. 2 tables N1 - Last updated - 2012-06-07 N1 - CODEN - RMINDF N1 - SubjectsTermNotLitGenreText - carcinogens; experimental studies; framework silicates; human ecology; laboratory studies; medical geology; minerals; pollutants; pollution; quartz; silica minerals; silicates; toxicity ER - TY - JOUR T1 - Assessment of the Haemolytic Activity of 2-Butoxyethanol and its Major Metabolite, Butoxyacetic Acid, in Various Mammals Including Humans AN - 21071872; 11126860 AB - 2-Butoxyethanol (BE) is a glycol ether produced in volumes exceeding 335 million pounds/year for industrial and domestic uses. BE causes acute haemolytic anaemia in rats and some other mammals. While BE is inactive in vitro, 2-butoxyacetic acid (BAA) is a potent haemolytic agent in vivo and in vitro. This finding suggests that metabolic activation of BE to BAA is required for haemolysis of erythrocytes to occur in vivo. Haemolysis of red blood cells (RBC) by BAA is preceded by swelling (increased mean cell volume [MCV] and haematocrit [HCT]). In an attempt to assess the potential risk to humans exposed to BE, studies were designed to determine the in vitro effect of BAA on RBCs from 10 mammalian species including humans. Blood samples from each mammalian species (n=3-5) were incubated with BAA at a final concentration of 0 (vehicle), 1 or 2 mM and kept at 37 degree C in a gently shaking water bath. Complete blood counts (CBCs) were measured at 0, 1, 2 and 4 h. BAA caused a time- and concentration-dependent increase in MCV and HCT of blood from rats, mice and hamsters (rodents), rabbits (lagomorphs), and baboons (primates). In contrast, blood from pigs (artiodactyis), dogs and cats (carnivores), guinea pigs (rodents/marsupials), and humans (primates), was minimally affected by BAA. These results were confirmed in guinea pigs and rats in vivo. Gavage administration of BE (250 mg kg super(-1)) to rats resulted in increased MCV and HCT followd by haemolysis (decreased RBCs). Identical treatment with BE resulted in no significant change in these parameters in guinea pigs. These data clearly demonstrated that BE-induced haemolytic anaemia is species-dependent. This information may prove important for selecting appropriate animal models for use in the assessment of the health risk to humans exposed to BE. Future studies will focus on the cellular basis of the differential sensitivity of RBCs from various mammals to BAA. JF - Human & Experimental Toxicology AU - Ghanayem, Burhan I AU - Sullivan, Chantal A AD - National Institute of Environmental Health Sciences, National Institutes of Health Research Triangle Park, NC 27709, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 305 EP - 311 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU UK VL - 12 IS - 4 SN - 0960-3271, 0960-3271 KW - Toxicology Abstracts KW - Papio KW - Data processing KW - Erythrocytes KW - Cell size KW - Carnivores KW - Glycol ethers KW - Anemia KW - Animal models KW - Metabolic activation KW - Primates KW - X 24350:Industrial Chemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/21071872?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Human+%26+Experimental+Toxicology&rft.atitle=Assessment+of+the+Haemolytic+Activity+of+2-Butoxyethanol+and+its+Major+Metabolite%2C+Butoxyacetic+Acid%2C+in+Various+Mammals+Including+Humans&rft.au=Ghanayem%2C+Burhan+I%3BSullivan%2C+Chantal+A&rft.aulast=Ghanayem&rft.aufirst=Burhan&rft.date=1993-01-01&rft.volume=12&rft.issue=4&rft.spage=305&rft.isbn=&rft.btitle=&rft.title=Human+%26+Experimental+Toxicology&rft.issn=09603271&rft_id=info:doi/10.1177%2F096032719301200409 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2009-11-01 N1 - Last updated - 2015-03-30 N1 - SubjectsTermNotLitGenreText - Data processing; Glycol ethers; Carnivores; Cell size; Erythrocytes; Animal models; Anemia; Metabolic activation; Papio; Primates DO - http://dx.doi.org/10.1177/096032719301200409 ER - TY - JOUR T1 - Human gene therapy AN - 19859630; 3737396 AB - The purpose of this review is to acquaint the reader with clinically relevant gene transfer procedures, and to discuss their current applications. We also discuss the ethical issues of human genetic engineering, and speculate as to what the future of this field might be in the next century. Other recent reviews on this subject can be found in various sources. JF - Annual Review of Biochemistry AU - Morgan, R A AU - Anderson, W F AD - Mol. Hematol. Branch, NHLBI/NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 191 EP - 217 VL - 62 SN - 0066-4154, 0066-4154 KW - man KW - gene therapy KW - reviews KW - Medical and Pharmaceutical Biotechnology Abstracts; Human Genome Abstracts KW - W 30965:Miscellaneous, Reviews KW - W3 33180:Gene based (protocols, clinical trials, and animal models) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/19859630?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annual+Review+of+Biochemistry&rft.atitle=Human+gene+therapy&rft.au=Morgan%2C+R+A%3BAnderson%2C+W+F&rft.aulast=Morgan&rft.aufirst=R&rft.date=1993-01-01&rft.volume=62&rft.issue=&rft.spage=191&rft.isbn=&rft.btitle=&rft.title=Annual+Review+of+Biochemistry&rft.issn=00664154&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2010-08-21 ER - TY - JOUR T1 - Anchored reference loci for comparative genome mapping in mammals. AN - 19792139; 2936208 AB - We propose here a list of 321 reference anchor loci suitable for comparative gene mapping in mammals and other vertebrate classes. We selected cloned mouse and human functional genes spaced an average of 5-10 centiMorgans throughout their respective genomes. We also attempted to include loci that are evolutionarily conserved and represented in comparative gene maps in other mammalian orders, particularly cattle and the domestic cat. We believe that the map may provide the basis for a unified approach to comparative analysis of mammalian species genomes. JF - Nature Genetics AU - O'Brien, S J AU - Womack, JE AU - Lyons, LA AU - Moore, K J AU - Jenkins, NA AU - Copeland, NG AD - Lab. Viral Carcinog., NCI-Frederick, MD 21702-1201, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 103 EP - 112 VL - 3 IS - 2 SN - 1061-4036, 1061-4036 KW - reference anchor loci KW - genomes KW - gene mapping KW - Mammalia KW - Human Genome Abstracts; Genetics Abstracts; Medical and Pharmaceutical Biotechnology Abstracts KW - G 07120:Recombinant DNA/Genetic engineering KW - W 30965:Miscellaneous, Reviews KW - W3 33130:Genetic based (PCR, etc.) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/19792139?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+Genetics&rft.atitle=Anchored+reference+loci+for+comparative+genome+mapping+in+mammals.&rft.au=O%27Brien%2C+S+J%3BWomack%2C+JE%3BLyons%2C+LA%3BMoore%2C+K+J%3BJenkins%2C+NA%3BCopeland%2C+NG&rft.aulast=O%27Brien&rft.aufirst=S&rft.date=1993-01-01&rft.volume=3&rft.issue=2&rft.spage=103&rft.isbn=&rft.btitle=&rft.title=Nature+Genetics&rft.issn=10614036&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2010-08-21 ER - TY - JOUR T1 - Molecular organization and chromosomal localization of six highly repeated DNA families in the bovine genome AN - 16953614; 3618756 AB - The genomic structure and cytogenetic position of five localized (satellite) and one dispersed highly repeated bovine DNA families were determined using Southern blotting and fluorescence in situ hybridization. Oligonucleotides were synthesized to published sequence data for all six repeats and either used directly as hybridization probes or as primers in PCR in order to obtain longer-sized probes. Results from Southern hybridization following digestion with 26 restriction enzymes revealed type A ladder patterns for all satellites, with evidence for novel subdomains demonstrated in the 1.709, 1.715 and 1.711b families. In situ hybridization localized all five satellite repeats to the centromeric regions of many or all autosomes. In addition, three of the satellites also hybridized interstitially. The dispersed bovine-Pst element hybridized intensely along all chromosomes except at autosomal centromeres. JF - Animal Biotechnology AU - Modi, W S AU - Gallagher, D S AU - Womack, JE AD - Biol. Carcinogen. Dev. Prog., Prog. Resour., Inc./DynCorp, NCI-FCRDC, Frederick, MD 21702-1201, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 143 EP - 161 VL - 4 IS - 2 SN - 1049-5398, 1049-5398 KW - Biotechnology and Bioengineering Abstracts; Genetics Abstracts; Agricultural and Environmental Biotechnology Abstracts KW - Southern blotting KW - organization KW - localization KW - fluorescence KW - genomes KW - DNA KW - W2 32340:Other peptides, proteins, amino acids KW - W 30965:Miscellaneous, Reviews KW - G 07414:GENERAL UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16953614?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Animal+Biotechnology&rft.atitle=Molecular+organization+and+chromosomal+localization+of+six+highly+repeated+DNA+families+in+the+bovine+genome&rft.au=Modi%2C+W+S%3BGallagher%2C+D+S%3BWomack%2C+JE&rft.aulast=Modi&rft.aufirst=W&rft.date=1993-01-01&rft.volume=4&rft.issue=2&rft.spage=143&rft.isbn=&rft.btitle=&rft.title=Animal+Biotechnology&rft.issn=10495398&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - Southern blotting; organization; localization; fluorescence; DNA; genomes ER - TY - JOUR T1 - A computer program for estimating individualized probabilities of breast cancer AN - 16952592; 3621240 AB - A computer program is presented for estimating the absolute risk of developing breast cancer over a specified age interval for women with combinations of five risk factors, namely age at menarche, age at first live birth, family history of breast cancer, number of previous breast biopsies, and presence of atypical hyperplasia in biopsy specimens. Statistical methods have been developed and applied to data from the Breast Cancer Detection and Demonstration Project to obtain (i) point estimates of absolute risk by combining relative risk estimates from case-control data and estimated composite incidence rates from cohort data, and (ii) confidence intervals by using implicit delta-method arguments. The program is interactive and easy to use and is therefore well suited to assist in medical counselling. For instance, women with high estimated risk might be advised to undergo a program of frequent surveillance with mammography. An executable version of IBM-compatible PCs is available from the author upon submission of a PC submission of a PC diskette formatted with MS-DOS. JF - Computers and Biomedical Research AU - Benichou, J AD - Biostat. Branch, NCI, 6130 Executive Blvd., EPN/403, Rockville, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 373 EP - 382 VL - 26 IS - 4 SN - 0010-4809, 0010-4809 KW - probability KW - risk factors KW - Risk Abstracts KW - computer programs KW - breast cancer KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16952592?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Computers+and+Biomedical+Research&rft.atitle=A+computer+program+for+estimating+individualized+probabilities+of+breast+cancer&rft.au=Benichou%2C+J&rft.aulast=Benichou&rft.aufirst=J&rft.date=1993-01-01&rft.volume=26&rft.issue=4&rft.spage=373&rft.isbn=&rft.btitle=&rft.title=Computers+and+Biomedical+Research&rft.issn=00104809&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - breast cancer; computer programs ER - TY - JOUR T1 - A comparison in chimpanzees of the immunogenicity and efficacy of live attenuated respiratory syncytial virus (RSV) temperature-sensitive mutant vaccines and vaccinia virus recombinants that express the surface glycoproteins of RSV AN - 16948819; 3614484 AB - Respiratory syncytial virus (RSV) is the most common cause of viral bronchiolitis and pneumonia in children. The present study compares the level of attenuation, genetic stability and efficacy of three conditional-lethal temperature-sensitive (ts) mutants of the RSV A2 wild-type virus, designated ts-1, ts-1-NG1, and ts-4, in seronegative chimpanzees and also compares their efficacy with that of vaccinia virus recombinants that express the surface glycoproteins of RSV. Each of the ts mutants was highly attenuated in the lower respiratory tract, but still retained the capacity to induce significant rhinorrhoea. Each of the three ts mutants underwent partial reversion to a non-ts (ts + ) phenotype during replication in a minority of the chimpanzees. The ts+ virus present in the upper respiratory tract of the chimpanzees did not spread to the lower respiratory tract and represented only a minority fraction of the virus present in the nasopharyngeal swab specimens. The ts mutants were highly immunogenic and provided resistance that effectively restricted RSV replication following virus challenge. In contrast, the vaccinia-RSV recombinants were less immunogenic. They protected the lungs of two of four chimpanzees challenged with RSV, but failed to protect the upper respiratory tract. The chimpanzee can serve as a model for the rapid evaluation of further attenuated live RSV vaccines. JF - Vaccine AU - Crowe, JE Jr AU - Collins, P L AU - London, W T AU - Chanock, R M AU - Murphy, B R AD - Resp. Viruses Sect., Lab. Infect. Dis., NIAID/NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 1395 EP - 1404 VL - 11 IS - 14 SN - 0264-410X, 0264-410X KW - Biotechnology and Bioengineering Abstracts; Medical and Pharmaceutical Biotechnology Abstracts; Virology & AIDS Abstracts; Immunology Abstracts KW - glycoproteins KW - expression KW - respiratory syncytial virus KW - vaccines KW - temperature-sensitive mutant KW - immunogenicity KW - Pan troglodytes KW - W3 33365:Vaccines (other) KW - F 06807:Active immunization KW - V 22097:Immunization: Vaccines & vaccination: Human KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16948819?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Vaccine&rft.atitle=A+comparison+in+chimpanzees+of+the+immunogenicity+and+efficacy+of+live+attenuated+respiratory+syncytial+virus+%28RSV%29+temperature-sensitive+mutant+vaccines+and+vaccinia+virus+recombinants+that+express+the+surface+glycoproteins+of+RSV&rft.au=Crowe%2C+JE+Jr%3BCollins%2C+P+L%3BLondon%2C+W+T%3BChanock%2C+R+M%3BMurphy%2C+B+R&rft.aulast=Crowe&rft.aufirst=JE&rft.date=1993-01-01&rft.volume=11&rft.issue=14&rft.spage=1395&rft.isbn=&rft.btitle=&rft.title=Vaccine&rft.issn=0264410X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - expression; glycoproteins; vaccines; temperature-sensitive mutant; immunogenicity; respiratory syncytial virus; Pan troglodytes ER - TY - JOUR T1 - Cell proliferation not associated with carcinogenesis in rodents and humans AN - 16943750; 3613786 AB - Cell proliferation has often been found to be associated with carcinogenesis in rodents and humans at different stages of the multistage carcinogenesis process. The multistage process includes initiation, promotion, and progression phases. At each phase, increasing the normal level of cell turnover of target cells may enhance carcinogenesis. However, we present evidence that normal levels of cell turnover, or increasing the rate of cell turnover at these different stages, do not necessarily lead to enhanced carcinogenesis. In normal tissues, the length of the cell cycle depends on the age of the host and varies from tissue to tissue. Tissues with normal short cell cycles, such as intestine and bone marrow, do not show a high rate of spontaneous tumors in most species. Cells with higher turnover should be more susceptible to carcinogens at the initiation stage of carcinogenesis if cell proliferation per se causes cancer and if these cells or their progeny survive. JF - Environmental Health Perspectives [ENVIRON. HEALTH PERSPECT.]. Vol. 101, no. 5 Suppl. 1993. AU - Ward, J M AU - Uno, H AU - Kurata, Y AU - Weghorst, C M AU - Jang, Ja-June AD - NCI-Frederick Cancer Res. and Dev. Cent., Fairview 201, Frederick, MD 21702 1201, USA Y1 - 1993 PY - 1993 DA - 1993 VL - 101 SN - 0091-6765, 0091-6765 KW - Toxicology Abstracts KW - cell proliferation KW - reviews KW - carcinogenesis KW - negative KW - Rodentia KW - man KW - X 24250:Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16943750?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/Toxicology+Abstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:book&rft.genre=book&rft.jtitle=&rft.atitle=&rft.au=Ward%2C+J+M%3BUno%2C+H%3BKurata%2C+Y%3BWeghorst%2C+C+M%3BJang%2C+Ja-June&rft.aulast=Ward&rft.aufirst=J&rft.date=1993-01-01&rft.volume=&rft.issue=&rft.spage=no.+5+Sul.&rft.isbn=&rft.btitle=Cell+proliferation+not+associated+with+carcinogenesis+in+rodents+and+humans&rft.title=Cell+proliferation+not+associated+with+carcinogenesis+in+rodents+and+humans&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Rodentia; cell proliferation; carcinogenesis; negative; man; reviews ER - TY - JOUR T1 - A comparison of diets of blacks and whites in three areas of the United States AN - 16939255; 3613270 AB - Dietary factors may contribute to the increased cancer risk of blacks. As a first step to explore this hypothesis, we examined food frequency data obtained by interview with 1,976 adults (881 blacks and 1,095 whites) randomly selected from three areas of the United States. The a priori hypothesis was that blacks were more likely to consume diets low in fruits and vegetables and/or high in fat, particularly saturated fat. Contrary to expectation, blacks were more frequent consumers of fruits and vegetables considered to be protective against cancer (e.g., citrus fruits, cruciferous vegetables, and vegetables rich in vitamins A and C). Intake of both total and saturated fat was slightly lower among blacks than whites. This analysis does not rule out a role for these dietary factors in the etiology of cancer but indicates that ascribing the excess cancer risk among blacks to their frequency of fruit and vegetable consumption or intake of fat per se is inadequate. This suggests that alternative dietary explanations for the racial disparity in cancer risk should be pursued in future studies. JF - Nutrition and Cancer AU - Swanson, CA AU - Gridley, G AU - Greenberg, R S AU - Schoenberg, J B AU - Swanson, G M AU - Brown, L M AU - Hayes, R AU - Silverman, D AU - Pottern, L AD - Epidemiol. and Biostat. Program, Div. Cancer Etiol., NCI, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 153 EP - 165 VL - 20 IS - 2 SN - 0163-5581, 0163-5581 KW - African Americans KW - Risk Abstracts KW - ethnic groups KW - USA KW - diets KW - cancer KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16939255?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nutrition+and+Cancer&rft.atitle=A+comparison+of+diets+of+blacks+and+whites+in+three+areas+of+the+United+States&rft.au=Swanson%2C+CA%3BGridley%2C+G%3BGreenberg%2C+R+S%3BSchoenberg%2C+J+B%3BSwanson%2C+G+M%3BBrown%2C+L+M%3BHayes%2C+R%3BSilverman%2C+D%3BPottern%2C+L&rft.aulast=Swanson&rft.aufirst=CA&rft.date=1993-01-01&rft.volume=20&rft.issue=2&rft.spage=153&rft.isbn=&rft.btitle=&rft.title=Nutrition+and+Cancer&rft.issn=01635581&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - USA; ethnic groups; diets; cancer ER - TY - JOUR T1 - Structure, absolute stereochemistry, and synthesis of conocurvone, a potent, novel HIV-inhibitory naphthoquinone trimer from a Conospermum sp AN - 16924927; 3599610 AB - Bioassay-guided fractionation provided conocurvone, a novel trimeric naphthoquinone derivation, as the active anti-HIV constituent of an extract from a Conospermum sp. The related naphthoquinone monomer teretifolione B (2) also was isolated from a Conospermum sp. extract. The absolute stereochemistry of 2 was established by X-ray crystallographic analysis of the p-bromobenzoate derivative 6. Base-catalyzed coupling of 2 equiv of teretifolione B (2) with the deoxy derivative B provided compound 1, which was identical in all respects with the natural product. While compound 2 was inactive against HIV, the natural and synthetic conocurvone (1) and the synthetic trimeric analog 4 were all active and equipotent, preventing the cytopathic effects and replication of HIV in human T-lymphoblastic cells (CEM-SS) over a concentration range of 0.02-50 mu M. JF - Journal of the American Chemical Society AU - Decosterd, LA AU - Parsons, L C AU - Gustafson, K R AU - Cardellina, JH II AU - McMahon, J B AU - Cragg, G M AU - Murata, Y AU - Pannell, L K AU - Rios Steiner, J AU - Clardy, J AU - Boyd, M R AD - Div. Cancer Treat., NCI, Build. 1052, Rm. 121, Frederick, MD 21702-1201, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 6673 EP - 6679 VL - 115 IS - 15 SN - 0002-7863, 0002-7863 KW - conocurvone KW - Conospermum KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Virology & AIDS Abstracts KW - DNA biosynthesis KW - inhibitors KW - X-ray crystallography KW - human immunodeficiency virus KW - N.M.R. KW - stereochemistry KW - synthesis KW - V 22002:AIDS: Molecular and in vitro aspects KW - A 01068:Antiviral & viricidal UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16924927?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+American+Chemical+Society&rft.atitle=Structure%2C+absolute+stereochemistry%2C+and+synthesis+of+conocurvone%2C+a+potent%2C+novel+HIV-inhibitory+naphthoquinone+trimer+from+a+Conospermum+sp&rft.au=Decosterd%2C+LA%3BParsons%2C+L+C%3BGustafson%2C+K+R%3BCardellina%2C+JH+II%3BMcMahon%2C+J+B%3BCragg%2C+G+M%3BMurata%2C+Y%3BPannell%2C+L+K%3BRios+Steiner%2C+J%3BClardy%2C+J%3BBoyd%2C+M+R&rft.aulast=Decosterd&rft.aufirst=LA&rft.date=1993-01-01&rft.volume=115&rft.issue=15&rft.spage=6673&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+American+Chemical+Society&rft.issn=00027863&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - human immunodeficiency virus; inhibitors; stereochemistry; synthesis; X-ray crystallography; N.M.R.; DNA biosynthesis ER - TY - JOUR T1 - Absence of 6-hydroxydopamine in the rat brain after treatment with stimulants and other dopaminergic agents: A mass fragmentographic study AN - 16902299; 3597043 AB - We used mass fragmentography to search for 6-OHDA in the rat frontal cortex and striatum after the administration of a number of drugs including 3,4-dihydroxyphenyl-L-alanine, methamphetamine, amphetamine, and cocaine, all of which increase synaptic dopamine. No 6-OHDA was detected after the acute systemic administration of these agents. Intraventricular administration of 6-OHDA produced measurable concentrations of 6-OHDA that were higher in the striatum than in the frontal cortex. We conclude that 6-OHDOPA can cross the blood-brain barrier and is converted to 6-OHDA in the brain; 6-OHDA is a substrate for monoamine oxidase(s) and therefore a search for its purported deaminated metabolite is warranted; and acute treatment with the above stimulants either does not lead to the formation of 6-OHDA or produces concentrations below the detection limit of the assay. JF - Journal of Neurochemistry AU - Karoum, F AU - Chrapusta, S J AU - Egan, M F AU - Wyatt, R J AD - Neuropsychiatr. Branch, Intramural Res. Program, Natl. Inst. Ment. Health, NIMH Neurosci. Cent. Saint Elizabeths, Washington, D.C. 20032, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 1369 EP - 1375 VL - 61 IS - 4 SN - 0022-3042, 0022-3042 KW - 3,4-dihydroxyphenylalanine KW - methamphetamine KW - amphetamine KW - cocaine KW - effects on KW - 6-hydroxydopamine KW - rats KW - Toxicology Abstracts; CSA Neurosciences Abstracts KW - levels KW - neostriatum KW - cortex (frontal) KW - N3 11106:Neurobiology of drug abuse KW - X 24180:Social poisons & drug abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16902299?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Neurochemistry&rft.atitle=Absence+of+6-hydroxydopamine+in+the+rat+brain+after+treatment+with+stimulants+and+other+dopaminergic+agents%3A+A+mass+fragmentographic+study&rft.au=Karoum%2C+F%3BChrapusta%2C+S+J%3BEgan%2C+M+F%3BWyatt%2C+R+J&rft.aulast=Karoum&rft.aufirst=F&rft.date=1993-01-01&rft.volume=61&rft.issue=4&rft.spage=1369&rft.isbn=&rft.btitle=&rft.title=Journal+of+Neurochemistry&rft.issn=00223042&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - cortex (frontal); neostriatum; levels ER - TY - JOUR T1 - Association of delayed conception with caffeine consumption AN - 16886980; 3801728 AB - This cross-sectional study investigated the relation between intake of caffeine-containing beverages and time to conception in a population of 1,909 married women in New Haven, Connecticut, between May 12, 1980 and March 12, 1982. Women were interviewed shortly after the first prenatal visit regarding the length of time taken to conceive the index pregnancy, consumption of caffeine during pregnancy, and other exposures occurring prior to and during pregnancy. In logistic regression analyses, intake of caffeine from coffee, tea, and caffeinated soft drinks was associated with an increased risk of a delay of conception of 1 year or more. Compared with no caffeine use, consumption of 1-150 mg/day of caffeine resulted in an odds ratio for delayed conception of 1.39 (95% confidence interval (CI) 0.90-2.13), consumption of 151-300 mg/day of caffeine was associated with an odds ratio of 1.88 (95% CI 1.13-3.11), and that of over 300 mg/day (the equivalent of approximately three cups of coffee) resulted in an odds ratio of 2.24 (95% CI 1.06-4.73), after controlling for last method of birth control used, parity, and number of cigarettes per day. Risks for coffee, tea, and colas were examined simultaneously in logistic models and were found not to improve the fit of a model that contained a variable for total caffeine intake from all sources. JF - American Journal of Epidemiology AU - Hatch, EE AU - Bracken, M B AD - Epidemiol. and Biostat. Prog., Div. Cancer Etiol., NCI, EPN 408, 6130 Executive Blvd., Rockville, MD 20852, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 1082 EP - 1092 VL - 138 IS - 12 SN - 0002-9262, 0002-9262 KW - caffeine KW - man KW - Toxicology Abstracts; Risk Abstracts KW - statistical analysis KW - USA, Connecticut, New Haven KW - fertility KW - females KW - reproduction KW - pregnancy KW - X 24120:Food, additives & contaminants KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16886980?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Epidemiology&rft.atitle=Association+of+delayed+conception+with+caffeine+consumption&rft.au=Hatch%2C+EE%3BBracken%2C+M+B&rft.aulast=Hatch&rft.aufirst=EE&rft.date=1993-01-01&rft.volume=138&rft.issue=12&rft.spage=1082&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - USA, Connecticut, New Haven; fertility; reproduction; pregnancy; statistical analysis; females; man ER - TY - JOUR T1 - A left-handed crossover involved in amidohydrolase catalysis. Crystal structure of Erwinia chrysanthemi L-asparaginase with bound L-aspartate AN - 16886452; 3577734 AB - The crystal structure of L-asparaginase from Erwinia chrysanthemi in the presence and absence of L-aspartate was determined at 1.8 angstroms resolution. Conserved residues in a left-handed crossover (a rare occurrence in protein structures) link pairs of dimers into the catalytically active tetrameric form of the enzyme. The structure of ErA containing bound aspartic acid shows that this unusual strand connectivity is an essential part of the active site architecture, responsible for releasing the product of the enzymatic hydrolysis. The orientation of the bound aspartate indicates for the first time a threonine residue as a catalytic nucleophile. JF - FEBS Letters AU - Miller, M AU - Rao, JKM AU - Wlodawer, A AU - Gribskov, M R AD - Macromol. Struct. Lab., NCI-FCRDC, ABL-Basic Res. Program, P.O. Box B, Frederick, MD 21702, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 275 EP - 279 VL - 328 IS - 3 SN - 0014-5793, 0014-5793 KW - L-asparaginase KW - L-aspartic acid KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts B: Bacteriology KW - purification KW - Erwinia chrysanthemi KW - crystal structure KW - A 01006:Enzymes & cofactors KW - J 02728:Enzymes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16886452?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FEBS+Letters&rft.atitle=A+left-handed+crossover+involved+in+amidohydrolase+catalysis.+Crystal+structure+of+Erwinia+chrysanthemi+L-asparaginase+with+bound+L-aspartate&rft.au=Miller%2C+M%3BRao%2C+JKM%3BWlodawer%2C+A%3BGribskov%2C+M+R&rft.aulast=Miller&rft.aufirst=M&rft.date=1993-01-01&rft.volume=328&rft.issue=3&rft.spage=275&rft.isbn=&rft.btitle=&rft.title=FEBS+Letters&rft.issn=00145793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Erwinia chrysanthemi; purification; crystal structure ER - TY - JOUR T1 - An immunochemical approach of identifying and characterizing protein targets of toxic reactive metabolites AN - 16873340; 3584092 JF - Chemical Research in Toxicology AU - Pohl, L R AD - Lab. Chem. Pharmacol., NHLBI, NIH, Build. 10, Room 8N 115, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 786 EP - 793 VL - 6 IS - 6 SN - 0893-228X, 0893-228X KW - targets KW - Toxicology Abstracts KW - identification KW - proteins KW - toxicants KW - methodology KW - immunochemistry KW - X 24221:Toxicity testing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16873340?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+Research+in+Toxicology&rft.atitle=An+immunochemical+approach+of+identifying+and+characterizing+protein+targets+of+toxic+reactive+metabolites&rft.au=Pohl%2C+L+R&rft.aulast=Pohl&rft.aufirst=L&rft.date=1993-01-01&rft.volume=6&rft.issue=6&rft.spage=786&rft.isbn=&rft.btitle=&rft.title=Chemical+Research+in+Toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - toxicants; identification; methodology; immunochemistry; proteins ER - TY - JOUR T1 - Biochemical and electron microscopy analysis of the endotoxin binding to microtubules in vitro AN - 16873231; 3584016 AB - The mechanisms involved in cellular activation and damage by bacterial endotoxins are not completely defined. In particular, there is little information about possible intracellular targets of endotoxins. Recently, the participation of a microtubule associated protein in endotoxin actions on macrophages has been suggested. In the present work, we have studied the effect of E. coli lipopolysaccharide on the polymerization of microtubular protein in vitro. Electrophoretic analysis of the polymerization mixtures showed that the endotoxin inhibited the polymerization when present at high concentrations. At lower concentrations, LPS selectively displaced the microtubule associated protein MAP-2 from the polymerized microtubules. Electron microscopy showed that LPS binds to microtubules of tubulin + MAPs and to microtubules of purified tubulin (without MAPs) polymerized with taxol. Gel filtration experiments confirmed the binding of LPS to tubulin, and by ligand blot assays an interaction LPS - MAP-2 was detected. The ability of LPS to interact with microtubular proteins suggests a possible participation of microtubules on the cellular effects of endotoxins. JF - Molecular and Cellular Biochemistry AU - Risco, C AU - Dominguez, JE AU - Bosch, MA AU - Carrascosa, J L AD - Struct. Biol. Sect., Lab. Math. Biol., NCI (NCI-FCRDC), Build. 538, Rm. 124, Frederick, MD 21702-1201, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 67 EP - 74 VL - 121 IS - 1 SN - 0300-8177, 0300-8177 KW - Toxicology Abstracts KW - microtubules KW - endotoxins KW - in vitro KW - binding KW - analysis KW - X 24171:Microbial UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16873231?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+Cellular+Biochemistry&rft.atitle=Biochemical+and+electron+microscopy+analysis+of+the+endotoxin+binding+to+microtubules+in+vitro&rft.au=Risco%2C+C%3BDominguez%2C+JE%3BBosch%2C+MA%3BCarrascosa%2C+J+L&rft.aulast=Risco&rft.aufirst=C&rft.date=1993-01-01&rft.volume=121&rft.issue=1&rft.spage=67&rft.isbn=&rft.btitle=&rft.title=Molecular+and+Cellular+Biochemistry&rft.issn=03008177&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - endotoxins; binding; analysis; microtubules; in vitro ER - TY - JOUR T1 - Retrotransfer of IncP plasmid R751 from Escherichia coli maxicells: Evidence for the genetic sufficiency of self-transferable plasmids for bacterial conjugation AN - 16861907; 3571042 AB - Gene transfer between organisms is a prime contributor to evolution. Bacterial conjugation is probably the most important mechanism by which genes are spread among prokaryotes and perhaps also contributes to eukaryotic evolution. Conjugation is mediated by plasmids. The mechanism of conjugation remains ill-understood despite progress in the identification, mapping and sequencing of genes required for plasmid transmission. All conjugation-specific genes (those required only for DNA transfer and establishment) identified to date map to plasmids. We found that IncP plasmids could enter and subsequently convert maxicells, which are trapped in a metabolic state that prevents de novo expression of chromosomal genes, into conjugative donors. This suggests that IncP plasmids encode not only necessary functions but indeed all functions specific to DNA transmission. Thus, like viruses, plasmids can convert non-viable cells into gene vectors. JF - Molecular Microbiology AU - Heinemann, JA AU - Ankenbauer, R G AD - NIH, NIAID, LMSF, Rocky Mountain Lab., Hamilton, MT 59840, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 57 EP - 62 VL - 10 IS - 1 SN - 0950-382X, 0950-382X KW - plasmid R751 KW - Biochemistry Abstracts 2: Nucleic Acids; Microbiology Abstracts B: Bacteriology KW - gene transfer KW - conjugation KW - Escherichia coli KW - role KW - plasmids KW - N 14673:Conjugation KW - J 02760:Plasmids UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16861907?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+Microbiology&rft.atitle=Retrotransfer+of+IncP+plasmid+R751+from+Escherichia+coli+maxicells%3A+Evidence+for+the+genetic+sufficiency+of+self-transferable+plasmids+for+bacterial+conjugation&rft.au=Heinemann%2C+JA%3BAnkenbauer%2C+R+G&rft.aulast=Heinemann&rft.aufirst=JA&rft.date=1993-01-01&rft.volume=10&rft.issue=1&rft.spage=57&rft.isbn=&rft.btitle=&rft.title=Molecular+Microbiology&rft.issn=0950382X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Escherichia coli; conjugation; gene transfer; plasmids; role ER - TY - JOUR T1 - A test for measuring growth responses of Mollicutes to serum and polyoxyethylene sorbitan AN - 16861625; 3570981 AB - A test is described that is useful for characterizing mollicutes in terms of the ability to maintain growth in medium containing 15 to 20% fetal bovine serum or in serum-free media with or without 0.04% Tween 80 (polyoxyethylene sorbitan). Representative Acholeplasma species maintained growth in serum-free medium, and about half of the strains tested grew well in Tween 80-supplemented medium. Representative Mycoplasma and Entomoplasma species did not maintain growth in either serum-free medium alone or when Tween 80 was added. Spiroplasma species and group representatives generally failed to sustain growth in serum-free medium with or without Tween 80, but at least four of the spiroplasmas tested maintained growth in serum-free medium. The representative Mesoplasma species grew in serum-free media only when Tween 80 was added, as did Mycoplasma lactucae. Although the test has obvious determinative uses for members of the class Mollicutes, it does not supplant the conventional methodology for assaying the cholesterol requirements of these organisms. JF - International Journal of Systematic Bacteriology AU - Rose, D L AU - Tully, J G AU - Bove, J M AU - Whitcomb, R F AD - Mycoplasma Sect., Frederick Cancer Res. and Dev. Cent., NIAID, Frederick, MD 21702, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 527 EP - 532 VL - 43 IS - 3 SN - 0020-7713, 0020-7713 KW - polyoxyethylene sorbitan KW - effects on KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts B: Bacteriology KW - Mollicutes KW - Acholeplasma KW - serum KW - Spiroplasma KW - Mycoplasma KW - growth KW - A 01115:Mycoplasmas KW - J 02722:Biodegradation, growth, nutrition and leaching UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16861625?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Systematic+Bacteriology&rft.atitle=A+test+for+measuring+growth+responses+of+Mollicutes+to+serum+and+polyoxyethylene+sorbitan&rft.au=Rose%2C+D+L%3BTully%2C+J+G%3BBove%2C+J+M%3BWhitcomb%2C+R+F&rft.aulast=Rose&rft.aufirst=D&rft.date=1993-01-01&rft.volume=43&rft.issue=3&rft.spage=527&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Systematic+Bacteriology&rft.issn=00207713&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Mycoplasma; Acholeplasma; Spiroplasma; Mollicutes; serum; growth ER - TY - JOUR T1 - Facilitation of cocaine kindling by glucocorticoids in rats AN - 16859239; 3566457 AB - We report that glucocorticoids significantly facilitated the development of cocaine-induced kindled seizures. These results suggest that glucocorticoids may have effects on the development of kindled seizures which are similar to those of the neuropeptide, corticotropin-releasing hormone (CRH), with which they show a close functional relationship. The results may be of interest in the light of data showing that glucocorticoids increase CRH expression in the central nucleus of the amygdala, which is an important site for the development of kindling. JF - Brain Research AU - Kling, MA AU - Smith, MA AU - Glowa, J R AU - Pluznik, D AU - Demas, J AU - DeBellis, MD AU - Gold, P W AU - Schulkin, J AD - Clin. Neuroendocrinol. Branch, NIMH, NIH Build.10, Rm. 3S-231, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 163 EP - 166 VL - 629 IS - 1 SN - 0006-8993, 0006-8993 KW - cocaine KW - glucocorticoids KW - rats KW - Toxicology Abstracts; CSA Neurosciences Abstracts KW - amygdala KW - kindling KW - potentiation KW - N3 11106:Neurobiology of drug abuse KW - X 24180:Social poisons & drug abuse KW - N3 11080:Neuroendocrinology KW - N3 11124:Mammalian neuropathology (except primates) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16859239?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+Research&rft.atitle=Facilitation+of+cocaine+kindling+by+glucocorticoids+in+rats&rft.au=Kling%2C+MA%3BSmith%2C+MA%3BGlowa%2C+J+R%3BPluznik%2C+D%3BDemas%2C+J%3BDeBellis%2C+MD%3BGold%2C+P+W%3BSchulkin%2C+J&rft.aulast=Kling&rft.aufirst=MA&rft.date=1993-01-01&rft.volume=629&rft.issue=1&rft.spage=163&rft.isbn=&rft.btitle=&rft.title=Brain+Research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - kindling; potentiation; amygdala ER - TY - JOUR T1 - Expression of the major outer membrane protein of Chlamydia trachomatis in Escherichia coli AN - 16859088; 3571093 AB - The major outer membrane protein (MOMP) of Chlamydia trachomatis was expressed in Escherichia coli. To assess whether it assembled into a conformationally correct structure at the cell surface, we characterized the recombinant MOMP (rMOMP) by Western immunoblot analysis, indirect immunofluorescence, and immunoprecipitation with monoclonal antibodies (MAbs) that recognize contiguous and conformational MOMP epitopes. Western blot analysis showed that most of the rMOMP comigrated with authentic monomer MOMP, indicating that its signal peptide was recognized and cleaved by E. coli. The rMOMP could not be detected on the cell surface of viable or formalin-killed E. coli organisms by indirect immunofluorescence staining with a MAb specific for a MOMP contiguous epitope. In contrast, the same MAb readily stained rMOMP-expressing E. coli cells that had been permeablized by methanol fixation. JF - Infection and Immunity AU - Manning, D S AU - Stewart, S J AD - Lab. Intracell. Parasit., Rocky Mountain Lab., NIAID, Hamilton, MT 59840, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 4093 EP - 4098 VL - 61 IS - 10 SN - 0019-9567, 0019-9567 KW - Microbiology Abstracts B: Bacteriology KW - expression KW - outer membranes KW - Escherichia coli KW - Chlamydia trachomatis KW - proteins KW - J 02727:Amino acids, peptides and proteins UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16859088?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Expression+of+the+major+outer+membrane+protein+of+Chlamydia+trachomatis+in+Escherichia+coli&rft.au=Manning%2C+D+S%3BStewart%2C+S+J&rft.aulast=Manning&rft.aufirst=D&rft.date=1993-01-01&rft.volume=61&rft.issue=10&rft.spage=4093&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Chlamydia trachomatis; Escherichia coli; outer membranes; proteins; expression ER - TY - JOUR T1 - Revised taxonomy of the class Mollicutes: Proposed elevation of a monophyletic cluster of arthropod-associated Mollicutes to ordinal rank (Entomoplasmatales ord. nov.), with provision for familial rank to separate species with nonhelical morphology (Entomoplasmataceae fam. nov.) from helical species (Spiroplasmataceae), and emended descriptions of the order Mycoplasmatales, family Mycoplasmataceae AN - 16857949; 3570982 AB - On the basis of recent phylogenetic studies of 47 species within the class Mollicutes and recent molecular and physiologic findings that distinguish a new group of non-sterol-requiring insect and plant mollicutes from Acholeplasma species, we propose a revised taxonomy of the class Mollicutes. Order I (Mycoplasmatales) is retained as described earlier, with provision for a single family (Mycoplasmataceae) and two genera (Mycoplasma and Ureaplasma) for classification of sterol-requiring mollicutes primarily associated with vertebrates. Emended descriptions of the order and family for the above taxa are hereby included. Proposed order II (Entomoplasmatales ord. nov.) contains subtaxa for either nonhelical (Entomoplasmataceae fam. nov.) or helical (Spiroplasmataceae) mollicutes; the latter family is hereby transferred from the order Mycoplasmatales. The new order and family permit designation and classification of a monophyletic cluster of mollicute strains associated primarily with arthropods. It is proposed that nonhelical, sterol-requiring insect and plant mollicutes previously designated Mycoplasma ellychniae, Mycoplasma melaleucae, Mycoplasma somnilux, Mycoplasma luminosum, and Mycoplasma lucivorax be transferred to Entomoplasma gen. nov., family Entomoplasmataceae fam. nov., as Entomoplasma ellychniae comb. nov., Entomoplasma melaleucae comb. nov., Entomoplasma somnilux comb. nov., Entomoplasma luminosum comb. nov., and Entomoplasma lucivorax comb. nov. Furthermore, the genus Mesoplasma gen. nov. within the family Entomoplasmataceae fam. nov. is proposed for four non-sterol-requiring insect and plant mollicutes. This designation requires the transfer of Acholeplasma florum, Acholeplasma entomophilum, Acholeplasma seiffertii, and Mycoplasma lactucae to Mesoplasma florum comb. nov., Mesoplasma entomophilum comb. nov., Mesoplasma seiffertii comb. nov., and Mesoplasma lactucae comb. nov., respectively. Previously established orders Acholeplasmatales and Anaeroplasmatales within the class Mollicutes are designated orders III and IV, respectively, in the proposed revision. Classification and characteristics of lower taxa within these two orders remain as previously given. The proposal outlined here does not consider the large cluster of nonculturable, arthropod-associated, plant-pathogenic mollicutes ("mycoplasma-like organisms") recently shown to be more closely related to members of the order Acholeplasmatales. JF - International Journal of Systematic Bacteriology AU - Tully, J G AU - Bove, J M AU - Laigret, F AU - Whitcomb, R F AD - Mycoplasma Sect., Frederick Cancer Res. and Dev. Cent., NIAID, Frederick, MD 21702, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 378 EP - 385 VL - 43 IS - 2 SN - 0020-7713, 0020-7713 KW - Entomoplasma KW - Microbiology Abstracts B: Bacteriology KW - Mollicutes KW - identification KW - Acholeplasma KW - taxonomy KW - Mycoplasma KW - J 02710:Identification, taxonomy and typing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16857949?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Systematic+Bacteriology&rft.atitle=Revised+taxonomy+of+the+class+Mollicutes%3A+Proposed+elevation+of+a+monophyletic+cluster+of+arthropod-associated+Mollicutes+to+ordinal+rank+%28Entomoplasmatales+ord.+nov.%29%2C+with+provision+for+familial+rank+to+separate+species+with+nonhelical+morphology+%28Entomoplasmataceae+fam.+nov.%29+from+helical+species+%28Spiroplasmataceae%29%2C+and+emended+descriptions+of+the+order+Mycoplasmatales%2C+family+Mycoplasmataceae&rft.au=Tully%2C+J+G%3BBove%2C+J+M%3BLaigret%2C+F%3BWhitcomb%2C+R+F&rft.aulast=Tully&rft.aufirst=J&rft.date=1993-01-01&rft.volume=43&rft.issue=2&rft.spage=378&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Systematic+Bacteriology&rft.issn=00207713&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Mycoplasma; Acholeplasma; Mollicutes; identification; taxonomy ER - TY - JOUR T1 - TnphoA-mediated disruption of K54 capsular polysaccharide genes in Escherichia coli confers serum sensitivity AN - 16857583; 3573317 AB - To assess whether non-K1, group 2 capsular serotypes are important in conferring serum resistance to extraintestinal isolates of Escherichia coli, a K54 blood isolate (CP9) was evaluated as a model pathogen. Transposon mutagenesis (TnphoA) was used to generate isogenic capsule-negative mutants. CP9 was resistant to the bactericidal effects of serum, growing in 80% serum. In contrast, all of the capsule-negative mutants had an increased sensitivity to 80% normal human serum, undergoing a 2- to 3-log kill over 3 h when starting inocula of 10 super(4) to 10 super(7) CFU/ml were used. The killing of the capsule-negative strains was mediated through the alternative complement pathway and not by lysozyme or beta-lysins. The protective effect of the K54 capsule against the bactericidal activity of serum was not through inhibition of the complement cascade, nor did it appear to be through a difference in the binding of C3. JF - Infection and Immunity AU - Russo, T A AU - Moffitt, M C AU - Hammer, CH AU - Frank, M M AD - Bact. Pathog. Unit, Lab. Clin. Invest., NIAID/NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 3578 EP - 3582 VL - 61 IS - 8 SN - 0019-9567, 0019-9567 KW - polysaccharides K54 KW - Microbiology Abstracts B: Bacteriology KW - genes KW - Escherichia coli KW - capsules KW - serum KW - antibacterial activity KW - J 02730:Carbohydrates KW - J 02740:Genetics and evolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16857583?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=TnphoA-mediated+disruption+of+K54+capsular+polysaccharide+genes+in+Escherichia+coli+confers+serum+sensitivity&rft.au=Russo%2C+T+A%3BMoffitt%2C+M+C%3BHammer%2C+CH%3BFrank%2C+M+M&rft.aulast=Russo&rft.aufirst=T&rft.date=1993-01-01&rft.volume=61&rft.issue=8&rft.spage=3578&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Escherichia coli; capsules; genes; serum; antibacterial activity ER - TY - JOUR T1 - Mutagenicity of chemicals added to foods AN - 16856103; 3568438 AB - Much attention has recently been brought to the fact that many natural components of the diet are mutagenic and/or carcinogenic. Approximately 2700 distinct chemical entities, chemical mixtures, and plant extracts are allowed as direct food additives by the US F.D.A. These include chemicals found in the body, natural components of foods, and synthetic chemicals. In addition to the chemicals among these additives that are mutagenic, there are a number of mutagens that are normally present in the plant products that are consumed as part of the normal diets. The mutagenicity in Salmonella of these food additives was identified using the National Toxicology Program and US E.P.A. Gene-Tox databases. Relatively few of the chemicals deliberately added to foods have been tested for mutagenicity. Among the chemicals tested, approximately 15% were mutagenic in Salmonella. The mutagens include both organic and inorganic substances. Many of the natural plant components, such as flavonoids, hydrazides, and tannins also have been shown to be mutagenic. However, these natural components are not considered as food additives. A large proportion of the mutagenic food additives appear to act through the generation of oxygen- or free radicals. Although the relationships between mutagenicity and carcinogenicity of electrophilic chemicals has been well studied, the potential hazard of low-level increases in free-radical generating substances on tumor incidences is unknown. JF - Mutation Research AU - Zeiger, E AD - Environ. Toxicol. Program, NIEHS (A0-01), P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 53 EP - 61 VL - 290 IS - 1 SN - 0027-5107, 0027-5107 KW - aldehydes KW - additives KW - food KW - free radicals KW - man KW - mutagenicity KW - Toxicology Abstracts; Human Genome Abstracts KW - X 24120:Food, additives & contaminants UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16856103?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutation+Research&rft.atitle=Mutagenicity+of+chemicals+added+to+foods&rft.au=Zeiger%2C+E&rft.aulast=Zeiger&rft.aufirst=E&rft.date=1993-01-01&rft.volume=290&rft.issue=1&rft.spage=53&rft.isbn=&rft.btitle=&rft.title=Mutation+Research&rft.issn=00275107&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - food; additives; free radicals; mutagenicity; man ER - TY - JOUR T1 - Estimating historical exposure to silica among mine and pottery workers in the People's Republic of China AN - 16851661; 3569839 AB - A quantitative retrospective exposure assessment method was developed for use in a nested case-control study of lung cancer among mine and pottery workers exposed to silica dust in the People's Republic of China. Exposure assessment was carried out in 20 mines (10 tungsten, 6 iron/copper, and 4 tin) and nine pottery factories. A job title dictionary was developed and used in both the collection of historical exposure information and work histories of 1,668 (316 cases and 1,352 controls) study subjects. Several data abstraction forms were developed to collect historical and current exposure information and employees' work histories, starting in 1950. A retrospective exposure matrix was developed on the basis of facility/job title/calendar year combinations using available historical exposure information and current exposure profiles. Information on the amount of respirable, thoracic, and free silica content in total dust was used in estimating exposure to silica. JF - American Journal of Industrial Medicine AU - Dosemeci, M AU - Chen, J-Q AU - Hearl, F AU - Chen, R-G AU - McCawley, M AU - Wu, Z AU - McLaughlin, J K AU - Peng, K-L AU - Chen, A-L AD - NCI/NIH, 6130 Executive Blvd., Room 418, Rockville, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 55 EP - 66 VL - 24 IS - 1 SN - 0271-3586, 0271-3586 KW - silica KW - lung cancer KW - respiratory diseases KW - silicon dioxide KW - respiratory tract diseases KW - Toxicology Abstracts; Health & Safety Science Abstracts KW - mining KW - historical account KW - occupational exposure KW - lung KW - dust KW - China, People's Rep. KW - cancer KW - H SI2.8.7:DUST KW - X 24152:Chronic exposure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16851661?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Industrial+Medicine&rft.atitle=Estimating+historical+exposure+to+silica+among+mine+and+pottery+workers+in+the+People%27s+Republic+of+China&rft.au=Dosemeci%2C+M%3BChen%2C+J-Q%3BHearl%2C+F%3BChen%2C+R-G%3BMcCawley%2C+M%3BWu%2C+Z%3BMcLaughlin%2C+J+K%3BPeng%2C+K-L%3BChen%2C+A-L&rft.aulast=Dosemeci&rft.aufirst=M&rft.date=1993-01-01&rft.volume=24&rft.issue=1&rft.spage=55&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Industrial+Medicine&rft.issn=02713586&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - China, People's Rep.; silica; dust; occupational exposure; mining; historical account; lung cancer; respiratory diseases; lung; cancer; respiratory tract diseases ER - TY - JOUR T1 - Dose-response relationships for the induction of P450 2B by 1,4-bis[2-(3,5-dichloropyridyloxy)] benzene (TCPOBOP) in rat and cultured rat hepatocytes AN - 16846895; 3567696 AB - The dose-response relationships for hepatic CYP2B induction by 1,4-bis[2-(3,5-dichloropyridyloxy)] benzene (TCPOBOP) were examined in the male F344/NCr rat. TCPOBOP, administered for 14 days at 0-1000 ppm in the diet, caused concentration-dependent induction of hepatic CYP2B1 protein and RNA, and of CYP2B-mediated catalytic activities (benzyloxy- and pentoxyresorufin O-dealkylation, and testosterone 16 beta -hydroxylation). ED sub(50) values for CYP2B induction were greater than or equal to 300 ppm dietary TCPOBOP. The maximal inductions observed were 66-88% of those resulting from exposure of the rats to 500 ppm dietary phenobarbital. The EC sub(50) values for hepatic CYP2B induction were 1.5-3.0 mu M (based on serum TCPOBOP) and 15-20 mu mol/kg liver. The maximal inductions of isozymes of the CYP3A subfamily, of microsomal epoxide hydrolase, and of glutathione S-transferases Ya/Yc and Yb sub(1)/Yb sub(2) in rats exposed to TCPOBOP were 58-74% of those resulting from exposure of the rats to 500 ppm dietary phenobarbital. JF - Xenobiotica AU - Nims, R W AU - Sinclair, PR AU - Sinclair, J F AU - Dragnev, KH AU - Jones, C R AU - Mellini, D W AU - Thomas, P E AU - Lubet, R A AD - Build. 538, Room 205E, NCI-Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702-1201, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 1411 EP - 1426 VL - 23 IS - 12 SN - 0049-8254, 0049-8254 KW - 1,4-bis [2-(3,5-dichloropyridyloxy)] benzene KW - cytochrome P450 2B KW - dose-response relationship KW - rats KW - Toxicology Abstracts KW - induction KW - hepatocytes KW - X 24240:Miscellaneous UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16846895?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=unknown&rft.jtitle=TDR+-+The+Drama+Review&rft.atitle=Books%3A+%22Spectacular+Suffering%3A+Theatre%2C+Fascism%2C+and+the+Holocaust%22%3B+%22Staging+the+Holocaust%3A+The+Shoah+in+Drama+and+Performance%22&rft.au=Mazer%2C+Sharon&rft.aulast=Mazer&rft.aufirst=Sharon&rft.date=2000-01-01&rft.volume=44&rft.issue=4&rft.spage=174&rft.isbn=&rft.btitle=&rft.title=TDR+-+The+Drama+Review&rft.issn=10542043&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - induction; hepatocytes ER - TY - JOUR T1 - Estrogen receptor status and dietary intakes in breast cancer patients AN - 16842492; 3782062 AB - We used data from a study of racial differences in cancer patient survival to examine the association between estrogen receptor status and the intake of nutrients and food groups among 689 black and white women, ages 20-79, with breast cancer newly diagnosed in 1985 and 1986. We reviewed medical records and collected interview data, including a 34-item food frequency questionnaire. Consistent with published reports, we found positive estrogen receptor status to be positively associated with age and inversely associated with parity and oral contraceptive use. Whites were more likely than blacks to have estrogen receptor-positive tumors. We examined eight nutrients and six food groups in multivariate analyses for association with estrogen receptor status. After adjusting for age, race, usual body mass index, and parity, a high percent of calories from fat was associated with estrogen receptor-positive cancer, and a high percentage of calories from carbohydrates was associated with estrogen receptor-negative breast cancer. These findings indicate that women with breast cancer who are on diets with a high percentage of calories from fat may be more likely to develop estrogen receptor-positive cancers. JF - Epidemiology AU - Harlan, L C AU - Coates, R J AU - Block, G AU - Greenberg, R S AU - Ershow, A AU - Forman, M AU - Austin, D F AU - Chen, V AU - Heymsfield, S B AD - Div. Cancer Prev. and Control, NCI, 9000 Rockville Pike, EPN 313, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 25 EP - 31 VL - 4 IS - 1 SN - 1044-3983, 1044-3983 KW - estrogens KW - estrogen receptors KW - dietary intake KW - breast KW - fat load KW - man KW - Toxicology Abstracts; Health & Safety Science Abstracts KW - diets KW - females KW - age KW - ethnic groups KW - nutrients KW - breast cancer KW - cancer KW - X 24120:Food, additives & contaminants KW - H SM10.21:CANCER UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16842492?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Epidemiology&rft.atitle=Estrogen+receptor+status+and+dietary+intakes+in+breast+cancer+patients&rft.au=Harlan%2C+L+C%3BCoates%2C+R+J%3BBlock%2C+G%3BGreenberg%2C+R+S%3BErshow%2C+A%3BForman%2C+M%3BAustin%2C+D+F%3BChen%2C+V%3BHeymsfield%2C+S+B&rft.aulast=Harlan&rft.aufirst=L&rft.date=1993-01-01&rft.volume=4&rft.issue=1&rft.spage=25&rft.isbn=&rft.btitle=&rft.title=Epidemiology&rft.issn=10443983&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - breast cancer; diets; nutrients; age; ethnic groups; cancer; females; dietary intake; breast; fat load; man ER - TY - JOUR T1 - A regulatory apparatus with DNA looping AN - 16838419; 3775980 AB - In this brief exposition, we will summarize new and fascinating aspects of negative control of transcription initiation using the galactose (gal) operon of Escherichia coli. JF - Indian journal of biochemistry and biophysics. New Delhi AU - Adhya, S AD - Lab. Mol. Biol., NCI/NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 247 EP - 251 VL - 30 IS - 5 SN - 0301-1208, 0301-1208 KW - galactose KW - Microbiology Abstracts B: Bacteriology; Biochemistry Abstracts 2: Nucleic Acids KW - reviews KW - gal operon KW - transcription initiation KW - gene regulation KW - Escherichia coli KW - J 02725:DNA KW - N 14100:Reviews KW - N 14662:Gene regulation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16838419?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Indian+journal+of+biochemistry+and+biophysics.+New+Delhi&rft.atitle=A+regulatory+apparatus+with+DNA+looping&rft.au=Adhya%2C+S&rft.aulast=Adhya&rft.aufirst=S&rft.date=1993-01-01&rft.volume=30&rft.issue=5&rft.spage=247&rft.isbn=&rft.btitle=&rft.title=Indian+journal+of+biochemistry+and+biophysics.+New+Delhi&rft.issn=03011208&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Escherichia coli; gene regulation; transcription initiation; gal operon; reviews ER - TY - JOUR T1 - Applications of computers to toxicological research AN - 16838316; 3561454 JF - Chemical Research in Toxicology AU - Wang, Shaomeng AU - Milne, GWA AD - Lab. Med. Chem., NCI/NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 748 EP - 753 VL - 6 IS - 6 SN - 0893-228X, 0893-228X KW - Toxicology Abstracts KW - toxicity testing KW - computers KW - reviews KW - X 24221:Toxicity testing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16838316?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+Research+in+Toxicology&rft.atitle=Applications+of+computers+to+toxicological+research&rft.au=Wang%2C+Shaomeng%3BMilne%2C+GWA&rft.aulast=Wang&rft.aufirst=Shaomeng&rft.date=1993-01-01&rft.volume=6&rft.issue=6&rft.spage=748&rft.isbn=&rft.btitle=&rft.title=Chemical+Research+in+Toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - toxicity testing; computers; reviews ER - TY - JOUR T1 - The taxol supply crisis. New NCI policies for handling the large-scale production of novel natural product anticancer and anti-HIV agents AN - 16838218; 3559758 AB - Over the past 30 years, the National Cancer Institute has been involved in the preclinical and/or clinical evaluation of the majority of those agents approved for the treatment of cancer. Many of the new agents under consideration in the NCI program are either natural products of derivatives of natural product leads, and of critical importance to their development is the issue of drug supply. In responding to the drug supply crisis which emerged with the demonstration of the clinical efficacy of taxol, the NCI has identified several important lessons for those interested in natural product drug discovery and development. As a result, the NCI has developed plans to avert similar supply crises in the future by initiating exploratory research projects for large-scale production of promising agents at the earliest possible point following the demonstration of confirmed antitumor activity. These plans, together with a review of the development of taxol, are presented in this paper. JF - Journal of Natural Products AU - Cragg, G M AU - Schepartz, SA AU - Suffness, M AU - Grever, M R AD - Dev. Ther. Prog., Div. Cancer Treatment, NCI/NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 1657 EP - 1668 VL - 56 IS - 10 SN - 0163-3864, 0163-3864 KW - taxol KW - Biotechnology and Bioengineering Abstracts; Medical and Pharmaceutical Biotechnology Abstracts KW - antiviral agents KW - human immunodeficiency virus KW - research programs KW - production KW - cancer KW - antitumor agents KW - W3 33370:Antibiotics KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16838218?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Natural+Products&rft.atitle=The+taxol+supply+crisis.+New+NCI+policies+for+handling+the+large-scale+production+of+novel+natural+product+anticancer+and+anti-HIV+agents&rft.au=Cragg%2C+G+M%3BSchepartz%2C+SA%3BSuffness%2C+M%3BGrever%2C+M+R&rft.aulast=Cragg&rft.aufirst=G&rft.date=1993-01-01&rft.volume=56&rft.issue=10&rft.spage=1657&rft.isbn=&rft.btitle=&rft.title=Journal+of+Natural+Products&rft.issn=01633864&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - antiviral agents; research programs; production; antitumor agents; cancer; human immunodeficiency virus ER - TY - JOUR T1 - Metabolism of the food-derived mutagen/carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) in nonhuman primates AN - 16836700; 3563489 AB - Metabolism of the food-derived heterocyclic amine mutagen/carcinogen 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) was examined in cynomolgus monkeys. [ super(3)H]PhIP (50 mu mol/kg, p.o.) was extensively metabolized, with only 1% of the dose excreted into the urine as parent compound. Four metabolites were isolated by HPLC and identified: PhIP-4'-O-glucuronide, PhIP-4'-sulfate, 4'-hydroxy-PhIP and a glucuronide conjugate of N-hydroxy-PhIP. All four metabolites were detected in urine, bile and plasma of monkeys. 4'-Hydroxy-PhIP and PhIP were found in feces. The major PhIP metabolite in urine, bile and plasma was PhIP-4'-sulfate. The presence of the glucuronide conjugate of N-hydroxy-PhIP in urine, bile and plasma, and the presence of PhIP-DNA adducts in white blood cells indicate that PhIP undergoes metabolic activation via N-hydroxylation in cynomolgus monkeys. The results suggest that PhIP is activated in vivo to genotoxic metabolites in nonhuman primates and thus is a potential carcinogen in this species. JF - Carcinogenesis AU - Snyderwine, E G AU - Buonarati, M H AU - Felton, J S AU - Turteltaub, K W AD - Lab. Exp. Carcinogen., Div. Cancer Etiol., NCI/NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 2517 EP - 2522 VL - 14 IS - 12 SN - 0143-3343, 0143-3343 KW - 2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine KW - Toxicology Abstracts KW - Macaca fascicularis KW - metabolism KW - food KW - derivatives KW - X 24120:Food, additives & contaminants UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16836700?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Metabolism+of+the+food-derived+mutagen%2Fcarcinogen+2-amino-1-methyl-6-phenylimidazo%5B4%2C5-b%5Dpyridine+%28PhIP%29+in+nonhuman+primates&rft.au=Snyderwine%2C+E+G%3BBuonarati%2C+M+H%3BFelton%2C+J+S%3BTurteltaub%2C+K+W&rft.aulast=Snyderwine&rft.aufirst=E&rft.date=1993-01-01&rft.volume=14&rft.issue=12&rft.spage=2517&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433343&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Macaca fascicularis; food; derivatives; metabolism ER - TY - JOUR T1 - Excretion of food-derived heterocyclic amine carcinogens into breast milk of lactating rats and formation of DNA adducts in the newborn AN - 16836240; 3561695 AB - The distribution, DNA adduction and excretion into breast milk of 2-amino-3-methylimidazo[4,5-f]quinoline (IQ), 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) were examined in lactating female F344 rats with 5 day old pups. Six hours after a single dose (10 mg/kg, p.o.) of radiolabeled IQ, MeIQx or PhIP to lactating dams, radioactivity in the dams was highest in the liver and kidney followed, in descending order, by the mammary gland, omental fact and brain. By 24 h after carcinogen administration, all tissues of the dams showed significantly reduced levels of radioactivity except for omental fat which changed only marginally from 6 to 24 h. super(32)P-Postlabeling analysis showed that the level of DNA adducts in mammary gland 6 h after dosing was 2.2, 0.7 and 0.2 adducts/10 super(7) nucleotides for PhIP, IQ and MeIQx respectively. In contrast, in hepatic DNA, the levels of IQ-DNA adducts (5.5 adducts /10 super(7) nucleotides) were 11-fold higher than those of PhIP or MeIQx. The stomach contents, liver, kidney and urine of pups pursed by dams given radiolabeled IQ, MeIQx or PhIP were radioactive, indicating that these carcinogens (and/or metabolites) were excreted into breast milk and absorbed by the pups. After a 6 h suckling period, the amount of PhIP-derived radioactivity in the stomach contents of the pups was similar to 10-fold higher than that seen with IQ or MeIQx. Urine from pups from the three groups was mutagenic in the Ames assay with Salmonella TA98 in the presence of an S9 activating system. IQ-, MeIQx- and PhIP-DNA adducts, at levels in the range of 0.25-0.46 adducts per 10 super(8) nucleotides, were detected in the livers of pups using the super(32)P-postlabeling method under intensification conditions. The results from this study indicate that breast milk is a route of exposure of the newborn to heterocyclic amines. The presence of DNA adducts in the tissues of pups further suggests that this route of exposure may have a carcinogenic consequence to the newborn. JF - Carcinogenesis AU - Ghoshal, A AU - Snyderwine, E G AD - Lab. Exp. Carcinog., NCI/NIH, Bethesda, MD 20892-0037, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 2199 EP - 2203 VL - 14 IS - 11 SN - 0143-3343, 0143-3343 KW - 2-amino-3-methylimidazo(4,5-f)quinoline KW - 2-amino-3,8-dimethylimidazo(4,5-f)quinoxaline KW - 2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine KW - rats KW - Toxicology Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - lactation KW - adducts KW - DNA KW - excretion KW - breast milk KW - X 24120:Food, additives & contaminants KW - N 14630:Chemical reactions & interactions, including effects of radiation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16836240?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Excretion+of+food-derived+heterocyclic+amine+carcinogens+into+breast+milk+of+lactating+rats+and+formation+of+DNA+adducts+in+the+newborn&rft.au=Ghoshal%2C+A%3BSnyderwine%2C+E+G&rft.aulast=Ghoshal&rft.aufirst=A&rft.date=1993-01-01&rft.volume=14&rft.issue=11&rft.spage=2199&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433343&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - DNA; adducts; excretion; breast milk; lactation ER - TY - JOUR T1 - Epidemic cholera in the Amazon: The challenge of preventing death AN - 16829468; 3562767 AB - Epidemic cholera struck Peru in January 1991, and spread rapidly. The national cholera case-fatality rate (CFR) was less than 1% in the first six months of the epidemic, but in some rural areas, the CFR exceeded 10%. We investigated cholera mortality in the rural Amazon region, an area with a CFR of 6.3%. We conducted a case-control study, comparing 29 decedents with 61 survivors of recent cholera-like diarrheal illness in 12 villages with a combined CFR of 13.5%. Of 29 decedents, 28 (96%) died in the village or en route to a health facility. Death occurred within 36 hours of illness onset for 83% of the decedents. In 11 (92%) villages, the first or second recognized case was fatal. Death was associated with receiving treatment only at home (odds ratio indeterminate; 95% confidence interval 3.5, indeterminate). Treatment with oral rehydration salts (ORS) was not protective against death for patients who received treatment only at home. Treatment with homemade sugar-salt solution (SSS) was also not protective; fewer than one-third of respondents knew the correct SSS recipe. Most decedents experienced multiple barriers to health care. Cholera victims died rapidly and early in village outbreaks, and few patients had access to health care. Provision of threatened villages with ORS supplies and education in their use before cholera strikes is essential to reducing cholera mortality in this region. JF - AM. J. TROP. MED. HYGIENE AU - Quick, R E AU - Vargas, R AU - Moreno, D AU - Mujica, O AU - Beingolea, L AU - Palacios, A M AU - Seminario, L AU - Tauxe, R V AD - Enteric Dis. Branch, Mailstop C09, Div. Bact. and Mycotic Dis., NCI/CDC, Atlanta, GA 30333, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 597 EP - 602 VL - 48 IS - 5 KW - Microbiology Abstracts B: Bacteriology KW - cholera KW - Vibrio cholerae KW - treatment KW - epidemics KW - Peru KW - man KW - J 02846:Gastrointestinal tract UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16829468?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AM.+J.+TROP.+MED.+HYGIENE&rft.atitle=Epidemic+cholera+in+the+Amazon%3A+The+challenge+of+preventing+death&rft.au=Quick%2C+R+E%3BVargas%2C+R%3BMoreno%2C+D%3BMujica%2C+O%3BBeingolea%2C+L%3BPalacios%2C+A+M%3BSeminario%2C+L%3BTauxe%2C+R+V&rft.aulast=Quick&rft.aufirst=R&rft.date=1993-01-01&rft.volume=48&rft.issue=5&rft.spage=597&rft.isbn=&rft.btitle=&rft.title=AM.+J.+TROP.+MED.+HYGIENE&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Vibrio cholerae; Peru; epidemics; cholera; treatment; man ER - TY - JOUR T1 - Sexual intercourse during pregnancy and preterm delivery: Effects of vaginal microorganisms AN - 16823220; 3559272 AB - Our aim was to investigate the influence of vaginal colonization with specific microorganisms on the relationship between sexual intercourse during pregnancy and preterm delivery. As part of a multicenter, prospective study interviews and physical examinations were conducted with and genital cultures were obtained from women seeking prenatal care from 23 to 26 weeks' gestation. At 31 to 36 weeks interviews were conducted with a randomly selected sample of these patients. Frequent intercourse (defined a priori once per week or more) at 23 to 26 weeks was associated with a significantly reduced risk of subsequent preterm delivery in women without Trichomonas vaginalis, Mycoplasma hominis, or bacterial vaginosis, possibly because of the relative health and lack of complications in the pregnancies of those women engaging in sexual intercourse. Frequent intercourse was not significantly associated with preterm delivery in women with T. vaginalis, M. hominis, or bacterial vaginosis. Neither T. vaginalis, M. hominis, nor bacterial vaginosis was associated with preterm delivery among women with infrequent intercourse at 23 to 26 weeks. However, T. vaginalis and M. hominis were risk factors for preterm delivery among those with frequent intercourse. Frequent sexual intercourse by itself is not associated with an increased risk of preterm birth. However, women who are colonized with specific microorganisms and who engage in frequent intercourse are at increased risk of preterm delivery. JF - AM. J. OBSTET. GYNECOL. AU - Read, J S AU - Klebanoff, MA AD - DESPR-NICHD-NIH, 6100 Executive Blvd., Rm. 7B03, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 514 EP - 519 VL - 168 IS - 2 SN - 0002-9378, 0002-9378 KW - delivery KW - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology KW - Trichomonas vaginalis KW - Mycoplasma hominis KW - colonization KW - sexual intercourse KW - pregnancy KW - premature KW - man KW - K 03090:Protozoa: human KW - J 02847:Genitourinary tract UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16823220?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AM.+J.+OBSTET.+GYNECOL.&rft.atitle=Sexual+intercourse+during+pregnancy+and+preterm+delivery%3A+Effects+of+vaginal+microorganisms&rft.au=Read%2C+J+S%3BKlebanoff%2C+MA&rft.aulast=Read&rft.aufirst=J&rft.date=1993-01-01&rft.volume=168&rft.issue=2&rft.spage=514&rft.isbn=&rft.btitle=&rft.title=AM.+J.+OBSTET.+GYNECOL.&rft.issn=00029378&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Trichomonas vaginalis; Mycoplasma hominis; man; pregnancy; sexual intercourse; premature; colonization ER - TY - JOUR T1 - A chemical screening strategy for the dereplication and prioritization of HIV-inhibitory aqueous natural products extracts AN - 16813518; 3553605 AB - A relatively high percentage (ca. 15%) of aqueous extracts from terrestrial plants, cyanobacteria, and marine invertebrates and algae has exhibited activity in the National Cancer Institute's primary AIDS-antiviral screen. By removal of anionic polysaccharides in a first stage of dereplication, we have eliminated from further consideration a considerable number of these extracts. However, a still substantial proportion of the active extracts remained, from which we wished to select and prioritize a small percentage for our detailed bioassay-directed fractionation studies. Therefore, a chemical screening protocol, utilizing various solid-phase extraction cartridges, has been developed for a second-stage dereplication and to assist in prioritization of these extracts for our further investigations. JF - Journal of Natural Products AU - Cardellina, JH II AU - Munro, MHG AU - Fuller, R W AU - Manfredi, K P AU - McKee, T C AU - Tischler, M AU - Bokesch, H R AU - Gustafson, K R AU - Beutler, JA AU - Boyd, M R AD - NCI, Build. 1052, Rm. 121, Frederick, MD 21702-1201, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 1123 EP - 1129 VL - 56 IS - 7 SN - 0163-3864, 0163-3864 KW - Biotechnology and Bioengineering Abstracts; ASFA Marine Biotechnology Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology; Medical and Pharmaceutical Biotechnology Abstracts; Virology & AIDS Abstracts KW - screening KW - antiviral agents KW - human immunodeficiency virus KW - inhibition KW - plants KW - Cyanophyta KW - marine organisms KW - V 22002:AIDS: Molecular and in vitro aspects KW - W3 33370:Antibiotics KW - A 01068:Antiviral & viricidal KW - Q4 27380:Pharmaceuticals KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16813518?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Natural+Products&rft.atitle=A+chemical+screening+strategy+for+the+dereplication+and+prioritization+of+HIV-inhibitory+aqueous+natural+products+extracts&rft.au=Cardellina%2C+JH+II%3BMunro%2C+MHG%3BFuller%2C+R+W%3BManfredi%2C+K+P%3BMcKee%2C+T+C%3BTischler%2C+M%3BBokesch%2C+H+R%3BGustafson%2C+K+R%3BBeutler%2C+JA%3BBoyd%2C+M+R&rft.aulast=Cardellina&rft.aufirst=JH&rft.date=1993-01-01&rft.volume=56&rft.issue=7&rft.spage=1123&rft.isbn=&rft.btitle=&rft.title=Journal+of+Natural+Products&rft.issn=01633864&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - screening; antiviral agents; inhibition; plants; marine organisms; human immunodeficiency virus; Cyanophyta ER - TY - JOUR T1 - Birth weight and perinatal mortality: The effect of maternal smoking AN - 16811690; 3549033 AB - Infants born to mothers who smoke are a few hundred grams smaller, on average, than the infants of nonsmokers. This effect on fetal growth is regarded as evidence of the reproductive toxicity of cigarette smoking. In this paper, data from nearly 260,000 births in the state of Missouri (1980-1984) were analyzed using a method based on adjustment to relative birth weight. Two additional effects of smoking are demonstrated with this analysis; i.e., smokers are at higher risk of delivering very small preterm infants, and their infants have higher perinatal mortality at every relative birth weight. The latter is not apparent on an absolute birth weight scale and thus is not generally recognized. A supplementary analysis of births at high altitude is carried out to suggest that effects on fetal growth can occur independently of effects on mortality. JF - American Journal of Epidemiology AU - Wilcox, A J AD - Epidemiol. Branch, NIEHS, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 1098 EP - 1104 VL - 137 IS - 10 SN - 0002-9262, 0002-9262 KW - Toxicology Abstracts KW - smoking KW - pregnancy KW - mortality KW - neonates KW - birth weight KW - man KW - X 24180:Social poisons & drug abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16811690?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Epidemiology&rft.atitle=Birth+weight+and+perinatal+mortality%3A+The+effect+of+maternal+smoking&rft.au=Wilcox%2C+A+J&rft.aulast=Wilcox&rft.aufirst=A&rft.date=1993-01-01&rft.volume=137&rft.issue=10&rft.spage=1098&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - smoking; birth weight; neonates; mortality; man; pregnancy ER - TY - JOUR T1 - Variation in the size of the ospA-containing linear plasmid, but not the linear chromosome, among the three Borrelia species associated with Lyme disease AN - 16802458; 3551144 AB - The aetiological agents of Lyme disease form a phylogenetically heterogeneous group, composed of three species, Borrelia burgdorferi, Borrelia garinii, and group VS461. We have compared the sizes of the linear plasmid that carries the genes encoding the major outer-surface proteins OspA and OspB as well as the size and structure of the chromosome among the Lyme disease spirochaetes. We have found differences in the sizes of the ospA-containing plasmids, but not the linear chromosomes among the three species. The ospA-containing plasmid size of 50 kb in B. burgdorferi isolates is significantly smaller than the size of 55 kb in B. garinii isolates and 56 kb in group VS461 isolates. The chromosome was found to be linear in all three Borrelia species, but not significantly different in size. JF - Microbiology AU - Samuels, D S AU - Marconi, R T AU - Garon, C F AD - Lab. Vectors and Pathogens, Rocky Mountain Lab., NIAID, Hamilton, MT 59840, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 2445 EP - 2449 VL - 139 IS - 10 SN - 0022-1287, 0022-1287 KW - ospA gene KW - Genetics Abstracts; Microbiology Abstracts B: Bacteriology KW - genes KW - variation KW - size KW - plasmids KW - Borrelia KW - Lyme disease KW - J 02760:Plasmids KW - G 07320:Bacterial genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16802458?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Microbiology&rft.atitle=Variation+in+the+size+of+the+ospA-containing+linear+plasmid%2C+but+not+the+linear+chromosome%2C+among+the+three+Borrelia+species+associated+with+Lyme+disease&rft.au=Samuels%2C+D+S%3BMarconi%2C+R+T%3BGaron%2C+C+F&rft.aulast=Samuels&rft.aufirst=D&rft.date=1993-01-01&rft.volume=139&rft.issue=10&rft.spage=2445&rft.isbn=&rft.btitle=&rft.title=Microbiology&rft.issn=00221287&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Borrelia; plasmids; size; variation; Lyme disease; genes ER - TY - JOUR T1 - Generation of free radicals from model lipid hydroperoxides and H sub(2)O sub(2) by Co(II) in the presence of cysteinyl and histidyl chelators AN - 16794012; 3541974 AB - Electron spin resonance spin trapping was utilized to investigate the generation of free radicals from cumene hydroperoxide (cumene-OOH), tert-butyl hydroperoxide (tert-butyl-OOH), and H sub(2)O sub(2) at pH 7.2 by Co(II) in the presence of cysteinyl and histidyl chelating agents. The spin trap used was 5,5-dimethyl-1-pyrroline N-oxide. Incubation of Co(II) with cumene-OOH or tert-butyl-OOH did not generate any detectable amounts of free radicals. However, in the presence of glutathione, cysteine, penicillamine, or N-acetylcysteine, Co(II) generated cumene-OOH-derived carbon-centered radicals, cumene alkoxyl radicals, and hydroxyl ( super( multiplied by )OH) radicals. Oxidized glutathione and cystine used instead of reduced glutathione or cysteine did not generate any free radical, indicating an important role of the -SH group in radical generation. While the addition of diethylenetriaminepentaacetic acid (DTPA) prevented radical generation, deferoxamine had only a slightly inhibitory effect. JF - Chemical Research in Toxicology AU - Shi, Xianglin AU - Dalal, N S AU - Kasprzak, K S AD - NCI, Build. 538, Room 205, Frederick, MD 21702, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 277 EP - 283 VL - 6 IS - 3 SN - 0893-228X, 0893-228X KW - hydroperoxides KW - cobalt (II) KW - hydrogen peroxide KW - generation KW - Toxicology Abstracts KW - lipids KW - metals KW - free radicals KW - X 24165:Biochemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16794012?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+Research+in+Toxicology&rft.atitle=Generation+of+free+radicals+from+model+lipid+hydroperoxides+and+H+sub%282%29O+sub%282%29+by+Co%28II%29+in+the+presence+of+cysteinyl+and+histidyl+chelators&rft.au=Shi%2C+Xianglin%3BDalal%2C+N+S%3BKasprzak%2C+K+S&rft.aulast=Shi&rft.aufirst=Xianglin&rft.date=1993-01-01&rft.volume=6&rft.issue=3&rft.spage=277&rft.isbn=&rft.btitle=&rft.title=Chemical+Research+in+Toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - lipids; free radicals; metals ER - TY - JOUR T1 - Interaction of group B streptococcal opacity variants with the host defense system AN - 16793905; 3547870 AB - Group B streptococci (GBS) demonstrate high-frequency phase variation of colony opacity. Colony opacity is a function of chain length, with opaque colonies consisting of GBS that form longer chains. Because opaque variants do not grow on standard streptococcal media, the role of opacity variation in GBS infection has not been studied. We have isolated stable variants from type III GBS that are either transparent (variants 1.2 and 1.3) or opaque (variants 1.1 and 1.5). In this study, we evaluated the interactions of these variants with different components of the host immune system both in vitro and in vivo. Opaque GBS were less immunogenic than transparent GBS. Opaque GBS were more susceptible to killing by polymorphonuclear neutrophils (PMNs) and could induce a chemiluminescent response of PMNs in the absence of antibody (Ab) or complement. Transparent GBS did not induce neutrophil chemiluminescence in the absence of Ab and complement. However, in the presence of Ab and complement, transparent GBS induced a stronger chemiluminescent response than did opaque GBS. Scanning electron micrographs of PMNs and GBS demonstrated differences in the attachment and engulfment of the different variants by the PMNs as well as different effects of the GBS on the PMNs themselves. Interactions with complement were affected by GBS opacity as well, with opaque variant 1.1 initiating complement activation in the absence of any Ab. The virulence of the GBS opacity variants was studied in vivo by inoculation of graded numbers of GBS into newborn mice. Transparent variants 1.2 and 1.3 were most virulent, with variant 1.1 intermediate and variant 1.5 minimally virulent. However, in mixed infections, variant 1.5 greatly enhanced the virulence of small numbers of transparent GBS. These results indicate that the opacity status of GBS can influence the interaction between the GBS and the host immune system. JF - Infection and Immunity AU - Pincus, SH AU - Cole, R L AU - Kamanga-Sollo, E AU - Fischer, SH AD - Lab. Microb. Struct. and Funct., Rocky Mountain Lab., NIAID, Hamilton, MT 59840, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 3761 EP - 3768 VL - 61 IS - 9 SN - 0019-9567, 0019-9567 KW - opaque KW - group B KW - mice KW - Immunology Abstracts; Microbiology Abstracts B: Bacteriology KW - immunogenicity KW - animal models KW - host-pathogen interactions KW - colonies KW - Streptococcus agalactiae KW - virulence KW - immune response KW - J 02833:Immune response and immune mechanisms KW - F 06008:Bacteria UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16793905?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Interaction+of+group+B+streptococcal+opacity+variants+with+the+host+defense+system&rft.au=Pincus%2C+SH%3BCole%2C+R+L%3BKamanga-Sollo%2C+E%3BFischer%2C+SH&rft.aulast=Pincus&rft.aufirst=SH&rft.date=1993-01-01&rft.volume=61&rft.issue=9&rft.spage=3761&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Streptococcus agalactiae; colonies; host-pathogen interactions; immunogenicity; immune response; virulence; animal models ER - TY - JOUR T1 - Enhancement by L-histidine of nickel (II)-induced DNA-protein cross-linking and oxidative DNA base damage in the rat kidney AN - 16792231; 3541996 AB - Formation of DNA-protein cross-links and oxidatively damaged DNA bases was investigated with the use of alkaline elution and gas chromatography/mass spectrometry techniques in the nuclei from kidneys of rats 3 and 18 h after a single iv injection of the Ni super(II)(His) sub(2) complex (NiHis), nickel(II) acetate (NiAcet), or L-histidine (His). Administration of 20 mu mol of NiHis/kg body wt caused the formation of DNA-protein cross-links and significantly increased levels of oxidatively damaged DNA bases, including 2,6-diamino-4-hydroxy-5-formamidopyrimidine (FapyGua; 3.5-fold vs the control value) 3 h postinjection and 8-oxoguanine (2.6-fold), cytosine glycol (2.5-fold), 8-oxoadenine (2-fold), and FapyGua (1.9-fold) 18 h postinjection. Injection of 20 mu mol of NiAcet/kg body wt enhanced the cross-linking to a lesser extent than NiHis and did not significantly increase the amounts of modified DNA bases over the control levels. JF - Chemical Research in Toxicology AU - Misra, M AU - Olinski, R AU - Dizdaroglu, M AU - Kasprzak, K S AD - NCI-FCRDC, Build. 538, Room 205, Frederick, MD 21702-1201, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 33 EP - 37 VL - 6 IS - 1 SN - 0893-228X, 0893-228X KW - histidine KW - nickel KW - rats KW - Biochemistry Abstracts 2: Nucleic Acids; Toxicology Abstracts KW - cross-linking KW - damage KW - bases KW - DNA KW - kidney KW - proteins KW - N 14630:Chemical reactions & interactions, including effects of radiation KW - X 24165:Biochemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16792231?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+Research+in+Toxicology&rft.atitle=Enhancement+by+L-histidine+of+nickel+%28II%29-induced+DNA-protein+cross-linking+and+oxidative+DNA+base+damage+in+the+rat+kidney&rft.au=Misra%2C+M%3BOlinski%2C+R%3BDizdaroglu%2C+M%3BKasprzak%2C+K+S&rft.aulast=Misra&rft.aufirst=M&rft.date=1993-01-01&rft.volume=6&rft.issue=1&rft.spage=33&rft.isbn=&rft.btitle=&rft.title=Chemical+Research+in+Toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - DNA; proteins; cross-linking; bases; damage; kidney ER - TY - JOUR T1 - Inhibition of HIV infection by baicalin-A flavonoid compound purified from chinese herbal medicine AN - 16791735; 3542878 AB - Baicalin (BA), (formulated as 7-D-glucuronic acid-5,6-dihydroxy-flavone), was purified from the plant Scutellaria Baicalensis Georgi. It has been used as a traditional Chinese herbal medicine. The inhibitory effect of BA against human immunodeficiency virus (HIV-1) infection and replication has been studied in vitro. The compound inhibits HIV-1 infection and replication as measured by: a quantitative focal syncytium formation on CEM-ss monolayer cells; and HIV-1 specific core antigen p24 expression and retroviral reverse transcriptase (RT) activity in the HIV-1-infected H9 cells. We have further demonstrated that the enzymatic activity of purified recombinant HIV-1/RT was inhibited by BA. In addition to lymphoid cell lines, the anti-HIV-1 activity of BA was also observed in cultures of primary human peripheral blood mononuclear cells infected with HIV-1 in vitro. Neither cytotoxic nor cytostatic effects on the indicator cells were found under the assay condition. This data suggests that BA may serve as a useful drug for the treatment and prevention of HIV infections. JF - Cellular & Molecular Biology Research AU - Li, B-Q AU - Fu, T AU - Yan, Y-D AU - Baylor, N W AU - Ruscetti, F W AU - Kung, H-F AD - BCDP, PRI/Dyn-Corp, NCI-FCRDC, P.O. Box B, Bldg. 560/31-76, Frederick, MD 21702-1201, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 119 EP - 124 VL - 39 IS - 2 SN - 0968-8773, 0968-8773 KW - 7-D-glucuronic acid-5,6-dihydroxy-flavone KW - Scutellaria baicalensis georgi KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Virology & AIDS Abstracts KW - DNA biosynthesis KW - human immunodeficiency virus 1 KW - inhibitors KW - infection KW - China, People's Rep. KW - V 22002:AIDS: Molecular and in vitro aspects KW - A 01068:Antiviral & viricidal UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16791735?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cellular+%26+Molecular+Biology+Research&rft.atitle=Inhibition+of+HIV+infection+by+baicalin-A+flavonoid+compound+purified+from+chinese+herbal+medicine&rft.au=Li%2C+B-Q%3BFu%2C+T%3BYan%2C+Y-D%3BBaylor%2C+N+W%3BRuscetti%2C+F+W%3BKung%2C+H-F&rft.aulast=Li&rft.aufirst=B-Q&rft.date=1993-01-01&rft.volume=39&rft.issue=2&rft.spage=119&rft.isbn=&rft.btitle=&rft.title=Cellular+%26+Molecular+Biology+Research&rft.issn=09688773&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - human immunodeficiency virus 1; China, People's Rep.; infection; inhibitors; DNA biosynthesis ER - TY - JOUR T1 - Functional toxicology: A new approach to detect biologically active xenobiotics AN - 16791709; 3541886 AB - The pervasiveness of chemicals in the environment with estrogenic activity and other biological functions recommends the development of new approaches to monitor and study them. Chemicals can be screened for activity in vitro using a panel of human or animal cells that have been transfected with a specific receptor and reporter gene; for example, the estrogen receptor. By using a variety of different receptors, the screening of xenobiotics for biological functions can be broad. Chemicals could then be classified by their function in vitro which, in some cases, may be a useful guide for toxicological studies. JF - Environmental Health Perspectives AU - McLachlan, JA AD - NIEHS, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 386 EP - 387 VL - 101 IS - 5 SN - 0091-6765, 0091-6765 KW - Toxicology Abstracts KW - toxicity testing KW - xenobiotics KW - X 24221:Toxicity testing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16791709?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Functional+toxicology%3A+A+new+approach+to+detect+biologically+active+xenobiotics&rft.au=McLachlan%2C+JA&rft.aulast=McLachlan&rft.aufirst=JA&rft.date=1993-01-01&rft.volume=101&rft.issue=5&rft.spage=386&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - xenobiotics; toxicity testing ER - TY - JOUR T1 - Trimethyltin-induced c-fos expression: Adolescent vs neonatal rat hippocampus AN - 16790632; 3541949 AB - In the adult animal, the immediate early genes such as c-fos and c-jun, and other activity-dependent genes such as ornithine decarboxylase (ODC) are induced within minutes to hours in response to perturbations to the cellular environment. We have examined the induction of these genes following acute exposure to trimethyltin (TMT) using Northern blot analysis. The induction of these genes within the hippocampus and the cerebellum was examined half an hour following acute exposure to TMT (4 mg/kg, sc). In the neonatal (PND 4) rat hippocampus, the basal expression of c-fos, c-jun, and ODC appeared to be unaltered following TMT exposure. However, in the adolescent (PND 35) rat, TMT exposure produced a dramatic induction of c-fos mRNA in the hippocampus within half an hour, while beta -actin expression remained constant. No TMT-induced changes in the expression of c-fos were seen in the cerebellum of adolescent animals. JF - Toxicology and Applied Pharmacology AU - Zawia, N H AU - Harry, G J AD - Dev. and Reprod. Toxicol. Group, Syst. Tox. Branch, NIEHS, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 99 EP - 102 VL - 121 IS - 1 SN - 0041-008X, 0041-008X KW - trimethyltin KW - c-fos gene KW - rats KW - tin KW - Toxicology Abstracts; CSA Neurosciences Abstracts KW - genes KW - neurotoxicity KW - induction KW - metals KW - hippocampus KW - gene expression KW - N3 11104:Mammals (except primates) KW - X 24165:Biochemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16790632?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+Applied+Pharmacology&rft.atitle=Trimethyltin-induced+c-fos+expression%3A+Adolescent+vs+neonatal+rat+hippocampus&rft.au=Zawia%2C+N+H%3BHarry%2C+G+J&rft.aulast=Zawia&rft.aufirst=N&rft.date=1993-01-01&rft.volume=121&rft.issue=1&rft.spage=99&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+Applied+Pharmacology&rft.issn=0041008X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - induction; gene expression; hippocampus; neurotoxicity; metals; genes ER - TY - JOUR T1 - Immunochemical detection of liver protein adducts of the nonsteroidal antiinflammatory drug diclofenac AN - 16787382; 3541933 AB - Serious idiosyncratic hepatic injury has been associated with the use of many nonsteroidal antiinflammatory drugs, including the widely prescribed agent diclofenac. In order to investigate the possibility that covalent protein adducts of reactive metabolites of diclofenac might be responsible for the hepatotoxicity produced by this drug, we have developed a polyclonal antibody that can recognize such adducts in tissues. Immunoblotting revealed that protein adducts of reactive metabolites of diclofenac of 50, 70, 110, and 140 kDa were formed in the livers of mice treated with diclofenac. In the future, it will be determined whether these adducts can cause hepatotoxicity by either a hypersensitivity or metabolic mechanism. Similar approaches may be used to study the protein adducts and mechanisms of hepatotoxicity of other nonsteroidal antiinflammatory drugs. JF - Chemical Research in Toxicology AU - Pumford, N R AU - Myers, T G AU - Davila, J C AU - Highet, RJ AU - Pohl, L R AD - Lab. Chem. Pharmacol., NHLBI, NIH, Build. 10, Rm. 8N 115, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 147 EP - 150 VL - 6 IS - 2 SN - 0893-228X, 0893-228X KW - diclofenac KW - Toxicology Abstracts KW - detection KW - antiinflammatory agents KW - adducts KW - liver KW - proteins KW - X 24114:Metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16787382?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+Research+in+Toxicology&rft.atitle=Immunochemical+detection+of+liver+protein+adducts+of+the+nonsteroidal+antiinflammatory+drug+diclofenac&rft.au=Pumford%2C+N+R%3BMyers%2C+T+G%3BDavila%2C+J+C%3BHighet%2C+RJ%3BPohl%2C+L+R&rft.aulast=Pumford&rft.aufirst=N&rft.date=1993-01-01&rft.volume=6&rft.issue=2&rft.spage=147&rft.isbn=&rft.btitle=&rft.title=Chemical+Research+in+Toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - proteins; adducts; detection; liver; antiinflammatory agents ER - TY - JOUR T1 - Effect of L-ascorbic acid pretreatment on cadmium toxicity in the male Fischer (F344/NCr) rat AN - 16784311; 3541585 AB - Some studies have indicated that cadmium-induced lethality and selective injurious effects to specific tissues, such as testes or liver, can be prevented by pretreatment with the antioxidant L-ascorbic acid (ascorbic acid). However, the basis of this tolerance is unclear. We examined the effects of ascorbic acid pretreatment on cadmium toxicity in male Fischer (F344/NCr) rats. Cadmium treatment alone (25 mu mol CdCl sub(2)/kg, s.c.) proved lethal, causing a 93% mortality within 72 h, but in rats pretreated with ascorbic acid (2 g/kg, s.c. 24, 12 and 1 h) cadmium-induced lethality was nearly prevented. Hepatic lesions, including hepatocellular necrosis, induced by cadmium were at least partially ameliorated by ascorbic acid pretreatment. Ascorbic acid pretreatment had no effect on cadmium-induced testicular lesions nor on cadmium content in testes, liver, kidney and urine. Ascorbic acid alone modestly increased hepatic metallothionein (MT), but not renal MT and had no effect on induction of hepatic or renal MT by cadmium. JF - Toxicology AU - Shiraishi, N AU - Uno, H AU - Waalkes, M P AD - Tumor, Pathol. and Pathog. Sect., Lab. Comp. Carcinog., Build. 538, Room 205E, NCI, Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702-1201, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 85 EP - 100 VL - 85 IS - 2-3 SN - 0300-483X, 0300-483X KW - ascorbic acid KW - cadmium KW - rats KW - heavy metals KW - Toxicology Abstracts KW - toxicity KW - X 24161:Acute exposure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16784311?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology&rft.atitle=Effect+of+L-ascorbic+acid+pretreatment+on+cadmium+toxicity+in+the+male+Fischer+%28F344%2FNCr%29+rat&rft.au=Shiraishi%2C+N%3BUno%2C+H%3BWaalkes%2C+M+P&rft.aulast=Shiraishi&rft.aufirst=N&rft.date=1993-01-01&rft.volume=85&rft.issue=2-3&rft.spage=85&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=0300483X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - toxicity ER - TY - JOUR T1 - Cancer among migrant and seasonal farmworkers: An epidemiologic review and research agenda AN - 16783426; 3541225 AB - There are an estimated three million hired migrant and seasonal farmworkers in the United States. Adults and children may be exposed to mutagenic and potentially carcinogenic pesticides during planting, weeding, thinning, and harvesting crops. Field conditions that provide little opportunity to wash skin or clothing to minimize pesticide absorption may intensify exposure. Little is known, however, about the occurrence of cancer in migrant or seasonal farmworkers. Most cancer epidemiologic research on agricultural populations has focussed on farm owner/operators. The few studies that have evaluated cancer in farmworkers suggest that, like farm owner/operators, they may be experiencing excesses of multiple myeloma and cancers of the stomach, prostate, and testis. A few studies suggest that the farmworkers may differ from farmers by experiencing excesses of cancers of the buccal cavity and pharynx, lung, and liver. Cervical cancer was elevated in female farmworkers in one study. Descriptive data and etiologic research on cancer among farmworkers and family members are urgently needed. Feasibility evaluations, however, should precede etiologic investigations because of possible difficulties in studying this population of workers. JF - American Journal of Industrial Medicine AU - Zahm, SH AU - Blair, A AD - Occup. Stud. Sect., NCI/NIH, Executive Plaza N., Rm. 418, Rockville, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 753 EP - 766 VL - 24 IS - 6 SN - 0271-3586, 0271-3586 KW - occupational health KW - agricultural practices KW - occupational hazards KW - Toxicology Abstracts; Health & Safety Science Abstracts KW - agriculture KW - epidemiology KW - mortality KW - pesticides KW - cancer KW - X 24132:Chronic exposure KW - H SE2.3:HAZARD DETERMINATION KW - H SM10.21:CANCER UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16783426?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Industrial+Medicine&rft.atitle=Cancer+among+migrant+and+seasonal+farmworkers%3A+An+epidemiologic+review+and+research+agenda&rft.au=Zahm%2C+SH%3BBlair%2C+A&rft.aulast=Zahm&rft.aufirst=SH&rft.date=1993-01-01&rft.volume=24&rft.issue=6&rft.spage=753&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Industrial+Medicine&rft.issn=02713586&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - agriculture; occupational health; mortality; cancer; epidemiology; pesticides; agricultural practices; occupational hazards ER - TY - JOUR T1 - Binding of the cationic dye, Janus green B, as a measure of the specific surface area of crystalline silica in aqueous suspension AN - 16782652; 3541581 AB - Twelve preparations of crystalline silica, with a wide range of particle sizes, were assayed by a new method, which measures surface adsorption of the cationic dye Janus green B to crystalline silica samples in a buffered aqueous suspension. The same samples were also assayed for total surface area by the Brunauer-Emmett-Teller (BET) method of surface adsorption of nitrogen gas. A strong linear correlation was found between the two methods of measurement (r = 0.977). Reproducible specific surface area measurements by the Janus green B adsorption method were made on 2-mg samples using ordinary visible wavelength spectrophotometric equipment, whereas the BET method necessitated sample sizes in excess of 100 mg and more specialized instrumentation. Five size-fractionated preparations from the same Min-U-Sil alpha -quartz sample showed an increase in BET surface area and Janus green B binding per unit weight with decreasing particle size. Comparison of surface areas for different preparations of crystalline silica is important in understanding the relative activities of these preparations in studies on mechanisms of silicosis and silica-induced lung cancer. JF - Toxicology and Applied Pharmacology AU - Daniel, L N AU - Mao, Yan AU - Vallyathan, V AU - Saffiotti, U AD - Lab. Exp. Pathol., NCI/NIH, Bethesda, MD 20892-0041, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 62 EP - 67 VL - 123 IS - 1 SN - 0041-008X, 0041-008X KW - Janus Green B KW - silicon dioxide KW - Toxicology Abstracts KW - methodology KW - measurement KW - surface area KW - X 24222:Analytical procedures UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16782652?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+Applied+Pharmacology&rft.atitle=Binding+of+the+cationic+dye%2C+Janus+green+B%2C+as+a+measure+of+the+specific+surface+area+of+crystalline+silica+in+aqueous+suspension&rft.au=Daniel%2C+L+N%3BMao%2C+Yan%3BVallyathan%2C+V%3BSaffiotti%2C+U&rft.aulast=Daniel&rft.aufirst=L&rft.date=1993-01-01&rft.volume=123&rft.issue=1&rft.spage=62&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+Applied+Pharmacology&rft.issn=0041008X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - surface area; measurement; methodology ER - TY - JOUR T1 - Reactions of the bioregulatory agent nitric oxide in oxygenated aqueous media: Determination of the kinetics for oxidation and nitrosation by intermediates generated in the NO/O sub(2) reaction AN - 16781709; 3541670 AB - The reaction kinetics of nitric oxide autoxidation in aerobic solutions were investigated by direct observation of the nitrite ion product and by trapping the strongly oxidizing and nitrosating intermediates formed in this reaction. The rate behavior observed for nitrite formation [rate = k sub(3)[O sub(2)][NO] super(2), k sub(3) = (6) x 10 super(6) M super(-2) s super(-1) at 22 degree C] was the same as found for oxidation of Fe(CN) sub(6) super(4-) and of 2,2'-azinobis(3-ethylbenzthiazoline-6-sulfonic acid) (ABTS) and as for the nitrosation of sulfanilamide. There was a slight decrease in k sub(3) to (3.5) x 10 super(6) M super(-2) s super(-1) at 37 degree C. The second-order dependency for NO was observed at NO concentrations as low as 3 mu M. The results of the competitive kinetics studies suggest that the key oxidizing intermediates, species which are both strong oxidants and nitrosating agents, are not one of those commonly proposed (NO sub(2), N sub(2)O sub(3), NO super(+), or O sub(2)NO super(-)) but are one or more as yet uncharacterized NO sub(x) species. JF - Chemical Research in Toxicology AU - Wink, DA AU - Darbyshire, J F AU - Nims, R W AU - Saavedra, JE AU - Ford, P C AD - Chem. Sect., Lab. Comp. Carcinog., NCI, Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 23 EP - 27 VL - 6 IS - 1 SN - 0893-228X, 0893-228X KW - nitric oxide KW - Toxicology Abstracts KW - oxidation KW - nitrosation KW - kinetics KW - X 24240:Miscellaneous UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16781709?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+Research+in+Toxicology&rft.atitle=Reactions+of+the+bioregulatory+agent+nitric+oxide+in+oxygenated+aqueous+media%3A+Determination+of+the+kinetics+for+oxidation+and+nitrosation+by+intermediates+generated+in+the+NO%2FO+sub%282%29+reaction&rft.au=Wink%2C+DA%3BDarbyshire%2C+J+F%3BNims%2C+R+W%3BSaavedra%2C+JE%3BFord%2C+P+C&rft.aulast=Wink&rft.aufirst=DA&rft.date=1993-01-01&rft.volume=6&rft.issue=1&rft.spage=23&rft.isbn=&rft.btitle=&rft.title=Chemical+Research+in+Toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - oxidation; nitrosation; kinetics ER - TY - JOUR T1 - Open-complex formation by the host initiator, DnaA, at the origin of P1 plasmid replication AN - 16781085; 3535054 AB - Replication of P1 plasmid requires both the plasmid-specific initiator, RepA, and the host initiator, DnaA. Here we show that DnaA can make the P1 origin reactive to the single-strand specific reagents KMnO sub(4) and mung bean nuclease. Addition of RepA further increased the KMnO sub(4) reactivity of the origin, although RepA alone did not influence the reaction. The increased reactivity implies that the two initiators interact in some way to alter the origin conformation. The KMnO sub(4) reactivity was restricted to one strand of the origin. We suggest that the roles of DnaA in P1 plasmid and bacterial replication are similar: origin opering and loading of the DnaB helicase. The strand-bias in chemical reactivity at the P1 origin most likely indicates that only one of the strands is used for the loading of DnaB, a scenario consistent with the unidirectional replication of the plasmid. JF - EMBO Journal AU - Mukhopadhyay, G AU - Carr, K M AU - Kaguni, J M AU - Chattoraj, D K AD - Lab. Biochem., NCI/NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 4547 EP - 4554 VL - 12 IS - 12 SN - 0261-4189, 0261-4189 KW - open-complex KW - plasmid P1 KW - DnaA protein KW - Microbiology Abstracts B: Bacteriology; Biochemistry Abstracts 2: Nucleic Acids KW - replication KW - role KW - plasmids KW - formation KW - J 02760:Plasmids KW - N 14650:General UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16781085?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=EMBO+Journal&rft.atitle=Open-complex+formation+by+the+host+initiator%2C+DnaA%2C+at+the+origin+of+P1+plasmid+replication&rft.au=Mukhopadhyay%2C+G%3BCarr%2C+K+M%3BKaguni%2C+J+M%3BChattoraj%2C+D+K&rft.aulast=Mukhopadhyay&rft.aufirst=G&rft.date=1993-01-01&rft.volume=12&rft.issue=12&rft.spage=4547&rft.isbn=&rft.btitle=&rft.title=EMBO+Journal&rft.issn=02614189&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - plasmids; replication; role; formation ER - TY - CONF T1 - Renal cell cancer and exposure to gasoline: A review AN - 16780266; 3538977 AB - A review of the epidemiology of renal cell cancer is presented. Risk factors for renal cell cancer such as cigarette smoking, obesity, diet, and use of analgestics and prescription diuretics are examined. Although uncommon, occupational risk factors are also reviewed. Studies examining gasoline exposure and renal cell cancer are evaluated, including investigations recently presented at a meeting on this topic. Overall, most studies find no link between gasoline exposure and renal cell cancer; moreover, the experimental evidence that initiated the health concern is no longer considered relevant to humans. Positive associations, however, reported in two recent studies prevent a firm conclusion of no risk for this exposure. JF - ENVIRON. HEALTH PERSPECT. SUPPL. AU - McLaughlin, J K Y1 - 1993 PY - 1993 DA - 1993 SP - 111 EP - 114 VL - 101 IS - 6 KW - man KW - gasoline KW - Risk Abstracts; Health & Safety Science Abstracts; Toxicology Abstracts KW - reviews KW - kidney KW - cancer KW - X 24250:Reviews KW - R2 23060:Medical and environmental health KW - H SM10.21:CANCER UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16780266?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=ENVIRON.+HEALTH+PERSPECT.+SUPPL.&rft.atitle=Renal+cell+cancer+and+exposure+to+gasoline%3A+A+review&rft.au=McLaughlin%2C+J+K&rft.aulast=McLaughlin&rft.aufirst=J&rft.date=1993-01-01&rft.volume=101&rft.issue=6&rft.spage=111&rft.isbn=&rft.btitle=&rft.title=ENVIRON.+HEALTH+PERSPECT.+SUPPL.&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 ER - TY - JOUR T1 - Immune-based therapeutics: Scientific rationale and the promising approaches to the treatment of the human immunodeficiency virus-infected individual AN - 16780060; 3540593 AB - The primary approach to therapy for infection with human immunodeficiency virus (HIV) continues to be centered around antiretroviral agents that have conferred significant clinical benefits. The considerable degree of immunologic dysfunction in HIV infection, however, has led to intense interest in methods of immune stimulation and reconstitution. Immunomodulatory intervention in HIV infection is highly controversial. Over the years a number of immunomodulatory agents-many with only a poor rationale for their clinical use-have been evaluated. In this review we concentrate on immunomodulatory approaches that are currently being investigated. We group these interventions, reviewing the rationale and clinical data for each category: passive immunity (administration of immunoglobulins and use of apheresis), thymic hormone treatment, cytokine treatment (administration of interleukins, tumor necrosis factor, and interferons), adoptive cellular immunity, and therapeutic vaccination. At present, the only interventions supported by data from well-controlled studies are the parenteral administration of interferon alpha to patients with HIV-associated Kaposi's sarcoma and the administration of pooled immunoglobulin (to decrease the rate of bacterial infections) to children who cannot take trimethoprim-sulfamethoxazole. However, several other approaches under development show promise in reversing some of the immune deficits of HIV infection. Clinical evaluation of these approaches should yield valuable insights into the immunopathogenesis of HIV infection, and these insights should facilitate the formulation of new modalities of treatment. JF - Clinical Infectious Diseases AU - Stein, D S AU - Timpone, J G AU - Gradon, JD AU - Kagan, J M AU - Schnittman, S M AD - Div. AIDS, NIAID/NIH, 6003 Executive Blvd., Rockville, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 749 EP - 771 VL - 17 IS - 4 SN - 1058-4838, 1058-4838 KW - Biotechnology and Bioengineering Abstracts; Medical and Pharmaceutical Biotechnology Abstracts; Virology & AIDS Abstracts KW - reviews KW - antiviral agents KW - alpha -interferon KW - human immunodeficiency virus KW - treatment KW - infection KW - immunotherapy KW - immunoregulation KW - man KW - W3 33150:Cytokine based KW - V 22003:AIDS: Immunological aspects KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16780060?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+Infectious+Diseases&rft.atitle=Immune-based+therapeutics%3A+Scientific+rationale+and+the+promising+approaches+to+the+treatment+of+the+human+immunodeficiency+virus-infected+individual&rft.au=Stein%2C+D+S%3BTimpone%2C+J+G%3BGradon%2C+JD%3BKagan%2C+J+M%3BSchnittman%2C+S+M&rft.aulast=Stein&rft.aufirst=D&rft.date=1993-01-01&rft.volume=17&rft.issue=4&rft.spage=749&rft.isbn=&rft.btitle=&rft.title=Clinical+Infectious+Diseases&rft.issn=10584838&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - reviews; alpha -interferon; antiviral agents; treatment; immunoregulation; immunotherapy; infection; man; human immunodeficiency virus ER - TY - JOUR T1 - Pharmacodynamics of cytochrome P450 2B induction by phenobarbital, 5-ethyl-5-phenylhydantoin, and 5-ethyl-5-phenyloxazolidinedione in the male rat liver or in cultured rat hepatocytes AN - 16778224; 3541656 AB - The pharmacodynamics of rat hepatic cytochrome P450 2B (P450 2B) induction by phenobarbital (PB) and two structural congeners, dl-5-ethyl 5-phenylhydantoin (EPH) and dl-5-ethyl 5-phenyloxazolidinedione (EPO), were investigated. The in vivo ED sub(50) values for P450 2B induction were similar to 110, similar to 100, and similar to 3000 dietary ppm (14 days administration) for PB, EPH, and EPO, respectively. The in vivo EC sub(50) values for P450 2B induction were similar to 9, similar to 6, and similar to 130 mu M (total serum) for PB, EPH, and EPO, respectively. In cultured rat hepatocytes, the ED sub(50) values for induction of (benzyloxy)resorufin O-dealkylation activity were 14.5, 14.2, and 108 mu M for PB, EPH, and EPO, respectively. These data indicate that pharmacodynamic results obtained with cultured hepatocytes represent a good qualitative and quantitative approximation of the in vivo hepatic responses in male rats caused by PB-type inducers. JF - Chemical Research in Toxicology AU - Nims, R W AU - Sinclair, PR AU - Sinclair, J F AU - Thomas, P E AU - Jones, C R AU - Mellini, D W AU - Syi, Jia-Lin AU - Lubet, R A AD - Chem. Sect., Lab. Comp. Carcinog., NCI, Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 188 EP - 196 VL - 6 IS - 2 SN - 0893-228X, 0893-228X KW - phenobarbital KW - 5-ethyl-5-phenylhydantoin KW - 5-ethyl-5-phenyloxazolidinedione KW - cytochrome P450 KW - rats KW - Toxicology Abstracts KW - induction KW - liver KW - X 24114:Metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16778224?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+Research+in+Toxicology&rft.atitle=Pharmacodynamics+of+cytochrome+P450+2B+induction+by+phenobarbital%2C+5-ethyl-5-phenylhydantoin%2C+and+5-ethyl-5-phenyloxazolidinedione+in+the+male+rat+liver+or+in+cultured+rat+hepatocytes&rft.au=Nims%2C+R+W%3BSinclair%2C+PR%3BSinclair%2C+J+F%3BThomas%2C+P+E%3BJones%2C+C+R%3BMellini%2C+D+W%3BSyi%2C+Jia-Lin%3BLubet%2C+R+A&rft.aulast=Nims&rft.aufirst=R&rft.date=1993-01-01&rft.volume=6&rft.issue=2&rft.spage=188&rft.isbn=&rft.btitle=&rft.title=Chemical+Research+in+Toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - induction; liver ER - TY - JOUR T1 - X-ray-induced chromatid damage in cells from Down syndrome and Alzheimer disease patients in relation to DNA repair and cancer proneness AN - 16777368; 3538011 AB - Frequencies of chromatid aberrations in response to G sub(2)-phase x-irradiation were compared in PHA-stimulated blood lymphocytes from healthy control subjects, Down syndrome (DS) patients, and Alzheimer disease (AD) patients. In cells arrested with Colcemid immediately (0-30 min) after x-irradiation, DS, AD, and control cells showed similar high frequencies of chromatid breaks and gaps, representing unrepaired DNA strand breaks. Frequencies had decreased in AD and control cells arrested 30-90 min after irradiation. However, DS cells had two- to three-fold higher frequencies than AD or control cells. This result indicates deficient repair of the DNA damage in DS cells. Similar responses were obtained with lymphocytes from four of seven DS parents tested and with skin fibroblasts from DS patients compared to age-matched controls. Addition of 1- beta -D-arabinofuranosylcytosine (ara-C), an inhibitor of the repair polymerase, after x-irradiation during G sub(2) phase increased the frequencies of chromatid breaks and gaps in lymphocytes from control and AD donors significantly more than in those from DS patients. This result indicates a deficiency in DS cells in incision at sites of x-ray-induced damage. Thus DS, like other cancer-prone genetic disorders, has alpha G sub(2)-phase DNA repair deficiency in strand break repair and also a second DNA repair deficiency in incision activity. JF - Cancer Genetics and Cytogenetics AU - Sanford, K K AU - Parshad, R AU - Price, F M AU - Tarone, R E AU - Schapiro, M B AD - Rm. 2D15, Build. 37, NCI/NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 25 EP - 30 VL - 70 IS - 1 SN - 0165-4608, 0165-4608 KW - Alzheimer's disease KW - DNA repair KW - Down's syndrome KW - X radiation KW - cancer KW - chromatids KW - damage KW - man KW - Toxicology Abstracts; Human Genome Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - X 24210:Radiation & radioactive materials KW - N 14652:DNA repair UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16777368?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Genetics+and+Cytogenetics&rft.atitle=X-ray-induced+chromatid+damage+in+cells+from+Down+syndrome+and+Alzheimer+disease+patients+in+relation+to+DNA+repair+and+cancer+proneness&rft.au=Sanford%2C+K+K%3BParshad%2C+R%3BPrice%2C+F+M%3BTarone%2C+R+E%3BSchapiro%2C+M+B&rft.aulast=Sanford&rft.aufirst=K&rft.date=1993-01-01&rft.volume=70&rft.issue=1&rft.spage=25&rft.isbn=&rft.btitle=&rft.title=Cancer+Genetics+and+Cytogenetics&rft.issn=01654608&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Down's syndrome; Alzheimer's disease; X radiation; DNA repair; chromatids; damage; cancer; man ER - TY - JOUR T1 - Structure-based inhibitors of HIV-1 protease AN - 16775020; 3737072 AB - This review discusses the current state of structural investigations of HIV-1 PR inhibitor complexes, concentrating on the structure of the enzyme, its mode of interaction with a variety of inhibitors, and the use of structure to design and discover novel lead compounds. JF - Annual Review of Biochemistry AU - Wlodawer, A AU - Erickson, J W AD - Macromol. Struct. Lab., NCI-FCRDC, ABL-Basic Res. Program, Frederick, MD 21702, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 543 EP - 585 VL - 62 SN - 0066-4154, 0066-4154 KW - proteinase KW - Biotechnology and Bioengineering Abstracts; Medical and Pharmaceutical Biotechnology Abstracts; Virology & AIDS Abstracts KW - reviews KW - human immunodeficiency virus 1 KW - inhibitors KW - V 22002:AIDS: Molecular and in vitro aspects KW - W 30965:Miscellaneous, Reviews KW - W3 33390:Products: Others UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16775020?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annual+Review+of+Biochemistry&rft.atitle=Structure-based+inhibitors+of+HIV-1+protease&rft.au=Wlodawer%2C+A%3BErickson%2C+J+W&rft.aulast=Wlodawer&rft.aufirst=A&rft.date=1993-01-01&rft.volume=62&rft.issue=&rft.spage=543&rft.isbn=&rft.btitle=&rft.title=Annual+Review+of+Biochemistry&rft.issn=00664154&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - reviews; inhibitors; human immunodeficiency virus 1 ER - TY - JOUR T1 - Mortality among workers at a nuclear power plant in the United States AN - 16774387; 3535715 AB - A second follow-up of 9,000 workers at the Calvert Cliffs Nuclear Power Plant (MD, USA) identified 346 deaths in the years 1969-88, 101 of which were attributed to malignant neoplasms. The original study had the primary purpose of assessing the feasibility of studies of workers based upon individual plant and Nuclear Regulatory Commission records. The average, cumulative, occupational dose through 1984 was low, only 21 mSv, but ranged up to 470 mSv, with 12 percent of the workers receiving more than 50 mSv. Mortality from most causes of death was low and there was a deficit of deaths from diseases of the circulatory system. Ionizing radiation exposures were not related to the probability of death from neoplasms generally or from any specific form of cancer. There were only two deaths from leukemia, whereas four were expected at population death rates. Larger numbers of workers, followed for longer periods of time, are needed to determine the mortality risk to workers in the nuclear power industry. JF - Cancer Causes & Control AU - Jablon, S AU - Boice, JD Jr AD - NCI/NIH, Radiat. Epidemiol. Branch, Executive Plaza N., No. 408, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 427 EP - 430 VL - 4 IS - 5 SN - 0957-5243, 0957-5243 KW - occupational hazards KW - occupational health KW - radiation dosimetry KW - Toxicology Abstracts; Risk Abstracts; Pollution Abstracts; Health & Safety Science Abstracts KW - radiation KW - USA, Maryland KW - mortality KW - nuclear power plants KW - cancer KW - R2 23080:Industrial and labor KW - X 24210:Radiation & radioactive materials KW - P 8000:RADIATION KW - H SM10.21:CANCER KW - P 6000:TOXICOLOGY AND HEALTH KW - H SI4.21:NUCLEAR POWER STATION SAFETY UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16774387?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Causes+%26+Control&rft.atitle=Mortality+among+workers+at+a+nuclear+power+plant+in+the+United+States&rft.au=Jablon%2C+S%3BBoice%2C+JD+Jr&rft.aulast=Jablon&rft.aufirst=S&rft.date=1993-01-01&rft.volume=4&rft.issue=5&rft.spage=427&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - USA, Maryland; nuclear power plants; occupational health; mortality; radiation dosimetry; cancer; radiation; occupational hazards ER - TY - JOUR T1 - Cytogenetic evidence for differences in DNA incision activity in xeroderma pigmentosum group A, C and D cells after X-irradiation during G sub(2) phase AN - 16753196; 3525324 AB - The capacity of cells to incise DNA to remove altered sites after DNA damage can be determined from the rate of DNA-strand break accumulation in the presence of an inhibitor of DNA-repair synthesis, such as 1- beta -D-arabinofuranosylcytosine (ara-C). Because each chromatid contains a single continuous molecule of double-stranded DNA, chromatid breaks and gaps, i.e., non-displaced breaks, represent unrepaired DNA-strand breaks. The accumulation of chromatid breaks and gaps after X-irradiation in the presence of ara-C thus provides a measure of DNA incision activity. Addition of ara-C to skin fibroblasts or stimulated blood lymphocytes from normal individuals at intervals after X-irradiation significantly increased frequencies of chromatid breaks and/or gaps. In contrast, addition of ara-C to XP cells of complementation groups A and D had a negligible effect and a significant but less than normal effect on XP cells of complementation group C and one sample of blood lymphocytes of undetermined complementation group. JF - Mutation Research AU - Parshad, R AU - Tarone, R E AU - Price, F M AU - Sanford, K K AD - Lab. Cell. and Mol. Biol., NCI/NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 149 EP - 155 VL - 294 IS - 2 SN - 0921-8262, 0921-8262 KW - Genetics Abstracts; Toxicology Abstracts KW - X radiation KW - lymphocytes KW - damage KW - xeroderma pigmentosum KW - fibroblasts KW - DNA KW - X 24210:Radiation & radioactive materials KW - G 07232:Radiation (X) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16753196?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutation+Research&rft.atitle=Cytogenetic+evidence+for+differences+in+DNA+incision+activity+in+xeroderma+pigmentosum+group+A%2C+C+and+D+cells+after+X-irradiation+during+G+sub%282%29+phase&rft.au=Parshad%2C+R%3BTarone%2C+R+E%3BPrice%2C+F+M%3BSanford%2C+K+K&rft.aulast=Parshad&rft.aufirst=R&rft.date=1993-01-01&rft.volume=294&rft.issue=2&rft.spage=149&rft.isbn=&rft.btitle=&rft.title=Mutation+Research&rft.issn=09218262&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - X radiation; DNA; damage; xeroderma pigmentosum; fibroblasts; lymphocytes ER - TY - JOUR T1 - Improved bacterial hosts for regulated expression of genes from lambda p sub(L) plasmid vectors AN - 16752964; 3525319 AB - The construction and use of a set of Escherichia coli strains with defective lambda prophages that facilitate expression of genes cloned in lambda P sub(L)-plasmid vectors is described. These bacteria allow high and regulated expression of such genes, whereas a kanamycin-resistance marker (Km super(R)) on the prophage allows easy identification and genetic transfer from strain to strain. Optimal conditions for examining gene expression with the p sub(L)-vector systems using these strains are discussed. JF - Gene AU - Patterson, T A AU - Costantino, N AU - Dasgupta, S AU - Court, D L AD - ABL-Basic Res. Program, NCI-FCRDC, P.O. Box B, Frederick, MD 21702-1201, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 83 EP - 87 VL - 132 IS - 1 SN - 0378-1119, 0378-1119 KW - PL plasmid vector KW - Genetics Abstracts; Microbiology Abstracts B: Bacteriology KW - gene transfer KW - defects KW - phage lambda KW - Escherichia coli KW - plasmids KW - gene expression KW - G 07321:GENERAL KW - J 02740:Genetics and evolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16752964?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gene&rft.atitle=Improved+bacterial+hosts+for+regulated+expression+of+genes+from+lambda+p+sub%28L%29+plasmid+vectors&rft.au=Patterson%2C+T+A%3BCostantino%2C+N%3BDasgupta%2C+S%3BCourt%2C+D+L&rft.aulast=Patterson&rft.aufirst=T&rft.date=1993-01-01&rft.volume=132&rft.issue=1&rft.spage=83&rft.isbn=&rft.btitle=&rft.title=Gene&rft.issn=03781119&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - phage lambda; Escherichia coli; defects; plasmids; gene expression; gene transfer ER - TY - JOUR T1 - Initiation of food supplements and stopping of breast-feeding as determinants of weanling shigellosis AN - 16751618; 3725032 AB - The association between the period elapsed since weaning and the risk of shigellosis was assessed between 1 November 1987 and 30 November 1989 for a cohort of 1085 Bangladeshi children aged <3 years. The children were followed for 1 month after exposure to Shigella spp. in their residential neighbourhoods, and the 268 who developed microbiologically confirmed (n = 118) or clinically presumptive (n = 150) shigellosis were compared with the 817 control children who did not develop either syndrome. No increase in risk was noted among breast-fed infants who received food supplements within the previous 3 months compared with those who had received supplements for longer (adjusted odds ratio (OR) = 1.2; 95% confidence interval (CI) = 0.4-3.0). However, compared with breast-fed children, nonbreast-fed children had an increased risk (adjusted OR = 2.0; 95% CI = 1.3-2.9; P <0.001), which was largely attributable to a substantially increased risk in the 3 months after stopping breast-feeding (adjusted OR = 6.6; 95% CI = 2.9-14.6; P <0.001). The early post-cessation risk was equivalent for confirmed and presumptive shigellosis, but was particularly pronounced among the severely malnourished (adjusted OR = 10.2; 95% CI = 3.1-33.3; P <0.001). This complex temporal pattern of risk highlights the need for precise definitions of weaning to facilitate identification of children at high risk for invasive diarrhoeal syndromes. JF - W H O Drug Information AU - Ahmed, F AU - Clemens, J D AU - Rao, M R AU - Khan, M R AU - Haque, E AD - DESPR, NICHD, 6100 Executive Plaza Build., Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 571 EP - 578 VL - 71 IS - 5 SN - 1010-9609, 1010-9609 KW - weanling diarrhea KW - Microbiology Abstracts B: Bacteriology KW - diarrhea KW - breast feeding KW - etiology KW - shigellosis KW - neonates KW - feeding behavior KW - man KW - risk factors KW - J 02846:Gastrointestinal tract UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16751618?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=W+H+O+Drug+Information&rft.atitle=Initiation+of+food+supplements+and+stopping+of+breast-feeding+as+determinants+of+weanling+shigellosis&rft.au=Ahmed%2C+F%3BClemens%2C+J+D%3BRao%2C+M+R%3BKhan%2C+M+R%3BHaque%2C+E&rft.aulast=Ahmed&rft.aufirst=F&rft.date=1993-01-01&rft.volume=71&rft.issue=5&rft.spage=571&rft.isbn=&rft.btitle=&rft.title=W+H+O+Drug+Information&rft.issn=10109609&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - shigellosis; risk factors; neonates; etiology; feeding behavior; man; breast feeding; diarrhea ER - TY - JOUR T1 - Diversity in the Chlamydia trachomatis histone homologue Hc2 AN - 16751313; 3521775 AB - Chlamydia trachomatis elementary bodies contain two developmentally expressed histone H1 homologues. An 18-kDa histone homologue, Hc1, is conserved among C. trachomatis serovars and C. psittaci. The other histone homologue, Hc2 (encoded by hctB), varies in size between C. trachomatis serovars but is present in reduced amounts or absent from C. psittaci. The variation in Hc2 size among C. trachomatis serovars was found to be due to internal deletions from a region of the hctB gene encoding lysine- and alanine-rich pentameric repeats. JF - Gene AU - Hackstadt, T AU - Brickman, T J AU - Barry, CE III AU - Sager, J AD - Lab. Intracell. Parasites, Rocky Mountain Lab., NIAID, Hamilton, MT 59840, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 137 EP - 141 VL - 132 IS - 1 SN - 0378-1119, 0378-1119 KW - histone Hc2 KW - histone Hc1 KW - Genetics Abstracts; Microbiology Abstracts B: Bacteriology; Biochemistry Abstracts 2: Nucleic Acids KW - diversity KW - genes KW - Chlamydia trachomatis KW - nucleotide sequence KW - N 14640:Structure & sequence KW - G 07321:GENERAL KW - J 02740:Genetics and evolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16751313?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gene&rft.atitle=Diversity+in+the+Chlamydia+trachomatis+histone+homologue+Hc2&rft.au=Hackstadt%2C+T%3BBrickman%2C+T+J%3BBarry%2C+CE+III%3BSager%2C+J&rft.aulast=Hackstadt&rft.aufirst=T&rft.date=1993-01-01&rft.volume=132&rft.issue=1&rft.spage=137&rft.isbn=&rft.btitle=&rft.title=Gene&rft.issn=03781119&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Chlamydia trachomatis; genes; nucleotide sequence; diversity ER - TY - JOUR T1 - Modulation of the H sub(2)O sub(2)-induced SOS response in Escherichia coli PQ300 by amino acids, metal chelators, antioxidants, and scavengers of reactive oxygen species AN - 16748777; 3520597 AB - The SOS chromotest is a simple colorimetric genotoxicity assay that monitors DNA repair by measuring the induction of the gene sfiA in Escherichia coli K-12. E. coli PQ300, a diagnostic SOS tester strain for the detection of oxidative genotoxins, carries a mutation in a key gene for antioxidative defense, oxyR. This mutation renders PQ300 more sensitive to oxidative genotoxins, particularly to H sub(2)O sub(2). We found that induction of the SOS response by H sub(2)O sub(2) in E. coli PQ300 is dependent on the composition of the incubation medium; a substantially reduced response was obtained in minimal phosphate buffered saline (PBS) as opposed to complex Luria broth (LB) medium. Supplementation of PBS with histidine or cysteine stimulated H sub(2)O sub(2)-induced SOS induction to levels exceeding those found in LB medium. JF - Environmental and Molecular Mutagenesis AU - Mueller, J AU - Janz, S AD - Lab. Genet., NCI/NIH, Build. 37, Rm. 2B09, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 157 EP - 163 VL - 22 IS - 3 SN - 0893-6692, 0893-6692 KW - SOS KW - scavengers KW - hydrogen peroxide KW - oxygen KW - Toxicology Abstracts; Genetics Abstracts KW - modulation KW - response KW - reactivity KW - antioxidants KW - amino acids KW - Escherichia coli KW - chelating agents KW - species KW - induction KW - mutagenicity testing KW - DNA repair KW - metals KW - X 24240:Miscellaneous KW - G 07221:Specific chemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16748777?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+and+Molecular+Mutagenesis&rft.atitle=Modulation+of+the+H+sub%282%29O+sub%282%29-induced+SOS+response+in+Escherichia+coli+PQ300+by+amino+acids%2C+metal+chelators%2C+antioxidants%2C+and+scavengers+of+reactive+oxygen+species&rft.au=Mueller%2C+J%3BJanz%2C+S&rft.aulast=Mueller&rft.aufirst=J&rft.date=1993-01-01&rft.volume=22&rft.issue=3&rft.spage=157&rft.isbn=&rft.btitle=&rft.title=Environmental+and+Molecular+Mutagenesis&rft.issn=08936692&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Escherichia coli; induction; modulation; response; amino acids; metals; chelating agents; antioxidants; reactivity; species; DNA repair; mutagenicity testing ER - TY - JOUR T1 - Enhanced expression of angiotensin II receptor subtypes and angiotensin converting enzyme in medroxyprogesterone-induced mouse mammary adenocarcinomas AN - 16747046; 3520648 AB - Angiotensin II receptors of the AT sub(1) subtype were very highly expressed in medroxyprogesterone-induced ductal adenocarcinomas of the mammary gland in BALB/c mice. AT sub(1) receptors are associated only to neoplastic epithelial cells. Lobular adenocarcinomas expressed very few AT sub(1) receptors and expressed AT sub(2) receptors only in areas corresponding to peritumoral connective tissue. Binding to angiotensin converting enzyme was present in all adenocarcinomas studied and was higher in ductal than in lobular adenocarcinomas. Normal mammary gland did not express either angiotensin II receptors or angiotensin converting enzyme. The present results are the first demonstration of angiotensin receptor subtypes and converting enzyme in mammary adenocarcinomas differentially expressed in tumors of ductal and lobular origin. Localization of receptor subtypes could be useful to study the differentiation of mammary cells during experimental mammary carcinogenesis in mice. JF - Biochemical and Biophysical Research Communications AU - Guerra, F K AU - Ciuffo, G M AU - Elizalde, P V AU - Charreau, E H AU - Saavedra, J M AD - Sect. Pharmacol., Lab. Clin. Sci., NIMH, 9000 Rockville Pike, Build. 10, Room 2D-45, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 93 EP - 99 VL - 193 IS - 1 SN - 0006-291X, 0006-291X KW - medroxyprogesterone KW - angiotensin II KW - mice KW - angiotensin converting enzyme KW - Toxicology Abstracts KW - adenocarcinoma KW - induction KW - receptors KW - X 24117:Biochemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16747046?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+and+Biophysical+Research+Communications&rft.atitle=Enhanced+expression+of+angiotensin+II+receptor+subtypes+and+angiotensin+converting+enzyme+in+medroxyprogesterone-induced+mouse+mammary+adenocarcinomas&rft.au=Guerra%2C+F+K%3BCiuffo%2C+G+M%3BElizalde%2C+P+V%3BCharreau%2C+E+H%3BSaavedra%2C+J+M&rft.aulast=Guerra&rft.aufirst=F&rft.date=1993-01-01&rft.volume=193&rft.issue=1&rft.spage=93&rft.isbn=&rft.btitle=&rft.title=Biochemical+and+Biophysical+Research+Communications&rft.issn=0006291X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - adenocarcinoma; induction; receptors ER - TY - JOUR T1 - MK-801, but not drugs acting at strychnine-insensitive glycine receptors, attenuate methamphetamine nigrostriatal toxicity AN - 16738190; 3518237 AB - Repeated administration of methamphetamine (METH) results in damage to nigrostriatal dopaminergic neurons. Both competitive N-methyl-D-aspartate (NMDA) receptor antagonists and use-dependent cation channel blockers attenuate METH-induced damage. The objectives of the present study were to examine whether comparable reductions in METH-induced damage could be obtained by compounds acting at strychnine-insensitive glycine receptors on the NMDA receptor complex. Four injections of METH resulted in a ) 70.9% depletion of striatal dopamine (DA) and ) 62.7% depletion of dihydroxyphenylacetic acid (DOPAC) content, respectively. A significant protection against METH-induced DA and DOPAC depletion was afforded by the use-dependent channel blocker, MK-801. The competitive glycine antagonist 7-chlorokynurenic acid (7-Cl-KA), the low efficacy glycine partial agonist (+)-3-amino-1-hydroxy-2-pyrrolidone ((+)-HA-966), and the high efficacy partial glycine agonist 1-aminocyclopropane-carboxylic acid (ACPC) were ineffective against METH-induced toxicity despite their abilities to attenuate glutamate-induced neurotoxicity under both in vivo and in vitro conditions. JF - Brain Research AU - Layer, R T AU - Bland, L R AU - Skolnick, P AD - NIDDK/NIH, Build. 8, Rm. 111, Bethesda, MD 20892-0008, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 38 EP - 44 VL - 625 IS - 1 SN - 0006-8993, 0006-8993 KW - MK-801 KW - methamphetamine KW - rats KW - dizocilpine KW - Toxicology Abstracts; CSA Neurosciences Abstracts KW - attenuation KW - neurotoxicity KW - substantia nigra KW - N3 11104:Mammals (except primates) KW - X 24180:Social poisons & drug abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16738190?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+Research&rft.atitle=MK-801%2C+but+not+drugs+acting+at+strychnine-insensitive+glycine+receptors%2C+attenuate+methamphetamine+nigrostriatal+toxicity&rft.au=Layer%2C+R+T%3BBland%2C+L+R%3BSkolnick%2C+P&rft.aulast=Layer&rft.aufirst=R&rft.date=1993-01-01&rft.volume=625&rft.issue=1&rft.spage=38&rft.isbn=&rft.btitle=&rft.title=Brain+Research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - attenuation; neurotoxicity; substantia nigra ER - TY - JOUR T1 - An adjustment in p-values for multiple endpoint testing AN - 16735548; 3510705 AB - In preclinical and pilot studies where various measurements are taken in order to gain an idea of the effectiveness or toxicity of an agent, it is important to control the overall Type I error rate when doing hypothesis testing. A review of some of the adjustments presently available in the literature is provided. Two adjustments to control the false-positive rate are proposed when the vector of test statistics is multivariate normal or asymptotically so. An example is used to illustrate the different techniques. JF - Drug Information Journal AU - Weller, E A AU - Chinchilli, V M AD - NCI, Cancer Stat. Branch, SEER Program, EPN Rm. 343J, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 695 EP - 703 VL - 27 IS - 3 SN - 0092-8615, 0092-8615 KW - multiple endpoint testing KW - Toxicology Abstracts KW - toxicity testing KW - statistics KW - X 24221:Toxicity testing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16735548?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Drug+Information+Journal&rft.atitle=An+adjustment+in+p-values+for+multiple+endpoint+testing&rft.au=Weller%2C+E+A%3BChinchilli%2C+V+M&rft.aulast=Weller&rft.aufirst=E&rft.date=1993-01-01&rft.volume=27&rft.issue=3&rft.spage=695&rft.isbn=&rft.btitle=&rft.title=Drug+Information+Journal&rft.issn=00928615&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - toxicity testing; statistics ER - TY - JOUR T1 - Studies on the mutagenic activation of heterocyclic amines by cynomolgus monkey, rat and human microsomes show that cynomolgus monkeys have a low capacity to N-oxidize the quinoxaline-type heterocyclic amines AN - 16733859; 3521380 AB - A number of mutagens and carcinogens have been isolated from cooked meats. In the current study we investigated the ability of hepatic microsomes from cynomolgus monkeys, Fischer-344 rats and humans to metabolically activate these compounds. Monkeys had almost no capacity to activate the quinoxaline-type compounds to mutagens in the Ames test relative to rats and humans but were able to activate the quinoline, pyridoindole and pyridoimidazole compounds. Differences in the mutagenicity of the quinoline and quinoxaline compounds by monkeys and rats was related to differences in cytochrome P-450-mediated N-oxidation between the species. This suggests that monkeys and rats may have different hepatic cytochrome P-450 isozymes, which are important for the metabolic activation of quinolines and quinoxalines, or that the orthologous monkey cytochromes show a select substrate specificity for the quinolines over the quinoxalines. JF - Cancer Letters AU - Davis, C D AU - Adamson, R H AU - Snyderwine, E G AD - Lab. Exp. Carcinog., Div. Cancer Etiol., NCI, NIH, Bethesda, MD 20892-0037, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 95 EP - 104 VL - 73 IS - 2-3 SN - 0304-3835, 0304-3835 KW - heterocyclic amines KW - monkeys KW - rats KW - Toxicology Abstracts KW - metabolic activation KW - microsomes KW - Macaca mulatta KW - mutagenicity KW - man KW - X 24240:Miscellaneous UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16733859?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Letters&rft.atitle=Studies+on+the+mutagenic+activation+of+heterocyclic+amines+by+cynomolgus+monkey%2C+rat+and+human+microsomes+show+that+cynomolgus+monkeys+have+a+low+capacity+to+N-oxidize+the+quinoxaline-type+heterocyclic+amines&rft.au=Davis%2C+C+D%3BAdamson%2C+R+H%3BSnyderwine%2C+E+G&rft.aulast=Davis&rft.aufirst=C&rft.date=1993-01-01&rft.volume=73&rft.issue=2-3&rft.spage=95&rft.isbn=&rft.btitle=&rft.title=Cancer+Letters&rft.issn=03043835&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Macaca mulatta; metabolic activation; mutagenicity; microsomes; man ER - TY - JOUR T1 - An extraintestinal, pathogenic isolate of Escherichia coli (O4/K54/H5) can produce a group 1 capsule which is divergently regulated from its constitutively produced group 2, K54 capsular polysaccharide AN - 16731279; 3515888 AB - We are studying an O4/K54/H5 Escherichia coli bacteremic isolate (CP9) as a model pathogen for extraintestinal infection. Its group 2, K54 capsular polysaccharide is an important virulence determinant and confers serum resistance. The effect of the group 1 capsule regulators, RcsA, RcsB, and Lon protease, on the regulation of CP9's capsular polysaccharides was assessed. It was established that in the presence of multicopy rcsA or with disruption of lon, CP9 can be induced to produce a group 1 capsule. RcsA, RcsB, and Lon are present in this K54 background and regulate group 1 capsule expression in a fashion similar to that described for K-12 strains. Two independent group 2 capsule gene protein fusions (cl1.29::TnphoA and cl1.137::TnphoA) were used to evaluate the effects of these regulators on group 2 K54 capsule production. Disruption of lon resulted in 1.9-fold (TR293 [cl1.29::TnphoA lon-146]) and 3.4-fold (TR1373 [cl1.137::TnphoA lon-146]) decreases in fusion activity at 28 degree C, relative to the baseline level. However, decreases in fusion activity at 42 degree C were only 1.2- and 1.4-fold, respectively. Inactivation of both lon and rcsA or lon and rcsB restored fusion activity to baseline levels at 28 degree C, but only a partial restoration of activity was seen at higher temperatures. To assess whether these differences in fusion activity reflected a functional change in capsule production, the effects of 80% normal human serum (NHS) were tested against CP9 and TR93 (lon-146). Since the group 2 K54 capsule protects against the bactericidal activity of 80% NHS, a decrease in its production results in an increase in serum sensitivity. Viable counts of CP9 increased 10-fold in 80% NHS over 3 h at 28 degree C, as expected. In contrast to CP9, TR93 (lon-146) incurred a 10-fold loss in viability under the same conditions. The levels of RcsA are increased in TR93 (lon-146) as a consequence of lon disruption; therefore, these results in conjunction with the cl1::TnphoA protein fusion data establish RcsA as a negative regulator of the group 2 K54 capsular polysaccharide. Its action appears to be mediated through RcsB and is greatest at 28 degree C but decreases at higher temperatures. The results also suggest the existence of another Lon-sensitive negative regulator of group 2 K54 capsule production, which is active at higher temperatures. JF - Journal of Bacteriology AU - Russo, T A AU - Singh, G AD - Bact. Pathog. Unit, Lab. Clin. Invest., NIAID/NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 7617 EP - 7623 VL - 175 IS - 23 SN - 0021-9193, 0021-9193 KW - K54 capsular polysaccharide KW - effects on KW - rcsA gene KW - rcsB gene KW - lon gene KW - Genetics Abstracts; Microbiology Abstracts B: Bacteriology KW - gene fusion KW - genes KW - Escherichia coli KW - production KW - J 02730:Carbohydrates KW - G 07321:GENERAL UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16731279?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Bacteriology&rft.atitle=An+extraintestinal%2C+pathogenic+isolate+of+Escherichia+coli+%28O4%2FK54%2FH5%29+can+produce+a+group+1+capsule+which+is+divergently+regulated+from+its+constitutively+produced+group+2%2C+K54+capsular+polysaccharide&rft.au=Russo%2C+T+A%3BSingh%2C+G&rft.aulast=Russo&rft.aufirst=T&rft.date=1993-01-01&rft.volume=175&rft.issue=23&rft.spage=7617&rft.isbn=&rft.btitle=&rft.title=Journal+of+Bacteriology&rft.issn=00219193&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Escherichia coli; production; genes; gene fusion ER - TY - JOUR T1 - Distribution and molecular analysis of Lyme disease spirochetes, Borrelia burgdorferi, isolated from ticks throughout California AN - 16730707; 3516309 AB - Previous studies describing the occurrence and molecular characteristics of Lyme disease spirochetes, Borrelia burgdorferi, from California have been restricted primarily to isolates obtained from the north coastal region of this large and ecologically diverse state. Our objective was to look for and examine B. burgdorferi organisms isolated from Ixodes pacificus ticks collected from numerous regions spanning most parts of California where this tick is found. All of the isolates were identified as B. burgdorferi by their protein profiles and reactivities with monoclonal and polyclonal antibodies, and all the isolates were typed by the polymerase chain reaction as North American-type spirochetes (B. burgdorferi sensu stricto). Although products of the ospAB locus were identified in protein analyses in all of the isolates, several isolates contained deleted forms of this locus that would result in the expression of chimeric OspA-OspB proteins. The analysis of OspC demonstrated that this protein was widely conserved among the isolates but was also quite variable in its molecular mass and the amount of it that was expressed. JF - Journal of Clinical Microbiology AU - Schwan, T G AU - Schrumpf, ME AU - Karstens, R H AU - Clover, J R AU - Wong, J AU - Daugherty, M AU - Struthers, M AU - Rosa, P A AD - Arthropod-Borne Dis. Sect., Lab. Vectors and Pathogens, Rocky Mountain Lab., NIAID, Hamilton, MT 59840, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 3096 EP - 3108 VL - 31 IS - 12 SN - 0095-1137, 0095-1137 KW - Microbiology Abstracts B: Bacteriology KW - Borrelia burgdorferi KW - USA, California KW - distribution KW - man KW - Lyme disease KW - J 02855:Human Bacteriology: Others UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16730707?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Clinical+Microbiology&rft.atitle=Distribution+and+molecular+analysis+of+Lyme+disease+spirochetes%2C+Borrelia+burgdorferi%2C+isolated+from+ticks+throughout+California&rft.au=Schwan%2C+T+G%3BSchrumpf%2C+ME%3BKarstens%2C+R+H%3BClover%2C+J+R%3BWong%2C+J%3BDaugherty%2C+M%3BStruthers%2C+M%3BRosa%2C+P+A&rft.aulast=Schwan&rft.aufirst=T&rft.date=1993-01-01&rft.volume=31&rft.issue=12&rft.spage=3096&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Microbiology&rft.issn=00951137&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Borrelia burgdorferi; USA, California; distribution; Lyme disease; man ER - TY - JOUR T1 - Generation of free radicals from hydrogen peroxide and lipid hydroperoxides in the presence of Cr(III) AN - 16730308; 3510661 AB - Free radical generation from H sub(2)O sub(2) and lipid hydroperoxides in the presence of Cr(III) was investigated by electron spin resonance (ESR) spin trapping methodology. Incubation of Cr(III) with H sub(2)O sub(2) at physiological pH generated hydroxyl ( multiplied by OH) radical, the yield of which reached saturation level in about 6 min. Deferoxamine reduced the multiplied by OH radical yield by only about 20%, diethylenetriamine pentaacetic acid (DTPA) reduced it by about 70%, while cysteine, glutathione, and NADH exhibited no significant effect. The yield of multiplied by OH radical formation also depended on the pH being 15 times higher at pH 10 than that at pH 7.2. At pH 3.0, multiplied by OH radical generation became nondetectable, and addition of H sub(2)O sub(2) to Cr(III) solution did not affect the intensity of the Cr(III) ESR signal while at pH 10, addition of H sub(2)O sub(2) reduced the Cr(III) intensity by about 40%, showing that reaction of Cr(III) with H sub(2)O sub(2) occurred only at higher pH. Incubation of Cr(III) with the model lipid hydroperoxides, cumene hydroperoxide and t-butyl hydroperoxide, generated lipid hydroperoxide-derived free radicals. JF - Archives of Biochemistry and Biophysics AU - Shi, X AU - Dalal, N S AU - Kasprzak, K S AD - Build. 538, Rm. 205, NCI, Frederick, MD 21702, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 294 EP - 299 VL - 302 IS - 1 SN - 0003-9861, 0003-9861 KW - hydrogen peroxide KW - chromium KW - generation KW - Toxicology Abstracts KW - carcinogenicity KW - mechanisms KW - free radicals KW - X 24165:Biochemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16730308?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+Biochemistry+and+Biophysics&rft.atitle=Generation+of+free+radicals+from+hydrogen+peroxide+and+lipid+hydroperoxides+in+the+presence+of+Cr%28III%29&rft.au=Shi%2C+X%3BDalal%2C+N+S%3BKasprzak%2C+K+S&rft.aulast=Shi&rft.aufirst=X&rft.date=1993-01-01&rft.volume=302&rft.issue=1&rft.spage=294&rft.isbn=&rft.btitle=&rft.title=Archives+of+Biochemistry+and+Biophysics&rft.issn=00039861&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - free radicals; carcinogenicity; mechanisms ER - TY - JOUR T1 - Occasional binges by moderate drinkers: Implications for birth outcomes AN - 16729849; 3511425 AB - We investigated the effects of occasional alcohol binges on birth outcomes in a cohort of live singletons born to 709 moderate drinkers recruited from a Seattle, WA, health maintenance organization before their sixth month of pregnancy. We compared infants of women with one or more binges in the month before pregnancy or in the first two trimesters with those whose mothers reported no binges in either period. Mean values of birthweight, length, head circumference, gestational age, intrauterine growth, and Apgar scores did not differ notably between the two groups. The risk of having an adverse neonatal discharge diagnosis initially appeared lower in infants of binging mothers, but this difference vanished after recategorization of the variable and control for confounding. Our results indicate that occasional binges, during a broad window of exposure and among otherwise moderate drinkers, do not adversely affect the birth outcomes examined here. JF - Epidemiology AU - Tolo, K-A AU - Little, R E AD - Epidemiol. Branch, Mail Drop A3-05, NIEHS, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 415 EP - 420 VL - 4 IS - 5 SN - 1044-3983, 1044-3983 KW - ethanol KW - moderate drinkers KW - outcome KW - Toxicology Abstracts KW - pregnancy KW - man KW - X 24180:Social poisons & drug abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16729849?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Epidemiology&rft.atitle=Occasional+binges+by+moderate+drinkers%3A+Implications+for+birth+outcomes&rft.au=Tolo%2C+K-A%3BLittle%2C+R+E&rft.aulast=Tolo&rft.aufirst=K-A&rft.date=1993-01-01&rft.volume=4&rft.issue=5&rft.spage=415&rft.isbn=&rft.btitle=&rft.title=Epidemiology&rft.issn=10443983&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - pregnancy; man ER - TY - JOUR T1 - Comparative carcinogenicity of polybrominated biphenyls with or without perinatal exposure in rats and mice AN - 16729801; 3511417 AB - Chronic toxicity and carcinogenicity studies of a polybrominated biphenyl mixture (PBB) were conducted in F344/N rats and B6C3F1 mice of each sex. The major objective of the study was to determine if exposure to PBB during the perinatal period, in addition to conventional exposure of animals for 2 years, enhances the sensitivity of the bioassay to identify the carcinogenic potential of this chemical. Perinatal exposure alone (through dietary administration of 10 ppm PBB to the dams) had no effect on the incidences of neoplasms in female F344/N rats, but in male rats, perinatal exposure was associated with a marginally increased incidence of hepatocellular adenomas that may have been related to chemical administration. In male and female B6C3F sub(1) mice, perinatal exposure to 30 ppm PBB resulted in significantly increased incidences of hepatocellular neoplasms. JF - Fundamental and Applied Toxicology AU - Chhabra, R S AU - Bucher, J R AU - Haseman, J K AU - Elwell, M R AU - Kurtz, P J AU - Carlton, B D AD - NIEHS, Research Triangle Park, NC 27709, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 451 EP - 460 VL - 21 IS - 4 SN - 0272-0590, 0272-0590 KW - polybrominated biphenyls KW - rats KW - mice KW - Toxicology Abstracts KW - carcinogenicity KW - X 24190:Polycyclic hydrocarbons UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16729801?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fundamental+and+Applied+Toxicology&rft.atitle=Comparative+carcinogenicity+of+polybrominated+biphenyls+with+or+without+perinatal+exposure+in+rats+and+mice&rft.au=Chhabra%2C+R+S%3BBucher%2C+J+R%3BHaseman%2C+J+K%3BElwell%2C+M+R%3BKurtz%2C+P+J%3BCarlton%2C+B+D&rft.aulast=Chhabra&rft.aufirst=R&rft.date=1993-01-01&rft.volume=21&rft.issue=4&rft.spage=451&rft.isbn=&rft.btitle=&rft.title=Fundamental+and+Applied+Toxicology&rft.issn=02720590&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - carcinogenicity ER - TY - JOUR T1 - The interplay of the GrpE heat shock protein and Mg super(2+) in RepA monomerization by DnaJ and DnaK AN - 16725010; 3516262 AB - Genetic and biochemical studies have established that the sole function of the Escherichia coli DnaJ, DnaK, and GrpE heat shock proteins in plasmid P1 DNA replication is to convert RepA dimers to monomers. Monomers bind avidly to oriP1 DNA and initiate DNA replication. However, with purified heat shock proteins, only DnaJ, DnaK, and ATP were required for the monomerization of RepA; GrpE was not required. We have found reaction conditions that mimic the physiological situation. Our results imply that GrpE facilitates the utilization of Mg super(2+) for an essential step in RepA activation. JF - Journal of Biological Chemistry AU - Skowyra, D AU - Wickner, S AD - Bldg. 37, Rm. 2D19, NCI/NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 25296 EP - 25301 VL - 268 IS - 34 SN - 0021-9258, 0021-9258 KW - GrpE protein KW - magnesium KW - interactions KW - RepA protein KW - DnaJ protein KW - DnaK protein KW - Microbiology Abstracts B: Bacteriology KW - Escherichia coli KW - J 02727:Amino acids, peptides and proteins UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16725010?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=The+interplay+of+the+GrpE+heat+shock+protein+and+Mg+super%282%2B%29+in+RepA+monomerization+by+DnaJ+and+DnaK&rft.au=Skowyra%2C+D%3BWickner%2C+S&rft.aulast=Skowyra&rft.aufirst=D&rft.date=1993-01-01&rft.volume=268&rft.issue=34&rft.spage=25296&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Escherichia coli ER - TY - JOUR T1 - Residual myelotoxicity of lindane in mice AN - 16724658; 3511407 AB - Lindane ( gamma -1,2,3,4,5,6-hexachlorocyclohexane), a widely used insecticide, may be found at low concentrations in the human diet. Male B6C3F sub(1) mice given lindane daily at doses of 20 and 40 mg/kg body wt by gavage in corn oil for 3 days had suppressed bone marrow cellularity, erythrocyte precursors, granulocyte-macrophage progenitor cells (CFU-GM), and residual progenitor cell damage, which could be demonstrated by two whole-body irradiations (WBI) at 200 rads. Lindane exposure for 10 consecutive days at doses of 0, 10, or 20 mg/kg did not cause clinical abnormality or changes in body weights, but there were dose-dependent decreases in marrow cellularity, in more pluripotent stem cells and in committed CFU-GMs, which returned to control values by 4 weeks. JF - Fundamental and Applied Toxicology AU - Hong, H L AU - Boorman, G A AD - Pathol. Branch, MD D2-05, Natl. Toxicol. Program, NIEHS, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 500 EP - 507 VL - 21 IS - 4 SN - 0272-0590, 0272-0590 KW - lindane KW - myelotoxicity KW - mice KW - pesticides (organochlorine) KW - Toxicology Abstracts KW - insecticides KW - bone marrow KW - X 24131:Acute exposure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16724658?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fundamental+and+Applied+Toxicology&rft.atitle=Residual+myelotoxicity+of+lindane+in+mice&rft.au=Hong%2C+H+L%3BBoorman%2C+G+A&rft.aulast=Hong&rft.aufirst=H&rft.date=1993-01-01&rft.volume=21&rft.issue=4&rft.spage=500&rft.isbn=&rft.btitle=&rft.title=Fundamental+and+Applied+Toxicology&rft.issn=02720590&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - insecticides; bone marrow ER - TY - JOUR T1 - Effect of a recombinant CD4-IgG on in vitro T helper cell function: Data from a phase I/II study of patients with AIDS AN - 16719940; 3509862 AB - Ten patients with AIDS were enrolled in a phase I/II protocol of recombinant CD4-IgG (rCD4-IgG) treatment. Patients' peripheral blood leukocytes (PBL) were tested before, during, and after therapy with rCD4-IgG for T helper (TH) cell function assessed by antigen- and mitogen-stimulated proliferation and interleukin-2 production in response to influenza A virus, allogeneic PBL (alloantigens), and phytohemagglutinin. Although clinal benefit was not evident, rCD4-IgG treatment was associated with rapid and potent improved TH cell function for two of three stimuli tested in 90% of the patients. These data are complemented by an in vitro experimental model that demonstrates the opposing immunologic effects of rgp120 and rCD4-IgG on TH cell function of PBL from uninfected individuals. Thus, restoration of TH cell function by rCD4-IgG in the absence of increased CD4 cells counts could be due to removal of an immunosuppressive factor, possibly gp120. These findings suggest that rCD-IgG can induce partial restoration of immune function in AIDS patients, even in the absence of apparent short-term clinical benefit. JF - Journal of Infectious Diseases AU - Clerici, M AU - Yarchoan, R AU - Blatt, S AU - Hendrix, C W AU - Ammann, A J AU - Broder, S AU - Shearer, G M AD - Exp. Immunol. Branch, NCI, Build. 10, Rm. 4B-17, NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 1012 EP - 1016 VL - 168 IS - 4 SN - 0022-1899, 0022-1899 KW - CD4 antigen KW - chimeric proteins KW - Biotechnology and Bioengineering Abstracts; Medical and Pharmaceutical Biotechnology Abstracts; Immunology Abstracts; Virology & AIDS Abstracts KW - recombinants KW - lymphocytes T KW - treatment KW - immunoglobulin G KW - fusion protein KW - man KW - acquired immune deficiency syndrome KW - W3 33160:Antibody based KW - F 06756:Function KW - W 30965:Miscellaneous, Reviews KW - V 22004:AIDS: Clinical aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16719940?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Infectious+Diseases&rft.atitle=Effect+of+a+recombinant+CD4-IgG+on+in+vitro+T+helper+cell+function%3A+Data+from+a+phase+I%2FII+study+of+patients+with+AIDS&rft.au=Clerici%2C+M%3BYarchoan%2C+R%3BBlatt%2C+S%3BHendrix%2C+C+W%3BAmmann%2C+A+J%3BBroder%2C+S%3BShearer%2C+G+M&rft.aulast=Clerici&rft.aufirst=M&rft.date=1993-01-01&rft.volume=168&rft.issue=4&rft.spage=1012&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - recombinants; lymphocytes T; treatment; fusion protein; immunoglobulin G; man; acquired immune deficiency syndrome ER - TY - JOUR T1 - Inhibition of rev activity and human immunodeficiency virus type 1 replication by antisense oligodeoxynucleotide phosphorothioate analogs directed against the rev-responsive element AN - 16718802; 3506103 AB - The interaction between the Rev protein of human immunodeficiency virus type 1 and its highly structured and conserved RNA target, the Rev-responsive element, is required for virus replication. We demonstrate that antisense oligodeoxynucleotide phosphorothioate analogs directed against the Rev-responsive element effectively inhibit Rev activity, as well as human immunodeficiency virus type 1 replication, and are candidates for antiviral therapy. JF - Journal of Virology AU - Li, G AU - Lisziewicz, J AU - Sun, D AU - Zon, G AU - Daefler, S AU - Wong-Staal, F AU - Gallo, R C AU - Klotman, ME AD - Lab. Tumor Cell Biol., NCI/NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 6882 EP - 6888 VL - 67 IS - 11 SN - 0022-538X, 0022-538X KW - Rev protein KW - oligodeoxyribonucleotide KW - Biotechnology and Bioengineering Abstracts; Medical and Pharmaceutical Biotechnology Abstracts; Virology & AIDS Abstracts KW - antiviral activity KW - replication KW - human immunodeficiency virus 1 KW - treatment KW - activity KW - V 22002:AIDS: Molecular and in vitro aspects KW - W 30965:Miscellaneous, Reviews KW - W3 33380:Antisense UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16718802?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Virology&rft.atitle=Inhibition+of+rev+activity+and+human+immunodeficiency+virus+type+1+replication+by+antisense+oligodeoxynucleotide+phosphorothioate+analogs+directed+against+the+rev-responsive+element&rft.au=Li%2C+G%3BLisziewicz%2C+J%3BSun%2C+D%3BZon%2C+G%3BDaefler%2C+S%3BWong-Staal%2C+F%3BGallo%2C+R+C%3BKlotman%2C+ME&rft.aulast=Li&rft.aufirst=G&rft.date=1993-01-01&rft.volume=67&rft.issue=11&rft.spage=6882&rft.isbn=&rft.btitle=&rft.title=Journal+of+Virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - antiviral activity; replication; treatment; activity; human immunodeficiency virus 1 ER - TY - JOUR T1 - N-acetylation phenotype and genotype and risk of bladder cancer in benzidine-exposed workers AN - 16716840; 3510179 AB - Several studies in subjects occupationally exposed to arylamine carcinogens have shown increased risks for bladder cancer associated with the slow acetylator phenotype. To follow up these reports, a case-control study of N-acetylation and bladder cancer risk was carried out among subjects occupationally exposed to benzidine, in benzidine dye production and use facilities in China. Thirty-eight bladder cancer cases and 43 controls from these factories were included for study of acetylation phenotype, by dapsone administration, and for polymorphisms in the NAT2 gene, by a polymerase chain reaction (PCR)-based test. In contrast to previous studies, no increase in bladder cancer risk was found for the slow N-acetylation phenotype (OR = 0.3; 95% CI = 0.1 - 1.3) or for slow N-acetylation-associated double mutations in NAT2 (OR = 0.5; 95% CI = 0.1 - 1.8). JF - Carcinogenesis AU - Hayes, R B AU - Bi, W AU - Rothman, N AU - Broly, F AU - Caporaso, N AU - Feng, P AU - You, Xiejun AU - Yin, Songnian AU - Woosley, R L AU - Meyer, U A AD - Environ. Epidemiol. Branch, NCI/NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 675 EP - 678 VL - 14 IS - 4 SN - 0143-3334, 0143-3334 KW - N-acetylation KW - man KW - phenotypes KW - genotypes KW - risks KW - bladder KW - benzidine KW - workers KW - Health & Safety Science Abstracts; Risk Abstracts; Toxicology Abstracts; Genetics Abstracts KW - occupational exposure KW - cancer KW - R2 23080:Industrial and labor KW - X 24155:Biochemistry KW - H SM10.21:CANCER KW - G 07221:Specific chemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16716840?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=N-acetylation+phenotype+and+genotype+and+risk+of+bladder+cancer+in+benzidine-exposed+workers&rft.au=Hayes%2C+R+B%3BBi%2C+W%3BRothman%2C+N%3BBroly%2C+F%3BCaporaso%2C+N%3BFeng%2C+P%3BYou%2C+Xiejun%3BYin%2C+Songnian%3BWoosley%2C+R+L%3BMeyer%2C+U+A&rft.aulast=Hayes&rft.aufirst=R&rft.date=1993-01-01&rft.volume=14&rft.issue=4&rft.spage=675&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - occupational exposure; cancer; man; phenotypes; genotypes; risks; bladder; workers ER - TY - JOUR T1 - TCDD-mediated changes in hepatic epidermal growth factor receptor may be a critical event in the hepatocarcinogenic action of TCDD AN - 16710918; 3705539 AB - 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a potent liver tumor promoter in rats, with females being more sensitive than males. The epidermal growth factor receptor (EGFR) pathway has been implicated in altered cell growth patterns induced by tumor promoters. We investigated hepatic EGFR levels in a two-stage initiation promotion model. The TCDD doses were chosen to encompass the dose range administered in a previous chronic bioassay currently used to determine the cancer potency commonly used for human health risk assessments. TCDD was administered biweekly by oral gavage to female Sprague-Dawley rats for 30 weeks following initiation by a single dose of diethylnitrosamine (DEN). TCDD-mediated decreased EGF receptor levels were demonstrated in intact but not ovariectomized animals, consistent with previous tumor data. Likewise, previous studies have shown that TCDD induces cell proliferation in intact rats but not ovariectomized rats. We report a significant dose-dependent decrease in plasma membrane EGF receptor maximum binding capacity in both initiated and non-initiated intact rats at TCDD doses equivalent to 3.5, 10.7, 35.7 and 125 ng/kg/day. There was a significant correlation between EGF receptor effects and liver TCDD concentration. The decrease in plasma membrane EGFR determined by equilibrium binding was confirmed quantitatively by EGF stimulation of EGFR autophosphorylation as well as qualitatively by immunohistochemical detection in control and treated rats. These results demonstrate that the observed down modulation of the EGFR by TCDD is ovarian-dependent and is a sensitive effect induced at dose levels associated with TCDD hepatocarcinogenicity in rodent bioassays. JF - Carcinogenesis AU - Sewall, CH AU - Lucier, G W AU - Tritscher, A M AU - Clark, G C AD - NIEHS, MD D4-04, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 1885 EP - 1893 VL - 14 IS - 9 SN - 0143-3334, 0143-3334 KW - TCDD KW - epidermal growth factor receptors KW - rats KW - Toxicology Abstracts KW - carcinogenicity KW - liver KW - X 24155:Biochemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16710918?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=TCDD-mediated+changes+in+hepatic+epidermal+growth+factor+receptor+may+be+a+critical+event+in+the+hepatocarcinogenic+action+of+TCDD&rft.au=Sewall%2C+CH%3BLucier%2C+G+W%3BTritscher%2C+A+M%3BClark%2C+G+C&rft.aulast=Sewall&rft.aufirst=CH&rft.date=1993-01-01&rft.volume=14&rft.issue=9&rft.spage=1885&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - liver; carcinogenicity ER - TY - JOUR T1 - Risk of silicosis in a cohort of white South African gold miners AN - 16703687; 3534423 AB - The risk of silicosis was investigated in a cohort of 2,235 white South African gold miners who had, on average, 24 years of net service from 1940 to the early 1970s and who were followed up to 1991 for radiological signs of onset of silicosis (ILO category 1/1 or more). There were 313 (14%) miners who developed signs of silicosis at an average age of 55.9 years. The latency period was largely independent of the cumulative dust exposure. In 57% of the silicotics, the radiological signs developed, on average, 7.4 years after mining exposure ceased. The risk of silicosis increased exponentially with the cumulative dust dose, the accelerated increase being after 7 mg/m super(3)-years. At the highest exposure level of 15 mg/m super(3)-years, which represents approximately 37 years of gold mining at an average respirable dust concentration of 0.4 mg/m super(3), the cumulative risk for silicosis reached 77%. In conclusion, the risk of silicosis was strongly dose dependent; however, the latency period was largely independent of the dose. JF - American Journal of Industrial Medicine AU - Hnizdo, E AU - Sluis-Cremer, G K AD - Epidemiol. Branch, NIEHS, Mail Drop A3-05, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 447 EP - 457 VL - 24 IS - 4 SN - 0271-3586, 0271-3586 KW - gold KW - Toxicology Abstracts; Risk Abstracts; Health & Safety Science Abstracts; Pollution Abstracts KW - mining KW - South Africa KW - occupational exposure KW - silicosis KW - dust KW - R2 23080:Industrial and labor KW - H SI2.8.7:DUST KW - P 6000:TOXICOLOGY AND HEALTH KW - X 24152:Chronic exposure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16703687?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Industrial+Medicine&rft.atitle=Risk+of+silicosis+in+a+cohort+of+white+South+African+gold+miners&rft.au=Hnizdo%2C+E%3BSluis-Cremer%2C+G+K&rft.aulast=Hnizdo&rft.aufirst=E&rft.date=1993-01-01&rft.volume=24&rft.issue=4&rft.spage=447&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Industrial+Medicine&rft.issn=02713586&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - South Africa; dust; occupational exposure; gold; mining; silicosis ER - TY - JOUR T1 - Evidence for two levels of control of P1 oriR and host oriC replication origins by DNA adenine methylation AN - 16700685; 3500674 AB - A mutant mini-P1 plasmid with increased copy number can be established in Dam super(-) strains of Escherichia coli, where mini-P1 plasmid replication is normally blocked. Comparison of this plasmid and a plasmid driven by the host oriC replication origin showed that both origins are subject to control by methylation at two different levels. First, both origins appear to be subject to negative acting at the level of hemimethylation. This probably involves the sequestration of the hemimethylated DNA produced by replication, as has been previously described for oriC. Second, both origins show a positive requirement for adenine methylation for efficient function in vivo. This conslusion is supported by the behavior of the P1 origin in an improved in vitro replication system. In vitro, where sequestraion of hemimethylated DNA is not expected to occur, the hemimethylated P1 origin DNA was fully functional as a template. However, the activity of fully unmethylated DNA was severely restricted in comparison with that of either of the methylated forms. This in vitro uncoupling of the two effects of origin methyaltion suggests that two separate mechanisms are involved. JF - Journal of Bacteriology AU - Abeles, A AU - Brendler, T AU - Austin, S AD - Lab. Chromosome Biol., ABL-Basic Res. Program, NCI-Frederick Cancer Res. and Dev. Cent., Frederick, MD 21701-1201, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 7801 EP - 7807 VL - 175 IS - 24 SN - 0021-9193, 0021-9193 KW - oriR KW - oriC KW - adenine KW - replication origins KW - plasmid P1 KW - Microbiology Abstracts B: Bacteriology; Biochemistry Abstracts 2: Nucleic Acids KW - methylation KW - DNA KW - plasmids KW - J 02725:DNA KW - N 14650:General UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16700685?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Bacteriology&rft.atitle=Evidence+for+two+levels+of+control+of+P1+oriR+and+host+oriC+replication+origins+by+DNA+adenine+methylation&rft.au=Abeles%2C+A%3BBrendler%2C+T%3BAustin%2C+S&rft.aulast=Abeles&rft.aufirst=A&rft.date=1993-01-01&rft.volume=175&rft.issue=24&rft.spage=7801&rft.isbn=&rft.btitle=&rft.title=Journal+of+Bacteriology&rft.issn=00219193&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - DNA; methylation; plasmids ER - TY - JOUR T1 - Heat shock proteins DnaJ, DnaK, and GrpE stimulate P1 plasmid replication by promoting initiator binding to the origin. AN - 16698755; 2981865 AB - Binding of the P1-encoded protein RepA to the origin of P1 plasmid replication is essential for initiation of DNA replication and for autoregulatory repression of the repA promoter. Previous studies have shown defects in both initiation and repression in hosts lacking heat shock proteins DnaJ, DnaK, and GrpE and have suggested that these proteins play a role in the RepA-DNA binding required for initiation and repression. In this study, using in vivo dimethyl sulfate footprinting, we have confirmed the roles of the three heat shock proteins in promoting RepA binding to the origin. The defects in both activities could be suppressed by increasing the concentration of wild-type RepA over the physiological level. We also isolated RepA mutants that were effective initiators and repressors without requiring the heat shock proteins. These data suggest that the heat shock proteins facilitate both repression and initiation by promoting only the DNA-binding activity of RepA. In a similar plasmid, F, initiator mutants that confer heat shock protein independence for replication were also found, but they were defective for repression. We propose that the initiator binding involved in repression and the initiator binding involved in initiation are similar in P1 but different in F. JF - Journal of Bacteriology AU - Sozhamannan, S AU - Chattoraj, D K AD - Lab. Biochem., NCI, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 3546 EP - 3555 VL - 175 IS - 11 SN - 0021-9193, 0021-9193 KW - plasmid P1 KW - Microbiology Abstracts B: Bacteriology KW - heat shock proteins KW - phage P1 KW - replication KW - DNA KW - Escherichia coli KW - binding KW - plasmids KW - J 02760:Plasmids UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16698755?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Bacteriology&rft.atitle=Heat+shock+proteins+DnaJ%2C+DnaK%2C+and+GrpE+stimulate+P1+plasmid+replication+by+promoting+initiator+binding+to+the+origin.&rft.au=Sozhamannan%2C+S%3BChattoraj%2C+D+K&rft.aulast=Sozhamannan&rft.aufirst=S&rft.date=1993-01-01&rft.volume=175&rft.issue=11&rft.spage=3546&rft.isbn=&rft.btitle=&rft.title=Journal+of+Bacteriology&rft.issn=00219193&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - phage P1; Escherichia coli; heat shock proteins; plasmids; replication; DNA; binding ER - TY - JOUR T1 - Fine-structure analysis of the P7 plasmid partition site. AN - 16698203; 2981869 AB - The par region of bacteriophage P7 is responsible for active partition of the P7 plasmid prophage into daughter cells. The cis-acting partition site was defined precisely as a 75-bp sequence that was necessary and sufficient to promote correct segregation of an unstable vector plasmid when the two P7 partition proteins, ParA and ParB, were supplied in trans. Roughly the same region was necessary to exert partition-mediated incompatibility. The minimal site contains an integration host factor (IHF) protein binding site bracketed by regions containing heptamer repeat sequences that individually bind ParB. An additional sequence forms the left boundary of the site. Site-directed mutations in the latter sequence, as well as the IHF motif and the rightmost ParB box, blocked site function. Although the P7 site shares 55% sequence identity with its counterpart in bacteriophage P1, functional interactions between the partition sites and the Par proteins of the two plasmids were entirely species specific in vivo. The P1 sequence has similar IHF and ParB binding motifs, but the left boundary sequence differs radically and may define a point of species-specific contact with the Par proteins. No evidence was found for the existence of a functional P7 analog of the P1 parS core, a small subregion of the P1 site that, in isolation, acts as an enfeebled partition site with modified incompatibility properties. JF - Journal of Bacteriology AU - Hayes, F AU - Davis, MA AU - Austin, S J AD - Lab. Chromosome Biol., ABL-Basic Res. Program, NCI-Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 3443 EP - 3451 VL - 175 IS - 11 SN - 0021-9193, 0021-9193 KW - phage P7 KW - plasmid P7 KW - Genetics Abstracts; Microbiology Abstracts B: Bacteriology KW - partition KW - genes KW - Escherichia coli KW - plasmids KW - analysis KW - J 02760:Plasmids KW - G 07200:P PLASMIDS UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16698203?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Bacteriology&rft.atitle=Fine-structure+analysis+of+the+P7+plasmid+partition+site.&rft.au=Hayes%2C+F%3BDavis%2C+MA%3BAustin%2C+S+J&rft.aulast=Hayes&rft.aufirst=F&rft.date=1993-01-01&rft.volume=175&rft.issue=11&rft.spage=3443&rft.isbn=&rft.btitle=&rft.title=Journal+of+Bacteriology&rft.issn=00219193&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Escherichia coli; plasmids; partition; genes; analysis ER - TY - JOUR T1 - Isolation of dnaJ, dnaK, and grpE homologues from Borrelia burgdorferi and complementation of Escherichia coli mutants. AN - 16697859; 2978939 AB - The heat-shock proteins DnaJ, DnaK, and GrpE are involved in the replication of various species of DNA in Escherichia coli , in addition to their roles in other processes, including protein disaggregation and export. We have cloned the Borrelia burgdorferi homologues of these genes. DNA sequence analysis revealed an open reading frame encoding a protein that is 62% identical to the E. coli DnaK protein. Genes homologous to the E. coli grpE and dnaJ genes, encoding products 28% and 39% identical to their homologues, are located up- and downstream, respectively, of the B. burgdorferi dnaK gene. No obvious promoters were detected in the sequenced DNA, although a potential transcription terminator was found downstream of the dnaJ gene, so these three genes may form an operon, perhaps with a fourth gene located upstream of the grpE gene. The grpE homologue complemented an E. coli grpE mutant and the dnaJ homologue complemented an E. coli dnaJ mutant, whereas the B. burgdorferi dnaK gene did not complement dnaK mutants. JF - Molecular Microbiology AU - Tilly, K AU - Hauser, R AU - Campbell, J AU - Ostheimer, G J AD - Lab. Microb. Struct. and Funct., Rocky Mountain Lab., NIAID/NIH, Hamilton, MT 59840, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 359 EP - 369 VL - 7 IS - 3 SN - 0950-382X, 0950-382X KW - dnaJ gene KW - dnaK gene KW - grpE gene KW - Genetics Abstracts; Microbiology Abstracts B: Bacteriology KW - heat shock proteins KW - complementation KW - Borrelia burgdorferi KW - genes KW - prediction KW - mutants KW - nucleotide sequence KW - amino acid sequence KW - Escherichia coli KW - G 07320:Bacterial genetics KW - J 02740:Genetics and evolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16697859?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+Microbiology&rft.atitle=Isolation+of+dnaJ%2C+dnaK%2C+and+grpE+homologues+from+Borrelia+burgdorferi+and+complementation+of+Escherichia+coli+mutants.&rft.au=Tilly%2C+K%3BHauser%2C+R%3BCampbell%2C+J%3BOstheimer%2C+G+J&rft.aulast=Tilly&rft.aufirst=K&rft.date=1993-01-01&rft.volume=7&rft.issue=3&rft.spage=359&rft.isbn=&rft.btitle=&rft.title=Molecular+Microbiology&rft.issn=0950382X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - Borrelia burgdorferi; Escherichia coli; heat shock proteins; genes; mutants; complementation; nucleotide sequence; amino acid sequence; prediction ER - TY - JOUR T1 - Oxidative DNA damage by crystalline silica. AN - 16697283; 2981082 AB - Using a simple DNA strand breakage assay, we detected the production of oxidant species, probably hydroxyl free radicals, in buffered suspensions of crystalline silica at pH 7.4 DNA damage was affected by the presence of oxygen and was accelerated by superoxide dismutase and by hydrogen peroxide. Deferoxamine blocked damage by hydrogen peroxide and silica but accelerated DNA damage by silica alone and by superoxide dismutase and silica. DNA damage was blocked by catalase and by the scavenging agents dimethyl sulfoxide and sodium benzoate. Chemical etching of crystalline silica to remove impurities by treatment of the surface with hydrofluoric acid resulted in markedly diminished DNA damaging ability. Even preparations of crystalline silica previously characterized as highly pure contained trace iron impurities in amounts significant enough to produce oxygen free radicals in aqueous suspension. Both superoxide and Fenton reaction oxidants were produced. We conclude that silica is able to mediate DNA strand breakage in vitro and that this DNA damage may be an important factor in silica toxicity. JF - Free Radical Biology & Medicine AU - Daniel, L N AU - Mao, Yan AU - Saffiotti, U AD - Lab. of Exp. Pathol., NCI, Build. 41, Room C-105, Bethesda, MD 20892-0041, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 463 EP - 472 VL - 14 IS - 5 SN - 0891-5849, 0891-5849 KW - silica KW - silicon dioxide KW - Biochemistry Abstracts 2: Nucleic Acids; Toxicology Abstracts KW - strands KW - breaks KW - DNA KW - in vitro KW - free radicals KW - N 14630:Chemical reactions & interactions, including effects of radiation KW - X 24155:Biochemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16697283?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Free+Radical+Biology+%26+Medicine&rft.atitle=Oxidative+DNA+damage+by+crystalline+silica.&rft.au=Daniel%2C+L+N%3BMao%2C+Yan%3BSaffiotti%2C+U&rft.aulast=Daniel&rft.aufirst=L&rft.date=1993-01-01&rft.volume=14&rft.issue=5&rft.spage=463&rft.isbn=&rft.btitle=&rft.title=Free+Radical+Biology+%26+Medicine&rft.issn=08915849&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - DNA; strands; breaks; free radicals; in vitro ER - TY - JOUR T1 - Production of recombinant proteins in high-density insect cell cultures AN - 16697251; 3503157 AB - The effect of the growth phase of Spodoptera frugiperda (Sf9) cells on the production of recombinant proteins ( beta -galactosidase and glucocerebrosidase) was investigated. Cells infected with the recombinant Autographa californica nuclear polyhedrosis virus at the late exponential and stationary phases yielded low quantities of expressed protein. Highest enzyme yields were obtained using Sf9 cells from the early exponential phase (0.9 mg beta -galactosidase/10 super(6) cells and 1.7 mu g glucocerebrosidase/10 super(6) cells). Infection of resuspension of cells collected from various phases of growth in fresh medium resulted in 75% restoration of maximal expression levels. This finding suggested either nutrient limitation or waste product accumulation as the cause of the decrease in productivity at the latter phases of growth. Further experiments revealed that the highest productivity levels could be obtained with cultures of Sf9 cells grown in a fermentor to a cell concentration of 4 x 10 super(6)/mL. The medium needed to be replaced prior to infection with the recombinant virus and supplemented with a mixture of glucose, L-glutamine, and yeastolate ultrafiltrate. JF - Biotechnology and Bioengineering AU - Reuveny, S AU - Kim, Y J AU - Kemp, C W AU - Shiloach, J AD - Biotechnol. Unit, LCDB, NIDDK, Natl. Inst. Health, Bldg. 6, Rm. B1-33, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 235 EP - 239 VL - 42 IS - 2 SN - 0006-3592, 0006-3592 KW - beta -galactosidase KW - glucocerebrosidase KW - Biotechnology and Bioengineering Abstracts; Entomology Abstracts; Agricultural and Environmental Biotechnology Abstracts KW - baculovirus KW - Spodoptera frugiperda KW - growth stage KW - batch culture KW - optimization KW - recombinant KW - Noctuidae KW - proteins KW - cell lines KW - Lepidoptera KW - productivity KW - Z 05161:Cell & tissue culture KW - W2 32340:Other peptides, proteins, amino acids KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16697251?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biotechnology+and+Bioengineering&rft.atitle=Production+of+recombinant+proteins+in+high-density+insect+cell+cultures&rft.au=Reuveny%2C+S%3BKim%2C+Y+J%3BKemp%2C+C+W%3BShiloach%2C+J&rft.aulast=Reuveny&rft.aufirst=S&rft.date=1993-01-01&rft.volume=42&rft.issue=2&rft.spage=235&rft.isbn=&rft.btitle=&rft.title=Biotechnology+and+Bioengineering&rft.issn=00063592&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - growth stage; batch culture; optimization; recombinant; proteins; cell lines; productivity; baculovirus; Spodoptera frugiperda; Noctuidae; Lepidoptera ER - TY - JOUR T1 - An approach to development of specific T-lymphocyte lines by use of preprocessed antigens in Plasmodium vinckei vinckei murine malaria. AN - 16697151; 2978569 AB - The development of parasite-specific T-cell lines represents one approach to the potential identification of relevant immunogens in erythrocytic malarial infection. However, the use of parasitized-erythrocyte lysates as antigens inhibits the proliferation of T cells. To circumvent this problem, we preincubated antigen-presenting cells (APCs) from spleens of malaria-naive, BALB/c mice with a Plasmodium vinckei vinckei (hereafter referred to as P. vinckei)-parasitized erythrocyte lysate. APCs were subsequently irradiated and washed prior to being incubated with T lymphocytes from P. vinckei-immune, histocompatible mice. After 8 to 10 cycles of antigenic stimulation and rest, two T-cell lines were analyzed. Both lines were predominantly CD4 super(+). Proliferation assays demonstrated marked lymphocyte blastogenesis to syngeneic but not allogeneic APCs that had preprocessed malarial antigen. Antigen incubated directly with T cells and nonpulsed APCs in vitro did not result in T-cell proliferation. Assays of interleukin-2 (IL-2), IL-4, IL-5, and gamma interferon were compatible with one cell line being predominantly T sub(H)1 and the other being T sub(H)2. Thus, APCs that have preprocessed malarial antigen and are free of extraneous parasite material induce highly reactive, antigen-specific, major histocompatibility complex-restricted T-cell lines that functionally appear capable of inducing humoral and/or cell-mediated immunity. JF - Infection and Immunity AU - Wasserman, G M AU - Kumar, S AU - Ahlers, J AU - Ramsdell, F AU - Berzofsky, JA AU - Miller, L H AD - Lab. Malaria Res., NIAID/NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 1958 EP - 1963 VL - 61 IS - 5 SN - 0019-9567, 0019-9567 KW - Plasmodium vinckei KW - Biotechnology and Bioengineering Abstracts; Agricultural and Environmental Biotechnology Abstracts; Immunology Abstracts; Microbiology Abstracts C: Algology, Mycology & Protozoology KW - lymphocytes T KW - development KW - malaria KW - cell lines KW - antigens KW - K 03086:Immunology & vaccination KW - F 06711:Monoclonal antibodies, hybridomas, antigens and antisera KW - W2 32340:Other peptides, proteins, amino acids KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16697151?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=An+approach+to+development+of+specific+T-lymphocyte+lines+by+use+of+preprocessed+antigens+in+Plasmodium+vinckei+vinckei+murine+malaria.&rft.au=Wasserman%2C+G+M%3BKumar%2C+S%3BAhlers%2C+J%3BRamsdell%2C+F%3BBerzofsky%2C+JA%3BMiller%2C+L+H&rft.aulast=Wasserman&rft.aufirst=G&rft.date=1993-01-01&rft.volume=61&rft.issue=5&rft.spage=1958&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - development; lymphocytes T; malaria; antigens; cell lines ER - TY - JOUR T1 - Induction and enhancement of immune responses to herpes simplex virus type 2 in humans by use of a recombinant glycoprotein D vaccine. AN - 16696979; 2978484 AB - A vaccine for a chronic or recurrent viral infection should induce immune responses that protect against primary disease or that augment preexisting defenses sufficiently to diminish the likelihood of disease recurrence or progression. Such a vaccine was sought for genital herpes, a sexually transmitted infection of epidemic proportion. Vaccine containing recombinant herpes simplex virus type 2 glycoprotein D expressed in CHO cells was given repeatedly and safely to 24 human volunteers. In previously uninfected subjects, the vaccine induced primary antigen-specific and neutralizing antibody responses nearing or exceeding those seen at entry in subjects with genital herpes. Primary cellular immune responses were also evoked. Either the quantity or mode of presentation of antigen permitted this vaccine to exhibit previously unachieved immunogenicity, which may prove adequate for antiviral immunoprophylaxis or treatment of genital herpes. JF - Journal of Infectious Diseases AU - Straus, SE AU - Savarese, B AU - Tigges, M AU - Freifeld, A G AU - Krause, PR AU - Margolis, D M AU - Meier, J L AU - Paar, D P AU - Adair, S F AD - Lab. Clin. Invest., Build. 10, Rm. 11N228, NIAID/NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 1045 EP - 1052 VL - 167 IS - 5 SN - 0022-1899, 0022-1899 KW - glycoprotein D KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Virology & AIDS Abstracts KW - herpes simplex virus 2 KW - vaccines KW - immune response KW - man KW - V 22097:Immunization: Vaccines & vaccination: Human KW - A 01097:Viruses UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16696979?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=unknown&rft.jtitle=Dance+Theatre+Journal&rft.atitle=The+Poised+Disturbances+of+Raimund+Hoghe&rft.au=Johnson%2C+Dominic&rft.aulast=Johnson&rft.aufirst=Dominic&rft.date=2005-01-01&rft.volume=21&rft.issue=2&rft.spage=36&rft.isbn=&rft.btitle=&rft.title=Dance+Theatre+Journal&rft.issn=02649160&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - herpes simplex virus 2; vaccines; immune response; man ER - TY - JOUR T1 - Chronic cannabinoid administration alters cannabinoid receptor binding in rat brain: A quantitative autoradiographic study AN - 16695778; 3502704 AB - The active ingredient of marijuana is (-)- Delta super(9)-tetrahydrocannabinol ( Delta super(9)-THC). Delta super(9)-THC and other natural and synthetic cannabinoids such as CP-55,940 inhibit spontaneous activity and produce catalepsy in animals in a receptor-mediated fashion. Tolerance develops to the motor effects of Delta super(9)-THC after repeated administration. To test the hypothesis that tolerance is mediated by changes in cannabinoid receptor binding characteristics, we used quantitative in vitro autoradiography of [ super(3)H]CP-55,940 binding to striatal brain sections from rats treated either chronically or acutely with Delta super(9)-THC, CP-55,940, or the inactive natural cannabinoid cannabidiol. The data suggest that tolerance to cannabinoids results at least in part from agonist-induced receptor down-regulation. JF - Brain Research AU - Oviedo, A AU - Glowa, J AU - Herkenham, M AD - Sect. Funct. Neuroanat., NIMH Build. 36, Rm. 2D15, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 293 EP - 302 VL - 616 IS - 1-2 SN - 0006-8993, 0006-8993 KW - cannabinoids KW - rats KW - Toxicology Abstracts; CSA Neurosciences Abstracts KW - chronic effects KW - localization KW - receptors KW - neostriatum KW - autoradiography KW - binding KW - N3 11106:Neurobiology of drug abuse KW - X 24180:Social poisons & drug abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16695778?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+Research&rft.atitle=Chronic+cannabinoid+administration+alters+cannabinoid+receptor+binding+in+rat+brain%3A+A+quantitative+autoradiographic+study&rft.au=Oviedo%2C+A%3BGlowa%2C+J%3BHerkenham%2C+M&rft.aulast=Oviedo&rft.aufirst=A&rft.date=1993-01-01&rft.volume=616&rft.issue=1-2&rft.spage=293&rft.isbn=&rft.btitle=&rft.title=Brain+Research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - chronic effects; receptors; binding; autoradiography; localization; neostriatum ER - TY - JOUR T1 - The galactose regulon of Escherichia coli AN - 16695190; 3054220 AB - Galactose transport and metabolism in Escherichia coli involves a multicomponent amphibolic pathway. Galactose transport is accomplished by two different galactose-specific transport systems. At least four of the genes and operons involved in galactose transport and metabolism have promoters containing similar regulatory sequences. These sequences are recognized by at least three regulators, Gal repressor (GalR), Gal isorepressor (GalS) and cAMP receptor protein (CRP), which modulate transcription from these promoters. The negative regulators, GalR and GalS, discriminate between utilization of the high-affinity (regulated by GalS) and low-affinity (regulated by GalR) transport systems, and modulate the expression of genes for galactose metabolism in an overlapping fashion. GalS is itself autogenously regulated and CRP dependent, while the gene for GalR is constitutive. The gal operon encoding the enzymes for galactose metabolism has two promoters regulated by CRP in opposite ways; one (P sub(1)) is stimulated and the other (P sub(2)) inhibited by CRP. Both promoters are strongly repressed by GalR but weakly by GalS. All but one of the constituent promoters of the gal regulon have two operators. The gal regulon has the potential to coordinate galactose metabolism and transport in a highly efficient manner, under a wide variety of conditions of galactose availability. JF - Molecular Microbiology AU - Weickert, MJ AU - Adhya, S AD - Lab. Mol. Biol., NCI/NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 245 EP - 251 VL - 10 IS - 2 SN - 0950-382X, 0950-382X KW - galactose KW - regulons KW - gal gene KW - Microbiology Abstracts B: Bacteriology KW - transport KW - genes KW - metabolism KW - Escherichia coli KW - J 02740:Genetics and evolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16695190?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+Microbiology&rft.atitle=The+galactose+regulon+of+Escherichia+coli&rft.au=Weickert%2C+MJ%3BAdhya%2C+S&rft.aulast=Weickert&rft.aufirst=MJ&rft.date=1993-01-01&rft.volume=10&rft.issue=2&rft.spage=245&rft.isbn=&rft.btitle=&rft.title=Molecular+Microbiology&rft.issn=0950382X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Escherichia coli; transport; metabolism; genes ER - TY - JOUR T1 - Overcoming multidrug resistance in human tumor cells using free and liposomally encapsulated antisense oligodeoxynucleotides AN - 16694655; 3501567 AB - Antisense oligonucleotides offer a molecular targeting tool for overcoming cellular multidrug resistance. In order to improve the in vitro and the in vivo transport of oligodeoxynucleotides, we developed a new liposomal delivery system, using the minimal volume entrapment (MVE) technique. We have demonstrated that cellular uptake and intracellular release of oligodeoxynucleotides were facilitated by delivery in liposomes. 15 mers cap phosphorothioate oligodeoxynucleotides complementary to the 5'end of the coding region or to a loop-forming site in the mdr-1 mRNA were encapsulated in liposomes by the MVE method. P-glycoprotein synthesis and doxorubicin resistance were greatly reduced by exposure of the multidrug resistant SKVLB cells to 5 mu M liposomally encapsulated oligonucleotide. A lower effect was observed when free oligodeoxynucleotides were used. Oligomers antisense to the loop-forming site appeared to be more effective and more specific in modulating multidrug resistance than oligomers with antisense sequence to the 5'end coding region. JF - Biochemical and Biophysical Research Communications AU - Thierry, A R AU - Rahman, A AU - Dritschilo, A AD - Lab. Tumor Cell Biol., NCI/NIH, Bldg. 37, 9000 Rockville Pike, Rockville, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 952 EP - 960 VL - 190 IS - 3 SN - 0006-291X, 0006-291X KW - drug delivery systems KW - oligodeoxyribonucleotides KW - Biotechnology and Bioengineering Abstracts; Medical and Pharmaceutical Biotechnology Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - cells KW - antisense KW - liposomes KW - drug resistance KW - tumors KW - N 14250:Biological properties KW - W 30965:Miscellaneous, Reviews KW - W3 33380:Antisense UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16694655?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+and+Biophysical+Research+Communications&rft.atitle=Overcoming+multidrug+resistance+in+human+tumor+cells+using+free+and+liposomally+encapsulated+antisense+oligodeoxynucleotides&rft.au=Thierry%2C+A+R%3BRahman%2C+A%3BDritschilo%2C+A&rft.aulast=Thierry&rft.aufirst=A&rft.date=1993-01-01&rft.volume=190&rft.issue=3&rft.spage=952&rft.isbn=&rft.btitle=&rft.title=Biochemical+and+Biophysical+Research+Communications&rft.issn=0006291X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - antisense; cells; liposomes; drug resistance; tumors ER - TY - JOUR T1 - Characterization of a monoclonal antibody against human prolactin receptors AN - 16686343; 3689793 AB - Tamoxifen is the first line of therapy for most human breast cancers. It not only works through the estrogen receptor but also can directly affect the binding of prolactin to its receptor. To define this latter mechanism, the nature of the prolactin receptor needs to be clearly defined. Monoclonal antibody (MAb) B6.2, an IgG sub(1) raised against a membrane-enriched fraction from metastatic human breast cancer cells, was as effective as polyclonal anti-prolactin receptor antibody in inhibiting the binding of prolactin to membranes from human tissue and to T47D human breast cancer cells. Control MAbs, MOPC-21 and the anti-NCA B1.1 MAb, had no effect on binding. Epidermal growth-factor receptors on these same cells were unaffected by B6.2. Prolactin-induced growth of the T47D cells was blocked by addition of B6.2 to the media while the control antibodies were without effect. Specific binding of B6.2 to the cells was completely inhibited by prolactin. Binding of both prolactin and B6.2 was inhibited by growing the T47D cells in the presence of tunicamycin A sub(1) under conditions where protein synthesis was not affected but glycosylation of proteins was. An affinity column of B6.2 was used to purify its antigen from T47D cells. The primary purification product, a M sub(r) 90,000 protein, specifically bound the lactogenic hormones human prolactin, human growth hormone and ovine prolactin but not the somatogenic hormone, bovine growth hormone and was precipitated by the polyclonal anti-prolactin receptor antibody but not by control MAbs. When tryptic and V8 digests of the B6.2 antigen and purified prolactin receptors were compared, identical electrophoretic profiles were obtained. Mouse 3T3 cells, when stably transfected with the gene for the long form of the human prolactin receptor, reacted with B6.2 and polyclonal anti-prolactin receptor antibody. Parental 3T3 cells, devoid of prolactin receptors, were negative for all antibodies tested. Thus, MAb B6.2 provides a useful tool for further studies on purification and characterization of these receptors from human tissues and may provide new insights into treatment for breast cancer. JF - International Journal of Cancer AU - Banerjee, R AU - Ginsburg, E AU - Vonderhaar, B K AD - Lab. Tumor Immunol. and Biol., NCI/NIH, Build. 10 Rm. 5B56, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 712 EP - 721 VL - 55 IS - 5 SN - 0020-7136, 0020-7136 KW - prolactin receptors KW - Biotechnology and Bioengineering Abstracts; Medical and Pharmaceutical Biotechnology Abstracts KW - metastases KW - malignancy KW - tumors KW - monoclonal antibodies KW - mammary gland KW - man KW - carcinoma KW - W3 33375:Antibodies KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16686343?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Cancer&rft.atitle=Characterization+of+a+monoclonal+antibody+against+human+prolactin+receptors&rft.au=Banerjee%2C+R%3BGinsburg%2C+E%3BVonderhaar%2C+B+K&rft.aulast=Banerjee&rft.aufirst=R&rft.date=1993-01-01&rft.volume=55&rft.issue=5&rft.spage=712&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - metastases; malignancy; tumors; monoclonal antibodies; mammary gland; man; carcinoma ER - TY - JOUR T1 - Specificity determinants of the P1 and P7 plasmid centromere analogs AN - 16685677; 3054102 AB - The cis-acting parS sites of P1 and P7 are similar in sequence and promote active partition of their respective plasmid prophages to daughter cells when the cognate Par proteins are supplied. Forty of the 94 relevant bases differ between the P1 and P7 parS sites, and the protein-site interactions show complete species specificity. A method was developed to predict which subset of the differing parS bases is responsible. When the four P1 bases thus identified were substituted into the P7 parS site, a complete switch to P1 specificity was observed. The P1-specific bases constitute two CG dinucleotide elements situated 66 bp apart. They lie within repeats of the TCGCCA sequence implicated in secondary contacts with the P1 ParB protein. The equivalent TC dinucleotides in the P7 site were found to be involved in P7 specificity. However, three other P7 bases can also contribute, including two in the heptamer repeats primarily responsible for ParB binding, and the P7-specific information shows some redundancy. The motifs containing the specificity dinucleotides and the primary ParB binding (heptamer) sites bear no obvious relationship of spacing or orientation to each other. For the ParB protein to contact both types of motif at the same time, the topology of the interaction must be complex. JF - Proceedings of the National Academy of Sciences, USA AU - Hayes, F AU - Austin, S J AD - Lab. Chromosome Biol., Advanced BioScience Lab.-Basic Res. Program, NCI-Frederick Cancer Res. Dev. Cent., Frederick, MD 21702, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 9228 EP - 9232 VL - 90 IS - 19 SN - 0027-8424, 0027-8424 KW - plasmid P1 KW - plasmid P7 KW - Microbiology Abstracts B: Bacteriology; Genetics Abstracts KW - centromeres KW - analogs KW - specificity KW - plasmids KW - determinants KW - J 02760:Plasmids KW - G 07203:Plasmids UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16685677?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.atitle=Specificity+determinants+of+the+P1+and+P7+plasmid+centromere+analogs&rft.au=Hayes%2C+F%3BAustin%2C+S+J&rft.aulast=Hayes&rft.aufirst=F&rft.date=1993-01-01&rft.volume=90&rft.issue=19&rft.spage=9228&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - plasmids; centromeres; analogs; specificity; determinants ER - TY - JOUR T1 - Activation of DNA binding by the monomeric form of the P1 replication initiator RepA by heat shock proteins DnaJ and DnaK AN - 16685173; 3054115 AB - RepA protein of plasmid P1 binds to arrays of 19 bp repeat sequences (iterons) and mediates initiation of replication and its control. Escherichia coli heat shock proteins DnaJ and DnaK can stimulate iteron binding activity of RepA in an ATP-dependent fashion. It has been proposed that RepA binds to DNA as monomers and that the stimulation in binding involves monomerization of RepA dimers which are inactive in the binding reaction. RepA-iteron and RepA-RepA interactions have been measured in this study to determine the equilibrium constants of the two reactions. The apparent K sub(D) value for RepA-iteron binding decreased from 10 nM to no more than 0.2 nM at increasing concentrations of the heat shock proteins. The stimulation of binding appears to be due to an increase in active RepA fraction and not to a change in the maximum binding capacity of the active species. This view was deduced from measurements of active RepA fraction, which increased in the presence of heat shock proteins, and from measurements of dissociation rate constants, which were independent of the heat shock protein concentrations. Accounting for the active fractions, the true K sub(D) value was estimated to be 0.10 ( plus or minus 0.09) nM in 20 mM Tris-HCl (pH 8), 100 mM NaCl, 40 mM KCl, 10 mM MgCl sub(2), 1 mM dithiothreitol, 0.1 mM EDTA, ATP (50 mu M), bovine serum albumin (50 mu g/ml), calf thymus DNA (50 mu g/ml) and glycerol (5%). The dissociation rate constant was 1.5 x 10 super(-2) s super(-1) and the calculated association rate constant was 1.5 x 10 super(8) M super(-1) s super(-1). Ultracentrifugation analyses of RepA at 15,000 r.p.m. in the above buffer but without ATP, bovine serum albumin, calf thymus DNA and glycerol, revealed that the protein was in monomer-dimer equilibrium with a K sub(D) of 2.6( plus or minus 0.2) mu M at 5 degree C. Therefore, at protein concentrations used in the binding reactions, RepA is monomeric (>99.5%), in confirmation of the earlier result that RepA binds as a monomer. It follows that the species that is stimulated to bind by the heat shock proteins is also a monomeric form of RepA. JF - Journal of Molecular Biology AU - DasGupta, S AU - Mukhopadhyay, G AU - Papp, P P AU - Lewis AU - Chattoraj, D K AD - Lab. Biochem., NCI, NCRR, NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 23 EP - 34 VL - 232 IS - 1 SN - 0022-2836, 0022-2836 KW - RepA protein KW - DnaJ protein KW - DnaK protein KW - plasmid P1 KW - Microbiology Abstracts B: Bacteriology; Biochemistry Abstracts 2: Nucleic Acids KW - replication KW - DNA KW - Escherichia coli KW - plasmids KW - binding KW - activation KW - J 02727:Amino acids, peptides and proteins KW - N 14940:Nucleic acid-binding proteins UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16685173?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Molecular+Biology&rft.atitle=Activation+of+DNA+binding+by+the+monomeric+form+of+the+P1+replication+initiator+RepA+by+heat+shock+proteins+DnaJ+and+DnaK&rft.au=DasGupta%2C+S%3BMukhopadhyay%2C+G%3BPapp%2C+P+P%3BLewis%3BChattoraj%2C+D+K&rft.aulast=DasGupta&rft.aufirst=S&rft.date=1993-01-01&rft.volume=232&rft.issue=1&rft.spage=23&rft.isbn=&rft.btitle=&rft.title=Journal+of+Molecular+Biology&rft.issn=00222836&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Escherichia coli; DNA; replication; binding; activation; plasmids ER - TY - JOUR T1 - Evaluation of a three-exposure mouse bone marrow micronucleus protocol: Results with 49 chemicals. AN - 16675516; 3038133 AB - Forty-nine chemicals were tested in a mouse bone marrow micronucleus test that employed three daily exposures by intraperitoneal injection. Bone marrow samples were obtained 24 hr following the final exposure. Twenty-five rodent carcinogens and 24 noncarcinogens were selected randomly from the 44 carcinogens and 29 noncarcinogens used by Tennant et al. to evaluate the performance of four in vitro genetic toxicity tests. As in that study of in vitro tests, the micronucleus tests were conducted with coded chemicals and test results (positive or negative) were determined prior to decoding. This study was conducted as part of an effort to assess the ability of the micronucleus test to discriminate between rodent carcinogens and noncarcinogens and to determine its potential role, in combination with other short-term tests, in identifying genotoxic chemicals that present a carcinogenic hazard. Nine chemicals were judged to be positive in the micronucleus test. This relatively low number of positive results, along with published and unpublished results from rodent micronucleus and chromosome aberration assays on several of these 49 chemicals, contributed to the conclusion that a single micronucleus test protocol is not adequate to detect all chemicals capable of inducing chromosomal damage in the bone marrow. However, a combination of two relatively simple assays such as the Salmonella and micronucleus tests can provide important information on the genetic toxicity of test chemicals and may provide guidance on the need for and the nature and extent of further toxicity studies. JF - Environmental and Molecular Mutagenesis AU - Shelby, MD AU - Erexson, G L AU - Hook, G J AU - Tice, R R AD - NIEHS, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 160 EP - 179 VL - 21 IS - 2 SN - 0893-6692, 0893-6692 KW - mice KW - Toxicology Abstracts; Genetics Abstracts KW - carcinogens KW - genotoxicity KW - micronuclei KW - comparison KW - bone marrow KW - G 07220:General theory/testing systems KW - X 24221:Toxicity testing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16675516?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+and+Molecular+Mutagenesis&rft.atitle=Evaluation+of+a+three-exposure+mouse+bone+marrow+micronucleus+protocol%3A+Results+with+49+chemicals.&rft.au=Shelby%2C+MD%3BErexson%2C+G+L%3BHook%2C+G+J%3BTice%2C+R+R&rft.aulast=Shelby&rft.aufirst=MD&rft.date=1993-01-01&rft.volume=21&rft.issue=2&rft.spage=160&rft.isbn=&rft.btitle=&rft.title=Environmental+and+Molecular+Mutagenesis&rft.issn=08936692&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - carcinogens; genotoxicity; comparison; bone marrow; micronuclei ER - TY - JOUR T1 - Enhancement of myelotoxicity induced by repeated irradiation in mice exposed to a mixture of groundwater contaminants. AN - 16674773; 3038161 AB - As part of a program on the toxicology of chemical mixtures at the National Institute of Environmental Health Sciences/National Toxicology Program (NIEHS/NTP), hematopoietic functions were studied in female B6C3F sub(1) mice treated with 0, 1%, and 5% of a chemical mixture stock of 25 groundwater contaminants in drinking water for 31.5 weeks. The toxicologic interaction between continuous exposure to groundwater contaminants and stress induced by multiple irradiation on hematopoiesis was investigated. Non-irradiated mice treated with 5% chemical mixture solution showed suppression of CFU-GM after 15.5 weeks and became progressively more affected (only 70% of controls by 31.5 weeks of treatment). The population of CFU-GM in mice treated with 5% chemical mixture for 4.5 weeks plus irradiation (1 week after first irradiation) was only 22% of the non-irradiated vehicle control group. This combined (i.e., chemical mixture plus irradiation) suppression of CFU-GM intensified after repeated irradiation until the number of CFU-GM was only 10.7% following the fourth irradiation at 25.5 weeks. JF - Archives of Toxicology AU - Hong, H L AU - Yang, RSH AU - Boorman, G A AD - NIEHS (MD D2-05), P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 358 EP - 364 VL - 67 IS - 5 SN - 0340-5761, 0340-5761 KW - myelotoxicity KW - mice KW - Toxicology Abstracts KW - radiation KW - contaminants KW - ground water KW - X 24240:Miscellaneous KW - X 24210:Radiation & radioactive materials UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16674773?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+Toxicology&rft.atitle=Enhancement+of+myelotoxicity+induced+by+repeated+irradiation+in+mice+exposed+to+a+mixture+of+groundwater+contaminants.&rft.au=Hong%2C+H+L%3BYang%2C+RSH%3BBoorman%2C+G+A&rft.aulast=Hong&rft.aufirst=H&rft.date=1993-01-01&rft.volume=67&rft.issue=5&rft.spage=358&rft.isbn=&rft.btitle=&rft.title=Archives+of+Toxicology&rft.issn=03405761&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - ground water; contaminants; radiation ER - TY - JOUR T1 - A recombinant form of Pseudomonas exotoxin A containing transforming growth factor alpha near its carboxyl terminus for the treatment of bladder cancer AN - 16670881; 3687205 AB - The epidermal growth factor receptor (EGFR) is overexpressed on the superficial layers of malignant urothelium and is suspected of playing a role in tumor progression. TP40 is a chimeric protein composed of transforming growth factor- alpha (TGF alpha ) fused to a modified form of Pseudomonas exotoxin A (PE) that is selectively cytotoxic to EGFR-bearing cells and is currently undergoing clinical study for the intravesical therapy of bladder cancer. We constructed a recombinant toxin PE35/TGF alpha -KDEL as an improved agent for the local therapy of EGFR-bearing bladder cancer. PE35/TGF alpha -KDEL does not require intracellular proteolysis to generate a carboxyl-terminal fragment capable of reaching the target cell cytosol and contains a modified carboxyl-terminal sequence KDEL, that increases toxin activity. These features make PE35/TGF alpha -KDEL from 10- to 700-fold more potent than TP40 on four human bladder cancer cell lines. PE35/TGF alpha -KDEL may be a useful agent for treatment of EGFR-bearing cancers. JF - Journal of Urology AU - Theuer, C P AU - Fitzgerald, D J AU - Pastan, I AD - Lab. Mol. Biol., NCI/NIH, Div. Cancer Biol., Diagn. and Cent., Build. 37, Rm. 4E16, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 1626 EP - 1632 VL - 149 IS - 6 SN - 0022-5347, 0022-5347 KW - chimeric proteins KW - exotoxin A KW - Biotechnology and Bioengineering Abstracts; Immunology Abstracts; Medical and Pharmaceutical Biotechnology Abstracts KW - urinary bladder KW - recombinants KW - treatment KW - malignancy KW - in vitro KW - Pseudomonas KW - proteolysis KW - growth factors KW - man KW - carcinoma KW - F 06818:Cancer immunotherapy KW - W3 33190:Therapy: Other KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16670881?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Urology&rft.atitle=A+recombinant+form+of+Pseudomonas+exotoxin+A+containing+transforming+growth+factor+alpha+near+its+carboxyl+terminus+for+the+treatment+of+bladder+cancer&rft.au=Theuer%2C+C+P%3BFitzgerald%2C+D+J%3BPastan%2C+I&rft.aulast=Theuer&rft.aufirst=C&rft.date=1993-01-01&rft.volume=149&rft.issue=6&rft.spage=1626&rft.isbn=&rft.btitle=&rft.title=Journal+of+Urology&rft.issn=00225347&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - urinary bladder; recombinants; treatment; in vitro; malignancy; proteolysis; growth factors; man; carcinoma; Pseudomonas ER - TY - JOUR T1 - 3-Nitropropionic acid is an indirect excitotoxin to cultured cerebellar granule neurons AN - 16668482; 3678813 AB - 3-Nitropropionic acid is a fungal neurotoxin preferentially affecting basal ganglia and hippocampus in laboratory animals. The ability of N-methyl-D-aspartate (NMDA) receptor agonists and antagonists to modify 3-nitropropionic acid toxicity was studied in cultured rat cerebellar granule neurons. Exposure of these neurons to 3-nitropropionic acid resulted in a concentration and time-dependent neurotoxicity. In contrast to glutamate toxicity, 3-nitropropionic acid toxicity was potentiated by preexposure to subtoxic concentrations of NMDA. Presumably, the 3-nitropropionic acid-induced energy depletion relieved the voltage-dependent Mg super(2+) block of the NMDA receptor and induced vulnerability to subtoxic concentrations of NMDA receptor agonists. MK-801 and 2-amino-5-phosphonovaleric acid (APV) delayed but did not prevent 3-nitropropionic acid toxicity, indicating that prolonged exposure to 3-nitropropionic acid ultimately resulted in histotoxic neuronal death. JF - European Journal of Pharmacology: (Environmental Toxicology and Pharmacology Section) AU - Weller, M AU - Paul, S M AD - Sect. Mol. Pharmacol., Clin. Neurosci. Branch, NIMH, Build. 49, Rm B1EE16, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 223 EP - 228 VL - 248 IS - 3 SN - 0926-6917, 0926-6917 KW - 3-nitropropionic acid KW - N-methyl-D-aspartic acid receptors KW - NMDA receptors KW - effects on KW - rats KW - Microbiology Abstracts C: Algology, Mycology & Protozoology; Toxicology Abstracts; CSA Neurosciences Abstracts KW - agonists KW - neurotoxicity KW - antagonists KW - neurons KW - cerebellum KW - N3 11104:Mammals (except primates) KW - K 03040:Fungi KW - X 24171:Microbial UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16668482?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+Journal+of+Pharmacology%3A+%28Environmental+Toxicology+and+Pharmacology+Section%29&rft.atitle=3-Nitropropionic+acid+is+an+indirect+excitotoxin+to+cultured+cerebellar+granule+neurons&rft.au=Weller%2C+M%3BPaul%2C+S+M&rft.aulast=Weller&rft.aufirst=M&rft.date=1993-01-01&rft.volume=248&rft.issue=3&rft.spage=223&rft.isbn=&rft.btitle=&rft.title=European+Journal+of+Pharmacology%3A+%28Environmental+Toxicology+and+Pharmacology+Section%29&rft.issn=09266917&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - neurotoxicity; agonists; antagonists; cerebellum; neurons ER - TY - JOUR T1 - X-ray-induced chromatid damage in relation to DNA repair and cancer incidence in family members. AN - 16667457; 3022240 AB - The cytogenetic response to G sub(2)-phase X-irradiation was examined in phytohemagglutinin-stimulated peripheral-blood lymphocytes from 69 individuals, a few of whom were cancer patients. The cancer patients had not received radiation or chemotherapy. The responses of cells arrested by Colcemid 30 to 90 min after X-irradiation (58R) could be divided into 2 distinct categories: 51 individuals had aberration frequencies typical of normal individuals in previous studies, while 18 others had a 2- to 3-fold higher frequency of chromatid breaks and gaps. Because chromatid breaks and gaps results from unrepaired DNA strand breaks, the first category may represent an efficient DNA repair phenotype, while the second may represent a deficient repair phenotype. The individuals with the deficient G sub(2) response reported having first- and second-degree relatives with a 3.6- and 2.2-fold higher mean frequency of cancer, respectively. The present results, together with those from earlier studies of families with a genetic disorder predisposing to cancer, suggest that this deficient cytogenetic response to G sub(2) phase X-irradiation is associated with a high risk of cancer. JF - International Journal of Cancer AU - Knight, R D AU - Parshad, R AU - Price, F M AU - Tarone, R E AU - Sanford, K K AD - Build. 37, Rm. 2D15, NCI/NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 589 EP - 593 VL - 54 IS - 4 SN - 0020-7136, 0020-7136 KW - DNA repair KW - X radiation KW - carcinoma KW - chromatids KW - damage KW - family studies KW - man KW - Human Genome Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Toxicology Abstracts KW - X 24210:Radiation & radioactive materials KW - N 14652:DNA repair UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16667457?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Cancer&rft.atitle=X-ray-induced+chromatid+damage+in+relation+to+DNA+repair+and+cancer+incidence+in+family+members.&rft.au=Knight%2C+R+D%3BParshad%2C+R%3BPrice%2C+F+M%3BTarone%2C+R+E%3BSanford%2C+K+K&rft.aulast=Knight&rft.aufirst=R&rft.date=1993-01-01&rft.volume=54&rft.issue=4&rft.spage=589&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - X radiation; chromatids; damage; DNA repair; carcinoma; family studies; man ER - TY - JOUR T1 - Dose response for TCDD promotion of hepatocarcinogenesis in rats initiated with DEN: Histologic, biochemical, and cell proliferation endpoints AN - 16659958; 3666437 AB - The present study examines the dose-response relationship for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) promotion of histologic and biochemical parameters by using a two-stage model for hepatocarcinogenesis in female Sprague-Dawley rats initiated with a single intraperitoneal dose of 175 mg of diethylnitrosamine (DEN)/kg body weight at 70 days of age. A significant body weight reduction was present in the noninitiated group that received 125 ng TCDD. Relative liver weight was statistically increased in initiated rats treated with greater than or equal to 10.7 ng TCDD and in noninitiated rats treated with greater than or equal to 35.7 ng TCDD. Histopathologic evidence of cytotoxicity was dose-related in all TCDD-treated groups. There was a statistically significant dose response in the bromodeoxyuridine (BrdU) S-phase labeling index (LI) in the DEN-initiated rats and a marginally significant trend in the saline-treated rats (p = 0.10), but proliferating cell nuclear antigen S-phase LI and growth fraction within altered hepatic foci showed no increase. JF - Environmental Health Perspectives AU - Maronpot, R R AU - Foley, J F AU - Takahashi, K AU - Goldsworthy, T AU - Clark, G AU - Tritscher, A AU - Portier, C AU - Lucier, G AD - NIEHS, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 634 EP - 642 VL - 101 IS - 7 SN - 0091-6765, 0091-6765 KW - TCDD KW - N-nitrosodiethylamine KW - rats KW - Toxicology Abstracts KW - cell proliferation KW - carcinogenesis KW - liver KW - X 24152:Chronic exposure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16659958?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Dose+response+for+TCDD+promotion+of+hepatocarcinogenesis+in+rats+initiated+with+DEN%3A+Histologic%2C+biochemical%2C+and+cell+proliferation+endpoints&rft.au=Maronpot%2C+R+R%3BFoley%2C+J+F%3BTakahashi%2C+K%3BGoldsworthy%2C+T%3BClark%2C+G%3BTritscher%2C+A%3BPortier%2C+C%3BLucier%2C+G&rft.aulast=Maronpot&rft.aufirst=R&rft.date=1993-01-01&rft.volume=101&rft.issue=7&rft.spage=634&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - liver; carcinogenesis; cell proliferation ER - TY - JOUR T1 - Effect of temperature and oxygen on cell growth and recombinant protein production in insect cell cultures. AN - 16657129; 3018636 AB - The effect of temperature and O sub(2) saturation on the production of recombinant proteins beta -galactosidase and human glucocerebrosidase by Spodoptera frugiperda) cells (Sf9) infected with recombinant Autographa californica nuclear polyhedrosis virus was investigated. The rates of cell growth, glucose consumption, O sub(2) consumption and product expression were measured at temperatures between 22 degree C and 35 degree C. The results indicated that possible O sub(2) limitation may be alleviated without compromising the maximum cell yield by lowering the incubation temperature from 27 degree C to 25 degree C. The expression level of the recombinant proteins at 27 degree C was similar to that obtained at 22 degree C and 25 degree C; lower protein yields were obtained at 30 degree C. An increase in temperature from 22 degree C to 27 degree C led to earlier production of the proteins and to an increase in the proportion of the product released outside the cells. JF - Applied Microbiology and Biotechnology AU - Reuveny, S AU - Kim, Y J AU - Kemp, C W AU - Shiloach, J AD - Biotechnol. Unit, LCDB, NIDDK, NIH, Build. 6, Rm. B1-33, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 619 EP - 623 VL - 38 IS - 5 SN - 0175-7598, 0175-7598 KW - oxygen KW - temperature KW - Biotechnology and Bioengineering Abstracts; Medical and Pharmaceutical Biotechnology Abstracts KW - Spodoptera frugiperda KW - Autographa californica KW - proteins KW - production KW - nuclear polyhedrosis virus KW - growth KW - W 30965:Miscellaneous, Reviews KW - W3 33220:Cell culture UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16657129?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Applied+Microbiology+and+Biotechnology&rft.atitle=Effect+of+temperature+and+oxygen+on+cell+growth+and+recombinant+protein+production+in+insect+cell+cultures.&rft.au=Reuveny%2C+S%3BKim%2C+Y+J%3BKemp%2C+C+W%3BShiloach%2C+J&rft.aulast=Reuveny&rft.aufirst=S&rft.date=1993-01-01&rft.volume=38&rft.issue=5&rft.spage=619&rft.isbn=&rft.btitle=&rft.title=Applied+Microbiology+and+Biotechnology&rft.issn=01757598&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - production; proteins; growth; Spodoptera frugiperda; Autographa californica; nuclear polyhedrosis virus ER - TY - JOUR T1 - Identification of a protein in several Borrelia species which is related to OspC of the Lyme disease spirochetes. AN - 16652754; 3038039 AB - Using oligonucleotide probes which have previously been shown to be specific for the ospC gene found in the Lyme disease spirochete species Borrelia burgdorferi, B. garinii , and group VS461, we detected an ospC homolog in other Borrelia species including B. coriaceae, B. hermsii, B. anserina, B. turicatae , and B. parkeri . In contrast to the Lyme disease spirochetes, which carry the ospC gene on a 26-kb circular plasmid, we mapped the gene in other Borrelia species to linear plasmids which varied in size among the isolates tested. Some isolates carry multiple copies of the gene residing on linear plasmids of different sizes. The analyses conducted here also demonstrate that these Borrelia species contain a linear chromosome. Northern (RNA) blot analyses demonstrated that the gene is transcriptionally expressed in all species examined. High levels of transcriptional expression were observed in some B. hermsii isolates. Transcriptional start site analyses revealed that the length of the untranslated leader sequence was identical to that observed in the Lyme disease spirochete species. By Western blotting (immunoblotting) with antiserum (polyclonal) raised against the OspC protein of B. burgdorferi , we detected an immunoreactive protein of the same molecular weight as the OspC found in Lyme disease spirochete species. The results presented here demonstrate the presence of a protein that is genetically and antigenically related to OspC which is expressed in all species of the genus Borrelia tested. JF - Journal of Clinical Microbiology AU - Marconi, R T AU - Samuels, D S AU - Schwan, T G AU - Garon, C F AD - Lab. Vectors and Pathog., Rocky Mountain Lab., NIAID, Hamilton, MT 59840, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 2577 EP - 2583 VL - 31 IS - 10 SN - 0095-1137, 0095-1137 KW - OspC protein KW - ospC gene KW - Microbiology Abstracts B: Bacteriology KW - isolation KW - genes KW - Borrelia KW - homology KW - probes KW - Lyme disease KW - J 02727:Amino acids, peptides and proteins KW - J 02740:Genetics and evolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16652754?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Clinical+Microbiology&rft.atitle=Identification+of+a+protein+in+several+Borrelia+species+which+is+related+to+OspC+of+the+Lyme+disease+spirochetes.&rft.au=Marconi%2C+R+T%3BSamuels%2C+D+S%3BSchwan%2C+T+G%3BGaron%2C+C+F&rft.aulast=Marconi&rft.aufirst=R&rft.date=1993-01-01&rft.volume=31&rft.issue=10&rft.spage=2577&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Microbiology&rft.issn=00951137&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Borrelia; homology; genes; isolation; probes; Lyme disease ER - TY - JOUR T1 - Morphologic and antigenic characterization of interferon gamma -mediated persistent Chlamydia trachomatis infection in vitro. AN - 16648054; 2992495 AB - An in vitro cell culture system was used to study the effect of interferon gamma (IFN- gamma ) on Chlamydia trachomatis growth and differentiation. The effect of IFN- gamma on chlamydiae was dose-dependent. IFN- gamma at 2 ng/ml completely inhibited chlamydial growth and differentiation; however, persistent infection was established when chlamydiae were cultured with IFN- gamma at 0.2 ng/ml. Persistent infection was characterized by the development of noninfectious atypical chlamydial forms from which infectious progeny could be recovered only when IFN- gamma was removed from the culture system. Analysis of persistently infected cells by immunofluorescent microscopy and immunoblotting with specific antibodies revealed that the atypical chlamydial forms had near-normal levels of the 60-kDa heat shock protein, an immunopathologic antigen, and a paucity of the major outer membrane protein, a protective antigen. Furthermore, steady-state levels of other outer membrane constituents, such as the 60-kDa cysteine-rich outer membrane protein and lipopolysaccharide, were greatly reduced. If IFN- gamma causes similar events to occur in vivo, then persistently infected cells could augment the pathogenesis of the chronic inflammatory sequelae that follow chlamydial infection by serving as depots of antigen capable of stimulating a sustained inflammatory response. JF - Proceedings of the National Academy of Sciences, USA AU - Beatty, W L AU - Byrne, GI AU - Morrison, R P AD - Lab. Intracell. Parasit., Rocky Mountain Lab., NIAID/NIH, Hamilton, MT 59840, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 3998 EP - 4002 VL - 90 IS - 9 SN - 0027-8424, 0027-8424 KW - Immunology Abstracts; Microbiology Abstracts B: Bacteriology KW - cell culture KW - inflammatory diseases KW - antigenic characteristics KW - Chlamydia trachomatis KW - morphology KW - persistent infection KW - gamma -interferon KW - J 02832:Antigenic properties and virulence KW - F 06801:Bacteria UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16648054?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.atitle=Morphologic+and+antigenic+characterization+of+interferon+gamma+-mediated+persistent+Chlamydia+trachomatis+infection+in+vitro.&rft.au=Beatty%2C+W+L%3BByrne%2C+GI%3BMorrison%2C+R+P&rft.aulast=Beatty&rft.aufirst=W&rft.date=1993-01-01&rft.volume=90&rft.issue=9&rft.spage=3998&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Chlamydia trachomatis; persistent infection; gamma -interferon; morphology; antigenic characteristics; cell culture; inflammatory diseases ER - TY - JOUR T1 - Polyamine-like actions of peptides derived from conantokin-G, an N-methyl-D-aspartate (NMDA) antagonist. AN - 16647192; 2995470 AB - Conantokins-T and -G are highly conserved polypeptides derived from Conus venoms. The N-methyl-D-aspartate (NMDA) antagonist properties of these compounds have been attributed to a potent noncompetitive inhibition of polyamine responses. Substitution of the highly conserved gamma -carboxyglutamate residues as well as modification of the N and C termini of conantokin-G abolished the inhibition of polyamine responses at the NMDA receptor complex. However, several of these modified polypeptides closely mimicked the neurochemical profile of polyamines at the NMDA receptor complex. One of these derivatives, Tyr super(0)-conantokin-G, was found to be the most potent compound exhibiting polyamine-like actions at the NMDA receptor complex described to date, similar to 7-fold more potent than spermine. Circular dichroism studies demonstrate a significant alpha -helical content in conantokin-G (27% in aqueous medium). However, this alpha -helicity is not sufficient for the NMDA antagonist action of the parent peptide and is neither necessary nor sufficient for the polyamine-like behavior of several conantokin-G analogs. The modified conantokin-G derivatives described in this report should be useful probes for examining the role of both polyamines and the polyamine recognition site in the operation of the NMDA receptor complex. JF - Journal of Biological Chemistry AU - Chandler, P AU - Pennington, M AU - Maccecchini, M-L AU - Nashed, N T AU - Skolnick, P AD - Lab. Neurosci., NIDDK/LN, NIH, Build. 8, Rm. 111, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 17173 EP - 17178 VL - 268 IS - 23 SN - 0021-9258, 0021-9258 KW - N-methyl-D-aspartate antagonist KW - NMDA KW - antagonists KW - biological poisons KW - conantokin-G KW - derivatives KW - polyamines KW - venom KW - Toxicology Abstracts; ASFA Marine Biotechnology Abstracts; ASFA 1: Biological Sciences & Living Resources KW - Marine KW - electrophysiology KW - polypeptides KW - receptors KW - pharmacology KW - Conus KW - Q4 27390:Toxins KW - Q1 08266:Physiology, biochemistry, biophysics KW - Q1 08625:Non-edible products KW - X 24173:Animals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16647192?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=Polyamine-like+actions+of+peptides+derived+from+conantokin-G%2C+an+N-methyl-D-aspartate+%28NMDA%29+antagonist.&rft.au=Chandler%2C+P%3BPennington%2C+M%3BMaccecchini%2C+M-L%3BNashed%2C+N+T%3BSkolnick%2C+P&rft.aulast=Chandler&rft.aufirst=P&rft.date=1993-01-01&rft.volume=268&rft.issue=23&rft.spage=17173&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2014-05-06 N1 - SubjectsTermNotLitGenreText - biological poisons; electrophysiology; polypeptides; receptors; pharmacology; venom; antagonists; derivatives; Conus; Marine ER - TY - JOUR T1 - Pesticide exposures and multiple myeloma in Iowa men. AN - 16644562; 2998097 AB - A population-based case-control study of 173 White men with multiple myeloma (MM) and 650 controls was conducted in Iowa (United States), an area with a large farming population, to evaluate the association between MM, agricultural risk factors, and exposure to individual pesticides. A slight nonsignificantly elevated risk for MM was seen among farmers. Although slight excesses were observed, there were no significant associations between MM and handling either classes of pesticides or specific pesticides. Thus, this study found little evidence to suggest an association between risk of MM and farming or pesticides. JF - Cancer Causes & Control AU - Brown, L M AU - Burmeister, L F AU - Everett, G D AU - Blair, A AD - Epidemiol. and Biostat. Program, NCI, Executive Plaza North, Rm. 415, Bethesda, MD 20014, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 153 EP - 156 VL - 4 IS - 2 SN - 0957-5243, 0957-5243 KW - exposure KW - multiple myeloma KW - relationship KW - man KW - Health & Safety Science Abstracts; Pollution Abstracts; Risk Abstracts; Toxicology Abstracts KW - occupational exposure KW - agriculture KW - epidemiology KW - USA, Iowa KW - pesticides KW - cancer KW - X 24132:Chronic exposure KW - R2 23060:Medical and environmental health KW - H SM10.21:CANCER KW - P 6000:TOXICOLOGY AND HEALTH UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16644562?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Causes+%26+Control&rft.atitle=Pesticide+exposures+and+multiple+myeloma+in+Iowa+men.&rft.au=Brown%2C+L+M%3BBurmeister%2C+L+F%3BEverett%2C+G+D%3BBlair%2C+A&rft.aulast=Brown&rft.aufirst=L&rft.date=1993-01-01&rft.volume=4&rft.issue=2&rft.spage=153&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - USA, Iowa; pesticides; epidemiology; occupational exposure; agriculture; cancer; exposure; multiple myeloma; relationship; man ER - TY - JOUR T1 - Stimulatory effect of the CYP1A1 inducer 2,3,7,8-tetrachlorodibenzo-p-dioxin on the reproduction of HIV-1 in human lymphoid cell cultures. AN - 16640055; 3032886 AB - 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) was an inducer of microsomal benzo( alpha )pyrene hydroxylase (AHH) and 7-ethoxyresorufin O-deethylase (EROD) in MT-4 human lymphoid cell culture. Incubation of MT-4 cells with TCDD at 10, 50 and 150 nM for 1.5 and 48 h followed by infection of the cells with human immunodeficiency virus 1 (HIV-1) was accompanied by a 3-6-fold increase in the activity of viral RNA-dependent DNA-polymerase. The most marked effect on reverse transcriptase activity occurred with 10 nM TCDD 5-9 days after HIV-1 infection. In the same period there was accumulation of viral protein, determined by ELISA, with a 4-8- fold increase in production of viral protein. The above effects of TCCD have been observed even when MT-4 cells were washed 1.5 h after beginning the incubation with TCDD. JF - Xenobiotica AU - Tsyrlov, IB AU - Pokrovsky, A AD - Lab. Mol. Carcinog., NCI/NIH, Build. 37, Room 3E-24, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 457 EP - 467 VL - 23 IS - 4 SN - 0049-8254, 0049-8254 KW - 2,3,7,8-tetrachlorodibenzo(p)dioxin KW - Virology & AIDS Abstracts; Toxicology Abstracts KW - cell culture KW - human immunodeficiency virus KW - reproduction KW - lymphoid cells KW - X 24155:Biochemistry KW - V 22002:AIDS: Molecular and in vitro aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16640055?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Xenobiotica&rft.atitle=Stimulatory+effect+of+the+CYP1A1+inducer+2%2C3%2C7%2C8-tetrachlorodibenzo-p-dioxin+on+the+reproduction+of+HIV-1+in+human+lymphoid+cell+cultures.&rft.au=Tsyrlov%2C+IB%3BPokrovsky%2C+A&rft.aulast=Tsyrlov&rft.aufirst=IB&rft.date=1993-01-01&rft.volume=23&rft.issue=4&rft.spage=457&rft.isbn=&rft.btitle=&rft.title=Xenobiotica&rft.issn=00498254&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - human immunodeficiency virus; reproduction; cell culture; lymphoid cells ER - TY - JOUR T1 - Behavioral and neuroendocrine effects of diethyl ether exposure in the mouse AN - 16637585; 3678187 AB - Diethyl ether has diverse behavioral effects and is known for its ability to stimulate stress hormones, yet little is known of the concentrations in which these effects occur. To more fully characterize these effects, adult male NIH mice were exposed to a range of concentrations of ether (1000-30000 ppm) in an inhalation chamber and both behavioral and neuroendocrine responses were assessed. When responding was maintained under FI-60 s schedules of milk presentation, 30-min exposures to 1000 ppm ether resulted in minimal behavioral effects, 3000-10000 ppm increased rates of responding over two-fold and higher concentrations decreased responding almost completely. Five-min exposures to the same range of concentrations resulted in concentration-related effects which were smaller than those produced by 30-min exposures. Exposure to a similar range of concentrations in naive mice increased adrenocorticotrophic hormone (ACTH) and corticosterone levels in a time- and concentration-dependent manner. Five-min exposures to 10000 ppm ether increased levels of ACTH from a baseline of 25.95 pg/ml to 310.5 pg/ml but did not affect corticosterone. Thirty-min exposures to the full range of concentrations of ether, increased corticosterone from control levels of 70 ng/ml to 418 ng/ml at 30000 ppm, and increased ACTH from control levels of 19.13 pg/ml to 80.5 pg/ml at 30000 ppm, in a concentration-dependent manner. The increase in ACTH for 30-min exposures was not as large as that observed for 5-min exposures at 10000 ppm, nor was it as large as that seen for corticosterone. The imidazobenzodiazepine, Ro 15-4513 decreased FI responding at doses greater than 3 mg/kg and attenuated the rate-increasing effects of diethyl ether at 1 mg/kg. Diethyl ether exhibits robust behavioral and neuroendocrine activating effects. JF - Neurotoxicology and Teratology AU - Glowa, J R AD - Behav. Pharmacol. and Toxicol. Unit, LMC/NIDDK, Build. 14D Rm. 311, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 215 EP - 221 VL - 15 IS - 4 SN - 0892-0362, 0892-0362 KW - ethyl ether KW - adrenocorticotropic hormone KW - corticosterone KW - mice KW - hypothalamic-pituitary-adrenal axis KW - Toxicology Abstracts; CSA Neurosciences Abstracts KW - solvents KW - X 24155:Biochemistry KW - N3 11080:Neuroendocrinology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16637585?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurotoxicology+and+Teratology&rft.atitle=Behavioral+and+neuroendocrine+effects+of+diethyl+ether+exposure+in+the+mouse&rft.au=Glowa%2C+J+R&rft.aulast=Glowa&rft.aufirst=J&rft.date=1993-01-01&rft.volume=15&rft.issue=4&rft.spage=215&rft.isbn=&rft.btitle=&rft.title=Neurotoxicology+and+Teratology&rft.issn=08920362&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - solvents ER - TY - JOUR T1 - Serum antibodies from halothane hepatitis patients react with the rat endoplasmic reticulum protein ERp72 AN - 16631523; 3674965 AB - Immunoblotting studies have previously shown that serum antibodies from halothane hepatitis patients react with several liver microsomal proteins that have been modified by the trifluoroacetyl halide metabolite of halothane. In this study, an 80-kDa protein recognized by the patients' antibodies has been purified from rat liver microsomes and characterized. When the purified trifluoroacetylated 80-kDa and native 80-kDa proteins were employed as test antigens in an enzyme-linked immunosorbent assay, serum antibodies from halothane hepatitis patients reacted with both of these proteins to a significantly greater extent than did serum antibodies from control patients. Amino acid sequence analyses of several hydrolytic peptide fragments of the 80-kDa protein showed that the protein was 99% identical to the deduced amino acid sequence of a murine cDNA of the luminal endoplasmic reticulum protein ERp72. These results indicate that trifluoroacetylated ERp72 in the liver of halothane hepatitis patients may induce immune responses against epitopes present on the covalently altered protein and those present on the native protein and may have a role in halothane hepatitis. In addition, immunoblot and immunohistochemical studies revealed that the 80-kDa protein was present in all tissues studied, but was in highest concentration in liver, adipose tissue, ovaries, and testes and was enriched in specific cells of some organs. In the future, these findings should help define the physiological function of ERp72. JF - Chemical Research in Toxicology AU - Pumford, N R AU - Martin, B M AU - Thomassen, D AU - Burris, JA AU - Kenna, J G AU - Martin, J L AU - Pohl, L R AD - Lab. Chem. Pharmacol., NHLBI, NIH, Build. 10, Rm. 8N 115, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 609 EP - 615 VL - 6 IS - 5 SN - 0893-228X, 0893-228X KW - halothane KW - ERp72 protein KW - rats KW - Immunology Abstracts; Toxicology Abstracts KW - side effects KW - antibodies KW - anesthetics KW - autoantibodies KW - immune response (humoral) KW - hepatitis KW - man KW - F 06877:Other KW - X 24113:Side effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16631523?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+Research+in+Toxicology&rft.atitle=Serum+antibodies+from+halothane+hepatitis+patients+react+with+the+rat+endoplasmic+reticulum+protein+ERp72&rft.au=Pumford%2C+N+R%3BMartin%2C+B+M%3BThomassen%2C+D%3BBurris%2C+JA%3BKenna%2C+J+G%3BMartin%2C+J+L%3BPohl%2C+L+R&rft.aulast=Pumford&rft.aufirst=N&rft.date=1993-01-01&rft.volume=6&rft.issue=5&rft.spage=609&rft.isbn=&rft.btitle=&rft.title=Chemical+Research+in+Toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - hepatitis; side effects; antibodies; man; anesthetics; immune response (humoral); autoantibodies ER - TY - JOUR T1 - Mycoplasmal pericarditis: Evidence of invasive disease. AN - 16631454; 3028050 AB - Although the pathogenic mycoplasmas usually infect the respiratory and urogenital tracts, these organisms also can cause disease in remote sites. Such infections are difficult to diagnose because of both the fastidious nature of the mycoplasmas and the failure to consider their presence. Pericarditis is an uncommonly diagnosed and rarely confirmed example of invasive mycoplasmal infection. As part of a prospective study of large pericardial effusions, we discovered two cases with Mycoplasma pneumoniae infection. Subsequently, two cases of pericarditis due to Mycoplasma hominis and one due to Ureaplasma urealyticum were diagnosed. For all five patients, cultures of pericardial tissue and/or fluid were positive. In addition, four of the five patients either were immunocompromised or had undergone cardiac surgery previously. Appropriate antibiotic therapy was uniformly effective. We report here our experience with mycoplasmal pericarditis, provide evidence of an invasive pathogenesis for this syndrome, and suggest that pericardial disease caused by these organisms may not be an uncommon finding when sought in an aggressive manner. JF - Clinical Infectious Diseases AU - Kenney, R T AU - Li, J S AU - Clyde, WA Jr AU - Wall, T C AU - O'Connor, C M AU - Campbell, P T AU - Van Trigt, P AU - Corey, G R AD - Lab. Parasitic Dis./NIAID/NIH, Build. 4, Rm. 126, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SN - 1058-4838, 1058-4838 KW - Microbiology Abstracts B: Bacteriology KW - pericarditis KW - Ureaplasma urealyticum KW - pathogenicity KW - Mycoplasma pneumoniae KW - diseases KW - Mycoplasma hominis KW - J 02855:Human Bacteriology: Others UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16631454?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+Infectious+Diseases&rft.atitle=Mycoplasmal+pericarditis%3A+Evidence+of+invasive+disease.&rft.au=Kenney%2C+R+T%3BLi%2C+J+S%3BClyde%2C+WA+Jr%3BWall%2C+T+C%3BO%27Connor%2C+C+M%3BCampbell%2C+P+T%3BVan+Trigt%2C+P%3BCorey%2C+G+R&rft.aulast=Kenney&rft.aufirst=R&rft.date=1993-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Clinical+Infectious+Diseases&rft.issn=10584838&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Mycoplasma pneumoniae; Mycoplasma hominis; Ureaplasma urealyticum; pericarditis; diseases; pathogenicity ER - TY - JOUR T1 - DNA response to bleomycin in mammalian cells with variable degrees of chromatin condensation. AN - 16626304; 3002994 AB - BLM induces DNA degradation in living cells. We used CHO cells with maximal chromatin compactness (cells synchronized in metaphase), cells with chromatin decondensed by Na butyrate treatments, and control cells with normal chromatin condensation in order to analyze the correlation between chromatin compactness, DNA sensitivity to BLM, efficiency of repair of BLM-induced DNA lesions, and cell viability. We found that the DNA sensitivity to BLM and the efficiency of DNA repair is inversely correlated with the degree of chromatin coiling. Cells with decondensed chromatin are those showing higher DNA sensitivity to BLM but also those having the best efficiency to mend the damage. Accordingly, these cells show an amount of residual DNA lesions and a curve of growth similar to that of control cells. The situation is just the opposite for metaphase cells. The DNA of these cells is more resistant to BLM, but the damage is poorly repaired. JF - Environmental and Molecular Mutagenesis AU - Lopez-Larraza, D M AU - Bianchi, N O AD - NIH, NCI, Bldg. 37, Rm. 3B12, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 258 EP - 264 VL - 21 IS - 3 SN - 0893-6692, 0893-6692 KW - bleomycin KW - Biochemistry Abstracts 2: Nucleic Acids; Toxicology Abstracts KW - response KW - DNA KW - antineoplastic drugs KW - mammalian cells KW - N 14630:Chemical reactions & interactions, including effects of radiation KW - X 24117:Biochemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16626304?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+and+Molecular+Mutagenesis&rft.atitle=DNA+response+to+bleomycin+in+mammalian+cells+with+variable+degrees+of+chromatin+condensation.&rft.au=Lopez-Larraza%2C+D+M%3BBianchi%2C+N+O&rft.aulast=Lopez-Larraza&rft.aufirst=D&rft.date=1993-01-01&rft.volume=21&rft.issue=3&rft.spage=258&rft.isbn=&rft.btitle=&rft.title=Environmental+and+Molecular+Mutagenesis&rft.issn=08936692&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - DNA; response; mammalian cells; antineoplastic drugs ER - TY - JOUR T1 - Environmental toxicology of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans. AN - 16625791; 3002894 AB - Few environmental compounds have generated as much interest and controversy within the scientific community and in the lay public as polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs). Their ubiquitous presence in the environment and the risk of accidental exposure has raised concern over a possible threat of PCDDs or PCDFs to human health. The most extensively studied and potent isomer is 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD or dioxin). Dioxin is a multisite toxicant in laboratory rodents resulting in a number of tissue-, species-, and sex-dependent responses. Much has been learned about the mechanism of dioxin's effects, especially for the induction of cytochrome P-450 enzymes. Binding of PCDDs and PCDFs to a receptor protein, termed the dioxin or Ah receptor, is necessary for most biological and toxic responses. JF - Environmental Health Perspectives AU - Vanden Heuvel, JP AU - Lucier, G AD - NIEHS, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 189 EP - 200 VL - 100 SN - 0091-6765, 0091-6765 KW - environmental health KW - PCDD KW - PCDF KW - humans KW - dioxin KW - polychlorinated dibenzo(p)dioxins KW - polychlorinated dibenzofurans KW - environmental hygiene KW - Toxicology Abstracts; Health & Safety Science Abstracts; Pollution Abstracts KW - toxicology KW - X 24156:Environmental impact KW - H SE4.20:POISONS AND POISONING KW - P 6000:TOXICOLOGY AND HEALTH UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16625791?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Environmental+toxicology+of+polychlorinated+dibenzo-p-dioxins+and+polychlorinated+dibenzofurans.&rft.au=Vanden+Heuvel%2C+JP%3BLucier%2C+G&rft.aulast=Vanden+Heuvel&rft.aufirst=JP&rft.date=1993-01-01&rft.volume=100&rft.issue=&rft.spage=189&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - toxicology; environmental health; PCDD; PCDF; humans; environmental hygiene ER - TY - JOUR T1 - Molecular cloning and expression of hctB encoding a strain-variant chlamydial histone-like protein with DNA-binding activity. AN - 16622373; 2992527 AB - Two DNA-binding proteins with similarity to eukaryotic histone H1 have been described in Chlamydia trachomatis . In addition to the 18-kDa histone H1 homolog Hc1, elementary bodies of C. trachomatis possess an antigenically related histone H1 homolog, which we have termed Hc2, that varies in apparent molecular mass among strains. We report the molecular cloning, expression, and nucleotide sequence of the hctB gene encoding Hc2 and present evidence for in vivo DNA-binding activity of the expressed product. Expression of Hc2 in Escherichia coli induces a compaction of bacterial chromatin that is distinct from that observed upon Hc1 expression. Moreover, isolated nucleoids from Hc2-expressing E. coli exhibit markedly reduced sensitivity to DNase I. These properties of Hc2 are consistent with a postulated role in establishing the nucleoid structure of elementary bodies. JF - Journal of Bacteriology AU - Brickman, T J AU - Barry, CE III AU - Hackstadt, T AD - Lab. Intracell. Parasites, Rocky Mount. Lab., NIAID, Hamilton, MT 59840, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 4274 EP - 4281 VL - 175 IS - 14 SN - 0021-9193, 0021-9193 KW - Hc2 protein KW - Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Microbiology Abstracts B: Bacteriology KW - elementary bodies KW - genes KW - DNA-binding protein KW - Chlamydia trachomatis KW - nucleotide sequence KW - gene expression KW - N 14640:Structure & sequence KW - G 07320:Bacterial genetics KW - J 02740:Genetics and evolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16622373?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Bacteriology&rft.atitle=Molecular+cloning+and+expression+of+hctB+encoding+a+strain-variant+chlamydial+histone-like+protein+with+DNA-binding+activity.&rft.au=Brickman%2C+T+J%3BBarry%2C+CE+III%3BHackstadt%2C+T&rft.aulast=Brickman&rft.aufirst=T&rft.date=1993-01-01&rft.volume=175&rft.issue=14&rft.spage=4274&rft.isbn=&rft.btitle=&rft.title=Journal+of+Bacteriology&rft.issn=00219193&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Chlamydia trachomatis; gene expression; nucleotide sequence; DNA-binding protein; genes; elementary bodies ER - TY - JOUR T1 - The effects of boric acid (BA) on testicular cells in culture. AN - 16616109; 3038099 AB - No effect of BA on the steroidogenic function of isolated Leydig cells was observed, supporting the contention of a CNS-mediated rather than a direct hormone effect. Since increased testicular cyclic AMP (cAMP) produces inhibited spermiation, and a role for the serine proteases plasminogen activators (PAs) in spermiation has been proposed, we evaluated both Sertoli cell cAMP accumulation in Sertoli-germ cell cocultures and the stage-specific secretion of PA activity in cultured seminiferous tubules after in vitro BA exposure, respectively. The results showed that the inhibited spermiation is not due to BA effects on either process. To address the atrophy, we evaluated BA effects in Sertoli-germ cell cocultures on 1) morphology/germ cell attachment, which might identify a target cell; 2) Sertoli cell energy metabolism, because lactate, secreted by Sertoli cells, is a preferred energy source for germ cells; and 3) DNA/RNA synthesis, because germ cells synthesize DNA/RNA and BA impairs nucleic acid synthesis in liver and may do so in testis. JF - Reproductive Toxicology AU - Ku, W W AU - Shih, L M AU - Chapin, R E AD - Natl. Inst. Environ. Health Sci. (NIEHS), P.O. Box 12233 MD E1-02, Research Triangle Park, NC 27709, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 321 EP - 331 VL - 7 IS - 4 SN - 0890-6238, 0890-6238 KW - boric acid KW - effects on KW - rats KW - Toxicology Abstracts KW - testes KW - tissue culture KW - X 24140:Cosmetics, toiletries & household products UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16616109?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Reproductive+Toxicology&rft.atitle=The+effects+of+boric+acid+%28BA%29+on+testicular+cells+in+culture.&rft.au=Ku%2C+W+W%3BShih%2C+L+M%3BChapin%2C+R+E&rft.aulast=Ku&rft.aufirst=W&rft.date=1993-01-01&rft.volume=7&rft.issue=4&rft.spage=321&rft.isbn=&rft.btitle=&rft.title=Reproductive+Toxicology&rft.issn=08906238&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - testes; tissue culture ER - TY - JOUR T1 - Smoking cessation after successful treatment of small-cell lung cancer is associated with fewer smoking-related second primary cancers AN - 16615554; 3640504 AB - Objective: To determine the incidence of second primary cancers developing in patients surviving free of cancer for 2 or more years after treatment for small-cell lung cancer and to assess the potential effect of smoking cessation. Results: Fifty-five patients (10%) were free of cancer 2 years after initiation of therapy. Eighteen of these patients developed one or more second primary cancers, including 13 who developed second primary non-small-cell lung cancer. The risk for any second primary cancer compared with that in the general population was increased four times with a relative risk of a second primary non-small-cell lung cancer of 16. Forty-three patients discontinued smoking within 6 months of starting treatment for small-cell lung cancer, and 12 continued to smoke. In those who stopped smoking at time of diagnosis, the relative risk of a second lung cancer was 11, whereas, in those who continued to smoke, it was 32. JF - Annals of Internal Medicine AU - Richardson, GE AU - Tucker, MA AU - Venzon, D J AU - Linnoila, R I AU - Phelps, R AU - Phares, J C AU - Edison, M AU - Ihde, D C AU - Johnson, B E AD - NCI-Navy Med. Oncol. Branch, Build. 8, Room 5101, Natl. Nav. Med. Cent., Bethesda, MD 20889-5101, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 383 EP - 390 VL - 119 IS - 5 SN - 0003-4819, 0003-4819 KW - Toxicology Abstracts KW - cigarettes KW - smoking KW - tobacco KW - man KW - cancer KW - X 24180:Social poisons & drug abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16615554?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+Internal+Medicine&rft.atitle=Smoking+cessation+after+successful+treatment+of+small-cell+lung+cancer+is+associated+with+fewer+smoking-related+second+primary+cancers&rft.au=Richardson%2C+GE%3BTucker%2C+MA%3BVenzon%2C+D+J%3BLinnoila%2C+R+I%3BPhelps%2C+R%3BPhares%2C+J+C%3BEdison%2C+M%3BIhde%2C+D+C%3BJohnson%2C+B+E&rft.aulast=Richardson&rft.aufirst=GE&rft.date=1993-01-01&rft.volume=119&rft.issue=5&rft.spage=383&rft.isbn=&rft.btitle=&rft.title=Annals+of+Internal+Medicine&rft.issn=00034819&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - smoking; cancer; man; cigarettes; tobacco ER - TY - JOUR T1 - Expression of Chinese hamster cAMP-dependent protein kinase in Escherichia coli results in growth inhibition of bacterial cells: A model system for the rapid screening of mutant type I regulatory subunits. AN - 16613335; 3033008 AB - The regulatory and catalytic subunits of cAMP-dependent protein kinase (PKA) were coexpressed within the same bacterial cell using a polycistronic bacterial T7 expression vector encoding Chinese hamster cDNAs for the type I regulatory (RI) and catalytic alpha (C alpha ) subunits of PKA. Basal expression of active RI/C alpha holoenzyme in the BL21(DE3) strain of Escherichia coli caused severe growth inhibition resulting in extremely small colony size. Several lines of evidence demonstrate that this growth inhibition requires active PKA subunits and cAMP: (i) this phenotype is dependent on cAMP since it is not seen in a strain lacking adenylyl cyclase activity, but the growth rate of these transformants is slower when exogenous cAMP is added; (ii) normal growth occurs when wild-type RI cDNA is replaced by a mutant RI cDNA encoding a RI protein with reduced cAMP binding; and (iii) the growth-inhibited phenotype of the transformed BL21(DE3) cells requires soluble, active C alpha protein. Holoenzyme expressed in bacteria is activated by cAMP, which stimulates phosphorylation of an endogenous 50-kDa protein that is missing in four host mutants selected for normal growth after transformation with PKA holoenzyme. A mutant RI cDNA library was generated by PCR random mutagenesis and screened by polycistronic expression in BL21(DE3) cells. The RI cDNA sequence from one revertant has base-pair substitutions creating two amino acid substitutions within the cAMP binding sites. The coexpression of the RI/C alpha subunits in BL21(DE3) bacterial cells provides a system for rapidly selecting mutations in the RI subunits of PKA. JF - Proceedings of the National Academy of Sciences, USA AU - Gosse, ME AU - Padmanabhan, A AU - Fleischmann, R D AU - Gottesman, M M AD - Lab. Cell Biol., NCI/NIH, Build. 37, Rm. 1B22, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 8159 EP - 8163 VL - 90 IS - 17 SN - 0027-8424, 0027-8424 KW - protein kinase KW - cyclic AMP KW - Microbiology Abstracts B: Bacteriology; Biochemistry Abstracts 2: Nucleic Acids KW - expression KW - inhibition KW - dependent KW - mutants KW - screening KW - regulatory subunits KW - Escherichia coli KW - growth KW - J 02728:Enzymes KW - N 14555:Miscellaneous UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16613335?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.atitle=Expression+of+Chinese+hamster+cAMP-dependent+protein+kinase+in+Escherichia+coli+results+in+growth+inhibition+of+bacterial+cells%3A+A+model+system+for+the+rapid+screening+of+mutant+type+I+regulatory+subunits.&rft.au=Gosse%2C+ME%3BPadmanabhan%2C+A%3BFleischmann%2C+R+D%3BGottesman%2C+M+M&rft.aulast=Gosse&rft.aufirst=ME&rft.date=1993-01-01&rft.volume=90&rft.issue=17&rft.spage=8159&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Escherichia coli; dependent; expression; growth; inhibition; regulatory subunits; mutants; screening ER - TY - JOUR T1 - Effect of 3-methylcholanthrene induction on the distribution and DNA adduction of 2-amino-3-methylimidazo(4,5-f)quinoline (IQ) in F344 rats. AN - 16611004; 3032912 AB - 3-Methylcholanthrene (3MC) is a potent inducer of the cytochrome P450IA family of enzymes that catalyses the metabolic activation of the food mutagen/carcinogen 2-amino-3-methylimidazo-(4,5-f)quinoline (IQ). We have examined the effect of pretreatment with 3MC on the distribution and DNA adduct formation of IQ in male Fischer F344 rats. 3 hr after a single dose of ( super(14)C)IQ (10 mg/kg body weight, by gavage), the level of radioactivity in extrahepatic tissues was 30-70% less in 3MC-pretreated rats than in vehicle control rats. Although the level of radioactivity in the liver did not change after 3MC pretreatment, IQ-DNA adduct levels, measured by the super(32)P-postlabelling method, were 60% lower in the livers of 3MC-pretreated rats than those of control rats, and 83-97% lower in extrahepatic tissues such as the kidneys, colon, small intestine, bladder, heart and lung. IQ-DNA adducts in the testes and brain were found in control rats but were not detected in 3MC-pretreated rats. The rate of removal of IQ-DNA adducts from the livers of control and 3MC-pretreated animals was the same from 3 to 48 hr. At 48 hr, the adduct level in 3MC-pretreated rats remained lower than that seen in the control rats. The data suggest that 3MC induction of the P450IA family of cytochromes in vivo results in an increased rate of IQ detoxification. JF - Food and Chemical Toxicology AU - Snyderwine, E G AU - Nouso, K AU - Schut, HAJ AD - Lab. Exp. Carcinog., Div. Cancer Etiol., NCI, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 415 EP - 423 VL - 31 IS - 6 SN - 0278-6915, 0278-6915 KW - 2-amino-3-methylimidazo(4,5-f)quinoline KW - 3-methylcholanthrene KW - rats KW - Biochemistry Abstracts 2: Nucleic Acids; Toxicology Abstracts KW - adducts KW - DNA KW - distribution KW - N 14630:Chemical reactions & interactions, including effects of radiation KW - X 24190:Polycyclic hydrocarbons UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16611004?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=TDR+-+The+Drama+Review&rft.atitle=Jewish+American+Performance%3A+%22This+Lovely+Land+Is+Mine%22%3A+%22Milk+and+Honey%27s%22+Restorative+Nostalgia+for+Israel&rft.au=Hillman%2C+Jessica&rft.aulast=Hillman&rft.aufirst=Jessica&rft.date=2011-10-01&rft.volume=55&rft.issue=3&rft.spage=31&rft.isbn=&rft.btitle=&rft.title=TDR+-+The+Drama+Review&rft.issn=10542043&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - distribution; DNA; adducts ER - TY - JOUR T1 - Mechanism of action of Pseudomonas exotoxin. Identification of a rate-limiting step. AN - 16598230; 3038095 AB - Pseudomonas exotoxin (PE) enters cells by receptor-mediated endocytosis and is cleaved by a cellular protease between Arg super(279) and Gly super(280) to produce an NH sub(2)-terminal fragment of 28 kDa which contains the toxin's binding domain and a COOH-terminal fragment of 37 kDa which has translocating and ADP-ribosylating activity. After proteolysis, the COOH-terminal fragment reaches the endoplasmic reticulum by retrograde transport where it translocates to the cytosol and inhibits protein synthesis by ADP-ribosylating elongation factor 2. To understand how the 37-kDa fragment functions, we focused on the role of specific amino acids located near its NH sub(2) terminus. We found that there was a 4-250-fold loss in toxic activity when tryptophan 281, leucine 284, or tyrosine 289 were changed to other residues. Mutations at these three positions did not interfere with the receptor binding, cell-mediated proteolytic cleavage, or ADP-ribosylating activity. To determine the role of these amino acids, a competition assay was devised in which the addition of excess PE Delta 553, a mutant form of PE that lacks ADP-ribosylation activity, competed efficiently for the toxicity of PE. Excess PE with mutations near the NH sub(2) terminus of the 37-kDa fragment competed poorly. This competition occurred after proteolysis since PEGly super(276), a mutant form of PE that is not cleaved, did not compete. We conclude that specific amino acids at the NH sub(2) terminus of the 37-kDa fragment interact in a saturable manner with an unknown intracellular component. JF - Journal of Biological Chemistry AU - Zdanovsky, A G AU - Chiron, M AU - Pastan, I AU - FitzGerald, D J AD - Lab. Mol. Biol., NCI, Div. Cancer Biol., Diagn. Cent., NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 21791 EP - 21799 VL - 268 IS - 29 SN - 0021-9258, 0021-9258 KW - Microbiology Abstracts B: Bacteriology; Toxicology Abstracts KW - reaction KW - mutation KW - rates KW - Pseudomonas KW - exotoxins KW - kinetics KW - activity KW - X 24171:Microbial KW - J 02823:In vitro and in vivo effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16598230?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=Mechanism+of+action+of+Pseudomonas+exotoxin.+Identification+of+a+rate-limiting+step.&rft.au=Zdanovsky%2C+A+G%3BChiron%2C+M%3BPastan%2C+I%3BFitzGerald%2C+D+J&rft.aulast=Zdanovsky&rft.aufirst=A&rft.date=1993-01-01&rft.volume=268&rft.issue=29&rft.spage=21791&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Pseudomonas; exotoxins; activity; kinetics; reaction; rates; mutation ER - TY - JOUR T1 - Guanylate kinase of Escherichia coli K-12. AN - 16597677; 2992005 AB - We have identified the gene gmk, in the same operon as rpoZ, spoT, and recG at about 82 minutes on the Escherichia coli chromosome. The gmk ( sub(-)G) sub(-)M)P sub(-)k)inase) gene encodes a peptide of 23,592 Da, possessing extensive similarity to the amino acid sequence of guanylate kinase from yeast. To confirm that gmk truly encodes guanylate kinase and to explore some of its enzymatic features, we have overproduced the product of gmk and purified it to homogeneity. Unlike guanylate kinases purified from eukaryotic sources, E. coli) guanylate kinase is multimeric, and ionic conditions dictate its protomeric state; under low ionic conditions it appears to be a tetramer while under high ionic conditions it is a dimer. Kinetic analysis reveals that guanylate kinase, again, unlike eukaryotic guanylate kinases, binds GMP cooperatively and that the observed cooperativity changes with ionic strength. JF - Journal of Biological Chemistry AU - Gentry, D AU - Bengra, C AU - Ikehara, K AU - Cashel, M AD - Build. 6B, Rm. 3B-316, Lab. Mol. Genet., NICHD, NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 14316 EP - 14321 VL - 268 IS - 19 SN - 0021-9258, 0021-9258 KW - guanylate kinase KW - gmk gene KW - predictions KW - Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Microbiology Abstracts B: Bacteriology KW - genes KW - nucleotide sequence KW - amino acid sequence KW - Escherichia coli KW - N 14640:Structure & sequence KW - J 02728:Enzymes KW - G 07321:GENERAL UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16597677?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=Guanylate+kinase+of+Escherichia+coli+K-12.&rft.au=Gentry%2C+D%3BBengra%2C+C%3BIkehara%2C+K%3BCashel%2C+M&rft.aulast=Gentry&rft.aufirst=D&rft.date=1993-01-01&rft.volume=268&rft.issue=19&rft.spage=14316&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Escherichia coli; genes; nucleotide sequence; amino acid sequence ER - TY - JOUR T1 - Racial differences in risk of oral and pharyngeal cancer: Alcohol, tobacco, and other determinants AN - 16596579; 3685498 AB - In the United States, Blacks have increasingly higher rates of oral and pharyngeal cancer (oral cancer) than Whites, but determinants of the racial disparity have not been clear. Differences with respect to alcohol consumption, especially among current smokers, emerged as the most important explanatory variables. After adjusting for smoking, heavy drinking ( greater than or equal to 30 drinks/week) resulted in a 17-fold increased risk among Blacks and a ninefold increase among Whites. Among drinkers, Blacks tended to drink more than Whites. Also, a higher percentage of Blacks (37%) than Whites (28%) were current smokers, although there were little or no racial differences in relative risks or patterns of use for other smoking variables, including number of cigarettes smoked per day, years of smoking, and age started smoking. From population-attributable risk calculations, we estimated that differences in alcohol and tobacco use account for the bulk of the higher incidence of oral cancer among Blacks in the United States and that, in the absence of alcohol and tobacco, the rates of this cancer according to race (Black, White) and gender would be nearly equal. JF - Journal of the National Cancer Institute AU - Day, G L AU - Blot, W J AU - Austin, D F AU - Bernstein, L AU - Greenberg, R S AU - Preston-Martin, S AU - Schoenberg, J B AU - Winn, D M AU - McLaughlin, J K AU - Fraumeni, JF Jr AD - NCI, 6130 Executive Blvd., EPN 415, Rockville, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 465 EP - 473 VL - 85 IS - 6 SN - 0027-8874, 0027-8874 KW - oral cavity KW - pharynx KW - man KW - race differences KW - ethanol KW - alcohol KW - Health & Safety Science Abstracts; Toxicology Abstracts KW - ethnic groups KW - USA KW - tobacco KW - cancer KW - X 24180:Social poisons & drug abuse KW - H SM10.21:CANCER UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16596579?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Racial+differences+in+risk+of+oral+and+pharyngeal+cancer%3A+Alcohol%2C+tobacco%2C+and+other+determinants&rft.au=Day%2C+G+L%3BBlot%2C+W+J%3BAustin%2C+D+F%3BBernstein%2C+L%3BGreenberg%2C+R+S%3BPreston-Martin%2C+S%3BSchoenberg%2C+J+B%3BWinn%2C+D+M%3BMcLaughlin%2C+J+K%3BFraumeni%2C+JF+Jr&rft.aulast=Day&rft.aufirst=G&rft.date=1993-01-01&rft.volume=85&rft.issue=6&rft.spage=465&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - USA; ethanol; tobacco; cancer; ethnic groups; alcohol; oral cavity; pharynx; man; race differences ER - TY - JOUR T1 - A new PCR based method for the generation of nested deletions. AN - 16596564; 3036958 AB - We have developed a simple, PCR-based protocol, random primed/anchored-PCR (RPA-PCR), that allows the selective amplification and efficient cloning of segments that are adjacent to any known sequence. We demonstrate that RPA-PCR can be used to prepare a nested set of evenly spaced deletions suitable for DNA sequencing. However, it should also be possible to use this technique for a number of other purposes: generating deletions for the analysis of eukaryotic promoters, extending cDNA clones in the 5' direction, cloning the insertion sites of retroviral proviruses and transposons, and analyzing intron/exon boundaries. JF - Nucleic Acids Research AU - Whitcomb, J M AU - Rashtchian, A AU - Hughes, SH AD - ABL-Basic Res. Program, NCI-Frederick Cancer Res. Dev. Cent., P.O. Box B, Frederick, MD 21702-1201, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 4143 EP - 4146 VL - 21 IS - 17 SN - 0305-1048, 0305-1048 KW - random primed/anchored KW - Biotechnology and Bioengineering Abstracts; Medical and Pharmaceutical Biotechnology Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - deletion KW - cloning KW - gene amplification KW - genes KW - DNA KW - polymerase chain reaction KW - methodology KW - N 14610:Occurrence, isolation & assay KW - W 30965:Miscellaneous, Reviews KW - W3 33055:Genetic engineering (general) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16596564?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+Acids+Research&rft.atitle=A+new+PCR+based+method+for+the+generation+of+nested+deletions.&rft.au=Whitcomb%2C+J+M%3BRashtchian%2C+A%3BHughes%2C+SH&rft.aulast=Whitcomb&rft.aufirst=J&rft.date=1993-01-01&rft.volume=21&rft.issue=17&rft.spage=4143&rft.isbn=&rft.btitle=&rft.title=Nucleic+Acids+Research&rft.issn=03051048&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - deletion; gene amplification; cloning; genes; DNA; methodology; polymerase chain reaction ER - TY - JOUR T1 - Testicular toxicity of boric acid (BA): Relationship of dose to lesion development and recovery in the F344 rat. AN - 16595267; 3032834 AB - High-dose boric acid (BA) produces testicular lesions in adult rats, characterized by inhibited spermiation followed by atrophy. The present study addressed whether inhibited spermiation can be separated from atrophy based on dose, compared testis boron (B) dosimetry to lesion development, determined how inhibited spermiation was reflected by common reproductive endpoints, and examined reversibility of the testicular lesions. In summary, 1) the different aspects of the BA-induced testicular lesion can be separated using different doses, 2) inhibited spermiation does not necessarily proceed to atrophy, and 3) there is no recovery from the atrophy despite the absence of testis B after treatment. The ability to separate inhibited spermiation from atrophy based on dose and testis B dosimetry will be useful in evaluating possible mechanisms. Furthermore, the presence of dividing spermatogonia during long-term BA-induced atrophy suggests that this model should be useful for identifying critical components involved in the reinitiation of spermatogenesis. JF - Reproductive Toxicology AU - Ku, W W AU - Chapin, R E AU - Wine, R N AU - Gladen, B C AD - Natl. Inst. Environ. Health Sci. (NIEHS), P.O. Box 12233 MD A2-02, Research Triangle Park, NC 27709, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 305 EP - 319 VL - 7 IS - 4 SN - 0890-6238, 0890-6238 KW - boric acid KW - rats KW - Toxicology Abstracts KW - lesions KW - dose-response effects KW - testes KW - X 24140:Cosmetics, toiletries & household products UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16595267?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Reproductive+Toxicology&rft.atitle=Testicular+toxicity+of+boric+acid+%28BA%29%3A+Relationship+of+dose+to+lesion+development+and+recovery+in+the+F344+rat.&rft.au=Ku%2C+W+W%3BChapin%2C+R+E%3BWine%2C+R+N%3BGladen%2C+B+C&rft.aulast=Ku&rft.aufirst=W&rft.date=1993-01-01&rft.volume=7&rft.issue=4&rft.spage=305&rft.isbn=&rft.btitle=&rft.title=Reproductive+Toxicology&rft.issn=08906238&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - lesions; testes; dose-response effects ER - TY - JOUR T1 - Antisera specific for carcinogen-DNA adducts and carcinogen-modified DNA: Applications for detection of xenobiotics in biological samples. AN - 16593687; 3022789 AB - The development of immunoassays and immunoaffinity chromatography methods for determination of carcinogen-DNA adducts and carcinogen-modified DNA samples rests upon eliciting and characterizing polyclonal and monoclonal antisera against these haptens. The use of such antisera has widespread application in investigating chronic carcinogen administration in animal models and in monitoring human tissues for evidence of carcinogen exposure. Radioimmunoassays and enzyme-linked immunosorbent assays developed with carcinogen-DNA adduct antisera are exceedingly sensitive, measuring 1 adduct in 10 super(8) nucleotides. Not only can DNA damage be quantified directly by immunoassay, but the antisera have also been used to isolate DNA adducts of a particular chemical class by immunoaffinity chromatography before application of more chemically-specific end-points. Both of these methodological approaches have made seminal contributions to the newly-emerging field of molecular epidemiology. JF - Mutation Research AU - Poirier, M C AD - Lab. Cell. Carcinog. and Tumor Promot., NCI, NIH, Build. 37, Room 3B25, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 31 EP - 38 VL - 288 IS - 1 SN - 0027-5107, 0027-5107 KW - biological samples KW - Biochemistry Abstracts 2: Nucleic Acids; Toxicology Abstracts KW - adducts KW - xenobiotics KW - radioimmunoassay KW - enzyme-linked immunosorbent assay KW - detection KW - DNA KW - N 14630:Chemical reactions & interactions, including effects of radiation KW - X 24222:Analytical procedures UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16593687?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutation+Research&rft.atitle=Antisera+specific+for+carcinogen-DNA+adducts+and+carcinogen-modified+DNA%3A+Applications+for+detection+of+xenobiotics+in+biological+samples.&rft.au=Poirier%2C+M+C&rft.aulast=Poirier&rft.aufirst=M&rft.date=1993-01-01&rft.volume=288&rft.issue=1&rft.spage=31&rft.isbn=&rft.btitle=&rft.title=Mutation+Research&rft.issn=00275107&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - DNA; adducts; radioimmunoassay; enzyme-linked immunosorbent assay; xenobiotics; detection ER - TY - JOUR T1 - Cell-cycle dependent micronucleus formation and mitotic disturbances induced by 5-azacytidine in mammalian cells. AN - 16593647; 3022828 AB - 5-Azacytidine was originally developed to treat human myelogenous leukemia. However, interest in this compound has expanded because of reports of its ability to affect cell differentiation and to alter eukaryotic gene expression. In an ongoing attempt to understand the biochemical effects of this compound, we examined the effects of 5-azacytidine on mitosis and on micronucleus formation in mammalian cells. In L5178Y mouse cells, 5-azacytidine induced micronuclei at concentrations at which we and others have already reported its mutagenicity at the tk locus. Using CREST staining and C-banding studies, we showed that the induced micronuclei contained mostly chromosomal fragments although some may have contained whole chromosomes. By incorporating BrdU into the DNA of SHE cells, we determined that micronuclei were induced only when the compound was added while the cells were in S phase. Microscopically visible effects due to 5-azacytidine treatment were not observed until anaphase of the mitosis following treatment or thereafter. JF - Mutation Research AU - Stopper, H AU - Koerber, C AU - Schiffmann, D AU - Caspary, W J AD - NIEHS, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 165 EP - 177 VL - 300 IS - 3-4 SN - 0027-5107, 0027-5107 KW - azacitidine KW - disturbances KW - Genetics Abstracts; Toxicology Abstracts KW - mitosis KW - mammalian cells KW - micronuclei KW - formation KW - X 24117:Biochemistry KW - G 07221:Specific chemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16593647?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutation+Research&rft.atitle=Cell-cycle+dependent+micronucleus+formation+and+mitotic+disturbances+induced+by+5-azacytidine+in+mammalian+cells.&rft.au=Stopper%2C+H%3BKoerber%2C+C%3BSchiffmann%2C+D%3BCaspary%2C+W+J&rft.aulast=Stopper&rft.aufirst=H&rft.date=1993-01-01&rft.volume=300&rft.issue=3-4&rft.spage=165&rft.isbn=&rft.btitle=&rft.title=Mutation+Research&rft.issn=00275107&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - micronuclei; formation; mitosis; mammalian cells ER - TY - JOUR T1 - Strategies for development of chemopreventive agents AN - 16586433; 3670960 AB - The Chemoprevention Branch at the National Cancer Institute has developed a systematic approach for the stepwise development of cancer chemopreventive drugs. This approach guides the development of an agent from discovery to public use. Initially, candidate drugs are identified through literature searches, from interested scientists, or from the general public. For each agent to be considered, all available information on that agent is assimilated in a master file. The agents are then scored by predetermined selection criteria, and prioritized. The priority list is reviewed by a Chemical Selection Committee, which recommends agents for initial preclinical testing, as follows. In vitro tests measure a transformation-related endpoint in epithelial cells or organ cultures derived from trachea, lung, skin, or mammary glands. Testing in animal models of carcinogenesis involves the same organs plus bladder and colon. Three species of animals and several different kinds of carcinogens are used. Agents that appear promising in these screens are then tested in animal efficacy studies that measure the effectiveness over a broader range of doses, measure blood levels, and evaluate combinations of agents. JF - Comments on Toxicology AU - Steele, V E AU - Boone, C W AU - Kelloff, G J AD - Chemoprev. Branch, Div. Cancer Prev. and Control, NCI, NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 427 EP - 435 VL - 4 IS - 5 SN - 0892-2101, 0892-2101 KW - Toxicology Abstracts KW - side effects KW - antineoplastic drugs KW - chemotherapy KW - X 24113:Side effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16586433?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Comments+on+Toxicology&rft.atitle=Strategies+for+development+of+chemopreventive+agents&rft.au=Steele%2C+V+E%3BBoone%2C+C+W%3BKelloff%2C+G+J&rft.aulast=Steele&rft.aufirst=V&rft.date=1993-01-01&rft.volume=4&rft.issue=5&rft.spage=427&rft.isbn=&rft.btitle=&rft.title=Comments+on+Toxicology&rft.issn=08922101&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - SuppNotes - Special issue: Antimutagens and anticarcinogens. N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - antineoplastic drugs; side effects; chemotherapy ER - TY - JOUR T1 - Current status of the mollicute flora of humans. AN - 16585286; 3028033 AB - Of the more than 20 species of mollicutes reported to be present in human tissues, 15 have been isolated more than once and are currently thought to typify mollicutes of human origin. In the past decade a number of new and potentially significant mollicutes have been added to the list of species inhabiting humans. As our understanding of the human mollicute flora increases, diagnostic and clinical advances should permit the identification and control of those species that are significant pathogens in human disease. JF - Clinical Infectious Diseases AU - Tully, J G AD - Mycoplasma Sect., NIAID, Build. 550, Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702, USA Y1 - 1993 PY - 1993 DA - 1993 VL - 17 SN - 1058-4838, 1058-4838 KW - Microbiology Abstracts B: Bacteriology KW - reviews KW - occurrence KW - microflora KW - pathogens KW - man KW - Mycoplasma KW - J 02841:Microflora UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16585286?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+Infectious+Diseases&rft.atitle=Current+status+of+the+mollicute+flora+of+humans.&rft.au=Tully%2C+J+G&rft.aulast=Tully&rft.aufirst=J&rft.date=1993-01-01&rft.volume=17&rft.issue=&rft.spage=no.+1+sul&rft.isbn=&rft.btitle=&rft.title=Clinical+Infectious+Diseases&rft.issn=10584838&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Mycoplasma; man; microflora; pathogens; occurrence; reviews ER - TY - JOUR T1 - Frequent occurrence of HIV-inhibitory sulphated polysaccharides in marine invertebrates. AN - 16577959; 3011484 AB - Aqueous extracts of many marine invertebrates have exhibited some activity in the National Cancer Institute's primary screen for anti-HIV cytopathicity. Using a variety of techniques, including gel permeation, size exclusion and ion exchange chromatography, toluidine blue metachromicity, super(13)C-NMR spectroscopy and combustion analyses, we have determined that this activity is largely due to sulphated polysaccharides. Because of the wide occurrence of this class of compounds in these organisms we sought a method for the rapid dereplication of sulphated polysaccharides. It was critical that the method selected for dereplication allow differentiation of anionic polysaccharides from the AIDS-antiviral chemotypes. After evaluating a variety of methods, we found that the most efficient strategy appeared to be precipitation of the polysaccharide fraction from aqueous ethanolic solutions of the crude aqueous extracts. JF - Antiviral Chemistry & Chemotherapy AU - Beutler, JA AU - McKee, T C AU - Fuller, R W AU - Tischler, M AU - Cardellina, J H AU - Snader, K M AU - McCloud, T G AU - Boyd, M R AD - Lab. Drug Discovery Res. Dev., Div. Cancer Treat., NCI, Build. 1052, Rm. 121, Frederick, MD 21702-1201, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 167 EP - 172 VL - 4 IS - 3 SN - 0956-3202, 0956-3202 KW - Reniochalina stalagmitis KW - Sigillina KW - antiviral activity KW - invertebrates KW - marine invertebrates KW - polysaccharides KW - Biotechnology and Bioengineering Abstracts; ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts A: Industrial & Applied Microbiology; Virology & AIDS Abstracts; Medical and Pharmaceutical Biotechnology Abstracts; ASFA Marine Biotechnology Abstracts KW - Ircinia felix KW - metabolites KW - Marine KW - Galaxea KW - Niphates digitalis KW - Pyrosoma KW - human immunodeficiency virus KW - marine environment KW - W3 33370:Antibiotics KW - A 01068:Antiviral & viricidal KW - Q1 08625:Non-edible products KW - Q4 27380:Pharmaceuticals KW - V 22100:Antiviral agents KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16577959?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antiviral+Chemistry+%26+Chemotherapy&rft.atitle=Frequent+occurrence+of+HIV-inhibitory+sulphated+polysaccharides+in+marine+invertebrates.&rft.au=Beutler%2C+JA%3BMcKee%2C+T+C%3BFuller%2C+R+W%3BTischler%2C+M%3BCardellina%2C+J+H%3BSnader%2C+K+M%3BMcCloud%2C+T+G%3BBoyd%2C+M+R&rft.aulast=Beutler&rft.aufirst=JA&rft.date=1993-01-01&rft.volume=4&rft.issue=3&rft.spage=167&rft.isbn=&rft.btitle=&rft.title=Antiviral+Chemistry+%26+Chemotherapy&rft.issn=09563202&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2014-05-06 N1 - SubjectsTermNotLitGenreText - metabolites; marine environment; polysaccharides; marine invertebrates; antiviral activity; Ircinia felix; Galaxea; Niphates digitalis; human immunodeficiency virus; Pyrosoma; Marine ER - TY - JOUR T1 - Hc1-mediated effects on DNA structure: a potential regulator of chlamydial development. AN - 16577494; 3007630 AB - Chlamydiae are obligate intracellular bacteria which undergo a unique developmental cycle, alternating between non-replicative elementary bodies (EBs) and replicative reticulate bodies (RBs). The transition from RB to EB is characterized by condensation of the chromosome into a dense nucleoid structure. The chlamydial histone homologue Hc1 is sufficient to induce formation of a similar structure in Escherichia coli . High-level Hc1 expression in E. coli is self-limiting and down-regulates transcription, translation, and replication at concentrations similar to those observed in chlamydial elementary bodies. Expression of Hc1 at sub-structural levels may have specific regulatory functions through its interaction with chromosomal DNA. In E. coli this is reflected in a dramatic shift in the pattern of gene expression. The differential expression of the outer membrane porin proteins OmpC and OmpF and analysis of lacZ fusions with promoter regions sensitive to supercoiling suggests that low-level Hc1 expression results in a net relaxation of chromosomal DNA. Topological analysis of plasmid DNA from both E. coli and Chlamydia trachomatis supports a decrease in superhelicity preceding nucleoid formation. In vitro analysis of purified Hc1-DNA interactions supports preferential binding based upon DNA conformation. These results suggest a dual role in which Hc1-mediated changes in gene expression may precede metabolic inactivity. JF - Molecular Microbiology AU - Barry, CE III AU - Brickman, T J AU - Hackstadt, T AD - Lab. Intracell. Parasites, Host-Parasite Interac. Sec., NIAID, Rocky Mountain Lab., Hamilton, MT 59840, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 273 EP - 283 VL - 9 IS - 2 SN - 0950-382X, 0950-382X KW - Microbiology Abstracts B: Bacteriology KW - structure KW - reticulate bodies KW - elementary bodies KW - development KW - DNA KW - regulators KW - Chlamydia KW - J 02725:DNA UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16577494?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+Microbiology&rft.atitle=Hc1-mediated+effects+on+DNA+structure%3A+a+potential+regulator+of+chlamydial+development.&rft.au=Barry%2C+CE+III%3BBrickman%2C+T+J%3BHackstadt%2C+T&rft.aulast=Barry&rft.aufirst=CE&rft.date=1993-01-01&rft.volume=9&rft.issue=2&rft.spage=273&rft.isbn=&rft.btitle=&rft.title=Molecular+Microbiology&rft.issn=0950382X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Chlamydia; development; regulators; elementary bodies; reticulate bodies; DNA; structure ER - TY - JOUR T1 - Alcohol-nutrient interactions: A critical component of physiological change. AN - 16576594; 2991829 AB - A critical component of alcohol research is to understand the mechanisms of its modulation of cell functions, and ultimately disease and tumor resistance, as well as other pathological consequences. Clearly, from in vitro studies, alcohol can affect the functioning of cells directly and through its metabolites. Inadequate intake, reduced bioavailability and decreased storage capacity for micronutrients coupled with increased excretion of nutrients in heavy alcohol users causes malnutrition. Undernutrition per se is associated with a multitude of physiological changes and disease states. Due to the high-energy content of alcoholic beverages other nutrients may be displaced from the diet, and chronic alcohol consumption may also result in secondary malnutrition due to maldigestion of malabsorption, caused by gastrointestinal complications. To increase appreciation of the importance of alcohol's modulation of nutritional state, and the subsequent effects of undernutrition, a symposium on alcohol, nutrition and biomedical changes was organized. JF - Alcohol and Alcoholism AU - Watson, R R AD - NIAAA Alcohol Res. Cent., Dep. Fam. and Community Med., Arizona Health Sci. Cent., Univ. Arizona, Tucson, AZ 85724, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 57 EP - 58 VL - 28 IS - 1 SN - 0735-0414, 0735-0414 KW - ethanol KW - Toxicology Abstracts KW - nutrients KW - physiology KW - diets KW - X 24180:Social poisons & drug abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16576594?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcohol+and+Alcoholism&rft.atitle=Alcohol-nutrient+interactions%3A+A+critical+component+of+physiological+change.&rft.au=Watson%2C+R+R&rft.aulast=Watson&rft.aufirst=R&rft.date=1993-01-01&rft.volume=28&rft.issue=1&rft.spage=57&rft.isbn=&rft.btitle=&rft.title=Alcohol+and+Alcoholism&rft.issn=07350414&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - diets; nutrients; physiology ER - TY - JOUR T1 - Differential effects of dietary beta -carotene on papilloma and carcinoma formation induced by an initiation-promotion protocol in SENCAR mouse skin. AN - 16571398; 2986698 AB - SENCAR mice were used to determine the effects of the provitamin A compound beta -carotene on papilloma formation and the conversion of papillomas to carcinomas in a two-stage protocol with one application of the initiator 7,12-dimethyl-benz(a)anthracene (DMBA, 20 mu g) and 20 weekly applications of the promoter 12-O-tetradecanoylphorbol-13-acetate (TPA, 2 mu g). In conclusion, dietary beta -carotene caused differential effects on papilloma and carcinoma yields and sex-dependent differences in papilloma formation in female and male SENCAR mice treated with DMBA and TPA in a two-stage carcinogenesis protocol. JF - Carcinogenesis AU - Chen, Li-Chuan AU - Sly, L AU - Jones, C S AU - Tarone, R AU - De Luca, LM AD - Differ. Control Section, Lab. Cell. Carcinog. Tumor Promot., Build. 37, Rm. 3A-17, NCI, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 713 EP - 717 VL - 14 IS - 4 SN - 0143-3334, 0143-3334 KW - beta -carotene KW - 9,10-dimethyl-1,2-benzanthracene KW - TPA KW - mice KW - Toxicology Abstracts KW - carcinogenesis KW - papilloma KW - formation KW - X 24120:Food, additives & contaminants UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16571398?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Differential+effects+of+dietary+beta+-carotene+on+papilloma+and+carcinoma+formation+induced+by+an+initiation-promotion+protocol+in+SENCAR+mouse+skin.&rft.au=Chen%2C+Li-Chuan%3BSly%2C+L%3BJones%2C+C+S%3BTarone%2C+R%3BDe+Luca%2C+LM&rft.aulast=Chen&rft.aufirst=Li-Chuan&rft.date=1993-01-01&rft.volume=14&rft.issue=4&rft.spage=713&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - papilloma; formation; carcinogenesis ER - TY - JOUR T1 - Variability of osp genes and gene products among species of lyme disease spirochetes. AN - 16567522; 2981791 AB - A comparison of the osp operon in 24 Lyme disease isolates, including representatives from each of the three established species, Borrelia burgdorferi, Borrelia garinii , and group VS461, was conducted. Several properties were assessed to determine whether the variability observed in this operon was reflective of the species of the isolate. At the transcriptional level, start site and Northern (RNA) blot analyses were conducted. B. garinii and VS461 group isolates were found to possess an untranslated leader sequence 6 nucleotides longer than that observed in B. burgdorferi isolates. By Northern blot analyses all Lyme disease isolates, except the B. garinii isolate VS102, were found to produce a polycistronic full-length ospAB message. Isolate VS102 produced a truncated message lacking the ospB portion of the transcript. Southern blot analyses suggest that the deletion occurred at the DNA level and was not due to a posttranscriptional event. Analysis of the outer surface proteins by two-dimensional gel electrophoresis demonstrated that the OspB isoelectric points were variable, with the OspB of B. garinii isolates exhibiting a pronounced acidic shift. The reactivity of different isolates to OspA and -B monoclonal antibodies and to a hyperimmune anti-ospAB serum was also variable. The results presented here demonstrate genotypic and phenotypic heterogeneity in the osp operon at both the inter- and intraspecies levels. The results have implications concerning the use of the osp genes or their gene products in the development of a Lyme disease vaccine, as diagnostic markers of Lyme disease, and in subtyping of Lyme disease isolates. JF - Infection and Immunity AU - Marconi, R T AU - Konkel, ME AU - Garon, C F AD - Lab. Vectors and Pathogens, Rocky Mountain Lab., NIAID, Hamilton, MT 59840, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 2611 EP - 2617 VL - 61 IS - 6 SN - 0019-9567, 0019-9567 KW - osp gene KW - Genetics Abstracts; Microbiology Abstracts B: Bacteriology KW - spirochetes KW - Borrelia burgdorferi KW - genes KW - Borrelia garinii KW - nucleotide sequence KW - heterogeneity KW - gene products KW - G 07320:Bacterial genetics KW - J 02740:Genetics and evolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16567522?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Variability+of+osp+genes+and+gene+products+among+species+of+lyme+disease+spirochetes.&rft.au=Marconi%2C+R+T%3BKonkel%2C+ME%3BGaron%2C+C+F&rft.aulast=Marconi&rft.aufirst=R&rft.date=1993-01-01&rft.volume=61&rft.issue=6&rft.spage=2611&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - Borrelia burgdorferi; Borrelia garinii; genes; gene products; nucleotide sequence; heterogeneity; spirochetes ER - TY - JOUR T1 - Directional actin polymerization associated with spotted fever group rickettsia infection of Vero cells. AN - 16545080; 2977975 AB - Members of the spotted fever group (SFG) of rickettsiae spread rapidly from cell to cell by an unknown mechanism(s). Staining of Rickettsia rickettsii-infected Vero cells with rhodamine phalloidin demonstrated unique actin filaments associated with one pole of intracellular rickettsiae. F-actin tails greater than 70 mu m in length were seen extending from rickettsiae. Treatment of infected cells with chloramphenicol eliminated rickettsia-associated F-actin tails, suggesting that de novo protein synthesis of one or more rickettsial proteins is required for tail formation. Rickettsiae were coated with F-actin as early as 15 min postinfection, and tail formation was detected by 30 min. A survey of virulent and avirulent species within the SFG rickettsiae demonstrated that all formed actin tails. Typhus group rickettsiae, which do not spread directly from cell to cell, lacked F-actin tails entirely or exhibited only very short tails. Transmission electron microscopy demonstrated fibrillar material in close association with R. rickettsii but not Rickettsia prowazekii. Biochemical evidence that actin polymerization plays a role in movement was provided by showing that transit of R. rickettsii from infected cells into the cell culture medium was inhibited by treatment of host cells with cytochalasin D. These data suggest that the cell-to-cell transmission of SFG rickettsiae may be aided by induction of actin polymerization in a fashion similar to that described for Shigella flexneri and Listeria monocytogenes. JF - Infection and Immunity AU - Heinzen, R A AU - Hayes, S F AU - Peacock, M G AU - Hackstadt, T AD - Host-Parasite Interactions Sect., Lab. Intracell. Parasites, Rocky Mountain Lab., NIAID, Hamilton, MT 59840, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 1926 EP - 1935 VL - 61 IS - 5 SN - 0019-9567, 0019-9567 KW - actin KW - Microbiology Abstracts B: Bacteriology KW - Vero cells KW - spotted fevers KW - polymerization KW - Rickettsia rickettsii KW - J 02721:Cell cycle, morphology and motility UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16545080?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Directional+actin+polymerization+associated+with+spotted+fever+group+rickettsia+infection+of+Vero+cells.&rft.au=Heinzen%2C+R+A%3BHayes%2C+S+F%3BPeacock%2C+M+G%3BHackstadt%2C+T&rft.aulast=Heinzen&rft.aufirst=R&rft.date=1993-01-01&rft.volume=61&rft.issue=5&rft.spage=1926&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - Rickettsia rickettsii; Vero cells; polymerization; spotted fevers ER - TY - JOUR T1 - Tri-primer PCR can distinguish free and cloned viral DNA in a single reaction. AN - 16544163; 2970523 AB - A polymerase chain reaction based method is described which distinguishes free and cloned JC virus (JCV) DNA in a single reaction. The method utilizes three primers and amplifies DNA fragments of two different sizes, one specific for free and another specific for pBR322 cloned viral DNA. The procedure was used to simultaneously detect the presence of free and contaminating clones JCV DNA in brain tissues. JF - Journal of Virological Methods AU - Ishaq, M AU - Stoner, G L AD - Build. 36, Rm. 4A-29, Lab. Exp. Neuropathol., NINDS/NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 95 EP - 98 VL - 42 IS - 1 SN - 0166-0934, 0166-0934 KW - amplification KW - Biochemistry Abstracts 2: Nucleic Acids; Microbiology Abstracts A: Industrial & Applied Microbiology; Virology & AIDS Abstracts KW - primers KW - cloning KW - JC virus KW - DNA KW - brain KW - contamination KW - polymerase chain reaction KW - N 14610:Occurrence, isolation & assay KW - A 01012:Nucleic acids & metabolites KW - V 22022:Virus assay UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16544163?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Virological+Methods&rft.atitle=Tri-primer+PCR+can+distinguish+free+and+cloned+viral+DNA+in+a+single+reaction.&rft.au=Ishaq%2C+M%3BStoner%2C+G+L&rft.aulast=Ishaq&rft.aufirst=M&rft.date=1993-01-01&rft.volume=42&rft.issue=1&rft.spage=95&rft.isbn=&rft.btitle=&rft.title=Journal+of+Virological+Methods&rft.issn=01660934&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - JC virus; polymerase chain reaction; DNA; primers; cloning; brain; contamination ER - TY - JOUR T1 - Identification and characterization of Lyme disease spirochetes, Borrelia burgdorferi sensu lato, isolated in Korea. AN - 16543962; 2974770 AB - Lyme disease spirochetes, Borrelia burgdorferi sensu lato, were identified and characterized for the first time in Korea. Four isolates, designated Konkuk-1, Konkuk-2, Kangwon-3, and KM-4, were made from midgut suspensions of three Ixodes ticks and heart tissue from one mouse, Apodemus agrarius , collected from Chungbuk and Kangwon provinces. The four Korean isolates and B. burgdorferi sensu lato from other geographic areas and biological sources were compared by using sodium dodecyl sulfate-polyacrylamide gel electrophoresis for protein profiles, Western blot (immunoblot) analysis for reactivities with monoclonal and polyclonal antibodies, and agarose gel electrophoresis for plasmid profiles. Two typing schemes using polymerase chain reaction identified three of the isolates as members of group VS461 and one, Kangwon-3, as Borrelia garinii . These results demonstrate the potential for human Lyme disease to occur in some provinces of Korea. JF - Journal of Clinical Microbiology AU - Park, K-H AU - Chang, W-H AU - Schwan, T G AD - Lab. Vectors and Pathogens, Rocky Mountain Lab., NIAID, Hamilton, MT 59840, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 1831 EP - 1837 VL - 31 IS - 7 SN - 0095-1137, 0095-1137 KW - Korea KW - Microbiology Abstracts B: Bacteriology KW - spirochetes KW - Apodemus agrarius KW - Borrelia burgdorferi KW - Borrelia garinii KW - DNA KW - monoclonal antibodies KW - geographical variations KW - J 02710:Identification, taxonomy and typing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16543962?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Clinical+Microbiology&rft.atitle=Identification+and+characterization+of+Lyme+disease+spirochetes%2C+Borrelia+burgdorferi+sensu+lato%2C+isolated+in+Korea.&rft.au=Park%2C+K-H%3BChang%2C+W-H%3BSchwan%2C+T+G&rft.aulast=Park&rft.aufirst=K-H&rft.date=1993-01-01&rft.volume=31&rft.issue=7&rft.spage=1831&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Microbiology&rft.issn=00951137&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Borrelia burgdorferi; Apodemus agrarius; Borrelia garinii; spirochetes; monoclonal antibodies; DNA; geographical variations ER - TY - JOUR T1 - Immunotoxins made with a recombinant form of Pseudomonas exotoxin A that do not require proteolysis for activity. AN - 16535638; 2963361 AB - We used recombinant DNA technology to construct a mutant form of Pseudomonas exotoxin A (PE) called cysPE35 that contains amino acids 280-364 and 381-613 of PE. cysPE35 begins at the native PE proteolytic cleavage site and contains a single cysteine residue at position 287 that can be used to conjugate the toxin to monoclonal antibodies (MAbs). Unlike immunotoxins containing larger mutant forms of PE, such as PE40 or PE38, immunotoxins containing cysPE35 linked through a disulfide bond do not require proteolysis to generate a toxin fragment able to translocate to the cytosol. We have constructed a mutant form of PE which must be coupled to MAbs through a disulfide bond to produce fully active immunotoxins that do not require proteolysis to generate a toxin fragment able to reach the cell cytosol. JF - Cancer Research AU - Theuer, C P AU - Kreitman, R J AU - FitzGerald, D J AU - Pastan, I AD - Lab. Mol. Biol., NCI/NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 340 EP - 347 VL - 53 IS - 2 SN - 0008-5472, 0008-5472 KW - exotoxin A KW - Immunology Abstracts; Microbiology Abstracts B: Bacteriology KW - conjugates KW - Pseudomonas KW - monoclonal antibodies KW - immunotoxins KW - formation KW - F 06793:Immunopharmacology KW - J 02823:In vitro and in vivo effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16535638?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Research&rft.atitle=Immunotoxins+made+with+a+recombinant+form+of+Pseudomonas+exotoxin+A+that+do+not+require+proteolysis+for+activity.&rft.au=Theuer%2C+C+P%3BKreitman%2C+R+J%3BFitzGerald%2C+D+J%3BPastan%2C+I&rft.aulast=Theuer&rft.aufirst=C&rft.date=1993-01-01&rft.volume=53&rft.issue=2&rft.spage=340&rft.isbn=&rft.btitle=&rft.title=Cancer+Research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Pseudomonas; conjugates; monoclonal antibodies; formation; immunotoxins ER - TY - JOUR T1 - Studies on the substrate specificity of the proteinase of equine infectious anemia virus using oligopeptide substrates. AN - 16520068; 2959382 AB - The proteinase of the equine anemia virus (EIAV), a lentivirus closely related to human immunodeficiency virus (HIV), was purified from concentrated virus. The specificity of the enzyme was characterized using oligopeptides representing naturally occurring cleavage sites in the Gag and Gag-Pol polyproteins. The length of the substrate binding pocket was found to be 1-2 residues longer than that of HIV proteinases. Although the EIAV and HIV proteinases cleaved most of the peptides at the same bond, some were hydrolyzed by only the EIAV enzyme. Oligopeptides representing cleavage sites in the nucleocapsid protein were also found to be substrates of the EIAV proteinase. However, these peptides were not hydrolyzed by the HIV proteinases. While peptides representing the corresponding sequences in the first cysteine arrays of the nucleocapsid proteins of HIV-1 and HIV-2 were substrates of the proteinases, peptides representing the homologous sequences in the second Cys arrays were resistant against the proteolytic attack. A three-dimensional model of the EIAV proteinase built on the basis of homology with HIV-1 proteinase was used to interpret the differences. In addition to the oligopeptides representing cleavage sites in the Gag and Gag-Pol polyproteins, the EIAV proteinase was also able to cleave an oligopeptide mimicking a cleavage site in the transmembrane protein. Our results suggest that the specificity of lentiviral proteinases share common characteristics, although substantial differences may exist in hydrolysis of some peptides. JF - Biochemistry (Washington) AU - Toezser, J AU - Friedman, D AU - Weber, I T AU - Blaha, I AU - Oroszlan, S AD - Lab. Mol. Virol. Carcinog., ABL-Basic Res. Program, NCI-Frederick Cancer Res. Dev. Cent., Frederick, MD 21702-1201, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 3347 EP - 3353 VL - 32 IS - 13 SN - 0006-2960, 0006-2960 KW - equine infectious anemia virus KW - oligopeptides KW - proteinase KW - substrate specificity KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Virology & AIDS Abstracts KW - V 22032:Viral proteins UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16520068?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemistry+%28Washington%29&rft.atitle=Studies+on+the+substrate+specificity+of+the+proteinase+of+equine+infectious+anemia+virus+using+oligopeptide+substrates.&rft.au=Toezser%2C+J%3BFriedman%2C+D%3BWeber%2C+I+T%3BBlaha%2C+I%3BOroszlan%2C+S&rft.aulast=Toezser&rft.aufirst=J&rft.date=1993-01-01&rft.volume=32&rft.issue=13&rft.spage=3347&rft.isbn=&rft.btitle=&rft.title=Biochemistry+%28Washington%29&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - substrate specificity ER - TY - JOUR T1 - New method for plague surveillance using polymerase chain reaction to detect Yersinia pestis in fleas. AN - 16518716; 2960577 AB - Yersinia pestis , the plague bacillus, infects a variety of mammals throughout the world and is transmitted by fleas. We developed a polymerase chain reaction (PCR) test using primers designed from the Y. pestis plasminogen activator gene to directly detect plague-infected fleas. As few as 10 Y. pestis cells were detected, even in the presence of flea tissue, by PCR and then agarose gel electrophoresis and ethidium bromide staining. The feasibility of the assay was demonstrated by using naturally infected Xenopsylla cheopis fleas. The detection of Y. pestis in fleas by PCR provides a rapid and sensitive way to monitor plague in wild animal populations, allowing public health officials to better assess the potential risk of transmission to humans. JF - Journal of Clinical Microbiology AU - Hinnebusch, J AU - Schwan, T G AD - Arthropod-Borne Dis. Sect., Lab. Vectors and Pathog., Rocky Mountain Lab., NIAID, Hamilton, MT 59840, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 1511 EP - 1514 VL - 31 IS - 6 SN - 0095-1137, 0095-1137 KW - fleas KW - Siphonoptera KW - Microbiology Abstracts B: Bacteriology KW - plague KW - screening KW - vector-borne diseases KW - Yersinia pestis KW - polymerase chain reaction KW - J 02862:Infection UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16518716?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Clinical+Microbiology&rft.atitle=New+method+for+plague+surveillance+using+polymerase+chain+reaction+to+detect+Yersinia+pestis+in+fleas.&rft.au=Hinnebusch%2C+J%3BSchwan%2C+T+G&rft.aulast=Hinnebusch&rft.aufirst=J&rft.date=1993-01-01&rft.volume=31&rft.issue=6&rft.spage=1511&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Microbiology&rft.issn=00951137&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Yersinia pestis; plague; polymerase chain reaction; screening; vector-borne diseases ER - TY - JOUR T1 - Regulation of expression of major outer surface proteins in Borrelia burgdorferi . AN - 16517378; 2962553 AB - We have characterized a Borrelia burgdorferi clone (CA-11 2A) that does not synthesize the major outer surface proteins, OspA and OspB. While the osp operon is intact and capable of expression, no mRNA transcript is detectable in this clone. These results suggest that osp operon expression in the B. burgdorferi clone can be regulated at the level of transcription. JF - Infection and Immunity AU - Margolis, N AU - Rosa, P A AD - Lab. Microb. Struct. Funct., Rocky Mountain Lab., NIAID, Hamilton, MT 59840, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 2207 EP - 2210 VL - 61 IS - 5 SN - 0019-9567, 0019-9567 KW - Microbiology Abstracts B: Bacteriology KW - expression KW - operons KW - Borrelia burgdorferi KW - outer membranes KW - gene regulation KW - proteins KW - J 02740:Genetics and evolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16517378?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Regulation+of+expression+of+major+outer+surface+proteins+in+Borrelia+burgdorferi+.&rft.au=Margolis%2C+N%3BRosa%2C+P+A&rft.aulast=Margolis&rft.aufirst=N&rft.date=1993-01-01&rft.volume=61&rft.issue=5&rft.spage=2207&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Borrelia burgdorferi; gene regulation; expression; outer membranes; proteins; operons ER - TY - JOUR T1 - Foraging behaviour and social group dynamics in Puget Sound killer whales. AN - 16512191; 2955400 AB - Social and foraging behaviour was investigated in a population of 82 killer whales, Orcinus orca , seasonally resident in the straits of Washington State and British Columbia. Killer whales in this population travel in stable pods and temporarily dissociate into subgroups. Associations in subgroups were determined by photographing individual whales. The relative geographical positions of subgroups were determined by compass triangulation on landmarks. These data were used to determine correlations between individual associations, habitat use and behaviour. Behaviour indicative of pursuing fish prey at the surface (termed fast non-directional) correlated with the whales slowing down, travelling in smaller subgroups, and decreasing the distance between subgroups. This behviour was not correlated with bottom topography, specific quadrats within the study areas, or the convergence of subgroups (which could be interpreted as group herding of prey). These data suggest that these killer whales may benefit from cooperative food searching, but not necessarily from cooperative food capture. Adult males, which are thought to remain within their natal pods, were most likely to travel and to exhibit fast non-directional behaviour when alone. JF - Animal Behaviour AU - Hoelzel, A R AD - Lab. Viral Carcinogenesis, NCI, Frederick, MD 21702, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 581 EP - 591 VL - 45 IS - 3 SN - 0003-3472, 0003-3472 KW - feeding behaviour KW - foraging behavior KW - marine mammals KW - social behaviour KW - Oceanic Abstracts; ASFA 1: Biological Sciences & Living Resources; Ecology Abstracts; Animal Behavior Abstracts KW - Orcinus orca KW - Marine KW - INE, USA, Washington, Puget Sound KW - O 1070:Ecology/Community Studies KW - Y 25457:Mammals (excluding primates) KW - D 04672:Mammals KW - Q1 08425:Nutrition and feeding habits UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16512191?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aecology&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Animal+Behaviour&rft.atitle=Foraging+behaviour+and+social+group+dynamics+in+Puget+Sound+killer+whales.&rft.au=Hoelzel%2C+A+R&rft.aulast=Hoelzel&rft.aufirst=A&rft.date=1993-01-01&rft.volume=45&rft.issue=3&rft.spage=581&rft.isbn=&rft.btitle=&rft.title=Animal+Behaviour&rft.issn=00033472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2014-05-06 N1 - SubjectsTermNotLitGenreText - social behaviour; marine mammals; feeding behaviour; foraging behavior; Orcinus orca; INE, USA, Washington, Puget Sound; Marine ER - TY - JOUR T1 - Exposure to FIV and FIPV in wild and captive cheetahs. AN - 16510067; 2953547 AB - Two RNA-containing viruses, feline infectious peritonitis virus (FIPV) and feline immunodeficiency virus (FIV), have been observed to infect cheetahs. Although both viruses cause lethal immunogenetic pathology in domestic cats, only FIPV had documented pathogenesis in cheetahs. We summarize and update here a worldwide survey of serum and plasma from cheetah and other nondomestic felids for antibodies to FIV and FIPV, based on Western blot and immunofluorescence assays. FIPV exposure shows an acute pattern with recognizable outbreaks in several zoological facilities, but is virtually nonexistent in sampled free-ranging populations of cheetahs. FIV is more endemic in certain natural cheetah populations, but infrequent in zoological collections. FIV exposure was also seen in lions, bobcats, leopards, snow leopards, and jaguars. FIV causes T-cell lymphocyte depletion and associated diseases in domestic cats, but there is little direct evidence for FIV pathology in exotic cats to date. Because of the parallels with a high incidence of simian immunodeficiency virus in free-ranging African primates without disease, the cat model may also reflect historic infections that have approached an evolutionary balance between the pathogen and immune defenses of their feline host species. JF - Zoo Biology AU - Brown, E W AU - Olmsted, R A AU - Martenson, J S AU - O'Brien, S J AD - Lab. Viral Carcinog., NCI, Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702-1201, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 135 EP - 142 VL - 12 IS - 1 SN - 0733-3188, 0733-3188 KW - Virology & AIDS Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology KW - feral populations KW - antibodies KW - geographical distribution KW - Acinonyx jubatus KW - feline immunodeficiency virus KW - feline infectious peritonitis virus KW - viruses KW - surveys KW - zoological gardens KW - V 22143:Epizootiology KW - A 01114:Viruses UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16510067?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Zoo+Biology&rft.atitle=Exposure+to+FIV+and+FIPV+in+wild+and+captive+cheetahs.&rft.au=Brown%2C+E+W%3BOlmsted%2C+R+A%3BMartenson%2C+J+S%3BO%27Brien%2C+S+J&rft.aulast=Brown&rft.aufirst=E&rft.date=1993-01-01&rft.volume=12&rft.issue=1&rft.spage=135&rft.isbn=&rft.btitle=&rft.title=Zoo+Biology&rft.issn=07333188&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - feline infectious peritonitis virus; feline immunodeficiency virus; Acinonyx jubatus; zoological gardens; feral populations; surveys; antibodies; geographical distribution; viruses ER - TY - JOUR T1 - Inhibition of HIV-1 infectivity by zinc-ejecting aromatic C-nitroso compounds. AN - 16498440; 2945609 AB - Retroviral nucleocapsid and gag-precursor proteins from all known strains of retroviruses contain one or two copies of an invariant sequence, Cys-X sub(2)-Cys-X sub(4)-His-X sub(4)-Cys, that is populated with zinc in mature particles. Modification of cysteine or histidine residues results in defective packaging of genomic viral RNA and formation of non-infectious particles, making these structures potentially attractive targets for antiviral therapy. We recently reported that aromatic C-nitroso ligands of poly(ADP-ribose) polymerase preferentially destabilize one of the two (Cys-X sub(2)-Cys-X sub(28)-His-X sub(2)-Cys) zinc-fingers with concomitant loss of enzymatic activity, coincidental with selective cytocidal action of the C-nitroso substituted ligands on cancer cells. Based on the occurrence of (3Cys, 1His) zinc-binding sites in both retroviral nucleocapsid and gag proteins and in poly(ADP-ribose) polymerase, we reasoned that the C-nitroso compounds may also have antiretroviral effects. Two such compounds, 3-nitrosobenzamide and 6-nitroso-1,2-benzopyrone, inhibit infection of human immunodeficiency virus HIV-1 in human lymphocytes and also eject zinc from isolated HIV-1 nucleocapsid zinc fingers and from intact HIV-1 virions. The design of zinc-ejecting agents that target retroviral zinc fingers represents a new approach to the chemotherapy to AIDS. JF - Nature AU - Rice, W G AU - Schaeffer, CA AU - Harten, B AU - Villinger, F AU - South, T L AU - Summers, M F AU - Henderson, LE AU - Bess, JW Jr AU - Arthur, LO AD - Lab. Antiviral Drug Mech., Program Resour. Inc./DynCorp, NCI-Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 473 EP - 475 VL - 361 IS - 6411 SN - 0028-0836, 0028-0836 KW - aromatic C-nitroso compounds KW - zinc KW - zinc finger KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Virology & AIDS Abstracts KW - antiviral agents KW - inhibition KW - human immunodeficiency virus KW - infection KW - binding KW - proteins KW - A 01068:Antiviral & viricidal KW - V 22004:AIDS: Clinical aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16498440?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature&rft.atitle=Inhibition+of+HIV-1+infectivity+by+zinc-ejecting+aromatic+C-nitroso+compounds.&rft.au=Rice%2C+W+G%3BSchaeffer%2C+CA%3BHarten%2C+B%3BVillinger%2C+F%3BSouth%2C+T+L%3BSummers%2C+M+F%3BHenderson%2C+LE%3BBess%2C+JW+Jr%3BArthur%2C+LO&rft.aulast=Rice&rft.aufirst=W&rft.date=1993-01-01&rft.volume=361&rft.issue=6411&rft.spage=473&rft.isbn=&rft.btitle=&rft.title=Nature&rft.issn=00280836&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - human immunodeficiency virus; infection; inhibition; binding; proteins; antiviral agents ER - TY - JOUR T1 - Metabolism and mode of selective inhibition of human immunodeficiency virus replication by 3'-azido-2',3'-dideoxy-5-iodouridine and 3'-azido-2',3'-dideoxy-5-bromouridine. AN - 16496119; 2945594 AB - 3'-Azido-2',3'-dideoxy-5-iodouridine (AzIdUrd) and 3'-azido-2',3'-dideoxy-5-bromouridine (AzBdUrd), previously shown to be potent and selective inhibitors of human immunodeficiency virus replication in vitro were minimally toxic to the uninfected human lymphoid cell line H9 (IC sub(50) = 197 and 590 mu M, respectively). Both compounds strongly inhibited the incorporation of ( super(3)H)thymidine but not ( super(3)H)deoxyadenosine into DNA, and we observed no significant inhibition of ( super(3)H)uridine incorporation into RNA or ( super(3)H)amino acid incorporation into protein. Exposure of H9 cells to AzIdUrd or AzBdUrd (100 mu M, 24 hr) and pulse-labeling with ( super(3)H)thymidine resulted in approximately 80% reduction in levels of tritiated dTMP, dTDP, and dTTP relative to control. ( super(125)I)AzIdUrd was phosphorylated rapidly in H9 cells with the monophosphate accounting for over 90% of total radioactivity. A relatively low but stable level of AzIdUTP was maintained over a 12-hr period. ( super(125)I)AzIdUrd was phosphorylated by a cell free extract of H9 cells at a rate approximately three times that of thymidine and its phosphorylation was inhibited by excess thymidine. AzIdUrd was found to be a competitive inhibitor of cytosolic thymidine kinase with a K sub(i) of 2.63 mu M and AzIdUMP a weak competitive inhibitor of thymidylate kinase with a K sub(i) of 55.3 mu M. Both AzIdUTP and AzBdUTP were potent competitive inhibitors of HIV-1 reverse transcriptase (K sub(i) = 0.028 and 0.043 mu M, respectively) and relatively poor inhibitors of H9 cell DNA polymerase alpha (K sub(i) = 42.0 and 42.7 mu M, respectively). Thus, the high therapeutic index of these compounds is due to the sensitivity of the viral reverse transcriptase, coupled with the relative insensitivity of the host cell DNA polymerase alpha . JF - Biochemical Pharmacology AU - August, E M AU - Qian, H-Y AU - Birks, E M AU - Thombre, U A AU - Lin, Tai-Shun AU - Prusoff, W H AD - Lab. Med. Chem., Dev. Ther. Program, NCI/NIH, Build. 37, Rm. 5E-10, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 223 EP - 230 VL - 45 IS - 1 SN - 0006-2952, 0006-2952 KW - 3'-azido-2',3'-dideoxy-5-iodouridine KW - 3'-azido-2',3'-dideoxy-5-bromouridine KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Virology & AIDS Abstracts KW - antiviral agents KW - replication KW - human immunodeficiency virus KW - inhibition KW - A 01068:Antiviral & viricidal KW - V 22004:AIDS: Clinical aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16496119?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+Pharmacology&rft.atitle=Metabolism+and+mode+of+selective+inhibition+of+human+immunodeficiency+virus+replication+by+3%27-azido-2%27%2C3%27-dideoxy-5-iodouridine+and+3%27-azido-2%27%2C3%27-dideoxy-5-bromouridine.&rft.au=August%2C+E+M%3BQian%2C+H-Y%3BBirks%2C+E+M%3BThombre%2C+U+A%3BLin%2C+Tai-Shun%3BPrusoff%2C+W+H&rft.aulast=August&rft.aufirst=E&rft.date=1993-01-01&rft.volume=45&rft.issue=1&rft.spage=223&rft.isbn=&rft.btitle=&rft.title=Biochemical+Pharmacology&rft.issn=00062952&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - human immunodeficiency virus; replication; inhibition; antiviral agents ER - TY - JOUR T1 - Transcriptional analyses and mapping of the ospC gene in Lyme disease spirochetes. AN - 16496042; 2941643 AB - In Lyme disease spirochetes, the ospC gene encodes a 22.7-kDa protein referred to as either the pC or the OspC protein. Using a variety of electrophoretic approaches followed by Southern blotting and probing with oligonucleotide probes, we mapped to ospC gene to a circular 26-kb plasmid. The ospC gene represents the first gene to be mapped to a circular plasmid in Lyme disease spirochetes. The occurrence of this gene in isolates belonging to each of the three Lyme disease-associated species, Borrelia burgdorferi, Borrelia garinii , and the VS461 group, was evaluated. Transcriptional start site analyses suggest that the gene may be under the control of multiple promoters that are highly similar in nucleotide sequence. JF - Journal of Bacteriology AU - Marconi, R T AU - Samuels, D S AU - Garon, C F AD - Lab. Vectors and Pathogens, Rocky Mountain Lab., NIAID, Hamilton, MT 59840, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 926 EP - 932 VL - 175 IS - 4 SN - 0021-9193, 0021-9193 KW - aspC gene KW - Biochemistry Abstracts 2: Nucleic Acids; Genetics Abstracts; Microbiology Abstracts B: Bacteriology KW - spirochetes KW - genes KW - gene mapping KW - analysis KW - Borrelia KW - transcription KW - Lyme disease KW - G 07320:Bacterial genetics KW - N 14540:Structure, sequence & physical properties KW - J 02740:Genetics and evolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16496042?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Bacteriology&rft.atitle=Transcriptional+analyses+and+mapping+of+the+ospC+gene+in+Lyme+disease+spirochetes.&rft.au=Marconi%2C+R+T%3BSamuels%2C+D+S%3BGaron%2C+C+F&rft.aulast=Marconi&rft.aufirst=R&rft.date=1993-01-01&rft.volume=175&rft.issue=4&rft.spage=926&rft.isbn=&rft.btitle=&rft.title=Journal+of+Bacteriology&rft.issn=00219193&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Borrelia; Lyme disease; spirochetes; transcription; analysis; gene mapping; genes ER - TY - JOUR T1 - In vitro anti-human immunodeficiency virus (HIV) activities of transition state mimetic HIV protease inhibitors containing allophenylnorstatine. AN - 16495996; 2945718 AB - Transition state mimetic tripeptide human immunodeficiency virus (HIV) protease inhibitors containing allophenylnorstatine ((2S,3S)-3-amino-2-hydroxy-4-phenylbutyric acid) were synthesized and tested for activity against HIV in vitro. Two compounds, KNI-227 and KNI-272, which were highly potent against HIV protease with little inhibition of other aspartic proteases, showed the most potent activity against the infectivity and cytopathic effect of a wide spectrum of HIV strains. As tested in target CD4 super(+) ATH8 cells, the 50% inhibitory concentrations of KNI-227 against HIV type 1 LAI (HIV-1 sub(LAI)), HIV-1 sub(RF), HIV-1 sub(MN), and HIV-2 sub(ROD) were 0.1, 0.02, 0.03, and 0.1 mu M, respectively, while those of KNI-272 were 0.1, 0.02, 0.04, and 0.1 mu M, respectively. Both agents completely blocked the replication of 3'-azido-2',3'-dideoxythymidine-sensitive and -insensitive clinical HIV-1 isolates at 0.08 mu M as tested in target phytohemagglutinin-activated peripheral blood mononuclear cells. The ratios of 50% cytotoxic concentrations to 50% inhibitory concentrations for KNI-227 and KNI-272 were similar to 2,500 and > 4,000, respectively, as assessed in peripheral blood mononuclear cells. Both compounds blocked the posttranscriptional cleavage of the p55 precursor protein to generate the mature p24 Gag protein in stably HIV-1-infected cells. The n-octanol-water partition coefficients of KNI-227 and KNI-272 were high, with log P sub(o/w) values of 3.79 and 3.56, respectively. Degradation of KNI-227 and KNI-272 in the presence of pepsin (1 mg/ml, pH 2.2) at 37 degree C for 24 h was negligible. Current data warrant further careful investigations toward possible clinical application of these two novel compounds. JF - Antimicrobial Agents & Chemotherapy AU - Kageyama, S AU - Mimoto, T AU - Murakawa, Y AU - Nomizu, M AU - Ford, H Jr AU - Shirasaka, T AU - Gulnik, S AU - Erickson, J AU - Mitsuya, H AD - Med. Branch, NCI, Bethesda, MD 29892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 810 EP - 817 VL - 37 IS - 4 SN - 0066-4804, 0066-4804 KW - proteinase KW - allophenylnorstatine KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Virology & AIDS Abstracts KW - antiviral activity KW - antiviral agents KW - human immunodeficiency virus 1 KW - inhibitors KW - peptides KW - A 01068:Antiviral & viricidal KW - V 22004:AIDS: Clinical aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16495996?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antimicrobial+Agents+%26+Chemotherapy&rft.atitle=In+vitro+anti-human+immunodeficiency+virus+%28HIV%29+activities+of+transition+state+mimetic+HIV+protease+inhibitors+containing+allophenylnorstatine.&rft.au=Kageyama%2C+S%3BMimoto%2C+T%3BMurakawa%2C+Y%3BNomizu%2C+M%3BFord%2C+H+Jr%3BShirasaka%2C+T%3BGulnik%2C+S%3BErickson%2C+J%3BMitsuya%2C+H&rft.aulast=Kageyama&rft.aufirst=S&rft.date=1993-01-01&rft.volume=37&rft.issue=4&rft.spage=810&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - human immunodeficiency virus 1; inhibitors; peptides; antiviral activity; antiviral agents ER - TY - JOUR T1 - Stimulation of acetylcholinesterase activity by triiodothyronine in the brain of Singi fish, Heteropneustes fossilis (Bloch). AN - 16493928; 2941895 AB - Three consecutive days of injections of triiodothyronine (T sub(3)) (0.038, 0.075, 0.15 and 1.54 nmoles/g) significantly elevated the acetylcholinesterase (AchE) activity in the brain of Singi fish, Heteropneustes fossilis) (Bloch). The higher doses of 0.075, 0.15 and 1.54 nmoles of T sub(3)/g induced a greater increase in enzyme activity than 0.038 nmoles/g. A T sub(3) dose of 0.019 nmoles/g was found to be ineffective. The T sub(3) action on AchE activity was blocked by cycloheximide. Thiourea treatment for 30 days decreased the AchE activity below the control level. This reduced level of the enzyme activity was brought back even above the control level by T sub(3) injections. It is, therefore, suggested that thyroid hormone is involved in the sustenance of AchE activity in fish brain. JF - Fish Physiology and Biochemistry AU - De, S AU - Dasmahapatra, A K AU - Medda, A K AD - CGLS, NIEHS, 600 E. Green Field Ave., Milwaukee, WI 53204 USA Y1 - 1993 PY - 1993 DA - 1993 SP - 419 EP - 424 VL - 10 IS - 5 SN - 0920-1742, 0920-1742 KW - 3,5,3'-triodothyronine KW - Heteropneustes fossilis KW - Singi fish KW - acetylcholinesterase KW - brain KW - enzymatic activity KW - hormones KW - metabolism KW - stimulation KW - thyroid KW - triiodothyronine KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; CSA Neurosciences Abstracts; ASFA 1: Biological Sciences & Living Resources KW - Q1 08346:Physiology, biochemistry, biophysics KW - N3 11070:Neurochemistry and cellular biology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16493928?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fish+Physiology+and+Biochemistry&rft.atitle=Stimulation+of+acetylcholinesterase+activity+by+triiodothyronine+in+the+brain+of+Singi+fish%2C+Heteropneustes+fossilis+%28Bloch%29.&rft.au=De%2C+S%3BDasmahapatra%2C+A+K%3BMedda%2C+A+K&rft.aulast=De&rft.aufirst=S&rft.date=1993-01-01&rft.volume=10&rft.issue=5&rft.spage=419&rft.isbn=&rft.btitle=&rft.title=Fish+Physiology+and+Biochemistry&rft.issn=09201742&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - metabolism; thyroid; enzymatic activity; brain; hormones; stimulation ER - TY - JOUR T1 - Diarylsulfones, a new chemical class of nonnucleoside antiviral inhibitors of human immunodeficiency virus type 1 reverse transcriptase. AN - 16493636; 2945660 AB - A series of variously substituted diarylsulfonates and related derivatives were found to prevent human immunodeficiency virus type 1 (HIV-1) replication and HIV-1-induced cell killing in vitro. One of the more potent derivatives, 2-nitrophenyl phenyl sulfone (NPPS), completely protected human CEM-SS lymphoblastoid cells from the cytopathic effects of HIV-1 in cell culture at 1 to 5 mu M concentrations. HIV-1 replication, as assessed by the production of infectious virions, viral p24 antigen and virion reverse transcriptase (RT), was inhibited by NPPS at similar concentrations. There was no evidence of direct cytotoxicity of the drug at concentrations below 100 mu M. A variety of other CD4 super(+) T-cell lines as well as cultures of peripheral blood leukocytes and monocytes were protected from HIV-1-induced cytopathicity and/or viral replication. NPPS also inhibited several distinctly different strains of HIV-1 but was ineffective against three strains of HIV-1. Biochemical studies revealed that NPPS inhibited HIV-1 RT but not HIV-2 RT. NPPS had no direct effect on HIV-1 virions, nor did it block the initial binding of HIV-1 to target cells. Time-limited treatments of cells with NPPS found that NPPS had to be present continuously in culture to provide maximum antiviral protection. In addition, HIV-1 replication in cells in which infection was already fully established or in chronically infected cells was also unaffected by NPPS. We conclude that NPPS acts in a reversible manner as a nonnucleoside HIV-1-specific RT inhibitor. Although markedly different in structure from a larger, structurally diverse group of known HIV-1-specific nonnucleoside RT inhibitors, NPPS shares several of the biological properties that characterize this emerging new pharmacologic class. JF - Antimicrobial Agents & Chemotherapy AU - McMahon, J B AU - Gulakowski, R J AU - Weislow, O S AU - Schultz, R J AU - Narayanan, V L AU - Clanton, D J AU - Pedemonte, R AU - Wassmundt, F W AU - Buckheit, RW Jr AD - Lab. Drug Discovery Res. and Dev., Dev. Ther. Program, Div. Cancer Treat., NCI-Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702-1201, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 754 EP - 760 VL - 37 IS - 4 SN - 0066-4804, 0066-4804 KW - RNA-directed DNA polymerase KW - diarylsulfones KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Virology & AIDS Abstracts KW - antiviral agents KW - human immunodeficiency virus 1 KW - inhibitors KW - A 01068:Antiviral & viricidal KW - V 22004:AIDS: Clinical aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16493636?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antimicrobial+Agents+%26+Chemotherapy&rft.atitle=Diarylsulfones%2C+a+new+chemical+class+of+nonnucleoside+antiviral+inhibitors+of+human+immunodeficiency+virus+type+1+reverse+transcriptase.&rft.au=McMahon%2C+J+B%3BGulakowski%2C+R+J%3BWeislow%2C+O+S%3BSchultz%2C+R+J%3BNarayanan%2C+V+L%3BClanton%2C+D+J%3BPedemonte%2C+R%3BWassmundt%2C+F+W%3BBuckheit%2C+RW+Jr&rft.aulast=McMahon&rft.aufirst=J&rft.date=1993-01-01&rft.volume=37&rft.issue=4&rft.spage=754&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - human immunodeficiency virus 1; inhibitors; antiviral agents ER - TY - JOUR T1 - Laboratory and clinical evaluation of conjugate vaccines composed of Staphylococcus aureus type 5 and type 8 capsular polysaccharides bound to Pseudomonas aeruginosa recombinant exoprotein A. AN - 16490608; 2943447 AB - The synthesis, standardization, and immunogenicity in young outbred mice and clinical evaluation in adult volunteers of investigated vaccines designed to induce serum antibodies to the type 5 and type 8 capsular polysaccharides (CPs) of Staphylococcus aureus are described. Conjugates composed of the type 5 CP and a sonicated preparation of a high-molecular-weight type 8 CP bound to a nontoxic recombinant protein derived from Pseudomonas aeruginosa exotoxin A (rEPA) were synthesized. The conjugates were nontoxic and elicited serum CP antibodies after two subcutaneous injections into young outbred mice; a third injection elicited a booster response. In summary, the type 5 and type 8 conjugates were safe and elicited biologically active antibodies to both the CP and rEPA components. JF - Infection and Immunity AU - Fattom, A AU - Schneerson, R AU - Watson, D C AU - Karakawa, W W AU - Fitzgerald, D AU - Pastan, I AU - Li, Xiuru AU - Shiloach, J AU - Bryla, DA AU - Robbins, J B AD - Lab. Dev. and Mol. Immunity, Lab. Mol. Biol., NICH and Hum. Dev., NCI, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 1023 EP - 1032 VL - 61 IS - 3 SN - 0019-9567, 0019-9567 KW - polysaccharides KW - exoprotein A KW - mice KW - Immunology Abstracts; Microbiology Abstracts B: Bacteriology KW - vaccines KW - binding KW - capsules KW - Pseudomonas KW - Staphylococcus aureus KW - J 02834:Vaccination and immunization KW - F 06807:Active immunization UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16490608?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Laboratory+and+clinical+evaluation+of+conjugate+vaccines+composed+of+Staphylococcus+aureus+type+5+and+type+8+capsular+polysaccharides+bound+to+Pseudomonas+aeruginosa+recombinant+exoprotein+A.&rft.au=Fattom%2C+A%3BSchneerson%2C+R%3BWatson%2C+D+C%3BKarakawa%2C+W+W%3BFitzgerald%2C+D%3BPastan%2C+I%3BLi%2C+Xiuru%3BShiloach%2C+J%3BBryla%2C+DA%3BRobbins%2C+J+B&rft.aulast=Fattom&rft.aufirst=A&rft.date=1993-01-01&rft.volume=61&rft.issue=3&rft.spage=1023&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Pseudomonas; Staphylococcus aureus; capsules; vaccines; binding ER - TY - JOUR T1 - Potential role for a FTZ-F1 steroid receptor superfamily member in the control of Drosophila metamorphosis. AN - 16485859; 2936976 AB - FTZ-F1, a member of the steroid receptor superfamily, has been implicated in the activation of the homeobox segmentation gene fushi tarazu early in Drosophila embryogenesis. We have cloned a developmental isoform of FTZ-F1 and found that it is expressed as a product of the previously identified, midprepupal chromosome puff at 75CD. The 75CD puff occurs in the midst of a period of intense puffing activity that is triggered in response to the steroid hormone ecdysone at the onset of metamorphosis. Indirect immunofluorescent staining for FTZ-F1 on Drosophila polytene chromosomes reveals binding to over 150 chromosomal targets, which include 75CD itself and prominent late prepupal puffs that are predicted to be regulated by midprepupal puff proteins. These results suggest a role for FTZ-F1 as a regulator of insect metamorphosis and underscore the repeated utilization of a regulatory protein for widely separate developmental pathways. JF - Proceedings of the National Academy of Sciences, USA AU - Lavorgna, G AU - Karim, F D AU - Thummel, C S AU - Wu, C AD - Lab. Biochem., NCI/NIH, Build. 37, Rm. 4C-09, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 3004 EP - 3008 VL - 90 IS - 7 SN - 0027-8424, 0027-8424 KW - Drosophila KW - FTZ-F1 protein KW - amino acid sequence KW - cDNA KW - embryogenesis KW - gene families KW - genes KW - metamorphosis KW - nucleotide sequence KW - prediction KW - proteins KW - steroid receptors KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Entomology Abstracts; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - N 14640:Structure & sequence KW - Z 05188:Growth & regeneration KW - G 07367:GENERAL UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16485859?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.atitle=Potential+role+for+a+FTZ-F1+steroid+receptor+superfamily+member+in+the+control+of+Drosophila+metamorphosis.&rft.au=Lavorgna%2C+G%3BKarim%2C+F+D%3BThummel%2C+C+S%3BWu%2C+C&rft.aulast=Lavorgna&rft.aufirst=G&rft.date=1993-01-01&rft.volume=90&rft.issue=7&rft.spage=3004&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - nucleotide sequence; cDNA; amino acid sequence; genes; gene families; prediction; metamorphosis; proteins; embryogenesis ER - TY - JOUR T1 - Protective effects of selenium on cadmium toxicity in rats: Role of altered toxicokinetics and metallothionein. AN - 16484257; 2934237 AB - Selenium prevents the toxicity of the carcinogenic metal cadmium through undefined mechanisms. In this study, we determined the effects of selenium on cadmium toxicokinetics and on the ability of cadmium to induce metallothionein, a metal-binding protein that is thought to confer tolerance to cadmium toxicity. To assess the acute protective effects of selenium, male Wistar (WF/NCr) rats were given selenium (as SeO sub(2); 10 mu mol/kg, sc) at -24, 0, and +24 h relative to cadmium (as CdCl sub(2); 45 mu mol/kg, sc). The results suggest selenium prevents acute cadmium toxicity through a mechanism that does not involve induction of metallothionein and in spite of a markedly enhanced retention of cadmium. JF - Journal of Toxicology and Environmental Health AU - Wahba, Z Z AU - Coogan, T P AU - Rhodes, S W AU - Waalkes, M P AD - Inorg. Carcinog. Sect., Lab. Comp. Carcinog., NCI-FCRDC, Build. 538, Rm., 205E, Frederick MD 21702, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 171 EP - 182 VL - 38 IS - 2 SN - 0098-4108, 0098-4108 KW - cadmium KW - selenium KW - metallothionein KW - rats KW - Toxicology Abstracts KW - protection KW - toxicity KW - role KW - kinetics KW - X 24163:Metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16484257?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Toxicology+and+Environmental+Health&rft.atitle=Protective+effects+of+selenium+on+cadmium+toxicity+in+rats%3A+Role+of+altered+toxicokinetics+and+metallothionein.&rft.au=Wahba%2C+Z+Z%3BCoogan%2C+T+P%3BRhodes%2C+S+W%3BWaalkes%2C+M+P&rft.aulast=Wahba&rft.aufirst=Z&rft.date=1993-01-01&rft.volume=38&rft.issue=2&rft.spage=171&rft.isbn=&rft.btitle=&rft.title=Journal+of+Toxicology+and+Environmental+Health&rft.issn=00984108&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - toxicity; protection; kinetics; role ER - TY - JOUR T1 - Comparative analysis of scrapie agent inactivation methods. AN - 16482867; 2929306 AB - A scrapie-infected hamster brain homogenate was subjected to several different potential inactivation methods. methods included autoclaving for various lengths of time, either alone or in combination with different concentrations of sodium hydroxide or LpH, an aqueous acid phenolic derivative (Calgon Vestal Laboratories in St. Louis, MO). Inactivation treatments utilizing either NaOH or LpH alone were also evaluated. It was determined that several of the treatments inactivated all of the detectable infectivity. JF - Journal of Virological Methods AU - Ernst AU - Race, R E AD - NIH/NIAID, Lab. Persistent Viral Dis., Rocky Mountain Lab., Hamilton, MT 59840, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 193 EP - 202 VL - 41 IS - 2 SN - 0166-0934, 0166-0934 KW - treatments KW - spongiform encephalopathy KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Virology & AIDS Abstracts KW - inactivation KW - neuropathology KW - autoclaves KW - scrapie KW - V 22144:Prophylaxis & control KW - A 01068:Antiviral & viricidal UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16482867?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Virological+Methods&rft.atitle=Comparative+analysis+of+scrapie+agent+inactivation+methods.&rft.au=Ernst%3BRace%2C+R+E&rft.aulast=Ernst&rft.aufirst=&rft.date=1993-01-01&rft.volume=41&rft.issue=2&rft.spage=193&rft.isbn=&rft.btitle=&rft.title=Journal+of+Virological+Methods&rft.issn=01660934&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - scrapie; inactivation; autoclaves; neuropathology ER - TY - JOUR T1 - Enzyme function of copper, zinc superoxide dismutase as a free radical generator. AN - 16471367; 2920161 AB - The peroxidative activity of Cu,Zn-containing superoxide dismutase (Cu,Zn-SOD) was studied by using a chromogen, 2,2'-azinobis-(3-ethylbenzthiazoline-6-sulfonate) (ABTS) which reacts with super(.)OH radicals to form ABTS super(+.), and the spin traps, N-tert-butyl- alpha -phenylnitrone (PBN) and 5,5-dimethyl-1-pyrroline N-oxide (DMPO). The formation of ABTS super(+.) in this study required both active Cu,Zn-SOD and H sub(2)O sub(2) and followed first order kinetics with respect to SOD and H sub(2)O sub(2). It showed a binding isotherm with ABTS that yielded a dissociation constant of ABTS-enzyme as K sub(d) = 7.1 plus or minus 0.5 mu M. The K sub(d) values for DMPO and PBN were obtained as 0.63 and 11 mM, respectively, by competition reactions. A radical scavenger, formate anion, inhibits the formation of ABTS super(+.), whereas ethanol does not. The results together indicate that DMPO and anionic scavengers have easy access inside the positively charged active channel of Cu,Zn-SOD and are thus in a position to intercept the newly formed super(.)OH radicals. PBN and ethanol, however, stay outside of the channel and are not able to compete with ABTS for super(.)OH radicals. JF - Journal of Biological Chemistry AU - Yim, Moon B AU - Chock, PBoon AU - Stadtman, E R AD - Lab. Biochem., NHLBI, NIH, Build. 3, Rm. 202, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 4099 EP - 4105 VL - 268 IS - 6 SN - 0021-9258, 0021-9258 KW - enzymatic activity KW - free radicals KW - generation KW - kinetics KW - superoxide dismutase KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16471367?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=Enzyme+function+of+copper%2C+zinc+superoxide+dismutase+as+a+free+radical+generator.&rft.au=Yim%2C+Moon+B%3BChock%2C+PBoon%3BStadtman%2C+E+R&rft.aulast=Yim&rft.aufirst=Moon&rft.date=1993-01-01&rft.volume=268&rft.issue=6&rft.spage=4099&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Switch in antiviral specificity of a GTPase upon translocation from the cytoplasm to the nucleus. AN - 16465444; 2924000 AB - The Mx2 protein of rats is a cytoplasmic GTPase that protects cells against vesicular stomatitis virus but not against influenza virus. Since vesicular stomatitis virus replicates in the cytoplasm and influenza virus replicates in the nucleus, it was possible that the antiviral specificity of rat Mx2 protein was determined solely by the protein's subcellular localization. Here, we found that, indeed, rat Mx2 protein lost its anti-vesicular stomatitis virus activity and gained anti-influenza virus activity when it was directed to the nucleus by way of a foreign nuclear-transport signal appended to its amino terminus. These data show that rat Mx2 protein possesses an antiviral activity that is revealed only when the protein is shuttled to the nucleus. JF - Journal of Virology AU - Johannes, L AU - Arnheiter, H AU - Meier, E AD - Lab. Viral Mol. Pathog., Build. 36, Rm. 5D04, NINDS/NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 1653 EP - 1657 VL - 67 IS - 3 SN - 0022-538X, 0022-538X KW - GTPase KW - nucleus KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Virology & AIDS Abstracts KW - antiviral activity KW - influenza virus KW - cytoplasm KW - vesicular stomatitis virus KW - translocation KW - A 01068:Antiviral & viricidal KW - V 22100:Antiviral agents UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16465444?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Virology&rft.atitle=Switch+in+antiviral+specificity+of+a+GTPase+upon+translocation+from+the+cytoplasm+to+the+nucleus.&rft.au=Johannes%2C+L%3BArnheiter%2C+H%3BMeier%2C+E&rft.aulast=Johannes&rft.aufirst=L&rft.date=1993-01-01&rft.volume=67&rft.issue=3&rft.spage=1653&rft.isbn=&rft.btitle=&rft.title=Journal+of+Virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - vesicular stomatitis virus; influenza virus; translocation; antiviral activity; cytoplasm ER - TY - JOUR T1 - Oncogene ect2 is related to regulators of small GTP-binding proteins. AN - 16464229; 2920783 AB - We have developed an efficient expression cloning system that allows rapid isolation of complementary DNAs able to induce the transformed phenotype. We searched for molecules expressed in epithelial cells and possessing transforming potential to fibroblasts, and cloned a cDNA for the normal receptor of a growth factor secreted by NIH/3T3 cells. Here we report a second novel transforming gene, ect2. The isolated cDNA is activated by amino-terminal truncation of the normal product. The Ect2 protein has sequence similarity within a central core of 255 amino acids with the products of the breakpoint cluster gene, bcr, the yeast cell cycle gene, CDC24, and the dbl oncogene. Each of these genes encodes regulatory molecules or effectors for Rho-like small GTP-binding proteins. The baculovirus-expressed Ect2 protein could bind highly specifically to Rho and Rac proteins, could bind highly specifically to Rho and Rac proteins, whereas the dbl product showed broader binding specificity to Rho family proteins. Thus ect2 is a new member of an expanding family, whose products have transforming properties and interact with Rho-like proteins of the Ras superfamily. JF - Nature AU - Miki, T AU - Smith, CL AU - Long, JE AU - Eva, A AU - Fleming, T P AD - Lab. Cell. and Mol. Biol., NCI/NIH, Build. 37-1E24, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 462 EP - 465 VL - 362 IS - 6419 SN - 0028-0836, 0028-0836 KW - CNDA KW - Ect2 protein KW - NIM 3T3 cells KW - amino acid sequence KW - bcr KW - cDNA KW - ect2 KW - gene products KW - genes KW - guanine nucleotide-binding protein KW - homology KW - nucleotide sequence KW - predictions KW - transformation KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Oncogenes & Growth Factors Abstracts KW - G 07398:GENERAL KW - N 14640:Structure & sequence KW - B 26320:Other oncogenes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16464229?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature&rft.atitle=Oncogene+ect2+is+related+to+regulators+of+small+GTP-binding+proteins.&rft.au=Miki%2C+T%3BSmith%2C+CL%3BLong%2C+JE%3BEva%2C+A%3BFleming%2C+T+P&rft.aulast=Miki&rft.aufirst=T&rft.date=1993-01-01&rft.volume=362&rft.issue=6419&rft.spage=462&rft.isbn=&rft.btitle=&rft.title=Nature&rft.issn=00280836&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - nucleotide sequence; cDNA; amino acid sequence; genes; homology; transformation; gene products ER - TY - JOUR T1 - A Borrelia burgdorferi homolog of the Escherichia coli rho gene. AN - 16461593; 2924786 AB - The Escherichia coli rho gene product causes termination of transcription at specific sites, is essential for growth and is an RNA-dependent adenosine triphosphatase. While searching for another B. burgdorferi gene, we isolated a clone that encoded an open reading frame (ORF) 58% identical to the E. coli Rho protein. Many of the amino acids thought to be involved in ATP binding and hydrolysis are conserved between the two proteins. JF - Nucleic Acids Research AU - Tilly, K AU - Campbell, J AD - Lab. Microb. Struct. and Function, Rocky Mountain Lab., NIAID, Hamilton, MT 59840, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 1040 VL - 21 IS - 4 SN - 0305-1048, 0305-1048 KW - Borrelia burgdorferi KW - Escherichia coli KW - amino acid sequence KW - gene products KW - genes KW - homology KW - nucleotide sequence KW - predictions KW - rho gene KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - N 14640:Structure & sequence KW - G 07320:Bacterial genetics KW - J 02740:Genetics and evolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16461593?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+Acids+Research&rft.atitle=A+Borrelia+burgdorferi+homolog+of+the+Escherichia+coli+rho+gene.&rft.au=Tilly%2C+K%3BCampbell%2C+J&rft.aulast=Tilly&rft.aufirst=K&rft.date=1993-01-01&rft.volume=21&rft.issue=4&rft.spage=1040&rft.isbn=&rft.btitle=&rft.title=Nucleic+Acids+Research&rft.issn=03051048&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - nucleotide sequence; amino acid sequence; genes; homology; gene products ER - TY - JOUR T1 - Crystallization and preliminary X-ray diffraction studies of dogfish C-reactive protein. AN - 16457525; 2915839 AB - Crystals of dogfish (Mustelus canis ) C-reactive protein were obtained through vapor phase equilibration using the sitting drop rod technique with ammonium sulfate as the precipitating agent. The space group was determined to be P1 (triclinic lattice) with unit cell dimensions of a = 82.91, b = 92.25 and c = 103.40 angstrom; alpha = 83.36 degree , beta = 89.76 degree , and gamma = 81.30 degree . These crystals diffract to about 2.6 angstrom resolution and contain two hexamers in the asymmetric unit. JF - Proteins: Structure, Function & Genetics AU - Samudzi, C T AU - Nguyen, N Y AU - Ronald Rubin, J AD - NCI, Frederick Cancer Res. and Dev. Cent., ABL-Basic Res. Program, P.O. Box B, Frederick, MD 21702, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 100 EP - 102 VL - 15 SN - 0887-3585, 0887-3585 KW - C-reactive protein KW - Mustelus canis KW - X-ray diffraction analysis KW - biochemical analysis KW - crystal structure KW - molecular structure KW - proteins KW - x ray diffraction KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Oceanic Abstracts; ASFA 1: Biological Sciences & Living Resources KW - Marine KW - Q1 08346:Physiology, biochemistry, biophysics KW - O 1050:Vertebrates, Urochordates and Cephalochordates UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16457525?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proteins%3A+Structure%2C+Function+%26+Genetics&rft.atitle=Crystallization+and+preliminary+X-ray+diffraction+studies+of+dogfish+C-reactive+protein.&rft.au=Samudzi%2C+C+T%3BNguyen%2C+N+Y%3BRonald+Rubin%2C+J&rft.aulast=Samudzi&rft.aufirst=C&rft.date=1993-01-01&rft.volume=15&rft.issue=&rft.spage=100&rft.isbn=&rft.btitle=&rft.title=Proteins%3A+Structure%2C+Function+%26+Genetics&rft.issn=08873585&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - biochemical analysis; molecular structure; proteins; X-ray diffraction analysis; Marine ER - TY - JOUR T1 - PAC-1: A mitogen-induced nuclear protein tyrosine phosphatase. AN - 16456425; 2918994 AB - Tyrosine phosphorylation of proteins is required for signal transduction in cells and for growth regulation. A mitogen-induced gene (PAC-1) has been cloned from human T cells and encodes a 32-kilodalton protein that contains a sequence that defines the enzymatic site of known protein phosphotyrosine phosphatases (PTPases). PAC-1 was predominantly expressed in hematopoietic tissues and localized to the nucleus in transfected COS-7 cells and in mitogen-stimulated T cells. JF - Science (Washington) AU - Rohan, P J AU - Davis, P AU - Moskaluk, CA AU - Kearns, M AU - Krutzsch, H AU - Siebenlist, U AU - Kelly, K AD - Lab. Pathol., NCI/NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 1763 EP - 1766 VL - 259 IS - 5102 SN - 0036-8075, 0036-8075 KW - PAC-1 protein KW - amino acid sequence KW - cloning KW - genes KW - induction KW - lymphocytes T KW - man KW - mitogens KW - prediction KW - protein-tyrosine-phosphatase KW - signal transduction KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Human Genome Abstracts; Genetics Abstracts; Immunology Abstracts KW - G 07240:Immunogenetics KW - F 06752:Biochemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16456425?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science+%28Washington%29&rft.atitle=PAC-1%3A+A+mitogen-induced+nuclear+protein+tyrosine+phosphatase.&rft.au=Rohan%2C+P+J%3BDavis%2C+P%3BMoskaluk%2C+CA%3BKearns%2C+M%3BKrutzsch%2C+H%3BSiebenlist%2C+U%3BKelly%2C+K&rft.aulast=Rohan&rft.aufirst=P&rft.date=1993-01-01&rft.volume=259&rft.issue=5102&rft.spage=1763&rft.isbn=&rft.btitle=&rft.title=Science+%28Washington%29&rft.issn=00368075&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - mitogens; cloning; lymphocytes T; genes; amino acid sequence; induction; prediction; signal transduction; man ER - TY - JOUR T1 - Detection and quantitation of heme-containing proteins by chemiluminescence. AN - 16451216; 2919888 AB - A commercial assay for chemiluminescence (CL) has recently been developed for visualizing horseradish peroxidase-conjugated probes for antibodies and nucleic acids. To assess the utility of CL for detecting the peroxidase activity of other heme-containing proteins, the sensitivity of CL and a standard chromogenic stain for visualizing heme-proteins in SDS-polyacrylamide electrophoretic gels were compared. The chromogenic stain, which uses 3,3',5,5'-tetramethylbenzidine for a dye, and CL had equal sensitivity in electrophoretic gels. In blotting assays, CL was 10- to 10,000-fold more sensitive for detecting samples including cytochrome C and blood. Scintillation spectroscopy of CL emitted by blood, urine containing supplemental blood, or urine from a patient with hematuria resulted in a linear relationship between peroxidase activity and concentration, allowing for quantitation of blood over a broad range of concentrations. These results indicate that CL can rapidly detect and quantitate heme-proteins. JF - Analytical Biochemistry AU - Dorward, D W AD - Lab. Vectors and Pathog., Rocky Mt. Lab., NIAID/NIH, Hamilton, MT 59840, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 219 EP - 223 VL - 209 IS - 2 SN - 0003-2697, 0003-2697 KW - chemiluminescence KW - containing KW - detection KW - heme KW - methods KW - proteins KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16451216?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Analytical+Biochemistry&rft.atitle=Detection+and+quantitation+of+heme-containing+proteins+by+chemiluminescence.&rft.au=Dorward%2C+D+W&rft.aulast=Dorward&rft.aufirst=D&rft.date=1993-01-01&rft.volume=209&rft.issue=2&rft.spage=219&rft.isbn=&rft.btitle=&rft.title=Analytical+Biochemistry&rft.issn=00032697&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Metabolism-based transformation of myoglobin to an oxidase by BrCCl sub(3) and molecular modeling of the oxidase form. AN - 16449552; 2919810 AB - We have used molecular modeling and the known structure of the protein-bound heme adduct to identify probable mechanisms for transformation of myoglobin to an oxidase. Based on these modeling studies, the most likely structure of the experimentally observed adduct involves ligation to the heme iron of the epsilon -nitrogen atom of histidine 97 and/or that of histidine 64. The model structures revealed access of solvent to the heme active site, which could facilitate oxygen reduction. The transformation of myoglobins and perhaps other hemoproteins to oxidases may have toxicological importance in causing the tissue damage resulting from exposure to various xenobiotics and endogenous chemicals as well as explaining how hemoproteins are inactivated during catalysis. JF - Journal of Biological Chemistry AU - Osawa, Y AU - Darbyshire, J F AU - Steinbach, P J AU - Brooks, B R AD - Lab. Chem. Pharmacol., NHLBI, NIH, Build. 10, Rm. 8N110, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 2953 EP - 2959 VL - 268 IS - 4 SN - 0021-9258, 0021-9258 KW - metabolism KW - molecular modelling KW - myoglobin KW - oxidase KW - transformation KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16449552?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=Metabolism-based+transformation+of+myoglobin+to+an+oxidase+by+BrCCl+sub%283%29+and+molecular+modeling+of+the+oxidase+form.&rft.au=Osawa%2C+Y%3BDarbyshire%2C+J+F%3BSteinbach%2C+P+J%3BBrooks%2C+B+R&rft.aulast=Osawa&rft.aufirst=Y&rft.date=1993-01-01&rft.volume=268&rft.issue=4&rft.spage=2953&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Characterization of a distinct binding site for the prokaryotic chaperone, GroEL, on a human granulocyte ribonuclease. AN - 16447612; 2920573 AB - Although ribonucleases fold into correct tertiary conformation in vitro guided solely by information contained in the primary amino acid sequence, it is not clear whether folding of these proteins proceeds unassisted in a complex intracellular environment. We describe here the specific and high affinity binding of groEL, the prokaryotic homolog of the heat shock protein 60 family of molecular chaperones, to recombinant eosinophil cationic protein and eosinophil-derived neurotoxin, two members of the human ribonuclease gene family. We have determined that groEL binds to a unique peptide sequence near the amino terminus of nascent eosinophil cationic protein that includes the first of eight cysteine residues. This binding site functions independently and can confer groEL binding activity on an unrelated carrier protein. GroEL dissociates from the binding site upon addition of ATP and Mg super(2+); no other cations or cofactors are necessary. JF - Journal of Biological Chemistry AU - Rosenberg, H F AU - Ackerman, S J AU - Tenen, D G AD - Lab. Host Defenses, Build. 10, Rm. 11N114, NIAID/NIH, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 4499 EP - 4503 VL - 268 IS - 6 SN - 0021-9258, 0021-9258 KW - GroEL protein KW - binding KW - granulocytes KW - man KW - ribonuclease KW - role KW - sites KW - synthesis KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16447612?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=Characterization+of+a+distinct+binding+site+for+the+prokaryotic+chaperone%2C+GroEL%2C+on+a+human+granulocyte+ribonuclease.&rft.au=Rosenberg%2C+H+F%3BAckerman%2C+S+J%3BTenen%2C+D+G&rft.aulast=Rosenberg&rft.aufirst=H&rft.date=1993-01-01&rft.volume=268&rft.issue=6&rft.spage=4499&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - von Hippel-Lindau syndrome: Cloning and identification of the plasma membrane Ca super(++)-transporting ATPase isoform 2 gene that resides in the von Hippel-Lindau gene region. AN - 16444897; 2911461 AB - We have isolated and analyzed full-length complementary DNA clones encoded by a 200-kilobase gene encompassing the D3S601 locus that resides in the von Hippel-Lindau (VHL) gene region. The deduced amino acid sequence showed 99% identity with the published sequence of the rat plasma membrane Ca super(++)-transporting ATPase isoform 2 complementary DNA, implying that we have cloned and positioned the human plasma membranes Ca super(++)-transporting ATPase isoform 2 gene within the VHL critical region. The gene is expressed in VHL target tissues and should be considered a potential candidate gene for the VHL disease. JF - Cancer Research AU - Latif, F AU - Duh, Fuh-Mei AU - Gnarra, J AU - Tory, K AU - Kuzmin, I AU - Yao, M AU - Stackhouse, T AU - Modi, W AU - Lerman, MI AD - Lab. Immunol., NCI Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702-1201, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 861 EP - 867 VL - 53 IS - 4 SN - 0008-5472, 0008-5472 KW - Ca super(2+)-transporting ATPase KW - amino acid sequence KW - cDNA KW - genes KW - isoforms KW - man KW - nucleotide sequence KW - predictions KW - von Hippel-Lindau disease KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Biochemistry Abstracts 2: Nucleic Acids; Biochemistry Abstracts 1: Biological Membranes (till 1993); Human Genome Abstracts; Genetics Abstracts KW - N 14640:Structure & sequence KW - G 07430:Chromosome studies/nucleotide sequence UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16444897?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Research&rft.atitle=von+Hippel-Lindau+syndrome%3A+Cloning+and+identification+of+the+plasma+membrane+Ca+super%28%2B%2B%29-transporting+ATPase+isoform+2+gene+that+resides+in+the+von+Hippel-Lindau+gene+region.&rft.au=Latif%2C+F%3BDuh%2C+Fuh-Mei%3BGnarra%2C+J%3BTory%2C+K%3BKuzmin%2C+I%3BYao%2C+M%3BStackhouse%2C+T%3BModi%2C+W%3BLerman%2C+MI&rft.aulast=Latif&rft.aufirst=F&rft.date=1993-01-01&rft.volume=53&rft.issue=4&rft.spage=861&rft.isbn=&rft.btitle=&rft.title=Cancer+Research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - nucleotide sequence; von Hippel-Lindau disease; cDNA; amino acid sequence; genes; isoforms; man ER - TY - JOUR T1 - A cohort study in Southern China of tin miners exposed to radon and radon decay products. AN - 16444837; 2911449 AB - Several studies of underground mines have demonstrated that exposure to radioactive radon gas (more precisely, super(222)Rn and its short-lived decay products) at levels historically found in mines increases the risk of lung cancer. We report on a historical cohort study of male employees of the Yunnan Tin Corporation in southern China. The cohort consists of 17,143 workers with 175,143 person-years of observation and 981 lung cancer events. Eighty percent of the workers were employed underground and exposed to radon. The excess relative risk increased linearly with exposure, rising 0.6% per working level month. In the mines, workers were also exposed to arsenic-containing dusts. Adjustment for arsenic exposure, a known lung carcinogen, reduced the effect of radon exposure to 0.2% per working level month. JF - Health Physics AU - Xuan, Xiang-Zhen AU - Lubin, J H AU - Li, Jun-Yao AU - Yang, Li-Fen AU - Luo, Qing Sheng AU - Yang, Lan AU - Wang, Jian-Zhang AU - Blot, W J AD - Biostat. Branch, NCI EPN, Rm. 403, 6130 Executive Blvd., Rockville, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 120 EP - 131 VL - 64 IS - 2 SN - 0017-9078, 0017-9078 KW - tin KW - radon KW - lung cancer KW - arsenic KW - Toxicology Abstracts; Risk Abstracts; Pollution Abstracts; Health & Safety Science Abstracts KW - occupational exposure KW - dust KW - mining KW - mortality KW - risk assessment KW - China, People's Rep. KW - R2 23080:Industrial and labor KW - X 24210:Radiation & radioactive materials KW - P 8000:RADIATION KW - H SI2.8.7:DUST KW - H SI2.9.1:RADIATION HAZARDS KW - H SM10.21:CANCER KW - P 6000:TOXICOLOGY AND HEALTH UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16444837?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+Physics&rft.atitle=A+cohort+study+in+Southern+China+of+tin+miners+exposed+to+radon+and+radon+decay+products.&rft.au=Xuan%2C+Xiang-Zhen%3BLubin%2C+J+H%3BLi%2C+Jun-Yao%3BYang%2C+Li-Fen%3BLuo%2C+Qing+Sheng%3BYang%2C+Lan%3BWang%2C+Jian-Zhang%3BBlot%2C+W+J&rft.aulast=Xuan&rft.aufirst=Xiang-Zhen&rft.date=1993-01-01&rft.volume=64&rft.issue=2&rft.spage=120&rft.isbn=&rft.btitle=&rft.title=Health+Physics&rft.issn=00179078&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - China, People's Rep.; mining; tin; radon; occupational exposure; lung cancer; arsenic; dust; mortality; risk assessment ER - TY - JOUR T1 - Effect of primer selection on spuriously generated deletion of a tandem repeat during PCR. AN - 16442802; 2912388 AB - In general, the PCR faithfully amplifies the DNA fragment contained between unique primer binding sites. However, we have found that priming at certain sites can give rise to an artifactual deletion of one copy of a tandem repeat contained within the region to be amplified. The human polyomavirus JC (JCV) is a 5130-bp circular DNA virus that circulates widely in the population and frequently establishes latency in the kidney. While amplifying the JCV (Mad-1) regulatory region by PCR, we observed that one primer pair produced an unexpected deletion of one of the 98-bp repeat units. JF - PCR Methods and Applications AU - Ishaq, M AU - Stoner, G L AD - Lab. Exp. Neuropathol., NINDS/NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 263 EP - 265 VL - 2 IS - 3 SN - 1054-9803, 1054-9803 KW - deletion KW - polymerase chain reaction KW - polyomavirus JC (human) KW - primers KW - tandem repeat KW - Biotechnology and Bioengineering Abstracts; Medical and Pharmaceutical Biotechnology Abstracts; Virology & AIDS Abstracts; Human Genome Abstracts; Genetics Abstracts KW - G 07313:Viruses KW - V 22112:Animal DNA tumor viruses KW - W 30965:Miscellaneous, Reviews KW - W3 33130:Genetic based (PCR, etc.) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16442802?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PCR+Methods+and+Applications&rft.atitle=Effect+of+primer+selection+on+spuriously+generated+deletion+of+a+tandem+repeat+during+PCR.&rft.au=Ishaq%2C+M%3BStoner%2C+G+L&rft.aulast=Ishaq&rft.aufirst=M&rft.date=1993-01-01&rft.volume=2&rft.issue=3&rft.spage=263&rft.isbn=&rft.btitle=&rft.title=PCR+Methods+and+Applications&rft.issn=10549803&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - deletion; primers; polymerase chain reaction ER - TY - JOUR T1 - Primary HIV-1 isolates refractory to neutralization by soluble CD4 are potently inhibited by CD4-Pseudomonas exotoxin. AN - 16438471; 2908939 AB - Despite the ability of soluble forms of CD4 (sCD4) and related CD4 derivatives to neutralize human immunodeficiency type 1 (HIV-1) infectivity in vitro, these agents have shown little evidence of efficacy in clinical trials with infected individuals. In this report we demonstrate that CD4-Pseudomonas exotoxin inhibits spreading infection by primary HIV-1 isolates known to be highly refractory to neutralization by soluble CD4; the observed potency is at least as great as for a prototype sCD4-sensitive, laboratory-adapted HIV-1 strain. Thus, the in vitro efficacy of a CD4-based agent, which acts by targeted killing of infected cells, appears not to be compromised by features which render primary HIV-1 isolates refractory to neutralization by sCD4 derivatives. These results have important conceptual and practical implications for CD4-based therapeutic strategies. JF - Virology AU - Kennedy, P E AU - Moss, B AU - Berger, E A AD - Lab. Viral Dis., NIAID-NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 375 EP - 379 VL - 192 IS - 1 SN - 0042-6822, 0042-6822 KW - CD4 antigen KW - Biotechnology and Bioengineering Abstracts; Medical and Pharmaceutical Biotechnology Abstracts; Virology & AIDS Abstracts; Immunology Abstracts KW - neutralization KW - lymphocytes T KW - human immunodeficiency virus 1 KW - inhibition KW - exotoxins KW - conjugates KW - Pseudomonas KW - man KW - W3 33160:Antibody based KW - V 22003:AIDS: Immunological aspects KW - W 30965:Miscellaneous, Reviews KW - F 06800:Viruses UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16438471?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Virology&rft.atitle=Primary+HIV-1+isolates+refractory+to+neutralization+by+soluble+CD4+are+potently+inhibited+by+CD4-Pseudomonas+exotoxin.&rft.au=Kennedy%2C+P+E%3BMoss%2C+B%3BBerger%2C+E+A&rft.aulast=Kennedy&rft.aufirst=P&rft.date=1993-01-01&rft.volume=192&rft.issue=1&rft.spage=375&rft.isbn=&rft.btitle=&rft.title=Virology&rft.issn=00426822&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - neutralization; lymphocytes T; inhibition; exotoxins; conjugates; man; human immunodeficiency virus 1; Pseudomonas ER - TY - JOUR T1 - Effect of Yersinia pestis infection on temperature preference and movement of the Oriental rat flea (Xenopsylla cheopis ) (Siphonaptera: Pulicidae). AN - 16430511; 2904858 AB - Previous laboratory studies have shown that inoculation of bacterial endotoxin into the hemocoel of some arthropods, or natural infection by a number of pathogens, causes them to seek out a higher ambient temperature. This phenomenon has been called behavioral fever. Yersinia pestis is an endotoxin-producing bacterium that relies on infection of fleas for transmission. Behavioral fever in fleas might enhance the transmission of plague if infected fleas were induced to seek out a warm-bodied host after the death of an infected host. Our study indicates that in thermal gradients Y. pestis infected Oriental rat fleas (Xenopsylla cheopis ) do not exhibit behavioral fever and in one experiment sought out a significantly lower temperature. JF - Journal of Medical Entomology AU - Thomas, R E AU - Karstens, R H AU - Schwan, T G AD - Lab. Vectors and Pathogens, Arthropod-Borne Infect. Dis. Sect., Rocky Mountain Lab., NIAID, U.S. Public Health Serv., 903 S. 4th St., Hamilton, MT 59840, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 209 EP - 213 VL - 30 IS - 1 SN - 0022-2585, 0022-2585 KW - Microbiology Abstracts B: Bacteriology; Entomology Abstracts KW - plague KW - orientation KW - Yersinia pestis KW - Pulicidae KW - temperature preferences KW - Xenopsylla cheopis KW - Siphonaptera KW - infection KW - movements KW - J 02870:Invertebrate bacteriology KW - Z 05206:Medical & veterinary entomology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16430511?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Medical+Entomology&rft.atitle=Effect+of+Yersinia+pestis+infection+on+temperature+preference+and+movement+of+the+Oriental+rat+flea+%28Xenopsylla+cheopis+%29+%28Siphonaptera%3A+Pulicidae%29.&rft.au=Thomas%2C+R+E%3BKarstens%2C+R+H%3BSchwan%2C+T+G&rft.aulast=Thomas&rft.aufirst=R&rft.date=1993-01-01&rft.volume=30&rft.issue=1&rft.spage=209&rft.isbn=&rft.btitle=&rft.title=Journal+of+Medical+Entomology&rft.issn=00222585&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Yersinia pestis; Xenopsylla cheopis; Pulicidae; Siphonaptera; infection; temperature preferences; orientation; movements; plague ER - TY - JOUR T1 - Biochemical analysis of Torso and D-raf during Drosophila embryogenesis: Implications for terminal signal transduction. AN - 16430106; 2902786 AB - Determination of anterior and posterior terminal structure of Drosophila embryos requires activation of two genes encoding putative protein kinases, torso and D-raf. We demonstrate that Torso has intrinsic tyrosine kinase activity and show that it is transiently tyrosine phosphorylated (activated) at syncytial blastoderm stages. This report provides the first biochemical analysis of the terminal signal transduction pathway in Drosophila embryos. JF - Molecular and Cellular Biology AU - Sprenger, F AU - Trosclair, M M AU - Morrsion, D K AD - Mol. Mech. Carcinog. Lab., ABL-Basic Res. Program, NCI-Frederick Cancer Res. and Dev. Cent., P.O. Box B, Frederick, MD 21702-1201, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 1163 EP - 1172 VL - 13 IS - 2 SN - 0270-7306, 0270-7306 KW - D-raf kinase KW - Drosophila KW - Torso kinase KW - embryogenesis KW - expression KW - function KW - signal transduction KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Entomology Abstracts KW - Z 05173:Biochemistry & metabolism (incl. fat body) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16430106?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+Cellular+Biology&rft.atitle=Biochemical+analysis+of+Torso+and+D-raf+during+Drosophila+embryogenesis%3A+Implications+for+terminal+signal+transduction.&rft.au=Sprenger%2C+F%3BTrosclair%2C+M+M%3BMorrsion%2C+D+K&rft.aulast=Sprenger&rft.aufirst=F&rft.date=1993-01-01&rft.volume=13&rft.issue=2&rft.spage=1163&rft.isbn=&rft.btitle=&rft.title=Molecular+and+Cellular+Biology&rft.issn=02707306&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - expression; signal transduction; embryogenesis; function ER - TY - JOUR T1 - A recombinant immunotoxin that is active on prostate cancer cells and that is composed of the Fv region of monoclonal antibody PR1 and a truncated form of Pseudomonas exotoxin. AN - 16426815; 2906546 AB - Monoclonal antibody PR1 binds to the surface of normal prostate cells and to adenocarcinomas of the prostate. The cDNAs coding for the heavy and light chain variable regions of monoclonal antibody PR1 were cloned by PCR techniques. A recombinant toxin was then constructed that has the heavy chain variable region of monoclonal antibody PR1 connected to the light chain variable region by a flexible peptide linker to create a single-chain Fv; the Fv in turn is fused to a truncated form of Pseudomonas exotoxin. JF - Proceedings of the National Academy of Sciences, USA AU - Brinkmann, U AU - Gallo, M AU - Brinkmann, E AU - Kunwar, S AU - Pastan, I AD - Lab. Mol. Biol., Div. Cancer Biol., Diagn. and Cent., NCI/NIH, Build. 37, Rm. 4E16, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 547 EP - 551 VL - 90 IS - 2 SN - 0027-8424, 0027-8424 KW - Fv KW - Biotechnology and Bioengineering Abstracts; Medical and Pharmaceutical Biotechnology Abstracts; Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - prostate KW - adenocarcinoma KW - fragments KW - exotoxins KW - Pseudomonas KW - monoclonal antibodies KW - man KW - immunotoxins KW - W3 33160:Antibody based KW - F 06711:Monoclonal antibodies, hybridomas, antigens and antisera KW - W 30965:Miscellaneous, Reviews KW - J 02823:In vitro and in vivo effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16426815?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.atitle=A+recombinant+immunotoxin+that+is+active+on+prostate+cancer+cells+and+that+is+composed+of+the+Fv+region+of+monoclonal+antibody+PR1+and+a+truncated+form+of+Pseudomonas+exotoxin.&rft.au=Brinkmann%2C+U%3BGallo%2C+M%3BBrinkmann%2C+E%3BKunwar%2C+S%3BPastan%2C+I&rft.aulast=Brinkmann&rft.aufirst=U&rft.date=1993-01-01&rft.volume=90&rft.issue=2&rft.spage=547&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - prostate; adenocarcinoma; fragments; exotoxins; monoclonal antibodies; man; immunotoxins; Pseudomonas ER - TY - JOUR T1 - Suppression of polymorphonuclear leukocyte bactericidal activity by suramin. AN - 16422118; 2905073 AB - Suramin is a polyanionic compound with potent antineoplastic properties. Because polymorphonuclear leukocytes (PMNs) are a crucial component of host defense against bacteria and fungi, the effects of suramin on PMN function were studied in vitro. PMNs from healthy donors were incubated with concentrations of suramin of 1 to 1,000 mu g/ml (within and exceeding the therapeutic range) for 30 min, and PMN functional parameters were subsequently assessed. Suramin had no effect on viability, chemotaxis to N-formylmethionyl leucyl phenylalanine, phagocytosis of Candida albicans , or superoxide anion production in response to phorbol myristate acetate and formylmethionyl leucyl phenylalanine. Fungicidal activity against C. albicans blastoconidia was unaffected at a suramin concentration of < 500 mu g/ml, whereas at higher concentrations a slight suppression was observed. Bactericidal activity against Staphylococcus aureus was significantly suppressed by concentrations of greater than or equal to 100 mu g/ml. Phagocytosis of S. aureus was also significantly impaired at lambda 10 mu g/ml. The presence of 10% human serum during pretreatment did not abrogate the suramin-induced suppression of bactericidal activity. Treatment of PMNs with granulocyte colony-stimulating factor (4,000 U/ml) for 30 min prior to the addition of suramin (250 mu g/ml) improved the bactericidal defect. The PMN functional impairment may be related to increased susceptibility to bacterial infections, and granulocyte colony-stimulating factor may improve the defect. JF - Antimicrobial Agents & Chemotherapy AU - Roilides, E AU - Paschalides, P AU - Freifeld, A AU - Pizzo, P A AD - Infect. Dis. Sect., Pediatr. Branch, NCI/NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 495 EP - 500 VL - 37 IS - 3 SN - 0066-4804, 0066-4804 KW - suramin KW - effects on KW - Toxicology Abstracts; Immunology Abstracts; Microbiology Abstracts B: Bacteriology KW - antibacterial activity KW - leukocytes (polymorphonuclear) KW - immune response KW - Staphylococcus aureus KW - X 24117:Biochemistry KW - J 02833:Immune response and immune mechanisms KW - F 06793:Immunopharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16422118?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antimicrobial+Agents+%26+Chemotherapy&rft.atitle=Suppression+of+polymorphonuclear+leukocyte+bactericidal+activity+by+suramin.&rft.au=Roilides%2C+E%3BPaschalides%2C+P%3BFreifeld%2C+A%3BPizzo%2C+P+A&rft.aulast=Roilides&rft.aufirst=E&rft.date=1993-01-01&rft.volume=37&rft.issue=3&rft.spage=495&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Staphylococcus aureus; leukocytes (polymorphonuclear); antibacterial activity; immune response ER - TY - JOUR T1 - Endogenous peptides bound to HLA-A3 possess a specific combination of anchor residues that permit identification of potential antigenic peptides. AN - 16411971; 2887679 AB - A motif specific to peptides that bind to the human class I major histocompatibility complex molecule HLA-A3 was identified by sequence analysis of HPLC fractions containing endogenous peptides. Twenty-six different sequences were obtained, 19 of which were nonamers. The majority of these endogenous peptide sequences contained Leu at position (P)2, while most sequences contained Tyr or Lys at P9. Phe was shared by 16 sequences at P3. Synthetic peptides corresponding to endogenous peptide sequences were shown to bind to HLA-A3. The importance of Leu at P2 and Tyr or Lys at P9 ("anchor" residues) for peptide binding to HLA-A3 was demonstrated by the following results: (i) peptides GLFGGGGGY, GLFGGGGGK, and GLGGGGFGY, but not GLFGGGGGV, specifically bound to HLA-A3 and (ii) six nonapeptides from within the influenza A nucleoprotein, matrix, and polymerase proteins, selected for synthesis based upon their possession of P2 and P9 anchor residues, were shown to bind HLA-A3. None of a set of eight peptides that bound to HLA-A2, or six that bound to HLA-B27, bound detectably to HLA-A3. JF - Proceedings of the National Academy of Sciences, USA AU - DiBrino, M AU - Parker, K C AU - Shiloach, J AU - Knierman, M AU - Lukszo, J AU - Turner, R V AU - Biddison, W E AU - Coligan, JE AD - Biol. Resour. Branch, NIAID, Build. 4, Rm. 413, NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 1508 EP - 1512 VL - 90 IS - 4 SN - 0027-8424, 0027-8424 KW - binding KW - cell lines KW - histocompatibility antigen HLA-A3 KW - interaction KW - man KW - peptides KW - sites KW - specificity KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - F 06825:Human UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16411971?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.atitle=Endogenous+peptides+bound+to+HLA-A3+possess+a+specific+combination+of+anchor+residues+that+permit+identification+of+potential+antigenic+peptides.&rft.au=DiBrino%2C+M%3BParker%2C+K+C%3BShiloach%2C+J%3BKnierman%2C+M%3BLukszo%2C+J%3BTurner%2C+R+V%3BBiddison%2C+W+E%3BColigan%2C+JE&rft.aulast=DiBrino&rft.aufirst=M&rft.date=1993-01-01&rft.volume=90&rft.issue=4&rft.spage=1508&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - sites; specificity; binding; peptides; interaction; man; cell lines ER - TY - JOUR T1 - Changes in drug sensitivity of human immunodeficiency virus type 1 during therapy with azidothymidine, dideoxycytidine, and dideoxyinosine: An in vitro comparative study. AN - 16411907; 2887662 AB - Human immunodeficiency virus type 1 (HIV-1) strains were isolated from nine patients before and after prolonged therapy with either an alternating regimen of 3'-azido-3'-deoxythymidine (AZT) and 2',3'-dideoxycytidine (ddC) (AZT/ddC) or 2',3'-dideoxyinosine (ddI) alone. All strains obtained from four patients who received AZT/ddC for up to 41 mo were highly insensitive to AZT in vitro. Only one strain obtained after AZT/ddC therapy showed reduced susceptibility to ddC in addition to AZT and had previously unreported amino acid substitutions in the viral polymerase-encoding pol region, whereas three other strains had one or more of the five previously reported AZT-related mutations. In five HIV-1 strains from patients who received ddI for up to 29 mo, no appreciable decrease in sensitivity to ddI was detected. Two strains isolated after ddI therapy had no significant amino acid mutations, although three strains had a mutation reportedly associated with ddI administration. The data suggest that HIV-1 develops reduced susceptibility to AZT more readily than to ddC and ddI and/or that the reduced susceptibility to ddC and ddI is modest in degree. JF - Proceedings of the National Academy of Sciences, USA AU - Shirasaka, T AU - Yarchoan, R AU - O'Brien, M C AU - Husson, R N AU - Anderson, B D AU - Kojima, E AU - Shimada, T AU - Broder, S AU - Mitsuya, H AD - Exp. Retrovirol. Sect., Med. Branch, NCI/NIH, Build. 10, Rm. 5A11, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 562 EP - 566 VL - 90 IS - 2 SN - 0027-8424, 0027-8424 KW - azidothymidine KW - dideoxycytidine KW - dideoxyinosine KW - Virology & AIDS Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Microbiology Abstracts A: Industrial & Applied Microbiology KW - sensitivity KW - drugs KW - human immunodeficiency virus 1 KW - comparison KW - therapy KW - N 14160:Biological properties KW - A 01068:Antiviral & viricidal KW - V 22004:AIDS: Clinical aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16411907?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.atitle=Changes+in+drug+sensitivity+of+human+immunodeficiency+virus+type+1+during+therapy+with+azidothymidine%2C+dideoxycytidine%2C+and+dideoxyinosine%3A+An+in+vitro+comparative+study.&rft.au=Shirasaka%2C+T%3BYarchoan%2C+R%3BO%27Brien%2C+M+C%3BHusson%2C+R+N%3BAnderson%2C+B+D%3BKojima%2C+E%3BShimada%2C+T%3BBroder%2C+S%3BMitsuya%2C+H&rft.aulast=Shirasaka&rft.aufirst=T&rft.date=1993-01-01&rft.volume=90&rft.issue=2&rft.spage=562&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - human immunodeficiency virus 1; drugs; sensitivity; therapy; comparison ER - TY - JOUR T1 - Identification of an RNA binding site for human thymidylate synthase. AN - 16411485; 2896657 AB - Previous studies from this laboratory have shown that human TS mRNA translation is regulated by its protein product in a negative autoregulatory manner. We identify an RNA binding site for TS protein located within the first 188 nt of RNA. A 36-nt RNA sequence contained within this 188-nt fragment, corresponding to nt 75-110 and including the translational initiation site, binds TS protein with an affinity similar to that of both the full-length and the 188-nt TS RNA sequences. Variant RNAs with either a deletion or a mutation at the translational initiation region are unable to compete for TS protein binding. UV crosslinking studies reveal that an RNA fragment of approximately equals 36 nt is protected from RNase T1 digestion by TS protein binding. A second TS protein-binding site is localized within the protein-coding region corresponding to nt 434-634. The findings demonstrate a specific interaction between human TS protein and its TS RNA and identify an RNA binding site that includes the translational initiation site. JF - Proceedings of the National Academy of Sciences, USA AU - Chu, E AU - Voeller, D AU - Koeller, D M AU - Drake, J C AU - Takimoto, CH AU - Maley, G F AU - Maley, F AU - Allegra, C J AD - Natl. Cancer Inst., Navy Med. Oncol. Branch, NCI/NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 517 EP - 521 VL - 90 IS - 2 SN - 0027-8424, 0027-8424 KW - RNA KW - binding KW - identification KW - man KW - sites KW - thymidylate synthase KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16411485?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.atitle=Identification+of+an+RNA+binding+site+for+human+thymidylate+synthase.&rft.au=Chu%2C+E%3BVoeller%2C+D%3BKoeller%2C+D+M%3BDrake%2C+J+C%3BTakimoto%2C+CH%3BMaley%2C+G+F%3BMaley%2C+F%3BAllegra%2C+C+J&rft.aulast=Chu&rft.aufirst=E&rft.date=1993-01-01&rft.volume=90&rft.issue=2&rft.spage=517&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Case report of anorexia nervosa associated with Wilson's disease. AN - 16410797; 2892269 AB - Wilson's disease is a recessively inherited disorder of copper metabolism with prominent hepatic, hematopoetic, central nervous system (CNS), and ocular involvement. Psychiatric manifestations are notoriously variable. The following case history of a patient with both anorexia nervosa and Wilson's disease is presented and discussed in the context of organic CNS lesions associated with anorexia nervosa-like syndromes. JF - International Journal of Eating Disorders AU - Gwirtsman, HE AU - Prager, J AU - Henkin, R AD - Mood, Anxiety, and Personality Disord. Res. Branch, Div. Clin. Res., NIMH, Rm. 10C-24, 5600 Fisher Lane, Rockville, MD 20857, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 241 EP - 244 VL - 13 IS - 2 SN - 0276-3478, 0276-3478 KW - eating disorders KW - anorexia nervosa KW - Wilson's disease KW - case reports KW - Health & Safety Science Abstracts KW - H SM10.8.6:DIET UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16410797?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Eating+Disorders&rft.atitle=Case+report+of+anorexia+nervosa+associated+with+Wilson%27s+disease.&rft.au=Gwirtsman%2C+HE%3BPrager%2C+J%3BHenkin%2C+R&rft.aulast=Gwirtsman&rft.aufirst=HE&rft.date=1993-01-01&rft.volume=13&rft.issue=2&rft.spage=241&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Eating+Disorders&rft.issn=02763478&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 ER - TY - JOUR T1 - RNA polymerase idling and clearance in gal promoters: Use of supercoiled minicircle DNA template made in vivo. AN - 16403251; 2889282 AB - We have developed an in vivo system to engender supercoiled "minicircle" DNA containing a single promoter by using the integrative recombination system of bacteriophage lambda . The resulting minicircle templates allow quantitative analysis of the stages of transcription initiation from a promoter, including synthesis of both full-length and aborted transcripts in the same reactions under physiological conditions. We have used such minicircle DNA templates to study in vitro transcription of the Escherichia coli gal promoter. The full-length transcripts from gal P1 and P2 promoters responded to cAMP-cAMP receptor protein in a manner identical to that observed in vivo. There is a 3.5-fold stimulation of P1 and almost total inhibition of P2 in the presence of cAMP. Thus, the unitary promoter system described here duplicates the in vivo physiology. JF - Proceedings of the National Academy of Sciences, USA AU - Choy, HE AU - Adhya, S AD - Lab. Mol. Biol., NCI/NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 472 EP - 476 VL - 90 IS - 2 SN - 0027-8424, 0027-8424 KW - DNA-directed RNA polymerase KW - gal promoter KW - Biochemistry Abstracts 2: Nucleic Acids; Microbiology Abstracts B: Bacteriology KW - templates KW - supercoiling KW - promoters KW - DNA KW - Escherichia coli KW - transcription KW - N 14555:Miscellaneous KW - J 02740:Genetics and evolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16403251?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.atitle=RNA+polymerase+idling+and+clearance+in+gal+promoters%3A+Use+of+supercoiled+minicircle+DNA+template+made+in+vivo.&rft.au=Choy%2C+HE%3BAdhya%2C+S&rft.aulast=Choy&rft.aufirst=HE&rft.date=1993-01-01&rft.volume=90&rft.issue=2&rft.spage=472&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - Escherichia coli; DNA; templates; supercoiling; promoters; transcription ER - TY - JOUR T1 - Recent incidence trends for breast cancer in women and the relevance of early detection: An update. AN - 16398426; 2888468 AB - The incidence of breast cancer in women has been rising dramatically in the United States since 1982, based on data collected by the Surveillance, Epidemiology, and End Results (SEER) program of the National Cancer Institute. An additional three years of incidence and mortality data are included in this update of the earlier analyses; however, the focus of this report remains on examining the steeply increasing incidence trend between 1982 and 1986. Over this period, incidence rates for in situ and localized invasive tumors increased among women age 50 and older, while rates for regional and distant tumors remained stable. Conclusions regarding improved cancer control await confirmation by reduced breast cancer mortality. JF - Ca a Cancer Journal for Clinicians AU - Miller, BA AU - Feuer, E J AU - Hankey, B F AD - Cancer Stat. Branch, Surveillance Program, NIH, NCI, EPN, Rm. 343J, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 27 EP - 41 VL - 43 IS - 1 SN - 0007-9235, 0007-9235 KW - early detection KW - Health & Safety Science Abstracts KW - breast cancer KW - USA KW - mortality KW - females KW - H SM10.21:CANCER UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16398426?accountid=14244 L2 - http://onlinelibrary.wiley.com/doi/10.3322/canjclin.43.1.27/pdf LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2012-02-28 N1 - SubjectsTermNotLitGenreText - USA; females; breast cancer; mortality ER - TY - JOUR T1 - A cyclophilin-related protein involved in the function of natural killer cells. AN - 16396969; 2884977 AB - Natural killer cells are non-major histocompatibility complex-restricted large granular lymphocytes that can recognize and destroy tumor cells without prior stimulation. A 150-kDa molecule on the surface of human natural killer cells was identified as a component of a putative tumor-recognition complex. We report here the isolation of cDNAs coding for the 150-kDa tumor-recognition molecule from human and mouse cDNA libraries. Comparison of the human and mouse predicted amino acid sequences revealed > 80% homology. JF - Proceedings of the National Academy of Sciences, USA AU - Anderson, S K AU - Gallinger, S AU - Roder, J AU - Frey, J AU - Young, HA AU - Ortaldo, J R AD - Lab. Exp. Immunol., NCI, Frederick Cancer Res. and Dev. Cent., Build. 560, Rm. 31-93, Frederick, MD 21702-1201, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 542 EP - 546 VL - 90 IS - 2 SN - 0027-8424, 0027-8424 KW - amino acid sequence KW - cloning KW - cyclophilin KW - function KW - genes KW - man KW - mice KW - natural killer cells KW - prediction KW - receptors KW - role KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Human Genome Abstracts; Genetics Abstracts; Immunology Abstracts KW - G 07430:Chromosome studies/nucleotide sequence KW - F 06780:Genetics KW - G 07240:Immunogenetics KW - F 06757:NK cells UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16396969?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.atitle=A+cyclophilin-related+protein+involved+in+the+function+of+natural+killer+cells.&rft.au=Anderson%2C+S+K%3BGallinger%2C+S%3BRoder%2C+J%3BFrey%2C+J%3BYoung%2C+HA%3BOrtaldo%2C+J+R&rft.aulast=Anderson&rft.aufirst=S&rft.date=1993-01-01&rft.volume=90&rft.issue=2&rft.spage=542&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - cloning; amino acid sequence; genes; natural killer cells; prediction; role; receptors; man; function ER - TY - JOUR T1 - Nodal is a novel TGF- beta -like gene expressed in the mouse node during gastrulation. AN - 16393049; 2889436 AB - We isolate a candidate for the mutated gene which encodes a new member of the transforming growth factor- beta (TGF- beta ) superfamily. Expression is first detected in primitive streak-stage embryos at about the time of mesoderm formation. It then becomes highly localized in the node at the anterior of the primitive streak. This region is analogous to chick Hensen's node and Xenopus dorsal lip (Spemann's organizer), which can induce secondary body axes when grafted into host embryos. Our findings suggest that this gene, named nodal, encodes a signalling molecule essential for mesoderm formation and subsequent organization of axial structures in early mouse development. JF - Nature AU - Zhou, Xunlei AU - Sasaki, H AU - Lowe, L AU - Hogan, BLM AU - Kuehn, M R AD - Exp. Immunol. Branch, NCI/NIH, Bethesda, MD 20892, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 543 EP - 547 VL - 361 IS - 6412 SN - 0028-0836, 0028-0836 KW - amino acid sequence KW - cDNA KW - gastrulation KW - gene products KW - genes KW - like KW - nodal gene KW - nucleotide sequence KW - predictions KW - transforming growth factor- beta KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - G 07398:GENERAL KW - N 14640:Structure & sequence UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16393049?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature&rft.atitle=Nodal+is+a+novel+TGF-+beta+-like+gene+expressed+in+the+mouse+node+during+gastrulation.&rft.au=Zhou%2C+Xunlei%3BSasaki%2C+H%3BLowe%2C+L%3BHogan%2C+BLM%3BKuehn%2C+M+R&rft.aulast=Zhou&rft.aufirst=Xunlei&rft.date=1993-01-01&rft.volume=361&rft.issue=6412&rft.spage=543&rft.isbn=&rft.btitle=&rft.title=Nature&rft.issn=00280836&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - nucleotide sequence; cDNA; amino acid sequence; genes; like; gene products ER - TY - JOUR T1 - Retrotransfer in Escherichia coli conjugation: Bidirectional exchange or de novo mating?. AN - 16382626; 2880020 AB - DNA can be transferred among eubacteria and to plants and fungi by related, plasmid-mediated processes collectively referred to as bacterial conjugation. Conjugation occurs between cells in contact with one another and results in the unidirectional delivery of DNA from a bacterial donor to a recipient. Recent experiments that have reexamined the directionality of DNA flow during conjugation have come to different conclusions, some suggesting that genetic material also flows from recipient cells into the donor and that this process, termed retrotransfer, is likewise directed by donor-encoded functions. Here we report that plasmid transmission from bacterial recipients to donors is not a donor-mediated event. Movement of genetic material from recipients to donors was inhibited by streptomycin, which does not inhibit the conjugative donor, indicating that retrotransfer requires gene expression in recipients. Furthermore, retrotransfer was reduced in matings mediated by plasmids that encode strong entry exclusion, to a similar degree as matings between two donors. Therefore we suggest that retrotransfer is in fact newly initiated conjugation between transconjugants and donors. JF - Journal of Bacteriology AU - Heinemann, JA AU - Ankenbauer, R G AD - Lab. Microb. Struct. and Funct., NIAID/NIH, Rocky Moutain Lab., Hamilton, MT 59840, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 583 EP - 588 VL - 175 IS - 3 SN - 0021-9193, 0021-9193 KW - Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Microbiology Abstracts B: Bacteriology KW - transfer KW - conjugation KW - DNA KW - Escherichia coli KW - N 14673:Conjugation KW - G 07320:Bacterial genetics KW - J 02740:Genetics and evolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16382626?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Bacteriology&rft.atitle=Retrotransfer+in+Escherichia+coli+conjugation%3A+Bidirectional+exchange+or+de+novo+mating%3F.&rft.au=Heinemann%2C+JA%3BAnkenbauer%2C+R+G&rft.aulast=Heinemann&rft.aufirst=JA&rft.date=1993-01-01&rft.volume=175&rft.issue=3&rft.spage=583&rft.isbn=&rft.btitle=&rft.title=Journal+of+Bacteriology&rft.issn=00219193&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Escherichia coli; DNA; transfer; conjugation ER - TY - JOUR T1 - Transplacental carcinogenicity of cisplatin: Initiation of skin tumors and induction of other preneoplastic and neoplastic lesions in SENCAR mice AN - 15615256; 3928930 AB - cis-Dichlorodiammineplatinum (cis-DDP), an anticancer agent sometimes used in pregnant women for the treatment of malignant ovarian and uterine tumors, was tested for transplacental carcinogenic and/or tumor-initiating effects in SENCAR mice. Pregnant mice were given a single i.p. injection of either cis-DDP (7.5 mg/kg body weight) in 2.5% NaCl or the same weight-adjusted volume of NaCl (5 ml/kg body weight) on day 17 of gestation. Offspring were delivered and raised by their natural mothers until weaning at 3 weeks of age. Starting at week 4, offspring in experimental groups received topical applications of 2 mu g 12-O-tetrade-canoylphorbol-13-acetate (TPA) in acetone twice a week for 20 weeks while those in control groups received only acetone (0.2 ml/application) for the same duration. The experiment was terminated at 25 weeks of age. A high incidence (18 of 37; 48.7%) of papillomas was observed in offspring exposed transplacentally to cis-DDP and postnatally to TPA, while only 10% (4 of 40) of offspring exposed to TPA alone developed such tumors (P < 0.0002). Although no skin tumors were observed without TPA promotion, transplacental administration of cis-DDP resulted in development of thymic lymphomas, lung tumors, and proliferative kidney lesions in offspring. These results provide the first evidence that cis-DDP can initiate and/or induce preneoplastic and neoplastic lesions in multiple tissues transplacentally.(DBO) JF - Cancer Research AU - Diwan, BA AU - Anderson, L M AU - Rehm, S AU - Rice, J M AD - Biol. Carcinog. and Dev. Program, PRI/DynCorp, NCI-FCRDC, Frederick, MD 21702-1201, USA Y1 - 1993 PY - 1993 DA - 1993 SP - 3874 EP - 3876 VL - 53 IS - 17 SN - 0008-5472, 0008-5472 KW - cisplatin KW - mice KW - Toxicology Abstracts KW - carcinogenesis KW - placenta KW - skin KW - X 24115:Pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15615256?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Research&rft.atitle=Transplacental+carcinogenicity+of+cisplatin%3A+Initiation+of+skin+tumors+and+induction+of+other+preneoplastic+and+neoplastic+lesions+in+SENCAR+mice&rft.au=Diwan%2C+BA%3BAnderson%2C+L+M%3BRehm%2C+S%3BRice%2C+J+M&rft.aulast=Diwan&rft.aufirst=BA&rft.date=1993-01-01&rft.volume=53&rft.issue=17&rft.spage=3874&rft.isbn=&rft.btitle=&rft.title=Cancer+Research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - carcinogenesis; skin; placenta ER - TY - JOUR T1 - Ovarian cancer: Age contrasts in incidence, histology, disease stage at diagnosis, and mortality AN - 1434024216; 18537398 AB - Background. Age comparisons for incidence, histology, disease stage at initial diagnosis, and mortality of more than 20,000 ovarian cancer patients diagnosed between 1973-1987 are the focus of this descriptive epidemiologic study. This paper highlights key issues and concerns regarding ovarian cancer in women 65 years and older as a frame of reference for the proceedings of the working conference, "Perspectives on Ovarian Cancer in Older-Aged Women," co-sponsored by the National Institute on Aging, National Cancer Institute, and American Cancer Society held at the National Institutes of Health, November, 1991. Methods. Data are from the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) Program and the National Center for Health Statistics. The SEER Program database represents approximately 9.6% of the U.S. population. Results. Ovarian cancer affects women in the age group 65 years and older more frequently than younger women. More than 48% of all ovarian cancers occur in women in this age group. Age-adjusted rates increase as age advances, peaking at 54.0 per 100,000 in the age group 75-79 years. Time trends also indicate increases in age-specific incidence rates. This malignancy takes its toll in mortality in women 65 years and older with 64% of all deaths due to this neoplasm (in 1989). Moreover, older women are more likely to be initially diagnosed with advanced disease. Conclusions. Important questions about ovarian cancer in older-aged women need urgent attention from the research community. New strategies for diagnostic leads have to be developed for older women. JF - Cancer AU - Yancik, Rosemary AD - National Institute on Aging, 9000 Rockville Pike, Building 31, Room 5C05, Bethesda, MD 20892. Y1 - 1993/01// PY - 1993 DA - Jan 1993 SP - 517 EP - 523 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 71 IS - S2 SN - 0008-543X, 0008-543X KW - Health & Safety Science Abstracts KW - Age KW - USA KW - Ovarian carcinoma KW - H 11000:Diseases/Injuries/Trauma UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434024216?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=Ovarian+cancer%3A+Age+contrasts+in+incidence%2C+histology%2C+disease+stage+at+diagnosis%2C+and+mortality&rft.au=Yancik%2C+Rosemary&rft.aulast=Yancik&rft.aufirst=Rosemary&rft.date=1993-01-01&rft.volume=71&rft.issue=S2&rft.spage=517&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/10.1002%2Fcncr.2820710205 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-09-01 N1 - Last updated - 2014-03-10 N1 - SubjectsTermNotLitGenreText - Ovarian carcinoma; USA DO - http://dx.doi.org/10.1002/cncr.2820710205 ER - TY - JOUR T1 - Regional alterations in the levels of brain biogenic amines, glutamate, GABA, and GAD activity due to chronic consumption of inorganic arsenic in developing and adult rats AN - 13695882; S199445627 AB - Results are reported from experiments on the effect of daily doses of arsenic (5 mg per kg body weight) on the levels of several amino acids and on enzyme activity in different regions of the brain of young rats (from day 2 up to 60 d old). The results were compared with those in adult rats. Although there were greater changes in amines and amino acids in the cerebellum, hypothalamus, and brainstem than in other regions of the brain, the animals showed no obvious morbidity or behavioural abnormalities. However there was a significant increase in the time required for learning in tests with a food reward. The possible mechanisms involved are discussed. JF - Bulletin of Environmental Contamination and Toxicology AU - Nagaraja, T N AU - Desiraju, T AD - National Institute of Mental Health and Neuro Sciences, Bangalore Y1 - 1993 PY - 1993 DA - 1993 SP - 100 EP - 107 VL - 50 IS - 1 SN - 0007-4861, 0007-4861 KW - Animals (see also individual groups below) KW - Enzymes (see also individual groups below) KW - Gaba KW - Hypothalamus KW - Inorganic -- (see also without this prefix) KW - Aqualine Abstracts KW - AQ 00008:Effects of Pollution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/13695882?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aaqualine&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bulletin+of+Environmental+Contamination+and+Toxicology&rft.atitle=Regional+alterations+in+the+levels+of+brain+biogenic+amines%2C+glutamate%2C+GABA%2C+and+GAD+activity+due+to+chronic+consumption+of+inorganic+arsenic+in+developing+and+adult+rats&rft.au=Nagaraja%2C+T+N%3BDesiraju%2C+T&rft.aulast=Nagaraja&rft.aufirst=T&rft.date=1993-01-01&rft.volume=50&rft.issue=1&rft.spage=100&rft.isbn=&rft.btitle=&rft.title=Bulletin+of+Environmental+Contamination+and+Toxicology&rft.issn=00074861&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2000-09-01 N1 - SuppNotes - Publication focus: Experimental. N1 - Last updated - 2011-12-12 ER - TY - JOUR T1 - Role of cysteine residues in the extracellular domain and exoplasmic loops of the transmembrane domain of the TSH receptor: effect of mutation to serine on TSH receptor activity and response to thyroid stimulating autoantibodies. AN - 73433232; 1336379 AB - The extracellular domain of the thyrotropin (TSH) receptor is the primary site with which TSH and receptor autoantibodies interact. Cysteines 494 or 569 in the 1st and 2nd exoplasmic loops, respectively, of the transmembrane domain of the TSH receptor are important in this process or in coupling ligand binding to signal generation. Thus, when either is mutated to serine, a receptor results which has no detectable TSH binding and no cAMP response to TSH or thyroid stimulating autoantibodies after transfection, despite the fact the mutant receptor is normally synthesized, processed, and integrated in the membrane, as evidenced by Western blotting using a TSH receptor-specific antibody. Additional site directed mutagenesis studies are performed in order to identify cysteine residues in the extracellular domain of the receptor which, with cysteines 494 and 569, are important for tertiary structure and receptor bioactivity. JF - Biochemical and biophysical research communications AU - Kosugi, S AU - Ban, T AU - Akamizu, T AU - Kohn, L D AD - Section on Cell Regulation, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/12/30/ PY - 1992 DA - 1992 Dec 30 SP - 1754 EP - 1762 VL - 189 IS - 3 SN - 0006-291X, 0006-291X KW - Autoantibodies KW - 0 KW - Receptors, Thyrotropin KW - Recombinant Proteins KW - Serine KW - 452VLY9402 KW - Thyrotropin KW - 9002-71-5 KW - Cyclic AMP KW - E0399OZS9N KW - Cysteine KW - K848JZ4886 KW - Index Medicus KW - Animals KW - Humans KW - Plasmids KW - Molecular Weight KW - Rats KW - Blotting, Western KW - Transfection KW - Recombinant Proteins -- metabolism KW - Kinetics KW - Binding, Competitive KW - Cyclic AMP -- metabolism KW - Recombinant Proteins -- chemistry KW - Cell Membrane -- metabolism KW - Graves Disease -- immunology KW - Cell Line KW - Thyroid Gland -- metabolism KW - Sequence Deletion KW - Mutagenesis, Site-Directed KW - Receptors, Thyrotropin -- metabolism KW - Receptors, Thyrotropin -- chemistry KW - Protein Structure, Secondary KW - Thyrotropin -- pharmacology KW - Autoantibodies -- metabolism KW - Thyrotropin -- metabolism KW - Receptors, Thyrotropin -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73433232?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+and+biophysical+research+communications&rft.atitle=Role+of+cysteine+residues+in+the+extracellular+domain+and+exoplasmic+loops+of+the+transmembrane+domain+of+the+TSH+receptor%3A+effect+of+mutation+to+serine+on+TSH+receptor+activity+and+response+to+thyroid+stimulating+autoantibodies.&rft.au=Kosugi%2C+S%3BBan%2C+T%3BAkamizu%2C+T%3BKohn%2C+L+D&rft.aulast=Kosugi&rft.aufirst=S&rft.date=1992-12-30&rft.volume=189&rft.issue=3&rft.spage=1754&rft.isbn=&rft.btitle=&rft.title=Biochemical+and+biophysical+research+communications&rft.issn=0006291X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-08 N1 - Date created - 1993-02-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modulation of ultraviolet light mutational hotspots by cellular stress. AN - 73429532; 1474574 AB - Stressful treatments of cells provoke broad, transient, changes in cellular physiology and gene expression. In addition to these effects, DNA-damaging agents often induce permanent change in the form of mutations. Mutational patterns in target genes typically show hotspots and coldspots, the molecular basis of which appears to lie in the sequence context of the particular site. We determined the mutational pattern in an ultraviolet light-modified (in vitro) marker gene in a shuttle vector passaged through repair deficient (xeroderma pigmentosum) cells and compared it with patterns obtained from cells exposed to stress imposed by a DNA-damaging agent or a calcium ionophore. We found that the mutational hotspot pattern was altered by both stress treatments. We conclude that the cellular environment can influence the probability of mutagenesis at specific sites and propose that some of these effects on mutagenesis are mediated by alterations in cellular calcium levels. JF - Journal of molecular biology AU - Seetharam, S AU - Seidman, M M AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, NIH, Bethesda, MD 20892. Y1 - 1992/12/20/ PY - 1992 DA - 1992 Dec 20 SP - 1031 EP - 1036 VL - 228 IS - 4 SN - 0022-2836, 0022-2836 KW - Ionomycin KW - 56092-81-0 KW - Methyl Methanesulfonate KW - AT5C31J09G KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Xeroderma Pigmentosum KW - DNA Repair -- radiation effects KW - Base Sequence KW - Tumor Cells, Cultured KW - Humans KW - Molecular Sequence Data KW - Ionomycin -- pharmacology KW - Calcium -- pharmacology KW - Radiation, Ionizing KW - Methyl Methanesulfonate -- pharmacology KW - Mutagenesis -- radiation effects KW - Mutagenesis -- drug effects KW - Ultraviolet Rays KW - DNA Damage -- physiology KW - DNA Damage -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73429532?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+molecular+biology&rft.atitle=Modulation+of+ultraviolet+light+mutational+hotspots+by+cellular+stress.&rft.au=Seetharam%2C+S%3BSeidman%2C+M+M&rft.aulast=Seetharam&rft.aufirst=S&rft.date=1992-12-20&rft.volume=228&rft.issue=4&rft.spage=1031&rft.isbn=&rft.btitle=&rft.title=Journal+of+molecular+biology&rft.issn=00222836&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-29 N1 - Date created - 1993-01-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Overexpression of metallothionein in Chinese hamster ovary cells and its effect on nitrogen mustard-induced cytotoxicity: role of gene-specific damage and repair. AN - 73424172; 1458473 AB - Overexpression of metallothionein in mammalian cells has been associated with protection from cytotoxic chemicals and acquired resistance of tumors to cytotoxic drugs. The mechanism of this effect, however, remains unclear. We have explored whether cytotoxicity of the bifunctional alkylating agent nitrogen mustard was correlated with the extent of DNA damage formation and repair in the metallothionein gene regions in Chinese hamster ovary cells. The DNA damage and repair were examined in metallothionein-overexpressing, cadmium-resistant Chinese hamster ovary cells, Cdr200T1, with or without zinc-induced transcriptional activation, and in the parental CHO-met- cell line. The zinc-induced Cdr200T1 cells tolerated significantly higher doses of nitrogen mustard than did the uninduced Cdr200T1 variant. The parental CHO-met- cells, which did not have any detectable metallothionein expression, were even more resistant to nitrogen mustard than the zinc-induced Cdr variants. Nitrogen mustard-induced N-alkylpurines were formed with a higher frequency in inactive genomic regions than in the active genes. The removal of N-alkylpurines was similar in the active MT I gene region in Cdr200T1 and the silent MT I gene region in the parental cells, and the expression of these genes was determined by Northern assay. The MT II gene-containing region was repaired less efficiently than the MT I gene, independently of zinc induction. Further, preferential repair of nitrogen mustard-induced N-alkylpurines were detected in a single copy of the essential active dihydrofolate reductase gene as compared to a downstream noncoding region. This preferential repair was unaffected by the presence of zinc. Neither damage formation nor repair kinetics in the MT gene regions seemed to parallel the observed spectrum of sensitivity to HN2. JF - Cancer research AU - Wassermann, K AU - Pirsel, M AU - Bohr, V A AD - Laboratory of Molecular Pharmacology, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1992/12/15/ PY - 1992 DA - 1992 Dec 15 SP - 6853 EP - 6859 VL - 52 IS - 24 SN - 0008-5472, 0008-5472 KW - Cadmium KW - 00BH33GNGH KW - Mechlorethamine KW - 50D9XSG0VR KW - Metallothionein KW - 9038-94-2 KW - Tetrahydrofolate Dehydrogenase KW - EC 1.5.1.3 KW - Zinc KW - J41CSQ7QDS KW - Index Medicus KW - Cadmium -- pharmacology KW - Animals KW - Zinc -- pharmacology KW - Transcription, Genetic -- drug effects KW - Cell Survival -- drug effects KW - Dose-Response Relationship, Drug KW - CHO Cells KW - Tetrahydrofolate Dehydrogenase -- genetics KW - Cricetinae KW - Alkylation KW - DNA Repair KW - DNA Damage KW - Metallothionein -- genetics KW - Mechlorethamine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73424172?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Overexpression+of+metallothionein+in+Chinese+hamster+ovary+cells+and+its+effect+on+nitrogen+mustard-induced+cytotoxicity%3A+role+of+gene-specific+damage+and+repair.&rft.au=Wassermann%2C+K%3BPirsel%2C+M%3BBohr%2C+V+A&rft.aulast=Wassermann&rft.aufirst=K&rft.date=1992-12-15&rft.volume=52&rft.issue=24&rft.spage=6853&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-08 N1 - Date created - 1993-01-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The proto-oncogenes c-fos and c-jun modulate thyroid hormone inhibition of human thyrotropin beta subunit gene expression in opposite directions. AN - 73392397; 1335239 AB - The sequence from -1 to +6 bp in the hTSH beta gene contains overlapping putative thyroid hormone and AP-1 response elements. We demonstrate interaction between the AP-1 constituents c-fos and c-jun and thyroid hormone receptor in this region by transient transfection experiments using a -125 to +37 bp hTSH beta fragment. T3 inhibition was completely abolished by c-jun, but increased threefold by c-fos. A single transversion mutation at +2 bp restored T3 inhibition in the presence of c-jun and markedly reduced binding of purified c-jun by gel mobility shift assay. Thus, c-fos and c-jun influence T3 inhibition of hTSH beta expression in opposite directions acting through a response element shared with thyroid hormone receptor. Control of the relative cellular levels of these two proto-oncogenes may play a major role in modulating thyroid hormone inhibitory responses. JF - Biochemical and biophysical research communications AU - Bodenner, D L AU - McClaskey, J H AU - Kim, M K AU - Mixson, A J AU - Weintraub, B D AD - Molecular and Cellular Endocrinology Branch (MCEB), National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/12/15/ PY - 1992 DA - 1992 Dec 15 SP - 1050 EP - 1056 VL - 189 IS - 2 SN - 0006-291X, 0006-291X KW - c-erbA KW - c-fos KW - c-jun KW - Proto-Oncogene Proteins KW - 0 KW - Proto-Oncogene Proteins c-fos KW - Proto-Oncogene Proteins c-jun KW - Receptors, Thyroid Hormone KW - Triiodothyronine KW - 06LU7C9H1V KW - Thyrotropin KW - 9002-71-5 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Gene Expression -- drug effects KW - Proto-Oncogene Proteins c-fos -- metabolism KW - Humans KW - Receptors, Thyroid Hormone -- metabolism KW - Receptors, Thyroid Hormone -- genetics KW - Proto-Oncogene Proteins -- metabolism KW - Proto-Oncogene Proteins c-jun -- metabolism KW - Proto-Oncogenes KW - Plasmids KW - Protein Binding KW - Mutagenesis KW - Pregnancy KW - Polymerase Chain Reaction KW - Base Sequence KW - Transfection KW - Placenta KW - DNA -- genetics KW - Molecular Sequence Data KW - Proto-Oncogene Proteins -- genetics KW - Cell Line KW - Female KW - Thyrotropin -- genetics KW - Triiodothyronine -- pharmacology KW - Genes, fos KW - Thyrotropin -- metabolism KW - Genes, jun UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73392397?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+and+biophysical+research+communications&rft.atitle=The+proto-oncogenes+c-fos+and+c-jun+modulate+thyroid+hormone+inhibition+of+human+thyrotropin+beta+subunit+gene+expression+in+opposite+directions.&rft.au=Bodenner%2C+D+L%3BMcClaskey%2C+J+H%3BKim%2C+M+K%3BMixson%2C+A+J%3BWeintraub%2C+B+D&rft.aulast=Bodenner&rft.aufirst=D&rft.date=1992-12-15&rft.volume=189&rft.issue=2&rft.spage=1050&rft.isbn=&rft.btitle=&rft.title=Biochemical+and+biophysical+research+communications&rft.issn=0006291X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-28 N1 - Date created - 1993-01-28 N1 - Date revised - 2017-01-13 N1 - Gene symbol - c-erbA; c-fos; c-jun N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human lipoprotein lipase: the loop covering the catalytic site is essential for interaction with lipid substrates. AN - 73390692; 1460010 AB - Lipoprotein lipase (LPL), a key enzyme which initiates the hydrolysis of triglycerides present in chylomicrons and very low density lipoproteins, consists of multiple functional domains which are necessary for normal activity. The catalytic domain of LPL mediates the esterase function of the enzyme but separate lipid binding sites have been proposed to be involved in the interaction of LPL with emulsified lipid substrates at the water-lipid interface. Like pancreatic lipase (PL), LPL contains a surface loop covering the catalytic pocket that may modulate access of the substrate to the active site of the enzyme. Secondary structural analysis of this loop reveals a helix-turn-helix motif with two short amphipathic helices that have hydrophobic moments of 0.64 and 0.68. In order to investigate the role of the loop in the initial interaction of LPL with its substrate, we utilized site-directed mutagenesis to generate eight constructs in which the amphipathic properties of the loop were altered and expressed them in human embryonal kidney-293 cells. Reducing the amphiphilicity without changing the predicted secondary structure of the loop abolished the ability of the lipase to hydrolyze emulsified, long chain fatty acid triglycerides (triolein) but not the water soluble substrate tributyrin. Replacing the loop of LPL with the loop of hepatic lipase, which differs in 15 of 22 amino acids but is also amphiphilic, led to the expression of an enzyme that retained both triolein and tributyrin hydrolyzing activity. Substitution of the LPL loop by a short four amino acid peptide, which may allow more direct access to the active site than the 22 amino acid loop, enhanced hydrolysis of short chain fatty acid triglycerides by more than 2-fold, while the ability to hydrolyze emulsified substrates was abolished. Thus, disruption of the amphipathic structure of the LPL loop selectively decreases the hydrolysis of emulsified lipid substrate without affecting the esterase or catalytic function of the enzyme. These studies establish that the loop with its two amphipathic helices is essential for hydrolysis of long chain fatty acid substrate by LPL providing new insight into the role of the LPL loop in lipid-substrate interactions. We propose that the interaction between the lipoprotein substrates and the amphipathic helices within this loop may in part determine lipase substrate specificity. JF - The Journal of biological chemistry AU - Dugi, K A AU - Dichek, H L AU - Talley, G D AU - Brewer, H B AU - Santamarina-Fojo, S AD - Molecular Disease Branch, National Heart, Lung and Blood Institute, Bethesda, Maryland 20892. Y1 - 1992/12/15/ PY - 1992 DA - 1992 Dec 15 SP - 25086 EP - 25091 VL - 267 IS - 35 SN - 0021-9258, 0021-9258 KW - Recombinant Proteins KW - 0 KW - Triglycerides KW - Triolein KW - 122-32-7 KW - Lipoprotein Lipase KW - EC 3.1.1.34 KW - tributyrin KW - S05LZ624MF KW - Index Medicus KW - Models, Molecular KW - Humans KW - Computer Graphics KW - Amino Acid Sequence KW - Pancreas -- enzymology KW - Binding Sites KW - Triolein -- metabolism KW - Mutagenesis, Site-Directed KW - Transfection KW - Recombinant Proteins -- metabolism KW - Genetic Vectors KW - Kinetics KW - Triglycerides -- metabolism KW - Kidney KW - Molecular Sequence Data KW - Substrate Specificity KW - Recombinant Proteins -- chemistry KW - Cell Line KW - Protein Structure, Secondary KW - Lipoprotein Lipase -- metabolism KW - Lipoprotein Lipase -- genetics KW - Lipoprotein Lipase -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73390692?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Human+lipoprotein+lipase%3A+the+loop+covering+the+catalytic+site+is+essential+for+interaction+with+lipid+substrates.&rft.au=Dugi%2C+K+A%3BDichek%2C+H+L%3BTalley%2C+G+D%3BBrewer%2C+H+B%3BSantamarina-Fojo%2C+S&rft.aulast=Dugi&rft.aufirst=K&rft.date=1992-12-15&rft.volume=267&rft.issue=35&rft.spage=25086&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-12 N1 - Date created - 1993-01-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Immunogenicity and safety of a recombinant vaccinia virus vaccine expressing the carcinoembryonic antigen gene in a nonhuman primate. AN - 73386488; 1458480 AB - We have previously reported the development of a recombinant vaccinia virus vaccine expressing the human carcinoembryonic antigen (CEA) gene, designated rV(NYC)-CEA. This construct has been shown to elicit specific anti-CEA immune responses and an antitumor effect in a murine tumor model. In the studies reported here, the safety and immunogenicity of this recombinant vaccinia virus were evaluated in a rhesus monkey model. Human CEA is a M(r) 180,000 glycoprotein expressed in approximately 90% of gastrointestinal carcinomas and in some breast and non-small cell lung carcinomas. This family also includes normal cross-reacting antigen (NCA). Rhesus monkeys, like humans, have some NCA on the surface of their granulocytes. Eight monkeys were immunized 3 or 4 times by skin scarification with the recombinant CEA vaccine and four monkeys received wild-type vaccinia virus as control. After three vaccinations, all rV(NYC)-CEA-vaccinated animals exhibited a strong anti-CEA antibody response as measured by enzyme-linked immunosorbent assay. The functional ability of these antibodies to mediate lysis of a CEA-bearing tumor cell was demonstrated using human effector cells. This response could be enhanced by interleukin 2. Cellular immunity to CEA was measured by delayed-type hypersensitivity upon intradermal challenge with purified CEA. Only those animals receiving the recombinant vaccine displayed significant anti-CEA responses. Furthermore, peripheral blood mononuclear cells from immunized monkeys were found to proliferate in response to CEA stimulation. All vaccinated monkeys developed local skin irritation at the site of the vaccination, regional lymphadenopathy, and low-grade fevers after immunization. Following immunization with rV(NYC)-CEA, the response was consistent with the usual constitutional symptoms seen with human smallpox virus immunization. Blood counts, differentials, and hepatic and renal chemistries remained normal in all animals throughout the study and for up to 1 year following the primary vaccination. No evidence of immunological cross-reactivity to NCA was found by either a fall in the granulocyte count or analyses for anti-NCA antibodies. Thus, the rV(NYC)-CEA vaccine appears to be safe in rhesus monkeys. The administration of a CEA recombinant vaccine to rhesus monkeys induces both a humoral and a cell-mediated immune response directed against human CEA. JF - Cancer research AU - Kantor, J AU - Irvine, K AU - Abrams, S AU - Snoy, P AU - Olsen, R AU - Greiner, J AU - Kaufman, H AU - Eggensperger, D AU - Schlom, J AD - Laboratory of Tumor Immunology and Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/12/15/ PY - 1992 DA - 1992 Dec 15 SP - 6917 EP - 6925 VL - 52 IS - 24 SN - 0008-5472, 0008-5472 KW - Antigens, Neoplasm KW - 0 KW - Carcinoembryonic Antigen KW - Cell Adhesion Molecules KW - Membrane Glycoproteins KW - Vaccines, Synthetic KW - Viral Vaccines KW - Ovalbumin KW - 9006-59-1 KW - Index Medicus KW - Ovalbumin -- immunology KW - Animals KW - Hypersensitivity, Delayed KW - Membrane Glycoproteins -- analysis KW - Macaca mulatta KW - Membrane Glycoproteins -- immunology KW - Male KW - Immunization KW - Vaccines, Synthetic -- toxicity KW - Vaccinia virus -- immunology KW - Carcinoembryonic Antigen -- analysis KW - Carcinoembryonic Antigen -- immunology KW - Vaccines, Synthetic -- immunology KW - Viral Vaccines -- immunology KW - Carcinoembryonic Antigen -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73386488?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Immunogenicity+and+safety+of+a+recombinant+vaccinia+virus+vaccine+expressing+the+carcinoembryonic+antigen+gene+in+a+nonhuman+primate.&rft.au=Kantor%2C+J%3BIrvine%2C+K%3BAbrams%2C+S%3BSnoy%2C+P%3BOlsen%2C+R%3BGreiner%2C+J%3BKaufman%2C+H%3BEggensperger%2C+D%3BSchlom%2C+J&rft.aulast=Kantor&rft.aufirst=J&rft.date=1992-12-15&rft.volume=52&rft.issue=24&rft.spage=6917&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-08 N1 - Date created - 1993-01-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression cloning of a human dual-specificity phosphatase. AN - 73380614; 1281549 AB - Using an expression cloning strategy, we isolated a cDNA encoding a human protein-tyrosine-phosphatase. Bacteria expressing the kinase domain of the keratinocyte growth factor receptor (bek/fibroblast growth factor receptor 2) were infected with a fibroblast cDNA library in a phagemid prokaryotic expression vector and screened with a monoclonal anti-phosphotyrosine antibody. Among several clones showing decreased anti-phosphotyrosine recognition, one displayed phosphatase activity toward the kinase in vitro. The 4.1-kilobase cDNA encoded a deduced protein of 185 amino acids with limited sequence similarity to the vaccinia virus phosphatase VH1. The purified recombinant protein dephosphorylated several activated growth factor receptors, as well as serine-phosphorylated casein, in vitro. Both serine and tyrosine phosphatase activities were completely abolished by mutagenesis of a single cysteine residue conserved in VH1 and the VH1-related (VHR) human protein. These properties suggest that VHR is capable of regulating intracellular events mediated by both tyrosine and serine phosphorylation. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Ishibashi, T AU - Bottaro, D P AU - Chan, A AU - Miki, T AU - Aaronson, S A AD - Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/12/15/ PY - 1992 DA - 1992 Dec 15 SP - 12170 EP - 12174 VL - 89 IS - 24 SN - 0027-8424, 0027-8424 KW - VHR KW - bek KW - RNA, Messenger KW - 0 KW - Phosphoserine KW - 17885-08-4 KW - Phosphotyrosine KW - 21820-51-9 KW - Tyrosine KW - 42HK56048U KW - Phosphoprotein Phosphatases KW - EC 3.1.3.16 KW - Index Medicus KW - Humans KW - Gene Expression KW - Amino Acid Sequence KW - RNA, Messenger -- genetics KW - Phosphoserine -- metabolism KW - Cloning, Molecular KW - Base Sequence KW - Sequence Alignment KW - Restriction Mapping KW - Molecular Sequence Data KW - Tyrosine -- metabolism KW - Tyrosine -- analogs & derivatives KW - Substrate Specificity KW - Phosphoprotein Phosphatases -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73380614?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Expression+cloning+of+a+human+dual-specificity+phosphatase.&rft.au=Ishibashi%2C+T%3BBottaro%2C+D+P%3BChan%2C+A%3BMiki%2C+T%3BAaronson%2C+S+A&rft.aulast=Ishibashi&rft.aufirst=T&rft.date=1992-12-15&rft.volume=89&rft.issue=24&rft.spage=12170&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-19 N1 - Date created - 1993-01-19 N1 - Date revised - 2017-01-13 N1 - Gene symbol - VHR; bek N1 - Genetic sequence - L05147; GENBANK N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1987 Mar;84(5):1182-6 [3469660] Science. 1988 Jul 1;241(4861):42-52 [3291115] Cell. 1992 Feb 7;68(3):407-10 [1310893] Anal Biochem. 1992 May 1;202(2):293-8 [1519755] Cell. 1991 Oct 4;67(1):189-96 [1655274] Science. 1991 Nov 22;254(5035):1146-53 [1659742] Oncogene. 1992 Jan;7(1):187-90 [1741163] Cell. 1991 Dec 20;67(6):1181-94 [1836978] Nature. 1991 Mar 28;350(6316):359-62 [1848923] Methods Enzymol. 1991;201:110-49 [1943760] Cell. 1990 Apr 20;61(2):203-12 [2158859] EMBO J. 1990 Oct;9(10):3241-52 [2170109] Cell. 1989 Jul 14;58(1):181-91 [2473838] Proc Natl Acad Sci U S A. 1989 Jul;86(14):5252-6 [2546149] Nature. 1989 Nov 2;342(6245):39-45 [2682257] Nucleic Acids Res. 1987 Oct 26;15(20):8125-48 [3313277] EMBO J. 1985 Dec 1;4(12):3145-51 [3841511] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] EMBO J. 1992 Jun;11(6):2123-9 [1318193] J Biol Chem. 1992 Jul 15;267(20):14373-81 [1321146] Trends Biochem Sci. 1992 Mar;17(3):114-9 [1412695] Science. 1991 Jul 26;253(5018):401-6 [1650499] Cell. 1991 Nov 15;67(4):661-73 [1657401] Cell. 1991 Nov 15;67(4):675-85 [1657402] EMBO J. 1990 Aug;9(8):2399-407 [1695146] Cell. 1991 Mar 8;64(5):903-14 [1825803] Nature. 1991 May 16;351(6323):242-5 [1828290] Science. 1991 Jan 4;251(4989):72-5 [1846048] Anal Biochem. 1991 Feb 1;192(2):262-7 [1852137] Proc Natl Acad Sci U S A. 1991 Jun 15;88(12):5167-71 [2052597] Oncogene. 1990 Apr;5(4):451-8 [2139203] J Biol Chem. 1990 Aug 5;265(22):12767-70 [2165484] J Mol Biol. 1990 Oct 5;215(3):403-10 [2231712] Mol Cell Biol. 1988 Dec;8(12):5541-4 [2468999] Gene. 1989 Nov 15;83(1):137-46 [2531695] Cell. 1989 Sep 22;58(6):1013-6 [2550140] J Biol Chem. 1988 May 15;263(14):6731-7 [2834387] Nature. 1970 Aug 15;227(5259):680-5 [5432063] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - From the National Institutes of Health. AN - 73300565; 1433750 JF - JAMA AU - Gordis, E AU - Alexander, D AD - National Institute on Alcohol Abuse and Alcoholism. Y1 - 1992/12/09/ PY - 1992 DA - 1992 Dec 09 SP - 3183 VL - 268 IS - 22 SN - 0098-7484, 0098-7484 KW - Abridged Index Medicus KW - Index Medicus KW - United States KW - Animals KW - Alcoholism -- diagnosis KW - Pregnancy Complications -- diagnosis KW - Humans KW - National Institutes of Health (U.S.) KW - Female KW - Pregnancy KW - Fetal Alcohol Spectrum Disorders -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73300565?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=JAMA&rft.atitle=From+the+National+Institutes+of+Health.&rft.au=Gordis%2C+E%3BAlexander%2C+D&rft.aulast=Gordis&rft.aufirst=E&rft.date=1992-12-09&rft.volume=268&rft.issue=22&rft.spage=3183&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-22 N1 - Date created - 1992-12-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutation of alanine 623 in the third cytoplasmic loop of the rat thyrotropin (TSH) receptor results in a loss in the phosphoinositide but not cAMP signal induced by TSH and receptor autoantibodies. AN - 73369653; 1332945 AB - Thyrotropin (TSH) and IgG preparations from patients with Graves' disease increase inositol phosphate as well as cAMP formation in Cos-7 cells transfected with rat TSH receptor cDNA. Mutation of alanine 623 in the carboxyl end of the third cytoplasmic loop of the TSH receptor, to lysine or glutamic acid, results in the loss of TSH- and Graves' IgG-stimulated inositol phosphate formation but not in stimulated cAMP formation. There is no effect of the mutations on basal or P2-purinergic receptor-mediated inositol phosphate formation. The mutations do not affect transfection efficiency or the synthesis, processing, or membrane integration of the receptor, as evidenced by the unchanged amount and composition of the TSH receptor forms on Western blots of membranes from transfected cells. The mutations increase the affinity of the TSH receptor for [125I]TSH and decrease Bmax; however, cells with an equivalently decreased Bmax as a result of transfection with lower levels of wild type receptor do not lose either TSH-induced inositol phosphate formation or cAMP signaling activity. Thus, in addition to discriminating between ligand-induced phosphatidylinositol bisphosphate and cAMP signals, the mutation appears to cause an altered receptor conformation which affects ligand binding to its large extracellular domain. JF - The Journal of biological chemistry AU - Kosugi, S AU - Okajima, F AU - Ban, T AU - Hidaka, A AU - Shenker, A AU - Kohn, L D AD - Cell Regulation Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/12/05/ PY - 1992 DA - 1992 Dec 05 SP - 24153 EP - 24156 VL - 267 IS - 34 SN - 0021-9258, 0021-9258 KW - Autoantibodies KW - 0 KW - Immunoglobulin G KW - Inositol Phosphates KW - Phosphatidylinositols KW - Receptors, Thyrotropin KW - Recombinant Proteins KW - Colforsin KW - 1F7A44V6OU KW - Thyrotropin KW - 9002-71-5 KW - Cholera Toxin KW - 9012-63-9 KW - Cyclic AMP KW - E0399OZS9N KW - Alanine KW - OF5P57N2ZX KW - Index Medicus KW - Animals KW - Inositol Phosphates -- metabolism KW - Humans KW - Immunoglobulin G -- pharmacology KW - Cholera Toxin -- pharmacology KW - Amino Acid Sequence KW - Rats KW - Colforsin -- pharmacology KW - Transfection KW - Recombinant Proteins -- metabolism KW - Kinetics KW - Binding, Competitive KW - Recombinant Proteins -- immunology KW - Molecular Sequence Data KW - Recombinant Proteins -- chemistry KW - Graves Disease -- immunology KW - Cell Line KW - Protein Conformation KW - Mutagenesis, Site-Directed KW - Signal Transduction -- physiology KW - Phosphatidylinositols -- metabolism KW - Thyrotropin -- pharmacology KW - Receptors, Thyrotropin -- physiology KW - Receptors, Thyrotropin -- immunology KW - Autoantibodies -- pharmacology KW - Signal Transduction -- drug effects KW - Cyclic AMP -- metabolism KW - Thyrotropin -- metabolism KW - Receptors, Thyrotropin -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73369653?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Mutation+of+alanine+623+in+the+third+cytoplasmic+loop+of+the+rat+thyrotropin+%28TSH%29+receptor+results+in+a+loss+in+the+phosphoinositide+but+not+cAMP+signal+induced+by+TSH+and+receptor+autoantibodies.&rft.au=Kosugi%2C+S%3BOkajima%2C+F%3BBan%2C+T%3BHidaka%2C+A%3BShenker%2C+A%3BKohn%2C+L+D&rft.aulast=Kosugi&rft.aufirst=S&rft.date=1992-12-05&rft.volume=267&rft.issue=34&rft.spage=24153&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-30 N1 - Date created - 1992-12-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human and Giardia ADP-ribosylation factors (ARFs) complement ARF function in Saccharomyces cerevisiae. AN - 73302210; 1447192 AB - ADP-ribosylation factors (ARFs) are approximately 20-kDa guanine nucleotide-binding proteins that stimulate the ADP-ribosyltransferase activity of cholera toxin in vitro. ARFs are highly conserved, ubiquitously expressed in eukaryotic cells and appear to be involved in vesicular protein transport. The two yeast ARFs are > 60% identical to mammalian ARFs and are essential for cell viability (Stearns, T., Kahn, R. A., Botstein, D., and Hoyt, M. A. (1990) Mol. Cell. Biol. 10, 6690-6699). Although the two yeast ARF proteins are 96% identical in amino acid sequence, the yeast ARF1 gene is constitutively expressed, whereas the ARF2 gene is repressed by glucose. Human ARF5 and ARF6 and a Giardia ARF differ substantially in size and amino acid identity from other mammalian and eukaryotic ARFs but will, as befits their designation, activate cholera toxin. Expression of human ARF5, ARF6, or Giardia ARF cDNA rescued the lethal yeast ARF double mutant (arf1, arf2). Strains rescued by human ARF5, ARF6, or Giardia ARF grew much more slowly than wild-type yeast or strains rescued with yeast ARF1. We infer from the impaired growth of these rescued strains that the homologous ARFs may have specific targeting information that does not interact effectively or efficiently with the yeast protein membrane trafficking system. JF - The Journal of biological chemistry AU - Lee, F J AU - Moss, J AU - Vaughan, M AD - Laboratory of Cellular Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/12/05/ PY - 1992 DA - 1992 Dec 05 SP - 24441 EP - 24445 VL - 267 IS - 34 SN - 0021-9258, 0021-9258 KW - ARF1 KW - ARF2 KW - Carrier Proteins KW - 0 KW - Oligodeoxyribonucleotides KW - Cholera Toxin KW - 9012-63-9 KW - Poly(ADP-ribose) Polymerases KW - EC 2.4.2.30 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - ADP-Ribosylation Factor 1 KW - EC 3.6.5.2 KW - ADP-Ribosylation Factors KW - Index Medicus KW - Animals KW - Humans KW - Cholera Toxin -- pharmacology KW - Plasmids KW - Poly(ADP-ribose) Polymerases -- metabolism KW - Cloning, Molecular KW - Genotype KW - Base Sequence KW - Restriction Mapping KW - Polymerase Chain Reaction -- methods KW - Molecular Sequence Data KW - Saccharomyces cerevisiae -- genetics KW - Saccharomyces cerevisiae -- metabolism KW - Carrier Proteins -- metabolism KW - Genes, Fungal KW - GTP-Binding Proteins -- metabolism KW - Carrier Proteins -- genetics KW - Giardia -- metabolism KW - Giardia -- genetics KW - GTP-Binding Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73302210?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Human+and+Giardia+ADP-ribosylation+factors+%28ARFs%29+complement+ARF+function+in+Saccharomyces+cerevisiae.&rft.au=Lee%2C+F+J%3BMoss%2C+J%3BVaughan%2C+M&rft.aulast=Lee&rft.aufirst=F&rft.date=1992-12-05&rft.volume=267&rft.issue=34&rft.spage=24441&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-30 N1 - Date created - 1992-12-30 N1 - Date revised - 2017-01-13 N1 - Gene symbol - ARF1; ARF2 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Opioid receptor mediation of the hypothermic response to caffeine. AN - 73399822; 1334837 AB - Caffeine and other methylxanthines induce a dose-dependent reduction in core body temperature in mice. These experiments investigated the effects of neurotransmitter and neuromodulator antagonists on caffeine-induced hypothermia. Pretreatment with the alpha 2-adrenoceptor antagonist, atipamezole; the beta-adrenoceptor antagonist, propranolol; the dopamine antagonist, haloperidol; or the benzodiazepine receptor antagonist, flumazenil had no intrinsic effects on core body temperature nor did they interact significantly with the hypothermic effects of caffeine. The alpha 1-adrenoceptor antagonist, prazosin and the 5-HT receptor antagonist, metergoline significantly enhanced the hypothermic effects of caffeine, probably involving a combined effect with their intrinsic hypothermic actions. Pretreatment with the opiate receptor antagonist, naloxone (3 mg/kg i.p.), had no intrinsic effect on core body temperature but attenuated the hypothermic effect of caffeine reflected in a parallel shift to the right in the caffeine dose-effect curve. The naloxone-induced attenuation of the hypothermic effects of caffeine was also seen to be dose-dependent. The results reveal that opiate receptors (but not adrenoceptors, 5-HT, dopamine or benzodiazepine receptors) may play a role in modulating the hypothermic action of caffeine and possibly other methylxanthines. JF - European journal of pharmacology AU - Durcan, M J AU - Morgan, P F AD - Laboratory of Neurogenetics, DICBR, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892. Y1 - 1992/12/02/ PY - 1992 DA - 1992 Dec 02 SP - 151 EP - 156 VL - 224 IS - 2-3 SN - 0014-2999, 0014-2999 KW - Receptors, Opioid KW - 0 KW - Sympatholytics KW - Metergoline KW - 1501393LY5 KW - Naloxone KW - 36B82AMQ7N KW - Caffeine KW - 3G6A5W338E KW - Flumazenil KW - 40P7XK9392 KW - Index Medicus KW - Sympatholytics -- pharmacology KW - Naloxone -- pharmacology KW - Animals KW - Metergoline -- pharmacology KW - Drug Interactions KW - Dose-Response Relationship, Drug KW - Mice KW - Male KW - Flumazenil -- pharmacology KW - Body Temperature -- drug effects KW - Caffeine -- pharmacology KW - Receptors, Opioid -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73399822?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+pharmacology&rft.atitle=Opioid+receptor+mediation+of+the+hypothermic+response+to+caffeine.&rft.au=Durcan%2C+M+J%3BMorgan%2C+P+F&rft.aulast=Durcan&rft.aufirst=M&rft.date=1992-12-02&rft.volume=224&rft.issue=2-3&rft.spage=151&rft.isbn=&rft.btitle=&rft.title=European+journal+of+pharmacology&rft.issn=00142999&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-28 N1 - Date created - 1993-01-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The current status of new platinum analogs. AN - 85259966; pmid-1462169 AB - Nine platinum analogs are currently in clinical development, including three that contain the diaminocyclohexane substituent and five that contain the cyclobutanedicarboxylato leaving group. Many of them have shown activity in at least one cisplatin (CDDP)-resistant cell line, most commonly L1210 murine leukemia. In addition, most were less nephrotoxic than CDDP in preclinical evaluations. While these agents share certain key structural similarities, there are important differences in their toxicity profiles that may be exploitable in future combination therapies. Though neuropathy has been a troubling toxicity with two of the three diaminocyclohexane (DACH) compounds, it differs in that it appears to be less chronic and cumulative with oxaliplatin (I-OHP), which is also associated with much less myelosuppression. Of the cyclobutanedicarboxylato compounds that are structurally related to carboplatin (CBDCA), there are several notable differences. For several compounds, isolated neutropenia has been dose-limiting and thrombocytopenia, which is common with CBDCA, has been uncommon. Like CBDCA, neurotoxicity has not been an issue with this group. Therefore, the potential for dose escalation with a colony stimulating factor (CSF) appears enhanced. Furthermore, promising early clinical leads, such as the substantial response rates in cervix and head and neck cancers with 254-S and in patients with colon cancer using circadian modulation of I-OHP, require careful evaluation. Preclinical synergy data are also cited that suggest other potential clinical leads. The development of a number of these agents has been complicated by unanticipated issues, including unexpected chronic dose-limiting neurotoxicity with ormaplatin (OP), formulation and stability problems with liposomal-neodecanoato-diaminocyclohexane platinum (II) (L-NDDP), and problematic nephrotoxicity with zeniplatin (ZP). However, several of these new compounds are likely to enter broader phase II and III development and should provide important information not only about the utility of the agents themselves but also about the predictive value of some of these preclinical models of CDDP resistance. JF - Seminars in Oncology AU - Christian, M C AD - Investigational Drug Branch, National Cancer Institute, Bethesda, MD 20892. PY - 1992 SP - 720 EP - 733 VL - 19 IS - 6 SN - 0093-7754, 0093-7754 KW - Drugs, Investigational KW - Neoplasms KW - Antineoplastic Agents KW - Chemistry, Pharmaceutical KW - Human KW - Animal KW - Cyclobutanes KW - Organoplatinum Compounds KW - Forecasting KW - Carboplatin UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85259966?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Seminars+in+Oncology&rft.atitle=The+current+status+of+new+platinum+analogs.&rft.au=Christian%2C+M+C&rft.aulast=Christian&rft.aufirst=M&rft.date=1992-12-01&rft.volume=19&rft.issue=6&rft.spage=720&rft.isbn=&rft.btitle=&rft.title=Seminars+in+Oncology&rft.issn=00937754&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - The management of subglottic stenosis in patients with Wegener's granulomatosis. AN - 85199591; pmid-1453838 AB - Wegener's granulomatosis (WG) is a multisystem inflammatory disease characterized by vasculitis, granuloma formation, and necrosis. Among 158 patients treated at the National Institutes of Health during the past 24 years, 145 (92%) had an otolaryngologic manifestation of their disease and 25 (16%) had subglottic stenosis (SGS). SGS varied from asymptomatic to life-threatening. Sixteen (80%) of 20 patients with fixed SGS required surgical intervention, including manual dilations, carbon-dioxide laser resections, and laryngotracheoplasty (LTP). LTP was performed with and without microvascular reconstruction. Thirteen of the patients required tracheostomy and all 13 were ultimately decannulated. Five patients who repeatedly failed dilations and/or endoscopic laser surgery underwent LTP. Since 1987, two patients have undergone LTP with microvascular free flaps. Both patients were subsequently decannulated. The authors' experience demonstrates that management of SGS in WG is complex, requiring individualized frequent multimodality interventions to achieve satisfactory results. Microvascular laryngotracheal reconstruction should be considered in the surgical armamentarium for patients with persistent stenoses. JF - The Laryngoscope AU - Lebovics, R S AU - Hoffman, G S AU - Leavitt, R Y AU - Kerr, G S AU - Travis, W D AU - Kammerer, W AU - Hallahan, C AU - Rottem, M AU - Fauci, A S AD - National Institute on Deafness and other Communication Disorders, National Institutes of Health, Bethesda, MD 20892. PY - 1992 SP - 1341 EP - 1345 VL - 102 IS - 12 Pt 1 SN - 0023-852X, 0023-852X KW - Tracheal Stenosis KW - Combined Modality Therapy KW - Cartilage KW - Human KW - Tracheostomy KW - Reoperation KW - Child KW - Surgical Flaps KW - Glucocorticoids KW - Dilatation KW - Glottis KW - Laryngostenosis KW - Laser Surgery KW - Adult KW - Larynx KW - Middle Age KW - Wegener's Granulomatosis KW - Adolescent KW - Trachea KW - Female KW - Male UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85199591?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Laryngoscope&rft.atitle=The+management+of+subglottic+stenosis+in+patients+with+Wegener%27s+granulomatosis.&rft.au=Lebovics%2C+R+S%3BHoffman%2C+G+S%3BLeavitt%2C+R+Y%3BKerr%2C+G+S%3BTravis%2C+W+D%3BKammerer%2C+W%3BHallahan%2C+C%3BRottem%2C+M%3BFauci%2C+A+S&rft.aulast=Lebovics&rft.aufirst=R&rft.date=1992-12-01&rft.volume=102&rft.issue=12+Pt+1&rft.spage=1341&rft.isbn=&rft.btitle=&rft.title=The+Laryngoscope&rft.issn=0023852X&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - A clinical staging classification for type C Niemann-Pick disease. AN - 85161545; pmid-1461380 AB - Analysis of the temporal sequence of neurologic events, neurophysiologic abnormalities, and longevity in 36 Niemann-Pick type C patients revealed two clinical subgroups with five stages of severity within each group. Patients with a preschool onset (group I; n = 18) had a higher mortality than did patients with a school-age onset (group II; n = 18). An asymptomatic phase (stage 0) was defined by biochemical and histopathologic evidence of disease. The initial manifestations of stage 1 were a movement disorder (group I) and cognitive difficulties (group II) accompanied by impaired vertical saccadic eye movements and abnormal acoustic reflexes. Stage 2 was characterized by the sequential occurrence of vertical supranuclear gaze palsy (VSGP), cognitive difficulties, and dysarthria in group I and a movement disorder, VSGP, and dysarthria in group II. Pyramidal tract signs and abnormal brainstem auditory evoked responses defined stage 3 in both groups. Stage 4 culminated in a nonambulant, vegetative state. JF - Neurology AU - Higgins, J J AU - Patterson, M C AU - Dambrosia J M AU - Pikus, A T AU - Pentchev, P G AU - Sato, S AU - Brady, R O AU - Barton, N W AD - Developmental and Metabolic Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. PY - 1992 SP - 2286 EP - 2290 VL - 42 IS - 12 SN - 0028-3878, 0028-3878 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85161545?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurology&rft.atitle=A+clinical+staging+classification+for+type+C+Niemann-Pick+disease.&rft.au=Higgins%2C+J+J%3BPatterson%2C+M+C%3BDambrosia+J+M%3BPikus%2C+A+T%3BPentchev%2C+P+G%3BSato%2C+S%3BBrady%2C+R+O%3BBarton%2C+N+W&rft.aulast=Higgins&rft.aufirst=J&rft.date=1992-12-01&rft.volume=42&rft.issue=12&rft.spage=2286&rft.isbn=&rft.btitle=&rft.title=Neurology&rft.issn=00283878&rft_id=info:doi/ LA - English DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Elasticity and active force generation of cochlear outer hair cells. AN - 85156107; pmid-1474231 AB - The cochlear outer hair cell is described by a cylindrical membrane model, characterized by area and shear moduli for a passive elastic element and an active tension element dependent on the membrane potential. In passive experiments, these moduli are determined from the pressure-strain relations. The area modulus obtained is 0.07 N m-1, similar to a lipid bilayer and the shear modulus is 0.007 N m-1. These moduli combined with previous active experiments show that the active tension is nearly isotropic and is about 1.6 x 10(-2) N m-1 V-1, resulting in a 0.5 nN/mV force per cell. This implies that the receptor potential for acoustical stimulation produces an active force comparable to the acoustic force applied to the basilar membrane per outer hair cell. This finding supports the hypothesis that the outer hair cell acts as feedback motor in the fine tuning mechanism of the mammalian ear. JF - The Journal of the Acoustical Society of America AU - Iwasa, Kuni H AU - Chadwick, R S AD - National Institute on Deafness and Other Communication Disorders PY - 1992 SP - 3169 EP - 3173 VL - 92 IS - 6 SN - 0001-4966, 0001-4966 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85156107?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+the+Acoustical+Society+of+America&rft.atitle=Elasticity+and+active+force+generation+of+cochlear+outer+hair+cells.&rft.au=Iwasa%2C+Kuni+H%3BChadwick%2C+R+S&rft.aulast=Iwasa&rft.aufirst=Kuni&rft.date=1992-12-01&rft.volume=92&rft.issue=6&rft.spage=3169&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+the+Acoustical+Society+of+America&rft.issn=00014966&rft_id=info:doi/ LA - English DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Regulation of bradykinin-induced phosphoinositide turnover in cultured cerebellar astrocytes: possible role of protein kinase C. AN - 73533603; 1338944 AB - Phosphoinositide hydrolysis was studied in primary cultures of rat cerebellar astrocytes prelabeled with [3H]myo-inositol. Among the agonists examined, the rank order of efficacies in causing phosphoinositide hydrolysis was bradykinin > endothelin-1 > ATP > norepinephrine. The bradykinin response was robust (24-fold increase) with EC50 value of 30 nM and saturating concentration of 1 microM. Preincubation of cells with pertussis toxin did not affect the activation of phosphoinositide turnover by bradykinin. Although short-term (within 90 min) treatment of cells with phorbol dibutyrate attenuated bradykinin-induced phosphoinositide breakdown, the inhibitory effect was lost after 3-6 h of phorbol dibutyrate treatment. Extended (24 h) preincubation resulted in a potentiation of bradykinin response. Homologous desensitization of bradykinin response was observed in cells prestimulated with bradykinin for up to 6 h. However, similar to the effect of phorbol dibutyrate, 24-h pretreatment with bradykinin selectively sensitized the response to bradykinin. Up-regulation of the bradykinin response was also observed in cells prestimulated with endothelin-1 or norepinephrine for 24 h, although these treatments resulted in only homologous desensitization to their own response. Our results suggest that cultured cerebellar astrocytes express bradykinin receptors coupled to phospholipase C and in these cells protein kinase C plays a more prominent role in the negative-feedback regulation of bradykinin-evoked phosphoinositide response. JF - Neurochemistry international AU - Lin, W W AU - Chuang, D M AD - Section on Molecular Neurobiology, NIMH, Bethesda, MD 20892. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 573 EP - 579 VL - 21 IS - 4 SN - 0197-0186, 0197-0186 KW - Endothelins KW - 0 KW - Phosphatidylinositols KW - Virulence Factors, Bordetella KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Pertussis Toxin KW - EC 2.4.2.31 KW - Bradykinin KW - S8TIM42R2W KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Rats KW - Virulence Factors, Bordetella -- pharmacology KW - Endothelins -- pharmacology KW - Animals KW - Rats, Sprague-Dawley KW - Norepinephrine -- pharmacology KW - Cells, Cultured KW - Phorbol 12,13-Dibutyrate -- pharmacology KW - Adenosine Triphosphate -- pharmacology KW - Phosphatidylinositols -- metabolism KW - Cerebellum -- drug effects KW - Astrocytes -- drug effects KW - Bradykinin -- pharmacology KW - Cerebellum -- metabolism KW - Astrocytes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73533603?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurochemistry+international&rft.atitle=Regulation+of+bradykinin-induced+phosphoinositide+turnover+in+cultured+cerebellar+astrocytes%3A+possible+role+of+protein+kinase+C.&rft.au=Lin%2C+W+W%3BChuang%2C+D+M&rft.aulast=Lin&rft.aufirst=W&rft.date=1992-12-01&rft.volume=21&rft.issue=4&rft.spage=573&rft.isbn=&rft.btitle=&rft.title=Neurochemistry+international&rft.issn=01970186&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-06-29 N1 - Date created - 1993-06-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Recombinant human growth hormone promotes human lymphocyte engraftment in immunodeficient mice and results in an increased incidence of human Epstein Barr virus-induced B-cell lymphoma. AN - 73508657; 1336993 AB - Recombinant human growth hormone (rhGH) previously has been demonstrated to promote human or mouse T-cell engraftment in immunodeficient mice. We then wanted to examine long-term effects of rhGH on human cell engraftment in these mice. Mice with severe combined immune deficiency (SCID) were given human peripheral blood lymphocytes or human bone marrow cells and daily injections of rhGH (20 micrograms ip every other day). Upon later assessment for engraftment by flow cytometric analysis, it was determined that rhGH strongly promoted human T-cell engraftment in the thymus and spleens of these mice. However, there was considerable variability in both the incidence and extent of engraftment which appears to be due to donor-to-donor variation. Additionally, rhGH promoted B lymphomagenesis in these mice since long-term treatment of these xenogeneic chimeras with rhGH resulted in the increased incidence of human Epstein-Barr virus (EBV)-infected B-cell lymphoma. Thus, while rhGH can be used to optimize human T-cell engraftment in SCID mice, it also increases the likelihood of B-cell lymphoma generation when the donor is EBV infected. The results suggest that the activation of human T cells by rhGH results in an increased ability of these cells to traffic to the peripheral lymphoid organs of the SCID mice and results in a lymphoid microenvironment conducive to the outgrowth of EBV-transformed B lymphocytes. JF - Brain, behavior, and immunity AU - Murphy, W J AU - Durum, S K AU - Anver, M AU - Frazier, M AU - Longo, D L AD - National Cancer Institute-Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 355 EP - 364 VL - 6 IS - 4 SN - 0889-1591, 0889-1591 KW - Recombinant Proteins KW - 0 KW - Growth Hormone KW - 9002-72-6 KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Herpesvirus 4, Human -- pathogenicity KW - Recombinant Proteins -- pharmacology KW - Lymphoid Tissue -- pathology KW - Humans KW - Bone Marrow Transplantation -- adverse effects KW - Mice KW - Lymphocytes -- microbiology KW - Mice, Inbred BALB C KW - Graft Survival -- drug effects KW - Stimulation, Chemical KW - Recombinant Proteins -- toxicity KW - Chimera KW - Mice, SCID -- immunology KW - Transplantation, Heterologous KW - Lymphocytes -- drug effects KW - Lymphoma, B-Cell -- microbiology KW - Lymphoma, B-Cell -- etiology KW - Severe Combined Immunodeficiency -- complications KW - Lymphocyte Transfusion KW - Growth Hormone -- pharmacology KW - Severe Combined Immunodeficiency -- immunology KW - Growth Hormone -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73508657?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain%2C+behavior%2C+and+immunity&rft.atitle=Recombinant+human+growth+hormone+promotes+human+lymphocyte+engraftment+in+immunodeficient+mice+and+results+in+an+increased+incidence+of+human+Epstein+Barr+virus-induced+B-cell+lymphoma.&rft.au=Murphy%2C+W+J%3BDurum%2C+S+K%3BAnver%2C+M%3BFrazier%2C+M%3BLongo%2C+D+L&rft.aulast=Murphy&rft.aufirst=W&rft.date=1992-12-01&rft.volume=6&rft.issue=4&rft.spage=355&rft.isbn=&rft.btitle=&rft.title=Brain%2C+behavior%2C+and+immunity&rft.issn=08891591&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-03 N1 - Date created - 1993-03-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Clozapine rechallenge after an episode of 'neuroleptic malignant syndrome'. AN - 73451057; 1362370 AB - Nine out of 4044 patients admitted to our institution between 1987 and 1990 suffered an episode of NMS. Neuroleptic rechallenge using clozapine for persisting psychiatric illness was tolerated by eight patients. Clozapine was discontinued in one older, high-risk patient because recurrence of NMS was anticipated. Clozapine should be considered a drug of choice for psychotic patients with a history of NMS. JF - The British journal of psychiatry : the journal of mental science AU - Weller, M AU - Kornhuber, J AD - National Institutes of Health, Clinical Neuroscience Branch, Bethesda, MD 20892. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 855 EP - 856 VL - 161 SN - 0007-1250, 0007-1250 KW - Antipsychotic Agents KW - 0 KW - Clozapine KW - J60AR2IKIC KW - Index Medicus KW - Humans KW - Adult KW - Middle Aged KW - Antipsychotic Agents -- adverse effects KW - Male KW - Female KW - Psychotic Disorders -- drug therapy KW - Clozapine -- therapeutic use KW - Neuroleptic Malignant Syndrome -- prevention & control KW - Clozapine -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73451057?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+British+journal+of+psychiatry+%3A+the+journal+of+mental+science&rft.atitle=Clozapine+rechallenge+after+an+episode+of+%27neuroleptic+malignant+syndrome%27.&rft.au=Weller%2C+M%3BKornhuber%2C+J&rft.aulast=Weller&rft.aufirst=M&rft.date=1992-12-01&rft.volume=161&rft.issue=&rft.spage=855&rft.isbn=&rft.btitle=&rft.title=The+British+journal+of+psychiatry+%3A+the+journal+of+mental+science&rft.issn=00071250&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-17 N1 - Date created - 1993-02-17 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Br J Psychiatry. 1993 Jul;163:121-2 [8102585] Br J Psychiatry. 1993 Apr;162:566 [8329060] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pneumocystis carinii induction of tumor necrosis factor-alpha by alveolar macrophages: modulation by pentamidine isethionate. AN - 73446368; 1487315 AB - Pneumocystis carinii, and the inflammatory response it provokes, together contribute to irreversible lung damage in immunocompromised patients. P. carinii cysts were found to be capable of inducing tumor necrosis factor-alpha (TNF) release from alveolar macrophages in a concentration-dependent manner. At physiologically achievable concentrations, pentamidine isethionate (pentamidine) substantially reduces such production. Pretreatment of alveolar macrophages (AM phi) with interferon-gamma (IFN-gamma) synergizes with P. carinii to produce increased levels of TNF, a condition which pentamidine was also able to antagonize. Pentamidine treatment did not interfere with the phagocytic ability of AM phi. Considering clinical reduction of TNF could lessen P. carinii pneumonia (PCP) induced inflammation, the efficacy of pentamidine in the treatment of PCP may be partially associated with its ability to inhibit the release of inflammatory mediators such as TNF. JF - Immunology letters AU - Corsini, E AU - Dykstra, C AU - Craig, W A AU - Tidwell, R R AU - Rosenthal, G J AD - Immunotoxicology Section, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 303 EP - 308 VL - 34 IS - 3 SN - 0165-2478, 0165-2478 KW - Tumor Necrosis Factor-alpha KW - 0 KW - Pentamidine KW - 673LC5J4LQ KW - Interferon-gamma KW - 82115-62-6 KW - L-Lactate Dehydrogenase KW - EC 1.1.1.27 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Sprague-Dawley KW - Rats, Inbred F344 KW - Pneumonia, Pneumocystis -- immunology KW - Interferon-gamma -- pharmacology KW - Disease Models, Animal KW - Phagocytosis -- immunology KW - Male KW - L-Lactate Dehydrogenase -- metabolism KW - Female KW - Macrophage Activation -- drug effects KW - Pneumocystis -- immunology KW - Pentamidine -- pharmacology KW - Tumor Necrosis Factor-alpha -- biosynthesis KW - Macrophages, Alveolar -- microbiology KW - Macrophages, Alveolar -- drug effects KW - Macrophages, Alveolar -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73446368?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Immunology+letters&rft.atitle=Pneumocystis+carinii+induction+of+tumor+necrosis+factor-alpha+by+alveolar+macrophages%3A+modulation+by+pentamidine+isethionate.&rft.au=Corsini%2C+E%3BDykstra%2C+C%3BCraig%2C+W+A%3BTidwell%2C+R+R%3BRosenthal%2C+G+J&rft.aulast=Corsini&rft.aufirst=E&rft.date=1992-12-01&rft.volume=34&rft.issue=3&rft.spage=303&rft.isbn=&rft.btitle=&rft.title=Immunology+letters&rft.issn=01652478&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-25 N1 - Date created - 1993-02-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Recent National Cancer Institute lymphoma trials of etoposide-containing combination chemotherapy. AN - 73444835; 1283467 AB - Short-course prednisone/doxorubicin/cyclophospha- mide/etoposide-cytarabine/bleomycin/vincristine/methotrexate (ProMACE-CytaBOM) contains the same drugs as standard ProMACE-CytaBOM but is delivered weekly for 16 weeks rather than 2 weeks out of 3 for 18 weeks. This results in a significant increase in dose intensity, ranging from 27% to 65% for all drugs. A total of 46 patients have been treated with short-course ProMACE-CytaBOM. The overall complete response rate of 91% and relapse rate of 17% compares favorably with results obtained using standard ProMACE-CytaBOM (86% and 27%, respectively). Toxicity was slightly greater with short-course therapy, but in general the regimen was well tolerated. Further dose intensification is possible in eligible patients by dose escalating myelotoxic drugs. A second strategy for augmenting the dose intensity is to deliver the drugs by continuous intravenous infusion. Infusional chemotherapy with doxorubicin/etoposide/vincristine/oral prednisone/bolus cyclophosphamide (EPOCH) results in significant antitumor activity in heavily pretreated patients with chemotherapy-resistant Hodgkin's disease and non-Hodgkin's lymphomas. Complete responses or partial responses were seen in 91% of 21 evaluable patients. JF - Seminars in oncology AU - Urba, W J AU - Wilson, W H AU - Duffey, P L AU - Wittes, R AU - Chabner, B A AU - Longo, D L AD - Clinical Services Program, Program Resources, Inc/DynCorp, NCI-FCRDC, Frederick, MD 21702. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 26 EP - 32 VL - 19 IS - 6 Suppl 13 SN - 0093-7754, 0093-7754 KW - Cytarabine KW - 04079A1RDZ KW - Bleomycin KW - 11056-06-7 KW - Vincristine KW - 5J49Q6B70F KW - Etoposide KW - 6PLQ3CP4P3 KW - Doxorubicin KW - 80168379AG KW - Cyclophosphamide KW - 8N3DW7272P KW - Prednisone KW - VB0R961HZT KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - United States KW - Cyclophosphamide -- administration & dosage KW - Bleomycin -- administration & dosage KW - Humans KW - National Institutes of Health (U.S.) KW - Vincristine -- administration & dosage KW - Clinical Trials as Topic KW - Doxorubicin -- administration & dosage KW - Cytarabine -- administration & dosage KW - Methotrexate -- administration & dosage KW - Prednisone -- administration & dosage KW - Etoposide -- administration & dosage KW - Lymphoma -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73444835?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Seminars+in+oncology&rft.atitle=Recent+National+Cancer+Institute+lymphoma+trials+of+etoposide-containing+combination+chemotherapy.&rft.au=Urba%2C+W+J%3BWilson%2C+W+H%3BDuffey%2C+P+L%3BWittes%2C+R%3BChabner%2C+B+A%3BLongo%2C+D+L&rft.aulast=Urba&rft.aufirst=W&rft.date=1992-12-01&rft.volume=19&rft.issue=6+Suppl+13&rft.spage=26&rft.isbn=&rft.btitle=&rft.title=Seminars+in+oncology&rft.issn=00937754&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-02 N1 - Date created - 1993-03-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interaction of pumiliotoxin B with an "alkaloid-binding domain" on the voltage-dependent sodium channel. AN - 73443602; 1336116 AB - The alkaloid pumiliotoxin B (PTX-B) "activates" voltage-dependent sodium channels in synaptoneurosomes and neuroblastoma cells. It appears that PTX-B activates sodium channels by interacting with a site that is allosterically coupled to other sites on the sodium channel, namely two scorpion toxin sites and the brevetoxin site. In guinea pig cortical synaptoneurosomes, alpha-scorpion toxin, beta-scorpion toxin, and brevetoxin induce a dose-dependent potentiation of PTX-B-induced 22Na+ influx. The synergism with beta-scorpion toxin differentiates PTX-B from the alkaloid veratridine, which induces an activation of sodium channels that is not affected by beta-scorpion toxin. PTX-B does not inhibit [3H]batrachotoxinin-A benzoate ([3H]BTX-B) binding to the alkaloid site on sodium channels. On the other hand, aconitine, which activates sodium channels and inhibits [3H]BTX-B binding, induces a 22Na+ influx that, like PTX-B-induced 22Na+ influx, is potentiated by alpha-scorpion toxin, beta-scorpion toxin, and brevetoxin. Inhibition of [3H]BTX-B binding by aconitine is reduced in the presence of PTX-B. Both a type I pyrethroid (allethrin) and a type II pyrethroid (fenvalerate) inhibit PTX-B- and PTX-B/alpha-scorpion toxin-mediated 22Na+ influx. Allethrin and fenvalerate also inhibit aconitine-mediated 22Na+ flux but not BTX-mediated 22Na+ influx. It is proposed that on the sodium channel there is an "alkaloid-binding domain" at which alkaloids exert stimulatory actions. However, depending on the region on the domain to which the binding occurs, different allosteric interactions with other sites can be observed. PTX-B is proposed to interact with a part of the alkaloid-binding domain that is shared by aconitine but not by batrachotoxin or veratridine, whereas aconitine interacts with a part of the domain shared by PTX-B and by batrachotoxin/veratridine. JF - Molecular pharmacology AU - Gusovsky, F AU - Padgett, W L AU - Creveling, C R AU - Daly, J W AD - Laboratory of Bioorganic Chemistry, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 1104 EP - 1108 VL - 42 IS - 6 SN - 0026-895X, 0026-895X KW - Alkaloids KW - 0 KW - Amphibian Venoms KW - Indolizines KW - Neurotoxins KW - Piperidines KW - Sodium Channels KW - pumiliotoxin B KW - 67016-65-3 KW - Index Medicus KW - Ion Channel Gating KW - Animals KW - Synaptosomes -- drug effects KW - Neurotoxins -- metabolism KW - Guinea Pigs KW - Neurotoxins -- pharmacology KW - Synaptosomes -- metabolism KW - Binding Sites KW - Amphibian Venoms -- chemistry KW - Alkaloids -- metabolism KW - Sodium Channels -- metabolism KW - Alkaloids -- pharmacology KW - Sodium Channels -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73443602?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+pharmacology&rft.atitle=Interaction+of+pumiliotoxin+B+with+an+%22alkaloid-binding+domain%22+on+the+voltage-dependent+sodium+channel.&rft.au=Gusovsky%2C+F%3BPadgett%2C+W+L%3BCreveling%2C+C+R%3BDaly%2C+J+W&rft.aulast=Gusovsky&rft.aufirst=F&rft.date=1992-12-01&rft.volume=42&rft.issue=6&rft.spage=1104&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmacology&rft.issn=0026895X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-08 N1 - Date created - 1993-02-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Antimetabolites. AN - 73430716; 1457523 AB - Research efforts over the past year further elucidate the determinants of sensitivity and mechanisms of resistance to the antimetabolites fluorouracil, methotrexate, and cytarabine. Progress has been made in clarifying the complex regulation of target enzyme expression for these antimetabolites. Advances in analytical methodology should facilitate quantitation of thymidylate synthase content in tumor tissue prior to and following fluorouracil-based therapy. Information concerning the basis for certain drug interactions may guide rational dose rates and schedules for clinical trials. A better understanding of the clinical pharmacology of these agents has suggested strategies to minimize their toxicity while maintaining therapeutic activity. JF - Current opinion in oncology AU - Chen, A P AU - Grem, J L AD - National Cancer Institute, Bethesda, Maryland. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 1089 EP - 1098 VL - 4 IS - 6 SN - 1040-8746, 1040-8746 KW - Cytarabine KW - 04079A1RDZ KW - Fluorouracil KW - U3P01618RT KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - Neoplasms -- drug therapy KW - Animals KW - Drug Interactions KW - Humans KW - Drug Resistance KW - Fluorouracil -- therapeutic use KW - Cytarabine -- therapeutic use KW - Methotrexate -- pharmacology KW - Methotrexate -- therapeutic use KW - Fluorouracil -- pharmacology KW - Fluorouracil -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73430716?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+opinion+in+oncology&rft.atitle=Antimetabolites.&rft.au=Chen%2C+A+P%3BGrem%2C+J+L&rft.aulast=Chen&rft.aufirst=A&rft.date=1992-12-01&rft.volume=4&rft.issue=6&rft.spage=1089&rft.isbn=&rft.btitle=&rft.title=Current+opinion+in+oncology&rft.issn=10408746&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-11 N1 - Date created - 1993-01-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evolving role of flucytosine in immunocompromised patients: new insights into safety, pharmacokinetics, and antifungal therapy. AN - 73430432; 1457631 AB - Flucytosine is an antifungal agent useful in combination with amphotericin B in the treatment of several deeply invasive mycoses. The potentially dose-limiting, hematologic, gastrointestinal, and hepatic toxicities of flucytosine lead to a reluctance to use it in myelosuppressed patients. To investigate the safety and tolerability of flucytosine in this setting, we evaluated its use in 17 patients with cancer or aplastic anemia during a 2 1/2-year period at our institution and reviewed the literature describing mechanisms of action, resistance, in vitro and in vivo antifungal activity, clinical antifungal activity, pharmacokinetics, and toxicity. The combination of amphotericin B plus flucytosine eradicated the mycosis in 12 (71%) of 17 patients, whereas 3 (18%) of 17 died of progressive fungal infection. Serial serum levels of flucytosine measured by a creatinine iminohydrolase assay permitted reliable dosage adjustment. During therapy, only 2 (12%) of 17 patients had elevated mean serum levels of flucytosine (> 100 micrograms/mL) and 3 (18%) other patients had transiently elevated levels. Paired serum samples (n = 45) obtained at steady state during therapy with orally administered flucytosine showed similar peak and trough levels. Adverse effects of flucytosine therapy included one case each of reversible nausea, diarrhea, elevated transaminase levels, and thrombocytopenia. No cases of bone marrow aplasia, enterocolitis, hepatitis, or death due to flucytosine toxicity were encountered. We conclude that flucytosine in combination with amphotericin B is well tolerated in myelosuppressed patients when serum flucytosine levels are serially monitored. JF - Clinical infectious diseases : an official publication of the Infectious Diseases Society of America AU - Francis, P AU - Walsh, T J AD - Infectious Disease Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 1003 EP - 1018 VL - 15 IS - 6 SN - 1058-4838, 1058-4838 KW - Amphotericin B KW - 7XU7A7DROE KW - Flucytosine KW - D83282DT06 KW - Index Medicus KW - Drug Therapy, Combination KW - Humans KW - Adult KW - Amphotericin B -- administration & dosage KW - Middle Aged KW - Adolescent KW - Male KW - Female KW - Amphotericin B -- therapeutic use KW - Child, Preschool KW - Flucytosine -- adverse effects KW - Mycoses -- drug therapy KW - Immunocompromised Host KW - Flucytosine -- pharmacokinetics KW - Flucytosine -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73430432?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+infectious+diseases+%3A+an+official+publication+of+the+Infectious+Diseases+Society+of+America&rft.atitle=Evolving+role+of+flucytosine+in+immunocompromised+patients%3A+new+insights+into+safety%2C+pharmacokinetics%2C+and+antifungal+therapy.&rft.au=Francis%2C+P%3BWalsh%2C+T+J&rft.aulast=Francis&rft.aufirst=P&rft.date=1992-12-01&rft.volume=15&rft.issue=6&rft.spage=1003&rft.isbn=&rft.btitle=&rft.title=Clinical+infectious+diseases+%3A+an+official+publication+of+the+Infectious+Diseases+Society+of+America&rft.issn=10584838&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-12 N1 - Date created - 1993-01-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - DNA polymerase action on benzo[a]pyrene-DNA adducts. AN - 73424066; 1473243 AB - A 16mer oligonucleotide containing a single guanine residue at nucleotide 13 from the 3' end was treated with the (+)-enantiomer of the 7,8-dihydrodiol 9,10-epoxide of benzo[a]pyrene (B[a]P). Oligonucleotides containing either an adduct in which the epoxide ring was opened trans or cis by the amino group of the guanine residue were separated by chromatography and identified by 32P postlabeling and circular dichroism spectroscopy. In the presence of nucleotide triphosphates and DNA polymerase (either Sequenase, version 2.0 or human polymerase alpha), it was found that the B[a]P adducts inhibited extension of an 11mer primer opposite the nucleotide 3' to the adduct in the template. Under various conditions, this inhibition was greater for the cis adduct than for the trans adduct. After a 10 min incubation with Sequenase, primer extension was reduced to approximately 20% of that seen with unmodified oligonucleotide by the trans adduct and was almost completely inhibited by the cis adduct. When a 12mer primer was used to examine nucleotide incorporation directly across from the guanine or adducted guanine residues, it was clear that deoxycytidylic acid was preferentially incorporated in all cases but that the incorporation was severely inhibited by both the cis and trans adducts. These findings suggest that a cis adduct is a more effective block to replication than a trans adduct, and that these adducts may not be very efficient mutagenic lesions. JF - Carcinogenesis AU - Hruszkewycz, A M AU - Canella, K A AU - Peltonen, K AU - Kotrappa, L AU - Dipple, A AD - Chemistry of Carcinogenesis Laboratory, NCI-Frederick Cancer Research and Development Center, MD 21702. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 2347 EP - 2352 VL - 13 IS - 12 SN - 0143-3334, 0143-3334 KW - DNA Adducts KW - 0 KW - Oligodeoxyribonucleotides KW - benzo(a)pyrene-DNA adduct KW - Benzo(a)pyrene KW - 3417WMA06D KW - 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide KW - 55097-80-8 KW - DNA KW - 9007-49-2 KW - DNA-Directed DNA Polymerase KW - EC 2.7.7.7 KW - Index Medicus KW - 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide -- toxicity KW - 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide -- metabolism KW - Stereoisomerism KW - Base Sequence KW - Electrophoresis, Polyacrylamide Gel KW - Spectrophotometry, Ultraviolet KW - Molecular Sequence Data KW - Chromatography, Thin Layer KW - Templates, Genetic KW - Molecular Conformation KW - Chromatography, High Pressure Liquid KW - DNA -- metabolism KW - DNA-Directed DNA Polymerase -- metabolism KW - Benzo(a)pyrene -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73424066?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=DNA+polymerase+action+on+benzo%5Ba%5Dpyrene-DNA+adducts.&rft.au=Hruszkewycz%2C+A+M%3BCanella%2C+K+A%3BPeltonen%2C+K%3BKotrappa%2C+L%3BDipple%2C+A&rft.aulast=Hruszkewycz&rft.aufirst=A&rft.date=1992-12-01&rft.volume=13&rft.issue=12&rft.spage=2347&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-03 N1 - Date created - 1993-02-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Conservation of a 23-kDa human transplantation antigen in mammalian species. AN - 73420178; 1282492 AB - A group of transplantation antigens, referred to as tum- antigens, were identified in mouse tumor cells that had been mutagenized to produce variant cells and were recognized by clonal cytolytic T lymphocytes (CTL). Alterations in these variant cells that were recognized by CTL resulted from point mutations in the genes of specific proteins. We have isolated human and bovine cDNA clones that encode the homologs of the mouse tum- antigen P198. This 23.6-kDa protein is highly basic with a predicted pI of 11.55. p23/P198 is highly conserved across mammalian species, with > 94% identity (97% including conservative substitutions) among the human, bovine, and mouse deduced amino acid sequences. The nucleotide sequences of both the coding and 5'- and 3'-untranslated regions from human, bovine, and mouse are also highly conserved with > 88% identity in the coding regions. Hybridization of poly(A)+ RNA from various mammalian sources with cDNA and oligonucleotides specific for the coding region identified two mRNAs of 1.2 and 0.8 kb, whereas probes specific for the 3'-untranslated region between two consensus polyadenylation signals hybridized with the 1.2-kb, but not the 0.8-kb, mRNA. The abundance of the 1.2-kb mRNA relative to that of the 0.8-kb species varied depending upon the cell type. A single predominant transcription initiation site was mapped by primer extension. These studies indicate that this highly basic 23.6-kDa protein is encoded by two major mRNA species that differ only in the length of their 3'-untranslated regions and that the mechanism that gives rise to these two mRNAs, utilization of alternative polyadenylation sites, is conserved across species.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Genomics AU - Price, S R AU - Nightingale, M S AU - Bobak, D A AU - Tsuchiya, M AU - Moss, J AU - Vaughan, M AD - Laboratory of Cellular Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 959 EP - 964 VL - 14 IS - 4 SN - 0888-7543, 0888-7543 KW - Antigens, Neoplasm KW - 0 KW - Histocompatibility Antigens KW - RNA, Messenger KW - tumor-associated transplantation antigen KW - Poly A KW - 24937-83-5 KW - RNA KW - 63231-63-0 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Sequence Homology, Nucleic Acid KW - Humans KW - T-Lymphocytes, Cytotoxic -- immunology KW - Amino Acid Sequence KW - Nucleic Acid Hybridization KW - Poly A -- metabolism KW - Base Sequence KW - Cattle KW - RNA, Messenger -- metabolism KW - RNA -- metabolism KW - Molecular Sequence Data KW - Sequence Homology, Amino Acid KW - Histocompatibility Antigens -- genetics KW - Antigens, Neoplasm -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73420178?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Genomics&rft.atitle=Conservation+of+a+23-kDa+human+transplantation+antigen+in+mammalian+species.&rft.au=Price%2C+S+R%3BNightingale%2C+M+S%3BBobak%2C+D+A%3BTsuchiya%2C+M%3BMoss%2C+J%3BVaughan%2C+M&rft.aulast=Price&rft.aufirst=S&rft.date=1992-12-01&rft.volume=14&rft.issue=4&rft.spage=959&rft.isbn=&rft.btitle=&rft.title=Genomics&rft.issn=08887543&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-10 N1 - Date created - 1993-02-10 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - X51528; GENBANK; X56932; MX56932; X56933 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Techniques to enhance compliance with disulfiram. AN - 73416954; 1471757 AB - Pharmacodynamic benefits of disulfiram in the treatment of alcoholism have yet to be clearly demonstrated. Nevertheless, research does suggest that disulfiram may well have positive effects on drinking if medicational compliance procedures are employed. This paper reviews research on four strategies for enhancing disulfiram compliance: implants, incentives, contracts, and patient information. Generalizations about the strategies are drawn and needs for future research are briefly addressed. JF - Alcoholism, clinical and experimental research AU - Allen, J P AU - Litten, R Z AD - Division of Clinical and Prevention Research, National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20857. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 1035 EP - 1041 VL - 16 IS - 6 SN - 0145-6008, 0145-6008 KW - Drug Implants KW - 0 KW - Disulfiram KW - TR3MLJ1UAI KW - Index Medicus KW - Patient Education as Topic KW - Drug Administration Schedule KW - Token Economy KW - Motivation KW - Behavior Therapy KW - Humans KW - Alcoholism -- rehabilitation KW - Disulfiram -- adverse effects KW - Disulfiram -- administration & dosage KW - Patient Compliance -- psychology KW - Alcoholism -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73416954?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcoholism%2C+clinical+and+experimental+research&rft.atitle=Techniques+to+enhance+compliance+with+disulfiram.&rft.au=Allen%2C+J+P%3BLitten%2C+R+Z&rft.aulast=Allen&rft.aufirst=J&rft.date=1992-12-01&rft.volume=16&rft.issue=6&rft.spage=1035&rft.isbn=&rft.btitle=&rft.title=Alcoholism%2C+clinical+and+experimental+research&rft.issn=01456008&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-27 N1 - Date created - 1993-01-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Proto-oncogene activation in liver tumors of hepatocarcinogenesis-resistant strains of mice. AN - 73412338; 1361883 AB - Activation of the ras family of oncogenes occurs frequently in liver tumors of the B6C3F1 mouse, a strain which is highly sensitive to hepatocarcinogenesis. Many other mouse strains are much more resistant to hepatocarcinogenesis; the aim of this study was to determine the frequency and pattern of oncogene activation in spontaneous and chemically induced liver tumors of three such strains, the C57BL/6J, the C57BL/6 x DBA/2 F1 hybrid (B6D2F1) and the C57BL/6 x Balb/c F1 hybrid (B6BCF1). The C57BL/6, DBA/2 and Balb/c strains are all relatively resistant to spontaneous hepatocarcinogenesis (1.5-3.6% of animals develop liver tumors in 2 years); with regard to chemically induced hepatocarcinogenesis the Balb/c is highly resistant, the C57BL/6 has low susceptibility and the DBA/2 has low to moderate susceptibility. The nude mouse tumorigenicity assay was used to search for activated oncogenes in 15 C57BL/6J liver tumors induced by a single neonatal dose of vinyl carbamate (VC, 0.15 mumol/g body weight). Three tumors contained H-ras genes activated by point mutations at codon 61 and one contained a non-ras oncogene. The polymerase chain reaction and allele-specific oligonucleotide hybridization were used to study H-ras mutations in spontaneous and VC-induced tumors from all three strains of mice. The frequency of H-ras codon 61 mutations in tumors induced by 0.15 mumol/g body weight VC in the C57BL/6J mouse (5/37) was similar to that in spontaneous tumors (2/9); surprisingly, tumors induced by a lower dose of VC (0.03 mumol/g body weight) had a higher frequency of H-ras mutations (12/28). The frequencies of H-ras activation detected in VC (0.03 mumol/g body weight)-induced tumors from the two F1 hybrids studied differed markedly. Only one VC-induced B6BCF1 tumor contained a mutated H-ras gene (1/10), whereas the majority of B6D2F1 tumors contained such mutations (23/33). Several spontaneous B6D2F1 liver tumors contained H-ras codon 61 mutations (6/15). Thus, H-ras activation frequency does not determine susceptibility to hepatocarcinogenesis in inbred mice and their F1 hybrids, since a relatively high frequency of H-ras mutations was observed in two resistant strains and a low frequency was found in the other strain. JF - Carcinogenesis AU - Stanley, L A AU - Devereux, T R AU - Foley, J AU - Lord, P G AU - Maronpot, R R AU - Orton, T C AU - Anderson, M W AD - NIEHS, Research Triangle Park, NC 27709. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 2427 EP - 2433 VL - 13 IS - 12 SN - 0143-3334, 0143-3334 KW - B-raf KW - H-ras KW - Codon KW - 0 KW - DNA, Neoplasm KW - Index Medicus KW - 3T3 Cells KW - Animals KW - Disease Susceptibility KW - Gene Expression KW - Mice KW - Mice, Nude KW - Polymerase Chain Reaction KW - Base Sequence KW - Transfection KW - Polymorphism, Restriction Fragment Length KW - Blotting, Southern KW - Point Mutation KW - Molecular Sequence Data KW - Mice, Inbred C57BL KW - Male KW - Genes, ras KW - Liver Neoplasms, Experimental -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73412338?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Proto-oncogene+activation+in+liver+tumors+of+hepatocarcinogenesis-resistant+strains+of+mice.&rft.au=Stanley%2C+L+A%3BDevereux%2C+T+R%3BFoley%2C+J%3BLord%2C+P+G%3BMaronpot%2C+R+R%3BOrton%2C+T+C%3BAnderson%2C+M+W&rft.aulast=Stanley&rft.aufirst=L&rft.date=1992-12-01&rft.volume=13&rft.issue=12&rft.spage=2427&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-03 N1 - Date created - 1993-02-03 N1 - Date revised - 2017-01-13 N1 - Gene symbol - B-raf; H-ras N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prolongation of graft survival in primate allograft transplantation by yttrium-90-labeled anti-Tac in conjunction with granulocyte colony-stimulating factor. AN - 73410212; 1281566 AB - High-affinity IL-2 receptors are expressed by T cells activated in response to foreign histocompatibility antigens but not by normal resting T cells. To exploit this difference in IL-2R expression, anti-Tac, a murine monoclonal antibody specific for the IL-2R alpha subunit, was used to inhibit organ allograft rejection. To enhance its effector function, anti-Tac was armed by chelation with yttrium-90, a pure beta-emitting radionuclide. Animals received no immunosuppression (n = 5, group I, controls), unmodified anti-Tac (n = 5, 1 mg/kg q.o.d., group II), or 90Y-anti-Tac (n = 5, 1.6 mCi/kg divided into four doses, group III). The animals in group IV (n = 4) were treated identically to those in group III with the exception that 5 micrograms/kg/dose of granulocyte colony-stimulating factor was administered intramuscularly on the days when the yttrium-90 was given and on postoperative days 12 through 35 in order to reduce hematopoietic toxicity. Mean graft survival +/- S.E.M. for the control group was 8.2 +/- 0.5 days as compared with 13.8 +/- 2.1 days (P < 0.05) for those monkeys treated with unmodified anti-Tac. Graft survival was further prolonged in animals of group III that received 90Y-anti-Tac, with a mean graft survival of 45.0 +/- 11.8 days; however, three of the five monkeys retained viable grafts within this group but died secondary to bone marrow suppression. In comparison, the monkeys in group IV that were treated with G-CSF in conjunction with 90Y-anti-Tac had a mean graft survival of 49.2 +/- 2.9 days. In contrast to group III there were no deaths in the group (IV) receiving G-CSF. Furthermore, animals in group IV had a reduced magnitude and shortened duration of irradiation-induced neutropenia when compared with that observed in group III animals that did not receive G-CSF. Thus, treatment with 90Y-anti-Tac in conjunction with G-CSF may have potential applications in organ transplantation and the treatment of IL-2 receptor-expressing neoplastic diseases. JF - Transplantation AU - Parenteau, G L AU - Dirbas, F M AU - Garmestani, K AU - Brechbiel, M W AU - Bukowski, M A AU - Goldman, C K AU - Clark, R AU - Gansow, O A AU - Waldmann, T A AD - Surgery Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 963 EP - 968 VL - 54 IS - 6 SN - 0041-1337, 0041-1337 KW - Antibodies, Monoclonal KW - 0 KW - Receptors, Interleukin-2 KW - Yttrium Radioisotopes KW - Granulocyte Colony-Stimulating Factor KW - 143011-72-7 KW - Index Medicus KW - Radiation Injuries, Experimental -- complications KW - Animals KW - Neutropenia -- etiology KW - Humans KW - Transplantation, Homologous KW - Haplorhini KW - Antibodies, Monoclonal -- toxicity KW - Graft Survival -- immunology KW - Antibodies, Monoclonal -- pharmacology KW - Granulocyte Colony-Stimulating Factor -- pharmacology KW - Receptors, Interleukin-2 -- immunology KW - Organ Transplantation KW - Graft Survival -- drug effects KW - Antibodies, Monoclonal -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73410212?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Transplantation&rft.atitle=Prolongation+of+graft+survival+in+primate+allograft+transplantation+by+yttrium-90-labeled+anti-Tac+in+conjunction+with+granulocyte+colony-stimulating+factor.&rft.au=Parenteau%2C+G+L%3BDirbas%2C+F+M%3BGarmestani%2C+K%3BBrechbiel%2C+M+W%3BBukowski%2C+M+A%3BGoldman%2C+C+K%3BClark%2C+R%3BGansow%2C+O+A%3BWaldmann%2C+T+A&rft.aulast=Parenteau&rft.aufirst=G&rft.date=1992-12-01&rft.volume=54&rft.issue=6&rft.spage=963&rft.isbn=&rft.btitle=&rft.title=Transplantation&rft.issn=00411337&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-19 N1 - Date created - 1993-01-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Toxicokinetics of cinnamaldehyde in F344 rats. AN - 73409402; 1473801 AB - The toxicokinetic profile of cinnamaldehyde (CNMA) was investigated in Fischer 344 rats. CNMA was found to be unstable in blood. After iv administration, a large fraction of CNMA was immediately oxidized to cinnamic acid. The biological half-life of CNMA after iv administration was found to be 1.7 hr. After administration by gavage of CNMA at 250 or 500 mg/kg body weight using corn oil as vehicle, the maximum blood concentrations of CNMA were in the order of 1 microgram/ml. These low blood concentrations were maintained over a 24-hr period after a dose of 500 mg/kg, which is relatively long considering the short (1.7 hr) biological half-life of CNMA. The estimated oral bioavailability of CNMA was less than 20% for both the 250 and 500 mg/kg doses. No CNMA was present in blood at any time in rats dosed with 50 mg CNMA/kg body weight. Only a small amount of the administered CNMA was excreted in rat urine as free cinnamic acid or beta-glucuronide-conjugated cinnamic acid. The majority of CNMA administered orally was excreted in urine as hippuric acid within 24 hr. The maximum excretion rate occurred at 8 hr after gavage. Hippuric acid recovered in 50-hr urine samples was found to be directly proportional to the oral dose of CNMA. JF - Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association AU - Yuan, J H AU - Dieter, M P AU - Bucher, J R AU - Jameson, C W AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 997 EP - 1004 VL - 30 IS - 12 SN - 0278-6915, 0278-6915 KW - Cinnamates KW - 0 KW - Hippurates KW - Acrolein KW - 7864XYD3JJ KW - cinnamic aldehyde KW - SR60A3XG0F KW - hippuric acid KW - TE0865N2ET KW - cinnamic acid KW - U14A832J8D KW - Index Medicus KW - Rats KW - Administration, Oral KW - Animals KW - Rats, Inbred F344 KW - Injections, Intravenous KW - Half-Life KW - Cinnamates -- urine KW - Male KW - Female KW - Hippurates -- urine KW - Biological Availability KW - Acrolein -- analogs & derivatives KW - Acrolein -- pharmacokinetics KW - Acrolein -- blood KW - Acrolein -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73409402?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Food+and+chemical+toxicology+%3A+an+international+journal+published+for+the+British+Industrial+Biological+Research+Association&rft.atitle=Toxicokinetics+of+cinnamaldehyde+in+F344+rats.&rft.au=Yuan%2C+J+H%3BDieter%2C+M+P%3BBucher%2C+J+R%3BJameson%2C+C+W&rft.aulast=Yuan&rft.aufirst=J&rft.date=1992-12-01&rft.volume=30&rft.issue=12&rft.spage=997&rft.isbn=&rft.btitle=&rft.title=Food+and+chemical+toxicology+%3A+an+international+journal+published+for+the+British+Industrial+Biological+Research+Association&rft.issn=02786915&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-03 N1 - Date created - 1993-02-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Qualitative and quantitative experimental models to aid in risk assessment for immunotoxicology. AN - 73408454; 1471226 AB - We have previously reported on the design and content of a screening battery using a "tier" approach for detecting potential immunosuppressive compounds in mice [1]. This battery was composed of various immune function, immunopathology and host resistance tests, the results of which could help establish the potential of chemical and biological agents to cause immunosuppression. The data from these studies, which now encompass over 50 compounds, have been analyzed in an attempt to improve future testing strategies and provide information to aid in the risk assessment process. Specifically, the following two issues will be addressed; what are the likelihood(s) for each of the individual tests and testing configurations to accurately identify immunotoxic compounds? and what are the quantitative and qualitative relationships between the immune tests and host resistance assays? JF - Toxicology letters AU - Luster, M I AU - Pait, D G AU - Portier, C AU - Rosenthal, G J AU - Germolec, D R AU - Comment, C E AU - Munson, A E AU - White, K AU - Pollock, P AD - Systems Toxicity Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 71 EP - 78 VL - 64-65 Spec No SN - 0378-4274, 0378-4274 KW - Immunosuppressive Agents KW - 0 KW - Index Medicus KW - Animals KW - Immunologic Tests KW - Risk Factors KW - Mice, Inbred C57BL KW - Mice KW - Immunosuppressive Agents -- toxicity KW - Toxicology -- methods KW - Immune Tolerance UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73408454?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+letters&rft.atitle=Qualitative+and+quantitative+experimental+models+to+aid+in+risk+assessment+for+immunotoxicology.&rft.au=Luster%2C+M+I%3BPait%2C+D+G%3BPortier%2C+C%3BRosenthal%2C+G+J%3BGermolec%2C+D+R%3BComment%2C+C+E%3BMunson%2C+A+E%3BWhite%2C+K%3BPollock%2C+P&rft.aulast=Luster&rft.aufirst=M&rft.date=1992-12-01&rft.volume=64-65+Spec+No&rft.issue=&rft.spage=71&rft.isbn=&rft.btitle=&rft.title=Toxicology+letters&rft.issn=03784274&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-25 N1 - Date created - 1993-01-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Analysis of phospholipid metabolism in murine keratinocytes transformed by the v-ras oncogene: relationship of phosphatidylinositol turnover and cytokine stimulation to the transformed phenotype. AN - 73407514; 1473246 AB - Introduction of a v-rasHa oncogene into cultured mouse keratinocytes by transduction with a defective retrovirus is sufficient to transform keratinocytes to the benign phenotype. Transduced keratinocytes overexpress TGF alpha and hyperproliferate in culture medium with 0.05 mM Ca2+. Whereas normal keratinocytes respond to elevated medium Ca2+ by cessation of proliferation and induction of terminal differentiation, v-rasHa keratinocytes are not induced to differentiate by Ca2+. We now demonstrate that v-rasHa keratinocytes have elevated basal levels of phosphatidylinositol, inositol phosphates and diacylglycerols in 0.05 mM Ca2+ medium. Basal turnover of phosphatidylcholine is not altered by the rasHa oncogene. The generation of inositol phosphates is even further stimulated in v-rasHa cells by an increase in extracellular Ca2+ or by exposure to aluminum fluoride. Thus, the v-rasHa gene product does not stimulate the inositol phospholipid pathway maximally and additional phosphatidylinositol is available for turnover in response to inducers of phospholipase C activity. TGF alpha and medium conditioned by v-rasHa keratinocytes, both of which stimulate proliferation of normal cells in 0.05 mM Ca2+, transiently increased phosphatidylinositol turnover in normal keratinocytes but did not inhibit Ca(2+)-induced terminal differentiation. In contrast, sustained elevation in basal phosphatidylinositol metabolism was produced by aluminum fluoride. Combined exposure to aluminum fluoride and exogenous TGF alpha caused hyperproliferation, resistance to Ca(2+)-induced differentiation and morphological changes identical to those of v-rasHa keratinocytes. These results provide a link between the biological consequences of v-rasHa gene expression and biochemical changes which are known to alter the keratinocyte phenotype. JF - Carcinogenesis AU - Lee, E AU - Punnonen, K AU - Cheng, C AU - Glick, A AU - Dlugosz, A AU - Yuspa, S H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, NIH, Bethesda, MD 20892. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 2367 EP - 2373 VL - 13 IS - 12 SN - 0143-3334, 0143-3334 KW - v-ras KW - Aluminum Compounds KW - 0 KW - Cytokines KW - Diglycerides KW - Phosphatidylinositols KW - Aluminum KW - CPD4NFA903 KW - Choline KW - N91BDP6H0X KW - Fluorides KW - Q80VPU408O KW - Calcium KW - SY7Q814VUP KW - aluminum fluoride KW - Z77H3IKW94 KW - Index Medicus KW - Animals KW - Fluorides -- toxicity KW - Cell Division -- drug effects KW - Choline -- metabolism KW - Aluminum -- toxicity KW - Mice KW - Mice, Inbred BALB C KW - Phenotype KW - Calcium -- metabolism KW - Transfection KW - Cells, Cultured KW - Cell Differentiation -- drug effects KW - Mutation KW - Diglycerides -- metabolism KW - Genes, ras KW - Phosphatidylinositols -- metabolism KW - Keratinocytes -- metabolism KW - Cytokines -- metabolism KW - Cell Transformation, Neoplastic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73407514?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Analysis+of+phospholipid+metabolism+in+murine+keratinocytes+transformed+by+the+v-ras+oncogene%3A+relationship+of+phosphatidylinositol+turnover+and+cytokine+stimulation+to+the+transformed+phenotype.&rft.au=Lee%2C+E%3BPunnonen%2C+K%3BCheng%2C+C%3BGlick%2C+A%3BDlugosz%2C+A%3BYuspa%2C+S+H&rft.aulast=Lee&rft.aufirst=E&rft.date=1992-12-01&rft.volume=13&rft.issue=12&rft.spage=2367&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-03 N1 - Date created - 1993-02-03 N1 - Date revised - 2017-01-13 N1 - Gene symbol - v-ras N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Proopiomelanocortin messenger RNA is decreased in the mediobasal hypothalamus of rats made dependent on ethanol. AN - 73404721; 1471770 AB - It is thought that certain actions of ethanol involve an interaction with endogenous opioids, including proopiomelanocortin-derived peptides such as beta-endorphin. To examine this possibility, we used a sensitive and specific assay for proopiomelanocortin mRNA to obtain an estimate of the activity of the endorphinergic system in the mediobasal hypothalamus and the pituitary of rats exposed for 10 days in an inhalation chamber to either ethanol or water. This protocol causes dependence in the ethanol-exposed group, as demonstrated by the presence of withdrawal seizures after cessation of treatment. While ethanol treatment did not affect proopiomelanocortin mRNA levels in the pituitary, the level in hypothalamus was significantly lower in the ethanol-treated animals than in controls. These results suggest that some effect of ethanol may involve the hypothalamic endorphinergic system. JF - Alcoholism, clinical and experimental research AU - Scanlon, M N AU - Lazar-Wesley, E AU - Grant, K A AU - Kunos, G AD - Laboratory of Physiologic and Pharmacologic Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 1147 EP - 1151 VL - 16 IS - 6 SN - 0145-6008, 0145-6008 KW - DNA Probes KW - 0 KW - RNA, Messenger KW - Pro-Opiomelanocortin KW - 66796-54-1 KW - Index Medicus KW - Rats KW - Animals KW - Alcohol Withdrawal Delirium -- genetics KW - Alcohol Withdrawal Delirium -- pathology KW - Rats, Wistar KW - Male KW - Alcoholism -- pathology KW - Pro-Opiomelanocortin -- genetics KW - RNA, Messenger -- genetics KW - Alcoholism -- genetics KW - Hypothalamus, Middle -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73404721?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcoholism%2C+clinical+and+experimental+research&rft.atitle=Proopiomelanocortin+messenger+RNA+is+decreased+in+the+mediobasal+hypothalamus+of+rats+made+dependent+on+ethanol.&rft.au=Scanlon%2C+M+N%3BLazar-Wesley%2C+E%3BGrant%2C+K+A%3BKunos%2C+G&rft.aulast=Scanlon&rft.aufirst=M&rft.date=1992-12-01&rft.volume=16&rft.issue=6&rft.spage=1147&rft.isbn=&rft.btitle=&rft.title=Alcoholism%2C+clinical+and+experimental+research&rft.issn=01456008&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-27 N1 - Date created - 1993-01-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Continuous lisuride effects on central dopaminergic mechanisms in Parkinson's disease. AN - 73398518; 1471868 AB - Effects of the long term, continuous administration of a dopamine agonist on motor response complications attending levodopa therapy were studied in 7 patients with advanced Parkinson's disease under controlled conditions. After a 3-month round-the-clock infusion of lisuride, the duration of antiparkinsonian action of levodopa increased by approximately 90%, and the therapeutic window for the acutely administered dopamine precursor widened by > 300%. These benefits were more than three times greater than those produced by 9 days of continuous levodopa administration. In contrast to the effects on levodopa pharmacodynamics, the continuous infusion of lisuride did not prolong its action, suggesting a lisuride effect on presynaptic as well as postsynaptic dopaminergic mechanisms. These results lend further support to the view that continuous dopamine replacement ameliorates motor fluctuations and peak-dose dyskinesias that complicate standard levodopa regimens. Our findings further suggest that alterations at both presynaptic and postsynaptic levels contributing to these motor complications tend to normalize with the more physiological stimulation afforded by continuous replacement strategies, especially when given chronically. JF - Annals of neurology AU - Baronti, F AU - Mouradian, M M AU - Davis, T L AU - Giuffra, M AU - Brughitta, G AU - Conant, K E AU - Chase, T N AD - Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 776 EP - 781 VL - 32 IS - 6 SN - 0364-5134, 0364-5134 KW - Receptors, Dopamine KW - 0 KW - Levodopa KW - 46627O600J KW - Lisuride KW - E0QN3D755O KW - Index Medicus KW - Drug Therapy, Combination KW - Analysis of Variance KW - Humans KW - Adult KW - Levodopa -- therapeutic use KW - Middle Aged KW - Receptors, Dopamine -- drug effects KW - Receptors, Dopamine -- physiology KW - Lisuride -- therapeutic use KW - Movement -- physiology KW - Parkinson Disease -- physiopathology KW - Lisuride -- adverse effects KW - Parkinson Disease -- drug therapy KW - Movement -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73398518?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+neurology&rft.atitle=Continuous+lisuride+effects+on+central+dopaminergic+mechanisms+in+Parkinson%27s+disease.&rft.au=Baronti%2C+F%3BMouradian%2C+M+M%3BDavis%2C+T+L%3BGiuffra%2C+M%3BBrughitta%2C+G%3BConant%2C+K+E%3BChase%2C+T+N&rft.aulast=Baronti&rft.aufirst=F&rft.date=1992-12-01&rft.volume=32&rft.issue=6&rft.spage=776&rft.isbn=&rft.btitle=&rft.title=Annals+of+neurology&rft.issn=03645134&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-25 N1 - Date created - 1993-01-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Family history, alcohol use and dependence symptoms among young adults in the United States. AN - 73397424; 1471758 AB - Drawing upon data from the National Longitudinal Survey of young adults, this paper examines the effects of family history of alcoholism and current alcohol use by the young adults. A multivariate analysis of the data from the study indicates that there are both main and interaction effects of family history and current alcohol use on dependence symptoms among the young adults. JF - Alcoholism, clinical and experimental research AU - Harford, T C AU - Parker, D A AU - Grant, B F AD - Division of Biometry and Epidemiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20857. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 1042 EP - 1046 VL - 16 IS - 6 SN - 0145-6008, 0145-6008 KW - Index Medicus KW - Humans KW - Child of Impaired Parents -- psychology KW - Longitudinal Studies KW - Socioeconomic Factors KW - Cross-Sectional Studies KW - Risk Factors KW - Adult KW - Incidence KW - Adolescent KW - Bias (Epidemiology) KW - United States -- epidemiology KW - Female KW - Male KW - Alcoholism -- epidemiology KW - Personality Development KW - Alcoholism -- genetics KW - Alcoholism -- psychology KW - Social Environment UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73397424?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcoholism%2C+clinical+and+experimental+research&rft.atitle=Family+history%2C+alcohol+use+and+dependence+symptoms+among+young+adults+in+the+United+States.&rft.au=Harford%2C+T+C%3BParker%2C+D+A%3BGrant%2C+B+F&rft.aulast=Harford&rft.aufirst=T&rft.date=1992-12-01&rft.volume=16&rft.issue=6&rft.spage=1042&rft.isbn=&rft.btitle=&rft.title=Alcoholism%2C+clinical+and+experimental+research&rft.issn=01456008&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-27 N1 - Date created - 1993-01-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - DSM-III-R and proposed DSM-IV alcohol abuse and dependence, United States 1988: a nosological comparison. AN - 73394320; 1471761 AB - The purpose of the present study was to compare DSM-III-R and the proposed DSM-IV (options 1 and 2) diagnostic criteria for alcohol abuse and dependence in a representative sample of the United States general population. Alcohol abuse and dependence diagnostic categories were contrasted in terms of prevalence and overlap. The prevalences of DSM-III-R and DSM-IV diagnoses of alcohol abuse and dependence combined were remarkably similar. However, disaggregation of abuse and dependence diagnoses showed that there were major discrepancies between the classification systems. Reasons for these discrepancies are discussed in terms of differences in the number of diagnostic criteria and the content of the DSM-III-R and DSM-IV abuse and dependence categories, the requirement for physiological dependence in DSM-IV classifications, the relationship between the abuse and dependence categories, and the impact of the duration criteria. JF - Alcoholism, clinical and experimental research AU - Grant, B F AD - Division of Biometry and Epidemiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20857. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 1068 EP - 1077 VL - 16 IS - 6 SN - 0145-6008, 0145-6008 KW - Ethanol KW - 3K9958V90M KW - Index Medicus KW - Alcohol Withdrawal Delirium -- classification KW - Diagnosis, Differential KW - Humans KW - Aged KW - Alcohol Withdrawal Delirium -- diagnosis KW - Psychometrics KW - Cross-Sectional Studies KW - Drug Tolerance KW - Ethanol -- adverse effects KW - Adult KW - Health Surveys KW - Incidence KW - Middle Aged KW - Adolescent KW - United States -- epidemiology KW - Male KW - Female KW - Alcoholism -- epidemiology KW - Alcoholism -- diagnosis KW - Alcoholism -- classification KW - Psychiatric Status Rating Scales -- statistics & numerical data UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73394320?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcoholism%2C+clinical+and+experimental+research&rft.atitle=DSM-III-R+and+proposed+DSM-IV+alcohol+abuse+and+dependence%2C+United+States+1988%3A+a+nosological+comparison.&rft.au=Grant%2C+B+F&rft.aulast=Grant&rft.aufirst=B&rft.date=1992-12-01&rft.volume=16&rft.issue=6&rft.spage=1068&rft.isbn=&rft.btitle=&rft.title=Alcoholism%2C+clinical+and+experimental+research&rft.issn=01456008&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-27 N1 - Date created - 1993-01-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Loss of N-myc function results in embryonic lethality and failure of the epithelial component of the embryo to develop. AN - 73388377; 1459449 AB - myc genes are thought to function in the processes of cellular proliferation and differentiation. To gain insight into the role of the N-myc gene during embryogenesis, we examined its expression in embryos during postimplantation development using RNA in situ hybridization. Tissue- and cell-specific patterns of expression unique to N-myc as compared with the related c-myc gene were observed. N-myc transcripts become progressively restricted to specific cell types, primarily to epithelial tissues including those of the developing nervous system and those in developing organs characterized by epithelio-mesenchymal interaction. In contrast, c-myc transcripts were confined to the mesenchymal compartments. These data suggest that c-myc and N-myc proteins may interact with different substrates in performing their function during embryogenesis and suggest further that there are linked regulatory mechanisms for normal expression in the embryo. We have mutated the N-myc locus via homologous recombination in embryonic stem (ES) cells and introduced the mutated allele into the mouse germ line. Live-born heterozygotes are under-represented but appear normal. Homozygous mutant embryos die prenatally at approximately 11.5 days of gestation. Histologic examination of homozygous mutant embryos indicates that several developing organs are affected. These include the central and peripheral nervous systems, mesonephros, lung, and gut. Thus, N-myc function is required during embryogenesis, and the pathology observed is consistent with the normal pattern of N-myc expression. Examination of c-myc expression in mutant embryos indicates the existence of coordinate regulation of myc genes during mouse embryogenesis. JF - Genes & development AU - Stanton, B R AU - Perkins, A S AU - Tessarollo, L AU - Sassoon, D A AU - Parada, L F AD - Molecular Embryology Section, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 2235 EP - 2247 VL - 6 IS - 12A SN - 0890-9369, 0890-9369 KW - myc KW - Index Medicus KW - Animals KW - Intestines -- embryology KW - Fetal Death -- genetics KW - Multigene Family KW - Stomach -- embryology KW - Transcription, Genetic KW - Mice KW - Intestines -- metabolism KW - Lung -- metabolism KW - Mutagenesis, Site-Directed KW - Genotype KW - Alleles KW - Urogenital System -- metabolism KW - Stomach -- metabolism KW - Urogenital System -- embryology KW - Blotting, Southern KW - Heterozygote KW - Nervous System -- metabolism KW - Nervous System -- embryology KW - Lung -- embryology KW - Gene Expression Regulation KW - Embryonic and Fetal Development -- genetics KW - Genes, myc -- physiology KW - Epithelium -- embryology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73388377?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Genes+%26+development&rft.atitle=Loss+of+N-myc+function+results+in+embryonic+lethality+and+failure+of+the+epithelial+component+of+the+embryo+to+develop.&rft.au=Stanton%2C+B+R%3BPerkins%2C+A+S%3BTessarollo%2C+L%3BSassoon%2C+D+A%3BParada%2C+L+F&rft.aulast=Stanton&rft.aufirst=B&rft.date=1992-12-01&rft.volume=6&rft.issue=12A&rft.spage=2235&rft.isbn=&rft.btitle=&rft.title=Genes+%26+development&rft.issn=08909369&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-13 N1 - Date created - 1993-01-13 N1 - Date revised - 2017-01-13 N1 - Gene symbol - myc N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - New antimetabolites in the treatment of human malignancies. AN - 73380616; 1361080 AB - Several new antimetabolites have been evaluated in clinical trials in recent years. Those with the most promising activity include the structurally related purine analogs fludarabine, 2-chlorodeoxyadenosine, and 2'-deoxycoformycin. These compounds have shown impressive activity against a broad spectrum of indolent lymphoproliferative disorders, including hairy-cell leukemia, chronic lymphocytic leukemia, and low-grade non-Hodgkin's lymphomas. They may also be useful in the treatment of acute leukemias. In contrast, they lack activity against common solid tumors. They have been generally well tolerated in large clinical trials; however, each of them is myelosuppressive and immunosuppressive. It is unlikely that any one of these drugs, when used as a single agent, will provide optimal therapy for any disease other than, possibly, hairy-cell leukemia. Combinations with other cytotoxic agents and biologics are in development, and perhaps they will lead to more effective regimens in the future. JF - Seminars in oncology AU - Cheson, B D AD - Medicine Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 695 EP - 706 VL - 19 IS - 6 SN - 0093-7754, 0093-7754 KW - Antimetabolites, Antineoplastic KW - 0 KW - Drugs, Investigational KW - Purines KW - Pentostatin KW - 395575MZO7 KW - Cladribine KW - 47M74X9YT5 KW - Vidarabine KW - FA2DM6879K KW - fludarabine KW - P2K93U8740 KW - Index Medicus KW - Vidarabine -- analogs & derivatives KW - Animals KW - Humans KW - Cladribine -- therapeutic use KW - Clinical Trials as Topic KW - Vidarabine -- pharmacology KW - Cladribine -- pharmacology KW - Pentostatin -- therapeutic use KW - Leukemia -- drug therapy KW - Lymphoma -- drug therapy KW - Forecasting KW - Vidarabine -- therapeutic use KW - Purines -- chemistry KW - Immunosuppression KW - Pentostatin -- pharmacology KW - Drugs, Investigational -- therapeutic use KW - Drugs, Investigational -- pharmacology KW - Antimetabolites, Antineoplastic -- therapeutic use KW - Antimetabolites, Antineoplastic -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73380616?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Seminars+in+oncology&rft.atitle=New+antimetabolites+in+the+treatment+of+human+malignancies.&rft.au=Cheson%2C+B+D&rft.aulast=Cheson&rft.aufirst=B&rft.date=1992-12-01&rft.volume=19&rft.issue=6&rft.spage=695&rft.isbn=&rft.btitle=&rft.title=Seminars+in+oncology&rft.issn=00937754&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-11 N1 - Date created - 1993-01-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Hair dye use and multiple myeloma in white men. AN - 73364389; 1456346 AB - In recent reports, multiple myeloma has been linked to use of hair coloring products containing mutagenic and carcinogenic chemicals. A population-based case-control study in Iowa of 173 White men with multiple myeloma and 650 controls obtained information on hair dye use. Risk of multiple myeloma was significantly elevated (OR = 1.9) among hair dye users and was greatest among those using hair dyes at least once a month for a year or more (OR = 4.3). These data, along with results from other studies, suggest that use of hair dyes contributes to the development of multiple myeloma. JF - American journal of public health AU - Brown, L M AU - Everett, G D AU - Burmeister, L F AU - Blair, A AD - Epidemiology and Biostatistics Program, National Cancer Institute, Bethesda, Md. 20892. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 1673 EP - 1674 VL - 82 IS - 12 SN - 0090-0036, 0090-0036 KW - Hair Dyes KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Aged KW - Population Surveillance KW - Registries KW - Logistic Models KW - Risk Factors KW - European Continental Ancestry Group KW - Adult KW - Surveys and Questionnaires KW - Case-Control Studies KW - Middle Aged KW - Residence Characteristics KW - Iowa -- epidemiology KW - Male KW - Multiple Myeloma -- chemically induced KW - Multiple Myeloma -- pathology KW - Multiple Myeloma -- epidemiology KW - Hair Dyes -- adverse effects KW - Hair Dyes -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73364389?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+public+health&rft.atitle=Hair+dye+use+and+multiple+myeloma+in+white+men.&rft.au=Brown%2C+L+M%3BEverett%2C+G+D%3BBurmeister%2C+L+F%3BBlair%2C+A&rft.aulast=Brown&rft.aufirst=L&rft.date=1992-12-01&rft.volume=82&rft.issue=12&rft.spage=1673&rft.isbn=&rft.btitle=&rft.title=American+journal+of+public+health&rft.issn=00900036&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-04 N1 - Date created - 1993-01-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Am J Ind Med. 1990;18(3):295-301 [2220834] Am J Public Health. 1992 Jul;82(7):990-7 [1609918] Am J Ind Med. 1982;3(2):169-71 [7137173] J Natl Cancer Inst. 1984 May;72(5):1051-7 [6585583] J Natl Cancer Inst. 1980 Oct;65(4):735-8 [6932526] Proc Natl Acad Sci U S A. 1975 Jun;72(6):2423-7 [1094469] Am J Ind Med. 1984;6(2):97-102 [6465143] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Barbiturates impair cerebral metabolism during hypothermic circulatory arrest. AN - 73358649; 1449298 AB - Barbiturates have been used as a method of cerebral protection in patients undergoing open heart operations. Phosphorus 31 nuclear magnetic resonance spectroscopy was used to assess barbiturate-induced alterations in the cerebral tissue energy state during cardiopulmonary bypass, hypothermic circulatory arrest, and subsequent reperfusion. Sheep were positioned in a 4.7-T magnet with a radiofrequency coil over the skull. Nuclear magnetic resonance spectra were obtained at 37 degrees C, during cardiopulmonary bypass before and after drug administration at 37 degrees C and 15 degrees C, throughout a 1-hour period of hypothermic circulatory arrest, and during a 2-hour reperfusion period. A group of animals (n = 8) was administered a bolus of sodium thiopental (40 mg/kg) during bypass at 37 degrees C followed by an infusion of 3.3 mg.kg-1 x min-1 until hypothermic arrest. A control group of animals (n = 8) received no barbiturate. The phosphocreatine/adenosine triphosphate ratio, reflecting tissue energy state, was lower during cardiopulmonary bypass at 15 degrees C in the treated animals compared with controls (1.06 +/- 0.08 versus 1.36 +/- 0.17; p < 0.001). Lower phosphocreatine/adenosine triphosphate ratios were observed throughout all periods of arrest and reperfusion in the barbiturate-treated animals compared with controls (p < or = 0.01). Thiopental prevented the increase in cerebral energy state normally observed with hypothermia and resulted in a decrease in the energy state of the brain during hypothermic circulatory arrest and subsequent reperfusion. These results suggest that thiopental administration before a period of hypothermic circulatory arrest may prove detrimental to the preservation of the energy state of the brain. JF - The Annals of thoracic surgery AU - Siegman, M G AU - Anderson, R V AU - Balaban, R S AU - Ceckler, T L AU - Clark, R E AU - Swain, J A AD - Surgery Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 1131 EP - 1136 VL - 54 IS - 6 SN - 0003-4975, 0003-4975 KW - Phosphocreatine KW - 020IUV4N33 KW - Thiopental KW - 76-75-5 KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Abridged Index Medicus KW - Index Medicus KW - Evaluation Studies as Topic KW - Animals KW - Sheep KW - Energy Metabolism KW - Magnetic Resonance Spectroscopy KW - Thiopental -- adverse effects KW - Heart Arrest, Induced -- methods KW - Hypothermia, Induced -- methods KW - Brain Chemistry KW - Brain -- drug effects KW - Phosphocreatine -- chemistry KW - Brain -- metabolism KW - Thiopental -- administration & dosage KW - Adenosine Triphosphate -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73358649?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Annals+of+thoracic+surgery&rft.atitle=Barbiturates+impair+cerebral+metabolism+during+hypothermic+circulatory+arrest.&rft.au=Siegman%2C+M+G%3BAnderson%2C+R+V%3BBalaban%2C+R+S%3BCeckler%2C+T+L%3BClark%2C+R+E%3BSwain%2C+J+A&rft.aulast=Siegman&rft.aufirst=M&rft.date=1992-12-01&rft.volume=54&rft.issue=6&rft.spage=1131&rft.isbn=&rft.btitle=&rft.title=The+Annals+of+thoracic+surgery&rft.issn=00034975&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-24 N1 - Date created - 1992-12-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phase II study of pentostatin and intermittent high-dose recombinant interferon alfa-2a in advanced mycosis fungoides/Sézary syndrome. AN - 73353079; 1453206 AB - This phase II study was undertaken to assess the efficacy and toxicity of alternating administration of pentostatin (deoxycoformycin [DCF]) and interferon alfa-2a (IFN) in patients with advanced or refractory mycosis fungoides (MF) or the Sézary syndrome (SS). Forty-one patients underwent therapy with alternating cycles of DCF 4 mg/m2 intravenously (IV) days 1 through 3 and IFN 10 million U/m2 intramuscularly (IM) day 22, and 50 million U/m2 intramuscularly (IM) days 23 through 26. Twenty-nine patients had not responded to prior chemotherapy or total-skin electron-beam irradiation (TSEB), six had not responded to topical therapies, and six had no previous treatment. Two patients achieved a complete response (CR) and 15 achieved a partial response (PR), for an overall response rate of 41% (95% confidence interval, 26% to 58%). No responses were observed in the seven patients with visceral involvement. The median progression-free survival of patients who responded was 13.1 months. IFN-related constitutional symptoms were reported in 39% of patients; severe toxicities included cardiomyopathy in one patient, acute and chronic pulmonary dysfunction in four, and reversible mental status changes in two. Seven patients developed herpes zoster during therapy and six had staphylococcal bacteremia. These results suggest that the combination of DCF and IFN is an active regimen in MF patients without visceral involvement. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Foss, F M AU - Ihde, D C AU - Breneman, D L AU - Phelps, R M AU - Fischmann, A B AU - Schechter, G P AU - Linnoila, I AU - Breneman, J C AU - Cotelingam, J D AU - Ghosh, B C AD - National Cancer Institute, National Institutes of Health, Bethesda, MD. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 1907 EP - 1913 VL - 10 IS - 12 SN - 0732-183X, 0732-183X KW - Interferon-alpha KW - 0 KW - Recombinant Proteins KW - Pentostatin KW - 395575MZO7 KW - interferon alfa-2a KW - 47RRR83SK7 KW - Index Medicus KW - Pentostatin -- administration & dosage KW - Neoplasm Staging KW - Interferon-alpha -- administration & dosage KW - Humans KW - Adult KW - Treatment Outcome KW - Middle Aged KW - Male KW - Female KW - Survival Analysis KW - Skin Neoplasms -- drug therapy KW - Sezary Syndrome -- drug therapy KW - Skin Neoplasms -- pathology KW - Sezary Syndrome -- pathology KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Mycosis Fungoides -- drug therapy KW - Mycosis Fungoides -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73353079?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=Phase+II+study+of+pentostatin+and+intermittent+high-dose+recombinant+interferon+alfa-2a+in+advanced+mycosis+fungoides%2FS%C3%A9zary+syndrome.&rft.au=Foss%2C+F+M%3BIhde%2C+D+C%3BBreneman%2C+D+L%3BPhelps%2C+R+M%3BFischmann%2C+A+B%3BSchechter%2C+G+P%3BLinnoila%2C+I%3BBreneman%2C+J+C%3BCotelingam%2C+J+D%3BGhosh%2C+B+C&rft.aulast=Foss&rft.aufirst=F&rft.date=1992-12-01&rft.volume=10&rft.issue=12&rft.spage=1907&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=0732183X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-07 N1 - Date created - 1993-01-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Didanosine use in the adult HIV patient. AN - 73345514; 1465232 AB - There have been reports in the medical community of hesitation regarding the administration of didanosine to adult HIV patients because of the fear of the documented toxicities associated with didanosine. The most worrisome toxicities include pancreatitis and peripheral neuropathy. With close observation and follow-up, these toxicities can almost always be avoided or easily reversed. This article attempts to allay these fears so that the practitioner can administer this effective antiretroviral confidently and safely. The development of nucleoside and the pharmacology of didanosine are discussed. Drug administration information is provided, including a description of the different forms of didanosine currently available. Guidelines for assessing toxicities associated with didanosine, as well as suggestions for patient education, are also provided. Data gathered at the National Cancer Institute in the phase I didanosine trial indicate that early detection and discontinuation of didanosine, in nearly all cases, can limit or lessen the extent of morbidity. JF - The Nurse practitioner AU - Shay, L E AU - Wyvill, K M AD - National Cancer Institute, Bethesda, Md. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 59 EP - 64 VL - 17 IS - 12 SN - 0361-1817, 0361-1817 KW - Didanosine KW - K3GDH6OH08 KW - Index Medicus KW - Nursing KW - AIDS/HIV KW - Patient Education as Topic KW - Drug Interactions KW - Humans KW - Adult KW - Nurse Practitioners KW - Didanosine -- therapeutic use KW - Acquired Immunodeficiency Syndrome -- drug therapy KW - Acquired Immunodeficiency Syndrome -- nursing KW - Didanosine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73345514?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Nurse+practitioner&rft.atitle=Didanosine+use+in+the+adult+HIV+patient.&rft.au=Shay%2C+L+E%3BWyvill%2C+K+M&rft.aulast=Shay&rft.aufirst=L&rft.date=1992-12-01&rft.volume=17&rft.issue=12&rft.spage=59&rft.isbn=&rft.btitle=&rft.title=The+Nurse+practitioner&rft.issn=03611817&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-21 N1 - Date created - 1993-01-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phosphorylation of Nck in response to a variety of receptors, phorbol myristate acetate, and cyclic AMP. AN - 73343592; 1333046 AB - The 47-kDa protein coimmunoprecipitated with phospholipase C (PLC)-gamma 1 by anti-PLC-gamma 1 monoclonal antibodies is proved to be Nck, a protein composed almost exclusively of one SH2 and three SH3 domains. Nck and PLC-gamma 1 are recognized by certain anti-PLC-gamma 1 monoclonal antibodies because Nck and PLC-gamma 1 share an epitope that likely is located in their SH3 domains. Nck is widely distributed in rat tissues, with an especially high level of expression in testes. The expression levels of Nck remains unchanged during the development of rat brain, whereas PLC-gamma 1 decreases during the same developmental period. Stimulation of A431 cells with epidermal growth factor elicits the tight association of Nck with the epidermal growth factor receptor and phosphorylation of Nck on both serine and tyrosine residues. The phosphorylation of Nck is also enhanced in response to stimulation of the nerve growth factor receptor in PC12 cells, the T-cell receptor complex in Jurkat cells, the membrane immunoglobulin M in Daudi cells, and the low-affinity immunoglobulin G receptor (Fc gamma RII) in U937 cells. The phosphorylation of Nck was also enhanced following treatment of A431 cells with phorbol 12-myristate 13-acetate or forskolin. These results suggest that Nck is a target for a variety of protein kinases that might modulate the postulated role of Nck as an adaptor for the physical and functional coordination of signalling proteins. JF - Molecular and cellular biology AU - Park, D AU - Rhee, S G AD - Laboratory of Biochemistry, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 5816 EP - 5823 VL - 12 IS - 12 SN - 0270-7306, 0270-7306 KW - Adaptor Proteins, Signal Transducing KW - 0 KW - Antibodies, Monoclonal KW - Nck protein KW - Oncogene Proteins KW - Proteins KW - Receptors, Cell Surface KW - Colforsin KW - 1F7A44V6OU KW - Threonine KW - 2ZD004190S KW - Serine KW - 452VLY9402 KW - Epidermal Growth Factor KW - 62229-50-9 KW - Cyclic AMP KW - E0399OZS9N KW - Type C Phospholipases KW - EC 3.1.4.- KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Immunoblotting KW - Threonine -- metabolism KW - Amino Acid Sequence KW - Organ Specificity KW - Precipitin Tests KW - Type C Phospholipases -- isolation & purification KW - Serine -- metabolism KW - Receptors, Cell Surface -- metabolism KW - Rats KW - Chromatography, Affinity KW - Rats, Sprague-Dawley KW - Colforsin -- pharmacology KW - Phosphorylation KW - Kinetics KW - Molecular Sequence Data KW - Cell Line KW - PC12 Cells KW - Epidermal Growth Factor -- physiology KW - Proteins -- isolation & purification KW - Oncogene Proteins -- isolation & purification KW - Cyclic AMP -- metabolism KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Proteins -- metabolism KW - Oncogene Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73343592?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+cellular+biology&rft.atitle=Phosphorylation+of+Nck+in+response+to+a+variety+of+receptors%2C+phorbol+myristate+acetate%2C+and+cyclic+AMP.&rft.au=Park%2C+D%3BRhee%2C+S+G&rft.aulast=Park&rft.aufirst=D&rft.date=1992-12-01&rft.volume=12&rft.issue=12&rft.spage=5816&rft.isbn=&rft.btitle=&rft.title=Molecular+and+cellular+biology&rft.issn=02707306&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-29 N1 - Date created - 1992-12-29 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Mol Cell Biol. 1989 Jul;9(7):2934-43 [2550789] Oncogene. 1988 Nov;3(5):491-5 [3078956] Cell. 1989 Jun 30;57(7):1109-22 [2472219] Nature. 1989 Dec 7;342(6250):624 [2594066] Nature. 1988 Mar 17;332(6161):269-72 [2831461] Nature. 1988 Sep 1;335(6185):90-3 [2842690] Science. 1988 Dec 23;242(4886):1697-700 [3201259] J Biol Chem. 1987 Jul 25;262(21):10035-8 [3611052] J Biol Chem. 1977 Feb 10;252(3):1102-6 [320200] Mol Cell Biol. 1992 Dec;12(12):5824-33 [1333047] Mol Cell Biol. 1992 Mar;12(3):981-90 [1372091] Proc Natl Acad Sci U S A. 1992 Apr 15;89(8):3659-63 [1373507] Trends Biochem Sci. 1991 Aug;16(8):297-301 [1659758] J Biol Chem. 1992 Jun 25;267(18):12393-6 [1319994] J Biol Chem. 1992 Jan 25;267(3):1496-501 [1370476] Nature. 1992 Mar 26;356(6367):285-6 [1372393] Nature. 1992 Mar 26;356(6367):340-4 [1372395] Mol Cell Biol. 1992 Dec;12(12):5843-56 [1448108] Proc Natl Acad Sci U S A. 1990 Apr;87(7):2638-42 [1690891] J Biol Chem. 1991 Jan 25;266(3):1359-62 [1703147] Cancer Cells. 1990 Oct;2(10):303-10 [1704247] Cell. 1991 Apr 5;65(1):91-104 [1707345] Science. 1991 May 3;252(5006):668-74 [1708916] Proc Natl Acad Sci U S A. 1991 Jun 15;88(12):5453-6 [1828897] Cell. 1991 Apr 5;65(1):75-82 [1849460] Proc Natl Acad Sci U S A. 1991 Apr 1;88(7):2745-9 [2011584] Cell. 1990 Apr 20;61(2):203-12 [2158859] Science. 1990 Nov 16;250(4983):979-82 [2173144] Proc Natl Acad Sci U S A. 1990 Jun;87(11):4358-62 [2190221] Nature. 1988 Mar 17;332(6161):272-5 [2450282] Science. 1988 Aug 19;241(4868):968-70 [2457254] Science. 1990 Jun 22;248(4962):1537-9 [1694307] Nature. 1991 Mar 14;350(6314):158-60 [1706478] Cell. 1991 May 3;65(3):435-41 [1708307] Cell. 1991 Jan 25;64(2):281-302 [1846320] Cell. 1991 Apr 5;65(1):83-90 [1849461] Nucleic Acids Res. 1990 Feb 25;18(4):1048 [2107526] J Biol Chem. 1990 Nov 15;265(32):19704-11 [2174051] Proc Natl Acad Sci U S A. 1990 Nov;87(21):8622-6 [2236073] J Biol Chem. 1988 Oct 5;263(28):14497-504 [2459119] Cell. 1989 Jun 30;57(7):1101-7 [2472218] Proc Natl Acad Sci U S A. 1988 Aug;85(15):5419-23 [2840660] Proc Natl Acad Sci U S A. 1989 Mar;86(5):1568-72 [2466293] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Occurrence of oval-type cells in hepatitis B virus-associated human hepatocarcinogenesis. AN - 73340832; 1280243 AB - Proliferation of a new population of epithelial cells with distinct structure, as well as cytokeratin and alpha-fetoprotein expression, was observed in nonneoplastic liver tissues from 14 cases (13 hepatitis B virus-positive) of human hepatocellular carcinoma. These cells were characterized by oval nuclei; scant, pale cytoplasm; small cell size; and cross-reaction with a monoclonal antibody against rat oval cells. These putative human oval cells were strongly positive for cytokeratin 19 and displayed considerable heterogeneity in alpha-fetoprotein and albumin expression. The oval cells were most prominent in actively regenerating nodules and in liver tissue surrounding the cancer. Oval cells and transitional types of cells appear to be the principal producers of alpha-fetoprotein in the regenerating liver. Cancer cells positive for cytokeratins 8, 18 and 19 were observed in half the hepatocellular carcinomas studied. The data suggest that a new cell population structurally similar to oval cells seen in early stages of chemical hepatocarcinogenesis in rats is consistently present in regenerating liver lesions associated with human hepatocellular carcinoma. Furthermore, it is possible that the proliferation of these oval-type cells may partly account for the elevation of serum alpha-fetoprotein frequently seen in precancerous stages of hepatitis B virus-associated human hepatocellular carcinoma. JF - Hepatology (Baltimore, Md.) AU - Hsia, C C AU - Evarts, R P AU - Nakatsukasa, H AU - Marsden, E R AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 1327 EP - 1333 VL - 16 IS - 6 SN - 0270-9139, 0270-9139 KW - Serum Albumin KW - 0 KW - alpha-Fetoproteins KW - Keratins KW - 68238-35-7 KW - Index Medicus KW - In Situ Hybridization KW - Serum Albumin -- analysis KW - Humans KW - Adult KW - Middle Aged KW - Keratins -- analysis KW - alpha-Fetoproteins -- genetics KW - Male KW - Female KW - alpha-Fetoproteins -- analysis KW - Cell Division KW - Liver Neoplasms -- pathology KW - Liver -- pathology KW - Hepatitis B -- complications KW - Liver Neoplasms -- complications KW - Hepatitis B -- pathology KW - Carcinoma, Hepatocellular -- surgery KW - Carcinoma, Hepatocellular -- complications KW - Carcinoma, Hepatocellular -- pathology KW - Liver Neoplasms -- surgery UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73340832?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hepatology+%28Baltimore%2C+Md.%29&rft.atitle=Occurrence+of+oval-type+cells+in+hepatitis+B+virus-associated+human+hepatocarcinogenesis.&rft.au=Hsia%2C+C+C%3BEvarts%2C+R+P%3BNakatsukasa%2C+H%3BMarsden%2C+E+R%3BThorgeirsson%2C+S+S&rft.aulast=Hsia&rft.aufirst=C&rft.date=1992-12-01&rft.volume=16&rft.issue=6&rft.spage=1327&rft.isbn=&rft.btitle=&rft.title=Hepatology+%28Baltimore%2C+Md.%29&rft.issn=02709139&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-29 N1 - Date created - 1992-12-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutational analysis of the fingers domain of human immunodeficiency virus type 1 reverse transcriptase. AN - 73336960; 1279205 AB - Using BspMI cassette vectors, we have constructed a series of mutations in human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) that cause specific amino acid substitutions within the polymerase domain. The RNA-dependent DNA polymerase, DNA-dependent DNA polymerase, and RNase H activities of the mutant RTs were assayed. The elucidation of the structure of HIV-1 RT makes it possible to determine the locations of specific mutations in the three-dimensional structure of HIV-1 RT [E. Arnold, A. Jacobo-Molina, R. G. Nanni, R. L. Williams, X. Lu, J. Ding, A. D. Clark, Jr., A. Zhang, A. L. Ferris, P. Clark, A. Hizi, and S. H. Hughes, Nature (London) 357:85-89, 1992; L. A. Kohlstaedt, J. Wang, J. M. Friedman, P. A. Rice, and T. A. Steitz, Science 256:1783-1790, 1992]. The mutations described in this report are between amino acids 25 and 81, within the "fingers" domain of RT (Kohlstaedt et al., Science 256:1783-1790, 1992). It has been suggested that this domain may play a role in positioning the template. Although the fingers domain does not contain the active site for polymerization, several of the mutations within this domain disrupt polymerase activity without significantly affecting RNase H activity. JF - Journal of virology AU - Boyer, P L AU - Ferris, A L AU - Hughes, S H AD - ABL-Basic Research Program, NCI-Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 7533 EP - 7537 VL - 66 IS - 12 SN - 0022-538X, 0022-538X KW - Recombinant Proteins KW - 0 KW - reverse transcriptase, Human immunodeficiency virus 2 KW - EC 2.7.7.- KW - HIV Reverse Transcriptase KW - EC 2.7.7.49 KW - RNA-Directed DNA Polymerase KW - Index Medicus KW - AIDS/HIV KW - Recombinant Proteins -- isolation & purification KW - Recombinant Proteins -- metabolism KW - Electrophoresis, Polyacrylamide Gel KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Molecular Weight KW - HIV-1 -- genetics KW - RNA-Directed DNA Polymerase -- isolation & purification KW - HIV-1 -- enzymology KW - RNA-Directed DNA Polymerase -- metabolism KW - RNA-Directed DNA Polymerase -- genetics KW - Mutagenesis, Insertional UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73336960?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Mutational+analysis+of+the+fingers+domain+of+human+immunodeficiency+virus+type+1+reverse+transcriptase.&rft.au=Boyer%2C+P+L%3BFerris%2C+A+L%3BHughes%2C+S+H&rft.aulast=Boyer&rft.aufirst=P&rft.date=1992-12-01&rft.volume=66&rft.issue=12&rft.spage=7533&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-15 N1 - Date created - 1992-12-15 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Virol. 1991 Sep;65(9):4887-92 [1714522] J Virol. 1991 Oct;65(10):5232-6 [1716689] Science. 1991 Sep 27;253(5027):1557-9 [1716788] EMBO J. 1991 Dec;10(12):3905-11 [1718745] Proc Natl Acad Sci U S A. 1991 Nov 1;88(21):9878-82 [1719542] Proc Natl Acad Sci U S A. 1991 Dec 15;88(24):11363-7 [1722328] J Virol. 1992 Jan;66(1):12-9 [1727474] Science. 1986 Mar 14;231(4743):1289-91 [2418504] Nature. 1987 Jun 25-Jul 1;327(6124):716-7 [2439916] EMBO J. 1987 Oct;6(10):3133-7 [2446866] Proc Natl Acad Sci U S A. 1988 Feb;85(4):1218-22 [2448794] Proc Natl Acad Sci U S A. 1988 Apr;85(8):2469-73 [2451824] EMBO J. 1988 Jan;7(1):239-43 [2452083] J Virol. 1988 Jul;62(7):2525-9 [2453682] Proc Natl Acad Sci U S A. 1989 May;86(9):3104-8 [2470090] Virology. 1989 May;170(1):326-9 [2470195] Proc Natl Acad Sci U S A. 1989 Jul;86(13):4803-7 [2472634] Science. 1989 Dec 1;246(4934):1155-8 [2479983] Science. 1988 Jun 10;240(4858):1427-35 [3287617] Nucleic Acids Res. 1981 Apr 24;9(8):1825-39 [6264395] J Virol. 1992 Feb;66(2):1031-9 [1370546] J Virol. 1992 May;66(5):3179-82 [1373206] Nature. 1992 May 7;357(6373):85-9 [1374166] Science. 1992 Jun 26;256(5065):1783-90 [1377403] Virology. 1990 Apr;175(2):575-80 [1691564] J Biol Chem. 1990 Jun 5;265(16):8986-8 [1693146] Virology. 1991 Jan;180(1):339-46 [1701948] AIDS Res Hum Retroviruses. 1990 Sep;6(9):1061-72 [1702298] Proc Natl Acad Sci U S A. 1991 Feb 15;88(4):1148-52 [1705027] FEBS Lett. 1991 May 6;282(2):231-4 [1709876] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Lithium-discontinuation-induced refractoriness: preliminary observations. AN - 73324147; 1443252 AB - The authors used a systematic life-chart methodology to observe four patients with bipolar disorder in whom long periods (6-15 years) of effective lithium prophylaxis were followed by relapses on lithium discontinuation. Once the drug was reinstituted, it was no longer effective. The incidence, predictors, and mechanisms underlying this phenomenon all require further systematic study. The current preliminary observations suggest an additional reason for caution when lithium discontinuation in the well-maintained patient is considered. JF - The American journal of psychiatry AU - Post, R M AU - Leverich, G S AU - Altshuler, L AU - Mikalauskas, K AD - Biological Psychiatry Branch, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 1727 EP - 1729 VL - 149 IS - 12 SN - 0002-953X, 0002-953X KW - Lithium KW - 9FN79X2M3F KW - Abridged Index Medicus KW - Index Medicus KW - Drug Therapy, Combination KW - Combined Modality Therapy KW - Risk Factors KW - Humans KW - Electroconvulsive Therapy KW - Recurrence KW - Substance Withdrawal Syndrome -- etiology KW - Lithium -- therapeutic use KW - Bipolar Disorder -- psychology KW - Substance Withdrawal Syndrome -- psychology KW - Bipolar Disorder -- prevention & control KW - Lithium -- adverse effects KW - Bipolar Disorder -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73324147?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+journal+of+psychiatry&rft.atitle=Lithium-discontinuation-induced+refractoriness%3A+preliminary+observations.&rft.au=Post%2C+R+M%3BLeverich%2C+G+S%3BAltshuler%2C+L%3BMikalauskas%2C+K&rft.aulast=Post&rft.aufirst=R&rft.date=1992-12-01&rft.volume=149&rft.issue=12&rft.spage=1727&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+psychiatry&rft.issn=0002953X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-22 N1 - Date created - 1992-12-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Am J Psychiatry. 1993 Nov;150(11):1756 [8214199] Am J Psychiatry. 1994 Oct;151(10):1522 [7993489] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutational analysis of human T-cell leukemia virus type I Tax: regions necessary for function determined with 47 mutant proteins. AN - 73319542; 1433511 AB - We have made 47 mutations that span the length of the human T-cell leukemia virus type I (HTLV-I) Tax open reading frame. Of the 47 mutations, 38 were substitutions of single amino acids, 5 were missense changes in two or more amino acids, and 4 were deletions. A subset of these mutations includes individual changes of all 26 naturally occurring serines to alanines. By assaying each mutant protein separately on the HTLV-I long terminal repeat (LTR) and the human immunodeficiency virus type 1 (HIV-1) LTR in parallel, we were able to identify regions of Tax selectively necessary for each promoter. A small region in the carboxyl terminus, amino acids 315 to 325, was found to be selectively important for activation of the HTLV-I LTR. Three changes at serine 113, serine 160, and serine 258 were found to specifically affect function on the HIV-1 LTR. Surprisingly, we found that the great preponderance of missense changes (32 of 42) in Tax did not affect function. JF - Journal of virology AU - Semmes, O J AU - Jeang, K T AD - Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 7183 EP - 7192 VL - 66 IS - 12 SN - 0022-538X, 0022-538X KW - env KW - gag KW - pol KW - tax KW - DNA, Viral KW - 0 KW - Gene Products, tax KW - Index Medicus KW - AIDS/HIV KW - HIV Long Terminal Repeat KW - Animals KW - Transfection KW - Subcellular Fractions -- metabolism KW - Repetitive Sequences, Nucleic Acid KW - Fluorescent Antibody Technique KW - DNA, Viral -- genetics KW - Transcriptional Activation KW - Cell Line KW - Sequence Deletion KW - DNA, Viral -- metabolism KW - Mutagenesis, Site-Directed KW - Genes, pX KW - Gene Products, tax -- analysis KW - Human T-lymphotropic virus 1 -- genetics KW - Gene Products, tax -- metabolism KW - Human T-lymphotropic virus 1 -- metabolism KW - Gene Products, tax -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73319542?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Mutational+analysis+of+human+T-cell+leukemia+virus+type+I+Tax%3A+regions+necessary+for+function+determined+with+47+mutant+proteins.&rft.au=Semmes%2C+O+J%3BJeang%2C+K+T&rft.aulast=Semmes&rft.aufirst=O&rft.date=1992-12-01&rft.volume=66&rft.issue=12&rft.spage=7183&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-15 N1 - Date created - 1992-12-15 N1 - Date revised - 2017-01-13 N1 - Gene symbol - env; gag; pol; tax N1 - SuppNotes - Cited By: Virology. 1992 Jun;188(2):754-64 [1585646] J Virol. 1989 Mar;63(3):1474-9 [2783740] Science. 1987 Dec 11;238(4833):1575-8 [2825351] Proc Natl Acad Sci U S A. 1988 Mar;85(5):1457-61 [2830620] J Virol. 1988 Apr;62(4):1339-46 [2831395] Cell. 1988 Jun 3;53(5):827-36 [2836068] Nature. 1988 Jun 23;333(6175):776-8 [2838755] Science. 1988 Jul 1;241(4861):89-92 [2838905] Proc Natl Acad Sci U S A. 1988 Nov;85(21):8291-5 [2847157] Proc Natl Acad Sci U S A. 1988 Nov;85(22):8526-30 [2847164] Lancet. 1985 Aug 24;2(8452):407-10 [2863442] Lancet. 1986 May 3;1(8488):1031-2 [2871307] Science. 1985 Jun 21;228(4706):1430-4 [2990028] Science. 1985 Jul 5;229(4708):54-8 [2990037] Science. 1985 Aug 16;229(4714):675-9 [2992082] Nucleic Acids Res. 1985 Dec 20;13(24):8749-64 [3001649] Proc Natl Acad Sci U S A. 1985 Dec;82(24):8359-63 [3001699] EMBO J. 1986 Mar;5(3):561-5 [3011413] Proc Natl Acad Sci U S A. 1986 Sep;83(17):6558-62 [3018737] J Virol. 1986 Nov;60(2):394-9 [3021974] Proc Natl Acad Sci U S A. 1986 Nov;83(21):8112-6 [3022280] EMBO J. 1986 Nov;5(11):2883-8 [3024966] Cell. 1987 Jan 30;48(2):343-50 [3026643] Nucleic Acids Res. 1986 Dec 22;14(24):9679-98 [3027659] Cell. 1987 Apr 10;49(1):47-56 [3030566] J Virol. 1987 May;61(5):1559-70 [3033283] Proc Natl Acad Sci U S A. 1988 Dec;85(24):9733-7 [3059351] J Virol. 1988 Dec;62(12):4499-509 [3263510] Virology. 1973 Aug;54(2):536-9 [4737663] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7415-9 [6261256] Proc Natl Acad Sci U S A. 1984 Apr;81(8):2534-7 [6326131] Science. 1984 Jul 27;225(4660):381-5 [6330891] Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] J Virol. 1992 Feb;66(2):1040-9 [1731090] Virology. 1992 Mar;187(1):316-20 [1736534] Proc Natl Acad Sci U S A. 1991 Dec 15;88(24):11445-9 [1763059] Virology. 1991 Mar;181(1):218-27 [1899734] EMBO J. 1991 Dec;10(12):3795-803 [1935901] J Virol. 1991 May;65(5):2612-21 [2016773] Virology. 1991 Jun;182(2):874-8 [2024503] Nucleic Acids Res. 1991 Apr 25;19 Suppl:2241-5 [2041810] J Virol. 1991 Aug;65(8):4525-8 [2072462] J Biol Chem. 1990 Nov 25;265(33):20285-92 [2243093] Genes Dev. 1990 Nov;4(11):1875-85 [2276622] Science. 1990 Mar 2;247(4946):1082-4 [2309119] EMBO J. 1990 Mar;9(3):957-64 [2311587] Proc Natl Acad Sci U S A. 1986 Dec;83(24):9759-63 [2432602] Mol Cell Biol. 1989 Apr;9(4):1733-45 [2786141] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - IL-3-dependent mast cells attach to plate-bound vitronectin. Demonstration of augmented proliferation in response to signals transduced via cell surface vitronectin receptors. AN - 73318690; 1385529 AB - The adhesive interactions of activated mast cells with the extracellular matrix play an important role in anchorage and cellular motility. In this report we demonstrate that IL-3-dependent bone marrow-derived mast cells adhere to plate-bound vitronectin with high affinity in a saturable and dose-dependent manner. This adhesion interaction is unique in that it does not require prior mast cell activation through Fc epsilon RI or after treatment with PMA. It is inhibited by divalent cation chelation and by competitive inhibition with a synthetic Arginine-Glycine-Aspartate-Serine tetrapeptide. Polyclonal antisera for alpha v beta 3, an integrin known to bind vitronectin, inhibits attachment to plate-bound vitronectin in a dose-dependent manner. Comparison of the adhesion interactions for vitronectin, fibronectin, and laminin indicate that adhesion to vitronectin is greater than that seen with either fibronectin or laminin, either in the presence or absence of PMA. FACS analysis using a monoclonal hamster anti-murine vitronectin receptor (alpha v) antibody followed by a fluorescein-conjugated rabbit anti-hamster IgG revealed no change in surface vitronectin receptor expression after Fc epsilon RI-mediated cell activation. Proliferation assays with correction for cell viability revealed a 25% increase in cell number above the maximal IL-3 response over a 24-h period of adhesion to a vitronectin-coated surface and a 41% increase over 96 h of adhesion to vitronectin. Binding to plate-bound vitronectin was not able to sustain cell viability in the absence of IL-3. Thus, IL-3-dependent bone marrow-derived mast cells adhere to vitronectin, an extracellular matrix protein present throughout connective tissues. This interaction generates a signal that results in the augmentation of the maximal IL-3-dependent mast cell proliferative response, thus demonstrating at least one way in which the interaction between mast cells and extracellular matrix alter the biologic responsiveness of the mast cell. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Bianchine, P J AU - Burd, P R AU - Metcalfe, D D AD - Mast Cell Physiology Section, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/12/01/ PY - 1992 DA - 1992 Dec 01 SP - 3665 EP - 3671 VL - 149 IS - 11 SN - 0022-1767, 0022-1767 KW - Fibronectins KW - 0 KW - Glycoproteins KW - Interleukin-3 KW - Laminin KW - Receptors, Cytoadhesin KW - Receptors, IgE KW - Receptors, Vitronectin KW - Vitronectin KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Laminin -- metabolism KW - Fibronectins -- metabolism KW - Mice KW - Mice, Inbred BALB C KW - Cells, Cultured KW - In Vitro Techniques KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Cell Adhesion -- drug effects KW - Receptors, IgE -- physiology KW - Signal Transduction KW - Cell Division KW - Receptors, Cytoadhesin -- physiology KW - Interleukin-3 -- physiology KW - Glycoproteins -- metabolism KW - Mast Cells -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73318690?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=IL-3-dependent+mast+cells+attach+to+plate-bound+vitronectin.+Demonstration+of+augmented+proliferation+in+response+to+signals+transduced+via+cell+surface+vitronectin+receptors.&rft.au=Bianchine%2C+P+J%3BBurd%2C+P+R%3BMetcalfe%2C+D+D&rft.aulast=Bianchine&rft.aufirst=P&rft.date=1992-12-01&rft.volume=149&rft.issue=11&rft.spage=3665&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.issn=00221767&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-21 N1 - Date created - 1992-12-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The presence in a mouse T cell line of a 97-kDa protein kinase C (PKC) with characteristics similar to known members of the novel PKC subgroup and its possible role in lymphocyte gene expression. AN - 73318648; 1431124 AB - The receptor for tumor-promoting phorbol esters has been shown to be the Ca+2/phospholipid dependent enzyme protein kinase C (PKC). There are two major groups of PKC, the conventional PKC isotypes alpha, beta I, beta II, gamma) and the novel Ca+2-independent PKC (delta, epsilon, zeta, eta). Phorbol esters previously have been demonstrated to increase human IFN-gamma gene expression after treatment of a murine T cell line (Cl 9) that has been transfected with human IFN-gamma genomic DNA. In contrast, treatment with Ca+2 ionophore alone or in combination with phorbol ester did not enhance IFN-gamma production in a synergistic manner above the level obtained with phorbol ester treatment alone. To determine whether the lack of effect of Ca+2 ionophore is due to a defect in PKC, we compared the level of PKC autophosphorylation in the mouse T cell line (Cl 9), a mouse epidermal cell line (JB6), and purified rat brain PKC by in vitro kinase assays. The results demonstrate that instead of the expected 80-kDa autophosphorylated PKC band seen in purified rat brain PKC or mouse JB6 cell lysates, only a novel 97-kDa Ca+2-independent phosphoprotein was observed in Cl 9 cells. To ascertain if there was any nucleic acid sequence similarity to PKC epsilon, we hybridized Cl 9 poly(A+) RNA with a cloned fragment of the PKC epsilon gene and observed two hybridizing RNA bands (4.4 and 4.0 kb). Our results suggest that the 97-kDa phosphoprotein is similar to, but not identical with, PKC epsilon and is the major PKC expressed in the Cl 9 murine T cell line. These data suggested that the 97-kDa PKC may be responsible for the induction of both the transfected human IFN-gamma gene and the endogenous murine IL-2R alpha-chain. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Simek, S L AU - Fields, A P AU - Colburn, N H AU - Winkler-Pickett, R AU - Young, H A AD - Laboratory of Viral Carcinogenesis, NCI-FCRDC, Frederick, MD 21702-1201. Y1 - 1992/12/01/ PY - 1992 DA - 1992 Dec 01 SP - 3542 EP - 3549 VL - 149 IS - 11 SN - 0022-1767, 0022-1767 KW - Isoenzymes KW - 0 KW - Phorbol Esters KW - Phosphoproteins KW - RNA, Messenger KW - Receptors, Interleukin-2 KW - Interferon-gamma KW - 82115-62-6 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Abridged Index Medicus KW - Index Medicus KW - Phorbol Esters -- pharmacology KW - Animals KW - Phosphorylation KW - Isoenzymes -- physiology KW - Receptors, Interleukin-2 -- physiology KW - Cells, Cultured KW - In Vitro Techniques KW - Gene Expression KW - Mice KW - Interferon-gamma -- physiology KW - Substrate Specificity KW - RNA, Messenger -- genetics KW - Phosphoproteins -- metabolism KW - Protein Kinase C -- genetics KW - T-Lymphocytes -- physiology KW - Protein Kinase C -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73318648?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=The+presence+in+a+mouse+T+cell+line+of+a+97-kDa+protein+kinase+C+%28PKC%29+with+characteristics+similar+to+known+members+of+the+novel+PKC+subgroup+and+its+possible+role+in+lymphocyte+gene+expression.&rft.au=Simek%2C+S+L%3BFields%2C+A+P%3BColburn%2C+N+H%3BWinkler-Pickett%2C+R%3BYoung%2C+H+A&rft.aulast=Simek&rft.aufirst=S&rft.date=1992-12-01&rft.volume=149&rft.issue=11&rft.spage=3542&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.issn=00221767&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-21 N1 - Date created - 1992-12-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential effects of tetanus toxin on inhibitory and excitatory neurotransmitter release from mammalian spinal cord cells in culture. AN - 73314114; 1359016 AB - The effect of tetanus toxin on depolarization-evoked and spontaneous synaptic release of inhibitory and excitatory neurotransmitters was examined in murine spinal cord cell cultures. Toxin action on the release of radiolabeled glycine and glutamate was followed over time intervals corresponding to the early phase of convulsant activity through the later phase of electrical quiescence. Tetanus toxin inhibited potassium-evoked release of [3H]glycine and [3H]glutamate in a time- and dose-dependent manner. Ninety minutes after the application of toxin (6 x 10(-10) M), the stimulated release of [3H]glycine was blocked completely, whereas stimulated release of [3H]glutamate was not blocked completely until 150-210 min after toxin application. Fragment C, the binding portion of the tetanus toxin molecule, had no effect on stimulated release of either transmitter. The spontaneous synaptic release of [3H]glycine was blocked totally within 90 min of toxin exposure. In contrast, the spontaneous release of [3H]glutamate, in toxin-exposed cultures, was elevated to nearly twice that of control cultures at this time. Thus, toxin-induced convulsant activity is characterized by a reduction in the spontaneous synaptic release of inhibitory neurotransmitter with a concomitant increase in the release of excitatory neurotransmitter, as well as the more rapid onset of blockade of depolarization-evoked release of inhibitory versus excitatory neurotransmitter. JF - Journal of neurochemistry AU - Williamson, L C AU - Fitzgerald, S C AU - Neale, E A AD - Laboratory of Developmental Neurobiology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 2148 EP - 2157 VL - 59 IS - 6 SN - 0022-3042, 0022-3042 KW - Glutamates KW - 0 KW - Neurotransmitter Agents KW - Tetanus Toxin KW - Tritium KW - 10028-17-8 KW - Glutamic Acid KW - 3KX376GY7L KW - Glycine KW - TE7660XO1C KW - Index Medicus KW - Animals KW - Dose-Response Relationship, Drug KW - Glycine -- metabolism KW - Mice KW - Pregnancy KW - Cells, Cultured KW - Glutamates -- metabolism KW - Mice, Inbred C57BL KW - Chromatography, Thin Layer KW - Time Factors KW - Fluorescent Antibody Technique KW - Female KW - Neurotransmitter Agents -- metabolism KW - Spinal Cord -- metabolism KW - Spinal Cord -- embryology KW - Tetanus Toxin -- pharmacology KW - Spinal Cord -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73314114?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neurochemistry&rft.atitle=Differential+effects+of+tetanus+toxin+on+inhibitory+and+excitatory+neurotransmitter+release+from+mammalian+spinal+cord+cells+in+culture.&rft.au=Williamson%2C+L+C%3BFitzgerald%2C+S+C%3BNeale%2C+E+A&rft.aulast=Williamson&rft.aufirst=L&rft.date=1992-12-01&rft.volume=59&rft.issue=6&rft.spage=2148&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurochemistry&rft.issn=00223042&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-22 N1 - Date created - 1992-12-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cytochrome P450IIE1 genetic polymorphisms, racial variation, and lung cancer risk. AN - 73307437; 1423319 AB - Cytochrome P450IIE1 is responsible for the activation of carcinogenic N-nitrosamines, benzene, urethane, and other low-molecular-weight compounds. Restriction fragment length polymorphisms (PstI and RsaI restriction enzymes) have been identified in the cytochrome P450IIE1 transcription regulatory region that may affect expression. This study describes the PstI and RsaI polymorphisms in different racial populations and in a case-control study of lung cancer. The allelic frequencies were markedly different in Japanese, African-Americans, and Caucasians: the PstI rare allele was present at a frequency of 2% in Caucasians, 5% in African-Americans, and 24% in Japanese (P < 0.05). For the RsaI rare allele, frequencies were 2% in Caucasians, 2% in African-Americans, and 27% in Japanese (P < 0.05). The assay was also applied to 128 individuals enrolled in a case-control study of lung cancer. Although limited in statistical power, the data indicate no evidence for an association in the aggregate of cytochrome P450IIE1 PstI [for which the odds ratio was 0.7 (95% confidence interval (C.I.) = 0.2-2.8)] or RsaI [for which the odds ratio was 0.9 (95% C.I. = 0.2-5.4)] restriction fragment length polymorphisms with lung cancer in this U.S. population. When analyzed by race, the lung cancer odds ratio for the PstI mutant allele in African-Americans was 0.19 (95% C.I. = 0.03-1.38), and in Caucasians it was 4.13 (95% C.I. = 0.34-48.8). For the RsaI mutant allele, the odds ratios were 0.20 (95% C.I. = 0.02-2.43) and 4.28 (95% C.I. = 0.35-50.6), respectively. The ethnic differences of these restriction fragment length polymorphisms might be related to genetic susceptibilities for lung cancer among Caucasians and for gastric or esophageal cancer among Japanese. JF - Cancer research AU - Kato, S AU - Shields, P G AU - Caporaso, N E AU - Hoover, R N AU - Trump, B F AU - Sugimura, H AU - Weston, A AU - Harris, C C AD - Laboratory of Human Carcinogenesis, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1992/12/01/ PY - 1992 DA - 1992 Dec 01 SP - 6712 EP - 6715 VL - 52 IS - 23 SN - 0008-5472, 0008-5472 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Cytochrome P-450 CYP2E1 KW - EC 1.14.13.- KW - Oxidoreductases, N-Demethylating KW - EC 1.5.- KW - Index Medicus KW - Genotype KW - Polymerase Chain Reaction KW - Odds Ratio KW - Humans KW - Case-Control Studies KW - Baltimore -- epidemiology KW - Japan -- ethnology KW - Oxidoreductases, N-Demethylating -- genetics KW - Lung Neoplasms -- enzymology KW - Alleles KW - Oxidoreductases, N-Demethylating -- chemistry KW - Cytochrome P-450 Enzyme System -- genetics KW - Polymorphism, Genetic -- genetics KW - Continental Population Groups KW - Cytochrome P-450 Enzyme System -- chemistry KW - Lung Neoplasms -- ethnology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73307437?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Cytochrome+P450IIE1+genetic+polymorphisms%2C+racial+variation%2C+and+lung+cancer+risk.&rft.au=Kato%2C+S%3BShields%2C+P+G%3BCaporaso%2C+N+E%3BHoover%2C+R+N%3BTrump%2C+B+F%3BSugimura%2C+H%3BWeston%2C+A%3BHarris%2C+C+C&rft.aulast=Kato&rft.aufirst=S&rft.date=1992-12-01&rft.volume=52&rft.issue=23&rft.spage=6712&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-16 N1 - Date created - 1992-12-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human immunodeficiency virus type 1 Rev activation can be achieved without Rev-responsive element RNA if Rev is directed to the target as a Rev/MS2 fusion protein which tethers the MS2 operator RNA. AN - 73300818; 1433526 AB - The posttranscriptional trans activation of unspliced or partially spliced human immunodeficiency virus RNAs by the Rev regulatory protein is crucial for virus replication and is dependent on sequence-specific RNA binding by Rev. The cognate RNA target of Rev is contained within a highly structured, 244-nucleotide Rev-responsive element (RRE) RNA in the viral env gene. Here, we show that specific interaction with the RRE is not an absolute requirement for Rev function. When the RRE is replaced by a heterologous MS2 phage operator sequence, Rev will facilitate the cytoplasmic expression of human immunodeficiency virus mRNAs containing this sequence if directed to the MS2 operator via the RNA binding motif of the MS2 phage coat protein (MS-C) as a Rev/MS-C fusion protein. Rev/MS-C efficiently activated both RRE and MS2 targets. A mutation in the MS2 operator that abolished the coat protein binding in vitro rendered the mutant RNA nonresponsive to the fusion protein in vivo. Notwithstanding that Rev can be tethered to the viral RNAs via another RNA binding motif, the structural integrity of the N terminus of Rev was still required for optimal trans activation. JF - Journal of virology AU - Venkatesan, S AU - Gerstberger, S M AU - Park, H AU - Holland, S M AU - Nam, Y AD - Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 7469 EP - 7480 VL - 66 IS - 12 SN - 0022-538X, 0022-538X KW - gag KW - Capsid Proteins KW - 0 KW - Gene Products, rev KW - Gene Products, tat KW - RNA, Messenger KW - RNA, Viral KW - RNA-Binding Proteins KW - Recombinant Fusion Proteins KW - rev Gene Products, Human Immunodeficiency Virus KW - tat Gene Products, Human Immunodeficiency Virus KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Index Medicus KW - AIDS/HIV KW - Animals KW - HeLa Cells KW - Models, Molecular KW - Open Reading Frames KW - Humans KW - Escherichia coli -- genetics KW - Plasmids KW - Chloramphenicol O-Acetyltransferase -- metabolism KW - Nucleic Acid Conformation KW - RNA Processing, Post-Transcriptional KW - Recombinant Fusion Proteins -- metabolism KW - Mutagenesis, Site-Directed KW - Chloramphenicol O-Acetyltransferase -- genetics KW - HIV Long Terminal Repeat KW - Base Sequence KW - Transfection KW - Restriction Mapping KW - Molecular Sequence Data KW - Gene Products, tat -- genetics KW - Cell Line KW - HIV-1 -- genetics KW - Gene Products, rev -- metabolism KW - RNA, Messenger -- metabolism KW - Gene Products, rev -- genetics KW - Capsid -- genetics KW - Capsid -- metabolism KW - RNA, Viral -- genetics KW - RNA, Messenger -- genetics KW - RNA, Viral -- metabolism KW - Genes, gag KW - Transcriptional Activation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73300818?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Human+immunodeficiency+virus+type+1+Rev+activation+can+be+achieved+without+Rev-responsive+element+RNA+if+Rev+is+directed+to+the+target+as+a+Rev%2FMS2+fusion+protein+which+tethers+the+MS2+operator+RNA.&rft.au=Venkatesan%2C+S%3BGerstberger%2C+S+M%3BPark%2C+H%3BHolland%2C+S+M%3BNam%2C+Y&rft.aulast=Venkatesan&rft.aufirst=S&rft.date=1992-12-01&rft.volume=66&rft.issue=12&rft.spage=7469&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-15 N1 - Date created - 1992-12-15 N1 - Date revised - 2017-01-13 N1 - Gene symbol - gag N1 - SuppNotes - Cited By: Nature. 1989 Mar 16;338(6212):254-7 [2784194] Cell. 1991 Apr 19;65(2):241-8 [2015625] Proc Natl Acad Sci U S A. 1989 Aug;86(16):6111-5 [2788283] J Virol. 1988 Jul;62(7):2498-501 [2836628] J Virol. 1986 Aug;59(2):284-91 [3016298] J Mol Biol. 1988 Dec 20;204(4):927-38 [3221400] Biochemistry. 1987 Mar 24;26(6):1563-8 [3297131] Nature. 1988 Jul 14;334(6178):165-7 [3386755] Biochemistry. 1983 May 24;22(11):2601-10 [6347247] EMBO J. 1992 Mar;11(3):1119-29 [1547776] J Virol. 1992 Apr;66(4):1849-55 [1548742] J Virol. 1992 Jun;66(6):3699-706 [1583728] Hum Immunol. 1991 Aug;31(4):229-35 [1655683] Cell. 1990 Feb 23;60(4):685-93 [1689218] Biochemistry. 1990 Dec 18;29(50):11051-7 [1703010] Science. 1991 May 24;252(5009):1167-71 [1709522] FASEB J. 1991 Jul;5(10):2361-8 [1712325] Proc Natl Acad Sci U S A. 1991 Sep 1;88(17):7734-8 [1715576] J Virol. 1992 Feb;66(2):1139-51 [1731093] J Virol. 1992 Mar;66(3):1809-13 [1738210] Virology. 1991 Aug;183(2):630-5 [1853565] Biochemistry. 1991 Jul 30;30(30):7527-34 [1854752] Annu Rev Biochem. 1991;60:577-630 [1883204] Cell. 1991 Aug 9;66(3):577-88 [1907891] Cell. 1991 Nov 1;67(3):529-36 [1934059] J Virol. 1991 Dec;65(12):7051-5 [1942257] Nucleic Acids Res. 1990 Dec 11;18(23):6903-7 [2124673] New Biol. 1991 Feb;3(2):142-50 [2065010] J Virol. 1991 Aug;65(8):4248-54 [2072452] New Biol. 1990 Jan;2(1):20-31 [2078551] J Virol. 1990 Nov;64(11):5360-6 [2120472] Proc Natl Acad Sci U S A. 1990 Jun;87(12):4571-5 [2191294] Proc Natl Acad Sci U S A. 1990 Oct;87(19):7593-7 [2217189] Proc Natl Acad Sci U S A. 1990 Oct;87(19):7598-602 [2217190] Proc Natl Acad Sci U S A. 1990 Oct;87(19):7787-91 [2217212] Genes Dev. 1990 Aug;4(8):1365-73 [2227414] J Virol. 1990 Dec;64(12):5966-75 [2243382] EMBO J. 1990 Dec;9(12):4155-60 [2249669] Cell. 1990 Jun 29;61(7):1271-6 [2364429] J Virol. 1990 Feb;64(2):881-5 [2404140] Cell. 1990 Feb 23;60(4):675-83 [2406030] Cell. 1989 Oct 20;59(2):273-82 [2478293] Nature. 1989 Dec 14;342(6251):816-9 [2481237] Nature. 1989 Dec 7;342(6250):714-6 [2556643] Cell. 1989 Dec 1;59(5):789-95 [2686839] Science. 1989 Dec 22;246(4937):1625-9 [2688093] Cell. 1989 Jun 30;57(7):1155-65 [2736624] Cell. 1989 Jul 14;58(1):205-14 [2752419] Trends Genet. 1991 Jan;7(1):9-14 [2003337] Proc Natl Acad Sci U S A. 1989 Mar;86(5):1495-9 [2784208] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutational inactivation of an inhibitory sequence in human immunodeficiency virus type 1 results in Rev-independent gag expression. AN - 73300697; 1433510 AB - We have characterized an inhibitory RNA element in the human immunodeficiency virus type 1 (HIV-1) gag coding sequence that prevents gag expression. The inhibition exerted by this element could be overcome by the presence of the Rev-responsive element in cis and of Rev protein in trans. To understand the mechanism of function, we inactivated the inhibitory element by mutagenesis while maintaining an intact gag coding region. A constitutive high level of Rev-independent gag expression was achieved only after the introduction of 28 point mutations over a large region of 270 nucleotides within the gag coding region. To our knowledge, this is the first demonstration of inactivation of a negative RNA element within a coding region without alteration of the expressed protein. Elimination of the inhibitory element in the p17gag region, named INS-1, offered the opportunity to detect a second inhibitory element in the gag-pol region. The presence of either INS element is sufficient to inhibit gag expression, demonstrating that multiple INS elements acting independently can inhibit HIV RNA expression. Expression of gag from Rous sarcoma virus, a retrovirus that does not require Rev-like regulatory proteins, revealed that the Rous sarcoma virus p19gag region does not contain inhibitory elements. These results demonstrate the presence of a strong inhibitory element acting at the level of mRNA and provide a general method for the removal of such elements from mRNA coding regions. The inhibitory element functions in the absence of any HIV-1 proteins, suggesting that cellular factors are responsible for this inhibition. JF - Journal of virology AU - Schwartz, S AU - Campbell, M AU - Nasioulas, G AU - Harrison, J AU - Felber, B K AU - Pavlakis, G N AD - Human Retrovirus Section, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 7176 EP - 7182 VL - 66 IS - 12 SN - 0022-538X, 0022-538X KW - gag KW - pol KW - tat KW - Gene Products, rev KW - 0 KW - RNA, Messenger KW - RNA, Viral KW - rev Gene Products, Human Immunodeficiency Virus KW - Index Medicus KW - AIDS/HIV KW - Base Sequence KW - RNA, Messenger -- metabolism KW - Transfection KW - Humans KW - Molecular Sequence Data KW - Genome, Viral KW - RNA, Messenger -- genetics KW - Plasmids KW - Genes, tat KW - Cell Line KW - HIV-1 -- genetics KW - Gene Expression Regulation, Viral KW - Gene Products, rev -- genetics KW - RNA, Viral -- genetics KW - RNA, Viral -- metabolism KW - Genes, gag KW - Genes, pol UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73300697?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Mutational+inactivation+of+an+inhibitory+sequence+in+human+immunodeficiency+virus+type+1+results+in+Rev-independent+gag+expression.&rft.au=Schwartz%2C+S%3BCampbell%2C+M%3BNasioulas%2C+G%3BHarrison%2C+J%3BFelber%2C+B+K%3BPavlakis%2C+G+N&rft.aulast=Schwartz&rft.aufirst=S&rft.date=1992-12-01&rft.volume=66&rft.issue=12&rft.spage=7176&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-15 N1 - Date created - 1992-12-15 N1 - Date revised - 2017-01-13 N1 - Gene symbol - gag; pol; tat N1 - Genetic sequence - L04602; GENBANK N1 - SuppNotes - Cited By: J Virol. 1990 Jul;64(7):3391-8 [2191150] Genes Dev. 1990 Jul;4(7):1158-71 [2145194] Proc Natl Acad Sci U S A. 1990 Oct;87(19):7598-602 [2217190] J Virol. 1990 Jun;64(6):2519-29 [2335812] J Virol. 1989 Apr;63(4):1669-76 [2538650] Cell. 1989 Aug 11;58(3):423-6 [2569361] Cell. 1989 Dec 1;59(5):789-95 [2686839] J Virol. 1989 Mar;63(3):1265-74 [2783738] Proc Natl Acad Sci U S A. 1989 Mar;86(5):1495-9 [2784208] Proc Natl Acad Sci U S A. 1988 Apr;85(7):2071-5 [2832844] Mol Cell Biol. 1987 Dec;7(12):4513-21 [3325826] Mol Cell Biol. 1987 Feb;7(2):725-37 [3821727] Virology. 1973 Apr;52(2):456-67 [4705382] Nature. 1984 Oct 4-10;311(5985):433-8 [6090941] Mol Cell Biol. 1992 Mar;12(3):1375-86 [1545819] J Virol. 1991 Mar;65(3):1653-7 [1825343] J Virol. 1991 Oct;65(10):5305-13 [1895385] Cell. 1991 Oct 4;67(1):169-78 [1913815] J Virol. 1991 Jun;65(6):3044-51 [2033665] Mol Cell Biol. 1990 Feb;10(2):696-704 [2153921] AIDS. 1990 Jun;4(6):499-509 [2201316] J Virol. 1990 Dec;64(12):6010-7 [2243384] J Virol. 1990 Sep;64(9):4093-8 [2384914] J Virol. 1989 Oct;63(10):4331-43 [2550669] Cell. 1989 Jun 30;57(7):1155-65 [2736624] Nature. 1989 Mar 16;338(6212):254-7 [2784194] Nature. 1988 Nov 24;336(6197):396-9 [3194021] Cell. 1986 Aug 29;46(5):659-67 [3488815] Proc Natl Acad Sci U S A. 1985 Jan;82(2):488-92 [3881765] J Virol. 1991 Nov;65(11):5732-43 [1656066] J Virol. 1992 Jan;66(1):150-9 [1727477] Mol Cell Biol. 1992 Jan;12(1):207-19 [1729599] Genes Dev. 1991 May;5(5):808-19 [1827422] Virology. 1991 Aug;183(2):677-86 [1830183] Genes Dev. 1991 Feb;5(2):221-31 [1899842] Genes Dev. 1991 Feb;5(2):232-43 [1995415] New Biol. 1990 Jan;2(1):20-31 [2078551] J Virol. 1990 Nov;64(11):5448-56 [2214021] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutational analysis of the octapeptide sequence motif at the NS1-NS2A cleavage junction of dengue type 4 virus. AN - 73300317; 1433515 AB - We have previously shown that proper processing of dengue type 4 virus NS1 from the NS1-NS2A region of the viral polyprotein requires a hydrophobic N-terminal signal and the downstream NS2A. Results from deletion analysis indicate that a minimum length of eight amino acids at the C terminus of NS1 is required for cleavage at the NS1-NS2A junction. Comparison of this eight-amino-acid sequence with the corresponding sequences of other flaviviruses suggests a consensus cleavage sequence of Met/Leu-Val-Xaa-Ser-Xaa-Val-Xaa-Ala. Site-directed mutagenesis was performed to construct mutants of NS1-NS2A that contained a single amino acid substitution at different positions of the consensus cleavage sequence or at the immediate downstream position. Three to eight different substitutions were made at each position. A total of 50 NS1-NS2A mutants were analyzed for their cleavage efficiency relative to that of the wild-type dengue type 4 virus sequence. As predicted, nearly all substitutions at positions P1, P3, P5, P7, and P8, occupied by conserved amino acids, yielded low levels of cleavage, with the exception that Pro or Ala substituting for Ser (P5) was tolerated. Substitutions of an amino acid at the remaining positions occupied by nonconserved amino acids generally yielded high levels of cleavage. However, some substitutions at nonconserved positions were not tolerated. For example, substitution of Gly or Glu for Gln (P4) and substitution of Val or Glu for Lys (P6) each yielded a low level of cleavage. Overall, these data support the proposed cleavage sequence motif deduced by comparison of sequences among the flaviviruses. This study also showed that in addition to the eight-amino-acid sequence, the amino acid immediately following the NS1-NS2A cleavage site plays a role in cleavage. JF - Journal of virology AU - Pethel, M AU - Falgout, B AU - Lai, C J AD - Molecular Viral Biology Section, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 7225 EP - 7231 VL - 66 IS - 12 SN - 0022-538X, 0022-538X KW - Codon KW - 0 KW - Oligodeoxyribonucleotides KW - Protein Sorting Signals KW - Viral Nonstructural Proteins KW - Index Medicus KW - Vaccinia virus -- genetics KW - Animals KW - Protein Sorting Signals -- metabolism KW - Codon -- genetics KW - Protein Sorting Signals -- genetics KW - Humans KW - Amino Acid Sequence KW - Structure-Activity Relationship KW - Base Sequence KW - Transfection KW - Restriction Mapping KW - Molecular Sequence Data KW - Cell Line KW - Mutagenesis, Site-Directed KW - Viral Nonstructural Proteins -- genetics KW - Viral Nonstructural Proteins -- analysis KW - Dengue Virus -- genetics KW - Dengue Virus -- metabolism KW - Viral Nonstructural Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73300317?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Mutational+analysis+of+the+octapeptide+sequence+motif+at+the+NS1-NS2A+cleavage+junction+of+dengue+type+4+virus.&rft.au=Pethel%2C+M%3BFalgout%2C+B%3BLai%2C+C+J&rft.aulast=Pethel&rft.aufirst=M&rft.date=1992-12-01&rft.volume=66&rft.issue=12&rft.spage=7225&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-15 N1 - Date created - 1992-12-15 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Annu Rev Microbiol. 1988;42:657-83 [3060004] Virology. 1987 Aug;159(2):217-28 [3039728] Science. 1985 Aug 23;229(4715):726-33 [4023707] Mol Cell Biol. 1985 Dec;5(12):3403-9 [3939316] Methods Enzymol. 1983;96:215-22 [6656631] J Virol. 1992 Mar;66(3):1535-42 [1531368] Virology. 1991 Dec;185(2):689-97 [1683727] J Gen Virol. 1991 Apr;72 ( Pt 4):851-8 [1826736] J Virol. 1991 Nov;65(11):6042-50 [1833562] J Virol. 1991 Feb;65(2):922-30 [1987379] J Virol. 1991 May;65(5):2467-75 [2016768] Virology. 1991 May;182(1):17-27 [2024462] Proc Natl Acad Sci U S A. 1991 Jun 15;88(12):5139-43 [2052593] Virology. 1990 Jan;174(1):250-63 [2136778] J Virol. 1990 Sep;64(9):4364-74 [2143543] J Virol. 1990 Sep;64(9):4573-7 [2143546] Proc Natl Acad Sci U S A. 1990 Nov;87(22):8898-902 [2147282] Clin Microbiol Rev. 1990 Oct;3(4):376-96 [2224837] Nature. 1990 Nov 1;348(6296):91-2 [2234068] Trends Biochem Sci. 1990 Nov;15(11):425-30 [2278102] Virology. 1990 Jun;176(2):643-7 [2345967] Virology. 1990 Jul;177(1):159-74 [2353452] J Virol. 1989 Aug;63(8):3345-52 [2501515] J Virol. 1989 May;63(5):1852-60 [2522997] Virology. 1989 Apr;169(2):354-64 [2523178] Proc Natl Acad Sci U S A. 1989 Aug;86(16):6126-30 [2548200] Virology. 1989 Nov;173(1):291-301 [2554575] J Virol. 1989 Oct;63(10):4199-209 [2674479] J Gen Virol. 1988 Jan;69 ( Pt 1):1-21 [2826659] Virology. 1988 Jan;162(1):167-80 [2827375] Virology. 1986 Nov;155(1):77-88 [3022479] Annu Rev Biochem. 1988;57:701-54 [3052288] J Virol. 1987 Dec;61(12):4019-22 [3316711] Virology. 1988 Sep;166(1):197-205 [3413985] Virology. 1987 Dec;161(2):497-510 [3686827] Nucleic Acids Res. 1989 May 25;17(10):3889-97 [2543956] Virology. 1989 Aug;171(2):637-9 [2548336] Gene. 1989 Feb 20;75(2):197-211 [2714651] J Gen Virol. 1988 Jan;69 ( Pt 1):23-34 [2826667] Virology. 1988 Jul;165(1):234-44 [3388770] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A new functional role for P-glycoprotein: efflux pump for benzo(alpha)pyrene in human breast cancer MCF-7 cells. AN - 73295427; 1358437 AB - We propose that the cellular burden of certain carcinogens may be mitigated by P-glycoprotein (P-gp), the putative drug efflux pump. In a series of multidrug resistant human breast cancer MCF-7 cells with increasing P-gp expression we examined this hypothesis using benzo(alpha)pyrene, a widely distributed environmental and dietary carcinogen. We found that multidrug resistant cells were cross-resistant to benzo(alpha)pyrene and the rates of efflux for benzo(alpha)pyrene were higher in multidrug resistant cells than in wild type cells. Evidence supporting the involvement of P-gp included the inhibition of azidopine binding to P-gp benzo(alpha)pyrene and the inhibition of benzo(alpha)pyrene efflux by Adriamycin and verapamil. Our findings suggest that P-gp may play a role in the cellular defense to carcinogens. The expression of P-gp and the modulation of its function may affect the susceptibility of normal tissues to transformation by carcinogens. JF - Cancer research AU - Yeh, G C AU - Lopaczynska, J AU - Poore, C M AU - Phang, J M AD - Laboratory of Nutritional and Molecular Regulation, National Cancer Institute, NIH, Frederick, Maryland 21702. Y1 - 1992/12/01/ PY - 1992 DA - 1992 Dec 01 SP - 6692 EP - 6695 VL - 52 IS - 23 SN - 0008-5472, 0008-5472 KW - Membrane Glycoproteins KW - 0 KW - Neoplasm Proteins KW - P-Glycoprotein KW - Benzo(a)pyrene KW - 3417WMA06D KW - Doxorubicin KW - 80168379AG KW - Verapamil KW - CJ0O37KU29 KW - Index Medicus KW - Tumor Cells, Cultured KW - Doxorubicin -- pharmacology KW - Doxorubicin -- metabolism KW - Humans KW - Verapamil -- metabolism KW - Drug Resistance KW - Nucleic Acid Hybridization KW - Verapamil -- pharmacology KW - Neoplasm Proteins -- physiology KW - Membrane Glycoproteins -- physiology KW - Breast Neoplasms -- metabolism KW - Neoplasm Proteins -- metabolism KW - Membrane Glycoproteins -- metabolism KW - Benzo(a)pyrene -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73295427?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=A+new+functional+role+for+P-glycoprotein%3A+efflux+pump+for+benzo%28alpha%29pyrene+in+human+breast+cancer+MCF-7+cells.&rft.au=Yeh%2C+G+C%3BLopaczynska%2C+J%3BPoore%2C+C+M%3BPhang%2C+J+M&rft.aulast=Yeh&rft.aufirst=G&rft.date=1992-12-01&rft.volume=52&rft.issue=23&rft.spage=6692&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-16 N1 - Date created - 1992-12-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - HLA association with response and toxicity in melanoma patients treated with interleukin 2-based immunotherapy. AN - 73288979; 1423301 AB - Peripheral blood lymphocytes from 146 patients with metastatic melanoma undergoing interleukin 2 (IL-2)-based immunotherapy were characterized for HLA A, B, Cw, DR, DQw, and DRw specificities. Patients had been enrolled into sequential treatment protocols with either IL-2 alone (28) or in combination with tumor-infiltrating lymphocytes (TILs) (86), alpha-interferon (26), lymphokine-activated killer cells (16), radiation therapy (7), cyclophosphamide (3), tumor necrosis factor (1), and interleukin 4 (1) for a total of 168 courses of therapy. HLA phenotype was then correlated with response rate and toxicity to IL-2. We noted: (a) a significant difference in the frequency of A11 (20.5% versus 10.2%; P < 0.05) allele between melanoma patients and the North American Caucasian population; (b) a significantly higher frequency of A11 phenotype among responders (40.5%) than in the melanoma patient population (20.5%; P < 0.01), which was even more obvious among patients responding to TIL therapy (47.4% versus 22.1%; P < 0.05); within TIL patients, responders also had an increased frequency of A19 (42.1% versus 25.6%; P < 0.05); (c) a correlation between the number of TILs received and response rate (P < 0.005); and (d) an association between DR4 haplotype and decreased tolerance to IL-2 among the patients receiving TILs (P = 0.01). These results suggest that, in melanoma patients, some HLA Class I specificities may predict for a greater likelihood of response to IL-2-based therapy, while HLA Class II phenotype correlates with tolerance to the combination of TIL and IL-2 therapy. JF - Cancer research AU - Marincola, F M AU - Venzon, D AU - White, D AU - Rubin, J T AU - Lotze, M T AU - Simonis, T B AU - Balkissoon, J AU - Rosenberg, S A AU - Parkinson, D R AD - Surgery Branch, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1992/12/01/ PY - 1992 DA - 1992 Dec 01 SP - 6561 EP - 6566 VL - 52 IS - 23 SN - 0008-5472, 0008-5472 KW - HLA Antigens KW - 0 KW - Interleukin-2 KW - Index Medicus KW - Phenotype KW - Drug Administration Schedule KW - Immunotherapy KW - Humans KW - Prognosis KW - Remission Induction KW - HLA Antigens -- genetics KW - Interleukin-2 -- adverse effects KW - Interleukin-2 -- therapeutic use KW - Melanoma -- therapy KW - Melanoma -- immunology KW - Lymphocytes, Tumor-Infiltrating -- transplantation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73288979?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=HLA+association+with+response+and+toxicity+in+melanoma+patients+treated+with+interleukin+2-based+immunotherapy.&rft.au=Marincola%2C+F+M%3BVenzon%2C+D%3BWhite%2C+D%3BRubin%2C+J+T%3BLotze%2C+M+T%3BSimonis%2C+T+B%3BBalkissoon%2C+J%3BRosenberg%2C+S+A%3BParkinson%2C+D+R&rft.aulast=Marincola&rft.aufirst=F&rft.date=1992-12-01&rft.volume=52&rft.issue=23&rft.spage=6561&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-16 N1 - Date created - 1992-12-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Cancer Res 1993 Aug 15;53(16):3846 Cancer Res 1993 Dec 15;53(24):6079 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - HIV and AIDS among Adolescents in the United States: Increasing Risk in the 1990s AN - 61316749; 9304145 AB - Epidemiological & surveillance data from the Centers for Disease Control, supplemented by secondary statistics & survey research, are presented to investigate US teenagers' HIV (human immunodeficiency virus)- & AIDS (acquired immune deficiency syndrome-related knowledge, beliefs, & behaviors. Findings suggest that because adolescents are engaged in higher risk behaviors, comprehensive prevention & treatment services incorporating self-protection tools (free condoms), outreach, information, & evaluation studies will help curb the spread of HIV infection. While African-American adolescents have a higher incidence of infection than other racial groups, total AIDS cases are highest among young white hemophiliacs or homosexuals. The most common risk behaviors are having unprotected sex &/or sharing contaminated drug injection equipment. Higher HIV infection rates for young females may reflect susceptibility to sexually transmitted diseases due to physiological immaturity. Factors that impede HIV/AIDS prevention & treatment efforts include psychological variables, low socioeconomic status, cultural barriers, health care inadequacies, & political pressures against public health policies favoring youth. 2 Tables, 2 Figures, 120 References. Adapted with permission of Academic Press. JF - Journal of Adolescence AU - Bowler, Suzanne AU - Sheon, Amy R AU - D'Angelo, Lawrence J AU - Vermund, Sten H AD - c/o Vermund -- NIAID/NIH, 6003 Executive Blvd Room 2A42 Bethesda MD 20892 Y1 - 1992/12// PY - 1992 DA - December 1992 SP - 345 EP - 371 VL - 15 IS - 4 SN - 0140-1971, 0140-1971 KW - acquired immune deficiency syndrome/human immunodeficiency virus, knowledge/beliefs/behavior, US adolescents KW - national surveillance/epidemiological/survey data KW - Risk KW - Public Health KW - Epidemiology KW - Acquired Immune Deficiency Syndrome KW - United States of America KW - Adolescents KW - article KW - 1939: the family and socialization; adolescence & youth KW - 2045: sociology of health and medicine; sociology of medicine & health care UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/61316749?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Asocabs&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Adolescence&rft.atitle=HIV+and+AIDS+among+Adolescents+in+the+United+States%3A+Increasing+Risk+in+the+1990s&rft.au=Bowler%2C+Suzanne%3BSheon%2C+Amy+R%3BD%27Angelo%2C+Lawrence+J%3BVermund%2C+Sten+H&rft.aulast=Bowler&rft.aufirst=Suzanne&rft.date=1992-12-01&rft.volume=15&rft.issue=4&rft.spage=345&rft.isbn=&rft.btitle=&rft.title=Journal+of+Adolescence&rft.issn=01401971&rft_id=info:doi/ LA - English DB - Sociological Abstracts N1 - Date revised - 2007-04-01 N1 - Last updated - 2016-09-28 N1 - CODEN - JOADE8 N1 - SubjectsTermNotLitGenreText - Acquired Immune Deficiency Syndrome; United States of America; Adolescents; Public Health; Risk; Epidemiology ER - TY - JOUR T1 - An epidemiological perspective of the relationship between physical activity and NIDDM: From activity assessment to intervention AN - 21109646; 11313101 AB - Abstract not available. JF - Diabetes - Metabolism: Research and Reviews (Print Edition) AU - Kriska, Andrea M AU - Bennett, Peter H AD - University of Pittsburgh, Department of Epidemiology and Phoenix Epidemiology and Clinical Research Branch, NIDDK; Phoenix, U.S.A. Y1 - 1992/12// PY - 1992 DA - Dec 1992 SP - 355 EP - 372 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 USA VL - 8 IS - 4 SN - 1520-7552, 1520-7552 KW - Physical Education Index KW - PE 030:Exercise, Health & Physical Fitness UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/21109646?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Diabetes+-+Metabolism%3A+Research+and+Reviews+%28Print+Edition%29&rft.atitle=An+epidemiological+perspective+of+the+relationship+between+physical+activity+and+NIDDM%3A+From+activity+assessment+to+intervention&rft.au=Kriska%2C+Andrea+M%3BBennett%2C+Peter+H&rft.aulast=Kriska&rft.aufirst=Andrea&rft.date=1992-12-01&rft.volume=8&rft.issue=4&rft.spage=355&rft.isbn=&rft.btitle=&rft.title=Diabetes+-+Metabolism%3A+Research+and+Reviews+%28Print+Edition%29&rft.issn=15207552&rft_id=info:doi/10.1002%2Fdmr.5610080404 LA - English DB - Physical Education Index N1 - Date revised - 2009-12-01 N1 - Last updated - 2011-12-14 DO - http://dx.doi.org/10.1002/dmr.5610080404 ER - TY - JOUR T1 - Obesity and Cardiovascular Disease Risk Factors in Black and White Girls: The NHLBI Growth and Health Study AN - 1298326406 JF - American Journal of Public Health Y1 - 1992/12/01/ PY - 1992 DA - 1992 Dec 01 SP - 1613 CY - New York, N.Y. PB - American Public Health Association VL - 82 IS - 12 SN - 0090-0036 KW - Social Affairs UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1298326406?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Apio&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Public+Health&rft.atitle=Obesity+and+Cardiovascular+Disease+Risk+Factors+in+Black+and+White+Girls%3A+The+NHLBI+Growth+and+Health+Study&rft.au=&rft.aulast=&rft.aufirst=&rft.date=1992-12-01&rft.volume=82&rft.issue=12&rft.spage=1613&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Public+Health&rft.issn=00900036&rft_id=info:doi/ DB - Periodicals Index Online N1 - Last updated - 2013-02-23 ER - TY - JOUR T1 - Botulinum Toxin AN - 1295096327 JF - Journal of Voice : Official Journal of the Voice Foundation Y1 - 1992/12/01/ PY - 1992 DA - 1992 Dec 01 SP - 394 CY - New York, N.Y. PB - Raven Press VL - 6 IS - 4 SN - 0892-1997 KW - Music UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1295096327?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Apio&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Voice+%3A+Official+Journal+of+the+Voice+Foundation&rft.atitle=Botulinum+Toxin&rft.au=&rft.aulast=&rft.aufirst=&rft.date=1992-12-01&rft.volume=6&rft.issue=4&rft.spage=394&rft.isbn=&rft.btitle=&rft.title=Journal+of+Voice+%3A+Official+Journal+of+the+Voice+Foundation&rft.issn=08921997&rft_id=info:doi/ DB - Periodicals Index Online N1 - Last updated - 2013-02-23 ER - TY - JOUR T1 - Striatal extracellular dopamine in conscious vs. anesthetized rats: effects of chloral hydrate anesthetic on responses to drugs of different classes. AN - 73421303; 1477724 AB - Many investigations using the microdialysis technique have been performed in anesthetized animals, both in this laboratory and elsewhere. Concern arises with this preparation that the anesthetic may compromise neuronal function, or that it may interact with test drugs affecting neurotransmitter overflow. In addition, in these studies the microdialysis probe typically is introduced into the brain on the day of testing, and data collection commences within an hour or two following probe insertion. It has been suggested that transmitter recovered in the perfusate probably represents leakage due to tissue damage as well as exocytotic release, and may not accurately reflect neuronal responses to the manipulations of interest. Such potential confounds present important implications for the interpretation of data from these studies. The present investigation examined the effects of chloral hydrate anesthetic on (1) basal dopamine (DA) overflow in the anterior striatum, and (2) DA responses to systemically delivered drugs of two different classes known to influence DA activity. Three putative indices of impulse-dependent release were measured: (a) the time course and stability of basal DA overflow over several hours; (b) sodium channel involvement by adding tetrodotoxin (TTX) to the artificial CSF; and (c) calcium channel involvement using magnesium (Mg) in a calcium-free perfusate. Basal DA levels became stable in both conscious and anesthetized preparations by the second hour after probe insertion. Levels of recovered DA overflow in the anterior striata of conscious rats were approximately double those in chloral hydrate-anesthetized rats. Consistent with other findings, this suggests a general depression of CNS function by chloral hydrate.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Brain research AU - Hamilton, M E AU - Mele, A AU - Pert, A AD - Biological Psychiatry Branch, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1992/11/27/ PY - 1992 DA - 1992 Nov 27 SP - 1 EP - 7 VL - 597 IS - 1 SN - 0006-8993, 0006-8993 KW - Chloral Hydrate KW - 418M5916WG KW - Morphine KW - 76I7G6D29C KW - Sodium KW - 9NEZ333N27 KW - Calcium KW - SY7Q814VUP KW - Dextroamphetamine KW - TZ47U051FI KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Rats KW - Animals KW - Rats, Sprague-Dawley KW - Drug Interactions KW - Dialysis KW - Calcium -- pharmacology KW - Male KW - Chromatography, High Pressure Liquid KW - Sodium -- pharmacology KW - Basal Metabolism -- drug effects KW - Corpus Striatum -- metabolism KW - Dopamine -- metabolism KW - Corpus Striatum -- drug effects KW - Morphine -- pharmacology KW - Dextroamphetamine -- pharmacology KW - Chloral Hydrate -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73421303?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research&rft.atitle=Striatal+extracellular+dopamine+in+conscious+vs.+anesthetized+rats%3A+effects+of+chloral+hydrate+anesthetic+on+responses+to+drugs+of+different+classes.&rft.au=Hamilton%2C+M+E%3BMele%2C+A%3BPert%2C+A&rft.aulast=Hamilton&rft.aufirst=M&rft.date=1992-11-27&rft.volume=597&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Brain+research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-09 N1 - Date created - 1993-02-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dual-target inhibition of HIV-1 in vitro by means of an adeno-associated virus antisense vector. AN - 73347344; 1359646 AB - An adeno-associated virus vector encoding an antisense RNA was used to transduce stable intracellular resistance to human immunodeficiency virus-1 (HIV-1) in human hemopoietic and non-hemopoietic cell lines. The antisense targets are present in all HIV-1 transcripts and include the TAR sequence, which is critical for transcription and virus replication, and the polyadenylation signal. Cell lines expressing antisense RNA showed up to 95 percent inhibition of gene expression directed by the HIV-1 long terminal repeat and greater than 99 percent reduction in infectious HIV-1 production, with no detectable cellular toxicity. Because of their efficient transcription and inability to recombine with HIV-1, adeno-associated virus vectors represent a promising form of anti-retroviral gene therapy. JF - Science (New York, N.Y.) AU - Chatterjee, S AU - Johnson, P R AU - Wong, K K AD - Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health, Rockville, MD 20852. Y1 - 1992/11/27/ PY - 1992 DA - 1992 Nov 27 SP - 1485 EP - 1488 VL - 258 IS - 5087 SN - 0036-8075, 0036-8075 KW - NeoR KW - Gene Products, tat KW - 0 KW - RNA, Antisense KW - RNA, Messenger KW - RNA, Viral KW - tat Gene Products, Human Immunodeficiency Virus KW - Neomycin KW - 1404-04-2 KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Index Medicus KW - AIDS/HIV KW - Humans KW - Drug Resistance, Microbial -- genetics KW - HIV Long Terminal Repeat -- genetics KW - CD4-Positive T-Lymphocytes -- microbiology KW - RNA, Messenger -- genetics KW - Neomycin -- pharmacology KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Virus Replication -- genetics KW - Base Sequence KW - Transfection KW - Molecular Sequence Data KW - RNA, Viral -- genetics KW - Gene Products, tat -- genetics KW - Cell Line KW - HIV-1 -- genetics KW - Dependovirus -- genetics KW - RNA, Antisense -- genetics KW - HIV-1 -- physiology KW - Genetic Vectors -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73347344?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science+%28New+York%2C+N.Y.%29&rft.atitle=Dual-target+inhibition+of+HIV-1+in+vitro+by+means+of+an+adeno-associated+virus+antisense+vector.&rft.au=Chatterjee%2C+S%3BJohnson%2C+P+R%3BWong%2C+K+K&rft.aulast=Chatterjee&rft.aufirst=S&rft.date=1992-11-27&rft.volume=258&rft.issue=5087&rft.spage=1485&rft.isbn=&rft.btitle=&rft.title=Science+%28New+York%2C+N.Y.%29&rft.issn=00368075&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-17 N1 - Date created - 1992-12-17 N1 - Date revised - 2017-01-13 N1 - Gene symbol - NeoR N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Post-transcriptional regulation of early T cell development by T cell receptor signals. AN - 73318249; 1439838 AB - During differentiation in the thymus, immature T cells progress through an ordered sequence of developmental stages that are best characterized by variable expression of the co-receptor molecules CD4 and CD8. Crosslinking of T cell receptor (TCR) molecules on precursor thymocytes was found to block their differentiation into CD4+CD8+ cells by eliminating messenger RNA's encoding two families of developmentally important molecules: the co-receptor molecules CD4 and CD8 and the recombination activating genes 1 and 2. TCR-induced post-transcriptional regulation in early thymocytes was specific for selective messenger RNA's, required protein synthesis, and was itself developmentally regulated. These data identify a post-transcriptional mechanism that is influenced by TCR signals and that regulates early thymocyte development. JF - Science (New York, N.Y.) AU - Takahama, Y AU - Singer, A AD - Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/11/27/ PY - 1992 DA - 1992 Nov 27 SP - 1456 EP - 1462 VL - 258 IS - 5087 SN - 0036-8075, 0036-8075 KW - RAG-1 KW - RAG-2 KW - Antigens, CD4 KW - 0 KW - Antigens, CD8 KW - Protein Synthesis Inhibitors KW - RNA, Messenger KW - Receptors, Antigen, T-Cell, alpha-beta KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Thymus Gland -- cytology KW - Animals KW - Fetus -- cytology KW - Mice KW - Antigens, CD8 -- genetics KW - RNA Processing, Post-Transcriptional -- physiology KW - Signal Transduction -- physiology KW - Protein-Tyrosine Kinases -- genetics KW - RNA, Messenger -- metabolism KW - Cell Differentiation -- physiology KW - Protein Synthesis Inhibitors -- pharmacology KW - Cells, Cultured KW - Antigens, CD4 -- genetics KW - Genes, RAG-1 -- genetics KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Thymus Gland -- embryology KW - Gene Rearrangement, T-Lymphocyte -- genetics KW - T-Lymphocytes -- cytology KW - T-Lymphocytes -- drug effects KW - Receptors, Antigen, T-Cell, alpha-beta -- genetics KW - Receptors, Antigen, T-Cell, alpha-beta -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73318249?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science+%28New+York%2C+N.Y.%29&rft.atitle=Post-transcriptional+regulation+of+early+T+cell+development+by+T+cell+receptor+signals.&rft.au=Takahama%2C+Y%3BSinger%2C+A&rft.aulast=Takahama&rft.aufirst=Y&rft.date=1992-11-27&rft.volume=258&rft.issue=5087&rft.spage=1456&rft.isbn=&rft.btitle=&rft.title=Science+%28New+York%2C+N.Y.%29&rft.issn=00368075&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-17 N1 - Date created - 1992-12-17 N1 - Date revised - 2017-01-13 N1 - Gene symbol - RAG-1; RAG-2 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Purification and characterization of the mouse mammary tumor virus protease expressed in Escherichia coli. AN - 73304083; 1331110 AB - The mouse mammary tumor virus (MMTV) protease gene was cloned into pGEX-2T, an Escherichia coli expression vector containing the glutathione S-transferase coding region of Schistosoma japonicum. The chimeric protein was formed by fusion of the glutathione S-transferase with a hexapeptide which contains a thrombin cleavage site, followed by the MMTV protease. Affinity chromatography on a glutathione-Sepharose 4B column was used to isolate the chimeric protein. After thrombin cleavage, the glutathione S-transferase and the protease were separated by gel filtration chromatography on a Sephadex G-75 column. The overall yield of the protease purification procedure was about 1 mg of protease/liter of culture, and the specific activity was 380 pmol/min.micrograms of enzyme. Like other retroviral proteases, the MMTV enzyme was active as a dimer, showed maximum activity at pH between 4 and 6, and could be inhibited by pepstatin A and a phosphinic acid derivative HIV-1 protease inhibitor. Enzymatic characterization of this protease reveals its broad specificity, showing a clear preference for the oligopeptide substrate mimicking the cleavage site at the amino-terminal end of the capsid protein (kcat/Km = 9725.5 M-1.s-1). The chimeric protein was also an active dimer and showed a similar Km (17 microM) for such an oligopeptide, although its kcat was about 10 times smaller. Autocatalytic processing of the MMTV protease was observed after expression of clones containing the natural cleavage site, as it occurs at the amino-terminal end of the viral protease, instead of the thrombin-sensitive sequence. JF - The Journal of biological chemistry AU - Menéndez-Arias, L AU - Young, M AU - Oroszlan, S AD - Laboratory of Molecular Virology and Carcinogenesis, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1992/11/25/ PY - 1992 DA - 1992 Nov 25 SP - 24134 EP - 24139 VL - 267 IS - 33 SN - 0021-9258, 0021-9258 KW - gag KW - pol KW - pro KW - Antibodies KW - 0 KW - Oligodeoxyribonucleotides KW - Peptides KW - Recombinant Fusion Proteins KW - Glutathione Transferase KW - EC 2.5.1.18 KW - Endopeptidases KW - EC 3.4.- KW - Index Medicus KW - AIDS/HIV KW - Peptides -- chemical synthesis KW - Animals KW - Recombinant Fusion Proteins -- isolation & purification KW - Schistosoma japonicum -- genetics KW - Glutathione Transferase -- isolation & purification KW - Recombinant Fusion Proteins -- metabolism KW - Chromatography, Gel KW - Genetic Vectors KW - Molecular Sequence Data KW - Osmolar Concentration KW - Immunoblotting KW - Glutathione Transferase -- metabolism KW - Cloning, Molecular -- methods KW - Peptides -- immunology KW - Peptides -- metabolism KW - Glutathione Transferase -- genetics KW - Amino Acid Sequence KW - Schistosoma japonicum -- enzymology KW - Plasmids KW - Chromatography, Affinity KW - Base Sequence KW - Kinetics KW - Polymerase Chain Reaction -- methods KW - Restriction Mapping KW - Substrate Specificity KW - Endopeptidases -- isolation & purification KW - Endopeptidases -- genetics KW - Endopeptidases -- metabolism KW - Escherichia coli -- genetics KW - Genes, Viral KW - Mammary Tumor Virus, Mouse -- enzymology KW - Mammary Tumor Virus, Mouse -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73304083?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Purification+and+characterization+of+the+mouse+mammary+tumor+virus+protease+expressed+in+Escherichia+coli.&rft.au=Men%C3%A9ndez-Arias%2C+L%3BYoung%2C+M%3BOroszlan%2C+S&rft.aulast=Men%C3%A9ndez-Arias&rft.aufirst=L&rft.date=1992-11-25&rft.volume=267&rft.issue=33&rft.spage=24134&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-22 N1 - Date created - 1992-12-22 N1 - Date revised - 2017-01-13 N1 - Gene symbol - gag; pol; pro N1 - Genetic sequence - D12751; GENBANK; D12752; D10519; D10518; D12750; D10517; D12749; D10520; L01464; D12753 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Nucleosome core binding region of chromosomal protein HMG-17 acts as an independent functional domain. AN - 73361384; 1453455 AB - Chromosomal proteins HMG-14 and HMG-17 have a modular structure. Here we examine whether the putative nucleosome-binding domain in these proteins can function as an independent module. Mobility shift assays with recombinant HMG-17 indicate that synthetic molecules can be used to analyze the interaction of this protein with the nucleosome core. Peptides corresponding to various regions of the protein have been synthesized and their interaction with nucleosome cores analyzed by mobility shift, thermal denaturation and DNase I digestion. A 30 amino acid long peptide, corresponding to the putative nucleosome-binding domain of HMG-17, specifically shifts the mobility of cores as compared to free DNA, elevates the tm of both the premelt and main melt of the cores and protects from DNase I digestion the same nucleosomal DNA sites as the intact protein. The binding of both the peptide and the intact protein is lost upon digestion of the histone tails by trypsin. The nucleosomal binding sites of the peptide appear identical to those of the intact protein. Thus, a region of the protein can acts as an independent functional domain. This supports the notion that HMG-14 and HMG-17 are modular proteins. This finding is relevant to the understanding of the function and evolution of HMG-14/-17, the only nucleosome core particle binding proteins known to date. JF - Journal of molecular biology AU - Crippa, M P AU - Alfonso, P J AU - Bustin, M AD - Laboratory of Molecular Carcinogenesis National Cancer Institute, National Institutes of Health Bethesda, MD 20892. Y1 - 1992/11/20/ PY - 1992 DA - 1992 Nov 20 SP - 442 EP - 449 VL - 228 IS - 2 SN - 0022-2836, 0022-2836 KW - High Mobility Group Proteins KW - 0 KW - Nucleosomes KW - Peptides KW - Recombinant Proteins KW - Deoxyribonuclease I KW - EC 3.1.21.1 KW - Index Medicus KW - Swine KW - Peptides -- chemical synthesis KW - Animals KW - Thermodynamics KW - Biological Evolution KW - Humans KW - Protein Denaturation KW - Peptides -- metabolism KW - Amino Acid Sequence KW - Binding Sites KW - Recombinant Proteins -- metabolism KW - Molecular Sequence Data KW - Sequence Homology, Amino Acid KW - Nucleosomes -- metabolism KW - High Mobility Group Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73361384?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+molecular+biology&rft.atitle=Nucleosome+core+binding+region+of+chromosomal+protein+HMG-17+acts+as+an+independent+functional+domain.&rft.au=Crippa%2C+M+P%3BAlfonso%2C+P+J%3BBustin%2C+M&rft.aulast=Crippa&rft.aufirst=M&rft.date=1992-11-20&rft.volume=228&rft.issue=2&rft.spage=442&rft.isbn=&rft.btitle=&rft.title=Journal+of+molecular+biology&rft.issn=00222836&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-31 N1 - Date created - 1992-12-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - National Cancer Institute's evaluation of unconventional cancer treatments. AN - 73291433; 1433356 JF - Journal of the National Cancer Institute AU - Hawkins, M J AU - Friedman, M A AD - Cancer Therapy Evaluation Program, National Cancer Institute, Bethesda, Md 20892. Y1 - 1992/11/18/ PY - 1992 DA - 1992 Nov 18 SP - 1699 EP - 1702 VL - 84 IS - 22 SN - 0027-8874, 0027-8874 KW - Hydrazines KW - 0 KW - hydrazine KW - 27RFH0GB4R KW - Index Medicus KW - United States KW - Hydrazines -- therapeutic use KW - Humans KW - National Institutes of Health (U.S.) KW - Clinical Protocols KW - Neoplasms -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73291433?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=National+Cancer+Institute%27s+evaluation+of+unconventional+cancer+treatments.&rft.au=Hawkins%2C+M+J%3BFriedman%2C+M+A&rft.aulast=Hawkins&rft.aufirst=M&rft.date=1992-11-18&rft.volume=84&rft.issue=22&rft.spage=1699&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-11 N1 - Date created - 1992-12-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Generation of free radicals from lipid hydroperoxides by Ni2+ in the presence of oligopeptides. AN - 73331939; 1332613 AB - The generation of free radicals from lipid hydroperoxides by Ni2+ in the presence of several oligopeptides was investigated by electron spin resonance (ESR) utilizing 5,5-dimethyl-1-pyrroline N-oxide (DMPO) as a spin trap. Incubation of Ni2+ with cumene hydroperoxide or t-butyl hydroperoxide did not generate any detectable free radical. In the presence of glycylglycylhistidine (GlyGlyHis), however, Ni2+ generated cumene peroxyl (ROO.) radical from cumene hydroperoxide, with the free radical generation reaching its saturation level within about 3 min. The reaction was first order with respect to both cumene hydroperoxide and Ni2+. Similar results were obtained using t-butyl hydroperoxide, but the yield of t-butyl peroxyl radical generation was about 7-fold lower. Other histidine-containing oligopeptides such as beta-alanyl-L-histidine (carnosine), gamma-aminobutyryl-L-histidine (homocarnosine), and beta-alanyl-3-methyl-L-histidine (anserine) caused the generation of both cumene alkyl (R.) and cumene alkoxyl (RO.) radicals in the reaction of Ni2+ with cumene hydroperoxide. Similar results were obtained using t-butyl hydroperoxide. Glutathione also caused generation of R. and RO. radicals in the reaction of Ni2+ with cumene hydroperoxide but the yield was approximately 25-fold greater than that produced by the histidine-containing peptides, except GlyGlyHis. The ratio of DMPO/R. and DMPO/RO. produced with glutathione and cumene hydroperoxide was approximately 3:1. Essentially the same results were obtained using t-butyl hydroperoxide except that the ratio of DMPO/R. to DMPO/RO. was approximately 1:1. The free radical generation from cumene hydroperoxide reached its saturation level almost instantaneously while in the case of t-butyl hydroperoxide, the saturation level was reached in about 3 min. In the presence of oxidized glutathione, the Ni2+/cumene hydroperoxide system caused DMPO/.OH generation from DMPO without forming free hydroxyl radical. Since glutathione, carnosine, homocarnosine, and anserine are considered to be cellular antioxidants, the present work suggests that instead of protecting against oxidative damage, these oligopeptides may facilitate the Ni(2+)-mediated free radical generation and thus may participate in the mechanism(s) of Ni2+ toxicity and carcinogenicity. JF - Archives of biochemistry and biophysics AU - Shi, X AU - Dalal, N S AU - Kasprzak, K S AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick Cancer Research and Development Center, Maryland 21702. Y1 - 1992/11/15/ PY - 1992 DA - 1992 Nov 15 SP - 154 EP - 162 VL - 299 IS - 1 SN - 0003-9861, 0003-9861 KW - Benzene Derivatives KW - 0 KW - Cyclic N-Oxides KW - Free Radicals KW - Lipid Peroxides KW - Oligopeptides KW - Peroxides KW - Spin Labels KW - 5,5-dimethyl-1-pyrroline-1-oxide KW - 7170JZ1QF3 KW - diglycyl-histidine KW - 7451-76-5 KW - Nickel KW - 7OV03QG267 KW - tert-Butylhydroperoxide KW - 955VYL842B KW - Glutathione KW - GAN16C9B8O KW - cumene hydroperoxide KW - PG7JD54X4I KW - Glutathione Disulfide KW - ULW86O013H KW - Index Medicus KW - Kinetics KW - Electron Spin Resonance Spectroscopy KW - Glutathione -- analogs & derivatives KW - Benzene Derivatives -- chemistry KW - Peroxides -- chemistry KW - Lipid Peroxides -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73331939?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+biochemistry+and+biophysics&rft.atitle=Generation+of+free+radicals+from+lipid+hydroperoxides+by+Ni2%2B+in+the+presence+of+oligopeptides.&rft.au=Shi%2C+X%3BDalal%2C+N+S%3BKasprzak%2C+K+S&rft.aulast=Shi&rft.aufirst=X&rft.date=1992-11-15&rft.volume=299&rft.issue=1&rft.spage=154&rft.isbn=&rft.btitle=&rft.title=Archives+of+biochemistry+and+biophysics&rft.issn=00039861&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-02 N1 - Date created - 1992-12-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transcription-repair coupling determines the strandedness of ultraviolet mutagenesis in Escherichia coli. AN - 73321927; 1438310 AB - We have analyzed the spectra of UV-induced mutations in the lacI gene of a wild-type and an mfd strain of Escherichia coli. mfd strains have been recently proposed to be deficient in a factor coupling DNA repair and transcription. Analysis of UV-induced mutations occurring at adjacent pyrimidines showed that mutations in the wild-type strain arose largely from the nontranscribed strand but arose predominantly from the transcribed strand in the mfd strain. The overall strand switch was 14-fold. One mutation, G.C-->A.T in the lacI initiation codon, showed a > 300-fold shift. No effect was observed for mutations at non-pyrimidine-pyrimidine sequences. These results provide in vivo evidence for a key role of the mfd gene in controlling the strandedness of mutagenesis and support the proposed role of the mfd gene product in directing DNA excision repair to the transcribed strand of a damaged gene. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Oller, A R AU - Fijalkowska, I J AU - Dunn, R L AU - Schaaper, R M AD - Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992/11/15/ PY - 1992 DA - 1992 Nov 15 SP - 11036 EP - 11040 VL - 89 IS - 22 SN - 0027-8424, 0027-8424 KW - lacI KW - mfd KW - DNA, Bacterial KW - 0 KW - Index Medicus KW - Base Sequence KW - Base Composition KW - DNA, Bacterial -- isolation & purification KW - DNA, Bacterial -- genetics KW - Molecular Sequence Data KW - Dose-Response Relationship, Radiation KW - Mutagenesis KW - Ultraviolet Rays KW - DNA Repair KW - Genes, Bacterial -- genetics KW - Escherichia coli -- genetics KW - Transcription, Genetic KW - Escherichia coli -- radiation effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73321927?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Transcription-repair+coupling+determines+the+strandedness+of+ultraviolet+mutagenesis+in+Escherichia+coli.&rft.au=Oller%2C+A+R%3BFijalkowska%2C+I+J%3BDunn%2C+R+L%3BSchaaper%2C+R+M&rft.aulast=Oller&rft.aufirst=A&rft.date=1992-11-15&rft.volume=89&rft.issue=22&rft.spage=11036&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-23 N1 - Date created - 1992-12-23 N1 - Date revised - 2017-01-13 N1 - Gene symbol - lacI; mfd N1 - SuppNotes - Cited By: Mol Gen Genet. 1977 Nov 14;156(2):133-40 [340899] Science. 1966 Jun 3;152(3727):1345-53 [5327888] Proc Natl Acad Sci U S A. 1991 Dec 15;88(24):11574-8 [1763073] Cell. 1990 May 18;61(4):675-84 [2188732] J Biol Chem. 1990 Dec 5;265(34):21330-6 [2250027] Nature. 1989 Nov 2;342(6245):95-8 [2554145] Mol Cell Biol. 1989 Mar;9(3):1277-83 [2725498] J Mol Biol. 1987 Nov 20;198(2):187-202 [2828636] Microbiol Rev. 1984 Mar;48(1):60-93 [6371470] J Biol Chem. 1984 Oct 25;259(20):12463-9 [6490626] Cancer Res. 1981 Mar;41(3):819-25 [7459869] J Biol Chem. 1956 Jan;218(1):97-106 [13278318] J Mol Biol. 1988 Oct 5;203(3):619-33 [3062175] Proc Natl Acad Sci U S A. 1986 Dec;83(23):8878-82 [3466163] Mutat Res. 1987 May;183(3):241-7 [3553916] Cell. 1986 May 9;45(3):417-23 [3698104] Gene. 1985;39(2-3):181-9 [4092929] Mutat Res. 1967 Jul-Aug;4(4):502-4 [4862435] Mutat Res. 1969 Sep-Oct;8(2):215-28 [4904138] Mutat Res. 1971 Sep;13(1):1-8 [4938962] Cell. 1983 May;33(1):13-7 [6380746] Nature. 1982 Jul 8;298(5870):189-92 [7045692] Proc Natl Acad Sci U S A. 1958 May;44(5):390-401 [16590211] Annu Rev Genet. 1978;12:329-63 [371526] Cold Spring Harb Symp Quant Biol. 1979;43 Pt 2:881-6 [385231] Genetics. 1991 Oct;129(2):317-26 [1660424] Proc Natl Acad Sci U S A. 1991 Sep 15;88(18):8232-6 [1896474] J Biol Chem. 1991 Jun 25;266(18):11766-73 [2050676] Environ Mol Mutagen. 1990;16(3):143-8 [2209571] Microbiol Rev. 1989 Mar;53(1):1-24 [2540407] Nucleic Acids Res. 1989 Jun 26;17(12):4433-9 [2664708] Mol Gen Genet. 1989 Nov;219(3):359-64 [2695824] J Biol Chem. 1989 Oct 25;264(30):18005-10 [2808361] J Mol Biol. 1986 May 20;189(2):273-84 [3018259] Proc Natl Acad Sci U S A. 1988 Nov;85(21):8126-30 [3054881] Proc Natl Acad Sci U S A. 1987 Sep;84(17):6220-4 [3306672] Proc Natl Acad Sci U S A. 1987 Jun;84(11):3782-6 [3473483] Carcinogenesis. 1987 Sep;8(9):1333-6 [3621470] Cell. 1987 Oct 23;51(2):241-9 [3664636] Cell. 1985 Feb;40(2):359-69 [3838150] Mol Gen Genet. 1974;133(4):283-91 [4612337] Nature. 1974 Jan 4;247(5435):35-6 [4808937] Annu Rev Microbiol. 1969;23:487-514 [4899079] Mutat Res. 1970 Apr;9(4):349-58 [4921214] Mutat Res. 1975 Jun;28(3):347-54 [1094281] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alanine scanning mutagenesis identifies surface amino acids on domain II of Pseudomonas exotoxin required for cytotoxicity, proper folding, and secretion into periplasm. AN - 73316546; 1429683 AB - Pseudomonas exotoxin A (PE) is a single polypeptide chain that contains 613 amino acids and is arranged into three major structural domains. Domain Ia is responsible for cell recognition, domain II for translocation of PE across the membrane, and domain III for ADP-ribosylation of elongation factor 2. Recombinant PE can be produced in Escherichia coli and is efficiently secreted into the periplasm when an OmpA signal sequence is present. To investigate the role of the amino acids located on the surface of domain II in the action of the toxin against mammalian cells, we substituted alanine for each of the 27 surface amino acids present in domain II. Surprisingly, all 27 mutant proteins had some alteration in cytotoxicity when tested on human A431 or MCF7 cells or mouse L929 cells. Native PE has a compact structure and therefore is relatively protease resistant and very little ADP-ribosylation activity is detected in the absence of the denaturing agents like urea and dithiothreitol. Several of the mutations resulted in altered protease sensitivity of the toxin. Seven of the mutant molecules exhibited ADP-ribosylation activity without urea and dithiothreitol, indicating they are partially unfolded. Out of these seven mutants, six had increased cytotoxic activity on at least one of the target cell lines and the other retained its native cytotoxic potency. JF - The Journal of biological chemistry AU - Kasturi, S AU - Kihara, A AU - FitzGerald, D AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/11/15/ PY - 1992 DA - 1992 Nov 15 SP - 23427 EP - 23433 VL - 267 IS - 32 SN - 0021-9258, 0021-9258 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - Recombinant Proteins KW - Virulence Factors KW - Adenosine Diphosphate Ribose KW - 20762-30-5 KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Chymotrypsin KW - EC 3.4.21.1 KW - Trypsin KW - EC 3.4.21.4 KW - Alanine KW - OF5P57N2ZX KW - Index Medicus KW - Chymotrypsin -- metabolism KW - Animals KW - Recombinant Proteins -- pharmacology KW - Humans KW - Escherichia coli -- genetics KW - Bacterial Toxins -- pharmacology KW - Mice KW - Adenosine Diphosphate Ribose -- metabolism KW - Structure-Activity Relationship KW - Mutagenesis, Site-Directed KW - Tumor Cells, Cultured KW - Cell Survival -- drug effects KW - Trypsin -- metabolism KW - Recombinant Proteins -- chemistry KW - Cell Line KW - Exotoxins -- genetics KW - Exotoxins -- pharmacology KW - Pseudomonas aeruginosa -- genetics KW - Protein Folding KW - Exotoxins -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73316546?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Alanine+scanning+mutagenesis+identifies+surface+amino+acids+on+domain+II+of+Pseudomonas+exotoxin+required+for+cytotoxicity%2C+proper+folding%2C+and+secretion+into+periplasm.&rft.au=Kasturi%2C+S%3BKihara%2C+A%3BFitzGerald%2C+D%3BPastan%2C+I&rft.aulast=Kasturi&rft.aufirst=S&rft.date=1992-11-15&rft.volume=267&rft.issue=32&rft.spage=23427&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-16 N1 - Date created - 1992-12-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Hepatocyte growth factor is a synergistic factor for the growth of hematopoietic progenitor cells. AN - 73308044; 1421367 AB - Bone marrow (BM) stromal cells, which include macrophages, fibroblasts, endothelial cells, and adipocytes, have been shown to produce several factors that modulate the growth of BM progenitors. Hepatocyte growth factor (HGF) is a fibroblast-derived factor and has recently been shown to be a ligand for the c-met proto-oncogene, a member of the receptor class of tyrosine kinases. c-met messenger RNA (mRNA) is predominantly expressed in epithelial cells, but has been detected in several murine hematopoietic progenitor cell lines, suggesting that HGF and met might function during hematopoiesis. Here, BM cells were found to express both met mRNA and protein. Moreover, HGF was shown to synergize with interleukin-3 and granulocyte-macrophage colony-stimulating factor to stimulate colony formation of hematopoietic progenitor cells in vitro. These results show that, in addition to its activity on epithelial cells, HGF is a new member of the functionally related group of factors that modulate hematopoiesis. JF - Blood AU - Kmiecik, T E AU - Keller, J R AU - Rosen, E AU - Vande Woude, G F AD - ABL-Basic Research Program, Program Resources, Inc/DynCorp, Inc, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21701. Y1 - 1992/11/15/ PY - 1992 DA - 1992 Nov 15 SP - 2454 EP - 2457 VL - 80 IS - 10 SN - 0006-4971, 0006-4971 KW - Interleukin-3 KW - 0 KW - Proto-Oncogene Proteins KW - RNA, Messenger KW - Hepatocyte Growth Factor KW - 67256-21-7 KW - Granulocyte-Macrophage Colony-Stimulating Factor KW - 83869-56-1 KW - Proto-Oncogene Proteins c-met KW - EC 2.7.10.1 KW - Abridged Index Medicus KW - Index Medicus KW - Bone Marrow Cells KW - Animals KW - Tumor Cells, Cultured KW - Interleukin-3 -- pharmacology KW - Gene Expression KW - Bone Marrow -- metabolism KW - Mice KW - RNA, Messenger -- genetics KW - Proto-Oncogene Proteins -- genetics KW - Granulocyte-Macrophage Colony-Stimulating Factor -- pharmacology KW - Drug Synergism KW - Cell Division KW - Hepatocyte Growth Factor -- pharmacology KW - Hepatocyte Growth Factor -- genetics KW - Hematopoietic Stem Cells -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73308044?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Blood&rft.atitle=Hepatocyte+growth+factor+is+a+synergistic+factor+for+the+growth+of+hematopoietic+progenitor+cells.&rft.au=Kmiecik%2C+T+E%3BKeller%2C+J+R%3BRosen%2C+E%3BVande+Woude%2C+G+F&rft.aulast=Kmiecik&rft.aufirst=T&rft.date=1992-11-15&rft.volume=80&rft.issue=10&rft.spage=2454&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=00064971&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-22 N1 - Date created - 1992-12-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Retinoid status and the control of keratin expression and adhesion during the histogenesis of squamous metaplasia of tracheal epithelium. AN - 73307051; 1384955 AB - We induced vitamin A depletion to define early and late changes during the histogenesis of squamous metaplasia of hamster tracheal epithelium. An early change is the "minimal morphological change" (MMC), in which the mucociliary epithelium is separated from the basement membrane by a continuous layer of basal cells. Immunohistochemistry showed an exclusive localization of the keratins K5 and K14 in basal cells of normal and MMC epithelia. At the MMC stage no staining was observed above the basal layer with antibodies to K5, but upon progression of the lesion to a squamous focus all cells from basal to terminally differentiated were positive for K5 and K14. In contrast, when we used antibodies to the keratins K6 or K13 all cells were negative in the normal epithelium and in the MMC epithelium. Successive layers of suprabasal squamous cells found in squamous metaplasia failed to express normal epidermal differentiation marker keratins K1 and K10 but expressed the proliferation marker keratin K6 and the internal stratified epithelium keratin K13, not normally found in the epidermis or in the trachea. Hamster tracheal epithelial cells could be maintained in culture in serum-free medium for at least 4 weeks in the presence of retinoic acid (RA). In non-RA-containing medium, cells from vitamin A-deficient hamsters showed markedly reduced growth and an increase in the expression of keratins K5, K6, K13, and K14. Since our previous work had implicated retinoids in the control of cell adhesiveness, we were interested to find out whether changes in cell adhesion occur in vitamin A-deficient hamster tracheal epithelial cells, compared to normal cells. Functional assays demonstrated that hamster tracheal epithelial cells, obtained from non-RA-treated tracheas or maintained in culture, displayed reduced attachment to laminin, compared to RA-treated cells. Immunofluorescence studies did not show a decrease either in the alpha 6 integrin subunit, which was localized in the basal aspect of basal cells, or in basement membrane laminin. However, the expression of laminin-binding protein 37 decreased as the epithelium changed from pseudostratified to stratified. Therefore, a coordinated pattern of changes in keratin gene expression, as well as in the expression of laminin-binding protein 37, the precursor to the cell surface laminin receptor 67LR, and in adhesive properties takes place in tracheal epithelium when its phenotype changes from mucociliary to the preneoplastic stage of squamous metaplasia. JF - Cancer research AU - Lancillotti, F AU - Darwiche, N AU - Celli, G AU - De Luca, L M AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/11/15/ PY - 1992 DA - 1992 Nov 15 SP - 6144 EP - 6152 VL - 52 IS - 22 SN - 0008-5472, 0008-5472 KW - Antibodies KW - 0 KW - Cell Adhesion Molecules KW - Laminin KW - Tretinoin KW - 5688UTC01R KW - Keratins KW - 68238-35-7 KW - Index Medicus KW - Animals KW - Cell Adhesion -- physiology KW - Laminin -- analysis KW - Amino Acid Sequence KW - Metaplasia -- etiology KW - Protein Binding KW - Blotting, Western KW - Fibroblasts -- pathology KW - Cells, Cultured KW - Laminin -- physiology KW - Molecular Sequence Data KW - Mesocricetus KW - Epithelium -- pathology KW - Immunohistochemistry KW - Male KW - Cricetinae KW - Tretinoin -- pharmacology KW - Vitamin A Deficiency -- physiopathology KW - Keratins -- physiology KW - Trachea -- pathology KW - Keratins -- analysis KW - Cell Adhesion Molecules -- analysis KW - Cell Adhesion Molecules -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73307051?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Retinoid+status+and+the+control+of+keratin+expression+and+adhesion+during+the+histogenesis+of+squamous+metaplasia+of+tracheal+epithelium.&rft.au=Lancillotti%2C+F%3BDarwiche%2C+N%3BCelli%2C+G%3BDe+Luca%2C+L+M&rft.aulast=Lancillotti&rft.aufirst=F&rft.date=1992-11-15&rft.volume=52&rft.issue=22&rft.spage=6144&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-09 N1 - Date created - 1992-12-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The stress response and the regulation of inflammatory disease. AN - 73280680; 1416562 AB - The molecular and biochemical bases for interactions between the immune and central nervous systems are described. Immune cytokines not only activate immune function but also recruit central stress-responsive neurotransmitter systems in the modulation of the immune response and in the activation of behaviors that may be adaptive during injury or inflammation. Peripherally generated cytokines, such as interleukin-1, signal hypothalamic corticotropin-releasing hormone (CRH) neurons to activate pituitary-adrenal counter-regulation of inflammation through the potent antiinflammatory effects of glucocorticoids. Corticotropin-releasing hormone not only activates the pituitary-adrenal axis but also sets in motion a coordinated series of behavioral and physiologic responses, suggesting that the central nervous system may coordinate both behavioral and immunologic adaptation during stressful situations. The pathophysiologic perturbation of this feedback loop, through various mechanisms, results in the development of inflammatory syndromes, such as rheumatoid arthritis, and behavioral syndromes, such as depression. Thus, diseases characterized by both inflammatory and emotional disturbances may derive from common alterations in specific central nervous system pathways (for example, the CRH system). In addition, disruptions of this communication by genetic, infectious, toxic, or pharmacologic means can influence the susceptibility to disorders associated with both behavioral and inflammatory components and potentially alter their natural history. These concepts suggest that neuropharmacologic agents that stimulate hypothalamic CRH might potentially be adjunctive therapy for illnesses traditionally viewed as inflammatory or autoimmune. JF - Annals of internal medicine AU - Sternberg, E M AU - Chrousos, G P AU - Wilder, R L AU - Gold, P W AD - National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1992/11/15/ PY - 1992 DA - 1992 Nov 15 SP - 854 EP - 866 VL - 117 IS - 10 SN - 0003-4819, 0003-4819 KW - Abridged Index Medicus KW - Index Medicus KW - United States KW - Hypothalamo-Hypophyseal System -- physiology KW - Humans KW - National Institutes of Health (U.S.) KW - Inflammation -- immunology KW - Pituitary-Adrenal System -- physiology KW - Psychoneuroimmunology KW - General Adaptation Syndrome -- immunology KW - Neuroimmunomodulation -- physiology KW - Neurosecretory Systems -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73280680?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+internal+medicine&rft.atitle=The+stress+response+and+the+regulation+of+inflammatory+disease.&rft.au=Sternberg%2C+E+M%3BChrousos%2C+G+P%3BWilder%2C+R+L%3BGold%2C+P+W&rft.aulast=Sternberg&rft.aufirst=E&rft.date=1992-11-15&rft.volume=117&rft.issue=10&rft.spage=854&rft.isbn=&rft.btitle=&rft.title=Annals+of+internal+medicine&rft.issn=00034819&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-16 N1 - Date created - 1992-11-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Oxidative stress induced by administration of the neuroleptic drug haloperidol is attenuated by higher doses of haloperidol. AN - 73397788; 1467970 AB - The effect of haloperidol administration on lipid peroxidation and glutathione/protein thiol homeostasis in the brain was examined 4 h following subcutaneous administration of a single dose of haloperidol; 1.0, 1.5, 2.0 or 2.5 mg/kg b.wt. Glutathione (GSH) levels decreased significantly in cortex, striatum and midbrain after haloperidol administration. Maximal decrease of GSH was observed in the striatum. The depleted GSH was recoverable as protein glutathione mixed disulfide (Pr-SSG) with concomitant loss of protein thiols (Pr-SH) in all the regions of the brain examined. Administration of 1.5 mg/kg b.wt. of haloperidol resulted in significant depletion of GSH in striatum and midbrain as compared to that after administration of the lower dose of 1.0 mg/kg b.wt. of haloperidol. However, administration of higher doses of haloperidol (2.0 and 2.5 mg/kg b.wt.) did not result in greater depletion of GSH; the GSH levels were not significantly different from that observed following the administration of 1.5 mg/kg b.wt. of haloperidol. However, Pr-SSG levels increased dose-dependently following haloperidol administration. The total GSH recovered as sum of GSH and Pr-SSG was significantly higher than controls in striatum and midbrain following administration of higher doses of haloperidol, namely, 2.0 and 2.5 mg/kg b.wt. The depleted GSH was not recoverable as glutathione disulfide (GSSG). GSSG levels were not significantly different from controls 4 h after administration of 1.5 mg/kg b.wt. of haloperidol. The levels of malondialdehyde (indicative of lipid peroxidation) increased significantly as compared to control levels (280-220%) following administration of 1.0 and 1.5 mg/kg b.wt. of haloperidol.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Brain research AU - Shivakumar, B R AU - Ravindranath, V AD - Department of Neurochemistry, National Institute of Mental Health and Neuro Sciences, Bangalore, India. Y1 - 1992/11/13/ PY - 1992 DA - 1992 Nov 13 SP - 256 EP - 262 VL - 595 IS - 2 SN - 0006-8993, 0006-8993 KW - Disulfides KW - 0 KW - Fluorescent Dyes KW - Malondialdehyde KW - 4Y8F71G49Q KW - Glutathione KW - GAN16C9B8O KW - Haloperidol KW - J6292F8L3D KW - Index Medicus KW - Animals KW - Cerebral Cortex -- drug effects KW - Cerebral Cortex -- metabolism KW - Corpus Striatum -- metabolism KW - Glutathione -- metabolism KW - Lipid Peroxidation -- drug effects KW - Disulfides -- metabolism KW - Homeostasis -- drug effects KW - Rats KW - Malondialdehyde -- metabolism KW - Oxidation-Reduction KW - Rats, Sprague-Dawley KW - Corpus Striatum -- drug effects KW - Stress, Physiological -- metabolism KW - Haloperidol -- pharmacology KW - Haloperidol -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73397788?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research&rft.atitle=Oxidative+stress+induced+by+administration+of+the+neuroleptic+drug+haloperidol+is+attenuated+by+higher+doses+of+haloperidol.&rft.au=Shivakumar%2C+B+R%3BRavindranath%2C+V&rft.aulast=Shivakumar&rft.aufirst=B&rft.date=1992-11-13&rft.volume=595&rft.issue=2&rft.spage=256&rft.isbn=&rft.btitle=&rft.title=Brain+research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-26 N1 - Date created - 1993-01-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Structural features of substituted purine derivatives compatible with depletion of human O6-alkylguanine-DNA alkyltransferase. AN - 73351962; 1447749 AB - A series of O6- and S6-substituted purine derivatives were tested for their ability to deplete the human DNA repair protein O6-alkylguanine-DNA alkyltransferase (AGT) in cell-free extracts from HT29 colon tumor cells and intact HT29 cells. The order of potency was O6-(p-Y-benzyl)-guanine (Y = H, F, Cl, and CH3) > O6-benzyl-2'-deoxyguanosine > O6-(p-Y-benzyl)guanosine (Y = H, Cl, and CH3) > or = a series of 9-substituted O6-benzylguanine derivatives > or = O6-allylguanine > O6-benzylhypoxanthine > O6-methylguanine. A series of 7-substituted O6-benzylguanine derivatives, 2-amino-6-(p-Y-benzylthio)purine (Y = H, CH3), 2-amino-6-[(p-nitrobenzyl)thio]-9-beta-D-ribofuranosylpurine, and 7-benzylguanine were inactive. It is concluded that for efficient AGT depletion, an allyl or benzyl group attached through exocyclic oxygen at position 6 of a 2-aminopurine derivative is required. Activity is preserved with a variety of substituent groups attached to position 9 while substitution at position 7 leads to a complete loss of activity. JF - Journal of medicinal chemistry AU - Moschel, R C AU - McDougall, M G AU - Dolan, M E AU - Stine, L AU - Pegg, A E AD - Chemistry of Carcinogenesis Laboratory, ABL-Basic Research Program, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland 21702. Y1 - 1992/11/13/ PY - 1992 DA - 1992 Nov 13 SP - 4486 EP - 4491 VL - 35 IS - 23 SN - 0022-2623, 0022-2623 KW - Purines KW - 0 KW - Methyltransferases KW - EC 2.1.1.- KW - O(6)-Methylguanine-DNA Methyltransferase KW - EC 2.1.1.63 KW - Index Medicus KW - Tumor Cells, Cultured -- drug effects KW - Humans KW - Tumor Cells, Cultured -- enzymology KW - DNA Repair -- drug effects KW - Structure-Activity Relationship KW - Purines -- chemical synthesis KW - Purines -- pharmacology KW - Methyltransferases -- metabolism KW - Purines -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73351962?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+medicinal+chemistry&rft.atitle=Structural+features+of+substituted+purine+derivatives+compatible+with+depletion+of+human+O6-alkylguanine-DNA+alkyltransferase.&rft.au=Moschel%2C+R+C%3BMcDougall%2C+M+G%3BDolan%2C+M+E%3BStine%2C+L%3BPegg%2C+A+E&rft.aulast=Moschel&rft.aufirst=R&rft.date=1992-11-13&rft.volume=35&rft.issue=23&rft.spage=4486&rft.isbn=&rft.btitle=&rft.title=Journal+of+medicinal+chemistry&rft.issn=00222623&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-28 N1 - Date created - 1992-12-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Current serum levels of 2,3,7,8-tetrachlorodibenzo-p-dioxin in phenoxy acid herbicide applicators and characterization of historical levels. AN - 73327309; 1433346 AB - Workers who sprayed phenoxy acid herbicides, especially those who sprayed before 1975, may have been exposed to significant amounts of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a potent animal carcinogen present in herbicide preparations as a contaminant. The aims of this study were (a) to determine serum levels of TCDD in a representative sample of workers occupationally exposed to the agent during the spraying of phenoxy acid herbicides; (b) to compare serum levels in workers exposed before 1965, when concentrations in herbicide products were unregulated and high, with levels in workers exposed after 1974, when concentrations were lower as a result of government regulations worldwide; and (c) to examine the correlation, if any, between serum levels and duration of employment in spraying. Thirty-seven subjects were randomly selected from a group of 654 men who had sprayed the herbicides 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) and 2,4-dichlorophenoxyacetic acid (2,4-D) in Australia for at least 12 months. The workers were classified as follows: eight who sprayed only before 1965, nine who sprayed only during the period after 1964 and before 1975, and 20 who sprayed during the period after 1974 and before 1991. Serum from the workers was analyzed for TCDD by high-resolution gas chromatography and high-resolution mass spectrometry at a detection limit of 0.6 parts per trillion (ppt) on a lipid-weight basis. In addition, rates of exposure to TCDD were estimated, as were TCDD serum concentrations at termination of employment and intensity of herbicide use. Only one worker, with a serum TCDD level of 34 ppt, had a serum level higher than the maximum level of 26 ppt reported for the general population. Assuming a half-life of 7.1 years, we estimated the mean exposure rates to be 2.7, 2.3, and 0.06 ppt/mo for the three epochs, respectively. We found the highest serum level of TCDD at the time of cessation of employment to be 329 ppt. Calendar period and intensity of use of 2,4,5-T and 2,4-D were statistically significant determinants of rate of exposure to TCDD, but 2,4-D was associated with exposure rate only for the pre-1975 periods. Estimated rates prior to 1965 were more than an order of magnitude higher than those after 1974. The highest estimated exposure rate was 20.7 ppt/mo, which suggests that some sprayers may have been exposed to levels comparable with those that produce cancer in laboratory animals. JF - Journal of the National Cancer Institute AU - Johnson, E S AU - Parsons, W AU - Weinberg, C R AU - Shore, D L AU - Mathews, J AU - Patterson, D G AU - Needham, L L AD - Division of Biometry and Risk Assessment, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709. Y1 - 1992/11/04/ PY - 1992 DA - 1992 Nov 04 SP - 1648 EP - 1653 VL - 84 IS - 21 SN - 0027-8874, 0027-8874 KW - Herbicides KW - 0 KW - Polychlorinated Dibenzodioxins KW - 2,4-Dichlorophenoxyacetic Acid KW - 2577AQ9262 KW - 2,4,5-Trichlorophenoxyacetic Acid KW - 9Q963S4YMX KW - Index Medicus KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Time Factors KW - Male KW - Occupational Exposure KW - Agriculture KW - Herbicides -- chemistry KW - Polychlorinated Dibenzodioxins -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73327309?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Current+serum+levels+of+2%2C3%2C7%2C8-tetrachlorodibenzo-p-dioxin+in+phenoxy+acid+herbicide+applicators+and+characterization+of+historical+levels.&rft.au=Johnson%2C+E+S%3BParsons%2C+W%3BWeinberg%2C+C+R%3BShore%2C+D+L%3BMathews%2C+J%3BPatterson%2C+D+G%3BNeedham%2C+L+L&rft.aulast=Johnson&rft.aufirst=E&rft.date=1992-11-04&rft.volume=84&rft.issue=21&rft.spage=1648&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-27 N1 - Date created - 1992-11-27 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: J Natl Cancer Inst. 1994 Jun 1;86(11):866-8 [8182768] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutations of p53 gene in hepatocellular carcinoma: roles of hepatitis B virus and aflatoxin contamination in the diet. AN - 73292255; 1279184 AB - Mutations of the p53 tumor suppressor gene have been reported in 50% of patients with hepatocellular carcinoma (HCC) from China and South Africa. These reports suggested an association of p53 mutations with high levels of aflatoxin in the diet. Most studies of p53 and HCC, however, have not fully evaluated the possible role of the hepatitis B virus (HBV). Aflatoxin is a substance produced by food mold that is known to cause HCC in experimental animals. The purpose of this study was to evaluate the relationship of p53 gene mutation to high or low levels of aflatoxin in the diet and to HBV infection. p53 protein and hepatitis B surface antigen (HBsAg) were evaluated by immunohistochemistry using the avidin-biotin-peroxidase system in paraffin-embedded specimens of HCC and of adjacent nontumorous liver tissue from 43 patients. Tissue specimens from three normal human livers were also evaluated. HCCs and adjacent nontumorous liver tissues were obtained from 23 patients from Qidong, China, where aflatoxin levels in the diet are high, and from 20 patients from two regions in the United States (patients from the National Institutes of Health, Bethesda, Md., and Kuakini Medical Center, Honolulu, Hawaii), where aflatoxin levels in the diet are low. Mutant p53 protein was detected in the nuclei of HCCs from 14 (61%) of 23 patients from China and from three (30%) of 10 patients and six (60%) of 10 patients, respectively, from the two regions of the United States. A statistically significant association between detection of mutant p53 protein in HCC cells and the detection of HBsAg in hepatocytes of the adjacent nontumorous liver tissue was observed in patients from China and the United States considered together. Mutations of the tumor suppressor gene p53 in hepatocellular carcinomas are not limited to patients from geographic regions where the ingestion of aflatoxin is high. In many patients, these mutations may be associated with HBV infection. The possible interaction of chronic HBV infection and p53 gene mutation, suggested by these data, indicates a mechanism by which HBV infection beginning early in life could contribute to the subsequent development of HCC. JF - Journal of the National Cancer Institute AU - Hsia, C C AU - Kleiner, D E AU - Axiotis, C A AU - Di Bisceglie, A AU - Nomura, A M AU - Stemmermann, G N AU - Tabor, E AD - Division of Cancer Etiology, National Cancer Institute, National Institutes of Health, Bethesda, Md 20892. Y1 - 1992/11/04/ PY - 1992 DA - 1992 Nov 04 SP - 1638 EP - 1641 VL - 84 IS - 21 SN - 0027-8874, 0027-8874 KW - Aflatoxins KW - 0 KW - Hepatitis B Surface Antigens KW - Tumor Suppressor Protein p53 KW - Index Medicus KW - Hepatitis B Surface Antigens -- analysis KW - Humans KW - Hawaii -- epidemiology KW - Cell Nucleus -- chemistry KW - Hepatitis B -- genetics KW - Aged KW - Cytoplasm -- chemistry KW - Tumor Suppressor Protein p53 -- analysis KW - Hepatitis B -- complications KW - China -- epidemiology KW - Adult KW - Food Contamination KW - Middle Aged KW - United States -- epidemiology KW - Staining and Labeling KW - Mutation KW - Immunohistochemistry KW - Male KW - Female KW - Hepatitis B -- epidemiology KW - Cocarcinogenesis KW - Genes, p53 -- drug effects KW - Carcinoma, Hepatocellular -- etiology KW - Carcinoma, Hepatocellular -- genetics KW - Genes, p53 -- genetics KW - Liver Neoplasms -- epidemiology KW - Hepatitis B virus -- physiology KW - Aflatoxins -- toxicity KW - Liver Neoplasms -- etiology KW - Carcinoma, Hepatocellular -- epidemiology KW - Liver Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73292255?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Mutations+of+p53+gene+in+hepatocellular+carcinoma%3A+roles+of+hepatitis+B+virus+and+aflatoxin+contamination+in+the+diet.&rft.au=Hsia%2C+C+C%3BKleiner%2C+D+E%3BAxiotis%2C+C+A%3BDi+Bisceglie%2C+A%3BNomura%2C+A+M%3BStemmermann%2C+G+N%3BTabor%2C+E&rft.aulast=Hsia&rft.aufirst=C&rft.date=1992-11-04&rft.volume=84&rft.issue=21&rft.spage=1638&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-27 N1 - Date created - 1992-11-27 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: J Natl Cancer Inst. 1992 Nov 4;84(21):1619-20 [1331479] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - ras oncogene activation and occupational exposures in acute myeloid leukemia. AN - 73276129; 1433344 AB - Epidemiologic studies of acute myeloid leukemias (AMLs) show small increases in risk of disease associated with certain occupations and chemical exposures. This study was designed to determine whether the presence of mutationally activated ras oncogenes in AML are associated with occupational and chemical exposures. We interviewed 62 patients with newly diagnosed AML (or their next-of-kin), all of whom were enrolled in a national multicenter clinical trial, and 630 healthy control subjects. DNA extracted from patients' pretreatment bone marrow samples was amplified by using the polymerase chain reaction and probed with allele-specific oligonucleotides for activating point mutations at the 12th, 13th, and 61st codons of three protooncogenes: H-ras (also known as HRAS), K-ras (also known as KRAS2), and N-ras (also known as NRAS). Patients with ras mutation-positive AML had a higher frequency (six of 10 patients) of working 5 or more years in an a priori high-risk occupation than did patients with ras mutation-negative AML (eight of 52; odds ratio [OR] = 6.8; 95% confidence interval [CI] = 1.3-36). Patients with ras mutation-positive AML were more likely than patients with ras mutation-negative AML to have breathed chemical vapor on the job (OR = 9.1; 95% CI = 1.3-64) or to have had skin contact with chemicals (OR = 6.9; 95% CI = 1.3-37). When ras-positive patients were compared with healthy control subjects, the ORs for occupation and occupational exposures remained elevated, while patients with ras mutation-negative AML showed no increased risk when compared with control subjects. Activation of ras proto-oncogenes may identify an etiologic subgroup of AML caused by occupation and chemical exposure. Disease etiology may be better understood if epidemiologic measures of exposure are integrated with molecular assays of the genetic defects responsible for cancer initiation and promotion. JF - Journal of the National Cancer Institute AU - Taylor, J A AU - Sandler, D P AU - Bloomfield, C D AU - Shore, D L AU - Ball, E D AU - Neubauer, A AU - McIntyre, O R AU - Liu, E AD - Environmental and Molecular Epidemiology Section, National Institute of Environmental Health Sciences, Research Triangle Park, N.C. 27709. Y1 - 1992/11/04/ PY - 1992 DA - 1992 Nov 04 SP - 1626 EP - 1632 VL - 84 IS - 21 SN - 0027-8874, 0027-8874 KW - H-ras KW - HRAS KW - K-ras KW - KRAS KW - N-ras KW - NRAS KW - Codon KW - 0 KW - Index Medicus KW - Acute Disease KW - Leukemia, Myelomonocytic, Acute -- chemically induced KW - Codon -- genetics KW - Leukemia, Erythroblastic, Acute -- chemically induced KW - Leukemia, Myelomonocytic, Acute -- epidemiology KW - Humans KW - Leukemia, Erythroblastic, Acute -- epidemiology KW - Leukemia, Myeloid, Acute -- chemically induced KW - Leukemia, Myelomonocytic, Acute -- genetics KW - Aged KW - Leukemia, Monocytic, Acute -- genetics KW - Codon -- drug effects KW - Leukemia, Monocytic, Acute -- chemically induced KW - Leukemia, Myeloid, Acute -- genetics KW - Leukemia, Myeloid, Acute -- epidemiology KW - Adult KW - Case-Control Studies KW - Leukemia, Erythroblastic, Acute -- genetics KW - Leukemia, Monocytic, Acute -- epidemiology KW - Middle Aged KW - Mutation KW - Male KW - Female KW - Occupational Exposure KW - Leukemia, Myeloid -- chemically induced KW - Leukemia, Myeloid -- epidemiology KW - Genes, ras -- genetics KW - Genes, ras -- drug effects KW - Leukemia, Myeloid -- genetics KW - Gene Expression Regulation, Leukemic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73276129?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=ras+oncogene+activation+and+occupational+exposures+in+acute+myeloid+leukemia.&rft.au=Taylor%2C+J+A%3BSandler%2C+D+P%3BBloomfield%2C+C+D%3BShore%2C+D+L%3BBall%2C+E+D%3BNeubauer%2C+A%3BMcIntyre%2C+O+R%3BLiu%2C+E&rft.aulast=Taylor&rft.aufirst=J&rft.date=1992-11-04&rft.volume=84&rft.issue=21&rft.spage=1626&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-27 N1 - Date created - 1992-11-27 N1 - Date revised - 2017-01-13 N1 - Gene symbol - H-ras; HRAS; K-ras; KRAS; N-ras; NRAS N1 - SuppNotes - Comment In: J Natl Cancer Inst. 1992 Nov 4;84(21):1614-5 [1433339] J Natl Cancer Inst. 1993 Jun 2;85(11):920-1 [8492321] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Idazoxan down-regulates beta-adrenoceptors on C6 glioma cells in vitro. AN - 73406660; 1361912 AB - Incubation of the C6 cells with 10 microM idazoxan (an alpha 2-adrenoceptor antagonist and putative antidepressant) for 5 days in vitro resulted in a 23% reduction of beta-adrenoceptor number and a 37% decrease in isoproterenol-induced cyclic AMP accumulation. In contrast, post-receptor stimulated cyclic AMP accumulation (by the use of forskolin or cholera toxin) was unaffected. The desensitization of the beta-adrenoceptor was accompanied by an increase in the KL/KH ratio for this receptor. Chronic in vitro treatment of C6 glioma cells with idazoxan did not significantly affect cholera or pertussis toxin catalyzed ribosylation of Gs and Gi/Go in these cells. Similarly, idazoxan did not alter either the basal levels of protein kinase C (PKC) alpha, or its cytoplasm to membrane translocation. These results suggest that idazoxan may have direct postsynaptic effects, the site of which may be at the level of receptor/G protein interaction. JF - European journal of pharmacology AU - Manji, H K AU - Chen, G AU - Bitran, J A AU - Gusovsky, F AU - Potter, W Z AD - Section on Clinical Pharmacology, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1992/11/02/ PY - 1992 DA - 1992 Nov 02 SP - 275 EP - 282 VL - 227 IS - 3 SN - 0014-2999, 0014-2999 KW - Adrenergic alpha-Antagonists KW - 0 KW - Dioxanes KW - Receptors, Adrenergic, beta KW - Colforsin KW - 1F7A44V6OU KW - Cholera Toxin KW - 9012-63-9 KW - Cyclic AMP KW - E0399OZS9N KW - Protein Kinase C KW - EC 2.7.11.13 KW - Isoproterenol KW - L628TT009W KW - Idazoxan KW - Y310PA316B KW - Index Medicus KW - Rats KW - Protein Kinase C -- metabolism KW - Animals KW - Colforsin -- pharmacology KW - Tumor Cells, Cultured -- metabolism KW - Down-Regulation KW - Cyclic AMP -- metabolism KW - Cholera Toxin -- pharmacology KW - Glioma -- metabolism KW - Autoradiography KW - Isoproterenol -- pharmacology KW - Receptors, Adrenergic, beta -- metabolism KW - Receptors, Adrenergic, beta -- drug effects KW - Dioxanes -- pharmacology KW - Adrenergic alpha-Antagonists -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73406660?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+pharmacology&rft.atitle=Idazoxan+down-regulates+beta-adrenoceptors+on+C6+glioma+cells+in+vitro.&rft.au=Manji%2C+H+K%3BChen%2C+G%3BBitran%2C+J+A%3BGusovsky%2C+F%3BPotter%2C+W+Z&rft.aulast=Manji&rft.aufirst=H&rft.date=1992-11-02&rft.volume=227&rft.issue=3&rft.spage=275&rft.isbn=&rft.btitle=&rft.title=European+journal+of+pharmacology&rft.issn=00142999&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-01 N1 - Date created - 1993-02-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phase I and II study of high-dose ifosfamide, carboplatin, and etoposide with autologous bone marrow rescue in lymphomas and solid tumors. AN - 85272716; pmid-1403054 AB - PURPOSE: High-dose chemotherapy produces durable disease-free remissions in a minority of patients with resistant lymphomas and solid tumors. In an attempt to improve on the available regimens, ifosfamide, carboplatin, and etoposide (ICE) were selected for a new high-dose regimen because of their favorable spectrum of nonhematopoietic toxicity and evidence of synergy in in vitro systems. PATIENTS AND METHODS: Forty-one patients with drug-resistant Hodgkin's and non-Hodgkin's lymphomas, and breast and testicular cancers were entered onto a phase I and II trial of a single course of ICE with autologous bone marrow rescue. Before transplantation, all patients received combination chemotherapy until maximal tumor response was achieved. RESULTS: Patients received total doses of ifosfamide from 10 to 18 g/m2, carboplatin from 0.9 to 1.98 g/m2, and etoposide from 0.6 to 1.5 g/m2 administered during a 4-day period, with a maximum-tolerated dose (MTD) of ifosfamide 16 g/m2, carboplatin 1.8 g/m2, and etoposide 1.5 g/m2. The dose-limiting toxicities included irreversible renal, cardiac, and CNS dysfunction. There were three toxic deaths (7%), and all occurred above the MTD. Thirteen patients who were treated at the MTD tolerated the regimen well; reversible renal dysfunction and grade 2 mucositis commonly were observed. Of 23 heavily pretreated patients with persistent disease at the time of transplant, 10 (43%) achieved complete remissions (CRs) and 11 (48%) achieved partial remissions (PRs). Hodgkin's and non-Hodgkin's lymphoma patients who were treated at or below the MTD had a median potential follow-up of 11.9 months, and 12-month progression-free survivals of 62% and 48%, respectively. CONCLUSION: High-dose ICE with bone marrow rescue was well tolerated with a high response rate, and should be considered for further testing. JF - Journal of Clinical Oncology AU - Wilson, W H AU - Jain, V AU - Bryant, G AU - Cowan, K H AU - Carter, C AU - Cottler-Fox, M AU - Goldspiel, B AU - Steinberg, S M AU - Longo, D L AU - Wittes R E AD - Medicine Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. PY - 1992 SP - 1712 EP - 1722 VL - 10 IS - 11 SN - 0732-183X, 0732-183X KW - Drug Administration Schedule KW - Combined Modality Therapy KW - Human KW - Aged KW - Carboplatin KW - Transplantation, Autologous KW - Neoplasms KW - Ifosfamide KW - Adult KW - Antineoplastic Combined Chemotherapy Protocols KW - Middle Age KW - Lymphoma KW - Etoposide KW - Male KW - Female KW - Survival Analysis KW - Bone Marrow Transplantation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85272716?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Clinical+Oncology&rft.atitle=Phase+I+and+II+study+of+high-dose+ifosfamide%2C+carboplatin%2C+and+etoposide+with+autologous+bone+marrow+rescue+in+lymphomas+and+solid+tumors.&rft.au=Wilson%2C+W+H%3BJain%2C+V%3BBryant%2C+G%3BCowan%2C+K+H%3BCarter%2C+C%3BCottler-Fox%2C+M%3BGoldspiel%2C+B%3BSteinberg%2C+S+M%3BLongo%2C+D+L%3BWittes+R+E&rft.aulast=Wilson&rft.aufirst=W&rft.date=1992-11-01&rft.volume=10&rft.issue=11&rft.spage=1712&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Oncology&rft.issn=0732183X&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Saccade-vergence interactions in humans. AN - 85239336; pmid-1479435 AB - 1. We recorded eye movements in four normal human subjects during refixations between targets calling for various combinations of saccades and vergence. We confirmed and extended prior observations of 1) transient changes in horizontal ocular alignment during both pure horizontal saccades (relative divergence followed by relative convergence) and pure vertical saccades (usually divergence for upward and convergence for downward saccades); 2) occasional, high-frequency (20-25 Hz), conjugate oscillations along the axis orthogonal to the main saccade; and 3) the speeding up of horizontal vergence by both horizontal and vertical saccades. 2. To interpret these findings, we developed a hypothesis for the generation of vergence to step changes in target depth, both with and without associated saccades. The essential features of this hypothesis are 1) the transient changes in horizontal ocular alignment during pure horizontal saccades reflect asymmetries in the mechanical properties of the lateral and medial rectus muscles causing adduction to lag abduction; 2) pure vergence movements in response to step changes in target depth are generated by a neural network that uses a desired change in vergence position as its input command and instantaneous vergence motor error (the difference between the desired change and the actual change in vergence) to drive vergence premoter neurons; and 3) the facilitation of horizontal vergence by saccades arises from nonlinear interactions in central premotor circuits. 3. The hypothetical network for generating pure vergence to step changes in target depth is analogous in structure to the local feedback model for the generation of saccades and has the same conceptual appeal. With the assumption of a single nonlinearity describing the relationship between a vergence motor error signal and the output of the neurons that generate promoter vergence velocity commands, this model generates pure vergence movements with peak velocity-amplitude relationships and trajectories that closely match those of experimental data. 4. Several types of models are proposed for the central, nonlinear interaction that occurs when saccades and vergence are combined. Common to all models is the idea that omnidirectional pause neurons (OPN), which are thought to gate activity for saccade burst neurons, also gate activity for saccade-related vergence. In one model we hypothesize the existence of a separate class of saccade-related vergence burst neurons, which generate premotor horizontal vergence commands but only during saccades. In a second model we hypothesize separate right eye and left eye saccadic burst neurons that receive not only conjugate, but also equal but oppositely directed vergence error signals.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Journal of Neurophysiology AU - Zee, D S AU - Fitzgibbon, E J AU - Optican, L M AD - Laboratory of Sensorimotor Research, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892. PY - 1992 SP - 1624 EP - 1641 VL - 68 IS - 5 SN - 0022-3077, 0022-3077 KW - Photic Stimulation KW - Convergence, Ocular KW - Support, U.S. Gov't, P.H.S. KW - Human KW - Neurons KW - Adult KW - Brain Stem KW - Middle Age KW - Feedback KW - Models, Neurological KW - Saccades UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85239336?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Neurophysiology&rft.atitle=Saccade-vergence+interactions+in+humans.&rft.au=Zee%2C+D+S%3BFitzgibbon%2C+E+J%3BOptican%2C+L+M&rft.aulast=Zee&rft.aufirst=D&rft.date=1992-11-01&rft.volume=68&rft.issue=5&rft.spage=1624&rft.isbn=&rft.btitle=&rft.title=Journal+of+Neurophysiology&rft.issn=00223077&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - An evaluation of laryngeal muscle activation in patients with voice tremor. AN - 85211845; pmid-1437206 AB - Eight patients with voice tremor were studied to characterize laryngeal muscle involvement. Electromyographic (EMG) recordings were made from intrinsic laryngeal muscles, simultaneously with some extrinsic laryngeal muscles, respiratory movement, and voice recordings during respiration, whisper, and phonation. Spectral measures were used to determine the tremor frequency and the prominence of spectral peaks in the EMG, respiratory and acoustic signals, while correlation coefficients were computed between pairs of tremulous EMG signals to measure the synchrony of tremor between muscles. The intrinsic laryngeal muscles were tremulous during respiration and speech, with the thyroarytenoid most often involved. Tremor was also detected in some of the extrinsic muscle recordings and the percentage of muscles with tremor was higher during phonation than during whisper or respiration. Time delays were found between tremor oscillations in laryngeal muscles. Because the thyroarytenoid was affected in all the patients studied, botulinum toxin injections may be beneficial in treatment of this voice disorder. JF - Otolaryngology--Head and Neck Surgery AU - Koda, J AU - Ludlow, C L AD - Voice and Speech Section, National Institute on Deafness and Other Communication Disorders, Bethesda, MD 20892. PY - 1992 SP - 684 EP - 696 VL - 107 IS - 5 SN - 0194-5998, 0194-5998 KW - Laryngeal Muscles KW - Speech Acoustics KW - Human KW - Electromyography KW - Sound Spectrography KW - Aged KW - Middle Age KW - Muscle Contraction KW - Voice Disorders KW - Tremor KW - Female UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85211845?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Otolaryngology--Head+and+Neck+Surgery&rft.atitle=An+evaluation+of+laryngeal+muscle+activation+in+patients+with+voice+tremor.&rft.au=Koda%2C+J%3BLudlow%2C+C+L&rft.aulast=Koda&rft.aufirst=J&rft.date=1992-11-01&rft.volume=107&rft.issue=5&rft.spage=684&rft.isbn=&rft.btitle=&rft.title=Otolaryngology--Head+and+Neck+Surgery&rft.issn=01945998&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Metabolism of the food mutagen 2-amino-3-methylimidazo[4,5-f]quinoline in nonhuman primates undergoing carcinogen bioassay. AN - 73510962; 1489936 AB - 2-Amino-3-methylimidazo[4.5-f]quinoline (IQ) is a potent bacterial mutagen and rodent carcinogen which also produces hepatocellular carcinoma in monkeys. The metabolism and disposition of this procarcinogen were investigated in monkeys undergoing carcinogen bioassay and in monkeys given an acute dose of IQ. Analysis of urine, feces, and bile revealed that IQ was extensively metabolized. A number of metabolites in urine were purified by high-performance liquid chromatography and characterized by 1H NMR and mass spectroscopy. Metabolites resulted from cytochrome P450-mediated ring oxidation at the C-5 position or N-demethylation. These metabolites could be further transformed by conjugation to sulfate or beta-glucuronic acid. Glucuronidation and sulfamate formation at the exocyclic amine group were other major routes of metabolism. Enteric bacteria also contributed to IQ biotransformation by forming the 7-oxo derivatives of IQ and N-demethyl-IQ. The metastable N2-glucuronide conjugate of the carcinogenic metabolite, 2-(hydroxyamino)-3-methylimidazo[4,5-f]quinoline, was found in urine. This indicates that metabolic activation through cytochrome P450-mediated N-oxidation occurs in vivo and that glucuronidation is a means of transport of the carcinogenic metabolite to extrahepatic tissues. JF - Chemical research in toxicology AU - Snyderwine, E G AU - Welti, D H AU - Fay, L B AU - Würzner, H P AU - Turesky, R J AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. PY - 1992 SP - 843 EP - 851 VL - 5 IS - 6 SN - 0893-228X, 0893-228X KW - Mutagens KW - 0 KW - Quinolines KW - 2-amino-3-methylimidazo(4,5-f)quinoline KW - 30GL3D3T0G KW - Index Medicus KW - Bile -- chemistry KW - Animals KW - Mass Spectrometry KW - Macaca fascicularis KW - Spectrophotometry, Ultraviolet KW - Salmonella typhimurium -- drug effects KW - Feces -- chemistry KW - Magnetic Resonance Spectroscopy KW - Oxidation-Reduction KW - Rats KW - Mutagenicity Tests KW - Macaca mulatta KW - Salmonella typhimurium -- genetics KW - Female KW - Male KW - Quinolines -- toxicity KW - Quinolines -- metabolism KW - Mutagens -- metabolism KW - Food Contamination -- analysis KW - Mutagens -- toxicity KW - Mutagens -- pharmacokinetics KW - Quinolines -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73510962?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+research+in+toxicology&rft.atitle=Metabolism+of+the+food+mutagen+2-amino-3-methylimidazo%5B4%2C5-f%5Dquinoline+in+nonhuman+primates+undergoing+carcinogen+bioassay.&rft.au=Snyderwine%2C+E+G%3BWelti%2C+D+H%3BFay%2C+L+B%3BW%C3%BCrzner%2C+H+P%3BTuresky%2C+R+J&rft.aulast=Snyderwine&rft.aufirst=E&rft.date=1992-11-01&rft.volume=5&rft.issue=6&rft.spage=843&rft.isbn=&rft.btitle=&rft.title=Chemical+research+in+toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-04 N1 - Date created - 1993-03-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dose selection for animal carcinogenicity studies: a practitioner's perspective. AN - 73510804; 1489921 JF - Chemical research in toxicology AU - Griesemer, R A AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. PY - 1992 SP - 737 EP - 741 VL - 5 IS - 6 SN - 0893-228X, 0893-228X KW - Carcinogens KW - 0 KW - Index Medicus KW - Animals KW - Humans KW - Species Specificity KW - Carcinogens -- toxicity KW - Carcinogenicity Tests UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73510804?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+research+in+toxicology&rft.atitle=Dose+selection+for+animal+carcinogenicity+studies%3A+a+practitioner%27s+perspective.&rft.au=Griesemer%2C+R+A&rft.aulast=Griesemer&rft.aufirst=R&rft.date=1992-11-01&rft.volume=5&rft.issue=6&rft.spage=737&rft.isbn=&rft.btitle=&rft.title=Chemical+research+in+toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-04 N1 - Date created - 1993-03-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Chem Res Toxicol. 1992 Nov-Dec;5(6):735-6 [1489920] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Relationship of H-ras-1, L-myc, and p53 polymorphisms with lung cancer risk and prognosis. AN - 73502131; 1486864 AB - Proto-oncogenes (H-ras-1 and L-myc) and tumor-suppressor gene (p53) loci have been implicated in lung carcinogenesis. DNA restriction fragment length polymorphisms at these gene loci are being evaluated in a case-control study as markers predictive of risk for cancer or of prognosis when cancer is present. The cases and controls had a cigarette-smoking history of 40 or more pack years or other abnormalities in pulmonary function tests, their ages were closely matched (64 years for cases and 61 years for controls) and the ratio of Caucasians to African Americans was close to unity (cases, 0.95:1.00, controls, 1.00:0.88). The H-ras-1 gene contains an insertion deletion polymorphism. Inheritance of rare H-ras-1 alleles, defined by MspI digestion, confers a relative risk for lung cancer of 2.0 (95% confidence interval, 0.5-7.3) for Caucasians and 3.2 (0.9-11.6) for African Americans (74 cases, 67 controls). The L-myc gene sequence has a restriction site (EcoR1) polymorphism between the second and third exons. Inheritance of restriction site-present alleles was reported to confer poor prognosis (presence of lymph node metastases) in Japanese lung cancer patients. This hypothesis was tested in both case-control study subjects (56 cases, 55 controls) and additional surgical cases (40), but no evidence was found to support the hypothesis in the U.S. population. The p53 gene is a tumor-suppressor gene that can encode either a proline or an arginine in the 72nd residue. No associations was found between the minor allele (proline) and diagnosis of lung cancer (76 cases, 68 controls).(ABSTRACT TRUNCATED AT 250 WORDS) JF - Environmental health perspectives AU - Weston, A AU - Caporaso, N E AU - Perrin, L S AU - Sugimura, H AU - Tamai, S AU - Krontiris, T G AU - Trump, B F AU - Hoover, R N AU - Harris, C C AD - Laboratory of Human Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 61 EP - 67 VL - 98 SN - 0091-6765, 0091-6765 KW - H-ras-1 KW - L-myc KW - p53 KW - Biomarkers, Tumor KW - 0 KW - Index Medicus KW - Smoking KW - Base Sequence KW - African Continental Ancestry Group -- genetics KW - Risk Factors KW - Humans KW - Prognosis KW - Molecular Sequence Data KW - Case-Control Studies KW - United States -- ethnology KW - European Continental Ancestry Group -- genetics KW - Biomarkers, Tumor -- genetics KW - Genes, ras -- genetics KW - Polymorphism, Genetic -- genetics KW - Genes, p53 -- genetics KW - Lung Neoplasms -- genetics KW - Genes, myc -- genetics KW - Lung Neoplasms -- ethnology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73502131?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Relationship+of+H-ras-1%2C+L-myc%2C+and+p53+polymorphisms+with+lung+cancer+risk+and+prognosis.&rft.au=Weston%2C+A%3BCaporaso%2C+N+E%3BPerrin%2C+L+S%3BSugimura%2C+H%3BTamai%2C+S%3BKrontiris%2C+T+G%3BTrump%2C+B+F%3BHoover%2C+R+N%3BHarris%2C+C+C&rft.aulast=Weston&rft.aufirst=A&rft.date=1992-11-01&rft.volume=98&rft.issue=&rft.spage=61&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-24 N1 - Date created - 1993-02-24 N1 - Date revised - 2017-01-13 N1 - Gene symbol - H-ras-1; L-myc; p53 N1 - SuppNotes - Cited By: Mol Cell Biol. 1987 Feb;7(2):961-3 [3547088] J Natl Cancer Inst. 1986 Sep;77(3):697-701 [3462411] Mol Carcinog. 1991;4(4):265-8 [1714739] Br J Cancer. 1990 Jun;61(6):809-12 [1973618] Birth Defects Orig Artic Ser. 1990;26(1):129-40 [2224075] Cancer Res. 1990 Mar 15;50(6):1857-62 [2407346] Proc Natl Acad Sci U S A. 1989 Jul;86(13):5099-103 [2567993] Oncogene. 1989 Jul;4(7):923-8 [2666911] Jpn J Cancer Res. 1988 Jun;79(6):674-6 [2900827] Am J Hum Genet. 1988 Apr;42(4):615-7 [3279763] J Cell Physiol Suppl. 1987;Suppl 5:75-81 [3316256] Am J Hum Genet. 1980 May;32(3):314-31 [6247908] Ann Intern Med. 1980 Jun;92(6):809-25 [6992681] J Natl Cancer Inst. 1990 Feb 7;82(3):238-9 [1967321] Int J Cancer. 1990 Jan 15;45(1):47-9 [1967596] Int J Cancer. 1990 Sep 15;46(3):411-5 [1975565] J Natl Cancer Inst. 1990 Aug 1;82(15):1264-72 [2374176] Nature. 1989 Dec 7;342(6250):705-8 [2531845] Int J Cancer. 1989 Mar 15;43(3):391-4 [2564378] Nature. 1985 Jan 31-Feb 6;313(6001):369-74 [2578622] Int J Cancer. 1987 Oct 15;40(4):474-8 [2889677] Proc Natl Acad Sci U S A. 1988 Apr;85(7):2353-6 [2895475] J Cell Biochem. 1986;30(4):319-29 [3011817] FEBS Lett. 1987 Jun 22;218(1):41-6 [3297784] Nature. 1984 Nov 8-14;312(5990):169-70 [6504125] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Quantitative two-dimensional gel electrophoresis analysis of human fibroblasts transformed by ras oncogenes. AN - 73501952; 1483428 AB - Quantitative two-dimensional gel electrophoresis was used to compare the cellular protein patterns of a normal foreskin-derived human fibroblasts cell line (LG1) and three immortal derivatives of LG1. One derivative, designated MSU-1.1 VO, was selected for its ability to grow in the absence of serum and is non-tumorigenic in athymic mice. The other two strains were selected for focus-formation following transfection with either Ha-ras or N-ras oncogenes and form high grade malignant tumors. Correspondence and cluster analysis provided a nonbiased estimate of the relative similarity of the different two-dimensional patterns. These techniques separated the gel patterns into three distinct classes: LG1, MSU-1.1 VO, and the ras transformed cell strains. The MSU-1.1 VO cells were more closely related to the parental LG1 than to the ras-transformed cells. The differences between the three classes were primarily quantitative in nature: 16% of the spots demonstrated statistically significant changes (P 2) in the rate of incorporation of radioactive amino acids. The patterns from the two ras-transformed cell strains were similar, and variations in the expression of proteins that occurred between the separate experiments obscured consistent differences between the Ha-ras and N-ras transformed cells. However, while only 9 out of 758 spots were classified as different (1%), correspondence analysis could consistently separate the two ras transformants. One of these spots was five times more intense in the Ha-ras transformed cells than the N-ras.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Electrophoresis AU - Miller, M J AU - Maher, V M AU - McCormick, J J AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-0037. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 862 EP - 870 VL - 13 IS - 11 SN - 0173-0835, 0173-0835 KW - Ha-ras KW - N-ras KW - Neoplasm Proteins KW - 0 KW - Proteins KW - Index Medicus KW - Humans KW - Electrophoresis, Gel, Two-Dimensional KW - Image Processing, Computer-Assisted KW - Fibroblasts -- metabolism KW - Genes, ras -- genetics KW - Cell Transformation, Neoplastic -- metabolism KW - Proteins -- analysis KW - Neoplasm Proteins -- analysis KW - Cell Transformation, Neoplastic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73501952?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Electrophoresis&rft.atitle=Quantitative+two-dimensional+gel+electrophoresis+analysis+of+human+fibroblasts+transformed+by+ras+oncogenes.&rft.au=Miller%2C+M+J%3BMaher%2C+V+M%3BMcCormick%2C+J+J&rft.aulast=Miller&rft.aufirst=M&rft.date=1992-11-01&rft.volume=13&rft.issue=11&rft.spage=862&rft.isbn=&rft.btitle=&rft.title=Electrophoresis&rft.issn=01730835&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-17 N1 - Date created - 1993-02-17 N1 - Date revised - 2017-01-13 N1 - Gene symbol - Ha-ras; N-ras N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chemoprevention of skin cancer in xeroderma pigmentosum. AN - 73487201; 1293159 AB - Xeroderma pigmentosum is a rare recessive disease with sun sensitivity, increased freckling and defective DNA repair. Xeroderma pigmentosum patients have more than a 1000-fold increased risk of developing skin cancer including basal cell carcinoma, squamous cell carcinoma and melanoma. We studied chemoprevention of new skin cancers with oral retinoids in xeroderma pigmentosum patients who had multiple skin cancers. Xeroderma pigmentosum patients were cleared of all pre-existing tumors surgically and then treated with high dose (2 mg/kg/day) oral isotretinoin (13-cis retinoic acid, Accutane) for two years and then for one year off treatment. Patients were examined at regular intervals for new tumor formation and for side effects. Five xeroderma pigmentosum patients had a total of 121 basal or squamous cell carcinomas in 2 years before treatment and only 25 tumors during 2 years of treatment. The tumor frequency increased 8.5-fold after the drug was discontinued (New Engl J Med 318: 1633-1637, 1988). Toxicity (cutaneous, triglyceride, liver-function or skeletal abnormalities) prompted subsequent use of a low dose protocol. Patients were treated initially with 0.5 mg/kg/day oral isotretinoin and the dose was increased sequentially to 1.0 or 1.5 mg/kg/day. We found that toxicity was less with the lower doses. The lowest effective, least toxic dose varied among the xeroderma pigmentosum patients. JF - The Journal of dermatology AU - Kraemer, K H AU - DiGiovanna, J J AU - Peck, G L AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 715 EP - 718 VL - 19 IS - 11 SN - 0385-2407, 0385-2407 KW - Isotretinoin KW - EH28UP18IF KW - Index Medicus KW - Administration, Oral KW - Carcinoma, Basal Cell -- prevention & control KW - Humans KW - Carcinoma, Squamous Cell -- complications KW - Adult KW - Carcinoma, Squamous Cell -- prevention & control KW - Middle Aged KW - Child KW - Carcinoma, Basal Cell -- complications KW - Adolescent KW - Male KW - Female KW - Xeroderma Pigmentosum -- pathology KW - Isotretinoin -- administration & dosage KW - Isotretinoin -- adverse effects KW - Skin Neoplasms -- complications KW - Xeroderma Pigmentosum -- complications KW - Skin Neoplasms -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73487201?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+dermatology&rft.atitle=Chemoprevention+of+skin+cancer+in+xeroderma+pigmentosum.&rft.au=Kraemer%2C+K+H%3BDiGiovanna%2C+J+J%3BPeck%2C+G+L&rft.aulast=Kraemer&rft.aufirst=K&rft.date=1992-11-01&rft.volume=19&rft.issue=11&rft.spage=715&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+dermatology&rft.issn=03852407&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-05 N1 - Date created - 1993-04-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Calcium-independent K(+)-selective channel from chromaffin granule membranes. AN - 73472199; 1283986 AB - Intact adrenal chromaffin granules and purified granule membrane ghosts were allowed to fuse with acidic phospholipid planar bilayer membranes in the presence of Ca2+ (1 mM). From both preparations, we were able to detect a large conductance potassium channel (ca. 160 pS in symmetrical 400 mM K+), which was highly selective for K+ over Na+ (PK/PNa = 11) as estimated from the reversal potential of the channel current. Channel activity was unaffected by charybdotoxin, a blocker of the [Ca2+]-activated K+ channel of large conductance. Furthermore, this channel proved quite different from the previously described channels from other types of secretory vesicle preparations, not only in its selectivity and conductance, but also in its insensitivity to both calcium and potential across the bilayer. We conclude that the chromaffin granule membrane contains a K(+)-selective channel with large conductance. We suggest that the role of this channel may include ion movement during granule assembly or recycling, and do not rule out events leading to exocytosis. JF - The Journal of membrane biology AU - Arispe, N AU - Pollard, H B AU - Rojas, E AD - Laboratory of Cell Biology and Genetics, National Institutes of Health, NIDDK, Bethesda, Maryland 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 191 EP - 202 VL - 130 IS - 2 SN - 0022-2631, 0022-2631 KW - Catecholamines KW - 0 KW - Potassium Channels KW - Scorpion Venoms KW - Charybdotoxin KW - 115422-61-2 KW - Sodium KW - 9NEZ333N27 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Exocytosis -- physiology KW - Cell Fractionation KW - Animals KW - Scorpion Venoms -- pharmacology KW - Cattle KW - Catecholamines -- metabolism KW - Adrenal Medulla -- chemistry KW - Membrane Potentials -- physiology KW - Adrenal Medulla -- ultrastructure KW - Sodium -- pharmacology KW - Chromaffin Granules -- physiology KW - Chromaffin Granules -- ultrastructure KW - Chromaffin Granules -- chemistry KW - Intracellular Membranes -- chemistry KW - Calcium -- physiology KW - Potassium Channels -- physiology KW - Intracellular Membranes -- physiology KW - Potassium Channels -- ultrastructure KW - Potassium Channels -- drug effects KW - Intracellular Membranes -- ultrastructure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73472199?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+membrane+biology&rft.atitle=Calcium-independent+K%28%2B%29-selective+channel+from+chromaffin+granule+membranes.&rft.au=Arispe%2C+N%3BPollard%2C+H+B%3BRojas%2C+E&rft.aulast=Arispe&rft.aufirst=N&rft.date=1992-11-01&rft.volume=130&rft.issue=2&rft.spage=191&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+membrane+biology&rft.issn=00222631&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-26 N1 - Date created - 1993-03-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Integrated approach for evaluating species and interindividual differences in responsiveness to dioxins and structural analogs. AN - 73460655; 1336723 AB - 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a ubiquitous environmental contaminant that is produced inadvertently during the synthesis of some organochlorine compounds, such as the chlorinated phenoxy pesticides. It is biologically and ecologically persistent, with an estimated half-life of 7 years in humans. It possesses high acute toxicity in rodents and is a carcinogen, teratogen, and immunotoxin. In chronic bioassays for carcinogenicity, TCDD at a dose of 10 ng/kg/day increases the incidence of liver tumors in female rats, making it one of the most potent animal carcinogens ever tested. A recent study in humans has shown an increase in the incidence of respiratory tract tumors in workers in chlorinated phenoxy herbicide plants. Considerable controversy and uncertainty remain, however, concerning its carcinogenic potency in humans and the reliability of using animal data to predict human risks. It is generally accepted that most, if not all, of the effects of TCDD require its binding to the Ah receptor. In addition to its toxic effects, TCDD produces a number of biochemical effects, such as induction of CYP1A1, downregulation of binding activity of the estrogen and epidermal growth factor (EGF) receptors, and changes in cytokine pathways. These effects suggest that the Ah receptor plays an important role in regulating the cell cycle. A number of structural analogs of TCDD, such as the polychlorinated dibenzofurans, also interact with the Ah receptor, and they produce the same spectrum of responses as TCDD in animal and cell models. The potency of these compounds is strongly correlated with their binding affinity to the Ah receptor.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Environmental health perspectives AU - Clark, G AU - Tritscher, A AU - Bell, D AU - Lucier, G AD - Laboratory of Biochemical Risk Analysis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 125 EP - 132 VL - 98 SN - 0091-6765, 0091-6765 KW - Biomarkers, Tumor KW - 0 KW - Isoenzymes KW - Polychlorinated Dibenzodioxins KW - Receptors, Aryl Hydrocarbon KW - Receptors, Drug KW - Epidermal Growth Factor KW - 62229-50-9 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Aryl Hydrocarbon Hydroxylases KW - EC 1.14.14.1 KW - Index Medicus KW - Animals KW - Liver -- enzymology KW - Disease Susceptibility KW - Dose-Response Relationship, Drug KW - Humans KW - Mice KW - Biomarkers, Tumor -- metabolism KW - Rats KW - Risk KW - Rats, Sprague-Dawley KW - Lymphocytes -- enzymology KW - Female KW - Cricetinae KW - Polychlorinated Dibenzodioxins -- adverse effects KW - Cytochrome P-450 Enzyme System -- metabolism KW - Neoplasms, Experimental -- metabolism KW - Isoenzymes -- metabolism KW - Polychlorinated Dibenzodioxins -- metabolism KW - Polychlorinated Dibenzodioxins -- analogs & derivatives KW - Receptors, Drug -- metabolism KW - Aryl Hydrocarbon Hydroxylases -- metabolism KW - Neoplasms, Experimental -- chemically induced KW - Neoplasms -- chemically induced KW - Polychlorinated Dibenzodioxins -- administration & dosage KW - Epidermal Growth Factor -- metabolism KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73460655?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Integrated+approach+for+evaluating+species+and+interindividual+differences+in+responsiveness+to+dioxins+and+structural+analogs.&rft.au=Clark%2C+G%3BTritscher%2C+A%3BBell%2C+D%3BLucier%2C+G&rft.aulast=Clark&rft.aufirst=G&rft.date=1992-11-01&rft.volume=98&rft.issue=&rft.spage=125&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-24 N1 - Date created - 1993-02-24 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Arch Toxicol. 1991;65(3):213-9 [1905127] Mol Pharmacol. 1991 Apr;39(4):495-501 [1850092] Cell Biol Toxicol. 1991 Jan;7(1):67-94 [2054688] Proc Natl Acad Sci U S A. 1990 Jul;87(14):5288-92 [2371271] Fundam Appl Toxicol. 1990 Jul;15(1):186-200 [2373298] Toxicology. 1989 Sep;58(1):57-69 [2554534] Am J Epidemiol. 1989 Jun;129(6):1187-200 [2729256] J Biol Chem. 1986 May 15;261(14):6352-65 [3009454] Toxicol Appl Pharmacol. 1987 Jun 30;89(2):256-68 [3037728] Mol Pharmacol. 1986 Apr;29(4):372-7 [3486342] Life Sci. 1974 Nov 1;15(9):1585-95 [4549995] Cancer Res. 1973 Jul;33(7):1654-6 [4721228] Annu Rev Pharmacol Toxicol. 1982;22:517-54 [6282188] Biochem Biophys Res Commun. 1983 Sep 15;115(2):611-7 [6312985] Toxicol Appl Pharmacol. 1978 May;44(2):335-56 [675706] FEBS Lett. 1990 Apr 9;263(1):131-3 [1691986] Mol Pharmacol. 1991 Jan;39(1):13-9 [1846217] Mol Pharmacol. 1991 Mar;39(3):307-13 [1848654] Science. 1991 May 17;252(5008):954-8 [1852076] Eur J Biochem. 1991 May 8;197(3):577-82 [2029891] Annu Rev Pharmacol Toxicol. 1990;30:251-77 [2188570] Cancer Res. 1989 Dec 1;49(23):6503-11 [2510927] Am J Ind Med. 1989;16(4):455-74 [2558567] Environ Health Perspect. 1987 Dec;76:79-87 [2834196] J Immunol. 1988 Feb 1;140(3):928-35 [3257509] Arch Toxicol. 1985 Feb;56(4):230-5 [3922334] Cancer Res. 1980 Oct;40(10):3616-20 [6108157] Cancer Res. 1982 Dec;42(12):5030-7 [6291746] Mol Pharmacol. 1980 Jan;17(1):86-94 [7383021] Mutat Res. 1977-1978;47(3-4):141-60 [99649] Toxicol Appl Pharmacol. 1978 Nov;46(2):279-303 [734660] Cancer Res. 1991 Mar 1;51(5):1391-7 [1671757] Toxicol Appl Pharmacol. 1991 Mar 15;108(1):129-39 [1672475] Am J Hum Genet. 1991 Apr;48(4):720-5 [1707592] Biochem Pharmacol. 1991 Jan 1;41(1):85-92 [1846074] Science. 1991 Feb 8;251(4994):624-6 [1846976] Mutat Res. 1991 Apr;247(2):259-66 [2011143] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A comparison of xenon-133 and xenon-127 for the determination of regional cerebral blood flow measured by dynamic SPECT. AN - 73448551; 1484910 AB - Phantom studies and cerebral blood flow (CBF) measurements in 11 normal subjects at rest were performed by single photon emission tomography (SPECT) with Xe-133 (16 mm full-width at half-maximum [FWHM] collimation) and Xe-127 (16 mm, 12 mm, and 9 mm FWHM collimation). The phantom results clearly illustrated the feasibility of Xe-127 studies and the advantage of Xe-127 over Xe-133 for equivalent patient dose exposures. CBF values obtained with Xe-127 were comparable to those of Xe-133 for the 16 mm collimator, although higher flow values were found with the better resolution, probably because of reduced partial volume effects. The correlations between the various groups of examinations were high, except for the Xe-133 and Xe-127 16 mm collimator groups. Xe-127 allows a considerable increase in the resolution of the images, while exposing the patient to a lower radiation dose. Potential limitations because of higher energy penetrating photons from Xe-127 were not observed in this specially shielded equipment. JF - Psychiatry research AU - Coppola, R AU - Marenco, S AU - Jones, D W AU - Berman, K F AU - Weinberger, D R AD - Clinical Brain Disorders Branch, NIMH Neuroscience Center, St. Elizabeths, Washington, DC 20032. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 187 EP - 200 VL - 45 IS - 3 SN - 0165-1781, 0165-1781 KW - Xenon Radioisotopes KW - 0 KW - Index Medicus KW - Radiation Dosage KW - Reference Values KW - Blood Flow Velocity -- physiology KW - Humans KW - Adult KW - Adolescent KW - Regional Blood Flow -- physiology KW - Male KW - Female KW - Models, Anatomic KW - Tomography, Emission-Computed, Single-Photon -- methods KW - Brain -- blood supply UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73448551?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychiatry+research&rft.atitle=A+comparison+of+xenon-133+and+xenon-127+for+the+determination+of+regional+cerebral+blood+flow+measured+by+dynamic+SPECT.&rft.au=Coppola%2C+R%3BMarenco%2C+S%3BJones%2C+D+W%3BBerman%2C+K+F%3BWeinberger%2C+D+R&rft.aulast=Coppola&rft.aufirst=R&rft.date=1992-11-01&rft.volume=45&rft.issue=3&rft.spage=187&rft.isbn=&rft.btitle=&rft.title=Psychiatry+research&rft.issn=01651781&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-17 N1 - Date created - 1993-02-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of proto-oncogene activation in carcinogenesis. AN - 73447098; 1486840 AB - The accumulation of genetic damage in the forms of activated proto-oncogenes and inactivated tumor-suppressor genes is the driving force in the evolution of a normal cell to a malignant cell. For example, both the activation of ras oncogenes and the inactivation of several suppressor genes, including p53, have been observed in the development of human colon and lung tumors. Point mutations in key codons can activate ras proto-oncogenes and inactivate the p53 suppressor gene. Thus, several critical genes for tumorigenesis are potential targets for carcinogens and radiation that can induce point mutations at low doses. The ras proto-oncogenes are targets for many genotoxic carcinogens. Activation of the ras gene is an early event--probably the "initiating" step--in the development of many chemical-induced rodent tumors. ras Oncogenes are observed in more human tumors and at a higher frequency than any other oncogene, and activation of the proto-oncogene may occur at various stages of the carcinogenic process. Numerous proto-oncogenes other than the ras genes have been shown to be activated in human tumors and to a lesser extent in rodent tumors. Mechanisms that induce aberrant expression of proto-oncogenes are gene amplification and chromosomal translocation or gene rearrangement. Amplification of proto-oncogenes and possibly gene overexpression during the absence of gene amplification occur in the development of many human tumors. For a specific tumor type, amplification of any one proto-oncogene may occur at a low frequency, but the frequency of tumors in which at least one proto-oncogene is amplified can be much higher. Proto-oncogene amplification is usually associated with late stages of tumor progression; however, amplified HER2/neu has been observed in early clinical stages of mammary neoplasia. Activation of proto-oncogenes by chromosomal translocation has been detected at a high frequency in several hematopoietic tumors. Non-ras genes have been detected by DNA transfection assays in both human and rodent tumors. For example, ret and trk genes were found to be activated by gene rearrangements in human papillary thyroid carcinomas. Several potentially new types of oncogenes have also been detected by DNA transfection assays. The etiology of the genetic alterations observed in most human tumors is unclear at present. Examples of ras gene activation and those documented for mutations in the p53 gene demonstrate that exogenous conditions can induce oncogenic mutants of normal genes. The genetic alterations observed in most human tumors are probably generated by both spontaneous events and exogenous conditions. JF - Environmental health perspectives AU - Anderson, M W AU - Reynolds, S H AU - You, M AU - Maronpot, R M AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 13 EP - 24 VL - 98 SN - 0091-6765, 0091-6765 KW - H-ras KW - HER2/neu KW - K-ras KW - L-myc KW - N-myc KW - N-ras KW - ax1 KW - c-abl KW - c-myc KW - c-raf KW - gip2 KW - hst-1 KW - int-2 KW - lca KW - neu KW - p-21 KW - p-53 KW - ret KW - trk KW - Index Medicus KW - Rats KW - Animals KW - Genes, ras -- genetics KW - Neoplasms, Experimental -- chemically induced KW - Neoplasms, Experimental -- genetics KW - Humans KW - Mice KW - Transcriptional Activation KW - Female KW - Proto-Oncogenes -- genetics KW - Neoplasms -- chemically induced KW - Neoplasms -- genetics KW - Gene Expression Regulation, Neoplastic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73447098?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Role+of+proto-oncogene+activation+in+carcinogenesis.&rft.au=Anderson%2C+M+W%3BReynolds%2C+S+H%3BYou%2C+M%3BMaronpot%2C+R+M&rft.aulast=Anderson&rft.aufirst=M&rft.date=1992-11-01&rft.volume=98&rft.issue=&rft.spage=13&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-24 N1 - Date created - 1993-02-24 N1 - Date revised - 2017-01-13 N1 - Gene symbol - H-ras; HER2/neu; K-ras; L-myc; N-myc; N-ras; ax1; c-abl; c-myc; c-raf; gip2; hst-1; int-2; lca; neu; p-21; p-53; ret; trk N1 - SuppNotes - Cited By: Mol Cell Biol. 1990 Jan;10(1):405-8 [2403644] Cancer Res. 1990 Jan 15;50(2):266-72 [2403837] Adv Cancer Res. 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15-21;306(5944):658-61 [6318112] Cell. 1984 Jan;36(1):93-9 [6319012] Proc Natl Acad Sci U S A. 1983 Nov;80(22):6922-6 [6417658] Proc Natl Acad Sci U S A. 1984 Aug;81(15):4940-4 [6589638] Curr Top Microbiol Immunol. 1989;148:93-114 [2684550] Science. 1987 Oct 23;238(4826):542-5 [2821624] N Engl J Med. 1988 Sep 1;319(9):525-32 [2841597] Mol Carcinog. 1988;1(1):4-6 [2855601] Proc Natl Acad Sci U S A. 1985 Jun;82(11):3849-53 [2987950] Nature. 1986 Jul 3-9;322(6074):78-80 [3014349] Proc Natl Acad Sci U S A. 1986 Jul;83(14):4993-7 [3014525] N Engl J Med. 1987 Oct 8;317(15):929-35 [3041218] Cancer Res. 1988 Oct 15;48(20):5738-41 [3048648] Oncogene. 1988 Nov;3(5):541-4 [3078959] Proc Natl Acad Sci U S A. 1987 Aug;84(16):5923-7 [3112776] Oncogene Res. 1988;3(1):77-86 [3144694] Nature. 1988 Dec 22-29;336(6201):790-2 [3205307] Cell. 1988 Apr 22;53(2):173-4 [3282673] Proc Natl Acad Sci U S A. 1988 Jul;85(14):5026-30 [3293047] Cancer Res. 1988 Jun 15;48(12):3341-6 [3370635] Nature. 1986 Jan 2-8;319(6048):73-7 [3510398] Science. 1987 Jan 16;235(4786):305-11 [3541204] Cancer Res. 1987 Jun 15;47(12):3212-9 [3581065] Cancer Res. 1990 Dec 15;50(24):7811-4 [2253224] Cancer Res. 1990 Jan 15;50(2):444-7 [2295084] Proc Natl Acad Sci U S A. 1990 Mar;87(5):1791-5 [2308938] Cancer Res. 1991 Jan 15;51(2):556-67 [1670762] Environ Health Perspect. 1991 Jun;93:19-25 [1773791] Cell. 1991 Jan 25;64(2):281-302 [1846320] Cancer Res. 1991 May 15;51(10):2605-10 [1850660] Nature. 1991 Jan 10;349(6305):117-27 [1898771] Cancer Res. 1987 Aug 15;47(16):4248-53 [2440561] Nature. 1989 Aug 31;340(6236):678-9 [2505083] Cancer Res. 1989 Oct 15;49(20):5505-8 [2529025] Cancer Res. 1989 May 15;49(10):2683-8 [2540905] Oncogene. 1989 Nov;4(11):1389-95 [2554239] Mol Carcinog. 1989;2(1):34-9 [2567173] Oncogene. 1989 Dec;4(12):1457-62 [2594368] Oncogene. 1989 Feb;4(2):159-64 [2648253] Proc Natl Acad Sci U S A. 1989 May;86(9):3070-4 [2654935] Cell. 1989 Jun 16;57(6):901-8 [2661014] Environ Health Perspect. 1989 May;81:33-7 [2667982] Nature. 1987 Jul 9-15;328(6126):170-2 [3600795] Cancer. 1987 Dec 1;60(11):2669-74 [3677003] Mol Cell Biol. 1986 Jul;6(7):2716-20 [3785207] N Engl J Med. 1985 Oct 31;313(18):1111-6 [4047115] Br J Cancer. 1983 Jul;48(1):1-15 [6191767] Nature. 1983 Jun 2-8;303(5916):401-6 [6304522] EMBO J. 1983;2(5):697-703 [6416831] Proc Natl Acad Sci U S A. 1983 Dec;80(24):7581-5 [6424112] Science. 1984 Jun 8;224(4653):1121-4 [6719137] Cancer Res. 1990 Sep 15;50(18):5911-8 [1975511] Cancer Res. 1990 Dec 15;50(24):8002-9 [1979253] Cancer Res. 1991 Feb 1;51(3):944-8 [1988136] Cell. 1991 Jan 25;64(2):235-48 [1988146] Cell. 1991 Jan 25;64(2):249-70 [1988147] Cell. 1991 Jan 25;64(2):271-80 [1988148] Cell. 1991 Jan 25;64(2):303-12 [1988149] Cell. 1991 Jan 25;64(2):313-26 [1988150] Br J Cancer. 1991 Jan;63(1):136-42 [1989653] Proc Natl Acad Sci U S A. 1991 Feb 15;88(4):1085-9 [1996309] Cancer Res. 1991 Feb 15;51(4):1148-53 [1997158] Cancer Res. 1991 Mar 1;51(5):1504-8 [1997190] Br J Cancer. 1991 Apr;63(4):573-8 [2021541] Cancer Res. 1991 May 15;51(10):2690-3 [2021946] Biochemistry. 1991 May 14;30(19):4637-48 [2029511] Int J Cancer. 1991 May 30;48(3):409-12 [2040536] Cancer Res. 1991 Jul 1;51(13):3617-20 [2054797] Proc Natl Acad Sci U S A. 1990 Jan;87(2):538-42 [2105486] Proc Natl Acad Sci U S A. 1990 Feb;87(3):1104-8 [2105496] Eur J Clin Invest. 1990 Jun;20(3):225-35 [2114981] Proc Natl Acad Sci U S A. 1990 Aug;87(15):5998-6002 [2116014] Science. 1990 Aug 10;249(4969):655-9 [2116665] Cancer Res. 1990 Feb 15;50(4):1121-4 [2153451] Mol Carcinog. 1990;3(5):296-301 [2173932] Br J Cancer. 1990 Mar;61(3):365-8 [2183872] Cell. 1990 Jun 1;61(5):759-67 [2188735] Cancer Res. 1990 Jul 1;50(13):4014-9 [2191770] Biochem Biophys Res Commun. 1990 Jun 29;169(3):1094-8 [2194452] Cancer Res. 1990 Aug 1;50(15):4818-23 [2196119] EMBO J. 1990 Aug;9(8):2351-9 [2196171] Oncogene. 1990 Jul;5(7):1037-43 [2197591] Cell. 1990 Aug 10;62(3):539-48 [2199064] N Engl J Med. 1990 Aug 30;323(9):561-5 [2199829] Cancer Res. 1990 Oct 1;50(19):6139-45 [2205377] Cancer Res. 1990 Oct 15;50(20):6701-7 [2208136] Nature. 1990 Nov 22;348(6299):334-6 [2250705] Oncogene. 1988 Dec;3(6):673-8 [2577869] Cancer Res. 1989 Jan 15;49(2):357-60 [2642738] Proc Natl Acad Sci U S A. 1989 Apr;86(7):2403-7 [2648401] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human cytochromes P450: evolution and cDNA-directed expression. AN - 73444412; 1486867 AB - As the first step in the process of carcinogenesis, most chemical carcinogens require metabolic activation by cytochromes P450 for conversion to highly reactive electrophiles that bind covalently to DNA. Studies in rodents suggest that low or high levels of expression of a single P450 can determine susceptibility or resistance to chemically induced cancer. Although rodent systems have been used to explore the molecular basis of chemical carcinogenesis and to identify chemicals capable of damaging genes and causing cancer, it has been understood that marked species differences exist in the expression, regulation, and catalytic activities of different P450s. Thus, large efforts are underway to study the catalytic activities of human P450s directly by expression of their cDNAs in cultured cells. Two systems are being used: a) transient high-level P450 production in HepG2 cells for analysis of catalytic activities, and b) stable expression in human B-lymphoblastoid cells to study promutagen and procarcinogen activation. These studies define the relative contributions of individual P450 forms to the activation of various chemical carcinogens. The B-lymphoblastoid cDNA expression system can also be used to determine whether a chemical will be hazardous or toxic to humans. The most intriguing aspects of P450s are the occurrence of human genetic polymorphisms in P450 expression, which could be a risk factor for chemical carcinogenesis. The best-studied P450 genetic polymorphism is the debrisoquine/sparteine polymorphism which is due to mutant CYP2D6 alleles. Four mutant alleles have been characterized that account for most of the defective CYP2D6 genes in Caucasians. These can be detected by polymerase chain reaction assays.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Environmental health perspectives AU - Gonzalez, F J AU - Gelboin, H V AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 81 EP - 85 VL - 98 SN - 0091-6765, 0091-6765 KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Animals KW - Biological Evolution KW - Humans KW - Substrate Specificity KW - Gene Expression Regulation, Enzymologic -- genetics KW - Cytochrome P-450 Enzyme System -- genetics KW - DNA -- genetics KW - Cytochrome P-450 Enzyme System -- chemistry KW - Cytochrome P-450 Enzyme System -- classification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73444412?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Human+cytochromes+P450%3A+evolution+and+cDNA-directed+expression.&rft.au=Gonzalez%2C+F+J%3BGelboin%2C+H+V&rft.aulast=Gonzalez&rft.aufirst=F&rft.date=1992-11-01&rft.volume=98&rft.issue=&rft.spage=81&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-24 N1 - Date created - 1993-02-24 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Clin Pharmacol Ther. 1991 Sep;50(3):233-8 [1680592] Annu Rev Biochem. 1980;49:315-56 [6996566] Chem Res Toxicol. 1991 Jul-Aug;4(4):391-407 [1912325] Biochemistry. 1991 Apr 2;30(13):3247-55 [2009263] Proc Natl Acad Sci U S A. 1990 Jun;87(12):4790-3 [2162057] Biochem Biophys Res Commun. 1990 Oct 30;172(2):737-44 [2241965] J Pharmacol Exp Ther. 1990 Jan;252(1):442-7 [2299601] Cancer Detect Prev. 1989;14(2):215-9 [2559797] Biochemistry. 1989 Jun 13;28(12):4993-9 [2669966] Pharmacol Rev. 1988 Dec;40(4):243-88 [3072575] DNA. 1988 Mar;7(2):79-86 [3267210] Xenobiotica. 1988 Feb;18(2):207-16 [3376492] Mol Pharmacol. 1986 Apr;29(4):405-10 [3517618] Mutat Res. 1984 Sep;128(2):221-30 [6088974] Chem Res Toxicol. 1991 Sep-Oct;4(5):566-72 [1793807] Pharmacogenetics. 1991 Oct;1(1):26-32 [1844820] Pharmacogenetics. 1991 Oct;1(1):4-19 [1844821] Carcinogenesis. 1991 Feb;12(2):355-9 [1899812] Biochemistry. 1990 Jun 12;29(23):5491-9 [1974816] DNA Cell Biol. 1991 Jan-Feb;10(1):1-14 [1991046] Carcinogenesis. 1991 Jul;12(7):1197-201 [2070484] Cancer Res. 1990 Apr 1;50(7):2060-3 [2180561] Trends Genet. 1990 Jun;6(6):182-6 [2196721] Biochemistry. 1990 Dec 25;29(51):11280-92 [2271712] Biochemistry. 1990 Feb 6;29(5):1322-9 [2322567] Biochemistry. 1989 Sep 5;28(18):7340-8 [2573390] Biochemistry. 1989 Oct 3;28(20):8060-6 [2574990] J Biol Chem. 1989 Jun 25;264(18):10388-95 [2732228] Nature. 1988 Feb 4;331(6155):442-6 [3123997] Biochemistry. 1988 Dec 13;27(25):9006-13 [3233219] Cancer Res. 1988 Mar 15;48(6):1499-504 [3345523] Mol Biol Evol. 1987 Nov;4(6):572-93 [3484338] Mutat Res. 1985 Jun-Jul;150(1-2):33-41 [3889618] J Biol Chem. 1985 Jul 25;260(15):9057-67 [4019462] Mol Pharmacol. 1991 Sep;40(3):375-82 [1896026] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Nickel(II)-mediated oxidative DNA base damage in renal and hepatic chromatin of pregnant rats and their fetuses. Possible relevance to carcinogenesis. AN - 73443179; 1489933 AB - DNA base damage was studied in renal and hepatic chromatin of nickel(II)-injected pregnant female F344/NCr rats and their fetuses under conditions leading to initiation of sodium barbital-promotable renal tumors, but not liver tumors, in the male offspring. Pregnant rats were given a total of 90 or 180 mumol of nickel(II) acetate/kg body wt in a single ip dose on day 17 or in 2 or 4 ip doses between days 12 and 18 of gestation. Control rats received 180 mumol of sodium acetate/kg body wt. The animals were killed 24 or 48 h after the last injection. Chromatin was isolated from livers and kidneys from both adults and fetuses and analyzed by gas chromatography/mass spectrometry with selected ion monitoring. Eleven products derived from the purine and pyrimidine bases in DNA bases were identified and quantified. These were the following: 5-hydroxy-5-methylhydantoin, 5-hydroxyhydantoin, 5-(hydroxymethyl)uracil, cytosine glycol, thymine glycol, 5,6-dihydroxycystosine, 4,6-diamino-5-formamidopyrimidine, 2,6-diamino-4-hydroxy-5-formamidopyrimidine, 8-hydroxyadenine, 2-hydroxyadenine, and 8-hydroxyguanine (8-OH-Gua). Nickel(II) exposure increased the content of these products, especially those derived from purines, in both renal and hepatic chromatin of pregnant rats. The major difference between these two organs was the content of 8-OH-Gua, which increased greatly in the kidney but remained unchanged in the liver.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Chemical research in toxicology AU - Kasprzak, K S AU - Diwan, B A AU - Rice, J M AU - Misra, M AU - Riggs, C W AU - Olinski, R AU - Dizdaroglu, M AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, FCRDC, Frederick, Maryland 21702. PY - 1992 SP - 809 EP - 815 VL - 5 IS - 6 SN - 0893-228X, 0893-228X KW - Carcinogens KW - 0 KW - Chromatin KW - Nickel KW - 7OV03QG267 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Rats KW - Oxidation-Reduction KW - Animals KW - Rats, Inbred F344 KW - Cell Nucleus -- ultrastructure KW - Gas Chromatography-Mass Spectrometry KW - Cell Nucleus -- drug effects KW - Male KW - Female KW - Pregnancy KW - Liver -- drug effects KW - DNA Damage KW - Chromatin -- drug effects KW - Kidney -- drug effects KW - Carcinogens -- toxicity KW - DNA -- chemistry KW - Nickel -- toxicity KW - Kidney -- chemistry KW - Liver -- chemistry KW - Fetus -- metabolism KW - DNA -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73443179?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+research+in+toxicology&rft.atitle=Nickel%28II%29-mediated+oxidative+DNA+base+damage+in+renal+and+hepatic+chromatin+of+pregnant+rats+and+their+fetuses.+Possible+relevance+to+carcinogenesis.&rft.au=Kasprzak%2C+K+S%3BDiwan%2C+B+A%3BRice%2C+J+M%3BMisra%2C+M%3BRiggs%2C+C+W%3BOlinski%2C+R%3BDizdaroglu%2C+M&rft.aulast=Kasprzak&rft.aufirst=K&rft.date=1992-11-01&rft.volume=5&rft.issue=6&rft.spage=809&rft.isbn=&rft.btitle=&rft.title=Chemical+research+in+toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-04 N1 - Date created - 1993-03-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - 16,16-dimethyl prostaglandin E2 modulates aflatoxin B1-induced injury of rat hepatocytes in primary culture: possible role of cAMP. AN - 73443090; 1336677 AB - The hepatocellular cytoprotective effects of 16,16-dimethyl prostaglandin E2 (dmPGE2), an analogue of PGE2, were investigated using primary cultures of rat hepatocytes and aflatoxin B1 as the hepatotoxin. Lactic dehydrogenase (LDH) release by hepatocytes was used as an index of hepatotoxicity. When aflatoxin-treated hepatocytes were co-cultured with 16,16-dmPGE2 (0.01-0.5 micrograms/mL) LDH release was significantly reduced and ultrastructural changes of hepatocellular injury were markedly diminished. The magnitude of the cytoprotective effect was not dependent on the concentration of the prostaglandin over the range tested. A significant cytoprotective effect was also induced when hepatocellular cyclic AMP (cAMP) levels were increased by the addition of dibutyl-cAMP. In contrast to 16,16-dmPGE2, PGF2 alpha Tromethamine, an analogue of PGF2 alpha, which does not stimulate cAMP, induced insignificant changes in cytoprotection. These findings indicate that only a low concentration of 16,16-dmPGE2 (> or = 0.01 micrograms/mL) is necessary to induce a maximal hepatocellular cytoprotective effect and suggest that this effect may be dependent on activation of cAMP. JF - Journal of gastroenterology and hepatology AU - Bergasa, N V AU - Vergalla, J AU - Cole, K E AU - Wahl, L M AU - Jones, E A AD - Liver Diseases Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. PY - 1992 SP - 608 EP - 613 VL - 7 IS - 6 SN - 0815-9319, 0815-9319 KW - Aflatoxin B1 KW - 9N2N2Y55MH KW - Cyclic AMP KW - E0399OZS9N KW - L-Lactate Dehydrogenase KW - EC 1.1.1.27 KW - 16,16-Dimethylprostaglandin E2 KW - M790V82VAC KW - Index Medicus KW - Rats KW - Animals KW - Rats, Sprague-Dawley KW - Cells, Cultured KW - In Vitro Techniques KW - Microscopy, Electron KW - Male KW - L-Lactate Dehydrogenase -- metabolism KW - Liver -- cytology KW - Aflatoxin B1 -- adverse effects KW - Liver -- drug effects KW - Cyclic AMP -- physiology KW - 16,16-Dimethylprostaglandin E2 -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73443090?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+gastroenterology+and+hepatology&rft.atitle=16%2C16-dimethyl+prostaglandin+E2+modulates+aflatoxin+B1-induced+injury+of+rat+hepatocytes+in+primary+culture%3A+possible+role+of+cAMP.&rft.au=Bergasa%2C+N+V%3BVergalla%2C+J%3BCole%2C+K+E%3BWahl%2C+L+M%3BJones%2C+E+A&rft.aulast=Bergasa&rft.aufirst=N&rft.date=1992-11-01&rft.volume=7&rft.issue=6&rft.spage=608&rft.isbn=&rft.btitle=&rft.title=Journal+of+gastroenterology+and+hepatology&rft.issn=08159319&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-25 N1 - Date created - 1993-02-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Polycyclic aromatic hydrocarbon-DNA adducts and the CYP1A1 restriction fragment length polymorphism. AN - 73442190; 1362539 AB - Human cancer risk assessment at a genetic level involves the investigation of carcinogen metabolism and DNA adduct formation. Wide interindividual differences in metabolism result in different DNA adduct levels. For this and other reasons, many laboratories have considered DNA adducts to be a measure of the biologically effective dose of a carcinogen. Techniques for studying DNA adducts using chemically specific assays are becoming available. A modification of the 32P-postlabeling assay for polycyclic aromatic hydrocarbon DNA adducts described here provides potential improvements in quantification. DNA adducts, however, reflect only recent exposure to carcinogens; in contrast, genetic testing for metabolic capacity indicates the extent to which carcinogens can be activated and exert genotoxic effects. Such studies may reflect both separate and integrated risk factors together with DNA adduct levels. A recently described restriction fragment length polymorphism for the CYP1A1, which codes for the cytochrome P450 enzyme primarily responsible for the metabolic activation of carcinogenic polycyclic aromatic hydrocarbons, has been found to be associated with lung cancer risk in a Japanese population. In a subset of individuals enrolled in a U.S. lung cancer case-control study, no association with lung cancer was found. JF - Environmental health perspectives AU - Shields, P G AU - Sugimura, H AU - Caporaso, N E AU - Petruzzelli, S F AU - Bowman, E D AU - Trump, B F AU - Weston, A AU - Harris, C C AD - Laboratory of Human Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 191 EP - 194 VL - 98 SN - 0091-6765, 0091-6765 KW - DNA, Neoplasm KW - 0 KW - Polycyclic Compounds KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Oxidoreductases KW - EC 1.- KW - Cytochrome P-450 CYP1A1 KW - EC 1.14.14.1 KW - Index Medicus KW - United States KW - Polymerase Chain Reaction KW - Polymorphism, Restriction Fragment Length KW - Blotting, Southern KW - Humans KW - Case-Control Studies KW - Japan KW - Oxidoreductases -- genetics KW - Cytochrome P-450 Enzyme System -- genetics KW - Lung Neoplasms -- genetics KW - DNA, Neoplasm -- genetics KW - Polycyclic Compounds -- metabolism KW - DNA, Neoplasm -- metabolism KW - Lung Neoplasms -- ethnology KW - Lung Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73442190?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Polycyclic+aromatic+hydrocarbon-DNA+adducts+and+the+CYP1A1+restriction+fragment+length+polymorphism.&rft.au=Shields%2C+P+G%3BSugimura%2C+H%3BCaporaso%2C+N+E%3BPetruzzelli%2C+S+F%3BBowman%2C+E+D%3BTrump%2C+B+F%3BWeston%2C+A%3BHarris%2C+C+C&rft.aulast=Shields&rft.aufirst=P&rft.date=1992-11-01&rft.volume=98&rft.issue=&rft.spage=191&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-24 N1 - Date created - 1993-02-24 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Natl Cancer Inst. 1990 Aug 15;82(16):1333-9 [2380990] FEBS Lett. 1990 Apr 9;263(1):131-3 [1691986] Cancer Res. 1988 Apr 15;48(8):2156-61 [3349485] Cancer Res. 1982 Dec;42(12):5030-7 [6291746] Proc Natl Acad Sci U S A. 1984 Sep;81(18):5623-7 [6435118] Int J Cancer. 1991 Jun 19;48(4):485-92 [2045196] Carcinogenesis. 1990 Feb;11(2):205-11 [2105856] Cancer Res. 1990 Oct 15;50(20):6580-4 [2208119] Cancer Res. 1989 Sep 1;49(17):4929-35 [2503247] Carcinogenesis. 1989 Sep;10(9):1567-77 [2670301] Nature. 1988 Dec 22-29;336(6201):790-2 [3205307] Cancer Lett. 1986 Mar;30(3):289-97 [3697947] Nature. 1983 Jun 9-15;303(5917):468-72 [6304528] Nature. 1984 Aug 16-22;310(5978):586-9 [6431299] Proc Natl Acad Sci U S A. 1981 Oct;78(10):6126-9 [7031643] Cancer Res. 1988 Apr 15;48(8):2288-91 [3127049] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Genetic monitoring of human polymorphic cancer susceptibility genes by polymerase chain reaction: application to glutathione transferase mu. AN - 73442106; 1486839 AB - Several genes involved in the metabolism of carcinogens have been found to be polymorphic in human populations and are associated with increased risk of cancer at some sites. This study focuses on the polymorphic enzyme glutathione transferase mu (GT mu). Smokers with low lymphocyte GT mu activity are at an approximately 2-fold higher risk for lung cancer and an approximately 3-fold higher risk for stomach and colon adenocarcinomas. Recent cloning and sequencing of the GST1 gene has allowed the development of convenient genotyping methods based on restriction fragment length polymorphisms (RFLP) or the polymerase chain reaction (PCR). The GST1 polymorphism has been shown to be a deletion of the gene locus. To detect the presence or absence of the gene we amplified exons 4-5 and/or exons 6-7 of the GST1 gene by PCR. PCR amplification produced bands of 215-bp or 273-bp from individuals with one or two copies of the GST1 allele and no band if the individual was homozygously deleted (0/0). In the exon 6-7 PCR, we co-amplified a 268-bp portion of the beta-globin gene as an internal reference standard for quantitative analysis of product yield. This allowed homozygote individuals (+/+) to be distinguished from heterozygotes (+/0). We have compared the GST1 genotype to lymphocyte GT mu activity measured on trans-stilbene oxide (TSO) in the lymphocytes of 45 individuals. Low GT mu activity (< 67 pmole/min/10(7) cells) was strongly associated (24/24) with the GST1 0/0 genotype. With the exception of one individual, activities greater than 67 pmole/min/10(7) were associated with the presence of the GST1 allele (20/21). Individuals with the highest GT-TSO activity were found to be homozygous for GST1. (+/+), while heterozygotes (+/0) generally had lower activity, suggesting a gene dosage effect in lymphocytes.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Environmental health perspectives AU - Bell, D A AU - Thompson, C L AU - Taylor, J AU - Miller, C R AU - Perera, F AU - Hsieh, L L AU - Lucier, G W AD - Laboratory of Biochemical Risk Analysis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 113 EP - 117 VL - 98 SN - 0091-6765, 0091-6765 KW - GST1 KW - Glutathione Transferase KW - EC 2.5.1.18 KW - Index Medicus KW - Genotype KW - Polymerase Chain Reaction KW - Humans KW - Lymphocytes -- enzymology KW - Polymorphism, Genetic KW - Glutathione Transferase -- metabolism KW - Glutathione Transferase -- genetics KW - Gene Deletion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73442106?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Genetic+monitoring+of+human+polymorphic+cancer+susceptibility+genes+by+polymerase+chain+reaction%3A+application+to+glutathione+transferase+mu.&rft.au=Bell%2C+D+A%3BThompson%2C+C+L%3BTaylor%2C+J%3BMiller%2C+C+R%3BPerera%2C+F%3BHsieh%2C+L+L%3BLucier%2C+G+W&rft.aulast=Bell&rft.aufirst=D&rft.date=1992-11-01&rft.volume=98&rft.issue=&rft.spage=113&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-24 N1 - Date created - 1993-02-24 N1 - Date revised - 2017-01-13 N1 - Gene symbol - GST1 N1 - SuppNotes - Cited By: Carcinogenesis. 1991 Dec;12(12):2269-75 [1747926] Carcinogenesis. 1991 Jan;12(1):25-8 [1988177] Biochem J. 1991 Mar 1;274 ( Pt 2):587-93 [2006920] Mutat Res. 1991 Apr;247(2):259-66 [2011143] Mutat Res. 1991 Apr;247(2):267-81 [2011144] Proc Natl Acad Sci U S A. 1991 May 15;88(10):4443-7 [2034681] Nucleic Acids Res. 1990 Feb 25;18(4):993-8 [2315049] J Biol Chem. 1990 Jun 5;265(16):9188-93 [2345169] Nucleic Acids Res. 1990 Jun 25;18(12):3670 [2362832] Mutat Res. 1988 Dec;202(2):343-61 [3057366] Proc Natl Acad Sci U S A. 1988 Oct;85(19):7293-7 [3174634] Nucleic Acids Res. 1988 Feb 11;16(3):1215 [3344216] Hum Genet. 1985;69(1):66-8 [3967891] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - DNA adduct measurements and tumor incidence during chronic carcinogen exposure in animal models: implications for DNA adduct-based human cancer risk assessment. AN - 73441731; 1489923 JF - Chemical research in toxicology AU - Poirier, M C AU - Beland, F A AD - Division of Cancer Etiology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. PY - 1992 SP - 749 EP - 755 VL - 5 IS - 6 SN - 0893-228X, 0893-228X KW - Carcinogens KW - 0 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Humans KW - Carcinogenicity Tests KW - Risk KW - Carcinogens -- metabolism KW - Neoplasms, Experimental -- chemically induced KW - DNA Damage KW - DNA -- metabolism KW - Carcinogens -- toxicity KW - Neoplasms, Experimental -- pathology KW - DNA -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73441731?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+research+in+toxicology&rft.atitle=DNA+adduct+measurements+and+tumor+incidence+during+chronic+carcinogen+exposure+in+animal+models%3A+implications+for+DNA+adduct-based+human+cancer+risk+assessment.&rft.au=Poirier%2C+M+C%3BBeland%2C+F+A&rft.aulast=Poirier&rft.aufirst=M&rft.date=1992-11-01&rft.volume=5&rft.issue=6&rft.spage=749&rft.isbn=&rft.btitle=&rft.title=Chemical+research+in+toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-03-04 N1 - Date created - 1993-03-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Chem Res Toxicol. 1992 Nov-Dec;5(6):735-6 [1489920] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Biomarkers in occupational cancer epidemiology: considerations in study design. AN - 73441404; 1486844 AB - Epidemiologic studies of occupational groups have been central to the identification of human carcinogens. The incorporation of a biochemical component into occupational studies of cancer can expand the possibilities for identifying human carcinogens and for understanding the disease process. Two epidemiologic studies of occupation and cancer which include evaluation of biomarkers are described. The association of acetylator phenotype with bladder cancer risk was studied in benzidine-exposed workers. The association of benzene-related leukopenia with leukemia is being studied in benzene-exposed workers. These investigations illustrate issues in the use of biomarkers in epidemiologic studies of cancer risk. Such studies require the identification and characterization of the population at risk. Disease susceptibility factors are amenable for inclusion in these studies and can be statistically modeled as exposure-effect modifiers. Biomarkers of exposure are mainly of importance in short-term longitudinal and cross-sectional studies of exposure and intermediate outcomes and for validation of other data sources. Several sources of error can affect the results of molecular epidemiologic studies. Aside from minimizing laboratory error, consideration must be given in the design and execution of these studies to potential problems in subject selection and field collection of biologic samples and other relevant data. JF - Environmental health perspectives AU - Hayes, R B AD - Environmental Epidemiology Branch, National Cancer Institute, Bethesda, MD 20895. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 149 EP - 154 VL - 98 SN - 0091-6765, 0091-6765 KW - Benzidines KW - 0 KW - Biomarkers, Tumor KW - benzidine KW - 2X02101HVF KW - Benzene KW - J64922108F KW - Index Medicus KW - Reproducibility of Results KW - Disease Susceptibility KW - Epidemiologic Methods KW - Risk Factors KW - Humans KW - Cohort Studies KW - Case-Control Studies KW - Male KW - Leukemia -- chemically induced KW - Biomarkers, Tumor -- analysis KW - Occupational Exposure -- adverse effects KW - Occupational Exposure -- analysis KW - Benzene -- adverse effects KW - Urinary Bladder Neoplasms -- chemically induced KW - Benzidines -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73441404?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Biomarkers+in+occupational+cancer+epidemiology%3A+considerations+in+study+design.&rft.au=Hayes%2C+R+B&rft.aulast=Hayes&rft.aufirst=R&rft.date=1992-11-01&rft.volume=98&rft.issue=&rft.spage=149&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-24 N1 - Date created - 1993-02-24 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1971 Apr;68(4):820-3 [5279523] Eur Urol. 1985;11(4):263-6 [4043164] J Chromatogr. 1981 Jan 2;222(1):61-70 [6783675] Am J Epidemiol. 1980 Oct;112(4):564-9 [7424903] Am J Ind Med. 1992;21(4):481-9 [1580253] Proc Natl Acad Sci U S A. 1991 Jun 15;88(12):5237-41 [1675794] Science. 1990 Nov 30;250(4985):1233-8 [1978757] J Natl Cancer Inst. 1990 Nov 21;82(22):1746-52 [2231769] Genome. 1989;31(2):590-3 [2517259] Environ Health Perspect. 1989 Jul;82:207-13 [2792042] Stat Med. 1989 Sep;8(9):1051-69; discussion 1071-3 [2799131] Am J Epidemiol. 1987 Oct;126(4):561-7 [3631048] Am J Epidemiol. 1985 Jun;121(6):783-90 [4014171] Ann Clin Res. 1985;17(3):96-9 [4051447] J Occup Med. 1967 Jun;9(6):277-85 [6026374] Lancet. 1982 Oct 16;2(8303):842-5 [6126711] Br J Clin Pharmacol. 1984 Apr;17(4):459-64 [6721992] Environ Res. 1982 Apr;27(2):241-54 [7084156] Br J Ind Med. 1954 Apr;11(2):75-104 [13149741] Br J Clin Pharmacol. 1978 Nov;6(5):421-7 [728285] Science. 1991 Jul 5;253(5015):49-53 [1905840] J Occup Med. 1990 Sep;32(9):917-8 [2074519] Eur J Clin Pharmacol. 1989;37(6):581-7 [2612554] Stat Med. 1989 Sep;8(9):1041-9; discussion 1071-3 [2799130] Am J Epidemiol. 1988 Mar;127(3):674-83 [3341366] J Chronic Dis. 1982;35(7):581-600 [6282919] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cytokine induction and therapeutic synergy with interleukin-2 against murine renal and colon cancers by xanthenone-4-acetic acid derivatives. AN - 73440796; 1477076 AB - Derivatives of xanthenone-4-acetic acid (XAA) have been found to have similar activity to flavone-8-acetic acid against transplantable solid tumors. Some of these compounds were compared to flavone acetic acid (FAA) in their ability to induce cytokines as well as to mediate antitumor effects against murine renal cancer (Renca) and a mouse colon cancer (MCA-38). 5-Methyl-XAA and 5-chloro-XAA proved to be more potent than FAA on a mg/kg basis for induction of the genes for IFN alpha, IFN gamma, and TNF alpha, and for IFN and TNF activities in the sera of treated mice. These effects were sharply dose dependent. On the other hand, 7-methyl-XAA, which has no antitumor activity, did not induce these genes. In addition, 5-methyl-XAA and 5-chloro-XAA but not 7-methyl-XAA synergized with recombinant human interleukin-2 (rhIL-2) for the treatment of Renca and MCA-38. Doses of the active derivatives that failed to induce cytokines also exhibited no therapeutic synergy with rhIL-2. These results suggest that at least some of the antitumor effects of these XAA derivatives are related to their ability to induce cytokines. JF - Journal of immunotherapy : official journal of the Society for Biological Therapy AU - Futami, H AU - Eader, L AU - Back, T T AU - Gruys, E AU - Young, H A AU - Wiltrout, R H AU - Baguley, B C AD - Laboratory of Experimental Immunology, PRI/DynCorp., Inc., National Cancer Institute-Frederick Cancer Research and Development Center, MD 21701-1013. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 247 EP - 255 VL - 12 IS - 4 SN - 1053-8550, 1053-8550 KW - Antineoplastic Agents KW - 0 KW - Cytokines KW - DNA Probes KW - Flavonoids KW - Interferon-alpha KW - Interleukin-2 KW - Recombinant Proteins KW - Tumor Necrosis Factor-alpha KW - Xanthenes KW - xanthenone-4-acetic acid KW - 35614-21-2 KW - Interferon-gamma KW - 82115-62-6 KW - flavone acetic acid KW - 87626-55-9 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Leukocytes -- metabolism KW - Animals KW - Drug Screening Assays, Antitumor KW - Recombinant Proteins -- pharmacology KW - Combined Modality Therapy KW - Interferon-gamma -- biosynthesis KW - Tumor Necrosis Factor-alpha -- biosynthesis KW - Mice KW - Mice, Inbred BALB C KW - Structure-Activity Relationship KW - Flavonoids -- therapeutic use KW - Interferon-alpha -- biosynthesis KW - DNA -- genetics KW - Mice, Inbred C57BL KW - Flavonoids -- pharmacology KW - Drug Synergism KW - Recombinant Proteins -- therapeutic use KW - Male KW - Interleukin-2 -- pharmacology KW - Kidney Neoplasms -- drug therapy KW - Kidney Neoplasms -- therapy KW - Xanthenes -- therapeutic use KW - Cytokines -- biosynthesis KW - Gene Expression Regulation, Neoplastic -- drug effects KW - Kidney Neoplasms -- blood KW - Colonic Neoplasms -- therapy KW - Interleukin-2 -- therapeutic use KW - Xanthenes -- pharmacology KW - Colonic Neoplasms -- drug therapy KW - Antineoplastic Agents -- therapeutic use KW - Antineoplastic Agents -- pharmacology KW - Colonic Neoplasms -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73440796?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunotherapy+%3A+official+journal+of+the+Society+for+Biological+Therapy&rft.atitle=Cytokine+induction+and+therapeutic+synergy+with+interleukin-2+against+murine+renal+and+colon+cancers+by+xanthenone-4-acetic+acid+derivatives.&rft.au=Futami%2C+H%3BEader%2C+L%3BBack%2C+T+T%3BGruys%2C+E%3BYoung%2C+H+A%3BWiltrout%2C+R+H%3BBaguley%2C+B+C&rft.aulast=Futami&rft.aufirst=H&rft.date=1992-11-01&rft.volume=12&rft.issue=4&rft.spage=247&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunotherapy+%3A+official+journal+of+the+Society+for+Biological+Therapy&rft.issn=10538550&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-05 N1 - Date created - 1993-02-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Positron emission tomography with 18F-dopa: interpretation and biological correlates in nonhuman primates. AN - 73437527; 1283014 AB - Positron emission tomography (PET) was carried out, with 18F-DOPA as a ligand, in normal control monkeys and "parkinsonian" monkeys who had been treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. The following approaches were used in data analysis: ratio of 18F accumulation in specific to nonspecific brain areas and 18F-DOPA influx constant obtained using either the actual plasma 18F-DOPA or the 18F activity in a nonspecific brain area as the input function. The results from these analyses were compared to one another and to biological parameters relevant to dopaminergic function. The striatum/cortex ratio and the rate constant calculated from plasma 18F-DOPA appeared to be the most sensitive analytic techniques. JF - Psychiatry research AU - Doudet, D J AU - Aigner, T G AU - McLellan, C A AU - Cohen, R M AD - Laboratory of Cerebral Metabolism, National Institute of Mental Health, NIH, Bethesda, MD 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 153 EP - 168 VL - 45 IS - 3 SN - 0165-1781, 0165-1781 KW - Receptors, Dopamine KW - 0 KW - fluorodopa F 18 KW - 2C598205QX KW - Methoxyhydroxyphenylglycol KW - 534-82-7 KW - Hydroxyindoleacetic Acid KW - 54-16-0 KW - Dihydroxyphenylalanine KW - 63-84-3 KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Carbidopa KW - MNX7R8C5VO KW - Dopamine KW - VTD58H1Z2X KW - Homovanillic Acid KW - X77S6GMS36 KW - Index Medicus KW - Methoxyhydroxyphenylglycol -- metabolism KW - Corpus Striatum -- diagnostic imaging KW - Animals KW - Carbidopa -- pharmacology KW - Hydroxyindoleacetic Acid -- metabolism KW - Macaca mulatta KW - Homovanillic Acid -- metabolism KW - Cerebral Cortex -- diagnostic imaging KW - Dihydroxyphenylalanine -- pharmacokinetics KW - Dihydroxyphenylalanine -- analogs & derivatives KW - Receptors, Dopamine -- drug effects KW - Parkinson Disease, Secondary -- chemically induced KW - Receptors, Dopamine -- physiology KW - Dopamine -- physiology KW - Tomography, Emission-Computed KW - Parkinson Disease, Secondary -- diagnostic imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73437527?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychiatry+research&rft.atitle=Positron+emission+tomography+with+18F-dopa%3A+interpretation+and+biological+correlates+in+nonhuman+primates.&rft.au=Doudet%2C+D+J%3BAigner%2C+T+G%3BMcLellan%2C+C+A%3BCohen%2C+R+M&rft.aulast=Doudet&rft.aufirst=D&rft.date=1992-11-01&rft.volume=45&rft.issue=3&rft.spage=153&rft.isbn=&rft.btitle=&rft.title=Psychiatry+research&rft.issn=01651781&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-17 N1 - Date created - 1993-02-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Stimulation of early gene expression by angiotensin II in bovine adrenal glomerulosa cells: roles of calcium and protein kinase C. AN - 73435962; 1336125 AB - The adrenal glomerulosa cell is a major site of action of angiotensin II (AII), which binds to AT1 receptors to stimulate phosphoinositide hydrolysis and Ca2+ mobilization, and the subsequent production of aldosterone. All also influences adrenal growth and proliferation and promotes thymidine incorporation in adrenocortical cells. In primary cultures of bovine glomerulosa cells, AII was found to induce the expression of several early growth response genes (c-fos, c-jun, JunB, and Krox 24). This effect of AII was dose-dependent and was blocked by [Sar1,IIe8] AII and the nonpeptide antagonist DuP 753, indicating that it is mediated by the AT1 subtype of the AII receptor. ACTH, which elevates cAMP in glomerulosa cells, was a relatively weak inducer of c-fos expression but was as potent as AII in stimulating the expression of JunB. ACTH did not further enhance the maximal effect of AII on c-fos expression. The role of the AII-induced cytoplasmic Ca2+ increase in generating the c-fos response was suggested by the ability of the Ca2+ ionophore ionomycin to induce c-fos expression. However, mobilization of intracellular Ca2+ by the Ca2+ ATPase inhibitor thapsigargin, as well as the stimulation of Ca2+ influx by depolarization with potassium, were less potent stimuli of c-fos expression. Omission of Ca2+ from the extracellular medium, which abolishes the plateau phase of the AII-induced Ca2+ signal without affecting the early increase due to Ca2+ mobilization, enhanced the early phase of the AII-induced c-fos response, indicating that Ca2+ also has an inhibitory effect on the early gene response. Activation of protein kinase C by phorbol 12-myristate, 13-acetate (PMA) also stimulated c-fos expression, but the combination of PMA and ionomycin did not further increase the c-fos response. Inhibition of protein kinase C by staurosporine, or its depletion by prolonged exposure to PMA, prevented the c-fos response to PMA but only partially inhibited the response to AII, suggesting the involvement of other factors in stimulus-transcription coupling from the AT1 receptor. JF - Molecular endocrinology (Baltimore, Md.) AU - Clark, A J AU - Balla, T AU - Jones, M R AU - Catt, K J AD - Endocrinology and Reproduction Research Branch, National Institutes of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 1889 EP - 1898 VL - 6 IS - 11 SN - 0888-8809, 0888-8809 KW - JunB KW - KROX 24 KW - c-fos KW - c-jun KW - Alkaloids KW - 0 KW - DNA-Binding Proteins KW - Imidazoles KW - Pyridines KW - Terpenes KW - Transcription Factors KW - Angiotensin II KW - 11128-99-7 KW - PD 123177 KW - 114785-12-5 KW - Ionomycin KW - 56092-81-0 KW - Thapsigargin KW - 67526-95-8 KW - Adrenocorticotropic Hormone KW - 9002-60-2 KW - 1-Sarcosine-8-Isoleucine Angiotensin II KW - 9088-01-1 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Staurosporine KW - H88EPA0A3N KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - 1-Sarcosine-8-Isoleucine Angiotensin II -- pharmacology KW - Imidazoles -- pharmacology KW - DNA-Binding Proteins -- genetics KW - Ionomycin -- pharmacology KW - Genes, fos -- drug effects KW - Transcription Factors -- genetics KW - Stimulation, Chemical KW - Base Sequence KW - Cattle KW - Cells, Cultured KW - Molecular Sequence Data KW - Enzyme Activation -- drug effects KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Adrenocorticotropic Hormone -- pharmacology KW - Alkaloids -- pharmacology KW - Genes, jun -- drug effects KW - Terpenes -- pharmacology KW - Pyridines -- pharmacology KW - Zona Glomerulosa -- drug effects KW - Protein Kinase C -- antagonists & inhibitors KW - Zona Glomerulosa -- metabolism KW - Calcium -- physiology KW - Gene Expression Regulation -- drug effects KW - Zona Glomerulosa -- cytology KW - Protein Kinase C -- physiology KW - Angiotensin II -- pharmacology KW - Angiotensin II -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73435962?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.atitle=Stimulation+of+early+gene+expression+by+angiotensin+II+in+bovine+adrenal+glomerulosa+cells%3A+roles+of+calcium+and+protein+kinase+C.&rft.au=Clark%2C+A+J%3BBalla%2C+T%3BJones%2C+M+R%3BCatt%2C+K+J&rft.aulast=Clark&rft.aufirst=A&rft.date=1992-11-01&rft.volume=6&rft.issue=11&rft.spage=1889&rft.isbn=&rft.btitle=&rft.title=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.issn=08888809&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-10 N1 - Date created - 1993-02-10 N1 - Date revised - 2017-01-13 N1 - Gene symbol - JunB; KROX 24; c-fos; c-jun N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential molecular mechanism of the estrogen action that regulates lactoferrin gene in human and mouse. AN - 73434069; 1480183 AB - The 5'-flanking region of the human lactoferrin gene was isolated from a human placental genomic library. This genomic clone contains a 16-kilobase pair (kbp) insert and produces seven fragments when digested with the SacI restriction enzyme. We sequenced one of the fragments that comprises 1294 bp of the 5'-flanking sequence, 79 bp of the first exon, and 690 bp of the first intron. A major transcription start site was mapped by primer extension. The region immediately upstream from the transcription initiation site following the first exon is abundant in G and C nucleotides. In the promoter and 5'-flanking region within a 300-bp stretch (-465 to -165) of the DNA, we found a noncanonical TATA box (ATAAA), CAAT-like sequence (CAAC) and sequences homologous to the consensus SP1 binding site, Pu.1/Sp.1 binding element (PU box), two half-palindromic estrogen response elements (EREs; GGTCA), an imperfect ERE (GGTCAAGGCGATC), and a sequence resembling the chicken ovalbumin upstream promoter transcription factor (COUP-TF) binding site (GTCTCACAGGTCA). The COUP-TF binding site and the imperfect ERE shared five nucleotides (GGTCA). With the exception of the two half-palindromic EREs, the elements with very well matched sequences were also found in the corresponding positions in the mouse lactoferrin gene. The synthetic oligonucleotide, including the 26 bp of COUP/ERE sequence, was cloned before the SV40 promoter in a chloramphenicol acetyltransferase reporter construct. These chimeric plasmids were transiently transfected into human endometrium carcinoma RL95-2 cells to assess hormone responsiveness. We found that the COUP/ERE element acted as an enhancer in response to estrogen stimulation. In vitro DNase I footprinting analysis showed binding of the estrogen receptor on the imperfect ERE. In contrast to the mouse lactoferrin COUP/ERE element, COUP-TF does not interact with this element, as demonstrated by band shift assay and site-directed mutagenesis. Therefore, the molecular mechanisms of the estrogen action that govern the lactoferrin gene expression differ between mouse and human. JF - Molecular endocrinology (Baltimore, Md.) AU - Teng, C T AU - Liu, Y AU - Yang, N AU - Walmer, D AU - Panella, T AD - Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 1969 EP - 1981 VL - 6 IS - 11 SN - 0888-8809, 0888-8809 KW - Estrogens KW - 0 KW - Receptors, Estrogen KW - DNA KW - 9007-49-2 KW - Lactoferrin KW - EC 3.4.21.- KW - Index Medicus KW - Animals KW - DNA -- metabolism KW - Humans KW - Amino Acid Sequence KW - Sequence Homology KW - Receptors, Estrogen -- metabolism KW - Endometrium -- metabolism KW - Base Sequence KW - Hyperplasia KW - Estrus KW - Sequence Alignment KW - Endometrium -- drug effects KW - Molecular Sequence Data KW - Endometrium -- pathology KW - Consensus Sequence KW - Species Specificity KW - Female KW - Promoter Regions, Genetic KW - Lactoferrin -- genetics KW - Estrogens -- pharmacology KW - Enhancer Elements, Genetic KW - Mice -- genetics KW - Gene Expression Regulation KW - Mice -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73434069?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.atitle=Differential+molecular+mechanism+of+the+estrogen+action+that+regulates+lactoferrin+gene+in+human+and+mouse.&rft.au=Teng%2C+C+T%3BLiu%2C+Y%3BYang%2C+N%3BWalmer%2C+D%3BPanella%2C+T&rft.aulast=Teng&rft.aufirst=C&rft.date=1992-11-01&rft.volume=6&rft.issue=11&rft.spage=1969&rft.isbn=&rft.btitle=&rft.title=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.issn=08888809&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-10 N1 - Date created - 1993-02-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A pilot study of the combination of interleukin-2-based immunotherapy and radiation therapy. AN - 73423373; 1477077 AB - A clinical trial was undertaken to evaluate the feasibility of combining radiation therapy and immunotherapy. Twenty-eight patients with metastatic cancer were treated with rapid fractionation radiation up to 2,000 cGy, followed within 24 h by a course of interleukin 2 (IL-2) at 720,000 IU/kg or tumor-infiltrating lymphocytes (TILs) and IL-2 at 720,000 IU/kg. All patients tolerated treatment without any apparent increase in toxicity referable to the irradiation. Four patients had significant shrinkage of tumor at the irradiated site. Only two patients showed significant tumor shrinkage both inside and outside of the irradiated field. While rapid fractionation radiation can be safely administered in combination with immunotherapy, we observed no apparent synergy in antitumor effect in this small number of patients. JF - Journal of immunotherapy : official journal of the Society for Biological Therapy AU - Lange, J R AU - Raubitschek, A A AU - Pockaj, B A AU - Spencer, W F AU - Lotze, M T AU - Topalian, S L AU - Yang, J C AU - Rosenberg, S A AD - Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 265 EP - 271 VL - 12 IS - 4 SN - 1053-8550, 1053-8550 KW - Immunologic Factors KW - 0 KW - Interleukin-2 KW - Recombinant Proteins KW - Index Medicus KW - Combined Modality Therapy KW - Radiotherapy Dosage KW - Humans KW - Adult KW - Recombinant Proteins -- adverse effects KW - Neoplasm Metastasis KW - Aged KW - Pilot Projects KW - Middle Aged KW - Recombinant Proteins -- therapeutic use KW - Male KW - Female KW - Interleukin-2 -- adverse effects KW - Radiotherapy, High-Energy -- adverse effects KW - Neoplasms -- pathology KW - Neoplasms -- radiotherapy KW - Lymphocytes, Tumor-Infiltrating -- drug effects KW - Interleukin-2 -- therapeutic use KW - Immunologic Factors -- therapeutic use KW - Immunotherapy, Adoptive KW - Neoplasms -- therapy KW - Lymphocytes, Tumor-Infiltrating -- transplantation KW - Immunologic Factors -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73423373?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunotherapy+%3A+official+journal+of+the+Society+for+Biological+Therapy&rft.atitle=A+pilot+study+of+the+combination+of+interleukin-2-based+immunotherapy+and+radiation+therapy.&rft.au=Lange%2C+J+R%3BRaubitschek%2C+A+A%3BPockaj%2C+B+A%3BSpencer%2C+W+F%3BLotze%2C+M+T%3BTopalian%2C+S+L%3BYang%2C+J+C%3BRosenberg%2C+S+A&rft.aulast=Lange&rft.aufirst=J&rft.date=1992-11-01&rft.volume=12&rft.issue=4&rft.spage=265&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunotherapy+%3A+official+journal+of+the+Society+for+Biological+Therapy&rft.issn=10538550&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-05 N1 - Date created - 1993-02-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of nitric oxide in antagonistic effects of transforming growth factor-beta and interleukin-1 beta on the beating rate of cultured cardiac myocytes. AN - 73414052; 1282674 AB - We have recently shown that transforming growth factor-beta (TGF beta) acts in an autocrine manner to maintain the beating rate of neonatal rat cardiac myocytes cultured in serum-free medium on cardiac fibroblast matrix. Interleukin-1 beta (IL-1 beta) suppresses the myocyte-beating rate, and TGF beta antagonizes this effect. We now show that TGF beta and IL-1 beta also have antagonistic effects on the secretion of nitric oxide (NO) by these myocytes, and that NO secretion, the activity of NO synthase (NOS), and expression of the inducible form of NOS correlate inversely with the effects of these two agents on the beating rate. Western blot analysis shows that treatment of myocytes with TGF beta antagonizes the induction of NOS after treatment with IL-1 beta. Release of NO, induced by IL-1 beta, is dependent upon the availability of the substrate, L-arginine, and is suppressed by a competitive inhibitor, NG-monomethyl-L-arginine. L-Arginine (> 0.25 mM) also suppresses, and NG-monomethyl-L-arginine (> 0.5 mM) enhances the myocyte-beating rate. Treatment with IL-1 beta, but not TGF beta, increases cellular cGMP, presumably by activation of guanylate cyclase by NO. Methylene blue, an inhibitor of guanylate cyclase, reverses the suppression of beating caused by IL-1 beta. Bacterial lipopolysaccharide, present in the serum-free medium, is a coinducer of NO secretion. The suppressive effects of NO on the beating rate can be overcome by altering either the set of cytokines employed to induce NO or the matrix on which the myocytes are cultured, demonstrating that additional parameters are also involved in regulation of the beating rate. JF - Molecular endocrinology (Baltimore, Md.) AU - Roberts, A B AU - Vodovotz, Y AU - Roche, N S AU - Sporn, M B AU - Nathan, C F AD - Laboratory of Chemoprevention, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 1921 EP - 1930 VL - 6 IS - 11 SN - 0888-8809, 0888-8809 KW - Culture Media KW - 0 KW - Interleukin-1 KW - Lipopolysaccharides KW - Transforming Growth Factor beta KW - Nitric Oxide KW - 31C4KY9ESH KW - Arginine KW - 94ZLA3W45F KW - Nitric Oxide Synthase KW - EC 1.14.13.39 KW - Amino Acid Oxidoreductases KW - EC 1.4.- KW - Guanylate Cyclase KW - EC 4.6.1.2 KW - Methylene Blue KW - T42P99266K KW - Index Medicus KW - Animals KW - Amino Acid Oxidoreductases -- metabolism KW - Arginine -- metabolism KW - Lipopolysaccharides -- pharmacology KW - Culture Media -- pharmacology KW - Rats KW - Animals, Newborn KW - Myocardium -- cytology KW - Heart Rate -- drug effects KW - Methylene Blue -- pharmacology KW - Guanylate Cyclase -- antagonists & inhibitors KW - Cells, Cultured KW - Drug Antagonism KW - Transforming Growth Factor beta -- pharmacology KW - Interleukin-1 -- pharmacology KW - Nitric Oxide -- metabolism KW - Myocardial Contraction -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73414052?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.atitle=Role+of+nitric+oxide+in+antagonistic+effects+of+transforming+growth+factor-beta+and+interleukin-1+beta+on+the+beating+rate+of+cultured+cardiac+myocytes.&rft.au=Roberts%2C+A+B%3BVodovotz%2C+Y%3BRoche%2C+N+S%3BSporn%2C+M+B%3BNathan%2C+C+F&rft.aulast=Roberts&rft.aufirst=A&rft.date=1992-11-01&rft.volume=6&rft.issue=11&rft.spage=1921&rft.isbn=&rft.btitle=&rft.title=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.issn=08888809&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-02-10 N1 - Date created - 1993-02-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of immune activation on quinolinic acid and neuroactive kynurenines in the mouse. AN - 73402635; 1465184 AB - Accumulation of quinolinic acid and neuroactive kynurenines derived from tryptophan are of potential significance in human neuropathologic diseases because of their neurotoxic and convulsant properties. Clinical studies have established that sustained elevations of quinolinic acid, L-kynurenine and kynurenic acid within the cerebrospinal fluid occur in patients with a broad spectrum of inflammatory diseases and correlate with markers of immune activation and interferon-gamma activity. The present study describes an animal model that replicates these clinical observations and investigates the role of interferon-gamma as a mediator between immune activation and increased kynurenine pathway metabolism. Marked elevations in quinolinic acid, L-kynurenine and 3-hydroxykynurenine as well as an increased ratio of quinolinic acid: kynurenic acid in brain occurred 24 h after systemic pokeweed mitogen administration to C57BL6 mice. In plasma, L-tryptophan and kynurenic acid levels were reduced by pokeweed mitogen, while the concentrations of L-kynurenine, 3-hydroxykynurenine and quinolinic acid were increased. Interferon-gamma, pokeweed mitogen and lipopolysaccharide induced indoleamine-2,3-dioxygenase, the first enzyme of the kynurenine pathway, and increased both L-kynurenine and quinolinic acid concentrations of brain and systemic tissues, particularly in the lung, gastrointestinal tract and spleen. In contrast, hepatic tryptophan-2,3-dioxygenase activity was either reduced or unaffected. Increases in kynurenine pathway metabolism were sustained in mice given daily injections of interferon-gamma for seven days and subsequent responses to interferon-gamma were further enhanced. In contrast, daily administration of lipopolysaccharide was associated with subsequent attenuated responsiveness (tolerance) to lipopolysaccharide, pokeweed mitogen and interferon-gamma. Systemic administration of a monoclonal antibody to mouse interferon-gamma either attenuated or abolished the responses of kynurenine pathway metabolism to pokeweed mitogen and interferon-gamma. We conclude that acute and chronic increases in quinolinic acid and neuroactive kynurenines follow immune stimulation in mice, and result from indoleamine-2,3-dioxygenase induction. The results demonstrate that interferon-gamma is an important mediator between immune stimulation and indoleamine-2,3-dioxygenase induction. These increases in kynurenine pathway metabolism closely parallel the responses documented in patients with a broad spectrum of inflammatory diseases. Mice treated with immune stimuli are a useful model to investigate the relationships between immune activation and kynurenine pathway metabolism. JF - Neuroscience AU - Saito, K AU - Markey, S P AU - Heyes, M P AD - Section on Analytical Biochemistry, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 25 EP - 39 VL - 51 IS - 1 SN - 0306-4522, 0306-4522 KW - Antibodies, Monoclonal KW - 0 KW - Lipopolysaccharides KW - Pokeweed Mitogens KW - Recombinant Proteins KW - Kynurenine KW - 343-65-7 KW - 3-hydroxykynurenine KW - 484-78-6 KW - Interferon-gamma KW - 82115-62-6 KW - Tryptophan KW - 8DUH1N11BX KW - Quinolinic Acid KW - F6F0HK1URN KW - Kynurenic Acid KW - H030S2S85J KW - Index Medicus KW - Animals KW - Brain -- drug effects KW - Lipopolysaccharides -- pharmacology KW - Kynurenic Acid -- metabolism KW - Brain -- metabolism KW - Mice KW - Lung -- metabolism KW - Tryptophan -- metabolism KW - Models, Biological KW - Lung -- drug effects KW - Mice, Inbred C57BL KW - Male KW - Immune System -- drug effects KW - Quinolinic Acid -- metabolism KW - Pokeweed Mitogens -- pharmacology KW - Kynurenine -- metabolism KW - Interferon-gamma -- pharmacology KW - Interferon-gamma -- immunology KW - Antibodies, Monoclonal -- pharmacology KW - Immune System -- physiology KW - Kynurenine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73402635?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroscience&rft.atitle=Effects+of+immune+activation+on+quinolinic+acid+and+neuroactive+kynurenines+in+the+mouse.&rft.au=Saito%2C+K%3BMarkey%2C+S+P%3BHeyes%2C+M+P&rft.aulast=Saito&rft.aufirst=K&rft.date=1992-11-01&rft.volume=51&rft.issue=1&rft.spage=25&rft.isbn=&rft.btitle=&rft.title=Neuroscience&rft.issn=03064522&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-15 N1 - Date created - 1993-01-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Nitroxide-mediated protection against X-ray- and neocarzinostatin-induced DNA damage. AN - 73392384; 1459474 AB - The stable free radical Tempol (4-hydroxy-2,2,6,6-tetramethyl-piperidinyloxy) has been shown to protect against X-ray-induced cytotoxicity and hydrogen peroxide- or xanthine oxidase-induced cytotoxicity and mutagenicity. The ability of Tempol to protect against X-ray- or neocarzinostatin (NCS)-induced mutagenicity or DNA double-strand breaks (dsb) was studied in Chinese hamster cells. Tempol (50 mM) provided a protection factor of 2.7 against X-ray-induced mutagenicity in Chinese hamster ovary (CHO) AS52 cells, with a protection factor against cytotoxicity of 3.5. Using the field inversion gel electrophoresis technique of measuring DNA dsb, 50 mM Tempol provides a threefold reduction in DNA damage at an X-ray dose of 40 Gy. For NCS-induced damage, Tempol increased survival from 9% to 80% at 60 ng/mL NCS and reduced mutation induction by a factor of approximately 3. DNA dsb were reduced by a factor of approximately 7 at 500 ng/mL NCS. Tempol is representative of a class of stable nitroxide free radical compounds that have superoxide dismutase-mimetic activity, can oxidize metal ions such as ferrous iron that are complexed to DNA, and may also detoxify radiation-induced organoperoxide radicals by competitive scvenging. The NCS chromophore is reduced by sulfhydryls to an active form. Electron spin resonance (ESR) spectroscopy shows that 2-mercaptoethanol-activated NCS reacts with Tempol 3.5 times faster than does unactivated NCS. Thus, Tempol appears to inactivate the NCS chromophore before a substantial amount of DNA damage occurs. JF - Free radical biology & medicine AU - DeGraff, W G AU - Krishna, M C AU - Kaufman, D AU - Mitchell, J B AD - Radiobiology Section, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 479 EP - 487 VL - 13 IS - 5 SN - 0891-5849, 0891-5849 KW - Cyclic N-Oxides KW - 0 KW - Radiation-Protective Agents KW - Spin Labels KW - DNA KW - 9007-49-2 KW - Zinostatin KW - 9014-02-2 KW - tempol KW - U78ZX2F65X KW - Index Medicus KW - Animals KW - X-Rays KW - Dose-Response Relationship, Drug KW - Kinetics KW - CHO Cells KW - Dose-Response Relationship, Radiation KW - Cell Line KW - Mutagenesis KW - Cricetinae KW - Cell Survival -- drug effects KW - DNA Damage KW - Cyclic N-Oxides -- pharmacology KW - Radiation-Protective Agents -- pharmacology KW - Cell Survival -- radiation effects KW - DNA -- radiation effects KW - Zinostatin -- pharmacology KW - DNA -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73392384?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Free+radical+biology+%26+medicine&rft.atitle=Nitroxide-mediated+protection+against+X-ray-+and+neocarzinostatin-induced+DNA+damage.&rft.au=DeGraff%2C+W+G%3BKrishna%2C+M+C%3BKaufman%2C+D%3BMitchell%2C+J+B&rft.aulast=DeGraff&rft.aufirst=W&rft.date=1992-11-01&rft.volume=13&rft.issue=5&rft.spage=479&rft.isbn=&rft.btitle=&rft.title=Free+radical+biology+%26+medicine&rft.issn=08915849&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-12 N1 - Date created - 1993-01-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cellular proliferation and genetic events involved in the genesis of Burkitt lymphoma (BL) in immune compromised patients. AN - 73368102; 1458449 AB - A mathematical model simulating lymphomagenesis based on the two-hit theory of carcinogenesis is presented by contrasting the biologic variables responsible for a high risk of developing Burkitt lymphoma (BL) in three immunosuppressed groups with that of nonendemic BL. In this model, the pro-B lymphocyte is considered to be the target for BL-specific translocations such as t(8;14). With repeated mitosis, the target cell pool expands in the high-risk individual, and, thereby, the opportunities for a spontaneous translocation to arise are increased. The chromosomal translocation endows the target cell with survival advantages, and, hence, lymphoma develops. Modeling results demonstrate that this increased cell proliferation is sufficient in accounting entirely for the increase in tumor prevalence. Preventing enhanced cellular proliferation by obviating immune deficiency and treating patients with agents that restore immunity or have antiviral and antiproliferative properties prior to conversion from polyclonal B-cell proliferation to monoclonal malignancy could obviate the development of BL. JF - Cancer genetics and cytogenetics AU - Ellwein, L B AU - Purtilo, D T AD - National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 42 EP - 48 VL - 64 IS - 1 SN - 0165-4608, 0165-4608 KW - Index Medicus KW - AIDS/HIV KW - Lymphoproliferative Disorders -- genetics KW - Genetic Linkage KW - X Chromosome KW - Humans KW - HIV Infections -- genetics KW - Gene Rearrangement KW - Child KW - B-Lymphocytes -- immunology KW - Cell Transformation, Neoplastic KW - Cell Division KW - Gene Expression Regulation, Neoplastic KW - Computer Simulation KW - Models, Genetic KW - Burkitt Lymphoma -- genetics KW - Immunocompromised Host UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73368102?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+genetics+and+cytogenetics&rft.atitle=Cellular+proliferation+and+genetic+events+involved+in+the+genesis+of+Burkitt+lymphoma+%28BL%29+in+immune+compromised+patients.&rft.au=Ellwein%2C+L+B%3BPurtilo%2C+D+T&rft.aulast=Ellwein&rft.aufirst=L&rft.date=1992-11-01&rft.volume=64&rft.issue=1&rft.spage=42&rft.isbn=&rft.btitle=&rft.title=Cancer+genetics+and+cytogenetics&rft.issn=01654608&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-12 N1 - Date created - 1993-01-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Estimating the prevalence of mental disorders in U.S. adults from the Epidemiologic Catchment Area Survey. AN - 73354845; 1454978 AB - The National Institute of Mental Health Epidemiologic Catchment Area Survey is a comprehensive, community-based survey of mental disorders and use of services by adults, ages 18 and older. Diagnoses are based on the criteria in the "Diagnostic and Statistical Manual of Mental Disorders," third edition, and were obtained in five communities in the United States through lay-interviewer administration of the National Institute of Mental Health Diagnostic Interview Schedule. Results from the survey provide the public health field with data on the prevalence and incidence of specific mental disorders in the community, unbiased by the treatment status of the sample. The population with disorders is estimated, and the survey findings that respond to some of the most common requests for information about the epidemiology of mental disorders in the United States are highlighted briefly. Based on the survey, it is estimated that one of every five persons in the United States suffers from a mental disorder in any 6-month period, and that one of every three persons suffers a disorder in his or her lifetime. Fewer than 20 percent of those with a recent mental disorder seek help for their problem, according to the survey. High rates of comorbid substance abuse and mental disorders were found, particularly among those who had sought treatment for their disorders. JF - Public health reports (Washington, D.C. : 1974) AU - Bourdon, K H AU - Rae, D S AU - Locke, B Z AU - Narrow, W E AU - Regier, D A AD - Division of Clinical Research, National Institute of Mental Health, Rockville, MD 20857. PY - 1992 SP - 663 EP - 668 VL - 107 IS - 6 SN - 0033-3549, 0033-3549 KW - Abridged Index Medicus KW - Index Medicus KW - Severity of Illness Index KW - Sex Factors KW - Mental Health Services -- statistics & numerical data KW - Humans KW - Substance-Related Disorders -- etiology KW - National Institute of Mental Health (U.S.) KW - Mental Health Services -- utilization KW - Ambulatory Care Facilities -- statistics & numerical data KW - Catchment Area (Health) KW - Comorbidity KW - Interview, Psychological KW - Patient Acceptance of Health Care -- statistics & numerical data KW - Health Surveys KW - Information Services -- statistics & numerical data KW - Hospitalization -- statistics & numerical data KW - Information Services -- utilization KW - United States -- epidemiology KW - Ambulatory Care Facilities -- utilization KW - Female KW - Male KW - Substance-Related Disorders -- epidemiology KW - Prevalence KW - Mental Disorders -- diagnosis KW - Mental Disorders -- therapy KW - Mental Disorders -- epidemiology KW - Population Surveillance UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73354845?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Public+health+reports+%28Washington%2C+D.C.+%3A+1974%29&rft.atitle=Estimating+the+prevalence+of+mental+disorders+in+U.S.+adults+from+the+Epidemiologic+Catchment+Area+Survey.&rft.au=Bourdon%2C+K+H%3BRae%2C+D+S%3BLocke%2C+B+Z%3BNarrow%2C+W+E%3BRegier%2C+D+A&rft.aulast=Bourdon&rft.aufirst=K&rft.date=1992-11-01&rft.volume=107&rft.issue=6&rft.spage=663&rft.isbn=&rft.btitle=&rft.title=Public+health+reports+%28Washington%2C+D.C.+%3A+1974%29&rft.issn=00333549&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-07 N1 - Date created - 1993-01-07 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Arch Gen Psychiatry. 1992 Jan;49(1):37-46 [1728250] JAMA. 1990 Nov 21;264(19):2511-8 [2232018] JAMA. 1989 Apr 21;261(15):2229-35 [2648043] Acta Psychiatr Scand. 1989 Feb;79(2):163-78 [2784251] Arch Gen Psychiatry. 1988 Dec;45(12):1069-77 [2848472] Arch Gen Psychiatry. 1984 Oct;41(10):983-9 [6477056] J Am Geriatr Soc. 1985 Apr;33(4):228-35 [3989183] Arch Gen Psychiatry. 1981 Apr;38(4):381-9 [6260053] Arch Gen Psychiatry. 1984 Oct;41(10):942-8 [6477054] Arch Gen Psychiatry. 1984 Oct;41(10):971-8 [6477055] Arch Gen Psychiatry. 1988 Nov;45(11):977-86 [3263101] N1 - Last updated - 2017-01-17 ER - TY - CONF T1 - Animal models of retrovirus-associated malignancies. AN - 73348923; 1360178 JF - Veterinary pathology AU - Cremer, K J AU - Gruber, J Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 572 EP - 578 VL - 29 IS - 6 KW - Index Medicus KW - Neoplasms, Experimental -- microbiology KW - Animals KW - Neoplasms -- veterinary KW - Retroviridae Infections -- veterinary KW - Retroviridae Infections -- microbiology KW - Disease Models, Animal KW - Neoplasms -- microbiology KW - Retroviridae Infections -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73348923?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=Veterinary+pathology&rft.atitle=Animal+models+of+retrovirus-associated+malignancies.&rft.au=Cremer%2C+K+J%3BGruber%2C+J&rft.aulast=Cremer&rft.aufirst=K&rft.date=1992-11-01&rft.volume=29&rft.issue=6&rft.spage=572&rft.isbn=&rft.btitle=&rft.title=Veterinary+pathology&rft.issn=03009858&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-28 N1 - Date created - 1992-12-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Activation of human peripheral blood T lymphocytes by pharmacological induction of protein-tyrosine phosphorylation. AN - 73328066; 1279675 AB - Protein-tyrosine kinase and protein-tyrosine phosphatase (PTPase) activities are essential for T-cell antigen receptor-mediated signaling. To assess the functional consequences of alteration of the levels of tyrosine phosphorylation in normal human T cells, the effects of vanadate and hydrogen peroxide were studied. In combination, these agents induced tyrosine phosphorylation of cellular substrates, elevated cytosolic free calcium, and induced interleukin 2 receptor (IL-2R) alpha chain expression but not IL-2 secretion. However, anti-CD28 antibody in combination with vanadate and hydrogen peroxide induced IL-2 secretion, consistent with the requirement for a costimulatory signal in the induction of this gene. The effects of vanadate and hydrogen peroxide were enhanced in the absence of the T-cell PTPase, CD45. Thus, acute pharmacologic manipulation of the level of tyrosine phosphorylation in normal T cells correlates with partial, but not full, activation of these cells; in concert with a costimulatory signal provided by perturbation of the CD28 molecule, the complete program of activation is initiated. These agents should prove useful in dissecting signaling pathways involved in the regulation of genes critical to the immune response. JF - Proceedings of the National Academy of Sciences of the United States of America AU - O'Shea, J J AU - McVicar, D W AU - Bailey, T L AU - Burns, C AU - Smyth, M J AD - Leukocyte Cell Biology Section, National Cancer Institute, Frederick, MD 21702-1201. Y1 - 1992/11/01/ PY - 1992 DA - 1992 Nov 01 SP - 10306 EP - 10310 VL - 89 IS - 21 SN - 0027-8424, 0027-8424 KW - Receptors, Interleukin-2 KW - 0 KW - Phosphotyrosine KW - 21820-51-9 KW - Vanadates KW - 3WHH0066W5 KW - Tyrosine KW - 42HK56048U KW - RNA KW - 63231-63-0 KW - Hydrogen Peroxide KW - BBX060AN9V KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Protein Tyrosine Phosphatases KW - EC 3.1.3.48 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Cytosol -- metabolism KW - Immunoblotting KW - Protein Tyrosine Phosphatases -- metabolism KW - Vanadates -- pharmacology KW - Humans KW - Receptors, Interleukin-2 -- biosynthesis KW - Hydrogen Peroxide -- pharmacology KW - Mice KW - Tyrosine -- analysis KW - RNA -- blood KW - Cells, Cultured KW - Kinetics KW - RNA -- isolation & purification KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Flow Cytometry KW - Gene Expression Regulation -- drug effects KW - Tyrosine -- analogs & derivatives KW - Cell Line KW - Receptors, Interleukin-2 -- drug effects KW - RNA -- genetics KW - Lymphocyte Activation KW - Calcium -- metabolism KW - T-Lymphocytes -- metabolism KW - T-Lymphocytes -- drug effects KW - Protein-Tyrosine Kinases -- metabolism KW - T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73328066?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Activation+of+human+peripheral+blood+T+lymphocytes+by+pharmacological+induction+of+protein-tyrosine+phosphorylation.&rft.au=O%27Shea%2C+J+J%3BMcVicar%2C+D+W%3BBailey%2C+T+L%3BBurns%2C+C%3BSmyth%2C+M+J&rft.aulast=O%27Shea&rft.aufirst=J&rft.date=1992-11-01&rft.volume=89&rft.issue=21&rft.spage=10306&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-11 N1 - Date created - 1992-12-11 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1991 Jul 15;88(14):6279-83 [2068107] Cell. 1991 Mar 8;64(5):875-8 [1848158] J Biol Chem. 1990 Feb 15;265(5):2896-902 [2154464] Nature. 1990 Jul 5;346(6279):66-8 [2164155] Proc Natl Acad Sci U S A. 1990 Oct;87(19):7722-6 [2217205] Cell. 1985 Jul;41(3):707-17 [2408760] Science. 1989 Apr 21;244(4902):339-43 [2540528] Cell. 1989 Sep 22;58(6):1055-65 [2550143] Biochemistry. 1989 Oct 31;28(22):8864-71 [2690951] J Immunol. 1988 Apr 15;140(8):2520-6 [2895789] J Biol Chem. 1982 Jul 10;257(13):7298-301 [6282838] J Immunol. 1992 Apr 15;148(8):2497-502 [1532816] Immunol Today. 1992 Feb;13(2):63-8 [1575894] Cell. 1991 Aug 23;66(4):685-96 [1652370] J Biol Chem. 1990 Jan 5;265(1):318-27 [1688431] Proc Natl Acad Sci U S A. 1990 Jul;87(14):5327-30 [1695377] Proc Natl Acad Sci U S A. 1991 Jan 15;88(2):350-4 [1703295] Nature. 1991 Mar 7;350(6313):62-6 [1706070] J Immunol. 1991 Oct 15;147(8):2461-6 [1717561] J Exp Med. 1991 Mar 1;173(3):721-30 [1847722] Proc Natl Acad Sci U S A. 1991 Mar 1;88(5):1741-5 [2000381] Science. 1990 Mar 30;247(4950):1584-7 [2138816] Immunol Today. 1990 Jun;11(6):211-6 [2162180] Annu Rev Immunol. 1990;8:421-52 [2188669] Cancer Res. 1989 Feb 15;49(4):780-5 [2463877] J Biol Chem. 1989 Jun 15;264(17):10126-32 [2542323] J Biol Chem. 1989 Jun 25;264(18):10836-42 [2786526] J Exp Med. 1986 Oct 1;164(4):1193-205 [3093626] Immunogenetics. 1981 Mar 1;12(5-6):511-23 [7194313] J Biol Chem. 1992 Mar 5;267(7):4924-9 [1537871] J Biol Chem. 1992 Apr 5;267(10):7154-9 [1551921] Proc Natl Acad Sci U S A. 1991 Aug 1;88(15):6575-9 [1650475] Proc Natl Acad Sci U S A. 1991 Mar 15;88(6):2037-41 [1672451] J Exp Med. 1991 Dec 1;174(6):1407-15 [1683892] J Immunol. 1990 Mar 1;144(5):1591-9 [1689750] Proc Natl Acad Sci U S A. 1990 Dec;87(23):9255-9 [1701256] J Immunol. 1991 Jan 1;146(1):206-10 [1701792] Cancer Cells. 1990 Oct;2(10):303-10 [1704247] Proc Natl Acad Sci U S A. 1991 Jul 1;88(13):5484-8 [1712101] Proc Natl Acad Sci U S A. 1991 Jun 15;88(12):5453-6 [1828897] J Immunol. 1991 Nov 1;147(9):3122-7 [1833464] Science. 1990 Jun 15;248(4961):1349-56 [2113314] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Combination treatment with azidothymidine and granulocyte colony-stimulating factor in children with human immunodeficiency virus infection. AN - 73315843; 1279153 AB - Bone marrow suppression is the major dose-limiting toxic effect of zidovudine (azidothymidine; AZT) in children with human immunodeficiency virus infection. We evaluated the effect of subcutaneously administered granulocyte colony-stimulating factor (G-CSF) in pediatric patients whose absolute neutrophil count was less than 0.8 x 10(9)/L during AZT therapy despite dosage reductions to 120 mg/m2 every 6 hours. Nineteen patients between 6 months and 20 years of age were treated with AZT and G-CSF and monitored for 2 to 12 months. All had previously shown improvement while receiving AZT but had required dosage reduction or discontinuation. By using a sliding dosing schedule of G-CSF, we attempted to maintain the absolute neutrophil count between 1.5 and 5.0 x 10(9)/L. Administration of G-CSF resulted in a significant increase in the median leukocyte count (2.0 x 10(9)/L to 4.14 x 10(9)/L; p = 0.004), and the median absolute neutrophil count (1.02 x 10(9)/L to 2.96 x 10(9)/L; p = 0.0006). G-CSF was well tolerated, but mild thrombocytopenia developed in nine children. Administration of G-CSF and AZT was discontinued in two patients because of continuing neutropenia. With doses of G-CSF ranging from 1 to 20 micrograms/kg per day, 17 of 19 patients were able to tolerate AZT at a dose of 120 to 180 mg/m2 every 6 hours. We conclude that G-CSF therapy enables patients who have had AZT-related neutropenia to receive therapeutic doses of AZT. JF - The Journal of pediatrics AU - Mueller, B U AU - Jacobsen, F AU - Butler, K M AU - Husson, R N AU - Lewis, L L AU - Pizzo, P A AD - Pediatric Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 797 EP - 802 VL - 121 IS - 5 Pt 1 SN - 0022-3476, 0022-3476 KW - Granulocyte Colony-Stimulating Factor KW - 143011-72-7 KW - Zidovudine KW - 4B9XT59T7S KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Infant KW - Drug Therapy, Combination KW - Neutrophils KW - Humans KW - Pilot Projects KW - Child KW - Adolescent KW - Male KW - Leukocyte Count KW - Female KW - Platelet Count KW - Child, Preschool KW - Zidovudine -- adverse effects KW - HIV Infections -- blood KW - HIV Infections -- therapy KW - Granulocyte Colony-Stimulating Factor -- adverse effects KW - Zidovudine -- administration & dosage KW - Granulocyte Colony-Stimulating Factor -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73315843?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+pediatrics&rft.atitle=Combination+treatment+with+azidothymidine+and+granulocyte+colony-stimulating+factor+in+children+with+human+immunodeficiency+virus+infection.&rft.au=Mueller%2C+B+U%3BJacobsen%2C+F%3BButler%2C+K+M%3BHusson%2C+R+N%3BLewis%2C+L+L%3BPizzo%2C+P+A&rft.aulast=Mueller&rft.aufirst=B&rft.date=1992-11-01&rft.volume=121&rft.issue=5+Pt+1&rft.spage=797&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pediatrics&rft.issn=00223476&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-18 N1 - Date created - 1992-12-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Childhood leukemia and neonatal exposure to lighting in nurseries. AN - 73301571; 1420860 JF - Cancer causes & control : CCC AU - Miller, R W AD - Clinical Epidemiology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 581 EP - 582 VL - 3 IS - 6 SN - 0957-5243, 0957-5243 KW - Index Medicus KW - Infant KW - Humans KW - Child KW - Adolescent KW - Child, Preschool KW - Lighting -- adverse effects KW - Infant, Newborn KW - Environmental Exposure KW - Nurseries KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73301571?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+causes+%26+control+%3A+CCC&rft.atitle=Childhood+leukemia+and+neonatal+exposure+to+lighting+in+nurseries.&rft.au=Miller%2C+R+W&rft.aulast=Miller&rft.aufirst=R&rft.date=1992-11-01&rft.volume=3&rft.issue=6&rft.spage=581&rft.isbn=&rft.btitle=&rft.title=Cancer+causes+%26+control+%3A+CCC&rft.issn=09575243&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-18 N1 - Date created - 1992-12-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Preferential and strand-specific DNA repair of (6-4) photoproducts detected by a photochemical method in the hamster DHFR gene. AN - 73299252; 1423865 AB - A non-enzymatic method that was previously shown to create single-strand DNA breaks at the location of (6-4) photoproducts in the overall genome was adapted to measure (6-4) photoproducts at the level of the gene. This approach employs a photoisomerization step that converts the (6-4) photoproduct into the Dewar valence photoisomer, which is more alkaline labile and allows for the creation of a single-strand DNA break at this site. These strand breaks were quantified via Southern analysis and the DNA repair of (6-4) photoproducts was measured over 2, 4 and 8 h after a UV dose of 40 J/m2. A comparison of repair efficiency in the actively transcribed dihydrofolate reductase (DHFR) gene, a transcriptionally inactive genomic region and the overall genome (as measured by radioimmunoassay) showed preferential repair of the active gene. The active DHFR gene showed 59% repair by 8 h compared to 33% repair in the inactive downstream region. Analysis of (6-4) photoproduct repair in the transcribed and non-transcribed strands of the DHFR gene indicate some strand specificity with 62% repair in the transcribed strand at 8 h compared with 43% repair in the non-transcribed strand. However, this strand bias is much less distinct than has been reported for the major UV photoproduct, the cyclobutane pyrimidine dimer. JF - Carcinogenesis AU - Link, C J AU - Mitchell, D L AU - Nairn, R S AU - Bohr, V A AD - Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 1975 EP - 1980 VL - 13 IS - 11 SN - 0143-3334, 0143-3334 KW - DHFR KW - Tetrahydrofolate Dehydrogenase KW - EC 1.5.1.3 KW - Index Medicus KW - Photochemistry KW - Animals KW - DNA Damage KW - Blotting, Southern KW - CHO Cells KW - Radioimmunoassay KW - Cricetinae KW - DNA Repair KW - Tetrahydrofolate Dehydrogenase -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73299252?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Preferential+and+strand-specific+DNA+repair+of+%286-4%29+photoproducts+detected+by+a+photochemical+method+in+the+hamster+DHFR+gene.&rft.au=Link%2C+C+J%3BMitchell%2C+D+L%3BNairn%2C+R+S%3BBohr%2C+V+A&rft.aulast=Link&rft.aufirst=C&rft.date=1992-11-01&rft.volume=13&rft.issue=11&rft.spage=1975&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-22 N1 - Date created - 1992-12-22 N1 - Date revised - 2017-01-13 N1 - Gene symbol - DHFR N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The relationship between three subtypes of the flushing response and DSM-III alcohol abuse in Japanese. AN - 73296844; 1434631 AB - This study examined the relationship between the flushing response and drinking patterns and DSM-III alcohol abuse among Japanese using data collected in the joint U.S.-Japan collaborative study. The flushing response was classified into the following three subtypes: typical flushing (always flushed in the face after drinking), atypical flushing (sometimes) and nonflushing (never). This study of male current drinkers showed that typical flushers drank less alcohol than did atypical and nonflushers, but there was no observed difference between the drinking patterns of atypical flushers and nonflushers. Although the relationship was less pronounced, a similar association was found for female current drinkers. The 12-month prevalence of DSM-III alcohol abuse was estimated to be highest among atypical flushers and lowest among typical flushers, with nonflushers in between for both genders. When daily alcohol consumption and other pertinent sociodemographic variables were controlled, logistic regression analyses revealed that the risk for alcohol abuse by men was approximately 3.0 times higher among atypical flushers and 1.7 times higher among nonflushers than among typical flushers. The corresponding risks for abuse by women were 7.8 (atypical flushers) and 2.8 (nonflushers) times higher. Possible explanations for these differences in drinking patterns and the risk for alcohol abuse among the three flushing subtypes and between genders are discussed. JF - Journal of studies on alcohol AU - Higuchi, S AU - Parrish, K M AU - Dufour, M C AU - Towle, L H AU - Harford, T C AD - Division of Biometry and Epidemiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20857. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 553 EP - 560 VL - 53 IS - 6 SN - 0096-882X, 0096-882X KW - Ethanol KW - 3K9958V90M KW - Index Medicus KW - Phenotype KW - Psychiatric Status Rating Scales KW - Humans KW - Adult KW - Middle Aged KW - Adolescent KW - Male KW - Japan KW - Female KW - Ethanol -- adverse effects KW - Flushing -- etiology KW - Alcohol Drinking -- ethnology KW - Alcoholism -- diagnosis KW - Cross-Cultural Comparison KW - Alcoholism -- ethnology KW - Alcohol Drinking -- adverse effects KW - Alcohol Drinking -- genetics KW - Alcoholism -- genetics KW - Ethnic Groups -- psychology KW - Alcoholism -- psychology KW - Flushing -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73296844?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+studies+on+alcohol&rft.atitle=The+relationship+between+three+subtypes+of+the+flushing+response+and+DSM-III+alcohol+abuse+in+Japanese.&rft.au=Higuchi%2C+S%3BParrish%2C+K+M%3BDufour%2C+M+C%3BTowle%2C+L+H%3BHarford%2C+T+C&rft.aulast=Higuchi&rft.aufirst=S&rft.date=1992-11-01&rft.volume=53&rft.issue=6&rft.spage=553&rft.isbn=&rft.btitle=&rft.title=Journal+of+studies+on+alcohol&rft.issn=0096882X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-08 N1 - Date created - 1992-12-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - 32P-postlabeling analysis of the formation and persistence of DNA adducts in mammary glands of parous and nulliparous mice treated with benzo[a]pyrene. AN - 73294738; 1423869 AB - The susceptibility of the rodent mammary gland to known chemical carcinogens can vary with the stage of gland development. Full-term pregnancy (parity) can confer permanent structural and functional changes in the gland that are associated with decreased breast cancer risk in humans and protection from mammary carcinogenesis in rodents. In this study, the formation and persistence of benzo[a]pyrene (B[a]P)-derived DNA adducts in vivo was determined in the abdominal mammary organs of adult nulliparous and parous BALB/c mice treated orally with the carcinogen. Mammary DNA isolated from animals in both groups revealed only one major adduct on TLC maps by P1-nuclease 32P-postlabeling analysis. The major adduct co-migrated with the (+)-enantiomer of anti-BPDE-dGp. Much lower levels of the (-)-enantiomer were detected. Most of the adduct quantitated was probably contributed by cells of the stromal compartment, since the gland-free organ (cleared fat pad) generated essentially equivalent profiles and level of adduct by 32P-postlabeling. Comparable levels of the B[a]P-derived adduct were observed in the intact mammary organ of both nulliparous and parous mice during a time course from 1 to 28 days after treatment. In both cases, adduct removal occurred exponentially with a half-life of approximately 16 days. The capacity for de novo formation of reactive metabolites by the mammary organ was demonstrated in vitro: digests of DNA from mammary mince exposed to B[a]P generated an adduct on TLC maps that also co-migrated with the (+)-anti-BPDE-dGp standard. Thus, our cumulative findings confirm the capacity of mammary cells to form potentially carcinogenic DNA adducts; however, the functional changes that occur in the mouse mammary gland as a result of parity did not influence the profile, level or persistence of adduct following exposure to a known carcinogen. Other factors, such as changes in mammary cell cycle kinetics or responsiveness to promotional stimuli may be more causally related to reduction in incidence of neoplasia observed in parous animals. JF - Carcinogenesis AU - Walker, M P AU - Jahnke, G D AU - Snedeker, S M AU - Gladen, B C AU - Lucier, G W AU - DiAugustine, R P AD - Laboratory of Biochemical Risk Analysis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 2009 EP - 2015 VL - 13 IS - 11 SN - 0143-3334, 0143-3334 KW - Phosphorus Radioisotopes KW - 0 KW - Benzo(a)pyrene KW - 3417WMA06D KW - Index Medicus KW - Parity KW - Animals KW - Stereoisomerism KW - Stromal Cells -- drug effects KW - Mice KW - Chromatography, Thin Layer KW - Mice, Inbred BALB C KW - Autoradiography KW - Female KW - Pregnancy KW - Mammary Glands, Animal -- drug effects KW - DNA Damage KW - Benzo(a)pyrene -- toxicity KW - Mammary Glands, Animal -- anatomy & histology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73294738?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=32P-postlabeling+analysis+of+the+formation+and+persistence+of+DNA+adducts+in+mammary+glands+of+parous+and+nulliparous+mice+treated+with+benzo%5Ba%5Dpyrene.&rft.au=Walker%2C+M+P%3BJahnke%2C+G+D%3BSnedeker%2C+S+M%3BGladen%2C+B+C%3BLucier%2C+G+W%3BDiAugustine%2C+R+P&rft.aulast=Walker&rft.aufirst=M&rft.date=1992-11-01&rft.volume=13&rft.issue=11&rft.spage=2009&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-22 N1 - Date created - 1992-12-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of transforming growth factor-beta in maintenance of function of cultured neonatal cardiac myocytes. Autocrine action and reversal of damaging effects of interleukin-1. AN - 73294643; 1430228 AB - The three isoforms of transforming growth factor-beta (TGF-beta) have previously been implicated in embryonic development of the heart as well as in repair of myocardial damage after ischemia/reperfusion injury. TGF-beta 1 has also been localized intracellularly to both mitochondria and contractile filaments of cardiac myocytes, although its role in these structures has not been defined. We now report that exogenous TGF-beta stabilizes the beating rate of neonatal rat cardiac myocytes cultured on fibroblast matrix, and sustains their spontaneous rhythmic beating in serum-free medium. Moreover, using blocking antibodies to TGF-beta, we show that endogenous TGF-beta secreted by these myocytes acts in an autocrine fashion to maintain their beating rate. In contrast, IL-1 beta, an inflammatory mediator secreted by immune cells during myocardial injury, inhibits the beating of cardiac myocytes, and TGF-beta can overcome this inhibition. The antagonistic effects of TGF-beta and IL-1 were not observed when the myocytes were cultured on gelatin, as compared to native fibroblast matrix. The data indicate that TGF-beta is an important regulator of contractile function of the heart and have significant implications for understanding cardiac physiology in health and disease. JF - The Journal of clinical investigation AU - Roberts, A B AU - Roche, N S AU - Winokur, T S AU - Burmester, J K AU - Sporn, M B AD - Laboratory of Chemoprevention, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 2056 EP - 2062 VL - 90 IS - 5 SN - 0021-9738, 0021-9738 KW - Interleukin-1 KW - 0 KW - Transforming Growth Factor beta KW - Abridged Index Medicus KW - Index Medicus KW - Rats KW - Animals KW - Heart Rate -- drug effects KW - Cells, Cultured KW - Myocardial Contraction -- drug effects KW - Animals, Newborn -- physiology KW - Transforming Growth Factor beta -- pharmacology KW - Heart -- drug effects KW - Interleukin-1 -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73294643?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+clinical+investigation&rft.atitle=Role+of+transforming+growth+factor-beta+in+maintenance+of+function+of+cultured+neonatal+cardiac+myocytes.+Autocrine+action+and+reversal+of+damaging+effects+of+interleukin-1.&rft.au=Roberts%2C+A+B%3BRoche%2C+N+S%3BWinokur%2C+T+S%3BBurmester%2C+J+K%3BSporn%2C+M+B&rft.aulast=Roberts&rft.aufirst=A&rft.date=1992-11-01&rft.volume=90&rft.issue=5&rft.spage=2056&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+clinical+investigation&rft.issn=00219738&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-22 N1 - Date created - 1992-12-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 1992 Feb 5;267(4):2588-93 [1370826] Growth Factors. 1989;2(1):61-71 [2483947] Development. 1990 Apr;108(4):645-56 [1696875] Am J Pathol. 1989 Sep;135(3):541-56 [2506756] J Cell Biol. 1989 Dec;109(6 Pt 1):3137-45 [2592419] J Cell Biol. 1989 Feb;108(2):661-9 [2645303] Dev Biol. 1989 Aug;134(2):392-401 [2744239] Science. 1988 Oct 7;242(4875):97-9 [3175638] J Immunol. 1988 Apr 1;140(7):2312-6 [3280680] J Cell Biol. 1988 Apr;106(4):1375-84 [3283153] Am J Pathol. 1988 May;131(2):199-205 [3358450] J Biol Chem. 1987 Dec 5;262(34):16724-9 [3500170] Anal Biochem. 1984 Sep;141(2):322-8 [6093627] Dev Biol. 1980 Sep;79(1):247-52 [7409323] Eur J Immunol. 1991 Jul;21(7):1635-9 [1829411] Cell Regul. 1991 Jun;2(6):467-77 [1883875] J Cell Biol. 1991 Jun;113(5):981-6 [2040651] Science. 1990 Jul 6;249(4964):61-4 [2164258] J Immunol. 1990 Oct 15;145(8):2514-9 [2212650] Blood. 1990 Dec 15;76(12):2466-9 [2265243] Biochem J. 1990 Aug 15;270(1):269-71 [2396988] J Biol Chem. 1989 Jan 5;264(1):380-8 [2491849] Proc Natl Acad Sci U S A. 1989 Sep;86(17):6753-7 [2549546] J Am Coll Cardiol. 1989 Jun;13(7):1637-52 [2656824] Growth Factors. 1988;1(1):91-9 [3078566] Am J Pathol. 1988 Nov;133(2):298-305 [3189508] J Cell Biol. 1987 Dec;105(6 Pt 2):2861-76 [3320058] Cell. 1987 Oct 23;51(2):189-97 [3499229] Proc Natl Acad Sci U S A. 1981 Sep;78(9):5339-43 [6975480] Proc Natl Acad Sci U S A. 1992 Jul 15;89(14):6290-4 [1631120] Science. 1991 Jun 21;252(5013):1705-8 [1646484] Exp Cell Res. 1991 Aug;195(2):376-85 [1649057] J Clin Invest. 1990 Feb;85(2):507-14 [1688886] Prog Growth Factor Res. 1991;3(1):1-26 [1777597] Cell. 1991 Feb 22;64(4):841-8 [1847668] Biochem Pharmacol. 1991 Sep 12;42(7):1323-7 [1930256] Proc Natl Acad Sci U S A. 1991 Feb 15;88(4):1516-20 [1996351] J Exp Med. 1990 Sep 1;172(3):737-44 [2143773] Annu Rev Cell Biol. 1990;6:597-641 [2177343] Ann N Y Acad Sci. 1990;580:225-32 [2186691] Biochem J. 1990 Nov 1;271(3):827-30 [2244882] Nature. 1990 Jul 19;346(6281):281-4 [2374594] J Biol Chem. 1989 Jan 5;264(1):389-92 [2462560] Ciba Found Symp. 1991;157:29-40; discussion 41-50 [1649036] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Subchronic toxicity of barium chloride dihydrate administered to rats and mice in the drinking water. AN - 73291649; 1426711 AB - Barium Chloride dihydrate (BaCl2.2H2O) was given for 92 days to B6C3F1 mice and Fischer 344/N rats in their drinking water at levels of 0, 125, 500, 1000, 2000, and 4000 ppm. The no-effect level for this study was 2000 ppm BaCl2.2H2O in the drinking water. At 4000 ppm, daily consumption for mice was 436 to 562 mg/kg barium, up to four times more chemical than rats. Mortality ranged from 60 to 70% in mice and from 10 to 30% in rats in the 4000 ppm groups. Deaths in mice were associated with a treatment-related renal toxicity. Renal lesions in rats were much less severe than in mice and did not contribute to the treatment-related deaths seen in the high dose group. Body weights of both species and sexes in the 4000 ppm groups were lower than controls at 92 days. Male and female rats in treated groups exhibited higher serum phosphorus than controls. Serum sodium, potassium, and calcium levels in rats were unchanged by barium treatment, as were hematological values. In both species at 4000 ppm, motor activity, grip strength, and thermal sensitivity were marginally affected. These effects were probably secondary changes resulting from BaCl2 toxicity observed at this dose level. In a mating trial, no anatomical effects on offspring of rats or mice were seen. Rats receiving 4000 ppm exhibited marginal reductions in pup weights. No effects were seen on reproductive indices. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Dietz, D D AU - Elwell, M R AU - Davis, W E AU - Meirhenry, E F AD - Division of Toxicology Research and Testing, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 527 EP - 537 VL - 19 IS - 4 SN - 0272-0590, 0272-0590 KW - Barium Compounds KW - 0 KW - Chlorides KW - Electrolytes KW - barium chloride KW - 0VK51DA1T2 KW - Barium KW - 24GP945V5T KW - Index Medicus KW - Animals KW - Kidney -- pathology KW - Reproduction -- drug effects KW - Kidney -- drug effects KW - Mice KW - Pregnancy KW - Electrolytes -- blood KW - Rats KW - Behavior, Animal -- drug effects KW - Mice, Inbred Strains KW - Rats, Inbred F344 KW - Drinking -- drug effects KW - Body Weight -- drug effects KW - Female KW - Male KW - Organ Size -- drug effects KW - Barium -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73291649?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.atitle=Subchronic+toxicity+of+barium+chloride+dihydrate+administered+to+rats+and+mice+in+the+drinking+water.&rft.au=Dietz%2C+D+D%3BElwell%2C+M+R%3BDavis%2C+W+E%3BMeirhenry%2C+E+F&rft.aulast=Dietz&rft.aufirst=D&rft.date=1992-11-01&rft.volume=19&rft.issue=4&rft.spage=527&rft.isbn=&rft.btitle=&rft.title=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.issn=02720590&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-22 N1 - Date created - 1992-12-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Anthrax toxin protective antigen is activated by a cell surface protease with the sequence specificity and catalytic properties of furin. AN - 73286904; 1438214 AB - Proteolytic cleavage of the protective antigen (PA) protein of anthrax toxin at residues 164-167 is necessary for toxic activity. Cleavage by a cellular protease at this sequence, Arg-Lys-Lys-Arg, normally follows binding of PA to a cell surface receptor. We attempted to identify this protease by determining its sequence specificity and catalytic properties. Semi-random cassette mutagenesis was used to generate mutants with replacements of residues 164-167 by Arg, Lys, Ser, or Asn. Analysis of 19 mutant proteins suggested that lethal factor-dependent toxicity required the sequence Arg-Xaa-Xaa-Arg. Based on these data, three additional mutants were constructed with the sequences Ala-Lys-Lys-Arg, Arg-Lys-Lys-Ala, and Arg-Ala-Ala-Arg. Of these mutant proteins, Arg-Ala-Ala-Arg was toxic, confirming that the cellular protease can recognize the sequence Arg-Xaa-Xaa-Arg. The mutant containing the sequence Ala-Lys-Lys-Arg was also toxic but required > 13 times more protein to produce equivalent toxicity. This sequence specificity is similar to that of the ubiquitous subtilisin-like protease furin, which is involved in processing of precursors of certain receptors and growth factors. Therefore we tested whether a recombinant soluble furin would cleave PA. This furin derivative efficiently cleaved native PA and the Arg-Ala-Ala-Arg mutant but not the nontoxic PA mutants. In addition, previously identified inhibitors of furin blocked cleavage of receptor-bound PA. These data imply that furin is the cellular protease that activates PA, and that nearly all cell types contain at least a small amount of furin exposed on their cell surface. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Klimpel, K R AU - Molloy, S S AU - Thomas, G AU - Leppla, S H AD - Laboratory of Microbial Ecology, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/11/01/ PY - 1992 DA - 1992 Nov 01 SP - 10277 EP - 10281 VL - 89 IS - 21 SN - 0027-8424, 0027-8424 KW - Antigens, Bacterial KW - 0 KW - Bacterial Toxins KW - Oligodeoxyribonucleotides KW - anthrax toxin KW - Endopeptidases KW - EC 3.4.- KW - Subtilisins KW - EC 3.4.21.- KW - Furin KW - EC 3.4.21.75 KW - Index Medicus KW - Animals KW - Base Sequence KW - Kinetics KW - Molecular Sequence Data KW - Escherichia coli -- genetics KW - Amino Acid Sequence KW - Substrate Specificity KW - Cell Line KW - Bacterial Toxins -- genetics KW - Bacterial Toxins -- metabolism KW - Cell Survival -- drug effects KW - Cell Membrane -- enzymology KW - Bacillus anthracis -- genetics KW - Endopeptidases -- metabolism KW - Bacterial Toxins -- pharmacology KW - Bacillus anthracis -- enzymology KW - Mutagenesis, Insertional KW - Subtilisins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73286904?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Anthrax+toxin+protective+antigen+is+activated+by+a+cell+surface+protease+with+the+sequence+specificity+and+catalytic+properties+of+furin.&rft.au=Klimpel%2C+K+R%3BMolloy%2C+S+S%3BThomas%2C+G%3BLeppla%2C+S+H&rft.aulast=Klimpel&rft.aufirst=K&rft.date=1992-11-01&rft.volume=89&rft.issue=21&rft.spage=10277&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-11 N1 - Date created - 1992-12-11 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Methods Enzymol. 1991;195:153-68 [1903483] Mol Microbiol. 1991 Jun;5(6):1501-6 [1787799] Infect Immun. 1991 Oct;59(10):3381-6 [1909998] J Biol Chem. 1991 Oct 25;266(30):20124-30 [1939073] Cell. 1991 Jul 12;66(1):1-3 [2070411] Mol Biol Rep. 1990 Nov;14(4):265-75 [2094803] J Biol Chem. 1990 Nov 25;265(33):20678-85 [2122978] J Cell Biol. 1990 Dec;111(6 Pt 2):2851-9 [2269657] Nucleic Acids Res. 1990 Feb 11;18(3):664 [2408021] Proc Natl Acad Sci U S A. 1989 Apr;86(7):2209-13 [2467303] Infect Immun. 1989 Jul;57(7):2107-14 [2499545] J Biol Chem. 1989 Jul 5;264(19):11099-102 [2500434] J Biol Chem. 1989 Nov 15;264(32):19103-7 [2509473] Biochem Biophys Res Commun. 1988 Dec 15;157(2):747-54 [3144277] J Biol Chem. 1986 Jun 5;261(16):7123-6 [3711080] Histochem J. 1980 Jul;12(4):419-34 [6160123] Proc Natl Acad Sci U S A. 1982 May;79(10):3162-6 [6285339] Exp Cell Res. 1982 Mar;138(1):175-82 [7067736] J Biol Chem. 1981 Sep 10;256(17):9068-76 [7263699] J Gen Microbiol. 1958 Aug;19(1):91-103 [13575758] J Gen Microbiol. 1962 Nov;29:517-21 [13989434] J Bacteriol. 1965 Jan;89:74-83 [14255684] J Biol Chem. 1992 Aug 15;267(23):16396-402 [1644824] J Biol Chem. 1991 Jul 5;266(19):12127-30 [1905715] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Currently used doses of omeprazole in Zollinger-Ellison syndrome are too high. AN - 73286693; 1426868 AB - The efficacy of omeprazole increases during the first few days of administration, suggesting that long-term maintenance dose requirements in patients with Zollinger-Ellison syndrome may be lower than those initially established by upward titration. Long-term maintenance doses of omeprazole were prospectively reduced in 37 patients who had been taking omeprazole for 22 +/- 4 months. Successful reduction was defined as reduction to 20 mg once or twice daily with an absence of symptoms, endoscopy without evidence of active acid-peptic disease, and a gastric acid output of < 10 mEq/h. Sixty-eight percent of patients (25/37) were successfully reduced to 20 mg of omeprazole once (18/24) or twice daily (7/13). Ninety-five percent of patients (20/21) without multiple endocrine neoplasia type I, severe gastroesophageal reflux disease, or previous partial gastrectomy had safe reductions of doses. It is concluded that the currently used omeprazole maintenance doses in patients with Zollinger-Ellison syndrome are too high and advocated that the initial dose still be established by acute daily upward titration followed by gradual reduction once control of acid output has been achieved. JF - Gastroenterology AU - Metz, D C AU - Pisegna, J R AU - Fishbeyn, V A AU - Benya, R V AU - Feigenbaum, K M AU - Koviack, P D AU - Jensen, R T AD - Digestive Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 1498 EP - 1508 VL - 103 IS - 5 SN - 0016-5085, 0016-5085 KW - Gastrins KW - 0 KW - Omeprazole KW - KG60484QX9 KW - Abridged Index Medicus KW - Index Medicus KW - Prospective Studies KW - Humans KW - Gastrins -- blood KW - Adult KW - Aged KW - Middle Aged KW - Longitudinal Studies KW - Stomach -- drug effects KW - Male KW - Female KW - Gastric Acid -- secretion KW - Zollinger-Ellison Syndrome -- drug therapy KW - Omeprazole -- adverse effects KW - Omeprazole -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73286693?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gastroenterology&rft.atitle=Currently+used+doses+of+omeprazole+in+Zollinger-Ellison+syndrome+are+too+high.&rft.au=Metz%2C+D+C%3BPisegna%2C+J+R%3BFishbeyn%2C+V+A%3BBenya%2C+R+V%3BFeigenbaum%2C+K+M%3BKoviack%2C+P+D%3BJensen%2C+R+T&rft.aulast=Metz&rft.aufirst=D&rft.date=1992-11-01&rft.volume=103&rft.issue=5&rft.spage=1498&rft.isbn=&rft.btitle=&rft.title=Gastroenterology&rft.issn=00165085&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-14 N1 - Date created - 1992-12-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pharmacologic maintenance of abstinence in patients with alcoholism: no efficacy of 5-hydroxytryptophan or levodopa. AN - 73275028; 1424429 AB - Pharmacologic enhancement of central nervous system serotonin and dopamine functions has been postulated to improve maintenance of abstinence in patients with alcoholism. To test this hypothesis, patients with alcoholism who completed a 42-day inpatient treatment program were randomized to be administered, in a double-blind fashion, either 5-hydroxytryptophan and carbidopa, levodopa and carbidopa, or placebo for 1 year. Eight of 31 patients who entered the analysis remained abstinent from alcohol for 1 year; however, there was no significant effect of the treatment condition on maintenance of abstinence. Baseline psychologic measures showed that patients who abstained from alcohol had more education and higher scores on memory function tests. Measures of cerebrospinal fluid obtained before the start of the study indicated that all patients who had higher concentrations of the dopamine metabolite homovanillic acid relapsed, suggesting that further research is needed to elucidate the role of dopamine in alcoholism. JF - Clinical pharmacology and therapeutics AU - George, D T AU - Lindquist, T AU - Rawlings, R R AU - Eckardt, M J AU - Moss, H AU - Mathis, C AU - Martin, P R AU - Linnoila, M AD - Laboratory of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 553 EP - 560 VL - 52 IS - 5 SN - 0009-9236, 0009-9236 KW - Levodopa KW - 46627O600J KW - 5-Hydroxytryptophan KW - C1LJO185Q9 KW - Carbidopa KW - MNX7R8C5VO KW - Abridged Index Medicus KW - Index Medicus KW - Drug Therapy, Combination KW - Memory KW - Educational Status KW - Analysis of Variance KW - Double-Blind Method KW - Humans KW - Adult KW - Middle Aged KW - Carbidopa -- therapeutic use KW - Neuropsychological Tests KW - Time Factors KW - Male KW - Female KW - Intelligence Tests KW - Alcoholism -- cerebrospinal fluid KW - Levodopa -- therapeutic use KW - 5-Hydroxytryptophan -- therapeutic use KW - Alcoholism -- psychology KW - Alcoholism -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73275028?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+pharmacology+and+therapeutics&rft.atitle=Pharmacologic+maintenance+of+abstinence+in+patients+with+alcoholism%3A+no+efficacy+of+5-hydroxytryptophan+or+levodopa.&rft.au=George%2C+D+T%3BLindquist%2C+T%3BRawlings%2C+R+R%3BEckardt%2C+M+J%3BMoss%2C+H%3BMathis%2C+C%3BMartin%2C+P+R%3BLinnoila%2C+M&rft.aulast=George&rft.aufirst=D&rft.date=1992-11-01&rft.volume=52&rft.issue=5&rft.spage=553&rft.isbn=&rft.btitle=&rft.title=Clinical+pharmacology+and+therapeutics&rft.issn=00099236&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-22 N1 - Date created - 1992-12-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Amino- and carboxy-terminal deletion mutants of Gs alpha are localized to the particulate fraction of transfected COS cells. AN - 73257100; 1400589 AB - To elucidate the structural basis for membrane attachment of the alpha subunit of the stimulatory G protein (Gs alpha), mutant Gs alpha cDNAs with deletions of amino acid residues in the amino and/or carboxy termini were transiently expressed in COS-7 cells. The particulate and soluble fractions prepared from these cells were analyzed by immunoblot using peptide specific antibodies to monitor distribution of the expressed proteins. Transfection of mutant forms of Gs alpha with either 26 amino terminal residues deleted (delta 3-28) or with 59 amino terminal residues deleted (delta 1-59) resulted in immunoreactive proteins which localized primarily to the particulate fraction. Similarly, mutants with 10 (delta 385-394), 32 (delta 353-384), or 42 (delta 353-394) amino acid residues deleted from the carboxy terminus also localized to the particulate fraction, as did a mutant form of Gs alpha lacking amino acid residues at both the amino and carboxy termini (delta 3-28)/(delta 353-384). Mutant and wild type forms of Gs alpha demonstrated a similar degree of tightness in their binding to membranes as demonstrated by treatment with 2.5 M NaCl or 6 M urea, but some mutant forms were relatively resistant compared with wild type Gs alpha to solubilization by 15 mM NaOH or 1% sodium cholate. We conclude that: (a) deletion of significant portions of the amino and/or carboxyl terminus of Gs alpha is still compatible with protein expression; (b) deletion of these regions is insufficient to cause cytosolic localization of the expressed protein. The basis of Gs alpha membrane targeting remains to be elucidated. JF - The Journal of cell biology AU - Juhnn, Y S AU - Jones, T L AU - Spiegel, A M AD - Molecular Pathophysiology Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 523 EP - 530 VL - 119 IS - 3 SN - 0021-9525, 0021-9525 KW - Macromolecular Substances KW - 0 KW - Oligodeoxyribonucleotides KW - DNA KW - 9007-49-2 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Index Medicus KW - Animals KW - Immunoblotting KW - Electrophoresis, Polyacrylamide Gel KW - Amino Acid Sequence KW - Mutagenesis KW - Rats KW - Cell Fractionation KW - Base Sequence KW - DNA -- genetics KW - Molecular Sequence Data KW - Cell Membrane -- metabolism KW - Cell Line KW - Transfection KW - GTP-Binding Proteins -- metabolism KW - GTP-Binding Proteins -- analysis KW - GTP-Binding Proteins -- genetics KW - Sequence Deletion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73257100?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+cell+biology&rft.atitle=Amino-+and+carboxy-terminal+deletion+mutants+of+Gs+alpha+are+localized+to+the+particulate+fraction+of+transfected+COS+cells.&rft.au=Juhnn%2C+Y+S%3BJones%2C+T+L%3BSpiegel%2C+A+M&rft.aulast=Juhnn&rft.aufirst=Y&rft.date=1992-11-01&rft.volume=119&rft.issue=3&rft.spage=523&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+cell+biology&rft.issn=00219525&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-25 N1 - Date created - 1992-11-25 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cell. 1992 Mar 6;68(5):911-22 [1547491] Proc Natl Acad Sci U S A. 1985 Jun;82(12):4095-9 [3923487] J Biol Chem. 1991 May 15;266(14):9009-15 [1851161] Annu Rev Biochem. 1991;60:349-400 [1909108] Proc Natl Acad Sci U S A. 1991 Nov 15;88(22):10054-8 [1946422] J Biol Chem. 1990 May 25;265(15):8458-62 [2111318] Proc Natl Acad Sci U S A. 1990 Aug;87(15):5873-7 [2116011] Nature. 1990 Nov 8;348(6297):125-32 [2122258] Proc Natl Acad Sci U S A. 1990 Jan;87(2):728-32 [2153964] Nature. 1990 Aug 16;346(6285):658-60 [2385292] FEBS Lett. 1989 Jun 5;249(2):189-94 [2500363] FEBS Lett. 1989 Jul 17;251(1-2):230-6 [2502436] Proc Natl Acad Sci U S A. 1989 Oct;86(20):7900-3 [2554294] J Biol Chem. 1987 Oct 15;262(29):14241-9 [2820999] Proc Natl Acad Sci U S A. 1986 Dec;83(23):8893-7 [3024154] Annu Rev Biochem. 1988;57:69-99 [3052287] Proc Natl Acad Sci U S A. 1986 Apr;83(7):2258-62 [3083418] Proc Natl Acad Sci U S A. 1987 Nov;84(21):7493-7 [3118369] J Biol Chem. 1988 Jun 25;263(18):8996-70 [3132454] Neuron. 1988 Jul;1(5):403-10 [3272174] Methods Enzymol. 1987;152:684-704 [3657593] J Biol Chem. 1984 Nov 25;259(22):13806-13 [6438083] Anal Biochem. 1976 May 7;72:248-54 [942051] J Biol Chem. 1992 Jan 15;267(2):1271-8 [1730649] Nature. 1991 Jan 10;349(6305):117-27 [1898771] Proc Natl Acad Sci U S A. 1990 Jan;87(2):568-72 [2105488] Proc Natl Acad Sci U S A. 1990 Aug;87(15):5868-72 [2116010] J Cell Biol. 1990 Oct;111(4):1427-35 [2120241] Proc Natl Acad Sci U S A. 1990 Oct;87(19):7673-7 [2217200] Biochem Biophys Res Commun. 1987 Nov 13;148(3):1398-405 [2446610] Biochem J. 1989 Jun 15;260(3):837-41 [2504150] Methods Enzymol. 1989;174:39-50 [2633031] J Biol Chem. 1988 Jul 25;263(21):10394-400 [2839488] J Biol Chem. 1986 Jan 15;261(2):631-7 [3079758] Annu Rev Biochem. 1987;56:615-49 [3113327] Biochemistry. 1988 Jul 12;27(14):4957-65 [3139030] J Biol Chem. 1987 Nov 15;262(32):15746-51 [3316207] J Biol Chem. 1991 Mar 25;266(9):5363-6 [1706334] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Abnormal processing of transfected plasmid DNA in cells from patients with ataxia telangiectasia. AN - 73254604; 1383810 AB - In order to assess spontaneous mutability and accuracy of DNA joining in ataxia telangiectasia, a disorder with spontaneous chromosome breakage, the replicating shuttle vector plasmid, pZ189, was transfected into SV40 virus-transformed fibroblasts from ataxia telangiectasia patients. The ataxia telangiectasia fibroblasts showed elevated frequency of micronuclei, a measure of chromosome breakage. The spontaneous mutation frequency was normal with circular plasmids passed through the ataxia telangiectasia line. These results were compared to those with transformed fibroblasts from a patient with xeroderma pigmentosum, and from a normal donor. Mutation analysis revealed spontaneous point mutations and deletions in the plasmids with all 3 cell lines, however, insertions or complex mutations were only detectable with the ataxia telangiectasia line. To assess DNA-joining ability, linear plasmids which require joining of the DNA ends by host cell enzymes for survival, were transfected into the cells. We found a 2.4-fold less efficient DNA joining in ataxia telangiectasia fibroblasts (p = 0.04) and a 2.0-fold higher mutation frequency (p less than 0.01) in the recircularized plasmids than with the normal line. Plasmid DNA joining and mutation frequency were normal with the xeroderma pigmentosum fibroblasts. These findings with the ataxia telangiectasia fibroblasts of abnormal types of spontaneous mutations in the transfected plasmid and inefficient, error-prone DNA joining may be related to the increased chromosome breakage in these cells. In contrast, an EB virus-transformed ataxia telangiectasia lymphoblast line with normal frequency of micronuclei showed normal types of spontaneous mutations in the transfected plasmid and normal frequency of DNA joining which was error-prone. These data indicate that mechanisms that produce chromosome breakage in ataxia telangiectasia cells can be reflected in processing of plasmid vectors. JF - Mutation research AU - Rünger, T M AU - Poot, M AU - Kraemer, K H AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 47 EP - 54 VL - 293 IS - 1 SN - 0027-5107, 0027-5107 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Micronucleus Tests KW - DNA Repair KW - Transfection KW - Simian virus 40 -- genetics KW - Humans KW - Xeroderma Pigmentosum -- genetics KW - Lymphocytes -- metabolism KW - Cell Nucleus KW - Cell Line, Transformed KW - Plasmids KW - Mutation KW - Fibroblasts -- metabolism KW - Ataxia Telangiectasia -- genetics KW - DNA -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73254604?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutation+research&rft.atitle=Abnormal+processing+of+transfected+plasmid+DNA+in+cells+from+patients+with+ataxia+telangiectasia.&rft.au=R%C3%BCnger%2C+T+M%3BPoot%2C+M%3BKraemer%2C+K+H&rft.aulast=R%C3%BCnger&rft.aufirst=T&rft.date=1992-11-01&rft.volume=293&rft.issue=1&rft.spage=47&rft.isbn=&rft.btitle=&rft.title=Mutation+research&rft.issn=00275107&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-06 N1 - Date created - 1992-11-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Nucleotide sequence changes in the polymerase basic protein 2 gene of temperature-sensitive mutants of influenza A virus. AN - 73252348; 1413525 AB - Influenza A viruses bearing temperature-sensitive (ts) mutations are restricted in replication in the respiratory tract of animals and humans and are therefore attenuated. Nucleotide sequences were determined for the RNA segment coding for the polymerase basic protein 2 (PB2) from a panel of 12 influenza A/Udorn/307/72 (H3N2) ts viruses, previously characterized to have a ts mutation in the PB2 gene. Each of the viruses with a ts mutation in the PB2 gene had a single amino acid change located at position 65, 100, 112, 174, 298, 310, 386, 391, 556, or 658 of the PB2 protein. The sites of the single mutations were scattered throughout the length of the protein and occurred in regions that are highly conserved among the influenza A virus PB2 predicted amino acid sequences. Interestingly, the substitution of aspartic acid for asparagine at position 556 was found to lie within a region that has homology with cap-binding motifs of human and yeast proteins. Taken together, the findings of lesion sites in the A/Udorn/307/72 PB2 gene and the three reported amino acid changes at positions 265, 417, and 512 for A/AA/6/60, A/WSN/33, and A/FPV/Ros/34 ts PB2 genes, respectively, indicate that the PB2 gene can sustain a viable ts mutation at different sites. This information will allow us to construct cloned cDNA copies of the A/Udorn/307/72 PB2 gene mutagenized at specific sites. Different configurations of two or more ts mutations may be incorporated into the cDNA PB2 gene constructs. We have a host-range reassortant virus that should permit rescue of in vitro-produced transcripts of the PB2 gene into infectious virus. The rescue of these mutated PB2 RNA segments into an infectious influenza A virus may lead to the development of live attenuated reassortant virus vaccines that are satisfactorily attenuated, genetically stable, and immunogenic in humans. JF - Virology AU - Lawson, C M AU - Subbarao, E K AU - Murphy, B R AD - Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 506 EP - 510 VL - 191 IS - 1 SN - 0042-6822, 0042-6822 KW - DNA, Viral KW - 0 KW - PB2 protein, Influenzavirus A KW - Viral Proteins KW - RNA Replicase KW - EC 2.7.7.48 KW - Index Medicus KW - Base Sequence KW - Temperature KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Sequence Homology, Amino Acid KW - Viral Proteins -- genetics KW - Influenza A virus -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73252348?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Virology&rft.atitle=Nucleotide+sequence+changes+in+the+polymerase+basic+protein+2+gene+of+temperature-sensitive+mutants+of+influenza+A+virus.&rft.au=Lawson%2C+C+M%3BSubbarao%2C+E+K%3BMurphy%2C+B+R&rft.aulast=Lawson&rft.aufirst=C&rft.date=1992-11-01&rft.volume=191&rft.issue=1&rft.spage=506&rft.isbn=&rft.btitle=&rft.title=Virology&rft.issn=00426822&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-16 N1 - Date created - 1992-11-16 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M91713; GENBANK; M91712 N1 - SuppNotes - Erratum In: Virology 1993 Jul;195(1):302 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Macrophage-tropic human immunodeficiency virus isolates from different patients exhibit unusual V3 envelope sequence homogeneity in comparison with T-cell-tropic isolates: definition of critical amino acids involved in cell tropism. AN - 73240004; 1404602 AB - Previous experiments indicate that the V3 hypervariable region of the human immunodeficiency virus (HIV) envelope protein influences cell tropism of infection; however, so far no consistent V3 sequence can account for macrophage or T-cell tropism. In these experiments, we studied infectious recombinant HIV clones constructed by using V3 region sequences of HIV isolates from 16 patients to search for sequences associated with cell tropism. Remarkable homology was seen among V3 sequences from macrophage-tropic clones from different patients, and a consensus V3 region sequence for patient-derived macrophage-tropic viruses was identified. In contrast, V3 sequences of T-cell-tropic clones from different patients were highly heterogeneous, and the results suggested that sequence diversity leading to T-cell tropism might be generated independently in each patient. Site-specific mutations identified amino acids at several positions on each side of the GPGR motif at the tip of the V3 loop as important determinants of tropism for T cells and macrophages. However, a wide variety of mutant V3 sequences induced macrophage tropism, as detected in vitro. Therefore, the homogeneity of macrophage-tropic patient isolates appeared to be the result of selection based on a biological advantage in vivo. JF - Journal of virology AU - Chesebro, B AU - Wehrly, K AU - Nishio, J AU - Perryman, S AD - Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, Hamilton, Montana 59840. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 6547 EP - 6554 VL - 66 IS - 11 SN - 0022-538X, 0022-538X KW - DNA, Recombinant KW - 0 KW - HIV Envelope Protein gp120 KW - Index Medicus KW - AIDS/HIV KW - Genetic Variation KW - Humans KW - Amino Acid Sequence KW - Organ Specificity KW - Selection, Genetic KW - Cloning, Molecular KW - Structure-Activity Relationship KW - Virulence KW - Mutagenesis, Site-Directed KW - Base Sequence KW - Molecular Sequence Data KW - Sequence Homology, Amino Acid KW - Macrophages -- microbiology KW - T-Lymphocytes -- microbiology KW - HIV Infections -- genetics KW - HIV Infections -- microbiology KW - HIV Envelope Protein gp120 -- genetics KW - HIV -- genetics KW - HIV -- pathogenicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73240004?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Macrophage-tropic+human+immunodeficiency+virus+isolates+from+different+patients+exhibit+unusual+V3+envelope+sequence+homogeneity+in+comparison+with+T-cell-tropic+isolates%3A+definition+of+critical+amino+acids+involved+in+cell+tropism.&rft.au=Chesebro%2C+B%3BWehrly%2C+K%3BNishio%2C+J%3BPerryman%2C+S&rft.aulast=Chesebro&rft.aufirst=B&rft.date=1992-11-01&rft.volume=66&rft.issue=11&rft.spage=6547&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-18 N1 - Date created - 1992-11-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Virology. 1992 Jul;189(1):103-10 [1376536] Nature. 1991 Jan 10;349(6305):167-9 [1986308] J Virol. 1992 Apr;66(4):2577-82 [1548783] Lancet. 1986 Sep 20;2(8508):660-2 [2429124] Proc Natl Acad Sci U S A. 1988 May;85(9):3198-202 [2452447] Proc Natl Acad Sci U S A. 1988 Jun;85(12):4478-82 [2454471] Proc Natl Acad Sci U S A. 1991 Apr 15;88(8):3097-101 [2014229] AIDS Res Hum Retroviruses. 1991 Jan;7(1):3-16 [2015114] AIDS. 1990 Mar;4(3):221-8 [2112397] J Virol. 1990 Jul;64(7):3280-8 [2112615] Nature. 1990 Nov 1;348(6296):69-73 [2172833] Science. 1990 Aug 24;249(4971):932-5 [2392685] JAMA. 1990 Mar 16;263(11):1497-501 [2407871] FEBS Lett. 1989 May 8;248(1-2):48-52 [2470618] J Virol. 1989 May;63(5):2118-25 [2564898] Science. 1988 Apr 1;240(4848):80-2 [2832945] N Engl J Med. 1985 Dec 12;313(24):1493-7 [2999591] Science. 1986 Jul 11;233(4760):215-9 [3014648] J Virol. 1986 Aug;59(2):284-91 [3016298] Science. 1986 Sep 5;233(4768):1089-93 [3016903] J Virol. 1988 Oct;62(10):3779-88 [3047430] JAMA. 1986 Nov 7;256(17):2360-4 [3639953] Science. 1987 May 15;236(4803):819-22 [3646751] J Virol. 1991 Dec;65(12):6931-41 [1658383] Proc Natl Acad Sci U S A. 1990 Dec;87(24):9938-42 [1702224] J Virol. 1991 Feb;65(2):736-42 [1702842] Science. 1991 Jul 5;253(5015):71-4 [1905842] J Virol. 1991 Nov;65(11):5782-9 [1920616] J Virol. 1991 Nov;65(11):6266-76 [1920632] J Acquir Immune Defic Syndr. 1991;4(1):69-75 [1984058] J Infect Dis. 1991 Jan;163(1):64-70 [1984477] J Virol. 1991 Jan;65(1):190-4 [1985197] J Virol. 1991 Jan;65(1):356-63 [1985204] Science. 1992 Feb 28;255(5048):1134-7 [1546316] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Regulation of IL-2 receptor subunit genes in human monocytes. Differential effects of IL-2 and IFN-gamma. AN - 73232348; 1383334 AB - We investigated the effects of IFN-gamma and IL-2 on IL-2R alpha and beta mRNA expression in human monocytes. Low basal expression of IL-2R beta mRNA was detected in fresh monocytes. Stimulation of monocytes with IL-2 induced a significant increase of IL-2R beta mRNA, but did not induce IL-2R alpha mRNA. In contrast, stimulation of monocytes with IFN-gamma-induced IL-2R alpha mRNA, but did not modify IL-2R beta mRNA. Five U/ml of IFN-gamma induced IL-2R alpha mRNA and 2.2 nM of IL-2 induced IL-2R beta mRNA, both within 3 h. Nuclear run-on experiments demonstrated that the induction of IL-2R alpha mRNA by IFN-gamma is controlled, at least in part, at the transcriptional level. In contrast, the enhancement of IL-2R beta mRNA by IL-2 is controlled at a posttranscriptional level and is associated with an increase in the half-life of IL-2R beta mRNA. The results of studies on the cytotoxic activity and on the expression of c-fms mRNA of monocytes activated by the combination of IFN-gamma and IL-2 show that pretreatment with IFN-gamma renders monocytes more sensitive to activation by IL-2. These results demonstrate that the IL-2R alpha and IL-2R beta subunits are induced by different lymphokines through distinct mechanisms and that both receptor subunits can influence the response of monocytes to IL-2. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Espinoza-Delgado, I AU - Longo, D L AU - Gusella, G L AU - Varesio, L AD - Immunobiology Section, National Cancer Institute, Frederick Cancer Research Development Center, MD 21702-1201. Y1 - 1992/11/01/ PY - 1992 DA - 1992 Nov 01 SP - 2961 EP - 2968 VL - 149 IS - 9 SN - 0022-1767, 0022-1767 KW - Antigens, CD KW - 0 KW - Antigens, CD14 KW - Antigens, CD56 KW - Antigens, Differentiation, Myelomonocytic KW - Antigens, Differentiation, T-Lymphocyte KW - Interleukin-2 KW - RNA, Messenger KW - Receptors, Interleukin-2 KW - Interferon-gamma KW - 82115-62-6 KW - Abridged Index Medicus KW - Index Medicus KW - Antigens, CD -- biosynthesis KW - Blotting, Northern KW - Humans KW - Antigens, Differentiation, T-Lymphocyte -- biosynthesis KW - Transcription, Genetic KW - RNA Processing, Post-Transcriptional KW - RNA, Messenger -- biosynthesis KW - Cells, Cultured KW - Antigens, Differentiation, Myelomonocytic -- biosynthesis KW - Flow Cytometry KW - Up-Regulation KW - Drug Synergism KW - Interleukin-2 -- pharmacology KW - Monocytes -- immunology KW - Gene Expression Regulation -- immunology KW - Receptors, Interleukin-2 -- biosynthesis KW - Monocytes -- metabolism KW - Interferon-gamma -- pharmacology KW - Receptors, Interleukin-2 -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73232348?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=Regulation+of+IL-2+receptor+subunit+genes+in+human+monocytes.+Differential+effects+of+IL-2+and+IFN-gamma.&rft.au=Espinoza-Delgado%2C+I%3BLongo%2C+D+L%3BGusella%2C+G+L%3BVaresio%2C+L&rft.aulast=Espinoza-Delgado&rft.aufirst=I&rft.date=1992-11-01&rft.volume=149&rft.issue=9&rft.spage=2961&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.issn=00221767&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-25 N1 - Date created - 1992-11-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Predominant usage of V beta 8.3 T cell receptor in a T cell line that induces experimental autoimmune uveoretinitis (EAU). AN - 73231952; 1382911 AB - Experimental autoimmune uveoretinitis (EAU) is a T cell-mediated autoimmune disease induced in animals by immunization with retinal proteins (or synthetic fragments derived from them) in adjuvant, and it is considered a model of human autoimmune diseases of the eye. To study the T cell clonotypes that may be involved in EAU, we analyzed the T cell repertoire of three related T cell lines: the pathogenic line LR16, specific to the major uveitogenic epitope of IRBP; its pathogenic subline J; and its nonpathogenic subline A. We examined the expression of the genes coding for the variable regions of the 20 known Lewis rat T cell antigen receptor (TCR) V beta families. The nonpathogenic subline was found to contain mostly T cells expressing V beta 5, V beta 8.2, and V beta 19 while the pathogenic subline consisted mainly of cells expressing V beta 8.3 TCRs. Genomic Southern blot analysis of DNA from the pathogenic subline showed that V beta 8.3-expressing T cells were the dominant clonotype, and DNA sequence analyses of V beta 8.3 cDNAs revealed that two V beta 8.3 TCRs were expressed in the pathogenic subline. One of the V beta 8.3 cDNAs encoded a variable region gene segment identical to previously reported rat V beta 8.3 TCR while the other differed by two amino acids in the second complementarity determining region (CDR2). Taken together with previous data showing overrepresentation of V beta 8-expression in T cell lines that induce EAU, but not in nonuveitogenic T cell lines, our results suggest that V beta 8.3-expressing T cells represent a pathogenic clonotype in IRBP-induced EAU. JF - Clinical immunology and immunopathology AU - Egwuagu, C E AU - Bahmanyar, S AU - Mahdi, R M AU - Nussenblatt, R B AU - Gery, I AU - Caspi, R R AD - Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 152 EP - 160 VL - 65 IS - 2 SN - 0090-1229, 0090-1229 KW - Eye Proteins KW - 0 KW - Receptors, Antigen, T-Cell, alpha-beta KW - Retinol-Binding Proteins KW - interstitial retinol-binding protein KW - RNA KW - 63231-63-0 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Rats, Inbred Lew KW - DNA -- analysis KW - Gene Expression KW - Transcription, Genetic KW - Amino Acid Sequence KW - Eye -- pathology KW - Rats KW - Base Sequence KW - Retinol-Binding Proteins -- immunology KW - Retinol-Binding Proteins -- genetics KW - Blotting, Southern KW - Lymphocyte Activation -- immunology KW - Immunotherapy, Adoptive KW - Molecular Sequence Data KW - RNA -- isolation & purification KW - Sequence Homology, Amino Acid KW - Cell Line KW - Uveitis -- immunology KW - Receptors, Antigen, T-Cell, alpha-beta -- genetics KW - Uveitis -- chemically induced KW - T-Lymphocytes -- immunology KW - Receptors, Antigen, T-Cell, alpha-beta -- biosynthesis KW - Autoimmune Diseases -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73231952?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+immunology+and+immunopathology&rft.atitle=Predominant+usage+of+V+beta+8.3+T+cell+receptor+in+a+T+cell+line+that+induces+experimental+autoimmune+uveoretinitis+%28EAU%29.&rft.au=Egwuagu%2C+C+E%3BBahmanyar%2C+S%3BMahdi%2C+R+M%3BNussenblatt%2C+R+B%3BGery%2C+I%3BCaspi%2C+R+R&rft.aulast=Egwuagu&rft.aufirst=C&rft.date=1992-11-01&rft.volume=65&rft.issue=2&rft.spage=152&rft.isbn=&rft.btitle=&rft.title=Clinical+immunology+and+immunopathology&rft.issn=00901229&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-17 N1 - Date created - 1992-11-17 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - S49031; GENBANK; M83092; S50001; S72771; S49029; X64095; X64096; S49998; S47168; X64094 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Separation of the transcriptional activation and replication functions of the bovine papillomavirus-1 E2 protein. AN - 73230966; 1327758 AB - Replication of bovine papillomavirus-1 (BPV-1) DNA requires two viral gene products, the E1 protein and the full-length E2 protein. The 48 kDa E2 protein is a site-specific DNA-binding protein that binds to several sites which lie adjacent to the BPV-1 origin of replication. The 85 amino acid C-terminal domain contains the specific DNA binding and dimerization properties of the protein. The approximately 200 amino acid N-terminal domain is crucial for transcriptional activation. Both of these domains are highly conserved among different papillomaviruses. An internal hinge region separates the two functional domains. The region varies in amino acid sequence and length among the E2 proteins of different papillomaviruses. A series of mutations were constructed within the E2 open reading frame which delete various regions of the conserved DNA binding and transactivation domains as well as the internal hinge region. Two mutated E2 proteins that lack portions of the conserved DNA-binding domain but which support DNA replication were identified using transient replication assays. These mutated E2 proteins were unable to function as transcriptional activators. Conversely, two E2 proteins containing large deletions of the hinge region were able to activate transcription, but were defective for replication. Thus, the replication and transactivation functions of the E2 protein are separable. JF - The EMBO journal AU - Winokur, P L AU - McBride, A A AD - Laboratory of Tumor Virus Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 4111 EP - 4118 VL - 11 IS - 11 SN - 0261-4189, 0261-4189 KW - DNA-Binding Proteins KW - 0 KW - E2 protein, Bovine papillomavirus KW - Trans-Activators KW - Viral Proteins KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Index Medicus KW - Animals KW - Base Sequence KW - Restriction Mapping KW - Molecular Sequence Data KW - Plasmids KW - Haplorhini KW - Cell Line KW - Sequence Deletion KW - Mutagenesis KW - Virus Replication KW - Viral Proteins -- genetics KW - Trans-Activators -- metabolism KW - DNA-Binding Proteins -- genetics KW - Bovine papillomavirus 1 -- physiology KW - Transcription, Genetic KW - Protein-Tyrosine Kinases -- metabolism KW - Transcriptional Activation KW - Protein-Tyrosine Kinases -- genetics KW - Trans-Activators -- genetics KW - Viral Proteins -- metabolism KW - Genes, Viral KW - Bovine papillomavirus 1 -- genetics KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73230966?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+EMBO+journal&rft.atitle=Separation+of+the+transcriptional+activation+and+replication+functions+of+the+bovine+papillomavirus-1+E2+protein.&rft.au=Winokur%2C+P+L%3BMcBride%2C+A+A&rft.aulast=Winokur&rft.aufirst=P&rft.date=1992-11-01&rft.volume=11&rft.issue=11&rft.spage=4111&rft.isbn=&rft.btitle=&rft.title=The+EMBO+journal&rft.issn=02614189&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-19 N1 - Date created - 1992-11-19 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1992 Jan 15;89(2):589-93 [1309949] J Virol. 1989 Dec;63(12):5076-85 [2555544] EMBO J. 1991 Dec;10(13):4321-9 [1661672] Cell. 1991 May 3;65(3):493-505 [1850324] J Virol. 1990 Feb;64(2):950-6 [2153256] Proc Natl Acad Sci U S A. 1989 Jan;86(2):510-4 [2536165] J Virol. 1989 Apr;63(4):1743-55 [2538655] Cell. 1989 Nov 3;59(3):541-51 [2553273] EMBO J. 1988 Feb;7(2):533-9 [2835232] J Virol. 1988 Sep;62(9):3143-50 [2841467] EMBO J. 1988 Sep;7(9):2815-22 [2846284] EMBO J. 1988 Dec 1;7(12):3807-16 [2850174] Proc Natl Acad Sci U S A. 1985 Feb;82(4):1030-4 [2983327] Nature. 1985 Dec 12-18;318(6046):575-7 [2999614] J Virol. 1986 Nov;60(2):626-34 [3021996] Mol Cell Biol. 1986 Nov;6(11):4077-87 [3025630] Proc Natl Acad Sci U S A. 1987 Mar;84(5):1215-8 [3029771] EMBO J. 1987 Jan;6(1):145-52 [3034572] Oncogene Res. 1988 May;2(4):385-401 [3041347] J Virol. 1991 Dec;65(12):6528-34 [1658358] Annu Rev Cell Biol. 1989;5:197-245 [2557059] EMBO J. 1988 Apr;7(4):1197-204 [2841117] Proc Natl Acad Sci U S A. 1988 Aug;85(16):5864-8 [2842752] J Virol. 1988 Oct;62(10):3608-13 [2843663] EMBO J. 1988 Sep;7(9):2823-9 [2846285] EMBO J. 1988 Dec 20;7(13):4245-53 [2854060] Cell. 1985 Aug;42(1):183-91 [2990724] EMBO J. 1985 Nov;4(11):2933-9 [2998767] J Virol. 1986 Jan;57(1):138-44 [3001340] Mol Cell Biol. 1986 Nov;6(11):3838-46 [3025615] Nature. 1987 Jan 1-7;325(6099):70-3 [3025749] J Virol. 1987 May;61(5):1630-8 [3033289] J Virol. 1987 Jul;61(7):2128-37 [3035214] Cell. 1987 Jul 3;50(1):69-78 [3036366] Cell. 1988 Mar 11;52(5):635-8 [3278812] Proc Natl Acad Sci U S A. 1981 May;78(5):2727-31 [6265905] Proc Natl Acad Sci U S A. 1982 Dec;79(23):7147-51 [6296820] Mol Cell Biol. 1986 Apr;6(4):1117-28 [3023870] J Virol. 1991 Oct;65(10):5314-22 [1654443] Cell. 1986 Jan 31;44(2):283-92 [3943125] J Virol. 1991 Feb;65(2):649-56 [1846189] EMBO J. 1991 Feb;10(2):449-57 [1846806] J Virol. 1990 Feb;64(2):944-9 [2153255] J Virol. 1990 Oct;64(10):5093-105 [2168988] Science. 1990 Dec 21;250(4988):1694-9 [2176744] Virology. 1989 Mar;169(1):236-8 [2538035] J Virol. 1989 Jul;63(7):3151-4 [2542621] Nature. 1991 Oct 17;353(6345):628-32 [1656277] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phase I and pharmacokinetic evaluation of all-trans-retinoic acid in pediatric patients with cancer. AN - 73228195; 1403049 AB - Recent reports of the dramatic antitumor effect of all-trans-retinoic acid (RA) in patients with acute promyelocytic leukemia (APL) have renewed interest in the oncologic indications for retinoids. Furthermore, a variety of pediatric tumors are responsive to RA in vitro, which provides additional rationale for a phase I evaluation of RA in children with cancer that is refractory to standard therapy. A phase I trial of RA administered orally twice daily for 28-day treatment courses was performed. Cohorts of at least three pediatric cancer patients were entered at successive RA dose levels (from 45 to 80 mg/m2/d) until dose-limiting toxicity (DLT) was consistently observed. The maximum-tolerated dose (MTD) of RA was 60 mg/m2/d. Three of eight patients at the 80-mg/m2/d dose level developed reversible pseudotumor cerebri that necessitated discontinuation of the agent. Both patients with APL achieved complete remission (CR), whereas no patients with solid tumors had objective responses. Pharmacokinetic studies demonstrated a relatively short terminal half-life for RA (45 minutes), with diminution in plasma levels after chronic dosing. The MTD and recommended phase II dose for RA in children is 60 mg/m2/d given twice daily. Reversible CNS toxicity related to RA-induced pseudotumor cerebri is dose-limiting. Two children with APL achieved a CR to RA, which supports the inclusion of pediatric patients in clinical trials that evaluate the use of RA for patients with APL. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Smith, M A AU - Adamson, P C AU - Balis, F M AU - Feusner, J AU - Aronson, L AU - Murphy, R F AU - Horowitz, M E AU - Reaman, G AU - Hammond, G D AU - Fenton, R M AD - Pediatric Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 1666 EP - 1673 VL - 10 IS - 11 SN - 0732-183X, 0732-183X KW - Capsules KW - 0 KW - Tretinoin KW - 5688UTC01R KW - Index Medicus KW - Administration, Oral KW - Drug Administration Schedule KW - Pseudotumor Cerebri -- chemically induced KW - Half-Life KW - Humans KW - Cohort Studies KW - Adult KW - Child KW - Adolescent KW - Child, Preschool KW - Neoplasms -- drug therapy KW - Tretinoin -- pharmacokinetics KW - Tretinoin -- therapeutic use KW - Tretinoin -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73228195?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=Phase+I+and+pharmacokinetic+evaluation+of+all-trans-retinoic+acid+in+pediatric+patients+with+cancer.&rft.au=Smith%2C+M+A%3BAdamson%2C+P+C%3BBalis%2C+F+M%3BFeusner%2C+J%3BAronson%2C+L%3BMurphy%2C+R+F%3BHorowitz%2C+M+E%3BReaman%2C+G%3BHammond%2C+G+D%3BFenton%2C+R+M&rft.aulast=Smith&rft.aufirst=M&rft.date=1992-11-01&rft.volume=10&rft.issue=11&rft.spage=1666&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=0732183X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-23 N1 - Date created - 1992-11-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: J Clin Oncol. 1992 Nov;10(11):1659-61 [1403047] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The enhanced mutagenic potential of the MucAB proteins correlates with the highly efficient processing of the MucA protein. AN - 73224271; 1400235 AB - Inducible mutagenesis in Escherichia coli requires the direct action of the chromosomally encoded UmuDC proteins or functional homologs found on certain naturally occurring plasmids. Although structurally similar, the five umu-like operons that have been characterized at the molecular level vary in their ability to enhance cellular and phage mutagenesis; of these operons, the mucAB genes from the N-group plasmid pKM101 are the most efficient at promoting mutagenesis. During the mutagenic process, UmuD is posttranslationally processed to an active form, UmuD'. To explain the more potent mutagenic efficiency of mucAB compared with that of umuDC it has been suggested that unlike UmuD, intact MucA is functional for mutagenesis. To examine this possibility, we have overproduced and purified the MucA protein. Although functionally similar to UmuD, MucA was cleaved much more rapidly both in vitro and in vivo than UmuD. In vivo, restoration of mutagenesis functions to normally nonmutable recA430, recA433, recA435, or recA730 delta(umuDC)595::cat strains by either MucA+ or mutant MucA protein correlated with the appearance of the cleavage product, MucA'. These results suggest that most of the differences in mutagenic phenotype exhibited by MucAB and UmuDC correlate with the efficiency of posttranslational processing of MucA and UmuD rather than an inherent activity of the unprocessed proteins. JF - Journal of bacteriology AU - Hauser, J AU - Levine, A S AU - Ennis, D G AU - Chumakov, K M AU - Woodgate, R AD - Section on Viruses and Cellular Biology, National Institute of Child Health and Human Development, Bethesda, Maryland. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 6844 EP - 6851 VL - 174 IS - 21 SN - 0021-9193, 0021-9193 KW - MucA KW - MucB KW - UmuD KW - umuC KW - Bacterial Proteins KW - 0 KW - MucA protein, Bacteria KW - Protein Precursors KW - Rec A Recombinases KW - EC 2.7.7.- KW - Peptide Hydrolases KW - EC 3.4.- KW - Index Medicus KW - Base Sequence KW - Protein Precursors -- metabolism KW - Bacteriophage lambda -- genetics KW - Molecular Sequence Data KW - Rec A Recombinases -- pharmacology KW - Structure-Activity Relationship KW - Protein Processing, Post-Translational -- drug effects KW - Escherichia coli -- metabolism KW - Bacterial Proteins -- genetics KW - Peptide Hydrolases -- metabolism KW - Bacterial Proteins -- metabolism KW - Escherichia coli -- genetics KW - Bacterial Proteins -- isolation & purification KW - Mutagenesis -- genetics KW - Peptide Hydrolases -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73224271?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+bacteriology&rft.atitle=The+enhanced+mutagenic+potential+of+the+MucAB+proteins+correlates+with+the+highly+efficient+processing+of+the+MucA+protein.&rft.au=Hauser%2C+J%3BLevine%2C+A+S%3BEnnis%2C+D+G%3BChumakov%2C+K+M%3BWoodgate%2C+R&rft.aulast=Hauser&rft.aufirst=J&rft.date=1992-11-01&rft.volume=174&rft.issue=21&rft.spage=6844&rft.isbn=&rft.btitle=&rft.title=Journal+of+bacteriology&rft.issn=00219193&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-25 N1 - Date created - 1992-11-25 N1 - Date revised - 2017-01-13 N1 - Gene symbol - MucA; MucB; UmuD; umuC N1 - SuppNotes - Cited By: J Bacteriol. 1991 May;173(9):2906-14 [1902211] Proc Natl Acad Sci U S A. 1984 Dec;81(24):7747-51 [6393125] Nucleic Acids Res. 1990 Sep 11;18(17):5045-50 [2129552] J Bacteriol. 1990 Jun;172(6):3030-6 [2188949] J Bacteriol. 1990 Nov;172(11):6223-31 [2228957] J Bacteriol. 1989 May;171(5):2415-23 [2651400] J Bacteriol. 1989 Oct;171(10):5753-5 [2676992] J Bacteriol. 1988 May;170(5):2163-73 [2834329] Proc Natl Acad Sci U S A. 1985 Jul;82(13):4336-40 [2989817] J Bacteriol. 1985 Dec;164(3):1366-9 [2999084] Proc Natl Acad Sci U S A. 1987 Jun;84(12):3987-91 [3108885] Proc Natl Acad Sci U S A. 1988 Mar;85(6):1811-5 [3279417] J Cell Sci Suppl. 1987;6:303-21 [3308922] Proc Natl Acad Sci U S A. 1985 Jun;82(12):4172-6 [3858873] Proc Natl Acad Sci U S A. 1985 Jun;82(12):4193-7 [3889923] Proc Natl Acad Sci U S A. 1984 Mar;81(5):1375-9 [6231641] Microbiol Rev. 1984 Mar;48(1):60-93 [6371470] Nature. 1982 Nov 18;300(5889):278-81 [6755263] Cell. 1982 May;29(1):11-22 [7049397] Proc Natl Acad Sci U S A. 1975 Mar;72(3):979-83 [165497] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Mol Gen Genet. 1978 Sep 20;165(1):87-93 [362169] J Bacteriol. 1979 Feb;137(2):830-8 [370103] J Bacteriol. 1976 Oct;128(1):271-82 [789333] Mutat Res. 1992 Mar;281(3):221-5 [1371846] Proc Natl Acad Sci U S A. 1991 Feb 15;88(4):1251-5 [1847514] J Bacteriol. 1991 Sep;173(18):5604-11 [1885540] Mol Gen Genet. 1991 Sep;229(1):81-5 [1910151] Biochimie. 1991 Apr;73(4):485-9 [1911949] J Bacteriol. 1990 Sep;172(9):4964-78 [2144275] J Biol Chem. 1990 Nov 25;265(33):20641-5 [2147025] J Bacteriol. 1990 Sep;172(9):4979-87 [2203737] Mol Gen Genet. 1990 Nov;224(2):169-76 [2277636] Proc Natl Acad Sci U S A. 1989 Oct;86(19):7301-5 [2552436] J Bacteriol. 1989 May;171(5):2533-41 [2651406] J Mol Biol. 1989 Dec 5;210(3):439-52 [2693734] J Mol Biol. 1987 Aug 5;196(3):497-504 [2960817] Proc Natl Acad Sci U S A. 1985 Jul;82(13):4331-5 [2989816] Gene. 1985;38(1-3):31-8 [2998948] Biochimie. 1982 Aug-Sep;64(8-9):633-6 [6814511] Mutat Res. 1981 May;81(3):265-75 [7029254] Mol Gen Genet. 1986 Nov;205(2):234-9 [3027502] Proc Natl Acad Sci U S A. 1988 Mar;85(6):1806-10 [3126496] Proc Natl Acad Sci U S A. 1985 May;82(10):3325-9 [3159017] Proc Natl Acad Sci U S A. 1988 Mar;85(6):1816-20 [3279418] Biochem J. 1986 Nov 15;240(1):1-12 [3548705] Methods Enzymol. 1979;68:482-92 [232223] Mol Gen Genet. 1977 Nov 14;156(2):121-31 [340898] Mol Gen Genet. 1976 Jun 15;145(3):303-6 [781517] Bacteriol Rev. 1976 Dec;40(4):869-907 [795416] Mol Gen Genet. 1991 Sep;229(1):10-6 [1654503] J Mol Biol. 1986 Nov 5;192(1):39-47 [3820305] Proc Natl Acad Sci U S A. 1985 Nov;82(22):7753-6 [3877933] Mol Gen Genet. 1984;196(2):364-6 [6092873] Mol Gen Genet. 1984;195(1-2):83-9 [6238224] Nucleic Acids Res. 1981 Aug 25;9(16):4149-61 [6272195] Biochimie. 1991 Apr;73(4):479-84 [1911948] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Independent and synergistic effects of disulfide bond formation, beta 2-microglobulin, and peptides on class I MHC folding and assembly in an in vitro translation system. AN - 73221849; 1401922 AB - We have examined the post-translational processing, intrachain disulfide bond formation, folding, and assembly of MHC class I H chains with beta 2-microglobulin after coupled in vitro translation of homogeneous mRNA and transport of nascent chains into canine microsomal vesicles. The formation of native alpha 3 domain conformation was dependent on conditions that optimized intrachain disulfide bond formation, and efficient folding of the alpha 1 alpha 2 domain required exposure to antigenic peptide. beta 2-microglobulin and peptide acted synergistically in forming native alpha 1 alpha 2 domain structure, and a small proportion of molecules with native alpha 1 alpha 2, but non-native alpha 3 structure were detected, indicating that alpha 3 domain folding is not an absolute prerequisite for the formation of native alpha 1 alpha 2 domain structure. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Ribaudo, R K AU - Margulies, D H AD - Molecular Biology Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/11/01/ PY - 1992 DA - 1992 Nov 01 SP - 2935 EP - 2944 VL - 149 IS - 9 SN - 0022-1767, 0022-1767 KW - Gene Products, gag KW - 0 KW - H-2 Antigens KW - Histocompatibility Antigen H-2D KW - Immediate-Early Proteins KW - Viral Proteins KW - beta 2-Microglobulin KW - cytomegalovirus immediate early phosphoprotein pp89 KW - gag Gene Products, Human Immunodeficiency Virus KW - p18 gag protein, Human immunodeficiency virus 1 KW - Glutathione KW - GAN16C9B8O KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Electrophoresis, Polyacrylamide Gel KW - Transcription, Genetic KW - Amino Acid Sequence KW - Mice KW - Mice, Inbred BALB C KW - Glutathione -- pharmacology KW - Cloning, Molecular KW - Protein Biosynthesis -- drug effects KW - Base Sequence KW - Microsomes -- physiology KW - In Vitro Techniques KW - Molecular Sequence Data KW - Mice, Inbred C57BL KW - Molecular Conformation KW - Drug Synergism KW - beta 2-Microglobulin -- pharmacology KW - Viral Proteins -- pharmacology KW - Protein Processing, Post-Translational KW - Gene Products, gag -- pharmacology KW - H-2 Antigens -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73221849?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=Independent+and+synergistic+effects+of+disulfide+bond+formation%2C+beta+2-microglobulin%2C+and+peptides+on+class+I+MHC+folding+and+assembly+in+an+in+vitro+translation+system.&rft.au=Ribaudo%2C+R+K%3BMargulies%2C+D+H&rft.aulast=Ribaudo&rft.aufirst=R&rft.date=1992-11-01&rft.volume=149&rft.issue=9&rft.spage=2935&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.issn=00221767&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-25 N1 - Date created - 1992-11-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Identification of conserved amino acid residues critical for human immunodeficiency virus type 1 integrase function in vitro. AN - 73221358; 1404595 AB - We have probed the structural organization of the human immunodeficiency virus type 1 integrase protein by limited proteolysis and the functional organization by site-directed mutagenesis of selected amino acid residues. A central region of the protein was relatively resistant to proteolysis. Proteins with altered amino acids in this region, or in the N-terminal part of the protein that includes a putative zinc-binding motif, were purified and assayed for 3' processing, DNA strand transfer, and disintegration activities in vitro. In general, these mutations had parallel effects on 3' processing and DNA strand transfer, suggesting that integrase may utilize a single active site for both reactions. The only proteins that were completely inactive in all three assays contained mutations at conserved amino acids in the central region, suggesting that this part of the protein may be involved in catalysis. In contrast, none of the mutations in the N-terminal region resulted in a protein that was inactive in all three assays, suggesting that this part of integrase may not be essential for catalysis. The disintegration reaction was particularly insensitive to these amino acid substitutions, indicating that some function that is important for 3' processing and DNA strand transfer may be dispensable for disintegration. JF - Journal of virology AU - Engelman, A AU - Craigie, R AD - Laboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 6361 EP - 6369 VL - 66 IS - 11 SN - 0022-538X, 0022-538X KW - Oligodeoxyribonucleotides KW - 0 KW - DNA Nucleotidyltransferases KW - EC 2.7.7.- KW - Integrases KW - Endopeptidases KW - EC 3.4.- KW - Index Medicus KW - AIDS/HIV KW - Peptide Mapping KW - DNA Mutational Analysis KW - Endopeptidases -- pharmacology KW - Amino Acid Sequence KW - Protein Binding KW - Structure-Activity Relationship KW - Mutagenesis, Site-Directed KW - Base Sequence KW - Molecular Sequence Data KW - Oligodeoxyribonucleotides -- metabolism KW - Sequence Homology, Amino Acid KW - Catalysis KW - HIV-1 -- genetics KW - Conserved Sequence -- genetics KW - DNA Nucleotidyltransferases -- genetics KW - HIV-1 -- enzymology KW - DNA Nucleotidyltransferases -- drug effects KW - DNA Nucleotidyltransferases -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73221358?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Identification+of+conserved+amino+acid+residues+critical+for+human+immunodeficiency+virus+type+1+integrase+function+in+vitro.&rft.au=Engelman%2C+A%3BCraigie%2C+R&rft.aulast=Engelman&rft.aufirst=A&rft.date=1992-11-01&rft.volume=66&rft.issue=11&rft.spage=6361&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-18 N1 - Date created - 1992-11-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: EMBO J. 1987 Jul;6(7):2077-84 [2820721] J Virol. 1984 Feb;49(2):471-8 [6319746] Science. 1986 Feb 7;231(4738):589-94 [3003905] J Virol. 1987 Feb;61(2):480-90 [3027377] AIDS Res Hum Retroviruses. 1987 Spring;3(1):57-69 [3040055] Gene. 1987;56(1):125-35 [3315856] J Biol Chem. 1987 Jul 25;262(21):10035-8 [3611052] Proc Natl Acad Sci U S A. 1972 Dec;69(12):3506-9 [4509307] Nature. 1981 Oct 15-21;293(5833):543-8 [6169994] Cell. 1983 Mar;32(3):853-69 [6299578] Mol Cell Biol. 1992 May;12(5):2331-8 [1314954] J Virol. 1992 Apr;66(4):2359-68 [1548767] Nucleic Acids Res. 1991 Dec 25;19(24):6691-8 [1662361] Nucleic Acids Res. 1990 Feb 25;18(4):733-8 [1690391] Cell. 1991 Dec 20;67(6):1211-21 [1760846] Proc Natl Acad Sci U S A. 1991 Feb 15;88(4):1339-43 [1847518] Nucleic Acids Res. 1991 Feb 25;19(4):851-60 [1850126] J Virol. 1991 Sep;65(9):4636-44 [1870194] Mol Microbiol. 1990 Oct;4(10):1771-7 [1963920] Virology. 1991 May;182(1):397-402 [2024476] Proc Natl Acad Sci U S A. 1990 Jul;87(13):5119-23 [2164223] Cell. 1990 Oct 5;63(1):87-95 [2170022] Science. 1990 Sep 28;249(4976):1555-8 [2171144] Virology. 1990 Nov;179(1):347-64 [2171210] Virology. 1990 Apr;175(2):391-409 [2183467] J Virol. 1990 Nov;64(11):5656-9 [2214031] Cell. 1986 May 9;45(3):375-85 [2421920] Proc Natl Acad Sci U S A. 1986 Oct;83(20):7648-52 [2429313] J Virol. 1989 Dec;63(12):5319-27 [2555556] Proc Natl Acad Sci U S A. 1989 Aug;86(15):5743-7 [2762293] Nature. 1989 Jun 1;339(6223):389-92 [2786147] J Virol. 1988 Mar;62(3):722-31 [2828667] Virology. 1985 Apr 30;142(2):357-77 [2997990] J Virol. 1986 Aug;59(2):284-91 [3016298] Nucleic Acids Res. 1986 Jul 25;14(14):5901-18 [3016667] Nature. 1987 Apr 16-22;326(6114):662-9 [3031510] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Virology. 1992 Jun;188(2):459-68 [1585629] Science. 1992 Feb 7;255(5045):723-6 [1738845] Cell. 1991 Jan 11;64(1):159-70 [1846087] Virology. 1988 Dec;167(2):634-8 [3059679] Nature. 1987 Apr 9-15;326(6113):610-3 [3104797] J Mol Biol. 1986 May 5;189(1):113-30 [3537305] Nucleic Acids Res. 1991 Jul 25;19(14):3821-7 [1861975] J Virol. 1991 Oct;65(10):5624-30 [1895409] EMBO J. 1991 Jan;10(1):25-33 [1989886] Cell. 1990 Aug 24;62(4):829-37 [2167180] Mol Microbiol. 1990 Jun;4(6):961-75 [2170815] J Virol. 1990 Dec;64(12):5750-6 [2173767] Curr Top Microbiol Immunol. 1990;157:19-48 [2203610] Virology. 1985 Jun;143(2):676-9 [2414914] J Virol. 1986 Nov;60(2):771-5 [2430111] Proc Natl Acad Sci U S A. 1985 May;82(10):3101-5 [2582407] Biochemistry. 1973 Feb 27;12(5):828-34 [4346923] J Virol. 1984 Oct;52(1):172-82 [6090694] Virology. 1984 Sep;137(2):358-70 [6091334] J Virol. 1984 Jan;49(1):214-22 [6197537] J Gen Virol. 1988 Jul;69 ( Pt 7):1695-710 [2899128] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A single amino acid substitution is sufficient to modify the mitogenic properties of the epidermal growth factor receptor to resemble that of gp185erbB-2. AN - 73219159; 1356764 AB - The epidermal growth factor (EGF) receptor (EGFR) and the erbB-2 gene product, gp185erbB-2, exhibit distinct abilities to stimulate mitogenesis in different target cells. By using chimeric molecules between these two receptors, we have previously shown that their intracellular juxtamembrane regions are responsible for this specificity. Here we describe a genetically engineered EGFR mutant containing a threonine for arginine substitution at position 662 in the EGFR juxtamembrane domain, corresponding to threonine 694 in gp185erbB-2. This mutant, designated EGFRThr662, displayed affinity for EGF binding and catalytic properties that were indistinguishable from those of the wild type EGFR. However, EGFRThr662 behaved much as gp185erbB-2 in a number of bioassays which readily distinguish between the mitogenic effects of EGFR and gp185erbB-2. Moreover, significant differences were detected in the pattern of intracellular proteins phosphorylated on tyrosine in vivo by EGFR and EGFRThr662 in response to EGF. Thus, small differences in the primary sequence of two closely related receptors have dramatic effects on their ability to couple with mitogenic pathways. JF - The EMBO journal AU - Di Fiore, P P AU - Helin, K AU - Kraus, M H AU - Pierce, J H AU - Artrip, J AU - Segatto, O AU - Bottaro, D P AD - Laboratory of Cellular and Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 3927 EP - 3933 VL - 11 IS - 11 SN - 0261-4189, 0261-4189 KW - EGFR KW - erbB-2 KW - Codon KW - 0 KW - Mitogens KW - Oligodeoxyribonucleotides KW - Proto-Oncogene Proteins KW - Threonine KW - 2ZD004190S KW - Epidermal Growth Factor KW - 62229-50-9 KW - Arginine KW - 94ZLA3W45F KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Receptor, Epidermal Growth Factor KW - Receptor, ErbB-2 KW - Thymidine KW - VC2W18DGKR KW - Index Medicus KW - 3T3 Cells KW - Animals KW - Codon -- genetics KW - Amino Acid Sequence KW - Mice KW - Thymidine -- metabolism KW - Mutagenesis, Site-Directed KW - Base Sequence KW - Phosphorylation KW - Transfection KW - Genetic Vectors KW - Kinetics KW - Molecular Sequence Data KW - Repetitive Sequences, Nucleic Acid KW - Signal Transduction KW - Protein-Tyrosine Kinases -- genetics KW - Receptor, Epidermal Growth Factor -- genetics KW - Receptor, Epidermal Growth Factor -- physiology KW - Protein-Tyrosine Kinases -- metabolism KW - Epidermal Growth Factor -- pharmacology KW - Proto-Oncogenes KW - Proto-Oncogene Proteins -- genetics KW - Epidermal Growth Factor -- metabolism KW - Proto-Oncogene Proteins -- physiology KW - DNA Replication -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73219159?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+EMBO+journal&rft.atitle=A+single+amino+acid+substitution+is+sufficient+to+modify+the+mitogenic+properties+of+the+epidermal+growth+factor+receptor+to+resemble+that+of+gp185erbB-2.&rft.au=Di+Fiore%2C+P+P%3BHelin%2C+K%3BKraus%2C+M+H%3BPierce%2C+J+H%3BArtrip%2C+J%3BSegatto%2C+O%3BBottaro%2C+D+P&rft.aulast=Di+Fiore&rft.aufirst=P&rft.date=1992-11-01&rft.volume=11&rft.issue=11&rft.spage=3927&rft.isbn=&rft.btitle=&rft.title=The+EMBO+journal&rft.issn=02614189&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-19 N1 - Date created - 1992-11-19 N1 - Date revised - 2017-01-13 N1 - Gene symbol - EGFR; erbB-2 N1 - SuppNotes - Cited By: Mol Cell Biol. 1992 Jan;12(1):128-35 [1729595] Anal Biochem. 1980 Sep 1;107(1):220-39 [6254391] J Biol Chem. 1990 Feb 25;265(6):3407-16 [2105948] Cell. 1990 Apr 20;61(2):203-12 [2158859] EMBO J. 1990 Dec;9(13):4375-80 [2176151] Science. 1990 Apr 6;248(4951):79-83 [2181668] Mol Cell Biol. 1990 Jun;10(6):2749-56 [2188097] EMBO J. 1989 Jan;8(1):167-73 [2565808] Cell. 1988 Aug 26;54(5):641-9 [2842060] Science. 1985 Dec 6;230(4730):1132-9 [2999974] Nature. 1984 May 31-Jun 6;309(5967):418-25 [6328312] Proc Natl Acad Sci U S A. 1981 Apr;78(4):2072-6 [7017722] Cell. 1977 May;11(1):223-32 [194704] Science. 1991 Nov 22;254(5035):1146-53 [1659742] Mol Cell Biol. 1991 Apr;11(4):2040-8 [1672440] Mol Cell Biol. 1991 Jun;11(6):3191-202 [1674818] Proc Natl Acad Sci U S A. 1985 Apr;82(7):1974-8 [2984676] Science. 1987 Jul 10;237(4811):178-82 [2885917] Mol Cell Biol. 1988 Jun;8(6):2302-8 [3136317] J Biol Chem. 1988 Sep 15;263(26):13152-8 [3138233] EMBO J. 1988 Oct;7(10):3053-60 [3181128] Science. 1988 Feb 5;239(4840):628-31 [3257584] J Biol Chem. 1988 Jul 5;263(19):9462-9 [3379075] Cell. 1987 Dec 24;51(6):1063-70 [3500791] Nature. 1984 Oct 4-10;311(5985):480-3 [6090944] J Biol Chem. 1991 Jan 5;266(1):637-44 [1845983] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - p53 mutation and protein accumulation during multistage human esophageal carcinogenesis. AN - 73216684; 1394236 AB - Preinvasive lesions of squamous cell carcinoma are well defined morphologically and provide a model for multistage carcinogenesis. Since alterations in the p53 tumor suppressor gene occur frequently in invasive esophageal squamous cell carcinoma, we examined a set of preinvasive lesions to investigate the timing of p53 mutation. Surgically resected tissues from nine patients with esophageal squamous cell carcinoma contained precursor lesions which had not yet invaded normal tissues. Immunohistochemistry showed high levels of p53 protein in both preinvasive lesions and invasive carcinomas in six cases; sequence analysis of all invasive tumors identified p53 missense mutations in two cases. Preinvasive lesions from both tumors with mutations plus one wild-type tumor were microdissected and sequenced. In one patient there were different mutations in the invasive carcinoma (codon 282, CGGarg > TGGtrp) and a preinvasive lesion (codon 272, GTGval > T/GTGleu/val). In a second case, an invasive carcinoma had a mutation in codon 175 (CGCarg > CAChis), and adjacent preinvasive lesions contained a wild-type sequence. A carcinoma and preinvasive lesion from the third case contained high levels of protein and a wild-type DNA sequence. Therefore, p53 mutation may precede invasion in esophageal carcinogenesis, and multifocal esophageal neoplasms may arise from independent clones of transformed cells. The timing of p53 protein accumulation is favorable for an intermediate biomarker in multistage esophageal carcinogenesis. JF - Cancer research AU - Bennett, W P AU - Hollstein, M C AU - Metcalf, R A AU - Welsh, J A AU - He, A AU - Zhu, S M AU - Kusters, I AU - Resau, J H AU - Trump, B F AU - Lane, D P AD - Laboratory of Human Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/11/01/ PY - 1992 DA - 1992 Nov 01 SP - 6092 EP - 6097 VL - 52 IS - 21 SN - 0008-5472, 0008-5472 KW - p53 KW - Codon KW - 0 KW - Tumor Suppressor Protein p53 KW - Index Medicus KW - Exons -- genetics KW - Base Sequence KW - Codon -- genetics KW - Humans KW - Molecular Sequence Data KW - Carcinoma in Situ -- pathology KW - Carcinoma in Situ -- genetics KW - Carcinoma, Squamous Cell -- metabolism KW - Precancerous Conditions -- metabolism KW - Tumor Suppressor Protein p53 -- metabolism KW - Precancerous Conditions -- pathology KW - Esophageal Neoplasms -- pathology KW - Precancerous Conditions -- genetics KW - Esophageal Neoplasms -- metabolism KW - Carcinoma, Squamous Cell -- pathology KW - Genes, p53 -- genetics KW - Carcinoma, Squamous Cell -- genetics KW - Esophageal Neoplasms -- genetics KW - Mutation -- genetics KW - Carcinoma in Situ -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73216684?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=p53+mutation+and+protein+accumulation+during+multistage+human+esophageal+carcinogenesis.&rft.au=Bennett%2C+W+P%3BHollstein%2C+M+C%3BMetcalf%2C+R+A%3BWelsh%2C+J+A%3BHe%2C+A%3BZhu%2C+S+M%3BKusters%2C+I%3BResau%2C+J+H%3BTrump%2C+B+F%3BLane%2C+D+P&rft.aulast=Bennett&rft.aufirst=W&rft.date=1992-11-01&rft.volume=52&rft.issue=21&rft.spage=6092&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-18 N1 - Date created - 1992-11-18 N1 - Date revised - 2017-01-13 N1 - Gene symbol - p53 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Fibrosarcoma cells transduced with the IL-6 gene exhibited reduced tumorigenicity, increased immunogenicity, and decreased metastatic potential. AN - 73200149; 1394227 AB - Murine fibrosarcoma cell lines transduced with retroviral vectors containing the murine interleukin 6 (IL-6) gene constitutively secreted IL-6. When injected s.c. into normal mice these IL-6-secreting tumors exhibited reduced tumorigenicity. This reduced tumorigenicity was not seen in nude or irradiated mice, implicating a T-cell-dependent, radiosensitive host response activated by the cytokine. Subcutaneous IL-6-secreting tumor did not retard the growth of distant deposits of wild-type tumor in the same host. However, animals rejecting IL-6-secreting tumors exhibited resistance to later challenge with wild-type tumor. When injected i.v. in an experimental metastasis model the IL-6-secreting tumors failed to or were extremely inefficient in giving rise to pulmonary nodules; this was observed in both normal and immunoincompetent mice, implicating a second, nonimmune mechanism affecting the growth of the tumor modified to secrete IL-6. JF - Cancer research AU - Mullen, C A AU - Coale, M M AU - Levy, A T AU - Stetler-Stevenson, W G AU - Liotta, L A AU - Brandt, S AU - Blaese, R M AD - Metabolism Branch, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1992/11/01/ PY - 1992 DA - 1992 Nov 01 SP - 6020 EP - 6024 VL - 52 IS - 21 SN - 0008-5472, 0008-5472 KW - Histocompatibility Antigens Class I KW - 0 KW - Interleukin-6 KW - Methylcholanthrene KW - 56-49-5 KW - Index Medicus KW - Animals KW - Histocompatibility Antigens Class I -- metabolism KW - Histocompatibility Antigens Class I -- immunology KW - Mice KW - Mice, Nude KW - Neoplasm Transplantation KW - Graft Rejection KW - Tumor Cells, Cultured KW - Transfection KW - Mice, Inbred C57BL KW - Neoplasm Metastasis KW - Immunocompromised Host KW - T-Lymphocytes -- immunology KW - Female KW - Interleukin-6 -- secretion KW - Skin Neoplasms -- immunology KW - Lung Neoplasms -- immunology KW - Skin Neoplasms -- secretion KW - Fibrosarcoma -- secretion KW - Skin Neoplasms -- pathology KW - Fibrosarcoma -- pathology KW - Lung Neoplasms -- secretion KW - Interleukin-6 -- physiology KW - Fibrosarcoma -- immunology KW - Fibrosarcoma -- chemically induced KW - Interleukin-6 -- genetics KW - Fibrosarcoma -- genetics KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73200149?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Fibrosarcoma+cells+transduced+with+the+IL-6+gene+exhibited+reduced+tumorigenicity%2C+increased+immunogenicity%2C+and+decreased+metastatic+potential.&rft.au=Mullen%2C+C+A%3BCoale%2C+M+M%3BLevy%2C+A+T%3BStetler-Stevenson%2C+W+G%3BLiotta%2C+L+A%3BBrandt%2C+S%3BBlaese%2C+R+M&rft.aulast=Mullen&rft.aufirst=C&rft.date=1992-11-01&rft.volume=52&rft.issue=21&rft.spage=6020&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-18 N1 - Date created - 1992-11-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER -