TY - JOUR T1 - The fluidity of DOPC bilayers and membrane fractions prepared from murine plasmacytoma cells is unchanged after incorporation of pristane (2,6,10,14-tetramethylpentadecane) as assessed by fluorescence polarization analysis. AN - 75517009; 1343851 AB - The nature of the plasmacytomagenic activity of pristane (2,6,10,14-tetramethylpentadecane) is poorly defined. However, evidence for tumor promoting properties of pristane has recently come forward that includes direct cellular effects on B lymphocytes; i.e., the plasmacytoma precursor cell. Bly et al. (Cancer Biochem. Biophys. 11, 1990, 145-154) observed changed membrane fluidities in lymphocytes after administration of pristane in vivo. We measured steady-state fluorescence polarization using DPH (1,6-diphenyl-1,3,5-hexatriene) and APCL (1-acyl-2-[12-(9-anthryl)-11-trans-dodecenoyl]-sn-glycero-3- phosphocholine) as probes in DOPC (L-alpha-dioleoylphosphatidylcholin) model membranes and membrane fractions derived from plasmacytoma cells after incorporation of pristane in vitro. In a previous investigation, we verified the in vitro uptake of pristane into DOPC bilayers under the conditions employed here (Gawrisch and Janz, Biochim. Biophys. Acta 1070, 1991, 409-418). However, neither in DOPC bilayers nor in plasmacytoma membrane fractions could we detect changes in fluorescence polarization after in vitro incorporation of pristane within reasonable error limits. Therefore, we suggest that the observed alterations in membrane fluidity in lymphocytes from pristane-treated animals are the indirect result of the in vivo treatment but not a direct effect of pristane on membrane fluidity. JF - Cancer biochemistry biophysics AU - Janz, S AU - Krumbiegel, M AU - Gawrisch, K AD - Laboratory of Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Md 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 85 EP - 92 VL - 13 IS - 2 SN - 0305-7232, 0305-7232 KW - Carcinogens KW - 0 KW - Lipid Bilayers KW - Phosphatidylcholines KW - Terpenes KW - Diphenylhexatriene KW - 1720-32-7 KW - pristane KW - 26HZV48DT1 KW - 1,2-oleoylphosphatidylcholine KW - H026DM5V6U KW - Index Medicus KW - Animals KW - Solubility KW - Tumor Cells, Cultured -- metabolism KW - Fluorescence Polarization KW - Tumor Cells, Cultured -- drug effects KW - Cell Membrane -- drug effects KW - Phosphatidylcholines -- chemistry KW - Mice KW - Lipid Bilayers -- chemistry KW - Cell Membrane -- metabolism KW - Terpenes -- toxicity KW - Terpenes -- administration & dosage KW - Plasmacytoma -- metabolism KW - Carcinogens -- administration & dosage KW - Plasmacytoma -- chemically induced KW - Membrane Fluidity -- physiology KW - Membrane Fluidity -- drug effects KW - Carcinogens -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75517009?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+biochemistry+biophysics&rft.atitle=The+fluidity+of+DOPC+bilayers+and+membrane+fractions+prepared+from+murine+plasmacytoma+cells+is+unchanged+after+incorporation+of+pristane+%282%2C6%2C10%2C14-tetramethylpentadecane%29+as+assessed+by+fluorescence+polarization+analysis.&rft.au=Janz%2C+S%3BKrumbiegel%2C+M%3BGawrisch%2C+K&rft.aulast=Janz&rft.aufirst=S&rft.date=1992-11-01&rft.volume=13&rft.issue=2&rft.spage=85&rft.isbn=&rft.btitle=&rft.title=Cancer+biochemistry+biophysics&rft.issn=03057232&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 - 2017-01-17 ER - TY - JOUR T1 - D2 dopamine receptor genotype and cerebrospinal fluid homovanillic acid, 5-hydroxyindoleacetic acid and 3-methoxy-4-hydroxyphenylglycol in alcoholics in Finland and the United States. AN - 73455172; 1283042 AB - If a genetic association between the D2 dopamine receptor genotype and alcoholism is mediated by altered dopamine function, then a stronger association might be found in alcoholics who are deviant in indices of dopamine function and by comparing alcoholics to nonalcoholics matched for ethnic origin. Therefore, we evaluated the D2/TaqI polymorphism in 29 impulsive violent alcoholic Finns, 17 nonimpulsive violent alcoholic Finns and 36 Finnish controls free of mental disorders, alcoholism and substance abuse. In 37 of the alcoholics, we measured cerebrospinal fluid (CSF) homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA) and 3-methoxy-4-hydroxyphenylglycol. There was no relationship between D2/Taq 1 genotype and concentrations of these monoamine metabolites in this group, which exhibits lower CSF HVA and 5-HIAA as compared to controls. There was also no genotypic difference between Finnish alcoholics and nonalcoholic controls. The lack of relationship between D2/Taq1 genotype and HVA concentration was replicated in 24 Caucasian alcoholics in the United States. JF - Acta psychiatrica Scandinavica AU - Goldman, D AU - Dean, M AU - Brown, G L AU - Bolos, A M AU - Tokola, R AU - Virkkunen, M AU - Linnoila, M AD - Laboratory of Neurogenetics, National Cancer Institute, Frederick, Maryland. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 351 EP - 357 VL - 86 IS - 5 SN - 0001-690X, 0001-690X KW - Receptors, Dopamine KW - 0 KW - Methoxyhydroxyphenylglycol KW - 534-82-7 KW - Hydroxyindoleacetic Acid KW - 54-16-0 KW - Homovanillic Acid KW - X77S6GMS36 KW - Index Medicus KW - United States KW - Genotype KW - Alleles KW - Methoxyhydroxyphenylglycol -- cerebrospinal fluid KW - Finland KW - Ethnic Groups KW - Polymorphism, Genetic -- genetics KW - Humans KW - Adult KW - Hydroxyindoleacetic Acid -- cerebrospinal fluid KW - Male KW - Homovanillic Acid -- cerebrospinal fluid KW - Alcoholism -- cerebrospinal fluid KW - Receptors, Dopamine -- genetics KW - Alcoholism -- genetics KW - Receptors, Dopamine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73455172?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+psychiatrica+Scandinavica&rft.atitle=D2+dopamine+receptor+genotype+and+cerebrospinal+fluid+homovanillic+acid%2C+5-hydroxyindoleacetic+acid+and+3-methoxy-4-hydroxyphenylglycol+in+alcoholics+in+Finland+and+the+United+States.&rft.au=Goldman%2C+D%3BDean%2C+M%3BBrown%2C+G+L%3BBolos%2C+A+M%3BTokola%2C+R%3BVirkkunen%2C+M%3BLinnoila%2C+M&rft.aulast=Goldman&rft.aufirst=D&rft.date=1992-11-01&rft.volume=86&rft.issue=5&rft.spage=351&rft.isbn=&rft.btitle=&rft.title=Acta+psychiatrica+Scandinavica&rft.issn=0001690X&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 - Pseudomonas exotoxin: recombinant conjugates as therapeutic agents. AN - 73447722; 1487051 JF - Biochemical Society transactions AU - FitzGerald, D J AU - Pastan, I AD - Department of Health and Human Services, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 731 EP - 734 VL - 20 IS - 4 SN - 0300-5127, 0300-5127 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - Immunotoxins KW - Recombinant Fusion Proteins 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 - Animals KW - Humans KW - Recombinant Fusion Proteins -- therapeutic use KW - Recombinant Proteins -- therapeutic use KW - Bacterial Toxins -- metabolism KW - Bacterial Toxins -- therapeutic use KW - Exotoxins -- metabolism KW - Immunotoxins -- therapeutic use KW - Immunotoxins -- metabolism KW - Pseudomonas aeruginosa KW - Exotoxins -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73447722?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Society+transactions&rft.atitle=Pseudomonas+exotoxin%3A+recombinant+conjugates+as+therapeutic+agents.&rft.au=FitzGerald%2C+D+J%3BPastan%2C+I&rft.aulast=FitzGerald&rft.aufirst=D&rft.date=1992-11-01&rft.volume=20&rft.issue=4&rft.spage=731&rft.isbn=&rft.btitle=&rft.title=Biochemical+Society+transactions&rft.issn=03005127&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 - 2017-01-17 ER - TY - JOUR T1 - Dying to be equal: women, alcohol, and cardiovascular disease. AN - 73363496; 1458038 AB - This data note explores the relationship of gender, alcohol consumption and premature death from cardiovascular disease (MCVD). Data on the 8164 deaths attributed to MCVD from the National Mortality Followback Study (NMFS) were analyzed controlling for gender and consumption. Women who are heavy drinkers die young at a rate equal to that of men who drink heavily. In light of this, we recommend that future research and preventive efforts in this area include females as subjects and alcohol as a major risk factor. JF - British journal of addiction AU - Hanna, E AU - Dufour, M C AU - Elliott, S AU - Stinson, F AU - Harford, T C AD - National Institute on Alcohol Abuse and Alcoholism, (NIAAA), Rockville, MD 20857. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 1593 EP - 1597 VL - 87 IS - 11 SN - 0952-0481, 0952-0481 KW - Index Medicus KW - Mortality KW - Attitude to Health KW - Humans KW - Adult KW - Health Promotion -- trends KW - Aged KW - Middle Aged KW - Male KW - Female KW - Cardiovascular Diseases -- mortality KW - Cardiovascular Diseases -- etiology KW - Women's Health KW - Cardiovascular Diseases -- classification KW - Alcoholism -- prevention & control KW - Alcoholism -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73363496?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+addiction&rft.atitle=Dying+to+be+equal%3A+women%2C+alcohol%2C+and+cardiovascular+disease.&rft.au=Hanna%2C+E%3BDufour%2C+M+C%3BElliott%2C+S%3BStinson%2C+F%3BHarford%2C+T+C&rft.aulast=Hanna&rft.aufirst=E&rft.date=1992-11-01&rft.volume=87&rft.issue=11&rft.spage=1593&rft.isbn=&rft.btitle=&rft.title=British+journal+of+addiction&rft.issn=09520481&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 treatment of Wegener's granulomatosis with glucocorticoids and methotrexate. AN - 73335088; 1445449 AB - To identify alternatives to daily low-dose cyclophosphamide (CYC) in the treatment of Wegener's granulomatosis (WG). An open-label pilot study of weekly low-dose methotrexate (MTX) plus glucocorticoids (GC) for treatment of patients with WG was performed. Twenty-nine patients who did not have immediately life-threatening disease were included. Outcome was determined by clinical characteristics, pathologic findings, course of illness, laboratory and radiographic findings, and successful withdrawal of GC therapy. Weekly administration of MTX (at a mean stable dosage of 20 mg) and GC resulted in marked improvement in 76% of the 29 patients. Remission was achieved in 69% of the patients, 7% improved but had intermittent smoldering disease that precluded total withdrawal of GC, and 17% had progressive disease within 2-6 months of starting the study treatment. Two patients who initially achieved remission later had relapses after GC was discontinued. Of those who remain in remission (mean followup time 14.5 months), 72% have not required GC for a mean period of 10 months. Although standard therapy for WG (daily CYC and GC) has dramatically improved outcome in this often-fatal disease, treatment morbidity has led to attempts to identify effective interventions that have less toxicity. Weekly low-dose MTX was shown in this study to be a feasible alternative to CYC in patients whose illness was not immediately life-threatening or in whom prior CYC treatment was ineffective or produced serious toxicity. Although these results are preliminary, they are encouraging and justify further studies in which MTX, CYC, and other alternative therapeutic approaches are compared concurrently. JF - Arthritis and rheumatism AU - Hoffman, G S AU - Leavitt, R Y AU - Kerr, G S AU - Fauci, A S AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 1322 EP - 1329 VL - 35 IS - 11 SN - 0004-3591, 0004-3591 KW - Antibodies, Antineutrophil Cytoplasmic KW - 0 KW - Autoantibodies KW - Glucocorticoids KW - Methotrexate KW - YL5FZ2Y5U1 KW - Abridged Index Medicus KW - Index Medicus KW - Drug Therapy, Combination KW - Treatment Failure KW - Prospective Studies KW - Humans KW - Adult KW - Autoantibodies -- analysis KW - Aged KW - Pilot Projects KW - Middle Aged KW - Recurrence KW - Male KW - Female KW - Remission Induction KW - Granulomatosis with Polyangiitis -- immunology KW - Methotrexate -- therapeutic use KW - Glucocorticoids -- therapeutic use KW - Granulomatosis with Polyangiitis -- drug therapy KW - Granulomatosis with Polyangiitis -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73335088?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+treatment+of+Wegener%27s+granulomatosis+with+glucocorticoids+and+methotrexate.&rft.au=Hoffman%2C+G+S%3BLeavitt%2C+R+Y%3BKerr%2C+G+S%3BFauci%2C+A+S&rft.aulast=Hoffman&rft.aufirst=G&rft.date=1992-11-01&rft.volume=35&rft.issue=11&rft.spage=1322&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 - 1992-12-07 N1 - Date created - 1992-12-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cholera toxin pretreatment protects against tumor necrosis factor lethality without compromising tumor response to therapy. AN - 73318779; 1444796 AB - Antitumor therapy with tumor necrosis factor is limited by systemic toxic effects. We studied whether cholera toxin, a bacterial exotoxin that adenosine diphosphate-ribosylates the alpha-subunit of Gs proteins, could separate the lethal from the antitumor effects of tumor necrosis factor. A single dose of intravenous cholera toxin protected non-tumor-bearing mice from a lethal dose of Escherichia coli endotoxin administered 6 or 24 hours later. On the basis of these results, tumor-bearing mice were randomized to receive either cholera toxin or saline, followed 6 hours later by either human tumor necrosis factor (400 micrograms/kg) or saline. Tumor-bearing mice pretreated with cholera toxin had (1) reduced treatment-related mortality (0/11 vs 5/11 for saline controls) and (2) tumor regression similar to that of controls. In a separate experiment in tumor-bearing mice, intravenous human tumor necrosis factor treatment induced an increase in serum levels of murine tumor necrosis factor to a peak of 500 pg/mL at 1 hour in saline-pretreated controls, while a similar increase could not be detected in those mice pretreated with cholera toxin. These results suggest that pretreatment with cholera toxin can reduce the endogenous tumor necrosis factor response to administered tumor necrosis factor and separate the lethal from the antitumor effects. Cholera toxin may prove to be a useful tool for investigating the mechanisms underlying the varied effects of tumor necrosis factor. JF - Archives of surgery (Chicago, Ill. : 1960) AU - Block, M I AU - Alexander, H R AU - Norton, J A AD - Surgical Metabolism Section, National Cancer Institute, National Institutes of Health, Bethesda, Md. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 1330 EP - 1334 VL - 127 IS - 11 SN - 0004-0010, 0004-0010 KW - Endotoxins KW - 0 KW - Tumor Necrosis Factor-alpha KW - Cholera Toxin KW - 9012-63-9 KW - Abridged Index Medicus KW - Index Medicus KW - Drug Therapy, Combination KW - Animals KW - Survival Rate KW - Infusions, Intravenous KW - Mice, Inbred C57BL KW - Escherichia coli KW - Endotoxins -- adverse effects KW - Disease Models, Animal KW - Mice KW - Drug Evaluation, Preclinical KW - Female KW - Sarcoma, Experimental -- drug therapy KW - Tumor Necrosis Factor-alpha -- administration & dosage KW - Cholera Toxin -- pharmacology KW - Cholera Toxin -- administration & dosage KW - Tumor Necrosis Factor-alpha -- adverse effects KW - Sarcoma, Experimental -- pathology KW - Sarcoma, Experimental -- mortality KW - Cholera Toxin -- therapeutic use KW - Tumor Necrosis Factor-alpha -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73318779?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cholera+toxin+pretreatment+protects+against+tumor+necrosis+factor+lethality+without+compromising+tumor+response+to+therapy.&rft.au=Block%2C+M+I%3BAlexander%2C+H+R%3BNorton%2C+J+A&rft.aulast=Block&rft.aufirst=M&rft.date=1992-11-01&rft.volume=127&rft.issue=11&rft.spage=1330&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 - 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 - Effects of MgCl2 on the release and recycling of heparan sulfate proteoglycans in a rat parathyroid cell line. AN - 73294301; 1416969 AB - Divalent cations, such as Mg2+, Ba2+, and Co2+, are known to mimic the effects of Ca2+ in parathyroid cells, but it is not clear whether the mechanism of their action is the same as that of Ca2+. We have shown that extracellular Ca2+ concentration ([Ca2+]e) regulates the distribution and recycling of cell-surface heparan sulfate (HS) proteoglycans in a rat parathyroid cell line; at normal to high [Ca2+]e (e.g., 2 mM) HS proteoglycans are primarily localized intracellularly, while at low [Ca2+]e (0.05 mM) they are translocated to the cell surface and rapidly recycle (Takeuchi, Y., Sakaguchi, K., Yanagishita, M., Aurbach, G. D., and Hascall, V. C., 1990, J. Biol. Chem. 265, 13661-13668). We now show that a high concentration of Mg2+ (8 mM) reduces the amount of recycling HS proteoglycans in low [Ca2+]e. However, the primary effects of high Ca2+ and high Mg2+ on the recycling HS proteoglycans are different. High [Ca2+]e causes translocation of HS proteoglycans to intracellular compartments, while high Mg2+ stimulates cleavage of their core proteins and subsequent shedding of HS proteoglycans into the medium, thereby depleting the recycling molecules. However, high Mg2+ does not induce shedding of HS proteoglycans in high [Ca2+]e. The effects of Ba2+ and Co2+ were similar to those of Mg2+, but Sr2+ showed no significant effects on HS proteoglycan translocation. Otherwise, 8 mM Mg2+ did not alter biosynthesis or intracellular catabolism of HS proteoglycans. These observations suggest that the recycling of HS proteoglycans in parathyroid cells is sensitive only to [Ca2+]e, whereas several other divalent cations can deplete the recycling HS proteoglycans by a distinctly different mechanism. Thus, the mechanism by which Ca2+ regulates the amounts of the recycling HS proteoglycans may be more physiological and play a functional role in parathyroid cells. JF - Archives of biochemistry and biophysics AU - Takeuchi, Y AU - Yanagishita, M AU - Hascall, V C AD - Bone Research Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/11/01/ PY - 1992 DA - 1992 Nov 01 SP - 371 EP - 379 VL - 298 IS - 2 SN - 0003-9861, 0003-9861 KW - Cations, Divalent KW - 0 KW - Heparan Sulfate Proteoglycans KW - Proteoglycans KW - Sulfates KW - Sulfur Radioisotopes KW - Magnesium Chloride KW - 02F3473H9O KW - Tritium KW - 10028-17-8 KW - Heparitin Sulfate KW - 9050-30-0 KW - Leucine KW - GMW67QNF9C KW - Calcium Chloride KW - M4I0D6VV5M KW - Glucosamine KW - N08U5BOQ1K KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Electrophoresis, Polyacrylamide Gel KW - Chromatography, Ion Exchange KW - Rats KW - Sulfates -- metabolism KW - Kinetics KW - Leucine -- metabolism KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Glucosamine -- metabolism KW - Calcium Chloride -- pharmacology KW - Cell Line KW - Cations, Divalent -- pharmacology KW - Proteoglycans -- biosynthesis KW - Heparitin Sulfate -- metabolism KW - Proteoglycans -- metabolism KW - Parathyroid Glands -- metabolism KW - Magnesium Chloride -- pharmacology KW - Proteoglycans -- isolation & purification KW - Heparitin Sulfate -- isolation & purification KW - Heparitin Sulfate -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73294301?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Effects+of+MgCl2+on+the+release+and+recycling+of+heparan+sulfate+proteoglycans+in+a+rat+parathyroid+cell+line.&rft.au=Takeuchi%2C+Y%3BYanagishita%2C+M%3BHascall%2C+V+C&rft.aulast=Takeuchi&rft.aufirst=Y&rft.date=1992-11-01&rft.volume=298&rft.issue=2&rft.spage=371&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 - 1992-11-13 N1 - Date created - 1992-11-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Changes in T-helper cell function in human immunodeficiency virus-infected children during didanosine therapy as a measure of antiretroviral activity. AN - 73281636; 1421391 AB - Didanosine has shown activity against the human immunodeficiency virus (HIV) in both children and adults. We prospectively assessed T-helper cell (Th) function as determined by in vitro interleukin-2 (IL-2) production in response to a panel of T-cell stimuli in 22 HIV-infected children before and during didanosine therapy and we correlated the incidence of opportunistic and recurrent bacterial infections with changes in p24 antigen and CD4 counts. Didanosine (270, 360, or 540 mg/m2/d) was administered orally for periods ranging from 8 to 40 weeks (mean, 24 weeks). Five of six asymptomatic patients (Centers for Disease Control P-1) compared with 6 of 16 symptomatic (P-2) patients exhibited improved Th function (greater than threefold increase in IL-2 production to at least 2 of the 4 stimuli) during therapy. Of 12 patients without infections during therapy, 9 (75%) showed improvement in Th function, compared with only 2 of 10 patients with infections (P = .03). Notably, the incidence of infections was not correlated with improvements in CD4 count or decreases in p24 antigen. Improvement in Th function during didanosine therapy is correlated with decreased incidence of infections. Assessment of Th function may provide an additional measurement of immunologic response to antiretroviral therapy. JF - Blood AU - Clerici, M AU - Roilides, E AU - Butler, K M AU - DePalma, L AU - Venzon, D AU - Shearer, G M AU - Pizzo, P A AD - Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/11/01/ PY - 1992 DA - 1992 Nov 01 SP - 2196 EP - 2202 VL - 80 IS - 9 SN - 0006-4971, 0006-4971 KW - Interleukin-2 KW - 0 KW - Didanosine KW - K3GDH6OH08 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Infant KW - Reference Values KW - Cells, Cultured KW - Humans KW - Adult KW - Interleukin-2 -- biosynthesis KW - Follow-Up Studies KW - Child KW - Adolescent KW - Male KW - Female KW - Child, Preschool KW - Didanosine -- toxicity KW - Didanosine -- therapeutic use KW - HIV Infections -- immunology KW - HIV Infections -- drug therapy KW - T-Lymphocytes, Helper-Inducer -- drug effects KW - T-Lymphocytes, Helper-Inducer -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73281636?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Changes+in+T-helper+cell+function+in+human+immunodeficiency+virus-infected+children+during+didanosine+therapy+as+a+measure+of+antiretroviral+activity.&rft.au=Clerici%2C+M%3BRoilides%2C+E%3BButler%2C+K+M%3BDePalma%2C+L%3BVenzon%2C+D%3BShearer%2C+G+M%3BPizzo%2C+P+A&rft.aulast=Clerici&rft.aufirst=M&rft.date=1992-11-01&rft.volume=80&rft.issue=9&rft.spage=2196&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=00064971&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-07 N1 - Date created - 1992-12-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Recombinant toxins containing the variable domains of the anti-Tac monoclonal antibody to the interleukin-2 receptor kill malignant cells from patients with chronic lymphocytic leukemia. AN - 73277002; 1421405 AB - We have previously shown that the variable domains of the monoclonal antibody anti-Tac [anti-Tac(Fv)] can be fused to derivatives of Pseudomonas exotoxin (PE) or diphtheria toxin (DT) to produce recombinant immunotoxins that kill interleukin-2 (IL-2) receptor-bearing cells. We now report that two of these single-chain recombinant immunotoxins, anti-Tac(Fv)-PE40KDEL and DT388-anti-Tac(Fv), are cytotoxic toward peripheral blood mononuclear cells (PBMCs) from patients with chronic lymphocytic leukemia (CLL). In anti-Tac(Fv)-PE40KDEL, anti-Tac(Fv) is genetically fused to the amino terminus of PE40KDEL, a recombinant form of PE which contains amino acids 253-608 of PE and the -KDEL mutation at the carboxyl terminus. In DT388-anti-Tac(Fv), anti-Tac(Fv) is fused to the carboxyl terminus of the first 388 amino acids of DT. PBMCs from 14 patients were incubated with the recombinant toxins for 60 hours, and [3H]-leucine incorporation was measured. Anti-Tac(Fv)-PE40KDEL was cytotoxic to 7 of the 14 patient samples, with half-maximal inhibition of protein synthesis (IC50) achieved at 1.2 to 9 ng/mL (1.8 to 13 x 10(-11) mol/L). DT388-anti-Tac(Fv) was cytotoxic to 11 of the 14 samples, with IC50s ranging from less than 1 to 250 ng/mL. DT388-IL-2, in which the first 388 amino acids of DT are attached to IL-2, was marginally cytotoxic toward only 4 of 13 CLL samples tested with IC50s ranging from 100 to 550 ng/mL. Trypan blue staining of cells from several patients indicated that inhibition of protein synthesis correlated with cell death. Binding assays using [3H]-anti-Tac indicated that the CLL cells from nine of the patients contained between 400 and 2,500 sites per cell. Cells from another patient, which were resistant to both anti-Tac(Fv)-PE40KDEL and DT388-anti-Tac(Fv), had less than 100 sites per cell. We conclude that anti-Tac(Fv)-PE40KDEL and DT388-anti-Tac(Fv) can kill CLL cells which have low numbers of IL-2 receptors, and should be investigated further for therapy of this disease. JF - Blood AU - Kreitman, R J AU - Chaudhary, V K AU - Kozak, R W AU - FitzGerald, D J AU - Waldman, T A AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/11/01/ PY - 1992 DA - 1992 Nov 01 SP - 2344 EP - 2352 VL - 80 IS - 9 SN - 0006-4971, 0006-4971 KW - Antibodies, Monoclonal KW - 0 KW - Bacterial Toxins KW - Exotoxins KW - Immunotoxins KW - Receptors, Interleukin-2 KW - Recombinant Fusion Proteins 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 - Abridged Index Medicus KW - Index Medicus KW - Recombinant Proteins -- pharmacology KW - Tumor Cells, Cultured KW - Cell Survival -- drug effects KW - Humans KW - Recombinant Fusion Proteins -- pharmacology KW - Aged KW - Middle Aged KW - Antibodies, Monoclonal -- pharmacology KW - Pseudomonas aeruginosa KW - Male KW - Female KW - Exotoxins -- genetics KW - Exotoxins -- pharmacology KW - Leukemia, Lymphocytic, Chronic, B-Cell -- blood KW - Monocytes -- pathology KW - Monocytes -- drug effects KW - Immunotoxins -- pharmacology KW - Receptors, Interleukin-2 -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73277002?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Recombinant+toxins+containing+the+variable+domains+of+the+anti-Tac+monoclonal+antibody+to+the+interleukin-2+receptor+kill+malignant+cells+from+patients+with+chronic+lymphocytic+leukemia.&rft.au=Kreitman%2C+R+J%3BChaudhary%2C+V+K%3BKozak%2C+R+W%3BFitzGerald%2C+D+J%3BWaldman%2C+T+A%3BPastan%2C+I&rft.aulast=Kreitman&rft.aufirst=R&rft.date=1992-11-01&rft.volume=80&rft.issue=9&rft.spage=2344&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=00064971&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-07 N1 - Date created - 1992-12-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Occupational risk factors for multiple myeloma among Danish men. AN - 73264400; 1420859 AB - A large population-based case-control study evaluated occupational exposures in 1,098 Danish males diagnosed with multiple myeloma from 1970 to 1984 and in 4,169 age- and gender-matched controls alive at the time of case-diagnosis. Industrial histories were obtained from the Supplementary Pension Fund which, since 1964, has recorded employments of adult Danes; occupation came from subjects' most recent tax records. Four industrial hygienists created a job-exposure matrix for 47 substances based on 15,000 unique industry/occupation combinations in subjects' histories. Risk of myeloma was significantly elevated among road and railroad workers, precision metalworkers, and workers in the transportation and communication industries. Risk increased significantly with duration of employment in: production of synthetic yarns, plastic packaging, and miscellaneous chemical compounds; fabricating structural metal and stationary tanks; body factories; electrical plants; and retail sale of paint and wallpaper. Risks of myeloma were elevated, though statistically nonsignificantly, in all categories of exposure to gasoline and engine exhausts. Risks rose with likelihood and duration of exposure to phthalates, and were statistically significant and nearly fivefold with probable exposure to vinyl chloride for five or more years. After adjusting for multiple exposures and disregarding exposures within 10 years of diagnosis (or selection as a control), probable exposure to vinyl chloride was associated with increased risk of myeloma, which rose to fivefold with longer exposure. Associations with gasoline, engine exhausts, and phthalates persisted, but were inconsistent with duration and probability of exposure. Previously reported associations with agriculture were not confirmed by these data. JF - Cancer causes & control : CCC AU - Heineman, E F AU - Olsen, J H AU - Pottern, L M AU - Gomez, M AU - Raffn, E AU - Blair, A AD - Environmental Epidemiology Branch, National Cancer Institute, Bethesda, MD 10892. Y1 - 1992/11// PY - 1992 DA - November 1992 SP - 555 EP - 568 VL - 3 IS - 6 SN - 0957-5243, 0957-5243 KW - Gasoline KW - 0 KW - Phthalic Acids KW - Smoke KW - phthalic acid KW - 6O7F7IX66E KW - Vinyl Chloride KW - WD06X94M2D KW - Index Medicus KW - Odds Ratio KW - Age Factors KW - Humans KW - Communication KW - Aged KW - Transportation KW - Aged, 80 and over KW - Risk Factors KW - Military Personnel KW - Case-Control Studies KW - Denmark -- epidemiology KW - Incidence KW - Middle Aged KW - Occupations KW - Time Factors KW - Chemical Industry KW - Male KW - Occupational Exposure KW - Multiple Myeloma -- epidemiology KW - Occupational Diseases -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73264400?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Occupational+risk+factors+for+multiple+myeloma+among+Danish+men.&rft.au=Heineman%2C+E+F%3BOlsen%2C+J+H%3BPottern%2C+L+M%3BGomez%2C+M%3BRaffn%2C+E%3BBlair%2C+A&rft.aulast=Heineman&rft.aufirst=E&rft.date=1992-11-01&rft.volume=3&rft.issue=6&rft.spage=555&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 - Partial characterization, progressive development and correlations of some neoplastic characters in 20-methylcholanthrene-induced transformed murine embryonal fibroblasts. AN - 73308605; 1423239 AB - Non-trypsinized primary fibroblast cells from 20-day-old Swiss mouse embryo was transformed by 20-methylcholanthrene (MCA) and was designated as CNCI-PM-20. The progressive development of some transformation related characters such as morphological alterations, reduced population doubling time, increased saturation density, reduced serum requirement, increased plating efficiency, loss of density dependent growth inhibition, anchorage-independent growth and tumorigenicity in mice clearly demonstrated the multistep process of carcinogenesis as well as the neoplastic nature of the cell line. Furthermore, the association of reduced requirement of serum and loss of density-dependent growth inhibition with tumorigenicity were also observed. Finally, anchorage-independent growth, greater malignant nature of transformed foci and increased number of giant cells may be required for tumorigenicity of this cell line. JF - Cancer letters AU - Mukherjee, P AU - Das, S K AD - Department of Tissue Culture, Chittaranjan National Cancer Institute (Research Unit), Calcutta, India. Y1 - 1992/10/30/ PY - 1992 DA - 1992 Oct 30 SP - 1 EP - 12 VL - 67 IS - 1 SN - 0304-3835, 0304-3835 KW - Methylcholanthrene KW - 56-49-5 KW - Index Medicus KW - Animals KW - Cell Count KW - Mice KW - Pregnancy KW - Neoplasm Transplantation KW - Fibroblasts -- pathology KW - Cells, Cultured KW - Blood Physiological Phenomena KW - Embryo, Mammalian KW - Female KW - Male KW - Cell Division KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73308605?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Partial+characterization%2C+progressive+development+and+correlations+of+some+neoplastic+characters+in+20-methylcholanthrene-induced+transformed+murine+embryonal+fibroblasts.&rft.au=Mukherjee%2C+P%3BDas%2C+S+K&rft.aulast=Mukherjee&rft.aufirst=P&rft.date=1992-10-30&rft.volume=67&rft.issue=1&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 - 1992-12-15 N1 - Date created - 1992-12-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - N-acetylaspartylglutamate acts as an agonist upon homomeric NMDA receptor (NMDAR1) expressed in Xenopus oocytes. AN - 73229693; 1356833 AB - The electrophysiological effects of N-acetylaspartylglutamate (NAAG), an endogenous peptide restrictively distributed in the central nervous system, were studied using Xenopus oocytes injected with RNAs transcribed from cloned glutamate receptor cDNAs. NAAG induced an inward current, dose dependently, in oocytes injected with RNA for an N-methyl-D-aspartate receptor subunit (NMDAR1). In contrast, the oocytes injected with RNAs for AMPA-selective glutamate receptors (GluR1, GluR3, GluR1+GluR2 and GluR2+GluR3) scarcely responded to NAAG, and the oocytes injected with RNA for kainate receptor (GluR6) did not respond to NAAG. The half-maximal response (ED50) value of NAAG on expressed NMDAR1 was 185 microM, which shows that NAAG is about 115-times less potent than L-glutamate (Glu), the ED50 of which value was 1.6 microM. The maximal current amplitude induced by NAAG was about 70% of that by Glu. NAAG-induced current in NMDAR1-injected oocytes was potentiated by glycine, dose-dependently antagonized by DL-2-amino-5-phosphonovaleric acid, and blocked by magnesium ions in a voltage-dependent fashion. These results suggest that NAAG is one of the endogenous agonists selective for NMDAR1. JF - FEBS letters AU - Sekiguchi, M AU - Wada, K AU - Wenthold, R J AD - Laboratory of Neurochemistry, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/10/26/ PY - 1992 DA - 1992 Oct 26 SP - 285 EP - 289 VL - 311 IS - 3 SN - 0014-5793, 0014-5793 KW - Dipeptides KW - 0 KW - Glutamates KW - Receptors, N-Methyl-D-Aspartate KW - Recombinant Proteins KW - isospaglumic acid KW - 1W8M12WXYL KW - Glutamic Acid KW - 3KX376GY7L KW - N-Methylaspartate KW - 6384-92-5 KW - 2-Amino-5-phosphonovalerate KW - 76726-92-6 KW - Kainic Acid KW - SIV03811UC KW - Index Medicus KW - Animals KW - Recombinant Proteins -- drug effects KW - Kainic Acid -- pharmacology KW - Dose-Response Relationship, Drug KW - Transcription, Genetic KW - Cloning, Molecular KW - Xenopus laevis KW - 2-Amino-5-phosphonovalerate -- pharmacology KW - Recombinant Proteins -- metabolism KW - Glutamates -- pharmacology KW - N-Methylaspartate -- pharmacology KW - Kinetics KW - Membrane Potentials -- drug effects KW - Female KW - Receptors, N-Methyl-D-Aspartate -- physiology KW - Oocytes -- drug effects KW - Oocytes -- physiology KW - Receptors, N-Methyl-D-Aspartate -- genetics KW - Dipeptides -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73229693?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FEBS+letters&rft.atitle=N-acetylaspartylglutamate+acts+as+an+agonist+upon+homomeric+NMDA+receptor+%28NMDAR1%29+expressed+in+Xenopus+oocytes.&rft.au=Sekiguchi%2C+M%3BWada%2C+K%3BWenthold%2C+R+J&rft.aulast=Sekiguchi&rft.aufirst=M&rft.date=1992-10-26&rft.volume=311&rft.issue=3&rft.spage=285&rft.isbn=&rft.btitle=&rft.title=FEBS+letters&rft.issn=00145793&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 - Angiogenin is a cytotoxic, tRNA-specific ribonuclease in the RNase A superfamily. AN - 73242915; 1400510 AB - Angiogenin is a 14.4-kDa human plasma protein with 65% homology to RNase A that retains the key active site residues and three of the four RNase A disulfide bonds. We demonstrate that recombinant angiogenin functions as a cytotoxic tRNA-specific RNase in cell-free lysates and when injected into Xenopus oocytes. Inhibition of protein synthesis by angiogenin correlates with degradation of endogenous oocyte tRNA. Exogenous, radiolabeled tRNA is also hydrolyzed by angiogenin, whereas oocyte rRNA and mRNA are not detectably degraded by angiogenin. Protein synthesis was restored to angiogenin-injected oocytes by injecting the RNase inhibitor RNasin plus total Xenopus or calf liver tRNAs, thereby demonstrating that the tRNA degradation induced by angiogenin was the sole cause of cytotoxicity. A similar tRNA-reversible inhibition of protein synthesis was seen in rabbit reticulocyte lysates. Angiogenin therefore appears to be a specific cellular tRNase, whereas five homologues in the RNase A superfamily lack angiogenin's specificity for tRNA. One of these homologues purified from human eosinophils, eosinophil-derived neurotoxin, nonspecifically degrades oocyte RNA similar to RNase A and is also cytotoxic at very low concentrations. JF - The Journal of biological chemistry AU - Saxena, S K AU - Rybak, S M AU - Davey, R T AU - Youle, R J AU - Ackerman, E J AD - Genetics and Biochemistry Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10/25/ PY - 1992 DA - 1992 Oct 25 SP - 21982 EP - 21986 VL - 267 IS - 30 SN - 0021-9258, 0021-9258 KW - Cytotoxins KW - 0 KW - Proteins KW - RNA, Transfer KW - 9014-25-9 KW - Ribonucleases KW - EC 3.1.- KW - angiogenin KW - EC 3.1.27.- KW - Ribonuclease, Pancreatic KW - EC 3.1.27.5 KW - Index Medicus KW - Protein Biosynthesis KW - Animals KW - Cattle KW - Blotting, Northern KW - Sequence Alignment KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Substrate Specificity KW - Sequence Homology, Amino Acid KW - Cell Survival KW - Cytotoxins -- classification KW - Cytotoxins -- metabolism KW - RNA, Transfer -- metabolism KW - Proteins -- classification KW - Ribonucleases -- genetics KW - Cytotoxins -- genetics KW - Ribonucleases -- metabolism KW - Ribonuclease, Pancreatic -- metabolism KW - Proteins -- metabolism KW - Proteins -- genetics KW - Ribonucleases -- classification KW - Ribonuclease, Pancreatic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73242915?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Angiogenin+is+a+cytotoxic%2C+tRNA-specific+ribonuclease+in+the+RNase+A+superfamily.&rft.au=Saxena%2C+S+K%3BRybak%2C+S+M%3BDavey%2C+R+T%3BYoule%2C+R+J%3BAckerman%2C+E+J&rft.aulast=Saxena&rft.aufirst=S&rft.date=1992-10-25&rft.volume=267&rft.issue=30&rft.spage=21982&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 - 1992-11-25 N1 - Date created - 1992-11-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Niacinamide blocks 3-acetylpyridine toxicity of cerebellar granule cells in vitro. AN - 73403985; 1361407 AB - 3-Acetylpyridine (3AP) is a potent neurotoxin when administered to laboratory animals. However, its neurotoxic effects have not been investigated extensively in vitro. Cultured cerebellar granule cells are killed by concentrations of 3AP of 0.1-1 mM (ED50 = 220 microM) but not by its 2-acetyl and 4-acetyl analogues. The toxicity of 3AP is enhanced by preexposure to subtoxic concentrations of N-methyl-D-aspartate (NMDA) and is unaffected by the NMDA receptor antagonists MK-801 or APV, as well as by deprenyl, mazindol, or tetrahydrofolic acid. However, 3AP toxicity is completely blocked by preincubating cerebellar granule cells with low concentrations of niacinamide. These data lead us to suggest that 3AP toxicity is due to the substitution of 3AP for niacinamide in the formation of niacinamide adenine dinucleotides (NAD(P)). JF - Brain research AU - Weller, M AU - Marini, A M AU - Paul, S M AD - Section on Molecular Pharmacology, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1992/10/23/ PY - 1992 DA - 1992 Oct 23 SP - 160 EP - 164 VL - 594 IS - 1 SN - 0006-8993, 0006-8993 KW - Excitatory Amino Acid Antagonists KW - 0 KW - Glutamates KW - Pyridines KW - Tetrahydrofolates KW - 3-acetylpyridine KW - 00QT8FX306 KW - Niacinamide KW - 25X51I8RD4 KW - Selegiline KW - 2K1V7GP655 KW - Glutamic Acid KW - 3KX376GY7L KW - 5,6,7,8-tetrahydrofolic acid KW - 43ZWB253H4 KW - N-Methylaspartate KW - 6384-92-5 KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - 2-Amino-5-phosphonovalerate KW - 76726-92-6 KW - Mazindol KW - C56709M5NH KW - Index Medicus KW - Rats KW - Animals KW - Selegiline -- pharmacology KW - Rats, Sprague-Dawley KW - Mazindol -- pharmacology KW - 2-Amino-5-phosphonovalerate -- pharmacology KW - N-Methylaspartate -- pharmacology KW - Tetrahydrofolates -- pharmacology KW - Glutamates -- toxicity KW - Drug Synergism KW - Dizocilpine Maleate -- pharmacology KW - Niacinamide -- pharmacology KW - Cerebellum -- cytology KW - Pyridines -- toxicity KW - Neurons -- drug effects KW - Cerebellum -- drug effects KW - Pyridines -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73403985?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Niacinamide+blocks+3-acetylpyridine+toxicity+of+cerebellar+granule+cells+in+vitro.&rft.au=Weller%2C+M%3BMarini%2C+A+M%3BPaul%2C+S+M&rft.aulast=Weller&rft.aufirst=M&rft.date=1992-10-23&rft.volume=594&rft.issue=1&rft.spage=160&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 - 1993-01-27 N1 - Date created - 1993-01-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dietary retinoids are essential for skin papilloma formation induced by either the two-stage or the complete tumorigenesis model in female SENCAR mice. AN - 73408606; 1451104 AB - Our previous work has shown that dietary retinoic acid (RA) is necessary for skin tumor formation induced by the two-stage protocol with the initiator 7,12-dimethylbenz[a]anthracene (DMBA) and the promoter 12-O-tetradecanoyl phorbol-13-acetate (TPA) (De Luca et al., Cancer Res., 36 (1976) 2334-2339). Here we report that retinoids are required for tumorigenesis by the two-stage as well as by the complete tumorigenesis protocol. Mice were treated with a single dose of DMBA (20 micrograms), followed by 20 applications of TPA (2 micrograms), or by 20 applications of DMBA (25 micrograms for 2 weeks and 51 micrograms thereafter). Regardless of the tumor induction protocol, tumor formation was inhibited by vitamin A-deficiency, while RA (3 micrograms/g of diet) or retinyl palmitate (RP, 6 micrograms/g) supplementation permitted the appearance of tumors. In addition, in comparison to the purified diets and regardless of their RA levels, the non-purified Purina chow diet enhanced tumor yield especially in the two-stage tumorigenesis protocol. This effect was less striking in mice with tumors induced by the complete tumorigenesis protocol. In summary, dietary retinoids are essential for skin tumor formation induced either by the two-stage or the complete tumorigenesis protocol. JF - Cancer letters AU - De Luca, L M AU - Sly, L AU - Jones, C S AU - Chen, L C AD - Differentiation Control Section, Laboratory of Cellular Carcinogenesis and Tumor Promotion National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/10/21/ PY - 1992 DA - 1992 Oct 21 SP - 233 EP - 239 VL - 66 IS - 3 SN - 0304-3835, 0304-3835 KW - Vitamin A KW - 11103-57-4 KW - retinol palmitate KW - 1D1K0N0VVC KW - 9,10-Dimethyl-1,2-benzanthracene KW - 57-97-6 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Mice, Inbred Strains KW - Animals KW - Vitamin A Deficiency -- physiopathology KW - Body Weight -- drug effects KW - Mice KW - Diet KW - Time Factors KW - Female KW - Tetradecanoylphorbol Acetate -- toxicity KW - Vitamin A -- analogs & derivatives KW - Vitamin A -- administration & dosage KW - Papilloma -- pathology KW - 9,10-Dimethyl-1,2-benzanthracene -- toxicity KW - Vitamin A -- toxicity KW - Skin Neoplasms -- chemically induced KW - Vitamin A -- pharmacology KW - Skin Neoplasms -- pathology KW - Papilloma -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73408606?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Dietary+retinoids+are+essential+for+skin+papilloma+formation+induced+by+either+the+two-stage+or+the+complete+tumorigenesis+model+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=1992-10-21&rft.volume=66&rft.issue=3&rft.spage=233&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 - 1993-01-07 N1 - Date created - 1993-01-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Not myositis. A series of chance encounters. AN - 73261734; 1404746 JF - JAMA AU - Plotz, P H AD - Connective Tissue Diseases Section, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Md 20892. Y1 - 1992/10/21/ PY - 1992 DA - 1992 Oct 21 SP - 2074 EP - 2077 VL - 268 IS - 15 SN - 0098-7484, 0098-7484 KW - Phosphofructokinase-1 KW - EC 2.7.1.11 KW - Abridged Index Medicus KW - Index Medicus KW - Diagnosis, Differential KW - Myxedema -- diagnosis KW - Humans KW - Phosphofructokinase-1 -- deficiency KW - Neuromuscular Diseases -- diagnosis KW - Aged KW - Arteritis -- pathology KW - Muscles -- blood supply KW - Arteritis -- diagnosis KW - Muscular Diseases -- diagnosis KW - Muscular Diseases -- chemically induced KW - Adult KW - Middle Aged KW - Muscles -- pathology KW - Female KW - Myositis -- diagnosis KW - Myositis -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73261734?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&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=Not+myositis.+A+series+of+chance+encounters.&rft.au=Plotz%2C+P+H&rft.aulast=Plotz&rft.aufirst=P&rft.date=1992-10-21&rft.volume=268&rft.issue=15&rft.spage=2074&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-04 N1 - Date created - 1992-11-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Construction of a new universal vector for insertional mutagenesis by homologous recombination. AN - 73242182; 1327975 AB - We describe here the construction of a vector (pSSC-9) which can be used for the insertional mutagenesis of any gene for which genomic sequences have been cloned. This vector contains a neomycin-resistance-encoding gene (neoR) which is driven by a modified thymidine kinase (tk) promoter for positive selection. Flanking neoR are two tk genes driven by their own promoters for negative selection of nonhomologous insertions. The neoR and tk cassettes are separated by four unique cloning sites on the right-hand side of the neoR cassette and three unique sites on the left-hand side. The vector also includes two SfiI sites, one on each side of the tk cassettes, for the excision of the cloned genomic DNA fragments along with the selectable markers. Electroporation of pSSC-9 into mouse embryonic stem (ES) cells and cultured diploid mouse adrenal Y-1 cells conferred resistance to G418 and sensitivity to ganciclovir in both cell lines. These results illustrate the expression of the positive and negative selectable markers in two different cell lines and thus suggest that the vector could be used in ES cells, as well as in cultured somatic cells. JF - Gene AU - Chauhan, S S AU - Gottesman, M M AD - Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/10/21/ PY - 1992 DA - 1992 Oct 21 SP - 281 EP - 285 VL - 120 IS - 2 SN - 0378-1119, 0378-1119 KW - neoR KW - tk KW - Recombinant Proteins KW - 0 KW - Phosphotransferases KW - EC 2.7.- KW - Thymidine Kinase KW - EC 2.7.1.21 KW - Kanamycin Kinase KW - EC 2.7.1.95 KW - Ganciclovir KW - P9G3CKZ4P5 KW - Index Medicus KW - Phosphotransferases -- analysis KW - Phosphotransferases -- genetics KW - Animals KW - Thymidine Kinase -- metabolism KW - Mice KW - Phosphotransferases -- metabolism KW - Base Sequence KW - Promoter Regions, Genetic KW - Tumor Cells, Cultured KW - Cell Survival -- drug effects KW - Recombinant Proteins -- metabolism KW - Thymidine Kinase -- analysis KW - Molecular Sequence Data KW - Recombinant Proteins -- analysis KW - Cell Line KW - Thymidine Kinase -- genetics KW - Ganciclovir -- pharmacology KW - Genetic Vectors KW - Recombination, Genetic KW - Mutagenesis, Insertional UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73242182?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gene&rft.atitle=Construction+of+a+new+universal+vector+for+insertional+mutagenesis+by+homologous+recombination.&rft.au=Chauhan%2C+S+S%3BGottesman%2C+M+M&rft.aulast=Chauhan&rft.aufirst=S&rft.date=1992-10-21&rft.volume=120&rft.issue=2&rft.spage=281&rft.isbn=&rft.btitle=&rft.title=Gene&rft.issn=03781119&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 - neoR; tk N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Risk of suicide among persons with AIDS. A national assessment. AN - 73230569; 1404744 AB - We sought to describe the rate, risk, trends, methods, and distribution of suicide among persons with the acquired immunodeficiency syndrome (AIDS) in the United States. We used National Center for Health Statistics multiple-cause mortality data from 1987 through 1989 to identify suicides among persons with AIDS (PWAs) and public-access AIDS surveillance data to determine person-years of observation of PWAs. Residents of the United States with death certificates indicating suicide. Death certificates indicating both AIDS and suicide. In 1987 through 1989, a total of 165 suicides among PWAs occurred in 45 states and the District of Columbia. All but one case were male. Among males the rate was 165 per 100,000 person-years of observation, 7.4-fold higher than among demographically similar men in the general population. Self-poisoning with drugs was both the most common method (35%) and the method with the highest standardized mortality ratio (35). Suicide risk for PWAs decreased significantly (P < .05) from 1987 to 1989. Persons with AIDS have an increased risk of suicide, and assessment of such risk should be a standard practice in their care. These assessments should be carefully considered when potentially lethal medications are prescribed. The declining trend in suicide rates between 1987 and 1989 is encouraging; possible causes include emerging therapies for human immunodeficiency virus/AIDS, better psychiatric care for these patients, and lessened social stigma against PWAs. JF - JAMA AU - Coté, T R AU - Biggar, R J AU - Dannenberg, A L AD - National Cancer Institute, Viral Epidemiology Section, Rockville, Md 20852. Y1 - 1992/10/21/ PY - 1992 DA - 1992 Oct 21 SP - 2066 EP - 2068 VL - 268 IS - 15 SN - 0098-7484, 0098-7484 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Risk Factors KW - Humans KW - Adult KW - Middle Aged KW - Adolescent KW - United States -- epidemiology KW - Male KW - Acquired Immunodeficiency Syndrome -- epidemiology KW - Suicide -- trends KW - Suicide -- statistics & numerical data KW - Suicide -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73230569?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Risk+of+suicide+among+persons+with+AIDS.+A+national+assessment.&rft.au=Cot%C3%A9%2C+T+R%3BBiggar%2C+R+J%3BDannenberg%2C+A+L&rft.aulast=Cot%C3%A9&rft.aufirst=T&rft.date=1992-10-21&rft.volume=268&rft.issue=15&rft.spage=2066&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-04 N1 - Date created - 1992-11-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: JAMA. 1993 Jun 9;269(22):2847-8 [8497086] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - High-performance liquid chromatographic separation of purine deoxyribonucleoside monophosphate-benzo[a]pyrene adducts. AN - 73401054; 1460077 AB - Chromatographic methods that allow the separation of adducts of purine nucleoside 3'-phosphates with the pure enantiomers of the anti-dihydrodiol epoxide of benzo[a]pyrene are developed. The optimization procedure includes evaluation of the effect of buffer molarity, the pH of the buffer, and the role of organic modifiers. The method can be utilized to prepare standards with known absolute configuration that can be further used in the Randerath 32P-postlabeling procedure. JF - Journal of chromatography AU - Peltonen, K AU - Canella, K AU - Dipple, A AD - Chemistry of Carcinogenesis Laboratory, NCI-Frederick Cancer Research and Development Center, MD 21702. Y1 - 1992/10/16/ PY - 1992 DA - 1992 Oct 16 SP - 247 EP - 254 VL - 623 IS - 2 KW - Acetonitriles KW - 0 KW - Furans KW - Nucleotides KW - Purine Nucleosides KW - Benzo(a)pyrene KW - 3417WMA06D KW - tetrahydrofuran KW - 3N8FZZ6PY4 KW - acetonitrile KW - Z072SB282N KW - Index Medicus KW - Stereoisomerism KW - Acetonitriles -- analysis KW - Nucleotides -- analysis KW - Furans -- analysis KW - Benzo(a)pyrene -- analysis KW - Chromatography, High Pressure Liquid -- methods KW - Purine Nucleosides -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73401054?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+chromatography&rft.atitle=High-performance+liquid+chromatographic+separation+of+purine+deoxyribonucleoside+monophosphate-benzo%5Ba%5Dpyrene+adducts.&rft.au=Peltonen%2C+K%3BCanella%2C+K%3BDipple%2C+A&rft.aulast=Peltonen&rft.aufirst=K&rft.date=1992-10-16&rft.volume=623&rft.issue=2&rft.spage=247&rft.isbn=&rft.btitle=&rft.title=Journal+of+chromatography&rft.issn=&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 - Preferential activation of [3H]phorbol-12,13-dibutyrate binding by AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) in neonatal striatal cell cultures. AN - 73355532; 1280525 AB - Activation of excitatory amino acid receptors increased [3H]phorbol-12,13-dibutyrate ([3H]PdBu) binding in four week cultures of striatal cells from postnatal day 7 rat pups (PN7), and in PN7 cells co-cultured the fourth week with striatal cells from postnatal day 1 rat pups. Kainate (KA), trans-1-amino-cyclopentyl-1,3-dicarboxylate (ACPD), and N-methyl-D-aspartate (NMDA) increased [3H]PdBu binding equally in both types of cultures, but alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) increased binding by 3-fold in the co-cultures. Thus, [3H]PdBu binding in these two types of striatal cultures offers a simple model system for studying the regulation of AMPA/KA receptor responses. JF - Brain research AU - McMillian, M AU - Hong, J S AU - Pennypacker, K R AD - Neuropharmacology Section, National Institute of Environmental Health Sciences, National Institute of Health, Research Triangle Park, NC 27709. Y1 - 1992/10/16/ PY - 1992 DA - 1992 Oct 16 SP - 307 EP - 310 VL - 593 IS - 2 SN - 0006-8993, 0006-8993 KW - Glial Fibrillary Acidic Protein KW - 0 KW - Neurotoxins KW - Cycloleucine KW - 0TQU7668EI KW - 1-amino-1,3-dicarboxycyclopentane KW - 111900-32-4 KW - Ibotenic Acid KW - 2552-55-8 KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - N-Methylaspartate KW - 6384-92-5 KW - alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid KW - 77521-29-0 KW - Phosphopyruvate Hydratase KW - EC 4.2.1.11 KW - Kainic Acid KW - SIV03811UC KW - Index Medicus KW - Animals KW - Kainic Acid -- pharmacology KW - Cycloleucine -- pharmacology KW - Cycloleucine -- analogs & derivatives KW - Neurotoxins -- pharmacology KW - Binding Sites KW - Rats KW - Animals, Newborn KW - Rats, Inbred F344 KW - Phosphopyruvate Hydratase -- analysis KW - Cells, Cultured KW - N-Methylaspartate -- pharmacology KW - Glial Fibrillary Acidic Protein -- analysis KW - Neurons -- metabolism KW - Phorbol 12,13-Dibutyrate -- metabolism KW - Ibotenic Acid -- analogs & derivatives KW - Neurons -- drug effects KW - Corpus Striatum -- metabolism KW - Neurons -- cytology KW - Ibotenic Acid -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73355532?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Preferential+activation+of+%5B3H%5Dphorbol-12%2C13-dibutyrate+binding+by+AMPA+%28alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic+acid%29+in+neonatal+striatal+cell+cultures.&rft.au=McMillian%2C+M%3BHong%2C+J+S%3BPennypacker%2C+K+R&rft.aulast=McMillian&rft.aufirst=M&rft.date=1992-10-16&rft.volume=593&rft.issue=2&rft.spage=307&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 - 1993-01-06 N1 - Date created - 1993-01-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Neural computing in cancer drug development: predicting mechanism of action. AN - 73257154; 1411538 AB - Described here are neural networks capable of predicting a drug's mechanism of action from its pattern of activity against a panel of 60 malignant cell lines in the National Cancer Institute's drug screening program. Given six possible classes of mechanism, the network misses the correct category for only 12 out of 141 agents (8.5 percent), whereas linear discriminant analysis, a standard statistical technique, misses 20 out of 141 (14.2 percent). The success of the neural net indicates several things. (i) The cell line response patterns are rich in information about mechanism. (ii) Appropriately designed neural networks can make effective use of that information. (iii) Trained networks can be used to classify prospectively the more than 10,000 agents per year tested by the screening program. Related networks, in combination with classical statistical tools, will help in a variety of ways to move new anticancer agents through the pipeline from in vitro studies to clinical application. JF - Science (New York, N.Y.) AU - Weinstein, J N AU - Kohn, K W AU - Grever, M R AU - Viswanadhan, V N AU - Rubinstein, L V AU - Monks, A P AU - Scudiero, D A AU - Welch, L AU - Koutsoukos, A D AU - Chiausa, A J AD - Laboratory of Mathematical Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/10/16/ PY - 1992 DA - 1992 Oct 16 SP - 447 EP - 451 VL - 258 IS - 5081 SN - 0036-8075, 0036-8075 KW - Alkylating Agents KW - 0 KW - Antineoplastic Agents KW - Growth Inhibitors KW - Index Medicus KW - Tumor Cells, Cultured -- drug effects KW - Neural Networks (Computer) KW - Humans KW - In Vitro Techniques KW - Databases, Factual KW - Drug Evaluation, Preclinical KW - Antineoplastic Agents -- classification KW - Drug Design UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73257154?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Neural+computing+in+cancer+drug+development%3A+predicting+mechanism+of+action.&rft.au=Weinstein%2C+J+N%3BKohn%2C+K+W%3BGrever%2C+M+R%3BViswanadhan%2C+V+N%3BRubinstein%2C+L+V%3BMonks%2C+A+P%3BScudiero%2C+D+A%3BWelch%2C+L%3BKoutsoukos%2C+A+D%3BChiausa%2C+A+J&rft.aulast=Weinstein&rft.aufirst=J&rft.date=1992-10-16&rft.volume=258&rft.issue=5081&rft.spage=447&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 - 1992-11-25 N1 - Date created - 1992-11-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mik-beta 1(Fv)-PE40, a recombinant immunotoxin cytotoxic toward cells bearing the beta-chain of the IL-2 receptor. AN - 73250491; 1401913 AB - Mik-beta 1 is a mAb that binds to the beta subunit of the IL-2R. We have constructed a recombinant single chain immunotoxin Mik-beta 1(Fv)-PE40 by genetically fusing the H and L V domains of Mik-beta 1 to each other via a peptide linker, and then to PE40, a derivative of Pseudomonas exotoxin. Mik-beta 1(Fv)-PE40 was selectively cytotoxic for cells expressing high levels of IL-2R beta (p75) subunit. Mik-beta 1(Fv)-PE40 was cytotoxic to the NK cell line YT-S, which expresses p75 but not p55 subunits, with an IC50 of 6 ng/ml. The ATL line HUT-102 was less sensitive, with an IC50 of 200 ng/ml. However, the IC50 could be lowered to 11 ng/ml when Mik-beta 1(Fv)-PE40 was allowed to bind to HUT-102 cells at 4 degrees C for 4 h before overnight incubation at 37 degrees C. An excess of Mik-beta 1 but not of anti-Tac, the anti-p55 mAb, prevented the cytotoxicity of Mik-beta 1(Fv)-PE40. We constructed a more active version of Mik-beta 1(Fv)-PE40, designated Mik-beta 1(Fv)-PE40KDEL, by converting the carboxyl-terminus of the toxin from -REDLK to -KDEL. Mik-beta 1(Fv)-PE40KDEL showed an IC50 of 2 ng/ml toward YT-S cells and 35 ng/ml toward HUT-102 cells. Binding studies using radioiodinated Mik-beta 1 showed that Mik-beta 1(Fv)-PE40 bound to the p75 receptor subunit with 11% of the affinity of the native Mik-beta 1 antibody. Mik-beta 1(Fv)-PE40 may be a useful reagent to study cells that express IL-2R, and it deserves further study as a possible treatment for cancers in which the malignant cells express high numbers of p75 subunit. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Kreitman, R J AU - Schneider, W P AU - Queen, C AU - Tsudo, M AU - Fitzgerald, D J AU - Waldmann, T A AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/10/15/ PY - 1992 DA - 1992 Oct 15 SP - 2810 EP - 2815 VL - 149 IS - 8 SN - 0022-1767, 0022-1767 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - Immunotoxins KW - Receptors, Interleukin-2 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 - Abridged Index Medicus KW - Index Medicus KW - Protein Biosynthesis KW - Base Sequence KW - Recombinant Proteins -- pharmacology KW - Humans KW - Temperature KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Cell Line KW - Immunotoxins -- chemistry KW - Exotoxins -- pharmacology KW - Immunotoxins -- genetics KW - Immunotoxins -- pharmacology KW - Receptors, Interleukin-2 -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73250491?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mik-beta+1%28Fv%29-PE40%2C+a+recombinant+immunotoxin+cytotoxic+toward+cells+bearing+the+beta-chain+of+the+IL-2+receptor.&rft.au=Kreitman%2C+R+J%3BSchneider%2C+W+P%3BQueen%2C+C%3BTsudo%2C+M%3BFitzgerald%2C+D+J%3BWaldmann%2C+T+A%3BPastan%2C+I&rft.aulast=Kreitman&rft.aufirst=R&rft.date=1992-10-15&rft.volume=149&rft.issue=8&rft.spage=2810&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 - 1992-11-13 N1 - Date created - 1992-11-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Targeting of the T-cell receptor zeta-chain gene in embryonic stem cells: strategies for generating multiple mutations in a single gene. AN - 73247261; 1409721 AB - The T-cell receptor zeta chain is a member of a family of related proteins that play a critical role in coupling cell-surface receptors to intracellular signaling pathways. To study the role of zeta chain in T-cell ontogeny, we generated targeted mutations of the zeta-chain gene in murine embryonic stem cells. The mutant alleles are predicted to result either in a null phenotype or in the synthesis of a truncated protein capable of supporting T-cell-receptor surface expression but deficient in transmembrane signaling. Both of these targeting events were recovered in a single electroporation experiment with either coelectroporation or a combination deletion/truncation construct. Our results suggest that similar approaches could be used to generate multiple single mutations, modifications of more than one site within a gene, or subtle alterations that rely upon coconversion with the selectable marker gene. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Love, P E AU - Tremblay, M L AU - Westphal, H AD - Laboratory of Mammalian Genes and Development, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/10/15/ PY - 1992 DA - 1992 Oct 15 SP - 9929 EP - 9933 VL - 89 IS - 20 SN - 0027-8424, 0027-8424 KW - Membrane Proteins KW - 0 KW - Oligodeoxyribonucleotides KW - Receptors, Antigen, T-Cell KW - antigen T cell receptor, zeta chain KW - Index Medicus KW - Animals KW - Base Sequence KW - Genes KW - Tumor Cells, Cultured KW - Transfection KW - Oligodeoxyribonucleotides -- chemistry KW - Restriction Mapping KW - Recombination, Genetic KW - In Vitro Techniques KW - Molecular Sequence Data KW - Mice KW - Teratoma KW - Sequence Deletion KW - DNA Mutational Analysis -- methods KW - Membrane Proteins -- genetics KW - Receptors, Antigen, T-Cell -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73247261?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Targeting+of+the+T-cell+receptor+zeta-chain+gene+in+embryonic+stem+cells%3A+strategies+for+generating+multiple+mutations+in+a+single+gene.&rft.au=Love%2C+P+E%3BTremblay%2C+M+L%3BWestphal%2C+H&rft.aulast=Love&rft.aufirst=P&rft.date=1992-10-15&rft.volume=89&rft.issue=20&rft.spage=9929&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 - 1992-11-17 N1 - Date created - 1992-11-17 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1975 Apr;72(4):1441-5 [1055416] Proc Natl Acad Sci U S A. 1984 May;81(10):3153-7 [6328502] Cell. 1992 Jan 10;68(1):83-95 [1531041] Cell. 1991 May 3;65(3):443-9 [1673361] Cell. 1991 Mar 8;64(5):891-901 [1705867] Proc Natl Acad Sci U S A. 1991 Dec 1;88(23):10730-4 [1720548] Proc Natl Acad Sci U S A. 1991 Apr 15;88(8):3084-7 [1826563] Proc Natl Acad Sci U S A. 1991 May 1;88(9):3837-41 [1827205] Cell. 1991 Mar 8;64(5):875-8 [1848158] Mol Cell Biol. 1991 May;11(5):2769-77 [1850104] Mol Cell Biol. 1991 Sep;11(9):4509-17 [1875936] Cell. 1991 Sep 6;66(5):1051-66 [1909605] Cell. 1991 Feb 22;64(4):693-702 [1997203] Proc Natl Acad Sci U S A. 1991 May 15;88(10):4294-8 [2034673] Cell. 1991 Jun 28;65(7):1153-63 [2065352] Science. 1990 Jun 8;248(4960):1227-30 [2112266] Nature. 1990 Aug 30;346(6287):847-50 [2202907] Cell. 1990 Sep 21;62(6):1073-85 [2205396] Annu Rev Cell Biol. 1990;6:403-31 [2275818] Nature. 1990 May 3;345(6270):78-80 [2330056] Science. 1990 Jul 13;249(4965):174-7 [2371564] Nature. 1989 Sep 14;341(6238):159-62 [2528695] Nature. 1989 Dec 14;342(6251):803-5 [2532305] EMBO J. 1989 Dec 1;8(12):3651-6 [2583115] Science. 1989 Jun 16;244(4910):1288-92 [2660260] Trends Genet. 1989 Mar;5(3):70-6 [2660363] Proc Natl Acad Sci U S A. 1989 Nov;86(22):8932-5 [2682666] Nature. 1989 Nov 23;342(6248):435-8 [2685607] Annu Rev Genet. 1989;23:199-225 [2694931] J Biol Chem. 1989 Aug 5;264(22):13252-7 [2787796] Cell. 1987 Nov 6;51(3):503-12 [2822260] Cell. 1989 Jan 27;56(2):313-21 [2912572] Proc Natl Acad Sci U S A. 1988 Nov;85(22):8583-7 [3186749] Cell. 1988 Jan 15;52(1):85-95 [3278811] Nucleic Acids Res. 1988 Feb 11;16(3):1215 [3344216] Nature. 1987 Mar 19-25;326(6110):292-5 [3821905] J Embryol Exp Morphol. 1985 Jun;87:27-45 [3897439] Mol Cell Biol. 1985 Apr;5(4):659-66 [3990687] Curr Opin Biotechnol. 1991 Dec;2(6):823-9 [1367955] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparison of src-family cDNAs reveals distinct mechanisms underlying focus formation in transfected fibroblasts. AN - 73231993; 1383216 AB - Despite the intensive study of both cellular transformation and src-family protein-tyrosine kinases, there have been no direct comparisons of transforming potency for normal members of this gene-family. In this study, the focus-forming activity of normal c-src, fyn, and lck cDNAs were compared in NIH 3T3 cell transfection assays. Focus formation was studied quantitatively, and individual foci were analyzed for phosphotyrosine content and expression of appropriate translational products. Each foci arising from c-src transfectants had a marked increase in phosphotyrosine content, and the majority of these foci expressed a c-src protein with an aberrant carboxyl terminus. Foci derived from lck transfectants also had a marked increase in phosphotyrosine content, and some foci expressed a lck protein with an aberrant carboxyl terminus. In contrast, foci from fyn-transfected cells were not distinguished from G418-selected mass cultures in terms of total phosphotyrosine content or expression of p59fyn. These studies support the previously published concept that overexpression of the normal fyn protein contributes to focus formation in transfected NIH 3T3 cells but suggest that the focus-forming activity observed after c-src or lck transfections is frequently attributable to mutational events. Because lck mutations have not been previously described in transformed foci, we characterized the lck transcript expressed in two foci and identified a novel point mutation that encodes a lck protein with increased in vivo kinase and focus-forming activity. JF - The Journal of biological chemistry AU - Sartor, O AU - McLellan, C A AU - Chiueh, T AD - Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/10/15/ PY - 1992 DA - 1992 Oct 15 SP - 21044 EP - 21051 VL - 267 IS - 29 SN - 0021-9258, 0021-9258 KW - c-src KW - fyn KW - lck KW - src KW - v-src KW - Oligodeoxyribonucleotides KW - 0 KW - Proto-Oncogene Proteins KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - FYN protein, human KW - EC 2.7.10.2 KW - Fyn protein, mouse KW - Lymphocyte Specific Protein Tyrosine Kinase p56(lck) KW - Oncogene Protein pp60(v-src) KW - Proto-Oncogene Proteins c-fyn KW - Proto-Oncogene Proteins pp60(c-src) KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Animals KW - 3T3 Cells KW - Chickens KW - Base Sequence KW - Transfection KW - Humans KW - Molecular Sequence Data KW - Gene Expression KW - Mice KW - Proto-Oncogene Proteins pp60(c-src) -- isolation & purification KW - Genes, src KW - Multigene Family KW - Proto-Oncogene Proteins -- isolation & purification KW - Proto-Oncogene Proteins pp60(c-src) -- genetics KW - Proto-Oncogene Proteins pp60(c-src) -- biosynthesis KW - Protein-Tyrosine Kinases -- isolation & purification KW - Proto-Oncogenes KW - Oncogene Protein pp60(v-src) -- biosynthesis KW - Proto-Oncogene Proteins -- biosynthesis KW - Protein-Tyrosine Kinases -- genetics KW - Protein-Tyrosine Kinases -- biosynthesis KW - Oncogene Protein pp60(v-src) -- isolation & purification KW - Proto-Oncogene Proteins -- genetics KW - Cell Transformation, Neoplastic KW - Oncogene Protein pp60(v-src) -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73231993?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Comparison+of+src-family+cDNAs+reveals+distinct+mechanisms+underlying+focus+formation+in+transfected+fibroblasts.&rft.au=Sartor%2C+O%3BMcLellan%2C+C+A%3BChiueh%2C+T&rft.aulast=Sartor&rft.aufirst=O&rft.date=1992-10-15&rft.volume=267&rft.issue=29&rft.spage=21044&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 - 1992-11-18 N1 - Date created - 1992-11-18 N1 - Date revised - 2017-01-13 N1 - Gene symbol - c-src; fyn; lck; src; v-src N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Thapsigargin defines the roles of cellular calcium in secretagogue-stimulated enzyme secretion from pancreatic acini. AN - 73231684; 1383205 AB - In the present study we used thapsigargin (TG), an inhibitor of microsomal calcium ATPase, to evaluate the roles of free cytoplasmic calcium and intracellular stored calcium in secretagogue-stimulated enzyme secretion from rat pancreatic acini. Using microspectrofluorimetry of fura-2-loaded pancreatic acini, we found that TG caused a sustained increase in free cytoplasmic calcium by mobilizing calcium from inositol 1,4,5-trisphosphate-sensitive intracellular stores and by increasing influx of extracellular calcium. TG also caused a small increase in basal amylase secretion, inhibited the stimulation of amylase secretion caused by secretagogues that increase inositol 1,4,5-trisphosphate, and potentiated the stimulation of amylase secretion caused by 12-O-tetradecanoylphorbol-13-acetate or secretagogues that increase cyclic adenosine 3',5'-monophosphate. Bombesin, which like TG increased free cytoplasmic calcium, also potentiated the stimulation of amylase secretion caused by secretagogues that increase cyclic adenosine 3',5'-monophosphate, but did not inhibit the stimulation of amylase secretion caused by secretagogues that increase inositol 1,4,5-trisphosphate. Finally, TG inhibited the sustained phase of cholecystokinin-stimulated amylase secretion and potentiated the time course of vasoactive intestinal peptide-stimulated amylase secretion. The present findings indicate that stimulation of amylase secretion by secretagogues that increase inositol 1,4,5-trisphosphate does not depend on increased free cytoplasmic calcium per se. In contrast, TG-induced potentiation of the stimulation of secretagogues that increase cellular cyclic adenosine 3',5'-monophosphate appears to result from increased free cytoplasmic calcium per se. JF - The Journal of biological chemistry AU - Metz, D C AU - Patto, R J AU - Mrozinski, J E AU - Jensen, R T AU - Turner, R J AU - Gardner, J D AD - Digestive Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10/15/ PY - 1992 DA - 1992 Oct 15 SP - 20620 EP - 20629 VL - 267 IS - 29 SN - 0021-9258, 0021-9258 KW - Terpenes KW - 0 KW - Secretin KW - 1393-25-5 KW - 8-Bromo Cyclic Adenosine Monophosphate KW - 23583-48-4 KW - Vasoactive Intestinal Peptide KW - 37221-79-7 KW - Calcimycin KW - 37H9VM9WZL KW - Thapsigargin KW - 67526-95-8 KW - Carbachol KW - 8Y164V895Y KW - Amylases KW - EC 3.2.1.- KW - Calcium-Transporting ATPases KW - EC 3.6.3.8 KW - Sincalide KW - M03GIQ7Z6P KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Bombesin KW - PX9AZU7QPK KW - Calcium KW - SY7Q814VUP KW - Fura-2 KW - TSN3DL106G KW - Index Medicus KW - Vasoactive Intestinal Peptide -- pharmacology KW - Animals KW - Spectrometry, Fluorescence KW - Calcimycin -- pharmacology KW - 8-Bromo Cyclic Adenosine Monophosphate -- pharmacology KW - Sincalide -- pharmacology KW - Rats KW - Rats, Sprague-Dawley KW - Cytoplasm -- metabolism KW - Kinetics KW - In Vitro Techniques KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Secretin -- pharmacology KW - Bombesin -- pharmacology KW - Carbachol -- pharmacology KW - Male KW - Calcium -- metabolism KW - Pancreas -- cytology KW - Calcium-Transporting ATPases -- antagonists & inhibitors KW - Terpenes -- pharmacology KW - Pancreas -- enzymology KW - Amylases -- secretion KW - Pancreas -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73231684?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Thapsigargin+defines+the+roles+of+cellular+calcium+in+secretagogue-stimulated+enzyme+secretion+from+pancreatic+acini.&rft.au=Metz%2C+D+C%3BPatto%2C+R+J%3BMrozinski%2C+J+E%3BJensen%2C+R+T%3BTurner%2C+R+J%3BGardner%2C+J+D&rft.aulast=Metz&rft.aufirst=D&rft.date=1992-10-15&rft.volume=267&rft.issue=29&rft.spage=20620&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 - 1992-11-18 N1 - Date created - 1992-11-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Activation of Ras by insulin in 3T3 L1 cells does not involve GTPase-activating protein phosphorylation. AN - 73223895; 1328223 AB - Insulin-induced differentiation of 3T3 L1 cells to adipocytes can be mimicked by the expression of transfected ras oncogenes but not of the tyrosine-kinase oncogenes src and trk. Expression of two different transfected, dominant inhibitory ras mutants resulted in significant inhibition of insulin-induced differentiation, suggesting that endogenous Ras proteins are mediators of insulin signaling in these cells. Exposure of untransfected 3T3 L1 cells to insulin resulted in significant formation of the active Ras.GTP complex, at levels comparable with those resulting from exposure to platelet-derived growth factor. However, whereas exposure of the same cells to platelet-derived growth factor resulted in significant tyrosine phosphorylation of the p21ras GTPase-activating protein (GAP), insulin-treated cells did not show any detectable levels of de novo GAP tyrosine phosphorylation. Interestingly, insulin caused tyrosine phosphorylation of the p62 polypeptide coprecipitated with GAP by anti-GAP antibodies. Insulin-induced activation of cytosolic MAP kinase activity in untransfected 3T3 L1 cells was also mimicked by Ras expression (in the absence of insulin) in the same cells transfected with an inducible ras construct. These results confirm that Ras proteins participate in insulin signaling pathways in these mammalian cells and indicate that activation of cytosolic MAP kinases is an early event occurring downstream from Ras activation. However, tyrosine phosphorylation of GAP appears not to be a significant upstream regulatory event in the activation of Ras by insulin. JF - The Journal of biological chemistry AU - Porras, A AU - Nebreda, A R AU - Benito, M AU - Santos, E AD - Laboratory of Cellular and Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10/15/ PY - 1992 DA - 1992 Oct 15 SP - 21124 EP - 21131 VL - 267 IS - 29 SN - 0021-9258, 0021-9258 KW - ras KW - src KW - trk KW - v-src KW - Ethers, Cyclic KW - 0 KW - GTPase-Activating Proteins KW - Insulin KW - Platelet-Derived Growth Factor KW - Proteins KW - Proto-Oncogene Proteins KW - ras GTPase-Activating Proteins KW - Guanosine Diphosphate KW - 146-91-8 KW - Okadaic Acid KW - 1W21G5Q4N2 KW - Dexamethasone KW - 7S5I7G3JQL KW - Guanosine Triphosphate KW - 86-01-1 KW - Protein Kinases KW - EC 2.7.- KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Receptor, trkA KW - Glycogen Synthase Kinase 3 KW - EC 2.7.11.26 KW - Phosphoprotein Phosphatases KW - EC 3.1.3.16 KW - Index Medicus KW - Animals KW - Platelet-Derived Growth Factor -- metabolism KW - Guanosine Diphosphate -- metabolism KW - Dexamethasone -- pharmacology KW - Platelet-Derived Growth Factor -- pharmacology KW - Genes, src -- drug effects KW - Guanosine Triphosphate -- metabolism KW - Phosphorylation KW - Adipose Tissue -- drug effects KW - Gene Expression Regulation -- drug effects KW - Adipose Tissue -- enzymology KW - Phosphoprotein Phosphatases -- antagonists & inhibitors KW - 3T3 Cells KW - Adipose Tissue -- cytology KW - Cell Differentiation KW - Mice KW - Ethers, Cyclic -- pharmacology KW - Protein Binding KW - Protein Kinases -- metabolism KW - Transfection KW - Proto-Oncogenes -- drug effects KW - Proto-Oncogene Proteins -- biosynthesis KW - Protein-Tyrosine Kinases -- genetics KW - Genes, ras -- drug effects KW - Protein-Tyrosine Kinases -- biosynthesis KW - Insulin -- pharmacology KW - Proto-Oncogene Proteins -- genetics KW - Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73223895?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Ras+by+insulin+in+3T3+L1+cells+does+not+involve+GTPase-activating+protein+phosphorylation.&rft.au=Porras%2C+A%3BNebreda%2C+A+R%3BBenito%2C+M%3BSantos%2C+E&rft.aulast=Porras&rft.aufirst=A&rft.date=1992-10-15&rft.volume=267&rft.issue=29&rft.spage=21124&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 - 1992-11-18 N1 - Date created - 1992-11-18 N1 - Date revised - 2017-01-13 N1 - Gene symbol - ras; src; trk; v-src N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential irreversible insertion of protein kinase C into phospholipid vesicles by phorbol esters and related activators. AN - 73223822; 1400402 AB - Incubation of protein kinase C (PKC) alpha with phorbol 12,13-dibutyrate and phospholipid vesicles promoted a time-dependent irreversible insertion of the enzyme into the vesicles and the generation of a calcium-independent kinase activity. Calcium neither caused insertion nor influenced the insertion induced by the phorbol ester. The effect was strongly dependent on the phosphatidylserine concentration in the vesicle and could also be supported by other anionic phospholipids. An analysis of the structure-activity relations of PKC activators for the calcium-independent kinase activity revealed marked relative differences in potencies for binding and for insertion. Compounds such as phorbol 13-myristate 12-acetate and mezerein were very efficient at inducing insertion. In contrast, 12-deoxyphorbol esters and diacylglycerol were relatively inefficient at inducing insertion, requiring higher concentrations than expected from their binding affinities. The insertion of PKC alpha depended substantially on the length of the aliphatic esters in the 12- and 13-positions of the phorbol derivatives, and once again, potencies for insertion and binding were not directly proportional. Our findings suggest two different sites for ligand interaction on the molecule of PKC alpha with different structure-activity requirements. We speculate that the differential ability of compounds to promote insertion could contribute to the documented marked differences in the biological behavior of PKC activators. JF - The Journal of biological chemistry AU - Kazanietz, M G AU - Krausz, K W AU - Blumberg, P M AD - Molecular Mechanisms of Tumor Promotion Section, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/10/15/ PY - 1992 DA - 1992 Oct 15 SP - 20878 EP - 20886 VL - 267 IS - 29 SN - 0021-9258, 0021-9258 KW - Liposomes KW - 0 KW - Phorbol Esters KW - Phospholipids KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 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 - Animals KW - Models, Structural KW - Phorbol 12,13-Dibutyrate -- metabolism KW - Enzyme Activation KW - Kinetics KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Calcium -- pharmacology KW - Protein Binding KW - Structure-Activity Relationship KW - Binding Sites KW - Protein Kinase C -- metabolism KW - Phorbol Esters -- pharmacology KW - Brain -- enzymology KW - Phospholipids -- pharmacology KW - Protein Kinase C -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73223822?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Differential+irreversible+insertion+of+protein+kinase+C+into+phospholipid+vesicles+by+phorbol+esters+and+related+activators.&rft.au=Kazanietz%2C+M+G%3BKrausz%2C+K+W%3BBlumberg%2C+P+M&rft.aulast=Kazanietz&rft.aufirst=M&rft.date=1992-10-15&rft.volume=267&rft.issue=29&rft.spage=20878&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 - 1992-11-18 N1 - Date created - 1992-11-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Sequence specificity of aflatoxin B1-induced mutations in a plasmid replicated in xeroderma pigmentosum and DNA repair proficient human cells. AN - 73200930; 1394191 AB - The mutagenic spectrum induced by aflatoxin-DNA lesions in DNA repair deficient and repair proficient human cells was investigated. The reactive metabolite aflatoxin B1-8,9-epoxide was synthesized and reacted in vitro with the shuttle vector plasmid pS189. Plasmids were transfected into human fibroblasts and allowed to replicate, and the recovered plasmids were screened in indicator bacteria for plasmid survival and mutations in the supF marker gene. Sequence data were obtained from 71 independently arising mutants recovered from DNA repair deficient xeroderma pigmentosum (XP) cells [XP12BE(SV40)] and 60 mutants recovered from a DNA repair proficient cell line (GM0637). Plasmid survival was lower and mutation frequency higher with the XP cells, and the mutation hotspots differed substantially for the 2 cell lines. Most mutations (> 90%) were base substitutions at G:C pairs, only about one-half of which were G:C-->T:A transversions, the expected predominant mutation. One-third of the mutations at GG sites and none of those at isolated Gs were G:C-->A:T transitions. Tandem base substitutions also occurred only at GG sites and were found only with XP cells. The location of mutation hotspots with either cell line did not correlate with the level of modification within the sequence as assessed by a DNA polymerase stop assay. These results suggest that the DNA repair deficiency associated with XP can influence not only the overall frequency of mutations but also the distribution of mutations within a gene. The finding of transition mutations exclusively at GG sites may be of predictive value in attempts to link dietary aflatoxin exposure to cancers associated with specific mutations in the c-ras oncogene and the p53 tumor suppressor gene. JF - Cancer research AU - Levy, D D AU - Groopman, J D AU - Lim, S E AU - Seidman, M M AU - Kraemer, K H AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/10/15/ PY - 1992 DA - 1992 Oct 15 SP - 5668 EP - 5673 VL - 52 IS - 20 SN - 0008-5472, 0008-5472 KW - X-gal KW - lac KW - supF KW - DNA-Binding Proteins KW - 0 KW - Aflatoxin B1 KW - 9N2N2Y55MH KW - Index Medicus KW - Genetic Vectors -- drug effects KW - Base Sequence -- drug effects KW - Mutagenicity Tests KW - Humans KW - Molecular Sequence Data KW - DNA-Binding Proteins -- genetics KW - DNA-Binding Proteins -- toxicity KW - Cell Line, Transformed KW - Xeroderma Pigmentosum -- pathology KW - Mutation -- drug effects KW - DNA Repair KW - Xeroderma Pigmentosum -- genetics KW - Aflatoxin B1 -- toxicity KW - Plasmids -- drug effects KW - Aflatoxin B1 -- genetics KW - DNA Replication -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73200930?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+of+aflatoxin+B1-induced+mutations+in+a+plasmid+replicated+in+xeroderma+pigmentosum+and+DNA+repair+proficient+human+cells.&rft.au=Levy%2C+D+D%3BGroopman%2C+J+D%3BLim%2C+S+E%3BSeidman%2C+M+M%3BKraemer%2C+K+H&rft.aulast=Levy&rft.aufirst=D&rft.date=1992-10-15&rft.volume=52&rft.issue=20&rft.spage=5668&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 - 1992-11-10 N1 - Date created - 1992-11-10 N1 - Date revised - 2017-01-13 N1 - Gene symbol - X-gal; lac; supF N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Quinolinic acid in culture media used for in vitro neurotoxicology studies. AN - 73449387; 1465223 AB - Serum from several species is frequently added to the incubation media of cells in vitro. The excitotoxin and N-methyl-D-aspartate receptor agonist quinolinic acid was found to be present in serum in concentrations ranging from 59 to 4895 nM. Some neuronal systems are reported to be particularly sensitive to the neurotoxic effects of quinolinic acid. Therefore, quinolinic acid in serum should be considered as a potentially confounding variable in neurotoxicology studies in vitro. JF - Neuroscience letters AU - Heyes, M P AD - Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1992/10/12/ PY - 1992 DA - 1992 Oct 12 SP - 234 EP - 235 VL - 145 IS - 2 SN - 0304-3940, 0304-3940 KW - Culture Media KW - 0 KW - Quinolinic Acid KW - F6F0HK1URN KW - Index Medicus KW - Swine KW - Rats KW - Animals KW - Chickens KW - Cattle KW - Goats KW - Sheep KW - Humans KW - Horses KW - Rabbits KW - Mice KW - Quinolinic Acid -- blood KW - Quinolinic Acid -- toxicity KW - Nervous System Diseases -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73449387?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+letters&rft.atitle=Quinolinic+acid+in+culture+media+used+for+in+vitro+neurotoxicology+studies.&rft.au=Heyes%2C+M+P&rft.aulast=Heyes&rft.aufirst=M&rft.date=1992-10-12&rft.volume=145&rft.issue=2&rft.spage=234&rft.isbn=&rft.btitle=&rft.title=Pediatric+Annals&rft.issn=00904481&rft_id=info:doi/10.3928%2F00904481-20131022-11 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 - Processing of hepatocyte growth factor to the heterodimeric form is required for biological activity. AN - 73221554; 1383032 AB - Hepatocyte growth factor is a plasminogen-like molecule with diverse biological effects. Although it is synthesized as a single chain polypeptide, it was originally purified as a disulfide-linked heterodimer which was generated by an internal proteolytic event. Subsequent work indicated that preparations consisting largely of the monomeric form also exhibited potent activity. By using a combination of protease inhibition and site-directed mutagenesis, we established that conversion of the single chain polypeptide to the heterodimer occurred during the bioassay and was required for mitogenic and motogenic activity. JF - FEBS letters AU - Gak, E AU - Taylor, W G AU - Chan, A M AU - Rubin, J S AD - Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/10/12/ PY - 1992 DA - 1992 Oct 12 SP - 17 EP - 21 VL - 311 IS - 1 SN - 0014-5793, 0014-5793 KW - Recombinant Proteins KW - 0 KW - Hepatocyte Growth Factor KW - 67256-21-7 KW - Aprotinin KW - 9087-70-1 KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Animals KW - Base Sequence KW - Recombinant Proteins -- biosynthesis KW - Aprotinin -- pharmacology KW - Molecular Sequence Data KW - Biological Assay KW - Protein Conformation KW - Protein Processing, Post-Translational -- drug effects KW - Hepatocyte Growth Factor -- pharmacology KW - Hepatocyte Growth Factor -- genetics KW - Hepatocyte Growth Factor -- metabolism KW - Cell Division -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73221554?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FEBS+letters&rft.atitle=Processing+of+hepatocyte+growth+factor+to+the+heterodimeric+form+is+required+for+biological+activity.&rft.au=Gak%2C+E%3BTaylor%2C+W+G%3BChan%2C+A+M%3BRubin%2C+J+S&rft.aulast=Gak&rft.aufirst=E&rft.date=1992-10-12&rft.volume=311&rft.issue=1&rft.spage=17&rft.isbn=&rft.btitle=&rft.title=FEBS+letters&rft.issn=00145793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-20 N1 - Date created - 1992-11-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Long-term proliferation of mouse primordial germ cells in culture. AN - 73270367; 1383830 AB - Primordial germ cells (PGCs) are first identifiable as a population of about eight alkaline phosphatase-positive cells in the 7.0 days postcoitum mouse embryo. During the next 6 days of development they proliferate to give rise to the 25,000 cells that will establish the meiotic population. Steel factor is required for PGC survival both in vivo and in vitro and together with leukaemia inhibitory factor stimulates PGC proliferation in vitro. In feeder-dependent culture, PGCs will proliferate for up to 7 days, but their numbers eventually decline and their proliferative capacity is only a fraction of that seen in vivo. Here we report a further factor that stimulates PGC proliferation in vitro, basic fibroblast growth factor (bFGF). Furthermore, bFGF, in the presence of steel factor and leukaemia inhibitory factor, stimulates long-term proliferation of PGCs, leading to the derivation of large colonies of cells. These embryonic germ cells resemble embryonic stem cells, pluripotent cells derived from preimplantation embryos, or feeder-dependent embryonal carcinoma cells, pluripotent stem cells of PGC-derived tumours (teratomas and teratocarcinomas). To our knowledge, these results provide the first system for long-term culture of PGCs. JF - Nature AU - Resnick, J L AU - Bixler, L S AU - Cheng, L AU - Donovan, P J AD - Mammalian Genetics Laboratory, ABL-Basic Research Program, NCI-FCRDC, Frederick, Maryland 21702-1201. Y1 - 1992/10/08/ PY - 1992 DA - 1992 Oct 08 SP - 550 EP - 551 VL - 359 IS - 6395 SN - 0028-0836, 0028-0836 KW - Growth Inhibitors KW - 0 KW - Hematopoietic Cell Growth Factors KW - Interleukin-6 KW - Leukemia Inhibitory Factor KW - Lif protein, mouse KW - Lymphokines KW - Stem Cell Factor KW - Fibroblast Growth Factor 2 KW - 103107-01-3 KW - Index Medicus KW - Fibroblast Growth Factor 2 -- pharmacology KW - Animals KW - Cells, Cultured KW - Lymphokines -- pharmacology KW - Growth Inhibitors -- pharmacology KW - Mice KW - Hematopoietic Cell Growth Factors -- pharmacology KW - Time Factors KW - Immunoenzyme Techniques KW - Cell Division KW - Germ Cells -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73270367?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Long-term+proliferation+of+mouse+primordial+germ+cells+in+culture.&rft.au=Resnick%2C+J+L%3BBixler%2C+L+S%3BCheng%2C+L%3BDonovan%2C+P+J&rft.aulast=Resnick&rft.aufirst=J&rft.date=1992-10-08&rft.volume=359&rft.issue=6395&rft.spage=550&rft.isbn=&rft.btitle=&rft.title=Nature&rft.issn=00280836&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-13 N1 - Date created - 1992-11-13 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Nature. 1992 Oct 8;359(6395):482-3 [1406966] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inhibition of mitogen-induced c-fos expression in melanoma cells by retinoic acid involves the serum response element. AN - 73241672; 1400313 AB - To investigate the mechanism(s) by which all-transretinoic acid (RA) inhibits cell growth, we studied its effect on the expression of c-fos and c-jun in B16 melanoma cells. RA differentially inhibited proto-oncogene induction by mitogens, such as phorbol 12-myristate 13-acetate and serum. Suppression of c-fos was achieved with doses of RA as low as 10(-10) M and required pretreatment of cells with RA for a minimum of 2 h. In contrast, inhibition of c-jun required pretreatment for greater than 16 h with at least 10(-8) M RA and coincided with the observed decrease in cell growth. RA blocked c-fos induction by inhibiting transcription. This inhibition of transcription occurs through the serum response element (SRE), since the SRE alone was sufficient to confer down-regulation by RA to a minimal c-fos promoter construct. Thus, the SRE plays a critical role in the suppression of c-fos transcription by RA. JF - The Journal of biological chemistry AU - Busam, K J AU - Roberts, A B AU - Sporn, M B AD - Laboratory of Chemoprevention, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10/05/ PY - 1992 DA - 1992 Oct 05 SP - 19971 EP - 19977 VL - 267 IS - 28 SN - 0021-9258, 0021-9258 KW - c-fos KW - c-jun KW - DNA-Binding Proteins KW - 0 KW - Mitogens KW - Nuclear Proteins KW - Serum Response Factor KW - Tretinoin KW - 5688UTC01R KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Melanoma, Experimental KW - Cell Division -- drug effects KW - Mice KW - Transcription, Genetic KW - Plasmids KW - Precipitin Tests KW - Promoter Regions, Genetic KW - Tumor Cells, Cultured KW - Down-Regulation KW - Genes, jun -- drug effects KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Tretinoin -- pharmacology KW - Regulatory Sequences, Nucleic Acid KW - Genes, fos KW - Gene Expression Regulation -- drug effects KW - Mitogens -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73241672?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Inhibition+of+mitogen-induced+c-fos+expression+in+melanoma+cells+by+retinoic+acid+involves+the+serum+response+element.&rft.au=Busam%2C+K+J%3BRoberts%2C+A+B%3BSporn%2C+M+B&rft.aulast=Busam&rft.aufirst=K&rft.date=1992-10-05&rft.volume=267&rft.issue=28&rft.spage=19971&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 - 1992-11-16 N1 - Date created - 1992-11-16 N1 - Date revised - 2017-01-13 N1 - Gene symbol - c-fos; c-jun N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Studies on p40, the leucine zipper motif-containing protein encoded by the first open reading frame of an active human LINE-1 transposable element. AN - 73232453; 1328181 AB - Full-length human LINE-1 retrotransposons encode p40 proteins with varying electrophoretic mobilities under denaturing conditions. The p40 expressed from the first open reading frame in the LINE-1 copy designated L1.2A co-electrophoreses with the endogenous p40 in human teratocarcinoma cells. This finding is consistent with previous data indicating that L1.2A is an active element. The amino acid sequence in the central region of the L1.2A p40 accounts, at least in part, for its characteristic mobility. This region includes sequences which can, in principle, form a leucine zipper. JF - The Journal of biological chemistry AU - Holmes, S E AU - Singer, M F AU - Swergold, G D AD - Laboratory of Biochemistry, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10/05/ PY - 1992 DA - 1992 Oct 05 SP - 19765 EP - 19768 VL - 267 IS - 28 SN - 0021-9258, 0021-9258 KW - DNA Transposable Elements KW - 0 KW - DNA-Binding Proteins KW - Oligonucleotides KW - Peptides KW - Proteins KW - L1Hs-encoded protein p40, human KW - 148349-28-4 KW - Index Medicus KW - Teratoma -- metabolism KW - Protein Biosynthesis KW - Blotting, Western KW - Base Sequence KW - Tumor Cells, Cultured KW - Open Reading Frames KW - Humans KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Leucine Zippers -- genetics KW - Peptides -- genetics KW - Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73232453?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Inhibition+of+HIVa1+Replication+by+Novel+Multitarget+Ribozymes&rft.au=CHEN%2C+CHANGaJIE%3BBanerjea%2C+Akhil+C%3BHaglund%2C+Karl%3BHarmison%2C+George+G%3BSchubert%2C+Manfred&rft.aulast=CHEN&rft.aufirst=CHANGaJIE&rft.date=1992-10-01&rft.volume=660&rft.issue=1&rft.spage=271&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+New+York+Academy+of+Sciences&rft.issn=00778923&rft_id=info:doi/10.1111%2Fj.1749-6632.1992.tb21081.x 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 - Calcium ionophore A23187 induces expression of the growth arrest and DNA damage inducible CCAAT/enhancer-binding protein (C/EBP)-related gene, gadd153. Ca2+ increases transcriptional activity and mRNA stability. AN - 73227601; 1400365 AB - gadd153 is a CCAAT/enhancer-binding protein (C/EBP)-related gene whose expression is induced in response to growth arrest and DNA damage. This investigation explored the possibility that Ca2+ might play a role in regulating expression of gadd 153. We have demonstrated that treatment of HeLa cells with the calcium ionophores A23187 and ionomycin leads to the induction of gadd153 mRNA. The induction was rapid; increases in mRNA were detected by 90 min of treatment, and near maximum levels were achieved within 5-h exposure to A23187. Elevated mRNA levels resulted from both an increase in the rate of gadd153 transcription and an increase in the stability of the gadd153 mRNA. The response was not dependent on protein kinase C nor was it coupled to c-fos expression. Buffering intracellular and extracellular Ca2+ by combined treatment with BAPTA-AM (acetoxymethyl ester form of bis(aminophenoxy)ethane N,N'-tetraacetic acid) and EGTA prevented the induction of gadd153 mRNA by A23187. In addition, these treatments prevented the induction of gadd153 mRNA in response to the DNA damaging agent methyl methanesulfonate. We conclude that intracellular Ca2+ plays a role in regulating gadd153 expression. More specifically, Ca2+ likely plays a role in the induction of gadd153 mRNA following DNA damage. JF - The Journal of biological chemistry AU - Bartlett, J D AU - Luethy, J D AU - Carlson, S G AU - Sollott, S J AU - Holbrook, N J AD - Laboratory of Molecular Genetics, National Institute on Aging, Baltimore, Maryland 21224. Y1 - 1992/10/05/ PY - 1992 DA - 1992 Oct 05 SP - 20465 EP - 20470 VL - 267 IS - 28 SN - 0021-9258, 0021-9258 KW - CCAAT-Enhancer-Binding Proteins KW - 0 KW - Cations, Divalent KW - DNA-Binding Proteins KW - Nuclear Proteins KW - Oligonucleotides KW - RNA, Messenger KW - 1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester KW - 139890-68-9 KW - Calcimycin KW - 37H9VM9WZL KW - Egtazic Acid KW - 526U7A2651 KW - DNA KW - 9007-49-2 KW - Methyl Methanesulfonate KW - AT5C31J09G KW - Protein Kinase C KW - EC 2.7.11.13 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Gene Expression -- drug effects KW - Egtazic Acid -- analogs & derivatives KW - HeLa Cells KW - Humans KW - Transcription, Genetic KW - RNA, Messenger -- genetics KW - Egtazic Acid -- chemistry KW - Methyl Methanesulfonate -- pharmacology KW - Protein Kinase C -- metabolism KW - Base Sequence KW - Kinetics KW - Molecular Sequence Data KW - Cell Division KW - Nuclear Proteins -- genetics KW - DNA Damage KW - DNA-Binding Proteins -- genetics KW - DNA-Binding Proteins -- biosynthesis KW - Calcium -- physiology KW - Nuclear Proteins -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73227601?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Calcium+ionophore+A23187+induces+expression+of+the+growth+arrest+and+DNA+damage+inducible+CCAAT%2Fenhancer-binding+protein+%28C%2FEBP%29-related+gene%2C+gadd153.+Ca2%2B+increases+transcriptional+activity+and+mRNA+stability.&rft.au=Bartlett%2C+J+D%3BLuethy%2C+J+D%3BCarlson%2C+S+G%3BSollott%2C+S+J%3BHolbrook%2C+N+J&rft.aulast=Bartlett&rft.aufirst=J&rft.date=1992-10-05&rft.volume=267&rft.issue=28&rft.spage=20465&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 - 1992-11-16 N1 - Date created - 1992-11-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Localized mutagenesis and evidence for post-transcriptional regulation of MAK3. A putative N-acetyltransferase required for double-stranded RNA virus propagation in Saccharomyces cerevisiae. AN - 73220003; 1339437 AB - The MAK3 gene of Saccharomyces cerevisiae is necessary for the propagation of the L-A double-stranded RNA virus and its satellites, such as M1 that encodes a killer toxin. We cloned the MAK3 gene based on its genetic map position using physically mapped lambda-clones covering nearly all of the yeast genome. The minimal sequence necessary to complement the mak3-1 mutation contained 3 open reading frames (ORFs). Only one (ORF3) was necessary to complement mak3-1. A deletion insertion mutant of ORF3 grew slowly on nonfermentable carbon sources, an effect not due simply to its loss of L-A. Although ORF3 alone is sufficient for MAK3 activity when expressed from an expression vector, in its native context an additional 669 base pairs 3' to the ORF and complementary to the gene for a non-histone protein are necessary for expression, but not for normal steady state transcript levels. This suggests a post-transcriptional control of MAK3 expression by the 3' region. The MAK3 protein has substantial homology with several N-acetyltransferases with consensus patterns h..h.h. . . Y..[HK]GI[AG][KR].Lh. . .h and h.h[DE]. . . .N..A. . .Y . . .GF. . . .. . . .Y . . [DE]G, (h = hydrophobic). Mutation of any of the underlined conserved residues (94GI----AA, 123N----A, 130Y----A, 134GF----SL, 144Y----A, and 149G----A) inactivated the gene, supporting the hypothesis that MAK3 encodes an N-acetyltransferase. JF - The Journal of biological chemistry AU - Tercero, J C AU - Riles, L E AU - Wickner, R B AD - Section on Genetics of Simple Eukaryotes, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10/05/ PY - 1992 DA - 1992 Oct 05 SP - 20270 EP - 20276 VL - 267 IS - 28 SN - 0021-9258, 0021-9258 KW - DNA, Fungal KW - 0 KW - Fungal Proteins KW - RNA, Double-Stranded KW - RNA, Messenger KW - Saccharomyces cerevisiae Proteins KW - Arylamine N-Acetyltransferase KW - EC 2.3.1.5 KW - MAK3 protein, S cerevisiae KW - EC 2.3.1.88 KW - Index Medicus KW - Virus Replication KW - Chromosome Walking KW - Open Reading Frames KW - Amino Acid Sequence KW - Plasmids KW - Chromosome Mapping KW - Cloning, Molecular KW - Base Sequence KW - RNA, Messenger -- metabolism KW - Restriction Mapping KW - Molecular Sequence Data KW - Sequence Homology, Amino Acid KW - Saccharomyces cerevisiae -- genetics KW - Gene Expression Regulation, Fungal KW - Fungal Proteins -- metabolism KW - RNA Viruses -- physiology KW - Saccharomyces cerevisiae -- enzymology KW - Fungal Proteins -- genetics KW - Arylamine N-Acetyltransferase -- metabolism KW - Mutagenesis KW - Arylamine N-Acetyltransferase -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73220003?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Localized+mutagenesis+and+evidence+for+post-transcriptional+regulation+of+MAK3.+A+putative+N-acetyltransferase+required+for+double-stranded+RNA+virus+propagation+in+Saccharomyces+cerevisiae.&rft.au=Tercero%2C+J+C%3BRiles%2C+L+E%3BWickner%2C+R+B&rft.aulast=Tercero&rft.aufirst=J&rft.date=1992-10-05&rft.volume=267&rft.issue=28&rft.spage=20270&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 - 1992-11-16 N1 - Date created - 1992-11-16 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - D11151; GENBANK; M93405; D11150; M95912; D11149; D10348; D10347; M96626; M95771; L05565 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inhibition of HIVa1 Replication by Novel Multitarget Ribozymes AN - 875089930; 14716928 AB - Abstract not available. JF - Annals of the New York Academy of Sciences AU - CHEN, CHANGaJIE AU - Banerjea, Akhil C AU - Haglund, Karl AU - Harmison, George G AU - Schubert, Manfred AD - Laboratory of Viral and Molecular Pathogenesis National Institute of Neurological Disorders and Stroke National Institutes of Health Bethesda, Maryland 20892 Y1 - 1992/10// PY - 1992 DA - Oct 1992 SP - 271 EP - 273 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 USA VL - 660 IS - 1 SN - 0077-8923, 0077-8923 KW - Biotechnology and Bioengineering Abstracts KW - Human immunodeficiency virus KW - Replication KW - Ribozymes KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/875089930?accountid=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=Annals+of+the+New+York+Academy+of+Sciences&rft.atitle=Inhibition+of+HIVa1+Replication+by+Novel+Multitarget+Ribozymes&rft.au=CHEN%2C+CHANGaJIE%3BBanerjea%2C+Akhil+C%3BHaglund%2C+Karl%3BHarmison%2C+George+G%3BSchubert%2C+Manfred&rft.aulast=CHEN&rft.aufirst=CHANGaJIE&rft.date=1992-10-01&rft.volume=660&rft.issue=1&rft.spage=271&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+New+York+Academy+of+Sciences&rft.issn=00778923&rft_id=info:doi/10.1111%2Fj.1749-6632.1992.tb21081.x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2015-03-19 N1 - SubjectsTermNotLitGenreText - Replication; Ribozymes; Human immunodeficiency virus DO - http://dx.doi.org/10.1111/j.1749-6632.1992.tb21081.x ER - TY - JOUR T1 - Specific Inhibition of Oncogene Expression in Vitro and in Vivo by Antisense Oligonucleotides AN - 875053905; 14716900 AB - Abstract not available. JF - Annals of the New York Academy of Sciences AU - Neckers, Len AU - Rosolen, Angelo AU - Fahmy, Brigid AU - Whitesell, Luke AD - Clinical Pharmacology Branch National Institutes of Health National Cancer Institute Bethesda, Maryland 20892 Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 37 EP - 44 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 USA VL - 660 IS - 1 SN - 0077-8923, 0077-8923 KW - Biotechnology and Bioengineering Abstracts; Oncogenes & Growth Factors Abstracts KW - Antisense oligonucleotides KW - Oncogenes KW - B 26660:Miscellaneous Oncogenes & Growth Factors KW - W 30940:Products UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/875053905?accountid=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=Annals+of+the+New+York+Academy+of+Sciences&rft.atitle=Specific+Inhibition+of+Oncogene+Expression+in+Vitro+and+in+Vivo+by+Antisense+Oligonucleotides&rft.au=Neckers%2C+Len%3BRosolen%2C+Angelo%3BFahmy%2C+Brigid%3BWhitesell%2C+Luke&rft.aulast=Neckers&rft.aufirst=Len&rft.date=1992-10-01&rft.volume=660&rft.issue=1&rft.spage=37&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+New+York+Academy+of+Sciences&rft.issn=00778923&rft_id=info:doi/10.1111%2Fj.1749-6632.1992.tb21055.x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2011-11-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Antisense oligonucleotides; Oncogenes DO - http://dx.doi.org/10.1111/j.1749-6632.1992.tb21055.x ER - TY - JOUR T1 - Focal transcranial magnetic stimulation and response bias in a forced-choice task. AN - 85264797; pmid-1431962 AB - The effects of transcranial magnetic stimulation were studied on the performance of a warned, forced-choice response time task by normal adults. The task consisted of extension of the index finger in response to the click produced by the discharge of the magnetic coil (go-signal). The subjects were asked to choose the right or left finger only after the go-signal was delivered. Single magnetic stimuli were delivered to the prefrontal or motor area, and in the control situation, away from the head. Magnetic stimulation affected hand preference only when it was delivered to the motor area. With stimulation of this area, subjects more often chose the hand contralateral to the site stimulated with response times that were mainly less than 200 ms. With longer response times (between 200 and 1100 ms), magnetic stimulation had no effect on hand preference regardless of the site stimulated. Stimulation of prefrontal areas yielded results similar to the control situation. These results suggest that response bias in this paradigm is caused by an effect of magnetic stimulation on neural structures within, or closely related to, the motor areas of the brain. Although the response bias was clear and predictable, the subjects were unaware of its existence. It is possible to influence endogenous processes of movement preparation externally without disrupting the conscious perception of volition. JF - Journal of Neurology, Neurosurgery, and Psychiatry AU - Brasil-Neto, J P AU - Pascual-Leone, A AU - Valls-Solé J AU - Cohen, L G AU - Hallett, M AD - Human Cortical Physiology Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. PY - 1992 SP - 964 EP - 966 VL - 55 IS - 10 SN - 0022-3050, 0022-3050 KW - Reference Values KW - Human KW - Prefrontal Cortex KW - Dominance, Cerebral KW - Motor Cortex KW - Choice Behavior KW - Adult KW - Psychomotor Performance KW - Bias (Epidemiology) KW - Laterality KW - Attention KW - Male KW - Female KW - Reaction Time KW - Electromagnetic Fields UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85264797?accountid=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+Neurology%2C+Neurosurgery%2C+and+Psychiatry&rft.atitle=Focal+transcranial+magnetic+stimulation+and+response+bias+in+a+forced-choice+task.&rft.au=Brasil-Neto%2C+J+P%3BPascual-Leone%2C+A%3BValls-Sol%C3%A9+J%3BCohen%2C+L+G%3BHallett%2C+M&rft.aulast=Brasil-Neto&rft.aufirst=J&rft.date=1992-10-01&rft.volume=55&rft.issue=10&rft.spage=964&rft.isbn=&rft.btitle=&rft.title=Journal+of+Neurology%2C+Neurosurgery%2C+and+Psychiatry&rft.issn=00223050&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Role of inferior temporal neurons in visual memory. II. Multiplying temporal waveforms related to vision and memory. AN - 85239839; pmid-1432085 AB - 1. In the companion paper we reported on the activity of neurons in the inferior temporal (IT) cortex during a sequential pattern matching task. In this task a sample stimulus was followed by a test stimulus that was either a match or a nonmatch. Many of the neurons encoded information about the patterns of both current and previous stimuli in the temporal modulation of their responses. 2. A simple information processing model of visual memory can be formed with just four steps: 1) encode the current stimulus; 2) recall the code of a remembered stimulus; 3) compare the two codes; 4) and decide whether they are similar or different. The analysis presented in the first paper suggested that some IT neurons were performing the comparison step of visual memory. 3. We propose that IT neurons participate in the comparison of temporal waveforms related to vision and memory by multiplying them together. This product could form the basis of a crosscorrelation-based comparison. 4. We tested our hypothesis by fitting a simple multiplicative model to data from IT neurons. The model generated waveforms in separate memory and visual channels. The waveforms arising from the two channels were then multiplied on a point by point basis to yield the output waveform. The model was fitted to the actual neuronal data by a gradient descent method to find the best fit waveforms that also had the lowest total energy. 5. The multiplicative model fit the neuronal responses quite well. The multiplicative model made consistently better predictions of the actual response waveforms than did an additive model. Furthermore, the fit was better when the actual relationship between the responses and the sample and test stimuli were preserved than when that relationship was randomized. 6. We infer from the superior fit of the multiplicative model that IT neurons are multiplying temporally modulated waveforms arising from separate visual and memory systems in the comparison step of visual memory. JF - Journal of Neurophysiology AU - Eskandar, E N AU - Optican, L M AU - Richmond, B J AD - Laboratory of Sensorimotor Research, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892. PY - 1992 SP - 1296 EP - 1306 VL - 68 IS - 4 SN - 0022-3077, 0022-3077 KW - Models, Psychological KW - Support, U.S. Gov't, P.H.S. KW - Animal KW - Decision Making KW - Cognition KW - Mathematics KW - Memory KW - Vision KW - Neurons KW - Pattern Recognition, Visual KW - Temporal Lobe KW - Macaca mulatta KW - Models, Neurological KW - Male KW - Female UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85239839?accountid=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=Role+of+inferior+temporal+neurons+in+visual+memory.+II.+Multiplying+temporal+waveforms+related+to+vision+and+memory.&rft.au=Eskandar%2C+E+N%3BOptican%2C+L+M%3BRichmond%2C+B+J&rft.aulast=Eskandar&rft.aufirst=E&rft.date=1992-10-01&rft.volume=68&rft.issue=4&rft.spage=1296&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 - Genetic aspects of idiopathic speech and language disorders. AN - 85203542; pmid-1408200 AB - At the outset of this article, we posed the question of whether or not the current evidence from genetic studies of DLD and stuttering indicate that it would be fruitful to conduct studies aimed at determining the gene location for each of these disorders. As we pointed out, because these are behavioral development disorders, phenotypic variations and changes in characteristics through the life span pose problems when attempting to determine who is and is not affected. Further, because these disorders can be either idiopathic or secondary to a variety of causes, any genetic study must rule out or take account of cases secondary to other factors. Few studies conducted thus far have taken these problems into account, and the results must be considered tentative. Given these reservations, the results certainly point to a genetic component in both disorders, although the data collected thus far on DLD suggest a mendelian form of transmission. If further more intensive studies continue to support this model for DLD, linkage studies on this disorder are likely to be productive. JF - Otolaryngologic Clinics of North America AU - Ludlow, Christy L AU - Dooman, A G AD - Laryngeal and Speech Section, National Institute of Neurological Disorders and Stroke PY - 1992 SP - 979 EP - 994 VL - 25 IS - 5 SN - 0030-6665, 0030-6665 KW - Speech Disorders KW - Human KW - Language Development Disorders KW - Articulation Disorders KW - Stuttering UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85203542?accountid=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=Otolaryngologic+Clinics+of+North+America&rft.atitle=Genetic+aspects+of+idiopathic+speech+and+language+disorders.&rft.au=Ludlow%2C+Christy+L%3BDooman%2C+A+G&rft.aulast=Ludlow&rft.aufirst=Christy&rft.date=1992-10-01&rft.volume=25&rft.issue=5&rft.spage=979&rft.isbn=&rft.btitle=&rft.title=Otolaryngologic+Clinics+of+North+America&rft.issn=00306665&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Neurotransmission in the auditory system. AN - 85203490; pmid-1357616 AB - Neurotransmitters and neuromodulators thought to be active on neurons in the cochlea, CN, and SOC have been reviewed. The variety of neurotransmitters and neuromodulators present and likely colocalized in these neurons are the chemical substrates that link morphologically and physiologically diverse neurons to process sound information. The impact of the limited number of neurotransmitters and neuromodulators in the auditory system is magnified by their interaction with structurally diverse receptors; thus great functional diversity is possible. Moreover, the effects of neurotransmitters and neuromodulators are not limited to synaptic transmission but serve as trophic agents for the establishment of neuronal circuitry during development and the rearrangement of synapses as a result of sensory experience or injury. An understanding of the neurochemical aspects of sensory processing at these diverse synapses then is of fundamental importance in understanding the organization of the auditory system. JF - Otolaryngologic Clinics of North America AU - Hunter, C AU - Doi, K AU - Wenthold, R J AD - Laboratory of Neurochemistry, National Institute on Deafness and other Communication Disorders, National Institutes of Health, Bethesda, Maryland. PY - 1992 SP - 1027 EP - 1052 VL - 25 IS - 5 SN - 0030-6665, 0030-6665 KW - Cochlea KW - Auditory Pathways KW - Human KW - Brain Stem KW - Neurotransmitters KW - Synaptic Transmission UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85203490?accountid=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=Otolaryngologic+Clinics+of+North+America&rft.atitle=Neurotransmission+in+the+auditory+system.&rft.au=Hunter%2C+C%3BDoi%2C+K%3BWenthold%2C+R+J&rft.aulast=Hunter&rft.aufirst=C&rft.date=1992-10-01&rft.volume=25&rft.issue=5&rft.spage=1027&rft.isbn=&rft.btitle=&rft.title=Otolaryngologic+Clinics+of+North+America&rft.issn=00306665&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Strategies for constructing a guinea pig organ of Corti cDNA library and its potential use. AN - 85200706; pmid-1408189 AB - Mutations of genes common to several tissues or organs can lead to cellular damage, which may result in hearing impairment as part of a syndromic disorder. Mutations of genes that are unique to the organ of Corti would have a high probability of causing nonsyndromic hearing impairment. It is expected that such genes are involved in auditory transduction as well as in maintaining specific hair cell and supporting cell functions in the organ of Corti. Cloning and describing genes involved with nonsyndromic hearing impairment thus require the construction of a guinea pig cDNA library of the organ of Corti. JF - Otolaryngologic Clinics of North America AU - Wilcox, E R AD - National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, Maryland. PY - 1992 SP - 1011 EP - 1016 VL - 25 IS - 5 SN - 0030-6665, 0030-6665 KW - RNA, Messenger KW - Hearing Disorders KW - Guinea Pigs KW - Animal KW - DNA KW - Escherichia coli KW - Amino Acid Sequence KW - Mutation KW - Gene Amplification KW - Organ of Corti KW - Gene Library UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85200706?accountid=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=Otolaryngologic+Clinics+of+North+America&rft.atitle=Strategies+for+constructing+a+guinea+pig+organ+of+Corti+cDNA+library+and+its+potential+use.&rft.au=Wilcox%2C+E+R&rft.aulast=Wilcox&rft.aufirst=E&rft.date=1992-10-01&rft.volume=25&rft.issue=5&rft.spage=1011&rft.isbn=&rft.btitle=&rft.title=Otolaryngologic+Clinics+of+North+America&rft.issn=00306665&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Single motor unit activity of human intrinsic laryngeal muscles during respiration. AN - 85175083; pmid-1416638 AB - Individual motor units in the thyroarytenoid (TA) and cricothyroid (CT) muscles were studied in 10 normal human volunteers during quiet respiration. Both tonic and phasic firing patterns were found in both TA and CT units. The rate of firing was higher during inhalation than during exhalation in phasic TA units and in tonic CT units. Tonically active units had a higher firing frequency than phasically active units in both TA and CT muscles. Phasically active units corresponded with the respiratory cycle, with firing associated with inhalation in both the TA and CT muscles. A variety of firing patterns were found between units in both the TA and CT muscles, and in one subject, units recorded from the same muscle had very different firing patterns. The results suggest that although laryngeal motoneurons are modulated by the respiratory cycle, they do not respond uniformly to respiration. JF - The Annals of Otology, Rhinology, and Laryngology AU - Chanaud, C M AU - Ludlow, C L AD - Voice and Speech Section, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, Maryland 20892. PY - 1992 SP - 832 EP - 840 VL - 101 IS - 10 SN - 0003-4894, 0003-4894 KW - Laryngeal Muscles KW - Humans KW - Respiration KW - Adult KW - Electromyography KW - Action Potentials KW - Middle Aged KW - Female KW - Male KW - Motor Neurons UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85175083?accountid=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+Annals+of+Otology%2C+Rhinology%2C+and+Laryngology&rft.atitle=Single+motor+unit+activity+of+human+intrinsic+laryngeal+muscles+during+respiration.&rft.au=Chanaud%2C+C+M%3BLudlow%2C+C+L&rft.aulast=Chanaud&rft.aufirst=C&rft.date=1992-10-01&rft.volume=101&rft.issue=10&rft.spage=832&rft.isbn=&rft.btitle=&rft.title=The+Annals+of+Otology%2C+Rhinology%2C+and+Laryngology&rft.issn=00034894&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Practical approach to diagnosis and management of hereditary hearing impairment (HHI). AN - 85155009; pmid-1425370 JF - Ear, Nose, and Throat Journal AU - Grundfast, K M AU - Lalwani, A K AD - Laboratory of Molecular Biology, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, Maryland. PY - 1992 SP - 479 EP - 84, 487 VL - 71 IS - 10 SN - 0145-5613, 0145-5613 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85155009?accountid=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=Ear%2C+Nose%2C+and+Throat+Journal&rft.atitle=Practical+approach+to+diagnosis+and+management+of+hereditary+hearing+impairment+%28HHI%29.&rft.au=Grundfast%2C+K+M%3BLalwani%2C+A+K&rft.aulast=Grundfast&rft.aufirst=K&rft.date=1992-10-01&rft.volume=71&rft.issue=10&rft.spage=479&rft.isbn=&rft.btitle=&rft.title=Ear%2C+Nose%2C+and+Throat+Journal&rft.issn=01455613&rft_id=info:doi/ LA - English DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Prophylaxis and therapy for Pneumocystis pneumonia--where are we? AN - 75533410; 1344666 AB - The armamentarium of drugs to treat and to prevent Pneumocystis pneumonia has expanded substantially over the past decade. In all patient populations trimethoprim-sulfamethoxazole is the preferred regimen for both acute treatment and prophylaxis. Clindamycin-primaquine and atovaquone are both effective agents for acute therapy but there are no data yet suggesting that they are preferable to trimethoprim-sulfamethoxazole. Corticosteroid therapy is now standard for severe AIDS-associated Pneumocystis pneumonia, and should probably be used in other patient populations with severe pneumocystis pneumonia as well. JF - Infectious agents and disease AU - Masur, H AD - Critical Care Medicine Department, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 270 EP - 278 VL - 1 IS - 5 SN - 1056-2044, 1056-2044 KW - Adrenal Cortex Hormones KW - 0 KW - Antifungal Agents KW - Naphthoquinones KW - Clindamycin KW - 3U02EL437C KW - Trimethoprim, Sulfamethoxazole Drug Combination KW - 8064-90-2 KW - Primaquine KW - MVR3634GX1 KW - Atovaquone KW - Y883P1Z2LT KW - Index Medicus KW - AIDS/HIV KW - AIDS-Related Opportunistic Infections -- drug therapy KW - Naphthoquinones -- therapeutic use KW - Antifungal Agents -- adverse effects KW - Humans KW - Trimethoprim, Sulfamethoxazole Drug Combination -- therapeutic use KW - Clinical Trials as Topic KW - AIDS-Related Opportunistic Infections -- prevention & control KW - Trimethoprim, Sulfamethoxazole Drug Combination -- adverse effects KW - Antifungal Agents -- therapeutic use KW - Drug Tolerance KW - Adrenal Cortex Hormones -- therapeutic use KW - Primaquine -- therapeutic use KW - Clindamycin -- therapeutic use KW - Pneumonia, Pneumocystis -- prevention & control KW - Pneumonia, Pneumocystis -- drug therapy KW - Pneumonia, Pneumocystis -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75533410?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Pesticides+and+non-Hodgkin%27s+lymphoma.&rft.au=Zahm%2C+S+H%3BBlair%2C+A&rft.aulast=Zahm&rft.aufirst=S&rft.date=1992-10-01&rft.volume=52&rft.issue=19+Suppl&rft.spage=5485s&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 - 1994-05-13 N1 - Date created - 1994-05-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Carcinogenicity of combined ultraviolet B radiation and psoralen plus ultraviolet A irradiation treatment of mice. AN - 75518825; 1342188 AB - Psoralen plus ultraviolet A (PUVA) therapy and UVB phototherapy are frequently used in the treatment of psoriasis and other skin diseases. Both treatments are thought to be carcinogenic, but little is known about their interaction in the induction of skin cancer. Tumors induced in mice treated with both PUVA and UVB, either given sequentially or concurrently, seemed to be more antigenic as a group than tumors treated by PUVA alone, as determined by their lower frequency of growth when transplanted into naive mice. In this study, we treated C3H mice with a subcarcinogenic dose of UVB radiation for 4 weeks, followed by PUVA treatment for 41 weeks (sequential experiment) or with both UVB radiation (minimal carcinogenic dose) and PUVA for 41 weeks (concurrent experiment) and monitored the development of skin cancers. Although a few tumors appeared earlier in the groups treated with both UVB and PUVA in both experiments, no significant differences were observed in the rate of tumor development in mice treated with UVB and PUVA versus those treated with PUVA alone. JF - Photodermatology, photoimmunology & photomedicine AU - Granstein, R D AU - Morison, W L AU - Kripke, M L AD - National Cancer Institute, Frederick Research Facility, Maryland. PY - 1992 SP - 198 EP - 202 VL - 9 IS - 5 SN - 0905-4383, 0905-4383 KW - Carcinogens KW - 0 KW - Methoxsalen KW - U4VJ29L7BQ KW - Index Medicus KW - Radiation Dosage KW - Probability KW - Animals KW - Carcinoma, Squamous Cell -- etiology KW - Germ-Free Life KW - Neoplasms, Radiation-Induced -- etiology KW - Thymectomy KW - Fibrosarcoma -- pathology KW - Mice KW - Fibrosarcoma -- etiology KW - Neoplasm Transplantation KW - Mice, Inbred Strains KW - X-Rays KW - Neoplasms, Radiation-Induced -- pathology KW - Carcinoma, Squamous Cell -- pathology KW - Mice, Inbred C3H KW - Female KW - Methoxsalen -- adverse effects KW - PUVA Therapy -- adverse effects KW - Skin Neoplasms -- etiology KW - Skin Neoplasms -- chemically induced KW - Ultraviolet Rays -- adverse effects KW - Skin Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75518825?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Photodermatology%2C+photoimmunology+%26+photomedicine&rft.atitle=Carcinogenicity+of+combined+ultraviolet+B+radiation+and+psoralen+plus+ultraviolet+A+irradiation+treatment+of+mice.&rft.au=Granstein%2C+R+D%3BMorison%2C+W+L%3BKripke%2C+M+L&rft.aulast=Granstein&rft.aufirst=R&rft.date=1992-10-01&rft.volume=9&rft.issue=5&rft.spage=198&rft.isbn=&rft.btitle=&rft.title=Photodermatology%2C+photoimmunology+%26+photomedicine&rft.issn=09054383&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-02-10 N1 - Date created - 1994-02-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pardaxin-stimulated calcium uptake in PC12 cells is blocked by cadmium and is not mediated by L-type calcium channels. AN - 75515192; 1285007 AB - Pardaxin is an excitatory neurotoxin which triggers neurotransmitter release as a result of voltage-dependent pore formation within the neuronal membrane. We have used several pharmacological manipulations of calcium influx to characterize pardaxin pore activity in PC12 cells in culture. Pardaxin stimulates the uptake of radioactive calcium into PC12 cells in a dose dependent fashion (ED50 of 0.4 microM). This stimulation is partially inhibited by nifedipine, a blocker of L-type calcium channels. Effective blockade of pardaxin stimulation was produced by the inorganic calcium channel blockers cadmium (IC50 of 10 microM) and nickel (2 mM). Homologous down regulation of L-calcium channels by the agonist Bay K-8644, inhibited the subsequent stimulation of calcium uptake by this drug, but not by pardaxin. A fluorometric analysis of pardaxin pore formation in unilamellar large liposomes indicates pardaxin pores are blocked by cadmium (10-200 microM). These data distinguish between pardaxin pores and L-type calcium channels in PC12 cells. We suggest pardaxin as a pharmacological ionophore tool to modulate neuronal calcium homeostasis and neurotransmitter release. JF - Journal of basic and clinical physiology and pharmacology AU - Nikodijevic, B AU - Nikodijevic, D AU - Lazarovici, P AD - Section on Growth Factors, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. PY - 1992 SP - 359 EP - 370 VL - 3 IS - 4 SN - 0792-6855, 0792-6855 KW - Calcium Channels KW - 0 KW - Calcium Radioisotopes KW - Fish Venoms KW - Liposomes KW - Cadmium KW - 00BH33GNGH KW - pardaxin KW - 67995-63-5 KW - 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester KW - 71145-03-4 KW - Nickel KW - 7OV03QG267 KW - Nifedipine KW - I9ZF7L6G2L KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Nifedipine -- pharmacology KW - Animals KW - Spectrometry, Fluorescence KW - Nickel -- pharmacology KW - Porosity KW - Liposomes -- metabolism KW - 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester -- pharmacology KW - Down-Regulation -- drug effects KW - Models, Biological KW - PC12 Cells KW - Calcium -- metabolism KW - Cadmium -- pharmacology KW - Calcium Channels -- metabolism KW - Fish Venoms -- antagonists & inhibitors KW - Calcium Channels -- drug effects KW - Fish Venoms -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75515192?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+basic+and+clinical+physiology+and+pharmacology&rft.atitle=Pardaxin-stimulated+calcium+uptake+in+PC12+cells+is+blocked+by+cadmium+and+is+not+mediated+by+L-type+calcium+channels.&rft.au=Nikodijevic%2C+B%3BNikodijevic%2C+D%3BLazarovici%2C+P&rft.aulast=Nikodijevic&rft.aufirst=B&rft.date=1992-10-01&rft.volume=3&rft.issue=4&rft.spage=359&rft.isbn=&rft.btitle=&rft.title=Journal+of+basic+and+clinical+physiology+and+pharmacology&rft.issn=07926855&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-20 N1 - Date created - 1993-10-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Analysis of human cytochrome P450 catalytic activities and expression. AN - 73533950; 1306334 AB - Cytochromes P450 are a large group of membrane-associated heme protein monooxygenases, most of which are responsible for metabolizing foreign compounds. Chemical carcinogens, which are ingested or absorbed into the body as inert forms, are metabolically activated by P450s to electrophilic metabolites capable of binding to and mutating DNA. Different P450 forms are responsible for activation of the various classes of chemical carcinogens including the arylamines, polycyclic aromatic hydrocarbons, nitrosamines and aflatoxins. Thus, the cellular constituency and levels of P450s could determine the fate of a particular carcinogen and the risk of humans to exposure. To study the catalytic activities of human P450s, human P450 cDNAs were cloned and expressed into active enzymes using cultured cells. By both transient and stable cDNA expression systems, several human P450s were found to be capable of metabolically-activating the human hepatocarcinogen aflatoxin B1. These cDNA expression systems can also be used to determine whether an unknown chemical will be activated by a human P450 and thus be toxic or mutagenic in humans. To assess the extent of interindividual variation in P450 expression, probes developed from P450 cDNAs are being used to quantify levels of P450 mRNAs in various human tissues. Studies using RNase protection revealed that the closely related CYP2B6 and CYP2B7 mRNAs could be independently quantified in liver and lung, respectively. This procedure can be used to examine expression of different P450 genes in banks of human tissue specimens. JF - The Tohoku journal of experimental medicine AU - Gonzalez, F J AU - Crespi, C L AU - Czerwinski, M AU - Gelboin, H V AD - Laboratory of Molecular Carcinogenesis, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 67 EP - 72 VL - 168 IS - 2 SN - 0040-8727, 0040-8727 KW - CYP2B KW - RNA, Messenger KW - 0 KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Ribonucleases KW - EC 3.1.- KW - Index Medicus KW - Sensitivity and Specificity KW - Reproducibility of Results KW - Multigene Family KW - Humans KW - Organ Specificity -- physiology KW - DNA -- genetics KW - Catalysis KW - Liver -- enzymology KW - RNA, Messenger -- metabolism KW - Cytochrome P-450 Enzyme System -- genetics KW - Liver -- metabolism KW - Cytochrome P-450 Enzyme System -- metabolism KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Lung -- enzymology KW - Lung -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73533950?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Tohoku+journal+of+experimental+medicine&rft.atitle=Analysis+of+human+cytochrome+P450+catalytic+activities+and+expression.&rft.au=Gonzalez%2C+F+J%3BCrespi%2C+C+L%3BCzerwinski%2C+M%3BGelboin%2C+H+V&rft.aulast=Gonzalez&rft.aufirst=F&rft.date=1992-10-01&rft.volume=168&rft.issue=2&rft.spage=67&rft.isbn=&rft.btitle=&rft.title=The+Tohoku+journal+of+experimental+medicine&rft.issn=00408727&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 - CYP2B N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evaluation of Telazol-xylazine as an anesthetic combination for use in Syrian hamsters. AN - 73397064; 1460851 AB - The availability of safe parenteral anesthetics for use in Syrian hamsters is limited. We evaluated the effects of Telazol-xylazine (TZX) combinations with respect to anesthetic efficacy and potential for tissue damage. Two dose levels of the combination were administered by both the intraperitoneal (IP) and intramuscular (IM) routes. TZX by the IM route failed to consistently produce anesthesia and caused gross and histopathologic muscle lesions. IP administration of 20 mg/kg Telazol combined with 10 mg/kg xylazine was adequate for restraint purposes. IP administration of 30 mg/kg Telazol combined with 10 mg/kg xylazine produced a safe, reliable level of surgical anesthesia without evidence of gross or histopathologic lesions. There was no nephrotoxicity at either concentration of the anesthetic. A dose level of TZX that provides safe parenteral anesthesia in Syrian hamsters was determined. JF - Laboratory animal science AU - Forsythe, D B AU - Payton, A J AU - Dixon, D AU - Myers, P H AU - Clark, J A AU - Snipe, J R AD - Comparative Medicine Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 497 EP - 502 VL - 42 IS - 5 SN - 0023-6764, 0023-6764 KW - Drug Combinations KW - 0 KW - tiletamine, zolazepam drug combination KW - Xylazine KW - 2KFG9TP5V8 KW - Tiletamine KW - 2YFC543249 KW - Zolazepam KW - G1R474U58U KW - Index Medicus KW - Muscular Diseases -- pathology KW - Animals KW - Rodent Diseases -- chemically induced KW - Muscular Diseases -- chemically induced KW - Injections, Intraperitoneal -- veterinary KW - Respiration -- drug effects KW - Injections, Intramuscular -- veterinary KW - Muscular Diseases -- veterinary KW - Rodent Diseases -- pathology KW - Female KW - Cricetinae KW - Xylazine -- administration & dosage KW - Anesthesia, General -- veterinary KW - Zolazepam -- toxicity KW - Zolazepam -- administration & dosage KW - Xylazine -- toxicity KW - Mesocricetus KW - Tiletamine -- toxicity KW - Tiletamine -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73397064?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+animal+science&rft.atitle=Evaluation+of+Telazol-xylazine+as+an+anesthetic+combination+for+use+in+Syrian+hamsters.&rft.au=Forsythe%2C+D+B%3BPayton%2C+A+J%3BDixon%2C+D%3BMyers%2C+P+H%3BClark%2C+J+A%3BSnipe%2C+J+R&rft.aulast=Forsythe&rft.aufirst=D&rft.date=1992-10-01&rft.volume=42&rft.issue=5&rft.spage=497&rft.isbn=&rft.btitle=&rft.title=Laboratory+animal+science&rft.issn=00236764&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-14 N1 - Date created - 1993-01-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Charybdotoxin, dendrotoxin and mast cell degranulating peptide block the voltage-activated K+ current of fibroblast cells stably transfected with NGK1 (Kv1.2) K+ channel complementary DNA. AN - 73356956; 1280351 AB - The blocking actions of the K+ channel toxins charybdotoxin, dendrotoxin and mast cell degranulating peptide were studied in B82 mouse fibroblast cells transformed to express NGK1 (Kv1.2) K+ channels. All three toxins were potent blockers of the K+ current in these cells, with KD values of 1.7, 2.8 and 185 nM, respectively. The toxin block exhibited a weak voltage-dependence with the degree of inhibition decreasing at positive membrane potentials. For charybdotoxin and dendrotoxin, reducing [K+]i did not increase the fractional block, demonstrating that the relief of block at positive membrane potentials is not due to displacement of the toxin molecules by outward flow of K+ ions. A voltage-jump protocol was used to determine the rates of binding and unbinding of dendrotoxin and mast cell degranulating peptide; binding of charybdotoxin was too rapid to be quantitatively evaluated in this manner. The binding rates (dendrotoxin, approximately 5 x 10(7)/M per s; mast cell degranulating peptide, approximately 0.8 x 10(7)/M per s) were largely voltage-independent, suggesting that association of the toxin molecules with the channel is diffusion limited. The rates of unbinding (dendrotoxin, approximately 0.3/s; mast cell degranulating peptide, approximately 3/s at +60 mV) of both toxins increased e-fold per approximately 40 mV change in membrane potential, thus accounting for the voltage-dependence of the equilibrium block. Internal perfusion with the three toxins failed to affect the K+ current (in contrast to internal tetraethylammonium which strongly blocked the current), indicating that the toxins exert their blocking action by binding to extracellular sites. JF - Neuroscience AU - Werkman, T R AU - Kawamura, T AU - Yokoyama, S AU - Higashida, H AU - Rogawski, M A AD - Neuronal Excitability Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 935 EP - 946 VL - 50 IS - 4 SN - 0306-4522, 0306-4522 KW - Elapid Venoms KW - 0 KW - Peptides KW - Potassium Channels KW - Scorpion Venoms KW - Charybdotoxin KW - 115422-61-2 KW - mast cell degranulating peptide KW - 32908-73-9 KW - dendrotoxin KW - 74811-93-1 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Fibroblasts -- drug effects KW - Mice KW - Fibroblasts -- metabolism KW - Ampicillin Resistance -- genetics KW - Transfection KW - Cells, Cultured KW - Extracellular Space -- metabolism KW - DNA -- genetics KW - Restriction Mapping KW - Membrane Potentials -- drug effects KW - Extracellular Space -- drug effects KW - Elapid Venoms -- pharmacology KW - Potassium Channels -- metabolism KW - Scorpion Venoms -- pharmacology KW - Potassium Channels -- drug effects KW - Peptides -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73356956?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Charybdotoxin%2C+dendrotoxin+and+mast+cell+degranulating+peptide+block+the+voltage-activated+K%2B+current+of+fibroblast+cells+stably+transfected+with+NGK1+%28Kv1.2%29+K%2B+channel+complementary+DNA.&rft.au=Werkman%2C+T+R%3BKawamura%2C+T%3BYokoyama%2C+S%3BHigashida%2C+H%3BRogawski%2C+M+A&rft.aulast=Werkman&rft.aufirst=T&rft.date=1992-10-01&rft.volume=50&rft.issue=4&rft.spage=935&rft.isbn=&rft.btitle=&rft.title=Neuroscience&rft.issn=03064522&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 - Effect of chronic consumption of methylparathion on rat brain regional acetylcholinesterase activity and on levels of biogenic amines. AN - 73356783; 1455421 AB - Wistar rat pups (female) were exposed to methylparathion (MPTH) by gastric intubation in single doses, or in a chronic regimen of different durations. A single dose of 1 mg MPTH/kg body weight in 15-day-old pups caused a significant decrease of acetylcholinesterase (AChE) activity in cerebellum (CE), motor cortex (MC) and brain stem (BS). The effect began to appear in about 20 min after administration, the peak effect was attained in 120 min and later on this waned off completely by 24 h. The effect was similar in young (15 days) and in adult (70 days) rats. A single dose of 0.2 mg MPTH/kg in 15 day old pups caused a reduction of AChE activity only in the BS, while a 0.1 mg MPTH/kg single dose given to 15-day-old pups caused no effect even in seven regions of the brain examined. Effect of low dose chronic administration of MPTH on AChE activity was also studied in CE, MC, BS, hippocampus (HI), striatum-accumbens (SA), spinal cord (SC) and also in the hypothalamus (HY). Administration of 0.1 mg MPTH/kg from second day to 15 days of age caused significant reduction of AChE activity in only 2 of the 7 brain regions studied. Administration of double the dose (0.2 mg MPTH/kg) and for a longer duration (2nd day to 150 days of age), caused a depression in all the brain regions studied. In all these regions, the levels of NA, DA and 5HT did practically not change. The results suggest that chronic consumption of MPTH leads to a moderate decrease of AChE activity in several brain regions. JF - Toxicology AU - Kumar, M V AU - Desiraju, T AD - Department of Neurophysiology, National Institute of Mental Health and Neurosciences, Bangalore, India. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 13 EP - 20 VL - 75 IS - 1 SN - 0300-483X, 0300-483X KW - Biogenic Amines KW - 0 KW - Cholinesterase Inhibitors KW - Serotonin KW - 333DO1RDJY KW - Methyl Parathion KW - 41BCL2O91D KW - Acetylcholinesterase KW - EC 3.1.1.7 KW - Dopamine KW - VTD58H1Z2X KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Aging -- metabolism KW - Animals KW - Central Nervous System -- metabolism KW - Drug Administration Schedule KW - Rectum KW - Body Temperature -- drug effects KW - Dose-Response Relationship, Drug KW - Dopamine -- metabolism KW - Aging -- physiology KW - Rats KW - Norepinephrine -- metabolism KW - Rats, Wistar KW - Serotonin -- metabolism KW - Time Factors KW - Female KW - Methyl Parathion -- toxicity KW - Brain -- enzymology KW - Biogenic Amines -- metabolism KW - Cholinesterase Inhibitors -- toxicity KW - Brain -- drug effects KW - Acetylcholinesterase -- metabolism KW - Brain -- metabolism KW - Acetylcholinesterase -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73356783?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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&rft.atitle=Effect+of+chronic+consumption+of+methylparathion+on+rat+brain+regional+acetylcholinesterase+activity+and+on+levels+of+biogenic+amines.&rft.au=Kumar%2C+M+V%3BDesiraju%2C+T&rft.aulast=Kumar&rft.aufirst=M&rft.date=1992-10-01&rft.volume=75&rft.issue=1&rft.spage=13&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=0300483X&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 - CONF T1 - U.S.-Japan seminar on "genomic instability during carcinogenesis and tumor progression". AN - 73353857; 1360469 JF - Japanese journal of cancer research : Gann AU - Harris, C C AU - Hirohashi, S Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 1108 EP - 1111 VL - 83 IS - 10 KW - Index Medicus KW - International Cooperation KW - Genes, Tumor Suppressor -- genetics KW - Humans KW - Mutation KW - Gene Amplification KW - Genome, Human KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73353857?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&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=Japanese+journal+of+cancer+research+%3A+Gann&rft.atitle=U.S.-Japan+seminar+on+%22genomic+instability+during+carcinogenesis+and+tumor+progression%22.&rft.au=Harris%2C+C+C%3BHirohashi%2C+S&rft.aulast=Harris&rft.aufirst=C&rft.date=1992-10-01&rft.volume=83&rft.issue=10&rft.spage=1108&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 - 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 - The LEC rat--an animal model for human hepatitis and hepatocellular carcinoma. AN - 73353781; 1333464 JF - Japanese journal of cancer research : Gann AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 VL - 83 IS - 10 SN - 0910-5050, 0910-5050 KW - c-fos KW - c-jun KW - c-myc KW - hts KW - Copper KW - 789U1901C5 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Mutant Strains KW - Humans KW - Copper -- metabolism KW - Hepatitis KW - Liver Neoplasms, Experimental -- genetics KW - Liver Neoplasms, Experimental -- etiology KW - Carcinoma, Hepatocellular -- etiology KW - Carcinoma, Hepatocellular -- genetics KW - Hepatitis, Animal -- genetics KW - Disease Models, Animal KW - Hepatitis, Animal -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73353781?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+LEC+rat--an+animal+model+for+human+hepatitis+and+hepatocellular+carcinoma.&rft.au=Thorgeirsson%2C+S+S&rft.aulast=Thorgeirsson&rft.aufirst=S&rft.date=1992-10-01&rft.volume=83&rft.issue=10&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 - 1992-12-31 N1 - Date created - 1992-12-31 N1 - Date revised - 2017-01-13 N1 - Gene symbol - c-fos; c-jun; c-myc; hts N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Therapy of patients with metastatic breast cancer with 5-fluorouracil, leucovorin and carboplatin. AN - 73349683; 1450439 AB - Thirty-four women with metastatic breast cancer were treated at the National Cancer Institute of the National Institutes of Health, with a regimen of leucovorin (L), 500 mg/m2 i.v. over 30 min, followed in 1 h by 5-fluorouracil (5-FU), 375 mg/m2 i.v. bolus on days 1-5, and carboplatin (CBDCA), 50-100 mg/m2 i.v. bolus on days 2-4, every 28 days. All patients had received previous combination chemotherapy with at least one regimen (29 patients with 5-FU-containing regimens). CBDCA, 100 mg/m2 on days 2-4, resulted in grade 4 neutropenia in 10 out of 11 patients associated with sepsis in all 10 patients. CBDCA, 75 mg/m2 (seven patients) and 50 mg/m2 (15 patients), resulted in grade 4 neutropenia in six and eight patients, and neutropenic sepsis in five and two cases, respectively. Grade 4 thrombocytopenia occurred in 10, five and two patients receiving 100, 75 and 50 mg/m2 of CBDCA, respectively. Other toxicities included grade 3/4 mucositis in 18 patients and grade 3/4 diarrhea in 10 patients. Twenty nine patients were evaluable for response, with one pathologic complete response (3%), two partial responses (6%), 18 stable disease (53%) and eight (24%) progressive disease. Sites of response included bone, viscera and soft tissue. The median time from entry on study to progression, for responders, was 15 months. When platinum-DNA adduct formation in peripheral white blood cells was analyzed in 27 patients at 24 h after drug administration, a significant correlation between adduct level and CBDCA cumulative dose was found.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Anti-cancer drugs AU - Pai, L H AU - Swain, S M AU - Venzon, D J AU - Reed, E AU - Poirier, M C AU - Gupta-Burt, S AU - Denicoff, A M AU - Allegra, C J AD - National Cancer Institute, National Institute of Health, Bethesda, MD 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 463 EP - 469 VL - 3 IS - 5 SN - 0959-4973, 0959-4973 KW - DNA, Neoplasm KW - 0 KW - Carboplatin KW - BG3F62OND5 KW - Leucovorin KW - Q573I9DVLP KW - Fluorouracil KW - U3P01618RT KW - Index Medicus KW - DNA, Neoplasm -- blood KW - Dose-Response Relationship, Drug KW - Humans KW - Leucovorin -- administration & dosage KW - Aged KW - Carboplatin -- administration & dosage KW - DNA, Neoplasm -- drug effects KW - Fluorouracil -- administration & dosage KW - Adult KW - Leukocytes, Mononuclear -- metabolism KW - Middle Aged KW - Carboplatin -- blood KW - Female KW - Breast Neoplasms -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Breast Neoplasms -- blood KW - Breast Neoplasms -- secondary UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73349683?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Therapy+of+patients+with+metastatic+breast+cancer+with+5-fluorouracil%2C+leucovorin+and+carboplatin.&rft.au=Pai%2C+L+H%3BSwain%2C+S+M%3BVenzon%2C+D+J%3BReed%2C+E%3BPoirier%2C+M+C%3BGupta-Burt%2C+S%3BDenicoff%2C+A+M%3BAllegra%2C+C+J&rft.aulast=Pai&rft.aufirst=L&rft.date=1992-10-01&rft.volume=3&rft.issue=5&rft.spage=463&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 - 1993-01-06 N1 - Date created - 1993-01-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of the cyclic adenosine 3',5'-monophosphate response element in efficient expression of the rat thyrotropin receptor promoter. AN - 73343691; 1333054 AB - The "minimal" promoter region of the TSH receptor gene, -195 to -39 basepairs (bp), exhibits basal promoter activity, thyroid specificity, and negative regulation by TSH via its cAMP signal. In FRT thyroid cells and by comparison to pTRCAT5'-199, 5'-deletion mutants of chloramphenicol acetyltransferase (CAT) constructs from -199 to -150 bp of the minimal promoter decrease basal CAT activity by 50%, whereas continued deletion to -146 bp increases activity more than 4-fold. Continued deletion to -131 bp results in basal activity less than that of the -199 bp construct. An octameric cAMP response element (CRE)-like sequence, TGAGGTCA, is within -146 to -131 bp and starts at -139 bp. Its mutation to a consensus CRE (TGACGTCA) or AP1 (TGAGTCA) site or mutation of several residues flanking its 3'-terminus can improve promoter activity as much as 8-fold compared to pTRCAT5'-199. A nonpalindromic mutation to CGAGGACA decreases basal promoter activity to the level of the 199-bp minimal promoter. The CRE-like sequence between -139 and -132 bp is a constitutive enhancer of promoter activity in FRT thyroid cells, since, ligated to a simian virus-40-promoter-driven CAT gene, it increases CAT activity in the absence of forskolin in proportion to copy number and independent of direction or position. It can, however, function as a cAMP-responsive CRE, as evidenced by the fact that forskolin increases the activity of the same simian virus-40-promoter-driven CAT gene constructs in Buffalo rat liver (BRL) cells. DNAase-I footprinting shows that the CRE region is protected by a purified binding region peptide of the CRE-binding protein, activating transcription factor-2, and recombinant AP1 (human c-jun) as well as by BRL, FRT, and FRTL-5 rat thyroid cell nuclear extracts. Gel mobility shift analyses show that multiple CRE-binding proteins in the BRL, FRT, and FRTL-5 cell nuclear extracts form complexes with the CRE-like site, that one of these is CRE-binding protein, and that all form complexes with mutant sequences of the CRE-like site in a manner that exactly parallels their effects on constitutive enhancer function in FRT thyroid cells. We show, therefore, that the CRE-like site in the minimal TSH receptor promoter functions as a constitutive enhancer of promoter activity in FRT thyroid cells yet is a cAMP-responsive CRE.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Molecular endocrinology (Baltimore, Md.) AU - Ikuyama, S AU - Shimura, H AU - Hoeffler, J P AU - Kohn, L D AD - Laboratory of Biochemistry and Metabolism, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 1701 EP - 1715 VL - 6 IS - 10 SN - 0888-8809, 0888-8809 KW - Oligodeoxyribonucleotides KW - 0 KW - Receptors, Thyrotropin KW - Recombinant Proteins KW - Thyrotropin KW - 9002-71-5 KW - Cyclic AMP KW - E0399OZS9N KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Index Medicus KW - Animals KW - Cell Nucleus -- metabolism KW - Thyroid Gland KW - Chloramphenicol O-Acetyltransferase -- metabolism KW - Binding Sites KW - Mutagenesis, Site-Directed KW - Rats KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Base Sequence KW - Transfection KW - Recombinant Proteins -- metabolism KW - Enhancer Elements, Genetic KW - Molecular Sequence Data KW - Cell Line KW - Sequence Deletion KW - Promoter Regions, Genetic KW - Thyrotropin -- pharmacology KW - Gene Expression Regulation KW - Cyclic AMP -- physiology KW - Receptors, Thyrotropin -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73343691?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+the+cyclic+adenosine+3%27%2C5%27-monophosphate+response+element+in+efficient+expression+of+the+rat+thyrotropin+receptor+promoter.&rft.au=Ikuyama%2C+S%3BShimura%2C+H%3BHoeffler%2C+J+P%3BKohn%2C+L+D&rft.aulast=Ikuyama&rft.aufirst=S&rft.date=1992-10-01&rft.volume=6&rft.issue=10&rft.spage=1701&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 - 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 - The effect of alcohol withdrawal on serum concentrations of Lp(a), apolipoproteins A-1 and B, and lipids. AN - 73336430; 1332524 AB - Moderate alcohol consumption is associated with a decreased risk of coronary artery disease. The mechanism of the putative protective effect of alcohol intake, however, remains elusive. Recent studies suggest that a ratio of apolipoprotein A-I/apolipoprotein B and Lp(a) are better indicators of the risk of atherosclerosis than total cholesterol and high density lipoprotein cholesterol. To assess the effect of alcohol on these analytes, we determined the concentration of Lp(a), apolipoprotein A-I, apolipoprotein B, total cholesterol, and high-density lipoprotein cholesterol, and calculated low-density lipoprotein cholesterol in serum of 12 patients meeting DSM-III-R criteria for alcohol dependence at the time of admission for treatment of alcohol withdrawal (before). The analyses were repeated after 4 weeks of supervised abstinence on a locked research unit (after). With abstinence, there was a significant increase in the concentration of Lp(a), the atherogenic index and the ratio of low-density to high-density lipoprotein cholesterol but a significant decrease in total cholesterol, high-density lipoprotein cholesterol, apolipoprotein A-I, and the apolipoprotein A-I/B ratio. Apolipoprotein B and low-density lipoprotein cholesterol showed no significant changes before and after alcohol abstinence. Thus, decreased Lp(a) and increased high-density lipoprotein cholesterol and apolipoprotein A-I may be factors mediating the putative protective effect of alcohol in coronary artery disease. JF - Alcoholism, clinical and experimental research AU - Huang, C M AU - Elin, R J AU - Ruddel, M AU - Schmitz, J AU - Linnoila, M AD - Clinical Pathology Department, Warren Grant Magnuson Clinical Center, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 895 EP - 898 VL - 16 IS - 5 SN - 0145-6008, 0145-6008 KW - Apolipoprotein A-I KW - 0 KW - Apolipoproteins B KW - Cholesterol, HDL KW - Cholesterol, LDL KW - Lipids KW - Lipoprotein(a) KW - Cholesterol KW - 97C5T2UQ7J KW - Index Medicus KW - Cholesterol, LDL -- blood KW - Cholesterol -- blood KW - Substance Abuse Treatment Centers KW - Cholesterol, HDL -- blood KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Liver Function Tests KW - Male KW - Female KW - Lipids -- blood KW - Alcoholism -- rehabilitation KW - Lipoprotein(a) -- blood KW - Alcohol Withdrawal Delirium -- blood KW - Apolipoprotein A-I -- metabolism KW - Apolipoproteins B -- metabolism KW - Alcoholism -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73336430?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+effect+of+alcohol+withdrawal+on+serum+concentrations+of+Lp%28a%29%2C+apolipoproteins+A-1+and+B%2C+and+lipids.&rft.au=Huang%2C+C+M%3BElin%2C+R+J%3BRuddel%2C+M%3BSchmitz%2C+J%3BLinnoila%2C+M&rft.aulast=Huang&rft.aufirst=C&rft.date=1992-10-01&rft.volume=16&rft.issue=5&rft.spage=895&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 - 1992-12-08 N1 - Date created - 1992-12-08 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Alcohol Clin Exp Res. 1993 Aug;17(4):926 [8214436] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Timed treatment of the arthritic diseases: a review and hypothesis. AN - 73336284; 1439846 AB - Evidence has been accumulating regarding the importance of biological rhythms in the diagnosis and treatment of a variety of diseases and disorders. Increasingly, the arthritides have shown statistically quantifiable rhythmic parameters. Included in the latter group are joint pain and joint size. In addition, a number of drugs used to treat rheumatic diseases have varying therapeutic and toxic effects based on the time of day of administration. Among these drug classes are nonsteroidal antiinflammatory drugs, glucocorticoids, and a number of cytostatic agents. In the last group of agents, experience in treating malignant disease suggests that time-specified treatment may reduce the toxic effects of low-dose cytostatic treatment of rheumatoid arthritis (RA) and related diseases. This article reviews that evidence and suggests a rationale for the timed treatment of RA with methotrexate. JF - Seminars in arthritis and rheumatism AU - Vener, K J AU - Reddy, A AD - National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 83 EP - 97 VL - 22 IS - 2 SN - 0049-0172, 0049-0172 KW - Anti-Inflammatory Agents KW - 0 KW - Anti-Inflammatory Agents, Non-Steroidal KW - Index Medicus KW - Animals KW - Anti-Inflammatory Agents, Non-Steroidal -- therapeutic use KW - Humans KW - Anti-Inflammatory Agents -- therapeutic use KW - Periodicity KW - Time Factors KW - Arthritis -- therapy KW - Arthritis -- physiopathology KW - Models, Theoretical UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73336284?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+arthritis+and+rheumatism&rft.atitle=Timed+treatment+of+the+arthritic+diseases%3A+a+review+and+hypothesis.&rft.au=Vener%2C+K+J%3BReddy%2C+A&rft.aulast=Vener&rft.aufirst=K&rft.date=1992-10-01&rft.volume=22&rft.issue=2&rft.spage=83&rft.isbn=&rft.btitle=&rft.title=Seminars+in+arthritis+and+rheumatism&rft.issn=00490172&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 - Toxicity and carcinogenicity studies of quercetin, a natural component of foods. AN - 73333144; 1459373 AB - Quercetin is a naturally occurring chemical found in our daily diet in fruits and vegetables. Toxicity and carcinogenicity studies of quercetin were conducted in male and female F344/N rats, under conditions which allowed comparison to results of approximately 400 previously tested chemicals. The chemical was administered in the feed for 2-years at concentrations of 0, 1000, 10,000, or 40,000 ppm, and the estimated dose delivered was approximately 40-1900 mg/kg/day. There were no treatment-related effects on survival and no treatment-related clinical signs of toxicity. The high-dose groups had reduced body weight gain in comparison to controls during the last half of the study. At interim evaluations at 6 and 15 months, treatment-related toxic lesions were not observed, but at 2 years toxic and neoplastic lesions were seen in the kidney of male rats, including increased severity of chronic nephropathy, hyperplasia, and neoplasia of the renal tubular epithelium. Under the conditions of these 2-year studies quercetin showed carcinogenic activity in the kidney of the male rat, causing primarily benign tumors of the renal tubular epithelium. Quercetin did not cause tumors at other sites. Quercetin is a genotoxic chemical, but the neoplastic response observed in the kidney may be due in part to a combination of nongenotoxic and genotoxic events. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Dunnick, J K AU - Hailey, J R AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 423 EP - 431 VL - 19 IS - 3 SN - 0272-0590, 0272-0590 KW - Carcinogens KW - 0 KW - Quercetin KW - 9IKM0I5T1E KW - Index Medicus KW - Eating -- drug effects KW - Animals KW - Liver -- pathology KW - Kidney -- pathology KW - Food Analysis KW - Neoplasms, Experimental -- pathology KW - Rats KW - Rats, Inbred F344 KW - Neoplasms, Experimental -- chemically induced KW - Body Weight -- drug effects KW - Female KW - Male KW - Organ Size -- drug effects KW - Quercetin -- toxicity KW - Carcinogens -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73333144?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Toxicity+and+carcinogenicity+studies+of+quercetin%2C+a+natural+component+of+foods.&rft.au=Dunnick%2C+J+K%3BHailey%2C+J+R&rft.aulast=Dunnick&rft.aufirst=J&rft.date=1992-10-01&rft.volume=19&rft.issue=3&rft.spage=423&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 - 1993-01-13 N1 - Date created - 1993-01-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression of acidic fibroblast growth factor in regenerating liver and during hepatic differentiation. AN - 73332987; 1279268 AB - Acidic fibroblast growth factor belongs to a family of growth factors that show a high affinity for heparin sulfate proteoglycans. In vitro, it participates in various cellular functions including proliferation, differentiation, angiogenesis, and cell migration, but in vivo, the physiologic role of this growth factor is still not clearly defined. The level of expression and also cellular distribution of transcripts for acidic fibroblast growth factor (aFGF) were studied in adult rat liver after partial hepatectomy and during hepatic differentiation in fetal, neonatal, and adult livers by Northern analysis and in situ hybridization techniques. After partial hepatectomy a significant increase in the transcripts for aFGF was observed at 24 hours, whereas at 4 and 12 hours after the operation, the level of transcripts were similar to those of sham-operated animals. In the postnatal liver a high level of aFGF expression was present when the most evident transition from 2 to 3 cell thick hepatic cords to normal hepatic structure is taking place (Ogawa K, Medine A, Farber E. Br J Cancer 1979;40: 782-90). In contrast during the prenatal period, when the liver is still a hemopoietic organ and only a small number of sinusoids are present, low level of aFGF transcripts could be found. Animals treated with 2-acetylaminofluorene and partial hepatectomy (Evarts RP, Nagy P, Marsden E, Thorgeirsson SS. Carcinogenesis 1987;8:1737-40) displayed a marked increase in hepatic aFGF transcripts at the peak of proliferation of primitive liver epithelial cells (oval cells) and perisinusoidal stellate cells (Ito cells) in addition to hepatocytes. In situ hybridization combined with immunocytochemistry using oval and Ito cell specific antibodies revealed the presence of transcripts both in oval cells and Ito cells. Basophilic areas composed of small hepatocytes had a 3-fold increase in the level of transcripts as compared with the surrounding hepatocytes. These experiments demonstrate that the expression of aFGF is highest during the late stages of hepatic morphogenesis in newborn animals as well as during hepatic differentiation in adult liver. JF - Laboratory investigation; a journal of technical methods and pathology AU - Marsden, E R AU - Hu, Z AU - Fujio, K AU - Nakatsukasa, H AU - Thorgeirsson, S S AU - Evarts, R P AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, Maryland. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 427 EP - 433 VL - 67 IS - 4 SN - 0023-6837, 0023-6837 KW - Reticulin KW - 0 KW - Fibroblast Growth Factor 1 KW - 104781-85-3 KW - Index Medicus KW - Rats KW - Histocytochemistry -- methods KW - Animals KW - Rats, Inbred F344 KW - Blotting, Northern KW - Cell Differentiation KW - Nucleic Acid Hybridization KW - Reticulin -- metabolism KW - Staining and Labeling KW - Male KW - Liver -- cytology KW - Fibroblast Growth Factor 1 -- metabolism KW - Liver -- metabolism KW - Liver Regeneration UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73332987?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Expression+of+acidic+fibroblast+growth+factor+in+regenerating+liver+and+during+hepatic+differentiation.&rft.au=Marsden%2C+E+R%3BHu%2C+Z%3BFujio%2C+K%3BNakatsukasa%2C+H%3BThorgeirsson%2C+S+S%3BEvarts%2C+R+P&rft.aulast=Marsden&rft.aufirst=E&rft.date=1992-10-01&rft.volume=67&rft.issue=4&rft.spage=427&rft.isbn=&rft.btitle=&rft.title=Laboratory+investigation%3B+a+journal+of+technical+methods+and+pathology&rft.issn=00236837&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-07 N1 - Date created - 1992-12-07 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Lab Invest. 1992 Oct;67(4):413-5 [1434525] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - An alternative hypothesis on the role of chemically induced protein droplet (alpha 2u-globulin) nephropathy in renal carcinogenesis. AN - 73325871; 1279759 AB - Based on associations between the accumulation of protein droplets containing alpha 2u-globulin in proximal tubular epithelial cells and increased incidences of renal tubular neoplasms in male rats, it has been suggested that the carcinogenicity of chemicals that cause alpha 2u-globulin nephropathy is unique to animals that synthesize this protein. Chemicals that caused alpha 2u-globulin nephropathy and renal carcinogenicity in male rats have not been shown to produce renal tumors in animals that lack the capability for hepatic alpha 2u-globulin synthesis, including female rats, male NBR rats, or mice of either sex. Because humans do not synthesize alpha 2u-globulin it has been suggested that chemicals which cause renal toxicity associated with alpha 2u-globulin accumulation do not pose an increased cancer risk to humans. In this review on the association between alpha 2u-globulin nephropathy and renal carcinogenesis, it is apparent that (a) there are data inconsistent with the hypothesis linking these occurrences, (b) alternative mechanisms of renal toxicity and carcinogenicity are plausible, (c) data on quantitative dose-response correspondences between the various stages of alpha 2u-globulin nephropathy and renal carcinogenicity are limited, and (d) a greater understanding of the molecular changes occurring during renal carcinogenesis is needed before assuming that the current hypothesis is correct. Future research aimed at resolving issues raised in this paper should help determine whether or not the association between alpha 2u-globulin nephropathy and renal carcinogenesis represents a cause-and-effect relationship. JF - Regulatory toxicology and pharmacology : RTP AU - Melnick, R L AD - Division of Biometry and Risk Assessment, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 111 EP - 125 VL - 16 IS - 2 SN - 0273-2300, 0273-2300 KW - Alpha-Globulins KW - 0 KW - Hydrocarbons KW - alpha 2u globulin KW - Index Medicus KW - Rats KW - Hyalin -- metabolism KW - Animals KW - Humans KW - Male KW - Hyalin -- drug effects KW - Female KW - Kidney Diseases -- metabolism KW - Kidney Neoplasms -- chemically induced KW - Kidney Diseases -- complications KW - Kidney Neoplasms -- etiology KW - Hydrocarbons -- toxicity KW - Alpha-Globulins -- metabolism KW - Kidney Diseases -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73325871?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=An+alternative+hypothesis+on+the+role+of+chemically+induced+protein+droplet+%28alpha+2u-globulin%29+nephropathy+in+renal+carcinogenesis.&rft.au=Melnick%2C+R+L&rft.aulast=Melnick&rft.aufirst=R&rft.date=1992-10-01&rft.volume=16&rft.issue=2&rft.spage=111&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 - 1992-12-23 N1 - Date created - 1992-12-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Regul Toxicol Pharmacol. 1992 Oct;16(2):109-10 [1438993] Regul Toxicol Pharmacol. 1993 Oct;18(2):357-64 [7506436] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Quinolinic acid and kynurenine pathway metabolism in inflammatory and non-inflammatory neurological disease. AN - 73313371; 1422788 AB - Neurological dysfunction, seizures and brain atrophy occur in a broad spectrum of acute and chronic neurological diseases. In certain instances, over-stimulation of N-methyl-D-aspartate receptors has been implicated. Quinolinic acid (QUIN) is an endogenous N-methyl-D-aspartate receptor agonist synthesized from L-tryptophan via the kynurenine pathway and thereby has the potential of mediating N-methyl-D-aspartate neuronal damage and dysfunction. Conversely, the related metabolite, kynurenic acid, is an antagonist of N-methyl-D-aspartate receptors and could modulate the neurotoxic effects of QUIN as well as disrupt excitatory amino acid neurotransmission. In the present study, markedly increased concentrations of QUIN were found in both lumbar cerebrospinal fluid (CSF) and post-mortem brain tissue of patients with inflammatory diseases (bacterial, viral, fungal and parasitic infections, meningitis, autoimmune diseases and septicaemia) independent of breakdown of the blood-brain barrier. The concentrations of kynurenic acid were also increased, but generally to a lesser degree than the increases in QUIN. In contrast, no increases in CSF QUIN were found in chronic neurodegenerative disorders, depression or myoclonic seizure disorders, while CSF kynurenic acid concentrations were significantly lower in Huntington's disease and Alzheimer's disease. In inflammatory disease patients, proportional increases in CSF L-kynurenine and reduced L-tryptophan accompanied the increases in CSF QUIN and kynurenic acid. These responses are consistent with induction of indoleamine-2,3-dioxygenase, the first enzyme of the kynurenine pathway which converts L-tryptophan to kynurenic acid and QUIN. Indeed, increases in both indoleamine-2,3-dioxygenase activity and QUIN concentrations were observed in the cerebral cortex of macaques infected with retrovirus, particularly those with local inflammatory lesions. Correlations between CSF QUIN, kynurenic acid and L-kynurenine with markers of immune stimulation (neopterin, white blood cell counts and IgG levels) indicate a relationship between accelerated kynurenine pathway metabolism and the degree of intracerebral immune stimulation. We conclude that inflammatory diseases are associated with accumulation of QUIN, kynurenic acid and L-kynurenine within the central nervous system, but that the available data do not support a role for QUIN in the aetiology of Huntington's disease or Alzheimer's disease. In conjunction with our previous reports that CSF QUIN concentrations are correlated to objective measures of neuropsychological deficits in HIV-1-infected patients, we hypothesize that QUIN and kynurenic acid are mediators of neuronal dysfunction and nerve cell death in inflammatory diseases. Therefore, strategies to attenuate the neurological effects of kynurenine pathway metabolites or attenuate the rate of their synthesis offer new approaches to therapy. JF - Brain : a journal of neurology AU - Heyes, M P AU - Saito, K AU - Crowley, J S AU - Davis, L E AU - Demitrack, M A AU - Der, M AU - Dilling, L A AU - Elia, J AU - Kruesi, M J AU - Lackner, A AD - Section on Analytical Biochemistry, NIMH, NIH, Bethesda, MD 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 1249 EP - 1273 VL - 115 ( Pt 5) SN - 0006-8950, 0006-8950 KW - Kynurenine KW - 343-65-7 KW - Quinolinic Acid KW - F6F0HK1URN KW - Kynurenic Acid KW - H030S2S85J KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Humans KW - Macaca KW - Kynurenic Acid -- metabolism KW - Aged KW - Simian Acquired Immunodeficiency Syndrome -- complications KW - Brain Diseases -- metabolism KW - Kynurenic Acid -- cerebrospinal fluid KW - HIV Infections -- metabolism KW - Middle Aged KW - Encephalitis -- metabolism KW - HIV Infections -- cerebrospinal fluid KW - Female KW - Male KW - Neuritis -- veterinary KW - Kynurenine -- cerebrospinal fluid KW - Quinolinic Acid -- cerebrospinal fluid KW - Quinolinic Acid -- metabolism KW - Nervous System Diseases -- metabolism KW - Neuritis -- metabolism KW - Neuritis -- etiology KW - Kynurenine -- metabolism KW - Neuritis -- cerebrospinal fluid KW - Nervous System Diseases -- cerebrospinal fluid UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73313371?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+%3A+a+journal+of+neurology&rft.atitle=Quinolinic+acid+and+kynurenine+pathway+metabolism+in+inflammatory+and+non-inflammatory+neurological+disease.&rft.au=Heyes%2C+M+P%3BSaito%2C+K%3BCrowley%2C+J+S%3BDavis%2C+L+E%3BDemitrack%2C+M+A%3BDer%2C+M%3BDilling%2C+L+A%3BElia%2C+J%3BKruesi%2C+M+J%3BLackner%2C+A&rft.aulast=Heyes&rft.aufirst=M&rft.date=1992-10-01&rft.volume=115+%28+Pt+5%29&rft.issue=&rft.spage=1249&rft.isbn=&rft.btitle=&rft.title=Brain+%3A+a+journal+of+neurology&rft.issn=00068950&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-10 N1 - Date created - 1992-12-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vivo evidence of hydroxyl radical formation after acute copper and ascorbic acid intake: electron spin resonance spin-trapping investigation. AN - 73313189; 1331758 AB - Copper has been suggested to facilitate oxidative tissue injury through a free radical-mediated pathway analogous to the Fenton reaction. By applying the ESR spin-trapping technique, evidence for hydroxyl radical formation in vivo was obtained in rats treated simultaneously with copper and ascorbic acid. A secondary radical spin-trapping technique was used in which the hydroxyl radical formed the methyl radical upon reaction with dimethylsulfoxide. The methyl radical was then detected by ESR spectroscopy as its adduct with the spin trap phenyl-N-t-butylnitrone (PBN). Because copper excreted into the bile from treated animals is expected to be maintained in the Cu(I) state (by ascorbic acid or glutathione), a chelating agent that would redox-stabilize it in the Cu(I) state was used to prevent ex vivo redox chemistry. Bile samples were collected directly into solutions of bathocuproinedisulfonic acid, a Cu(I)-stabilizing agent, and 2,2'-dipyridyl, a Fe(II)-stabilizing agent. If these precautions were not taken, radical adducts were generated ex vivo and could be mistaken for radical adducts generated in vivo and excreted into the bile. Besides the PBN/.CH3 adduct, three other radical adducts were produced in vivo and excreted in bile. JF - Molecular pharmacology AU - Kadiiska, M B AU - Hanna, P M AU - Hernandez, L 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. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 723 EP - 729 VL - 42 IS - 4 SN - 0026-895X, 0026-895X KW - Free Radicals KW - 0 KW - Hydroxides KW - Copper KW - 789U1901C5 KW - Iron KW - E1UOL152H7 KW - Ascorbic Acid KW - PQ6CK8PD0R KW - Index Medicus KW - Rats KW - Bile -- chemistry KW - Animals KW - Rats, Sprague-Dawley KW - Electron Spin Resonance Spectroscopy KW - Bile -- metabolism KW - Time Factors KW - Male KW - Iron -- metabolism KW - Hydroxides -- chemistry KW - Ascorbic Acid -- chemistry KW - Copper -- toxicity KW - Copper -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73313189?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=In+vivo+evidence+of+hydroxyl+radical+formation+after+acute+copper+and+ascorbic+acid+intake%3A+electron+spin+resonance+spin-trapping+investigation.&rft.au=Kadiiska%2C+M+B%3BHanna%2C+P+M%3BHernandez%2C+L%3BMason%2C+R+P&rft.aulast=Kadiiska&rft.aufirst=M&rft.date=1992-10-01&rft.volume=42&rft.issue=4&rft.spage=723&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 - 1992-12-01 N1 - Date created - 1992-12-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Major depression: its recognition and treatment. Part 1: First-generation antidepressants. AN - 73296865; 1442526 JF - American pharmacy AU - Grothe, D R AU - Cohen, L J AD - National Institute of Mental Health, National Institutes of Health, Bethesda, Md. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 33 EP - 40 VL - NS32 IS - 10 SN - 0160-3450, 0160-3450 KW - Antidepressive Agents KW - 0 KW - Index Medicus KW - Humans KW - Antidepressive Agents -- blood KW - Depressive Disorder -- physiopathology KW - Depressive Disorder -- drug therapy KW - Antidepressive Agents -- therapeutic use KW - Antidepressive Agents -- adverse effects KW - Depressive Disorder -- classification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73296865?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+pharmacy&rft.atitle=Major+depression%3A+its+recognition+and+treatment.+Part+1%3A+First-generation+antidepressants.&rft.au=Grothe%2C+D+R%3BCohen%2C+L+J&rft.aulast=Grothe&rft.aufirst=D&rft.date=1992-10-01&rft.volume=NS32&rft.issue=10&rft.spage=33&rft.isbn=&rft.btitle=&rft.title=American+pharmacy&rft.issn=01603450&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 - The effect of sodium selenite on cell proliferation and transformation of primary rat tracheal epithelial cells. AN - 73289324; 1330341 AB - The effects of sodium selenite (Na2SeO3) on cell proliferation and the development of preneoplastic transformed variants were studied in primary cultures of rat tracheal epithelial cells. Results revealed a biphasic effect of Na2SeO3 on cell proliferation: at concentrations between 6 x 10(-8) and 6 x 10(-6) M, it stimulated and at concentrations of approximately 2 x 10(-5) and above it inhibited cell proliferation (presumably due to toxicity). Nontoxic concentrations of Na2SeO3 (6 x 10(-8) -6 x 10(-7) M) significantly reduced the spontaneous transformation frequency. Transformation induced by the tobacco-specific nitrosamine 4-(methyl-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) was effectively inhibited by nontoxic as well as toxic concentrations of Na2SeO3. Treatment of cultures with Na2SeO3 after cessation of NNK exposure, i.e. during the selection period, also significantly reduced the transformation frequency. These experiments show that the inhibition of transformation by Na2SeO3 is not the result of an antiproliferative effect. They further indicate that the inhibitory effect occurs even when the chemical treatment occurs during the 'postinitiation' phase. Thus the inhibition of transformation by Na2SeO3 cannot solely be explained by its effects on drug metabolism. JF - Carcinogenesis AU - Zhu, S AU - Gray, T E AU - Nettesheim, P AD - Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 1725 EP - 1729 VL - 13 IS - 10 SN - 0143-3334, 0143-3334 KW - Anticarcinogenic Agents KW - 0 KW - Carcinogens KW - Nitrosamines KW - 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone KW - 7S395EDO61 KW - Selenium KW - H6241UJ22B KW - Sodium Selenite KW - HIW548RQ3W KW - Index Medicus KW - Rats KW - Animals KW - Epithelial Cells KW - Cells, Cultured KW - Anticarcinogenic Agents -- pharmacology KW - Cell Division -- drug effects KW - Epithelium -- pathology KW - Epithelium -- drug effects KW - Trachea -- pathology KW - Selenium -- pharmacology KW - Cell Transformation, Neoplastic -- drug effects KW - Trachea -- cytology KW - Trachea -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73289324?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+effect+of+sodium+selenite+on+cell+proliferation+and+transformation+of+primary+rat+tracheal+epithelial+cells.&rft.au=Zhu%2C+S%3BGray%2C+T+E%3BNettesheim%2C+P&rft.aulast=Zhu&rft.aufirst=S&rft.date=1992-10-01&rft.volume=13&rft.issue=10&rft.spage=1725&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-27 N1 - Date created - 1992-11-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Plasmacytomagenesis in mice: model of neoplastic development dependent upon chromosomal translocations. AN - 73288294; 1423827 AB - Three model systems of plasmacytomagenesis that are associated with mutations that affect c-myc transcription were discussed. Plasmacytoma induction by chronic peritoneal irritation induced by non-metabolized paraffin oils or plastic objects is strongly influenced by the immune status of the host. BALB/cAn mice must be exposed to natural environmental antigens to develop a high incidence of plasmacytomas. This may be related to T-cell priming. BALB/cAn mice raised under strict SPF conditions are refractory to plasmacytoma induction by pristane. The genotype of the mouse plays an important role in the chronic peritoneal irritation model of plasmacytomagenesis in mice. Only a few of the standard inbred strains are susceptible, notably BALB/cAn and NZB/B1. The genetic basis of susceptibility and resistance has been studied in crosses and congenic strains involving the susceptible BALB/cAn and resistant DBA/2 strains. While several genes play a role in determining resistance at least one resistance gene located on the distal end of Chr 4 reduces the incidence by at least 50% as determined in the BALB/cAn.DBA/2 Fv-1n/n congenic strain. The action of susceptibility and resistance genes is not known; hypothetically these genes could play a role in plasmacytomagenesis by increasing the probabilities of illegitimate exchanges between genes or by influencing the formation of mutations in genes that regulate mitotic cycling. Plasmacytomas appear to develop in the chronic inflammatory tissues induced by these agents. Fundamental unanswered questions are whether these inflammatory tissues provide products such as oxidants in vivo that damage DNA and promote mutagenesis. In the mouse there is a resident self-renewing B cell population that is CD5+. These B cells, which are known to be precursors of normal lamina propria IgA-secreting plasma cells, are directly in contact with the chronic inflammatory process induced by pristane; they may be targets in plasmacytomagenesis. The plasmacytomas that develop by the peritoneal mode of induction all have chromosomal translocations that directly or indirectly activate c-myc. The predominant MACTR found in 90% of these tumors is T(12;15) in which a heavy-chain switch region sequence is joined to the 5' region of c-myc. The evidence strongly suggests that the translocation develops in a late mature B cell that is in the process of isotype switching. An unanswered question is whether the switching associated T(12;15) takes place in a B cell that is exposed to the inflammatory microenvironment.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Carcinogenesis AU - Potter, M AU - Wiener, F AD - DCBDC, National Cancer Institute, National Institutes of Health, Bethesda, MD. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 1681 EP - 1697 VL - 13 IS - 10 SN - 0143-3334, 0143-3334 KW - E&mgr;-bcl-2 KW - E&mgr;-v-abl KW - Ld-IL-6 KW - PVA-1 KW - c-myc KW - Index Medicus KW - Animals KW - Mice, Inbred C3H KW - Mice KW - Mice, Transgenic KW - Mice, Inbred BALB C KW - Models, Biological KW - Mice, Inbred DBA KW - Translocation, Genetic -- genetics KW - Plasmacytoma -- etiology KW - Plasmacytoma -- genetics KW - Chromosomes -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73288294?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Plasmacytomagenesis+in+mice%3A+model+of+neoplastic+development+dependent+upon+chromosomal+translocations.&rft.au=Potter%2C+M%3BWiener%2C+F&rft.aulast=Potter&rft.aufirst=M&rft.date=1992-10-01&rft.volume=13&rft.issue=10&rft.spage=1681&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-27 N1 - Date created - 1992-11-27 N1 - Date revised - 2017-01-13 N1 - Gene symbol - E&mgr;-bcl-2; E&mgr;-v-abl; Ld-IL-6; PVA-1; c-myc N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The prevalence of illicit drug use in six metropolitan areas in the United States: results from the 1991 National Household Survey on Drug Abuse. AN - 73272065; 1422110 AB - National levels and trends of illicit drug use in the general population are well documented. However, little is known about how this phenomenon is distributed among various subnational areas such as state, metropolitan area, and other local areas. The sample design from the National Household Survey on Drug Abuse (NHSDA) was recently expanded such that estimates from several large metropolitan areas could be produced with reasonable precision. The prevalence of illicit drug use is examined in six large metropolitan areas of the United States. These findings indicate that, in some cases, drug use varies considerably by metropolitan area. JF - British journal of addiction AU - Hughes, A L AD - National Institute on Drug Abuse, Division of Epidemiology and Prevention Research, Rockville, Maryland 20857. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 1481 EP - 1485 VL - 87 IS - 10 SN - 0952-0481, 0952-0481 KW - Street Drugs KW - 0 KW - Index Medicus KW - Cross-Sectional Studies KW - Humans KW - Incidence KW - United States -- epidemiology KW - Population Surveillance KW - Urban Population -- statistics & numerical data KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73272065?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+addiction&rft.atitle=The+prevalence+of+illicit+drug+use+in+six+metropolitan+areas+in+the+United+States%3A+results+from+the+1991+National+Household+Survey+on+Drug+Abuse.&rft.au=Hughes%2C+A+L&rft.aulast=Hughes&rft.aufirst=A&rft.date=1992-10-01&rft.volume=87&rft.issue=10&rft.spage=1481&rft.isbn=&rft.btitle=&rft.title=British+journal+of+addiction&rft.issn=09520481&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-04 N1 - Date created - 1992-12-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Intravenous administration of recombinant human macrophage colony-stimulating factor to patients with metastatic cancer: a phase I study. AN - 73258423; 1403042 AB - Recombinant human macrophage colony-stimulating factor (M-CSF) has been shown to stimulate specifically macrophage lineage differentiation in vitro and to induce cells capable of antitumor activity alone or in combination with an antibody. The administration of M-CSF to mice has demonstrated antitumor therapeutic effects in vivo. Therefore, a phase I trial of M-CSF administration to patients with metastatic cancer was undertaken. M-CSF was given by intermittent intravenous bolus infusion every 8 hours for 7 days; the treatment cycle was repeated once after a week of rest. Cohorts of three patients underwent dose escalation from 10 to 100,000 micrograms/m2/d; 23 patients received 27 courses of M-CSF administration. All patients had metastatic solid tumors refractory to conventional therapy, including renal cell carcinoma (RCC) (nine), melanoma (seven), and colorectal carcinoma (seven). Treatment-related toxicity was minimal; five patients developed transient signs of ocular or periorbital inflammation, with iridocyclitis as the most severe manifestation. At the highest doses, platelet counts decreased with therapy (but remained > 100,000/mm3) and the absolute monocyte count increased during the course of therapy. Only at 30,000 and 100,000 micrograms/m2/d was treatment limited because of toxicity (iritis and malaise). Pharmacokinetic studies demonstrated up to a 1,000-fold increase in circulating serum M-CSF after bolus infusion; half-life varied from 1 to 6 hours. Complete regression of mediastinal adenopathy and multiple pulmonary metastases were observed in one patient with RCC. Recombinant M-CSF can be administered safely to patients with metastatic cancer at doses that demonstrate biologic activity. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Sanda, M G AU - Yang, J C AU - Topalian, S L AU - Groves, E S AU - Childs, A AU - Belfort, R AU - de Smet, M D AU - Schwartzentruber, D J AU - White, D E AU - Lotze, M T AD - Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 1643 EP - 1649 VL - 10 IS - 10 SN - 0732-183X, 0732-183X KW - Recombinant Proteins KW - 0 KW - Macrophage Colony-Stimulating Factor KW - 81627-83-0 KW - Index Medicus KW - Infusions, Intravenous KW - Humans KW - Adult KW - Treatment Outcome KW - Recombinant Proteins -- adverse effects KW - Neoplasm Metastasis KW - Aged KW - Middle Aged KW - Recombinant Proteins -- administration & dosage KW - Male KW - Female KW - Neoplasms -- drug therapy KW - Macrophage Colony-Stimulating Factor -- administration & dosage KW - Macrophage Colony-Stimulating Factor -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73258423?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Intravenous+administration+of+recombinant+human+macrophage+colony-stimulating+factor+to+patients+with+metastatic+cancer%3A+a+phase+I+study.&rft.au=Sanda%2C+M+G%3BYang%2C+J+C%3BTopalian%2C+S+L%3BGroves%2C+E+S%3BChilds%2C+A%3BBelfort%2C+R%3Bde+Smet%2C+M+D%3BSchwartzentruber%2C+D+J%3BWhite%2C+D+E%3BLotze%2C+M+T&rft.aulast=Sanda&rft.aufirst=M&rft.date=1992-10-01&rft.volume=10&rft.issue=10&rft.spage=1643&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 - 1992-10-30 N1 - Date created - 1992-10-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Noncompetitive inhibition of N-methyl-D-aspartate by conantokin-G: evidence for an allosteric interaction at polyamine sites. AN - 73257409; 1328523 AB - Conantokins T and G are polypeptide toxins present in snails of the genus Conus. These substances were recently reported to act as N-methyl-D-aspartate (NMDA) antagonists. In the present study, we examined the possible mechanisms producing this antagonism. Conantokin-G inhibited spermine- and spermidine-stimulated [3H]MK-801 binding to extensively washed rat forebrain membranes in a noncompetitive manner with IC50 values of approximately 507 and approximately 946 nM, respectively. In contrast, glutamate-enhanced [3H]MK-801 binding was unaffected by conantokin-G concentrations of less than or equal to 20 microM. At concentrations greater than or equal to 5 microM, conantokin-G effected a modest, noncompetitive inhibition of glycine-stimulated [3H]MK-801 binding and also produced a small enhancement of basal [3H]MK-801 binding. Conantokin-G reduced (IC50 approximately 1.08 microM) the NMDA-stimulated accumulation of cyclic GMP in cerebellar granule cell cultures to basal values, but did not affect kainate-mediated increases in cyclic GMP. These findings indicate that conantokin-G acts as a noncompetitive NMDA antagonist through an allosteric inhibition of polyamine responses. The neurochemical profile of this polypeptide is distinct from previously described noncompetitive NMDA antagonists. JF - Journal of neurochemistry AU - Skolnick, P AU - Boje, K AU - Miller, R AU - Pennington, M AU - Maccecchini, M L AD - Laboratory of Neuroscience, NIDDK, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 1516 EP - 1521 VL - 59 IS - 4 SN - 0022-3042, 0022-3042 KW - Conotoxins KW - 0 KW - Mollusk Venoms KW - Peptides, Cyclic KW - Polyamines KW - N-Methylaspartate KW - 6384-92-5 KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - conotoxin GV KW - 93438-65-4 KW - Cyclic GMP KW - H2D2X058MU KW - Index Medicus KW - Osmolar Concentration KW - Animals KW - Dizocilpine Maleate -- metabolism KW - Prosencephalon -- metabolism KW - Dizocilpine Maleate -- antagonists & inhibitors KW - Granulocytes -- metabolism KW - Binding Sites KW - Cerebellum -- metabolism KW - Rats KW - Rats, Sprague-Dawley KW - Cerebellum -- cytology KW - Cyclic GMP -- metabolism KW - Male KW - Polyamines -- pharmacology KW - Mollusk Venoms -- pharmacology KW - N-Methylaspartate -- antagonists & inhibitors KW - Polyamines -- metabolism KW - Peptides, Cyclic -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73257409?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Noncompetitive+inhibition+of+N-methyl-D-aspartate+by+conantokin-G%3A+evidence+for+an+allosteric+interaction+at+polyamine+sites.&rft.au=Skolnick%2C+P%3BBoje%2C+K%3BMiller%2C+R%3BPennington%2C+M%3BMaccecchini%2C+M+L&rft.aulast=Skolnick&rft.aufirst=P&rft.date=1992-10-01&rft.volume=59&rft.issue=4&rft.spage=1516&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 - 1992-10-26 N1 - Date created - 1992-10-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Vimentin metaplasia in renal cortical tubules of preneoplastic, neoplastic, aging, and regenerative lesions of rats and humans. AN - 73252098; 1415487 AB - Vimentin expression was studied immunohistochemically in renal cortical tubules of untreated male rats of various ages, rats exposed to toxins (barbital sodium, folic acid) and carcinogens (streptozotocin, N-bis(2-hydroxypropyl)nitrosamine, barbital sodium, and in humans of various ages with or without renal epithelial tumors. Fetal, neonatal, and young adult rats did not express vimentin in renal cortical tubules. Regenerative renal tubular lesions from rats with aging nephropathy and from rats with toxic nephropathy both expressed vimentin. Mitogenic lesions induced by folic acid at 24 hours, however, were not immunoreactive for vimentin. Carcinogen-induced preneoplastic renal cortical tubular lesions in rats were most often focally immunoreactive whereas strong vimentin expression was found in almost all induced renal tumors. In kidneys of three children (younger than 2 years of age), vimentin was not found in renal cortical tubular cells except in rare individual cells in one case. Vimentin was abundant in basophilic regenerative tubules in kidneys of aged individuals, however. Most (7/10) human renal carcinomas and latent preneoplastic or neoplastic renal tubular lesions found incidentally at autopsy (2/4) showed vimentin expression. The authors suggest that the switching to vimentin expression in phenotypically normal renal cortical tubular cells in rats and humans, which do not usually express the intermediate filament protein vimentin, should be considered vimentin metaplasia. Vimentin expression is dissociated from increased cell proliferation in hyperplastic and neoplastic lesions, however. Instead the degree of dedifferentiation of the tubule cells and changes in phenotype were associated with vimentin expression. JF - The American journal of pathology AU - Ward, J M AU - Stevens, J L AU - Konishi, N AU - Kurata, Y AU - Uno, H AU - Diwan, B A AU - Ohmori, T AD - Tumor Pathology and Pathogenesis Section, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702-1201. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 955 EP - 964 VL - 141 IS - 4 SN - 0002-9440, 0002-9440 KW - Vimentin KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Rats KW - Animals, Newborn KW - Animals KW - Age Factors KW - Humans KW - Regeneration KW - Aged KW - Fetus -- metabolism KW - Male KW - Kidney Neoplasms -- metabolism KW - Vimentin -- metabolism KW - Kidney Tubules -- metabolism KW - Precancerous Conditions -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73252098?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Vimentin+metaplasia+in+renal+cortical+tubules+of+preneoplastic%2C+neoplastic%2C+aging%2C+and+regenerative+lesions+of+rats+and+humans.&rft.au=Ward%2C+J+M%3BStevens%2C+J+L%3BKonishi%2C+N%3BKurata%2C+Y%3BUno%2C+H%3BDiwan%2C+B+A%3BOhmori%2C+T&rft.aulast=Ward&rft.aufirst=J&rft.date=1992-10-01&rft.volume=141&rft.issue=4&rft.spage=955&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 - 1992-11-03 N1 - Date created - 1992-11-03 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Environ Health Perspect. 1991 Jun;93:233-46 [1773795] Acta Pathol Jpn. 1982 Jul;32(4):585-93 [7113698] Mutat Res. 1991 Jun;248(2):239-60 [2046683] IARC Sci Publ. 1990;(99):301-44 [2093652] Exp Pathol. 1990;40(4):301-12 [2098275] Carcinogenesis. 1990 Dec;11(12):2149-56 [2148284] Dev Biol. 1985 Apr;108(2):481-90 [2416612] Lab Invest. 1987 Jun;56(6):642-53 [2439772] Am J Pathol. 1987 Oct;129(1):1-8 [2444108] Biochem Biophys Res Commun. 1988 Dec 30;157(3):1316-22 [2462870] Acta Pathol Jpn. 1989 Nov;39(11):731-6 [2618660] FASEB J. 1989 Aug;3(10):2141-50 [2666230] Fundam Appl Toxicol. 1989 Aug;13(2):332-40 [2792600] Br J Cancer. 1978 Jul;38(1):1-23 [356869] J Histochem Cytochem. 1991 Jun;39(6):741-8 [1709656] Histochem J. 1991 Jan;23(1):13-21 [1938467] Prog Exp Tumor Res. 1991;33:1-20 [2028021] Histopathology. 1991 Apr;18(4):315-22 [2071090] J Cancer Res Clin Oncol. 1990;116(4):372-8 [2143998] Toxicol Lett. 1990 Sep;53(1-2):121-6 [2219151] Am J Clin Pathol. 1987 Sep;88(3):286-96 [2443000] Cancer Res. 1988 Apr 15;48(8):1996-2004 [2450643] Jpn J Cancer Res. 1989 Aug;80(8):771-7 [2511186] Histochemistry. 1989;90(6):489-96 [2715055] Virchows Arch B Cell Pathol Incl Mol Pathol. 1986;51(5):385-404 [2876545] Crit Rev Toxicol. 1988;19(2):147-83 [3069333] Histochemistry. 1988;89(1):81-90 [3366668] Lab Invest. 1968 Jul;19(1):92-6 [5671357] Am J Pathol. 1984 Feb;114(2):309-21 [6320650] Eur J Cell Biol. 1984 May;34(1):137-43 [6428888] Lab Invest. 1992 Apr;66(4):474-84 [1374823] Lab Invest. 1991 Jul;65(1):74-86 [1712875] Vet Pathol. 1989 Jan;26(1):6-10 [2913704] Crit Rev Toxicol. 1987;17(4):279-343 [3308322] J Cell Sci Suppl. 1987;8:293-312 [3332664] J Urol. 1971 Oct;106(4):503-6 [4330359] Lab Invest. 1983 Sep;49(3):317-26 [6193332] Lab Invest. 1984 May;50(5):552-9 [6201675] Histochemistry. 1983;77(3):365-94 [6345481] Cancer Res. 1991 Apr 1;51(7):1922-9 [2004377] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Identification of nitroxide radioprotectors. AN - 73251821; 1410280 AB - The nitroxide Tempol, a stable free radical, has recently been shown to protect mammalian cells against several forms of oxidative stress including radiation-induced cytotoxicity. To extend this observation, six additional water-soluble nitroxides with different structural features were evaluated for potential radioprotective properties using Chinese hamster V79 cells and clonogenic assays. Nitroxides (10 mM) were added 10 min prior to radiation exposure and full radiation dose-response curves were determined. In addition to Tempol, five of the six nitroxides afforded in vitro radioprotection. The best protectors were found to be the positively charged nitroxides, Tempamine and 3-aminomethyl-PROXYL, with protection factors of 2.3 and 2.4, respectively, compared with Tempol, which had a protection factor of 1.3. 3-Carboxy-PROXYL, a negatively charged nitroxide, provided minimal protection. DNA binding characteristics as studied by nonequilibrium dialysis of DNA with each of the nitroxides demonstrated that Tempamine and 3-amino-methyl-PROXYL bound more strongly to DNA than did Tempol. Since DNA is assumed to be the target of radiation-induced cytotoxicity, differences in protection may be explained by variabilities in affinity of the protector for the target. This study establishes nitroxides as a general class of new nonthiol radioprotectors and suggests other parameters that may be exploited to find even better nitroxide-induced radioprotection. JF - Radiation research AU - Hahn, S M AU - Wilson, L AU - Krishna, C M AU - Liebmann, J AU - DeGraff, W AU - Gamson, J AU - Samuni, A AU - Venzon, D AU - Mitchell, J B AD - Radiobiology Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 87 EP - 93 VL - 132 IS - 1 SN - 0033-7587, 0033-7587 KW - Cyclic N-Oxides KW - 0 KW - Protein Synthesis Inhibitors KW - Pyrrolidines KW - Radiation-Protective Agents KW - Spin Labels KW - tempamine KW - 14691-88-4 KW - 2,2,5,5-tetramethyl-1-pyrrolidinyloxy-3-carboxylic acid KW - 2154-68-9 KW - 3-cyano-2,2,5,5-tetramethyl-1-pyrrolidinyl-N-oxyl KW - 2154-70-3 KW - Triacetoneamine-N-Oxyl KW - 2896-70-0 KW - 3-carbamoyl-2,2,5,5-tetramethyl-1-pyrrolidinyl-N-oxyl KW - 4399-80-8 KW - 3-aminomethyl-2,2,5,5-tetramethyl-1-pyrrolidinyl-N-oxyl KW - 54606-49-4 KW - tempol KW - U78ZX2F65X KW - Index Medicus KW - Space life sciences KW - Animals KW - Protein Synthesis Inhibitors -- pharmacology KW - Cell Survival -- drug effects KW - Dose-Response Relationship, Radiation KW - Cell Survival -- radiation effects KW - Cell Line KW - Cricetinae KW - Cyclic N-Oxides -- pharmacology KW - Triacetoneamine-N-Oxyl -- pharmacology KW - Pyrrolidines -- pharmacology KW - Radiation-Protective Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73251821?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Identification+of+nitroxide+radioprotectors.&rft.au=Hahn%2C+S+M%3BWilson%2C+L%3BKrishna%2C+C+M%3BLiebmann%2C+J%3BDeGraff%2C+W%3BGamson%2C+J%3BSamuni%2C+A%3BVenzon%2C+D%3BMitchell%2C+J+B&rft.aulast=Hahn&rft.aufirst=S&rft.date=1992-10-01&rft.volume=132&rft.issue=1&rft.spage=87&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 - 1992-11-20 N1 - Date created - 1992-11-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Who will relapse? Symptoms of nicotine dependence predict long-term relapse after smoking cessation. AN - 73247482; 1401396 AB - Results of a prospective examination (N = 618) of factors associated with smoking relapse are reported. At 1-year follow-up, a modified version of the Fagerstrom Tolerance Questionnaire (Dependence Index; DI) and a measure of craving entered the logistic model (odds ratio of 2.7 [p less than .001]). At Year 2, only the DI entered the model (odds ratio of 2.2 [p less than .001]). The ability of signal detection analysis (SDA) to produce clinically useful decision rules was also examined. At Year 1, SDA produced 1 subgroup with a 25% nonrelapse rate and another with a 9% nonrelapse rate (odds ratio of 3.4 [p less than .001]). At Year 2, SDA produced 1 subgroup with a nonrelapse rate of 19% and another with a nonrelapse rate of 7% (odds ratio of 3.0 [p less than .001]). The use of signal detection methods may help clinicians to identify those at greater or lesser risk of relapse. JF - Journal of consulting and clinical psychology AU - Killen, J D AU - Fortmann, S P AU - Kraemer, H C AU - Varady, A AU - Newman, B AD - National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 797 EP - 801 VL - 60 IS - 5 SN - 0022-006X, 0022-006X KW - Nicotine KW - 6M3C89ZY6R KW - Index Medicus KW - Combined Modality Therapy KW - Behavior Therapy KW - Risk Factors KW - Humans KW - Adult KW - Recurrence KW - Male KW - Female KW - Smoking Cessation -- psychology KW - Substance Withdrawal Syndrome -- prevention & control KW - Nicotine -- adverse effects KW - Smoking -- adverse effects KW - Nicotine -- administration & dosage KW - Substance Withdrawal Syndrome -- psychology KW - Smoking -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73247482?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+consulting+and+clinical+psychology&rft.atitle=Who+will+relapse%3F+Symptoms+of+nicotine+dependence+predict+long-term+relapse+after+smoking+cessation.&rft.au=Killen%2C+J+D%3BFortmann%2C+S+P%3BKraemer%2C+H+C%3BVarady%2C+A%3BNewman%2C+B&rft.aulast=Killen&rft.aufirst=J&rft.date=1992-10-01&rft.volume=60&rft.issue=5&rft.spage=797&rft.isbn=&rft.btitle=&rft.title=Journal+of+consulting+and+clinical+psychology&rft.issn=0022006X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-12 N1 - Date created - 1992-11-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Conservation of mouse alpha A-crystallin promoter activity in chicken lens epithelial cells. AN - 73241701; 1404419 AB - Previous transfection experiments have shown that 162 base pairs (bp) of the 5' flanking sequence of the chicken alpha A-crystallin gene are required for promoter activity in primary chicken lens epithelial cells (PLE), while only 111 bp of the 5' flanking sequence are needed for activity of the mouse alpha A-crystallin promoter in transfected chicken PLE cells or in a SV40 T-antigen-transformed transfected mouse lens epithelial cell line (alpha TN4-1). The effect of site-directed mutations covering positions -111 to -34 of the mouse alpha A-crystallin promoter fused to the bacterial chloramphenicol acetyltransferase (CAT) gene was compared in transfected chicken PLE cells and mouse alpha TN4-1 cells; selected mutations were also examined in a nontransformed rabbit lens epithelial cell line (N/N1003A). In general, the same mutations reduced promoter activity in the transfected lens cells from all three species, although differences were noted. The mutations severely affected regions -111/-106 and -69/-40 regions in all the transfected cells examined; by contrast, mutations at positions -105/-99 and -87/-70 had a somewhat greater effect in the chicken PLE than the mouse alpha TN4-1 cells, while mutations of the -93/-88 sequence reduced expression in the alpha TN4-1 but not the PLE cells. A partial cDNA with sequence similarity to alpha A-CRYPB1 of the mouse has been isolated from a chicken lens library; mouse alpha A-CRYBP1 is a putative transcription factor which binds to the -66/-55 sequence of the mouse alpha A-crystallin promoter.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Journal of molecular evolution AU - Donovan, D M AU - Sax, C M AU - Klement, J F AU - Li, X AU - Chepelinsky, A B AU - Piatigorsky, J AD - Laboratory of Molecular and Developmental Biology, NEI, NIH, Bethesda, MD 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 337 EP - 345 VL - 35 IS - 4 SN - 0022-2844, 0022-2844 KW - Crystallins KW - 0 KW - Recombinant Fusion Proteins KW - Index Medicus KW - Animals KW - Plasmids -- genetics KW - Chick Embryo KW - Amino Acid Sequence KW - Mice KW - Cloning, Molecular KW - Mutagenesis, Site-Directed KW - Polymerase Chain Reaction KW - Base Sequence KW - Transfection KW - Blotting, Southern KW - Cells, Cultured KW - Molecular Sequence Data KW - Lens, Crystalline -- metabolism KW - Lens, Crystalline -- cytology KW - Recombinant Fusion Proteins -- genetics KW - Crystallins -- chemistry KW - Promoter Regions, Genetic -- genetics KW - Crystallins -- genetics KW - Recombinant Fusion Proteins -- chemistry KW - Gene Expression Regulation -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73241701?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Conservation+of+mouse+alpha+A-crystallin+promoter+activity+in+chicken+lens+epithelial+cells.&rft.au=Donovan%2C+D+M%3BSax%2C+C+M%3BKlement%2C+J+F%3BLi%2C+X%3BChepelinsky%2C+A+B%3BPiatigorsky%2C+J&rft.aulast=Donovan&rft.aufirst=D&rft.date=1992-10-01&rft.volume=35&rft.issue=4&rft.spage=337&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 - 1992-10-26 N1 - Date created - 1992-10-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pelvic radioiodine uptake in a rectal wall teratoma after thyroidectomy for papillary carcinoma. AN - 73232268; 1403156 AB - A 30-yr-old woman with previously resected papillary thyroid carcinoma was found to have a pelvic lesion which concentrated radioiodine. By performing simultaneous 131I whole-body and 99mTc-methylene diphosphonate bone scans, we found the lesion to be in soft tissue between the sacrum and bladder. Radioiodine therapy was postponed so that the lesion, a benign teratoma of the rectal wall, could be surgically removed. Prior to laparotomy, the patient received a second tracer dose of 131I so that the lesion could be located at surgery with a hand-held gamma detector. A postoperative whole-body 131I scan confirmed that the lesion had been removed, thus reducing the absorbed radiation that would have been received by the ovaries during radioiodine therapy. Although the lesion contained both thyroid and gastric epithelium, accumulated 131I was limited to the area with thyroid follicles. JF - Journal of nuclear medicine : official publication, Society of Nuclear Medicine AU - Lakshmanan, M AU - Reynolds, J C AU - Del Vecchio, S AU - Merino, M J AU - Norton, J A AU - Robbins, J AD - Clinical Endocrinology Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 1848 EP - 1850 VL - 33 IS - 10 SN - 0161-5505, 0161-5505 KW - Iodine Radioisotopes KW - 0 KW - Technetium Tc 99m Medronate KW - X89XV46R07 KW - Index Medicus KW - Thyroidectomy KW - Intraoperative Care KW - Humans KW - Adult KW - Bone and Bones -- diagnostic imaging KW - Female KW - Radionuclide Imaging KW - Rectal Neoplasms -- diagnostic imaging KW - Neoplasms, Multiple Primary -- diagnostic imaging KW - Carcinoma, Papillary -- surgery KW - Dermoid Cyst -- diagnostic imaging KW - Thyroid Neoplasms -- surgery KW - Sigmoid Neoplasms -- diagnostic imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73232268?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+nuclear+medicine+%3A+official+publication%2C+Society+of+Nuclear+Medicine&rft.atitle=Pelvic+radioiodine+uptake+in+a+rectal+wall+teratoma+after+thyroidectomy+for+papillary+carcinoma.&rft.au=Lakshmanan%2C+M%3BReynolds%2C+J+C%3BDel+Vecchio%2C+S%3BMerino%2C+M+J%3BNorton%2C+J+A%3BRobbins%2C+J&rft.aulast=Lakshmanan&rft.aufirst=M&rft.date=1992-10-01&rft.volume=33&rft.issue=10&rft.spage=1848&rft.isbn=&rft.btitle=&rft.title=Journal+of+nuclear+medicine+%3A+official+publication%2C+Society+of+Nuclear+Medicine&rft.issn=01615505&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 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Molecular and genetic analysis of liver oncogenesis in transforming growth factor alpha transgenic mice. AN - 73230037; 1394122 AB - Overexpression of a transforming growth factor alpha (TGF-alpha) transgene induced the development of liver tumors in 69 of 93 (74%) adult male mice. To identify factors associated with oncogenesis, liver tumors from transgenic animals were characterized at the molecular level. TGF-alpha RNA transcripts were elevated in 17 of 25 (68%) liver tumors, relative to adjacent nontumorous tissue. Expression of the endogenous c-myc and insulin-like growth factor II genes was enhanced in 7 of 19 (37%) and 12 of 16 (75%) tumors, respectively. In contrast, epidermal growth factor receptor RNA levels were unchanged or reduced in all liver tumors, and mutations were not detected in either the Ha-ras or Ki-ras genes. The occurrence of liver tumors in castrated TGF-alpha transgenic mice was reduced about 7-fold, while in ovariectomized transgenic animals the incidence was increased about 6-fold. The progeny of a cross between CD1-derived TGF-alpha transgenic (MT42) and C57BL/6 mice exhibited no reduction in tumor burden (83%); however, the incidence of tumor formation in MT42 x FVB/N offspring was substantially lower (19%). We conclude that in these transgenic mice TGF-alpha promotes tumor formation and appears to play a major role in tumor progression. Moreover, other factors that may collaborate in TGF-alpha-induced hepatocarcinogenesis include c-myc, insulin-like growth factor II, sex hormones, and the genetic background upon which the transgene operates. JF - Cancer research AU - Takagi, H AU - Sharp, R AU - Hammermeister, C AU - Goodrow, T AU - Bradley, M O AU - Fausto, N AU - Merlino, G AD - Laboratory of Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/10/01/ PY - 1992 DA - 1992 Oct 01 SP - 5171 EP - 5177 VL - 52 IS - 19 SN - 0008-5472, 0008-5472 KW - Ha-ras KW - IGF-II KW - Ki-ras KW - TGF-&agr; KW - c-myc KW - DNA, Neoplasm KW - 0 KW - Gonadal Steroid Hormones KW - Growth Substances KW - RNA, Neoplasm KW - Transforming Growth Factor alpha KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Disease Models, Animal KW - Mice KW - RNA, Neoplasm -- genetics KW - Mice, Transgenic KW - Growth Substances -- physiology KW - Phenotype KW - Base Sequence KW - Gene Expression -- genetics KW - DNA -- genetics KW - Molecular Sequence Data KW - Mice, Inbred C57BL KW - DNA, Neoplasm -- genetics KW - Gonadal Steroid Hormones -- physiology KW - Female KW - Male KW - Liver Neoplasms, Experimental -- genetics KW - Oncogenes -- genetics KW - Transforming Growth Factor alpha -- genetics KW - Liver Neoplasms, Experimental -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73230037?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Molecular+and+genetic+analysis+of+liver+oncogenesis+in+transforming+growth+factor+alpha+transgenic+mice.&rft.au=Takagi%2C+H%3BSharp%2C+R%3BHammermeister%2C+C%3BGoodrow%2C+T%3BBradley%2C+M+O%3BFausto%2C+N%3BMerlino%2C+G&rft.aulast=Takagi&rft.aufirst=H&rft.date=1992-10-01&rft.volume=52&rft.issue=19&rft.spage=5171&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 - 1992-10-29 N1 - Date created - 1992-10-29 N1 - Date revised - 2017-01-13 N1 - Gene symbol - Ha-ras; IGF-II; Ki-ras; TGF-&agr;; c-myc N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Stimulus deprivation increases pineal Gs alpha and G beta. AN - 73226351; 1402887 AB - Denervation and other forms of stimulus deprivation cause an increase in the magnitude of subsequent responses, a phenomenon commonly referred to as denervation supersensitivity. This has been well demonstrated with the cyclic AMP response to norepinephrine in the pineal gland. In the present report, we address the question of whether stimulus deprivation alters alpha and beta subunits of the GTP binding regulatory protein that stimulates adenylyl cyclase activity (Gs). Stimulus deprivation of the pineal gland was produced by denervation (superior cervical ganglionectomy), decentralization of the superior cervical ganglia, or by exposure of the animal to continuous lighting. All increased both the alpha and beta subunits of Gs (Gs alpha and G beta) by up to fourfold, as estimated using semiquantitative western blot technology. These effects were detectable after 1 day of stimulus deprivation and were sustained for 2 weeks. The stimulatory effects of constant light-induced stimulus deprivation were also apparent by measuring cholera toxin-dependent ADP-ribosylation of Gs alpha, which revealed a four-fold increase in the amount of labeled substrate. The results of in vivo studies were confirmed with in vitro studies, which demonstrated a spontaneous increase in both Gs alpha and G beta during 72 h of organ culture. The constant light-induced increases in both Gs alpha and G beta were prevented by continuous administration of isoproterenol (0.3 mg/kg/day), supporting the suggestion that adrenergic stimulation controls the levels of Gs alpha and G beta. These studies indicate that stimulus deprivation increases both Gs alpha and G beta.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Journal of neurochemistry AU - Babila, T AU - Klein, D C AD - Section on Neuroendocrinology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 1356 EP - 1362 VL - 59 IS - 4 SN - 0022-3042, 0022-3042 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 - Isoproterenol KW - L628TT009W KW - Index Medicus KW - Rats KW - Animals KW - Rats, Sprague-Dawley KW - Ganglionectomy KW - Cholera Toxin -- pharmacology KW - Adenosine Diphosphate Ribose -- metabolism KW - Organ Culture Techniques KW - Male KW - Isoproterenol -- pharmacology KW - Pineal Gland -- metabolism KW - GTP-Binding Proteins -- metabolism KW - Ganglia, Sympathetic -- physiology KW - GTP-Binding Proteins -- chemistry KW - Light UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73226351?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Stimulus+deprivation+increases+pineal+Gs+alpha+and+G+beta.&rft.au=Babila%2C+T%3BKlein%2C+D+C&rft.aulast=Babila&rft.aufirst=T&rft.date=1992-10-01&rft.volume=59&rft.issue=4&rft.spage=1356&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 - 1992-10-26 N1 - Date created - 1992-10-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inflammatory and toxic myopathies. AN - 73224375; 1327303 AB - The major advances in the immunopathogenesis and treatment of inflammatory myopathies, and the main criteria that distinguish polymyositis (PM) from dermatomyositis (DM) or inclusion-body myositis (IBM) are presented. The origin and implications of the amyloid and ubiquitin deposits found within the vacuolated fibers of patients with IBM are considered. The pathogenesis of human immunodeficiency virus (HIV) and human T-cell lymphotrophic virus (HTLV)-I-associated PM is presented, and the role of retroviruses in triggering PM, even in the absence of detectable viral genome within the muscle fibers, is discussed. In addition, three toxic myopathies with distinct morphologic, biochemical, or molecular characteristics, caused by zidovudine [azidothymidine (AZT) myopathy], the cholesterol-lowering-agent myopathy (CLAM), and the combination of blocking agents with corticosteroids are presented. JF - Current opinion in neurology and neurosurgery AU - Dalakas, M C AD - Neuromuscular Diseases Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 645 EP - 654 VL - 5 IS - 5 SN - 0951-7383, 0951-7383 KW - Adrenal Cortex Hormones KW - 0 KW - Hypolipidemic Agents KW - Zidovudine KW - 4B9XT59T7S KW - Pancuronium KW - J76UF062FS KW - Index Medicus KW - AIDS/HIV KW - Pancuronium -- adverse effects KW - Diagnosis, Differential KW - Zidovudine -- adverse effects KW - Humans KW - Biopsy KW - Muscles -- pathology KW - Hypolipidemic Agents -- adverse effects KW - Adrenal Cortex Hormones -- adverse effects KW - Dermatomyositis -- chemically induced KW - Dermatomyositis -- pathology KW - Polymyositis -- pathology KW - Polymyositis -- etiology KW - Polymyositis -- chemically induced KW - Inclusion Bodies -- ultrastructure KW - Dermatomyositis -- etiology KW - Myositis -- pathology KW - Myositis -- chemically induced KW - Myositis -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73224375?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Inflammatory+and+toxic+myopathies.&rft.au=Dalakas%2C+M+C&rft.aulast=Dalakas&rft.aufirst=M&rft.date=1992-10-01&rft.volume=5&rft.issue=5&rft.spage=645&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 - 1992-11-20 N1 - Date created - 1992-11-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - N omega-amino-L-arginine, an inhibitor of nitric oxide synthase, raises vascular resistance but increases mortality rates in awake canines challenged with endotoxin. AN - 73224000; 1383377 AB - Inhibitors of nitric oxide synthase (NOS) have been reported to increase mean arterial pressure in animal models of sepsis and recently have been given to patients in septic shock. However, controlled studies to determine the effects of these agents on cardiovascular function and survival in awake animal models of sepsis have not been reported. To examine the therapeutic potential of NOS inhibition in septic shock, we challenged canines with endotoxin (2 or 4 mg/kg i.v.) and treated them with either normal saline or N omega-amino-L-arginine (10 or 1 mg/kg/h), the most specific inhibitor available for the isoform of NOS implicated in septic shock. Endotoxemic animals treated with N omega-amino-L-arginine (n = 11) had higher systemic and pulmonary vascular resistance indices (SVRI and PVRI, p less than or equal to 0.033) and decreased heart rates (p = 0.009), cardiac indices (CI, p = 0.01), oxygen delivery indices (p = 0.027), and oxygen consumption indices (p = 0.046) compared with controls (n = 6). Moreover, N omega-amino-L-arginine increased mortality rates after endotoxin challenge (10 of 11 vs. 1 of 6 controls, p = 0.005). Administration of L-arginine did not improve survival or alter the cardiopulmonary effects of N omega-amino-L-arginine, which suggests that inhibition of NOS may not have been competitive. In normal animals, N omega-amino-L-arginine alone (n = 3) increased SVRI (p = 0.0008) and mean arterial pressure (p = 0.016), and decreased CI (p = 0.01) compared with saline-treated controls (n = 3), but, at the high dose, also produced neuromuscular rigidity and seizure-like activity that was not apparent in the endotoxemic model. Thus, the mortality rate from endotoxemia increased either because of NOS inhibition per se or because of properties unique to N omega-amino-L-arginine, or both. JF - The Journal of experimental medicine AU - Cobb, J P AU - Natanson, C AU - Hoffman, W D AU - Lodato, R F AU - Banks, S AU - Koev, C A AU - Solomon, M A AU - Elin, R J AU - Hosseini, J M AU - Danner, R L AD - Department of Critical Care Medicine, Warren G. Magnusen Clinical Center, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/10/01/ PY - 1992 DA - 1992 Oct 01 SP - 1175 EP - 1182 VL - 176 IS - 4 SN - 0022-1007, 0022-1007 KW - Endotoxins KW - 0 KW - N(G)-aminoarginine KW - 57444-72-1 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 - Animals KW - Oxygen Consumption -- drug effects KW - Heart Rate -- drug effects KW - Analysis of Variance KW - Pulmonary Circulation -- drug effects KW - Dogs KW - Heart -- drug effects KW - Time Factors KW - Amino Acid Oxidoreductases -- antagonists & inhibitors KW - Arginine -- toxicity KW - Vascular Resistance -- drug effects KW - Shock, Septic -- physiopathology KW - Shock, Septic -- blood KW - Endotoxins -- toxicity KW - Arginine -- analogs & derivatives KW - Arginine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73224000?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=N+omega-amino-L-arginine%2C+an+inhibitor+of+nitric+oxide+synthase%2C+raises+vascular+resistance+but+increases+mortality+rates+in+awake+canines+challenged+with+endotoxin.&rft.au=Cobb%2C+J+P%3BNatanson%2C+C%3BHoffman%2C+W+D%3BLodato%2C+R+F%3BBanks%2C+S%3BKoev%2C+C+A%3BSolomon%2C+M+A%3BElin%2C+R+J%3BHosseini%2C+J+M%3BDanner%2C+R+L&rft.aulast=Cobb&rft.aufirst=J&rft.date=1992-10-01&rft.volume=176&rft.issue=4&rft.spage=1175&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 - 1992-11-02 N1 - Date created - 1992-11-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: N Engl J Med. 1975 Nov 6;293(19):970-6 [1101063] Am J Physiol. 1966 Apr;210(4):817-20 [5906810] Lancet. 1991 Dec 21-28;338(8782-8783):1555-7 [1683974] Proc Natl Acad Sci U S A. 1990 Dec;87(24):10043-7 [1702214] Epilepsy Res. 1991 Mar;8(2):142-8 [1712286] Lancet. 1991 Dec 21-28;338(8782-8783):1557-8 [1720856] Br J Pharmacol. 1991 Apr;102(4):967-73 [1855125] Am J Physiol. 1991 Aug;261(2 Pt 2):R323-8 [1877690] Br J Pharmacol. 1991 May;103(1):1218-24 [1908734] Br J Pharmacol. 1990 Dec;101(4):815-20 [2085706] Nature. 1990 May 10;345(6271):161-3 [2110626] Ann Intern Med. 1990 Aug 1;113(3):227-42 [2197912] Chest. 1990 Dec;98(6):1480-7 [2245691] Proc Natl Acad Sci U S A. 1990 May;87(9):3629-32 [2333306] Biochem Biophys Res Commun. 1989 Apr 28;160(2):881-6 [2719705] Am J Physiol. 1988 Mar;254(3 Pt 2):H558-69 [3279822] Surgery. 1986 Feb;99(2):140-53 [3511560] Crit Care Med. 1985 Feb;13(2):85-90 [3967509] N Engl J Med. 1982 Nov 11;307(20):1225-30 [6752708] Lancet. 1992 Feb 15;339(8790):435 [1346701] Eur J Pharmacol. 1991 Aug 6;200(2-3):375-6 [1664333] Br J Pharmacol. 1991 May;103(1):1047-52 [1678981] J Natl Cancer Inst. 1990 May 2;82(9):726-8 [1691302] Biochem Biophys Res Commun. 1991 May 15;176(3):1136-41 [1710109] Epilepsy Res. 1991 Mar;8(2):134-41 [1712285] Biochem Biophys Res Commun. 1991 Aug 15;178(3):823-9 [1714727] Br J Pharmacol. 1991 Sep;104(1):21-4 [1723915] J Appl Physiol (1985). 1991 May;70(5):2155-63 [1864798] Biochem Biophys Res Commun. 1991 Aug 15;178(3):1135-40 [1872835] Crit Care Med. 1991 Sep;19(9):1146-51 [1884613] J Clin Invest. 1991 Jun;87(6):1964-8 [2040689] Biochem Biophys Res Commun. 1991 Jun 14;177(2):828-33 [2049105] J Natl Cancer Inst. 1990 May 2;82(9):772-6 [2109093] Biochem Biophys Res Commun. 1990 Apr 30;168(2):458-65 [2159292] Am J Physiol. 1990 Oct;259(4 Pt 2):H1038-43 [2221111] Biochem Biophys Res Commun. 1990 Nov 15;172(3):1132-8 [2244897] Biochem Biophys Res Commun. 1990 Mar 30;167(3):1037-43 [2322257] Biochem Biophys Res Commun. 1990 Jul 16;170(1):96-103 [2372300] J Exp Med. 1989 Mar 1;169(3):823-32 [2647895] Proc Natl Acad Sci U S A. 1988 Nov;85(22):8664-7 [3263652] Nature. 1987 Jun 11-17;327(6122):524-6 [3495737] Crit Care Med. 1987 Oct;15(10):923-9 [3652707] J Clin Invest. 1986 Jul;78(1):259-70 [3722379] J Pharmacol Exp Ther. 1991 Jun;257(3):1208-15 [1646327] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phase I study of continuous-infusion soluble CD4 as a single agent and in combination with oral dideoxyinosine therapy in children with symptomatic human immunodeficiency virus infection. AN - 73222934; 1357124 AB - To determine the safety and pharmacokinetics of recombinant soluble CD4 (sCD4) administered by continuous intravenous infusion to children with symptomatic human immunodeficiency virus type 1 infection, we conducted a phase I study at the National Cancer Institute. Three dose levels of sCD4 were evaluated: 100, 300, and 1000 micrograms/kg per day. After an initial 12 weeks of treatment with sCD4 alone, dideoxyinosine at a dose of 90 mg/m2 every 8 hours was added and subjects were observed for an additional 12 weeks. Combination therapy was continued in patients in whom it was well tolerated. In addition to toxicity and pharmacokinetic monitoring, surrogate markers of antiviral activity were evaluated. Eleven children were enrolled in the study. During the 12 weeks of treatment with sCD4 alone, and during subsequent sCD4 plus dideoxyinosine combination therapy, no significant toxic reaction attributable to sCD4 or dideoxyinosine was encountered. Low-level anti-CD4 antibodies developed in two patients. Steady-state sCD4 levels increased proportionately at higher doses. The CD4 cell counts and serum p24 antigen levels did not provide evidence of antiviral activity. We conclude that sCD4 was well tolerated at doses up to 1000 micrograms/kg per day when administered by continuous intravenous infusion; however, evidence of in vivo antiviral activity was not observed in this study. JF - The Journal of pediatrics AU - Husson, R N AU - Chung, Y AU - Mordenti, J AU - Butler, K M AU - Chen, S AU - Duliege, A M AU - Brouwers, P AU - Jarosinski, P AU - Mueller, B U AU - Ammann, A AD - Pediatric Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 627 EP - 633 VL - 121 IS - 4 SN - 0022-3476, 0022-3476 KW - Antigens, CD4 KW - 0 KW - Antigens, Viral KW - Recombinant Proteins KW - Didanosine KW - K3GDH6OH08 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Infusions, Intravenous KW - Humans KW - Recombinant Proteins -- pharmacokinetics KW - Child KW - CD4-Positive T-Lymphocytes KW - Leukocyte Count KW - Child, Preschool KW - Drug Therapy, Combination KW - Infant KW - Drug Evaluation KW - Treatment Outcome KW - Adolescent KW - Recombinant Proteins -- therapeutic use KW - Recombinant Proteins -- administration & dosage KW - Male KW - Antigens, Viral -- blood KW - Female KW - Didanosine -- therapeutic use KW - Acquired Immunodeficiency Syndrome -- immunology KW - Didanosine -- administration & dosage KW - Antigens, CD4 -- therapeutic use KW - Antigens, CD4 -- administration & dosage KW - Acquired Immunodeficiency Syndrome -- drug therapy KW - Didanosine -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73222934?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Phase+I+study+of+continuous-infusion+soluble+CD4+as+a+single+agent+and+in+combination+with+oral+dideoxyinosine+therapy+in+children+with+symptomatic+human+immunodeficiency+virus+infection.&rft.au=Husson%2C+R+N%3BChung%2C+Y%3BMordenti%2C+J%3BButler%2C+K+M%3BChen%2C+S%3BDuliege%2C+A+M%3BBrouwers%2C+P%3BJarosinski%2C+P%3BMueller%2C+B+U%3BAmmann%2C+A&rft.aulast=Husson&rft.aufirst=R&rft.date=1992-10-01&rft.volume=121&rft.issue=4&rft.spage=627&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 - 1992-11-13 N1 - Date created - 1992-11-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dose-dependent smooth muscle cell proliferation induced by thermal injury with pulsed infrared lasers. AN - 73221222; 1394931 AB - Recently, laser-heated and radio frequency-heated balloon angioplasty techniques have been proposed as a means to treat or minimize dissection and elastic recoil but have been associated with a high rate of clinical restenosis. Similarly, pulsed laser angioplasty techniques proposed to minimize thermal injury while ablating obstructing atheroma have failed to reduce clinical restenosis. Because "hot balloon" and pulsed laser angioplasty create both mechanical and thermal injury, it has been difficult to discern the cause of the smooth muscle cell (SMC) proliferation resulting in restenosis and whether such magnitude of proliferation is predictable and dose related. This study was undertaken to explore these issues. Localized thermal lesions accompanying efficient ablation were created with a pulsed Tm:YAG laser in nine rabbit aortas, which consistently led to a focal proliferation of SMC that filled the ablated region by 4 weeks. Transcutaneous Ho:YAG pulsed laser irradiation at multiple independent sites of 24 central rabbit ear arteries without ablation led to brief approximately 30 degrees C thermal transients and thermal damage to the artery wall resulting in significant neointimal proliferation by 3 weeks and a mean cross-sectional narrowing of 59 +/- 17% at a dose of 390 mJ/mm2. Acute and chronic responses to varying total energy deposition were studied by histology after the rabbits were killed at 2 hours to 4 weeks. Arterial segments midway between laser injuries were unaffected and served as internal controls. Neointimal proliferation at 3 weeks after laser injury exhibited a clear dose dependence. Mean cross-sectional narrowing increased from 34 +/- 10% to 85 +/- 15% as laser fluence increased from 240 mJ/cm2 to 640 mJ/cm2 (r = 0.84). Similarly, cross-sectional narrowing caused by SMC neointimal proliferation increased from 20 +/- 10% to 77 +/- 17% for a fixed surface irradiation as the depth of the most superficial arterial media decreased from 600 microns to 330 microns (r = 0.94). Thermal injury to the arterial wall is a potent stimulus for SMC proliferation and may necessitate reduction in laser or thermal energy used for angioplasty. Moreover, a dose-response relation exists between the degree of thermal injury and SMC proliferative response. Hence, this technique could be used as a practical model of restenosis suitable for screening therapies for inhibition of SMC proliferation. JF - Circulation AU - Douek, P C AU - Correa, R AU - Neville, R AU - Unger, E F AU - Shou, M AU - Banai, S AU - Ferrans, V J AU - Epstein, S E AU - Leon, M B AU - Bonner, R F AD - National Center for Research Resources, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md. 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 1249 EP - 1256 VL - 86 IS - 4 SN - 0009-7322, 0009-7322 KW - Abridged Index Medicus KW - Index Medicus KW - Aorta -- radiation effects KW - Animals KW - Ear -- blood supply KW - Arteries -- radiation effects KW - Aorta -- pathology KW - Rabbits KW - Dose-Response Relationship, Radiation KW - Arteries -- pathology KW - Cell Division -- radiation effects KW - Burns -- pathology KW - Infrared Rays KW - Muscle, Smooth, Vascular -- radiation effects KW - Muscle, Smooth, Vascular -- pathology KW - Laser Therapy -- methods KW - Laser Therapy -- adverse effects KW - Burns -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73221222?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Circulation&rft.atitle=Dose-dependent+smooth+muscle+cell+proliferation+induced+by+thermal+injury+with+pulsed+infrared+lasers.&rft.au=Douek%2C+P+C%3BCorrea%2C+R%3BNeville%2C+R%3BUnger%2C+E+F%3BShou%2C+M%3BBanai%2C+S%3BFerrans%2C+V+J%3BEpstein%2C+S+E%3BLeon%2C+M+B%3BBonner%2C+R+F&rft.aulast=Douek&rft.aufirst=P&rft.date=1992-10-01&rft.volume=86&rft.issue=4&rft.spage=1249&rft.isbn=&rft.btitle=&rft.title=Circulation&rft.issn=00097322&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-13 N1 - Date created - 1992-11-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pesticides and non-Hodgkin's lymphoma. AN - 73219755; 1394159 AB - The incidence of non-Hodgkin's lymphoma (NHL) has increased over 50% in the last 15 years. This paper reviews the possible role of pesticides in this increase. While small increases in risk of NHL among farmers have been observed in general occupational surveys, recent studies focusing on specific pesticides have observed much larger risks. Frequent use of phenoxyacetic acid herbicides, in particular, 2,4-dichlorophenoxyacetic acid, has been associated with 2- to 8-fold increases of NHL in studies conducted in Sweden, Kansas, Nebraska, Canada, and elsewhere. Canine malignant lymphoma has also been associated with dog owner use of 2,4-dichlorophenoxyacetic acid and commercial lawn pesticide treatments. There are much fewer data linking NHL to other types of pesticides, but triazine herbicides, organophosphate insecticides, fungicides, and fumigants have also been associated with increased risk of NHL. Pesticide exposures are not limited to agricultural populations but are widespread in the general population through use on lawns, golf courses, rights-of-way, and elsewhere. Since the use of pesticides, particularly phenoxy herbicides, has increased dramatically preceding and during the time period in which the incidence of NHL has increased, they could have contributed to the rising incidence of NHL. JF - Cancer research AU - Zahm, S H AU - Blair, A AD - Occupational Studies Section, National Cancer Institute, Rockville, Maryland 20892. Y1 - 1992/10/01/ PY - 1992 DA - 1992 Oct 01 SP - 5485s EP - 5488s VL - 52 IS - 19 Suppl SN - 0008-5472, 0008-5472 KW - Pesticides KW - 0 KW - Index Medicus KW - Humans KW - Lymphoma, Non-Hodgkin -- epidemiology KW - Agricultural Workers' Diseases -- epidemiology KW - Agricultural Workers' Diseases -- chemically induced KW - Lymphoma, Non-Hodgkin -- chemically induced KW - Pesticides -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73219755?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Pesticides+and+non-Hodgkin%27s+lymphoma.&rft.au=Zahm%2C+S+H%3BBlair%2C+A&rft.aulast=Zahm&rft.aufirst=S&rft.date=1992-10-01&rft.volume=52&rft.issue=19+Suppl&rft.spage=5485s&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 - 1992-10-29 N1 - Date created - 1992-10-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Monovalent immunotoxin containing truncated form of Pseudomonas exotoxin as potent antitumor agent. AN - 73219586; 1394141 AB - Recombinant truncated forms of Pseudomonas exotoxin A that lack the cell binding domain of Pseudomonas exotoxin A were coupled to an F(ab') fragment of a monoclonal antibody HB21 directed against the human transferrin receptor. One of these was NlysPE40. The other, NlysPE38QQR, has two amino groups on residues near the NH2-terminus and has no amino groups near the COOH-terminus. The proteins were linked by a stable thioether bond that connected the sulfhydryl group present in the hinge region of the antibody fragment to an amino group on the toxin. The F(ab')-PE40 immunotoxin, containing NlysPE40, exhibited potent cytotoxic activity on human carcinoma cell lines with a concentration of immunotoxin at which isotope incorporation falls by 50% when compared to nontreated cells (ID50) of 5.3 pM (0.5 ng/ml) on both the epidermoid carcinoma A431 and on the colon carcinoma Colo205. Immunotoxins made with whole antibody were considerably less active, with an ID50 of 15.9 pM (3.1 ng/ml) on these cell lines. F(ab')-PE38QQR, the immunotoxin containing NlysPE38QQR, was found to be the most active agent with an ID50 of 1.05 pM (0.1 ng/ml) on A431 cells. The greater cytotoxicity of immunotoxins containing fragmented antibody was probably due to the higher binding affinity of F(ab') conjugates in comparison to whole antibody conjugates to the transferrin receptor. The increase in cytotoxic activity of the immunotoxin made with NlysPE38QQR than that with NlysPE40 may reflect selective coupling of the toxin through NH2-terminal amino groups. The monovalent and divalent immunotoxins had dose-dependent antitumor effects on human epidermoid carcinoma xenografts in nude mice. A431 tumors completely regressed in all animals at a total dose of 105 pmol (10 micrograms) of F(ab')-PE38QQR and of 154 pmol (30 micrograms) of IgG-PE38QQR. Furthermore, the F(ab') immunotoxin was less toxic to mice than the conjugate containing IgG (840 pmol or 80 micrograms of total dose causing measurable adverse effects versus 208 pmol or 40 micrograms, respectively). Thus, a truncated Pseudomonas exotoxin A molecule coupled to the F(ab') fragment of an antibody is more active and less toxic in mice than an immunotoxin made with a whole antibody. Therefore, the therapeutic index for the monovalent immunotoxin is about four times better than that for the divalent immunotoxin. JF - Cancer research AU - Debinski, W AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1992/10/01/ PY - 1992 DA - 1992 Oct 01 SP - 5379 EP - 5385 VL - 52 IS - 19 SN - 0008-5472, 0008-5472 KW - Antibodies, Monoclonal KW - 0 KW - Antineoplastic Agents KW - Bacterial Toxins KW - Exotoxins KW - Immunoglobulin Fragments KW - Immunotoxins KW - Peptide Fragments KW - Receptors, Transferrin 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 - Neoplasm Transplantation KW - Animals KW - Immunoglobulin Fragments -- administration & dosage KW - Antibodies, Monoclonal -- metabolism KW - Humans KW - Immunoglobulin Fragments -- metabolism KW - Mice, Nude KW - Mice KW - Neoplasms, Experimental -- drug therapy KW - Neoplasms, Experimental -- pathology KW - Female KW - Antibodies, Monoclonal -- administration & dosage KW - Receptors, Transferrin -- metabolism KW - Peptide Fragments -- metabolism KW - Exotoxins -- pharmacology KW - Peptide Fragments -- pharmacology KW - Antineoplastic Agents -- metabolism KW - Exotoxins -- metabolism KW - Immunotoxins -- metabolism KW - Immunotoxins -- administration & dosage KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73219586?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Monovalent+immunotoxin+containing+truncated+form+of+Pseudomonas+exotoxin+as+potent+antitumor+agent.&rft.au=Debinski%2C+W%3BPastan%2C+I&rft.aulast=Debinski&rft.aufirst=W&rft.date=1992-10-01&rft.volume=52&rft.issue=19&rft.spage=5379&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 - 1992-10-29 N1 - Date created - 1992-10-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Myalgia and elevated creatine kinase activity associated with subcutaneous injections of diluent. AN - 73216396; 1403405 AB - A 16-year-old boy with short stature and mild primary hypothyroidism received subcutaneous injections of either recombinant human growth hormone or placebo in diluent that contained glycerol and m-cresol as a preservative. While he was receiving the study drug, myalgia developed and serum creatine kinase values were elevated. Both resolved when injections were stopped and recurred when injections of diluent alone were given. The myalgia and elevated creatine kinase activity were apparently caused by a component of the diluent. JF - The Journal of pediatrics AU - Bach, M A AU - Blum, D M AU - Rose, S R AU - Charnas, L R AD - Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 650 EP - 651 VL - 121 IS - 4 SN - 0022-3476, 0022-3476 KW - Cresols KW - 0 KW - Preservatives, Pharmaceutical KW - Growth Hormone KW - 9002-72-6 KW - Creatine Kinase KW - EC 2.7.3.2 KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Growth Hormone -- administration & dosage KW - Injections, Subcutaneous KW - Adolescent KW - Male KW - Creatine Kinase -- blood KW - Muscular Diseases -- chemically induced KW - Pain -- chemically induced KW - Muscular Diseases -- enzymology KW - Cresols -- adverse effects KW - Preservatives, Pharmaceutical -- adverse effects KW - Pain -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73216396?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Myalgia+and+elevated+creatine+kinase+activity+associated+with+subcutaneous+injections+of+diluent.&rft.au=Bach%2C+M+A%3BBlum%2C+D+M%3BRose%2C+S+R%3BCharnas%2C+L+R&rft.aulast=Bach&rft.aufirst=M&rft.date=1992-10-01&rft.volume=121&rft.issue=4&rft.spage=650&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 - 1992-11-13 N1 - Date created - 1992-11-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comments on occupational and environmental factors in the origin of non-Hodgkin's lymphoma. AN - 73212177; 1394163 AB - The review of the literature regarding non-Hodgkin's lymphoma and occupational and environmental factors presented at this workshop suggested associations with viruses, solvents, and hair dyes. A population-based case-control study among men from Iowa and Minnesota notes similar associations. Workers engaged in metal working, hair care, painting, and dry cleaning experienced nonsignificant excesses. Risks from specific exposures showed some variation by histological type. Both follicular and diffuse non-Hodgkin's lymphoma were associated with benzene. The diffuse type was linked to solvents other than benzene and formaldehyde, while the follicular was excessive among workers exposed to oils and greases. JF - Cancer research 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 - 1992/10/01/ PY - 1992 DA - 1992 Oct 01 SP - 5501s EP - 5502s VL - 52 IS - 19 Suppl SN - 0008-5472, 0008-5472 KW - Index Medicus KW - Risk Factors KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Minnesota -- epidemiology KW - Male KW - Iowa -- epidemiology KW - Lymphoma, Non-Hodgkin -- epidemiology KW - Occupational Diseases -- etiology KW - Lymphoma, Non-Hodgkin -- etiology KW - Occupational Diseases -- epidemiology KW - Lymphoma, Non-Hodgkin -- chemically induced KW - Occupational Diseases -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73212177?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Comments+on+occupational+and+environmental+factors+in+the+origin+of+non-Hodgkin%27s+lymphoma.&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=1992-10-01&rft.volume=52&rft.issue=19+Suppl&rft.spage=5501s&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 - 1992-10-29 N1 - Date created - 1992-10-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Radiation and non-Hodgkin's lymphoma. AN - 73206085; 1394160 AB - Lymphomas are rarely, if ever, found to be in excess following exposure to ionizing radiation. Hodgkin's disease has never been linked to radiation, and the evidence for non-Hodgkin's lymphoma (NHL) is very weak. Low doses of radiation from diagnostic X-ray procedures or from occupational exposures do not appear to cause NHL. Mortality studies of atomic bomb survivors in Japan and other epidemiological studies with quantitative estimates of radiation dose also fail to find dose-response relationships. NHL may arise infrequently following high-dose, possibly near lethal, radiation treatments. Immunosuppression associated with the disease being treated, such as Hodgkin's disease, may contribute to the development of NHL. If radiation does not cause NHL, at least not by its accepted mechanism of action of breaking chromosomes, creating rearrangements, gene deletions, and mutations, perhaps other environmental mutagens and clastogens should not be considered likely causes of NHL. JF - Cancer research AU - Boice, J D AD - Radiation Epidemiology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/10/01/ PY - 1992 DA - 1992 Oct 01 SP - 5489s EP - 5491s VL - 52 IS - 19 Suppl SN - 0008-5472, 0008-5472 KW - Index Medicus KW - Humans KW - Lymphoma, Non-Hodgkin -- epidemiology KW - Neoplasms, Radiation-Induced -- etiology KW - Neoplasms, Radiation-Induced -- epidemiology KW - Lymphoma, Non-Hodgkin -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73206085?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Radiation+and+non-Hodgkin%27s+lymphoma.&rft.au=Boice%2C+J+D&rft.aulast=Boice&rft.aufirst=J&rft.date=1992-10-01&rft.volume=52&rft.issue=19+Suppl&rft.spage=5489s&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 - 1992-10-29 N1 - Date created - 1992-10-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - New sites of proviral integration associated with murine promonocytic leukemias and evidence for alternate modes of c-myb activation. AN - 73177064; 1527851 AB - Murine promonocytic leukemias involving insertional mutagenesis of the c-myb locus can be induced by replication-competent retroviruses. In previously studied promonocytic leukemic cells induced by Moloney murine leukemia virus (called MML), the provirus has been invariably integrated upstream of exons 3 or 4 and the leukemic cells expressed aberrant RNAs with fused virus-myb sequences. Furthermore, Myb expressed by these cells has been shown to be truncated by 47 or 71 amino acids. The present report examines the mechanisms of myb activation in leukemias induced by two other retroviruses, amphotropic virus 4070A and Friend strain FB29 (the leukemias are called AMPH-ML and FB-ML, respectively). This study revealed two additional c-myb proviral insertion sites in these promonocytic leukemias. One FB-ML had a proviral integration in exon 9, and expressed a C-terminally truncated Myb protein of 47 kDa similar to that previously demonstrated to be expressed in the myelomonocytic cell lines NFS60 and VFL-2. However, a sequence of reverse-transcribed and amplified RNA from this leukemia demonstrated that the truncation involved a loss of 248 amino acids compared with a loss of 240 amino acids in the myelomonocytic cell lines. Another leukemia had a provirus integrated in the 5' end of c-myb upstream of exon 2 (in the first intron) and produced a Myb protein that was indistinguishable on sodium dodecyl sulfate-polyacrylamide gel electrophoresis from normal Myb. This latter leukemia (FB-ML R1-4-10) expressed Myb with the smallest N-terminal truncation observed so far in promonocytic leukemias; translation begins at an ATG within c-myb exon 2, leading to loss of only 20 amino acids from the N terminus. Unlike the proteins produced in Moloney murine leukemia virus-induced promonocytic leukemias (MML) that have larger truncations, this protein has an intact DNA binding region and does not contain N-terminal amino acids encoded by gag. However, this protein is similar to all N-terminally truncated Mybs so far studied, in that the truncation resulted in deletion of a casein kinase II phosphorylation site which has been proposed to be involved in regulation of DNA binding. JF - Journal of virology AU - Mukhopadhyaya, R AU - Wolff, L AD - Laboratory of Genetics, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 6035 EP - 6044 VL - 66 IS - 10 SN - 0022-538X, 0022-538X KW - c-myb KW - gag KW - Proto-Oncogene Proteins KW - 0 KW - Proto-Oncogene Proteins c-myb KW - DNA KW - 9007-49-2 KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Index Medicus KW - Animals KW - Blotting, Northern KW - Transcription, Genetic KW - Amino Acid Sequence KW - Mice KW - Precipitin Tests KW - Plasmids KW - Mice, Inbred DBA KW - Polymerase Chain Reaction KW - Base Sequence KW - Oncogenes KW - Tumor Cells, Cultured KW - Blotting, Southern KW - Molecular Sequence Data KW - Genes, gag KW - Female KW - Protein-Tyrosine Kinases -- genetics KW - Proviruses -- physiology KW - Proto-Oncogene Proteins -- metabolism KW - Protein-Tyrosine Kinases -- metabolism KW - Virus Integration KW - Proto-Oncogene Proteins -- genetics KW - Leukemia, Experimental -- microbiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73177064?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=New+sites+of+proviral+integration+associated+with+murine+promonocytic+leukemias+and+evidence+for+alternate+modes+of+c-myb+activation.&rft.au=Mukhopadhyaya%2C+R%3BWolff%2C+L&rft.aulast=Mukhopadhyaya&rft.aufirst=R&rft.date=1992-10-01&rft.volume=66&rft.issue=10&rft.spage=6035&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 - 1992-10-19 N1 - Date created - 1992-10-19 N1 - Date revised - 2017-01-13 N1 - Gene symbol - c-myb; gag N1 - SuppNotes - Cited By: Nucleic Acids Res. 1982 Jan 22;10(2):459-72 [7063411] J Immunol. 1978 Aug;121(2):641-7 [308074] Nucleic Acids Res. 1991 Dec 25;19(24):6950 [1762923] Nature. 1990 Apr 5;344(6266):517-22 [2157164] J Virol. 1990 Jan;64(1):155-60 [2403439] J Virol. 1987 Sep;61(9):2754-63 [2441077] J Virol. 1989 Apr;63(4):1630-40 [2538646] EMBO J. 1989 Jun;8(6):1767-75 [2670561] J Virol. 1988 Apr;62(4):1423-32 [2831403] J Virol. 1987 Jul;61(7):2339-43 [2884332] Virology. 1985 Feb;141(1):110-8 [2983493] Proc Natl Acad Sci U S A. 1986 Jul;83(14):5010-4 [3014527] Proc Natl Acad Sci U S A. 1986 Jul;83(13):4685-9 [3088565] Cell. 1988 Jan 29;52(2):185-95 [3277717] Virology. 1970 Dec;42(4):1136-9 [4099080] Nucleic Acids Res. 1984 Jan 25;12(2):857-72 [6694911] J Virol. 1992 Jan;66(1):512-23 [1309260] J Virol. 1991 Jul;65(7):3607-16 [1645785] EMBO J. 1991 Mar;10(3):655-64 [1825810] Genes Dev. 1990 Dec;4(12B):2235-41 [2279697] Nature. 1990 Feb 15;343(6259):662-5 [2406607] Anal Biochem. 1987 Apr;162(1):156-9 [2440339] 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] Oncogene Res. 1989;4(4):259-69 [2549488] J Virol. 1987 Dec;61(12):3721-5 [2824810] J Immunol. 1988 Jul 15;141(2):681-9 [2838552] Biotechniques. 1988 Feb;6(2):114-6 [2908499] Nucleic Acids Res. 1989 Mar 11;17(5):2141 [2928127] Proc Natl Acad Sci U S A. 1986 May;83(10):3204-8 [3010282] Nucleic Acids Res. 1986 Jul 11;14(13):5309-20 [3016644] Mol Cell Biol. 1986 Feb;6(2):380-92 [3023843] Proc Natl Acad Sci U S A. 1988 Aug;85(15):5698-702 [3165197] J Virol. 1985 Jun;54(3):864-8 [3999195] Nature. 1981 Oct 15-21;293(5833):543-8 [6169994] J Virol. 1981 Sep;39(3):777-91 [6270351] Erratum In: J Virol 1993 May;67(5):2960 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Reduced fertility among women employed as dental assistants exposed to high levels of nitrous oxide. AN - 73163748; 1298226 AB - Fertility is reduced in female rats exposed to levels of nitrous oxide similar to those found in some dental offices. Epidemiologic studies have suggested an association between exposure to mixed anesthetic gases and impaired fertility. We investigated the effects of occupational exposure to nitrous oxide on the fertility of female dental assistants. Screening questionnaires were mailed to 7000 female dental assistants, ages 18 to 39, registered by the California Department of Consumer Affairs. Sixty-nine percent responded. Four hundred fifty-nine women were determined to be eligible, having become pregnant during the previous four years for reasons unrelated to the failure of birth control, and 91 percent of these women completed telephone interviews. Detailed information was collected on exposure to nitrous oxide and fertility (measured by the number of menstrual cycles without contraception that the women required to become pregnant). After controlling for covariates, we found that women exposed to high levels of nitrous oxide were significantly less fertile than women who were unexposed or exposed to lower levels of nitrous oxide. The effect was evident only in the 19 women with five or more hours of exposure per week. These women were only 41 percent (95 percent confidence interval, 23 to 74 percent; P less than 0.003) as likely as unexposed women to conceive during each menstrual cycle. Occupational exposure to high levels of nitrous oxide may adversely affect women's ability to become pregnant. JF - The New England journal of medicine AU - Rowland, A S AU - Baird, D D AU - Weinberg, C R AU - Shore, D L AU - Shy, C M AU - Wilcox, A J AD - Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992/10/01/ PY - 1992 DA - 1992 Oct 01 SP - 993 EP - 997 VL - 327 IS - 14 SN - 0028-4793, 0028-4793 KW - Nitrous Oxide KW - K50XQU1029 KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Adult KW - Surveys and Questionnaires KW - Retrospective Studies KW - Adolescent KW - Female KW - Occupational Exposure KW - Nitrous Oxide -- adverse effects KW - Dental Assistants KW - Fertility -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73163748?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Reduced+fertility+among+women+employed+as+dental+assistants+exposed+to+high+levels+of+nitrous+oxide.&rft.au=Rowland%2C+A+S%3BBaird%2C+D+D%3BWeinberg%2C+C+R%3BShore%2C+D+L%3BShy%2C+C+M%3BWilcox%2C+A+J&rft.aulast=Rowland&rft.aufirst=A&rft.date=1992-10-01&rft.volume=327&rft.issue=14&rft.spage=993&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 - 1992-10-06 N1 - Date created - 1992-10-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: N Engl J Med. 1993 Jan 28;328(4):284-5 [8418413] N Engl J Med. 1993 Jan 28;328(4):284 [8466571] N Engl J Med. 1992 Oct 1;327(14):1026-7 [1518538] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Adolescent Nonsexual and Sex-Related Problem Behaviors AN - 61289152; 93Z8385 AB - Data from a subsample (N = 1,197 males [Ms] & 1,834 females [Fs], 75% white & 25% black) of the 1980 National Longitudinal Survey of Youth are drawn on to compare the involvement in problem behaviors of those who were: (1) virgins, (2) sexually experienced but never pregnant, & (3) pregnant or parents. Logistic regression analyses reveal that, after controlling for the effects of sociodemographic status, age, school status, & frequency of attendance at religious services, sexually experienced, never pregnant adolescents are more likely than virgins to have been involved in four types of nonsexual problem behaviors. However, pregnant/parenting adolescents are no more likely to engage in such behaviors than are their experienced but never pregnant peers. For Ms, but not for Fs, early age at first intercourse is associated with increased involvement in problem behaviors. Implications for policy & interventions for adolescents at risk are discussed. 4 Tables, 1 Appendix, 82 References. Adapted from the source document. JF - Journal of Adolescent Research AU - Ketterlinus, Robert D AU - Lamb, Michael E AU - Nitz, Katherine AU - Elster, Arthur B AD - NIH/NICHD, 9190 Rockville Pike BSA Bldg #333 Bethesda MD 20892-9901 Y1 - 1992/10// PY - 1992 DA - October 1992 SP - 431 EP - 456 VL - 7 IS - 4 SN - 0743-5584, 0743-5584 KW - problem behaviors, virgin/sexually experienced/pregnant/parenting adolescents KW - 1980 national survey data KW - black/white males/females KW - Sexual Behavior KW - Black White Differences KW - Sex Differences KW - Parenthood KW - Virginity KW - Sexual Reproduction KW - Adolescents KW - article KW - 1939: the family and socialization; adolescence & youth UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/61289152?accountid=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+Adolescent+Research&rft.atitle=Adolescent+Nonsexual+and+Sex-Related+Problem+Behaviors&rft.au=Ketterlinus%2C+Robert+D%3BLamb%2C+Michael+E%3BNitz%2C+Katherine%3BElster%2C+Arthur+B&rft.aulast=Ketterlinus&rft.aufirst=Robert&rft.date=1992-10-01&rft.volume=7&rft.issue=4&rft.spage=431&rft.isbn=&rft.btitle=&rft.title=Journal+of+Adolescent+Research&rft.issn=07435584&rft_id=info:doi/ LA - English DB - Sociological Abstracts N1 - Date revised - 2007-04-01 N1 - Last updated - 2016-09-28 N1 - CODEN - JADREZ N1 - SubjectsTermNotLitGenreText - Adolescents; Black White Differences; Sex Differences; Sexual Behavior; Virginity; Sexual Reproduction; Parenthood ER - TY - JOUR T1 - Analysis of the backbone dynamics of the ribonuclease H domain of the human immunodeficiency virus reverse transcriptase using 15N relaxation measurements. AN - 73210893; 1382587 AB - The backbone dynamics of the uniformly 15N-labeled ribonuclease H (RNase H) domain of human immunodeficiency virus (HIV-1) reverse transcriptase have been investigated using two-dimensional inverse-detected heteronuclear 15N-1HNMR spectroscopy. 15N T1, T2, and nuclear Overhauser enhancement (NOE) data were obtained for 107 out of a total of 134 backbone amide groups. The overall rotational correlation time (tau R) for the protein at 26 degrees C is 10.4 ns. The backbone N-H vectors for all the measurable residues exhibit very fast motions on a time scale of less than or equal to 20 ps. The 15N relaxation data for only 14 residues can be explained by this single internal motion alone. A further 39 residues display a second motion on a time scale ranging from 28.8 ps to 3.9 ns, while another 15 residues are characterized by an additional motion on the 170-ns to 2.25-ms time scale resulting in 15N T2 exchange line broadening. There are 39 residues that exhibit both the additional 15N T2 exchange line broadening and the slow (28.8 ps-3.9 ns) internal motion. Thus, the RNase H domain experiences extensive mobility throughout its structure as evidenced by the 93 residues which exhibit multiple modes of motion. Distinctly mobile regions of the protein are identified by large decreases in the overall order parameter (S2) and correspond to the C-terminal residues and the loop regions between beta-strands beta 1 and beta 2 and between alpha-helix alpha B and beta-strand beta 4.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Biochemistry AU - Powers, R AU - Clore, G M AU - Stahl, S J AU - Wingfield, P T AU - Gronenborn, A AD - Laboratory of Chemical Physics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/09/29/ PY - 1992 DA - 1992 Sep 29 SP - 9150 EP - 9157 VL - 31 IS - 38 SN - 0006-2960, 0006-2960 KW - Nitrogen Isotopes KW - 0 KW - Recombinant Proteins KW - HIV Reverse Transcriptase KW - EC 2.7.7.49 KW - RNA-Directed DNA Polymerase KW - Ribonuclease H KW - EC 3.1.26.4 KW - Index Medicus KW - AIDS/HIV KW - Mutagenesis, Site-Directed KW - Magnetic Resonance Spectroscopy -- methods KW - Models, Molecular KW - Recombinant Proteins -- chemistry KW - Protein Conformation KW - Ribonuclease H -- chemistry KW - RNA-Directed DNA Polymerase -- chemistry KW - HIV-1 -- enzymology KW - RNA-Directed DNA Polymerase -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73210893?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Analysis+of+the+backbone+dynamics+of+the+ribonuclease+H+domain+of+the+human+immunodeficiency+virus+reverse+transcriptase+using+15N+relaxation+measurements.&rft.au=Powers%2C+R%3BClore%2C+G+M%3BStahl%2C+S+J%3BWingfield%2C+P+T%3BGronenborn%2C+A&rft.aulast=Powers&rft.aufirst=R&rft.date=1992-09-29&rft.volume=31&rft.issue=38&rft.spage=9150&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-13 N1 - Date created - 1992-11-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Controlled trial of pulse methylprednisolone versus two regimens of pulse cyclophosphamide in severe lupus nephritis. AN - 73196845; 1356175 AB - Pulse cyclophosphamide is more effective than prednisone alone in preventing renal failure in lupus nephritis. We undertook a randomised, controlled trial to find out whether pulse methylprednisolone could equal pulse cyclophosphamide in preserving renal function in patients with lupus nephritis, and whether there was a difference between long and short courses of pulse cyclophosphamide in preventing exacerbations. 65 patients (60 female, 5 male; median [range] age 29 [10-48] years) with severe lupus nephritis were assigned randomly to monthly pulse methylprednisolone for 6 months (25 patients), monthly pulse cyclophosphamide for 6 months (20), or monthly cyclophosphamide for 6 months followed by quarterly pulse cyclophosphamide for 2 additional years (20). Patients treated with pulse methylprednisolone had a higher probability of doubling serum creatinine than those treated with long-course cyclophosphamide (p less than 0.04). Risk of doubling creatinine was not significantly different between short and long course cyclophosphamide. However, patients treated with short-course cyclophosphamide had a higher probability of exacerbations than those treated with long-course cyclophosphamide (p less than 0.01). An extended course of pulse cyclophosphamide is more effective than 6 months of pulse methylprednisolone in preserving renal function in patients with severe lupus nephritis. Addition of a quarterly maintenance regimen to monthly pulse cyclophosphamide reduces the rate of exacerbations. JF - Lancet (London, England) AU - Boumpas, D T AU - Austin, H A AU - Vaughn, E M AU - Klippel, J H AU - Steinberg, A D AU - Yarboro, C H AU - Balow, J E AD - Kidney Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland 20892. Y1 - 1992/09/26/ PY - 1992 DA - 1992 Sep 26 SP - 741 EP - 745 VL - 340 IS - 8822 SN - 0140-6736, 0140-6736 KW - Cyclophosphamide KW - 8N3DW7272P KW - Creatinine KW - AYI8EX34EU KW - Methylprednisolone KW - X4W7ZR7023 KW - Abridged Index Medicus KW - Index Medicus KW - Drug Administration Schedule KW - Humans KW - Adult KW - Treatment Outcome KW - Middle Aged KW - Child KW - Adolescent KW - Creatinine -- blood KW - Recurrence KW - Male KW - Female KW - Survival Analysis KW - Cyclophosphamide -- administration & dosage KW - Methylprednisolone -- administration & dosage KW - Lupus Nephritis -- drug therapy KW - Lupus Nephritis -- blood KW - Methylprednisolone -- adverse effects KW - Cyclophosphamide -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73196845?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Lancet+%28London%2C+England%29&rft.atitle=Controlled+trial+of+pulse+methylprednisolone+versus+two+regimens+of+pulse+cyclophosphamide+in+severe+lupus+nephritis.&rft.au=Boumpas%2C+D+T%3BAustin%2C+H+A%3BVaughn%2C+E+M%3BKlippel%2C+J+H%3BSteinberg%2C+A+D%3BYarboro%2C+C+H%3BBalow%2C+J+E&rft.aulast=Boumpas&rft.aufirst=D&rft.date=1992-09-26&rft.volume=340&rft.issue=8822&rft.spage=741&rft.isbn=&rft.btitle=&rft.title=Lancet+%28London%2C+England%29&rft.issn=01406736&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of conserved threonine and tyrosine residues in acetylcholine binding and muscarinic receptor activation. A study with m3 muscarinic receptor point mutants. AN - 73185356; 1527051 AB - Structure-function relationship studies of the m3 muscarinic acetylcholine receptor have recently identified a series of threonine and tyrosine residues (all located within the hydrophobic receptor core) that are critically involved in acetylcholine binding (Wess, J., Gdula, D., and Brann, M.R. (1991) EMBO J. 10, 3729-3734). To gain further insight into the functional roles of these amino acids, the agonist binding properties of six rat m3 muscarinic receptor point mutants, in which the critical threonine and tyrosine residues had been individually replaced by alanine and phenylalanine, respectively, were studied in greater detail following their transient expression in COS-7 cells. The binding profiles of a series of acetylcholine derivatives suggest that the altered threonine and tyrosine residues are primarily involved in the interaction of the acetylcholine ester moiety with the receptor protein. The two m3 receptor point mutants, Thr234----Ala and Tyr506----Phe, which showed the most pronounced decreases in acetylcholine binding affinities (approximately 40-60-fold as compared with the wild-type receptor), were stably expressed in CHO cells for further functional analysis. Both mutant receptors were found to be severely impaired in their ability to stimulate agonist-dependent phosphatidylinositol hydrolysis. Consistent with this observation, acetylcholine binding to the two mutant receptors was not significantly affected by addition of the GTP analog Gpp(NH)p (5'-guanylyl imidodiphosphate). Our data suggest that Thr234 and Tyr506 (located within transmembrane domains V and VI, respectively), which are conserved among all muscarinic receptors (m1-m5), may play an important role in agonist-induced muscarinic receptor activation. JF - The Journal of biological chemistry AU - Wess, J AU - Maggio, R AU - Palmer, J R AU - Vogel, Z AD - National Institute of Neurological Disorders and Stroke, Laboratory of Molecular Biology, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/09/25/ PY - 1992 DA - 1992 Sep 25 SP - 19313 EP - 19319 VL - 267 IS - 27 SN - 0021-9258, 0021-9258 KW - Inositol Phosphates KW - 0 KW - Receptors, Muscarinic KW - Threonine KW - 2ZD004190S KW - Guanylyl Imidodiphosphate KW - 34273-04-6 KW - Tyrosine KW - 42HK56048U KW - Acetylcholine KW - N9YNS0M02X KW - Index Medicus KW - Animals KW - Threonine -- metabolism KW - Inositol Phosphates -- metabolism KW - Amino Acid Sequence KW - Structure-Activity Relationship KW - Mutagenesis, Site-Directed KW - Rats KW - Guanylyl Imidodiphosphate -- metabolism KW - In Vitro Techniques KW - Molecular Sequence Data KW - CHO Cells KW - Tyrosine -- metabolism KW - Signal Transduction KW - Cricetinae KW - Acetylcholine -- metabolism KW - Receptors, Muscarinic -- chemistry KW - Receptors, Muscarinic -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73185356?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+conserved+threonine+and+tyrosine+residues+in+acetylcholine+binding+and+muscarinic+receptor+activation.+A+study+with+m3+muscarinic+receptor+point+mutants.&rft.au=Wess%2C+J%3BMaggio%2C+R%3BPalmer%2C+J+R%3BVogel%2C+Z&rft.aulast=Wess&rft.aufirst=J&rft.date=1992-09-25&rft.volume=267&rft.issue=27&rft.spage=19313&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 - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cytotoxic ribonuclease chimeras. Targeted tumoricidal activity in vitro and in vivo. AN - 73176371; 1527074 AB - Monoclonal antibodies to the transferrin receptor or to the T cell antigen, CD5, were chemically linked to mammalian RNase A and found to specifically inhibit protein synthesis in antigen-positive cells. Antibody-mediated specificity of these cytotoxic ribonuclease chimeras (CRCs) was demonstrated in three ways. 1) Toxicity was due to the chemical linkage of RNase to antibody, as the individual components added separately or in combination did not inhibit protein synthesis; 2) the anti-transferrin receptor CRCs inhibited protein synthesis in those cells expressing the human transferrin receptor (K562, U251, Jurkat cells) but had no detectable toxicity to cells lacking the human transferrin receptor (Vero or NIH 3T3 cells); 3) free antibody to either the human transferrin receptor (454A12 or 5E-9) or to the T cell antigen, CD5 (T101), blocked the cytotoxicity of the respective CRC. Two CRC species, designated P1 and P2, that differed in size and stoichiometry of RNase A to antibody, were purified by size-exclusion high performance liquid chromatography. The higher molecular weight P1 conjugate had an IC50 of 20-30 nM, whereas the P2 conjugate had a higher IC50 of 300-500 nM. Bioactivity could be reversibly increased more than 10-fold by freezing. The cytotoxicity of the CRCs was examined in vivo in a solid tumor animal model. Intratumoral injections of an anti-transferrin receptor CRC into established U251 human glioblastoma tumors grown in the flanks of nude mice prevented tumor growth, whereas RNase A mixed with antibody was ineffective. CRCs, therefore, express cytotoxicity in vitro and in vivo. Mammalian nucleases coupled to antibodies may be utilized as cell type-selective cytotoxins and have potential as pharmacologic reagents. The systemic toxicity and immunogenicity observed with mammalian derived cytotoxins may be significantly less than that of the currently employed plant- and bacterial-derived immunotoxins. JF - The Journal of biological chemistry AU - Newton, D L AU - Ilercil, O AU - Laske, D W AU - Oldfield, E AU - Rybak, S M AU - Youle, R J AD - National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/09/25/ PY - 1992 DA - 1992 Sep 25 SP - 19572 EP - 19578 VL - 267 IS - 27 SN - 0021-9258, 0021-9258 KW - Antibodies, Monoclonal KW - 0 KW - Antineoplastic Agents KW - Cross-Linking Reagents KW - Cytotoxins KW - Immunotoxins KW - Receptors, Transferrin KW - Ribonucleases KW - EC 3.1.- KW - Index Medicus KW - Neoplasm Transplantation KW - Protein Biosynthesis KW - Animals KW - Tumor Cells, Cultured KW - In Vitro Techniques KW - Receptors, Transferrin -- immunology KW - Mice, Nude KW - Mice KW - Immunotoxins -- chemistry KW - Ribonucleases -- toxicity KW - Cell Survival -- drug effects KW - Ribonucleases -- chemistry KW - Antibodies, Monoclonal -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73176371?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cytotoxic+ribonuclease+chimeras.+Targeted+tumoricidal+activity+in+vitro+and+in+vivo.&rft.au=Newton%2C+D+L%3BIlercil%2C+O%3BLaske%2C+D+W%3BOldfield%2C+E%3BRybak%2C+S+M%3BYoule%2C+R+J&rft.aulast=Newton&rft.aufirst=D&rft.date=1992-09-25&rft.volume=267&rft.issue=27&rft.spage=19572&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 - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cytochrome P450-benzphetamine interactions in the endoplasmic reticulum: studies using a monoclonal antibody to P450b. AN - 73203422; 1390673 AB - A monoclonal antibody (MAb) to phenobarbital-induced rat cytochrome P450b was used to study the interaction of the substrate benzphetamine (Bz) with cytochromes P450 in liver microsomes. Binding of Bz to liver microsomes from phenobarbital-treated rats was monitored by the substrate-induced type I spectral change. The MAb maximally inhibited this spectral change by 49%, providing a probe to distinguish MAb-specific P450b from other Bz-binding P450s. Thermodynamic parameters of the interaction were determined in the absence and presence of MAb. The MAb did not influence the spin-state equilibrium of substrate-free P450b, but it increased the low spin content of substrate-bound P450b. The MAb also decreased the affinity of both high and low spin P450b for Bz. The temperature dependence of the Bz-binding interactions revealed a transition near 20 degrees C. Fluorescence polarization measurements of the membrane probe 1,6-diphenyl-1,3,5-hexatriene also revealed a transition at this temperature. The MAb comparably inhibited Bz binding to high spin P450b in the low and high temperature regions, whereas MAb inhibition of Bz binding to low spin P450b was greater in the low temperature region than in the high temperature region. These results indicate temperature-dependent changes in membrane structure that modulate both Bz binding to P450b and MAb-P450b-Bz interactions. These results also demonstrate the utility of MAbs for evaluating P450-substrate binding microequilibria of MAb-specific P450s in the presence of other P450s while in the natural membrane environment of the endoplasmic reticulum. JF - Biochemistry AU - Omata, Y AU - Friedman, F K AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/09/22/ PY - 1992 DA - 1992 Sep 22 SP - 8862 EP - 8867 VL - 31 IS - 37 SN - 0006-2960, 0006-2960 KW - Antibodies, Monoclonal KW - 0 KW - Benzphetamine KW - 0M3S43XK27 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - benzphetamine N-demethylase KW - EC 1.14.14.1 KW - Oxidoreductases, N-Demethylating KW - EC 1.5.- KW - Index Medicus KW - Rats KW - Antigen-Antibody Reactions KW - Animals KW - Rats, Sprague-Dawley KW - Viscosity KW - Thermodynamics KW - Spectrum Analysis KW - Binding, Competitive KW - Temperature KW - Endoplasmic Reticulum -- enzymology KW - Microsomes, Liver -- enzymology KW - Oxidoreductases, N-Demethylating -- immunology KW - Cytochrome P-450 Enzyme System -- immunology KW - Cytochrome P-450 Enzyme System -- metabolism KW - Benzphetamine -- metabolism KW - Oxidoreductases, N-Demethylating -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73203422?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cytochrome+P450-benzphetamine+interactions+in+the+endoplasmic+reticulum%3A+studies+using+a+monoclonal+antibody+to+P450b.&rft.au=Omata%2C+Y%3BFriedman%2C+F+K&rft.aulast=Omata&rft.aufirst=Y&rft.date=1992-09-22&rft.volume=31&rft.issue=37&rft.spage=8862&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-26 N1 - Date created - 1992-10-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A transient transfection system for identifying biosynthesized proteins processed and presented to class I MHC restricted T lymphocytes. AN - 73252118; 1401939 AB - CD8+ cytotoxic T lymphocytes (CTL) constitute a major portion of immune responses to foreign and self antigens. CTL recognize class I major histocompatibility complex molecules complexed to peptides of 8-10 residues derived from cytosolic proteins. To understand CTL responses to these antigens and to manipulate CTL responses optimally, it is necessary to identify the specific peptides recognized by CTL. The methods currently used for this purpose have significant drawbacks. We describe a plasmid transfection method that results in significant lysis of histocompatible target cells. Influenza virus-specific CTLs specifically lysed target cells that were transfected with plasmids bearing cDNAs encoding full length gene products, fragments containing the region that encodes the CTL epitope, or even a ten residue peptide. This significantly lessens the time and effort required to define genes, and gene segments that contain CTL epitopes. JF - Journal of immunological methods AU - Eisenlohr, L C AU - Yewdell, J W AU - Bennink, J R AD - Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892. Y1 - 1992/09/18/ PY - 1992 DA - 1992 Sep 18 SP - 131 EP - 138 VL - 154 IS - 1 SN - 0022-1759, 0022-1759 KW - Histocompatibility Antigens Class I KW - 0 KW - Index Medicus KW - Animals KW - Vaccinia virus KW - Mice KW - Antigen-Presenting Cells -- immunology KW - Plasmids KW - Orthomyxoviridae Infections -- immunology KW - Fluorescent Antibody Technique KW - Cell Line KW - Cytotoxicity Tests, Immunologic -- methods KW - Transfection KW - Histocompatibility Antigens Class I -- immunology KW - T-Lymphocytes, Cytotoxic -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73252118?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+immunological+methods&rft.atitle=A+transient+transfection+system+for+identifying+biosynthesized+proteins+processed+and+presented+to+class+I+MHC+restricted+T+lymphocytes.&rft.au=Eisenlohr%2C+L+C%3BYewdell%2C+J+W%3BBennink%2C+J+R&rft.aulast=Eisenlohr&rft.aufirst=L&rft.date=1992-09-18&rft.volume=154&rft.issue=1&rft.spage=131&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunological+methods&rft.issn=00221759&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-26 N1 - Date created - 1992-10-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Photosensitization by anticancer agents. 11. Mechanisms of photosensitization of human leukemic cells by diaminoanthraquinones: singlet oxygen and radical reactions. AN - 73314683; 1331388 AB - The synthesis of several aminoanthraquinone derivatives (AAQs), designed to suppress the dark toxicity and to promote more efficient cancer cell photosensitization for potential use in photodynamic therapy (PDT), is described. The following AAQs were synthesized: 1-NH2-4,5-(MeO)2-AQ (1), 1,5-(NH2)2-4,8-(MeO)2-AQ (2), 1,8-(NH2)2-4,5-(MeO)2-AQ (3), and 1,5-(NHPhMe)2-4,8-(MeO)2-AQ (8). The agents exhibit strong absorption in the region 480-620 nm. Possible mechanisms of photosensitization were studied by measuring 1O2 phosphorescence at 1270 nm, detecting superoxide radicals employing an electron paramagnetic resonance (EPR)-spin trapping technique, and measuring oxygen consumption during the photo-oxidation of a representative biological electron donor, NADH. Strong phosphorescence from 1O2 was observed upon illumination of 2 and 3 in C6H6 (quantum yield of 0.25 and 0.5 respectively), and in EtOH (quantum yield of 0.23 and 0.34). The 1-amino-AQ (1) was the weakest 1O2 sensitizer, with quantum yield of 0.13 in benzene. No phosphorescence was observed in EtOH. A superoxide radical was detected as a spin adduct of 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) in irradiated benzene solutions of 1, 2 or 3 and DMPO. AAQs 2 and 3 sensitized photo-oxidation of NADH in H2O/EtOH mixture with the intermediacy of singlet oxygen as judged by the effect of sodium azide on the photostimulated oxygen consumption. Evolution of O2 upon addition of catalase to the illuminated solution confirmed the ultimate formation of hydrogen peroxide. These findings suggested that the (di)amino-dimethoxyanthraquinones might exert photosensitization via both Type I and Type II mechanisms. The AAQs were tested for their ability to photosensitize K562 human chronic myeloid leukemic cells in culture. Viability was measured using the 3,4,5-diethylthiazol-2,5-diphenyl tetrazolium blue assay, and DNA and possible membrane damage were assessed. The results from illuminating cells with light > 475 nm show that for the 1,5-compounds, the presence of methoxy substituents at 4,8 positions reduces the dark toxicity from ID50 of 23 to 250 microM and for the 1,8-compounds correspondingly from ID50 of 53 to > 300 microM. In the 1,5-series this decrease of the dark toxicity is accompanied by an increase in light-induced dose modification from 8.85 to 14.4. Differences exist in the mechanisms of cytotoxicity between the prototype phenolic AAQs and their methoxy counterparts. It appears that the cytotoxic action of the latter causes cell damage by the formation of a high proportion of alkali labile sites in addition to frank strand breaks.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Journal of photochemistry and photobiology. B, Biology AU - Reszka, K J AU - Bilski, P AU - Chignell, C F AU - Hartley, J A AU - Khan, N AU - Souhami, R L AU - Mendonca, A J AU - Lown, J W AD - Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992/09/15/ PY - 1992 DA - 1992 Sep 15 SP - 317 EP - 335 VL - 15 IS - 4 SN - 1011-1344, 1011-1344 KW - Anthraquinones KW - 0 KW - Antineoplastic Agents KW - Free Radicals KW - Radiation-Sensitizing Agents KW - Cycloleucine KW - 0TQU7668EI KW - NAD KW - 0U46U6E8UK KW - Singlet Oxygen KW - 17778-80-2 KW - Oxygen KW - S88TT14065 KW - Index Medicus KW - Oxygen Consumption -- drug effects KW - Humans KW - Oxygen -- metabolism KW - Photochemotherapy KW - Free Radicals -- metabolism KW - Structure-Activity Relationship KW - NAD -- metabolism KW - Tumor Cells, Cultured KW - Electron Spin Resonance Spectroscopy KW - Kinetics KW - Leukemia, Myelogenous, Chronic, BCR-ABL Positive KW - Spectrophotometry KW - Cycloleucine -- metabolism KW - Radiation-Sensitizing Agents -- chemistry KW - Cell Survival -- drug effects KW - DNA Damage KW - Radiation-Sensitizing Agents -- pharmacology KW - Radiation-Sensitizing Agents -- chemical synthesis KW - Anthraquinones -- chemical synthesis KW - Anthraquinones -- pharmacology KW - Antineoplastic Agents -- chemical synthesis KW - Anthraquinones -- chemistry KW - Antineoplastic Agents -- chemistry KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73314683?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+photochemistry+and+photobiology.+B%2C+Biology&rft.atitle=Photosensitization+by+anticancer+agents.+11.+Mechanisms+of+photosensitization+of+human+leukemic+cells+by+diaminoanthraquinones%3A+singlet+oxygen+and+radical+reactions.&rft.au=Reszka%2C+K+J%3BBilski%2C+P%3BChignell%2C+C+F%3BHartley%2C+J+A%3BKhan%2C+N%3BSouhami%2C+R+L%3BMendonca%2C+A+J%3BLown%2C+J+W&rft.aulast=Reszka&rft.aufirst=K&rft.date=1992-09-15&rft.volume=15&rft.issue=4&rft.spage=317&rft.isbn=&rft.btitle=&rft.title=Journal+of+photochemistry+and+photobiology.+B%2C+Biology&rft.issn=10111344&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 - Interleukin 10 inhibits macrophage microbicidal activity by blocking the endogenous production of tumor necrosis factor alpha required as a costimulatory factor for interferon gamma-induced activation. AN - 73183991; 1528880 AB - Interleukin 10 (IL-10) inhibits interferon gamma-induced macrophage activation for cytotoxicity against larvae of the human parasite Schistosoma mansoni by suppressing production of the toxic effector molecule nitric oxide (NO). In this study, the mechanism of IL-10 action was identified as inhibition of endogenous tumor necrosis factor alpha (TNF-alpha) production by interferon gamma-activated macrophages. TNF-alpha appears to serve as a cofactor for interferon gamma-mediated activation, since both schistosomulum killing and NO production were inhibited by anti-TNF-alpha antibody, whereas TNF-alpha alone was unable to stimulate these macrophage functions. IL-10 blocked TNF-alpha production by interferon gamma-treated macrophages at the levels of both protein and mRNA synthesis. Addition of exogenous TNF-alpha reversed IL-10-mediated suppression of macrophage cytotoxic activity as well as NO production. Likewise, addition of a macrophage-triggering agent (bacterial lipopolysaccharide or muramyl dipeptide), which induced the production of TNF-alpha, also reversed the suppressive effect of IL-10 on cytotoxic function. In contrast to IL-10, two other cytokines, IL-4 and transforming growth factor beta, which also inhibit macrophage activation for schistosomulum killing and NO production, did not substantially suppress endogenous TNF-alpha production. These results, therefore, describe a separate pathway by which macrophage microbicidal function is inhibited by the down-regulatory cytokine IL-10. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Oswald, I P AU - Wynn, T A AU - Sher, A AU - James, S L AD - Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20814. Y1 - 1992/09/15/ PY - 1992 DA - 1992 Sep 15 SP - 8676 EP - 8680 VL - 89 IS - 18 SN - 0027-8424, 0027-8424 KW - Cytokines KW - 0 KW - Lipopolysaccharides KW - Oligodeoxyribonucleotides KW - RNA, Messenger KW - Recombinant Proteins KW - Transforming Growth Factor beta KW - Tumor Necrosis Factor-alpha KW - Interleukin-10 KW - 130068-27-8 KW - Interleukin-4 KW - 207137-56-2 KW - Nitric Oxide KW - 31C4KY9ESH KW - Acetylmuramyl-Alanyl-Isoglutamine KW - 53678-77-6 KW - Interferon-gamma KW - 82115-62-6 KW - Index Medicus KW - Transforming Growth Factor beta -- pharmacology KW - Animals KW - Cytokines -- genetics KW - Lipopolysaccharides -- administration & dosage KW - Interleukin-4 -- pharmacology KW - Gene Expression KW - Nitric Oxide -- metabolism KW - RNA, Messenger -- genetics KW - Base Sequence KW - Acetylmuramyl-Alanyl-Isoglutamine -- pharmacology KW - Oligodeoxyribonucleotides -- chemistry KW - Schistosoma mansoni -- immunology KW - Immunity, Cellular -- drug effects KW - Molecular Sequence Data KW - Macrophages -- immunology KW - Interleukin-10 -- pharmacology KW - Interferon-gamma -- pharmacology KW - Tumor Necrosis Factor-alpha -- biosynthesis KW - Cytotoxicity, Immunologic -- drug effects KW - Macrophage Activation -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73183991?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+10+inhibits+macrophage+microbicidal+activity+by+blocking+the+endogenous+production+of+tumor+necrosis+factor+alpha+required+as+a+costimulatory+factor+for+interferon+gamma-induced+activation.&rft.au=Oswald%2C+I+P%3BWynn%2C+T+A%3BSher%2C+A%3BJames%2C+S+L&rft.aulast=Oswald&rft.aufirst=I&rft.date=1992-09-15&rft.volume=89&rft.issue=18&rft.spage=8676&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 - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Methods Enzymol. 1986;132:649-58 [3102898] Immunol Rev. 1987 Jun;97:5-27 [2957307] Biochem Biophys Res Commun. 1988 Nov 30;157(1):87-94 [3196352] Eur J Immunol. 1988 Oct;18(10):1587-92 [3142779] Immunol Rev. 1992 Jun;127:183-204 [1354651] J Immunol. 1992 Mar 15;148(6):1792-6 [1541819] J Immunol. 1992 Jun 1;148(11):3578-82 [1588047] Int Immunol. 1992 May;4(5):563-9 [1627494] J Exp Med. 1991 Oct 1;174(4):915-24 [1655948] Int Immunol. 1990;2(9):821-32 [1703785] J Immunol. 1991 Oct 1;147(7):2391-7 [1717559] J Immunol. 1992 Jan 15;148(2):568-74 [1729374] J Exp Med. 1992 Jan 1;175(1):169-74 [1730915] J Exp Med. 1991 Dec 1;174(6):1549-55 [1744584] J Immunol. 1991 May 15;146(10):3444-51 [1827484] J Immunol. 1991 Dec 1;147(11):3815-22 [1940369] J Exp Med. 1991 Nov 1;174(5):1209-20 [1940799] J Immunol. 1990 Dec 15;145(12):4290-7 [2124240] Science. 1990 Jun 8;248(4960):1230-4 [2161559] J Exp Med. 1989 Dec 1;170(6):2081-95 [2531194] J Immunol. 1989 Dec 15;143(12):4208-12 [2592772] J Immunol. 1981 Jul;127(1):179-83 [7240741] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Induction of erythroid differentiation and fetal hemoglobin production in human leukemic cells treated with phenylacetate. AN - 73183771; 1381630 AB - There is considerable interest in identifying nontoxic differentiation inducers for the treatment of various malignant and nonmalignant blood disorders, including inborn beta-chain hemoglobinopathies. Using the human leukemic K562 cell line as a model, we explored the efficacy of phenylacetate, an amino acid derivative with a low toxicity index when administered to humans. Treatment of K562 cultures with pharmacologically attainable concentrations of phenylacetate resulted in erythroid differentiation, evident by the reduced growth rate and increased hemoglobin production. The effect was time- and dose-dependent, further augmented by glutamine starvation (phenylacetate is known to deplete circulating glutamine in vivo), and reversible upon cessation of treatment. Molecular analysis showed that phenylacetate induced gamma globin gene expression with subsequent accumulation of the fetal form of hemoglobin (HbF). Interestingly, the addition of phenylacetate to antitumor agents of clinical interest, eg, hydroxyurea and 5-azacytidine, caused superinduction of HbF biosynthesis. The results suggest that phenylacetate, used alone or in combination with other drugs, might offer a safe and effective new approach to treatment of some hematopoietic neoplasms and severe hemoglobinopathies. JF - Blood AU - Samid, D AU - Yeh, A AU - Prasanna, P AD - Clinical Pharmacology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/09/15/ PY - 1992 DA - 1992 Sep 15 SP - 1576 EP - 1581 VL - 80 IS - 6 SN - 0006-4971, 0006-4971 KW - Phenylacetates KW - 0 KW - decitabine KW - 776B62CQ27 KW - Fetal Hemoglobin KW - 9034-63-3 KW - Azacitidine KW - M801H13NRU KW - Hydroxyurea KW - X6Q56QN5QC KW - Abridged Index Medicus KW - Index Medicus KW - Azacitidine -- pharmacology KW - Leukemia, Experimental KW - Humans KW - Azacitidine -- analogs & derivatives KW - Cell Division -- drug effects KW - Cell Differentiation KW - Hydroxyurea -- pharmacology KW - Phenylacetates -- pharmacology KW - Tumor Cells, Cultured -- metabolism KW - Tumor Cells, Cultured -- drug effects KW - Fetal Hemoglobin -- biosynthesis KW - Erythroid Precursor Cells -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73183771?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+arthritis+and+rheumatism&rft.atitle=Timed+treatment+of+the+arthritic+diseases%3A+a+review+and+hypothesis.&rft.au=Vener%2C+K+J%3BReddy%2C+A&rft.aulast=Vener&rft.aufirst=K&rft.date=1992-10-01&rft.volume=22&rft.issue=2&rft.spage=83&rft.isbn=&rft.btitle=&rft.title=Seminars+in+arthritis+and+rheumatism&rft.issn=00490172&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-13 N1 - Date created - 1992-10-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Reversal by nickel(II) of inhibitory effects of some scavengers of active oxygen species upon hydroxylation of 2'-deoxyguanosine in vitro. AN - 73201466; 1327552 AB - Effects of ethanol (EtOH), mannitol (Man), L-histidine (His) and glutathione (GSH) on the oxidation of 2'-deoxyguanosine (dG) to its 8-hydroxy derivative (8-OH-dG) with H2O2 plus L-ascorbic acid (Ascb) in the absence and presence of Ni(II) were investigated in order to unveil the nature of active oxygen species involved in that oxidation. In the absence of Ni(II), production of 8-OH-dG was inhibited by His much greater than GSH greater than or equal to GSSG (oxidized glutathione) much greater than EtOH, but not by Man. The latter tended to enhance the production of 8-OH-dG. In the presence of Ni(II), the inhibition by His, GSH and GSSG, but not EtOH, was prevented. The results indicate involvement of a 'crypto-hydroxyl' radical as the dG oxidizing species in both the absence and presence of Ni(II). Also, the results provide evidence that Ni(II) complexes with His, GSH and GSSG may lack antioxidant capacity. Moreover, the Ni(II) complex with His was found capable of enhancing 8-OH-dG production by the Ascb+H2O2 system to a greater extent than Ni(II) alone. Likewise, although to a lesser extent, the formation of 8-OH-dG was enhanced by the combination of Ni(II) and Man which do not form complexes at pH 7.4. Since His is a major Ni(II) carrier in animal tissues, the dG oxidation enhancing capacity of the Ni(II) complex with His may contribute to the toxic and carcinogenic effects of Ni(II). JF - Chemico-biological interactions AU - Kasprzak, K S AU - North, S L AU - Hernandez, L AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick, MD 21702. Y1 - 1992/09/14/ PY - 1992 DA - 1992 Sep 14 SP - 11 EP - 19 VL - 84 IS - 1 SN - 0009-2797, 0009-2797 KW - Free Radical Scavengers KW - 0 KW - Hydroxides KW - Hydroxyl Radical KW - 3352-57-6 KW - Ethanol KW - 3K9958V90M KW - Mannitol KW - 3OWL53L36A KW - Histidine KW - 4QD397987E KW - Nickel KW - 7OV03QG267 KW - Hydrogen Peroxide KW - BBX060AN9V KW - Deoxyguanosine KW - G9481N71RO KW - Glutathione KW - GAN16C9B8O KW - Ascorbic Acid KW - PQ6CK8PD0R KW - Oxygen KW - S88TT14065 KW - Index Medicus KW - Oxidation-Reduction KW - Ethanol -- pharmacology KW - Hydrogen Peroxide -- metabolism KW - Hydroxides -- metabolism KW - Ascorbic Acid -- metabolism KW - Mannitol -- pharmacology KW - Glutathione -- pharmacology KW - Hydroxylation KW - Histidine -- pharmacology KW - Deoxyguanosine -- metabolism KW - Nickel -- pharmacology KW - Oxygen -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73201466?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemico-biological+interactions&rft.atitle=Reversal+by+nickel%28II%29+of+inhibitory+effects+of+some+scavengers+of+active+oxygen+species+upon+hydroxylation+of+2%27-deoxyguanosine+in+vitro.&rft.au=Kasprzak%2C+K+S%3BNorth%2C+S+L%3BHernandez%2C+L&rft.aulast=Kasprzak&rft.aufirst=K&rft.date=1992-09-14&rft.volume=84&rft.issue=1&rft.spage=11&rft.isbn=&rft.btitle=&rft.title=Chemico-biological+interactions&rft.issn=00092797&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-26 N1 - Date created - 1992-10-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Solid phase synthesis of the proteinase of bovine leukemia virus. Comparison of its specificity to that of HIV-2 proteinase. AN - 73174200; 1325379 AB - The 126-residue proteinase (PR) of bovine leukemia virus (BLV) was synthesized by solid-phase peptide synthesis and its activity was shown using various oligopeptide substrates representing cleavage sites in BLV, human T-cell leukemia virus type 1 (HTLV-1), murine leukemia virus (MuLV) and human immunodeficiency virus type 1 (HIV-1). The specificity of the BLV PR was also compared to that of chemically synthesized human immunodeficiency virus type 2 (HIV-2) PR. Many of the peptides were cleaved at the expected site, however, 6 out of 15 were hydrolyzed only by one of the PRs. Furthermore, one BLV peptide was processed differently by the two enzymes. These results, together with the relative activities and the lack of inhibition of BLV PR by two HIV-1 PR inhibitors, suggest that the BLV PR specificity is substantially different from that of HIV PRs. JF - FEBS letters AU - Bláha, I AU - Tözsér, J AU - Kim, Y AU - Copeland, T D AU - Oroszlan, S AD - Laboratory of Molecular Virology and Carcinogenesis, NCI-Frederick Cancer Research and Development Center, MD 21702. Y1 - 1992/09/14/ PY - 1992 DA - 1992 Sep 14 SP - 389 EP - 393 VL - 309 IS - 3 SN - 0014-5793, 0014-5793 KW - Endopeptidases KW - EC 3.4.- KW - Aspartic Acid Endopeptidases KW - EC 3.4.23.- KW - HIV Protease KW - p16 protease, Human immunodeficiency virus 2 KW - Index Medicus KW - AIDS/HIV KW - Sequence Alignment KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Substrate Specificity KW - Chromatography, High Pressure Liquid KW - Endopeptidases -- chemical synthesis KW - Leukemia Virus, Bovine -- enzymology KW - Endopeptidases -- metabolism KW - Aspartic Acid Endopeptidases -- metabolism KW - Aspartic Acid Endopeptidases -- chemical synthesis KW - Aspartic Acid Endopeptidases -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73174200?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FEBS+letters&rft.atitle=Solid+phase+synthesis+of+the+proteinase+of+bovine+leukemia+virus.+Comparison+of+its+specificity+to+that+of+HIV-2+proteinase.&rft.au=Bl%C3%A1ha%2C+I%3BT%C3%B6zs%C3%A9r%2C+J%3BKim%2C+Y%3BCopeland%2C+T+D%3BOroszlan%2C+S&rft.aulast=Bl%C3%A1ha&rft.aufirst=I&rft.date=1992-09-14&rft.volume=309&rft.issue=3&rft.spage=389&rft.isbn=&rft.btitle=&rft.title=FEBS+letters&rft.issn=00145793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-06 N1 - Date created - 1992-10-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The effect of dilauroyl-L-3-phosphatidylcholine on the interaction between cytochrome P-450 1A1 and benzo[a]pyrene. AN - 73156705; 1516694 AB - Fluorescence quenching of benzo[a]pyrene (BP) by cytochrome P-450 1A1 was used to probe the effect of the lipid, dilauroyl-L-3-phosphatidylcholine, on this substrate-enzyme interaction. In the presence of lipid, a monoclonal antibody to this P-450 maximally inhibited BP binding at an antibody-to-P-450 ratio of 1:2, corresponding to an antibody crosslinked P-450 complex. The antibody did not inhibit BP binding in the absence of lipid. These results indicate that when P-450 is subjected to the orientational constraints imposed by antibody-mediated crosslinking, the lipid alters the conformation or quaternary structure of the P-450 oligomer in a manner which changes its affinity for BP. JF - FEBS letters AU - Omata, Y AU - Friedman, F K AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/09/14/ PY - 1992 DA - 1992 Sep 14 SP - 249 EP - 252 VL - 309 IS - 3 SN - 0014-5793, 0014-5793 KW - Antibodies, Monoclonal KW - 0 KW - Phosphatidylcholines KW - 1,2-dilauroylphosphatidylcholine KW - 18285-71-7 KW - Benzo(a)pyrene KW - 3417WMA06D KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Rats KW - Animals KW - Antibodies, Monoclonal -- metabolism KW - Binding, Competitive KW - Cytochrome P-450 Enzyme System -- immunology KW - Cytochrome P-450 Enzyme System -- metabolism KW - Phosphatidylcholines -- pharmacology KW - Benzo(a)pyrene -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73156705?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FEBS+letters&rft.atitle=The+effect+of+dilauroyl-L-3-phosphatidylcholine+on+the+interaction+between+cytochrome+P-450+1A1+and+benzo%5Ba%5Dpyrene.&rft.au=Omata%2C+Y%3BFriedman%2C+F+K&rft.aulast=Omata&rft.aufirst=Y&rft.date=1992-09-14&rft.volume=309&rft.issue=3&rft.spage=249&rft.isbn=&rft.btitle=&rft.title=FEBS+letters&rft.issn=00145793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-06 N1 - Date created - 1992-10-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Efficacy of atovaquone in treatment of toxoplasmosis in patients with AIDS. The NIAID-Clinical Center Intramural AIDS Program. AN - 73140488; 1355212 AB - Atovaquone (formerly 566C80) is a hydroxynaphthoquinone with potent activity against Toxoplasma in vitro and in laboratory animals. Eight patients with AIDS and presumed or biopsy confirmed toxoplasmosis who were intolerant of or had not responded to standard therapies were treated with oral atovaquone 750 mg four times a day. Seven patients showed radiographic improvement; the other remained radiographically stable. Six patients died 6-60 weeks after enrollment with no clinical (six) or necropsy (three) evidence of recurrent toxoplasmosis; two patients relapsed at 10 and 32 weeks. Toxicity was mild: only one patient required temporary discontinuation of drug due to a rash. Atovaquone is a well-tolerated drug that appears to be an effective alternative for patients with toxoplasmosis who are intolerant of standard therapies. JF - Lancet (London, England) AU - Kovacs, J A AD - Critical Care Medicine Department, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/09/12/ PY - 1992 DA - 1992 Sep 12 SP - 637 EP - 638 VL - 340 IS - 8820 SN - 0140-6736, 0140-6736 KW - Anti-Infective Agents KW - 0 KW - Naphthoquinones KW - Atovaquone KW - Y883P1Z2LT KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Magnetic Resonance Imaging KW - Administration, Oral KW - Humans KW - Adult KW - Enzyme-Linked Immunosorbent Assay KW - Middle Aged KW - Biopsy KW - Recurrence KW - Male KW - Naphthoquinones -- therapeutic use KW - Anti-Infective Agents -- therapeutic use KW - Acquired Immunodeficiency Syndrome -- complications KW - Naphthoquinones -- administration & dosage KW - Naphthoquinones -- pharmacology KW - Toxoplasmosis, Cerebral -- drug therapy KW - Anti-Infective Agents -- administration & dosage KW - Toxoplasmosis, Cerebral -- etiology KW - Anti-Infective Agents -- pharmacology KW - Toxoplasmosis, Cerebral -- diagnosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73140488?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Lancet+%28London%2C+England%29&rft.atitle=Efficacy+of+atovaquone+in+treatment+of+toxoplasmosis+in+patients+with+AIDS.+The+NIAID-Clinical+Center+Intramural+AIDS+Program.&rft.au=Kovacs%2C+J+A&rft.aulast=Kovacs&rft.aufirst=J&rft.date=1992-09-12&rft.volume=340&rft.issue=8820&rft.spage=637&rft.isbn=&rft.btitle=&rft.title=Lancet+%28London%2C+England%29&rft.issn=01406736&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-01 N1 - Date created - 1992-10-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Multitarget-ribozyme directed to cleave at up to nine highly conserved HIV-1 env RNA regions inhibits HIV-1 replication--potential effectiveness against most presently sequenced HIV-1 isolates. AN - 19713262; 8744700 AB - Several mono-, di-, tetra-, penta- and nonaribozymes were developed. These multitarget-ribozymes were targeted to cleave HIV-1 env RNA at up to nine different conserved sites. Each multitarget-ribozyme consisted of a chain of up to nine hammerhead motifs, each flanked by a different targeting sequence. The multitarget-ribozymes were functional in vitro and gave rise to multiple, specific partial and/or complete RNA digestion products. Per RNA copy, multitarget-ribozymes were more efficient than monoribozymes or ribozymes targeting a subset of the same sites. In contrast to monoribozymes, a 400nt nonaribozyme, targeted to cleave at nine different sites within a 1.3kb HIV-1 env RNA substrate, was active and showed the same specificity of cleavage when it was part of a large 3.3kb transcript. We conclude that multitarget-ribozymes retain the specificity of monoribozymes, but they are more efficient per ribozyme RNA copy and they remain active when they are part of a large transcript. A tetra-, penta- or nonaribozyme under control of the SV40 late promoter, the beta-actin gene promoter or the HIV-1 LTR, respectively, were cotransfected with the infectious HIV-1 DNA clone pNL4-3 into permissive HeLa T4 cells. Each cotransfection resulted in a specific inhibition of HIV-1 replication as determined by syncytia formation and p24 antigen release. In addition, coexpression of the nonaribozyme with an HIV-1 env RNA transcript resulted in the specific dramatic reduction of the env transcript. We conclude that the multitarget-ribozymes are also functional intracellularly. A nucleotide sequence comparison of the target sites indicates that the multitarget-ribozymes could potentially be effective against all thirty HIV-1 isolates presently sequenced. Their use may help to slow the selection of viral escape mutants and thereby prolong their effectiveness. We anticipate that multitarget-ribozymes will also be more effective in the successful targeting of less variable cellular RNAs. Images JF - Nucleic Acids Research AU - Chen, C J AU - Banerjea, A C AU - Harmison, G G AU - Haglund, K AU - Schubert, M AD - Laboratory of Viral and Molecular Pathogenesis, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/09/11/ PY - 1992 DA - 1992 Sep 11 SP - 4581 EP - 4589 PB - Oxford University Press, Oxford Journals, Great Clarendon Street VL - 20 IS - 17 SN - 0305-1048, 0305-1048 KW - Virology & AIDS Abstracts; Biotechnology and Bioengineering Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - p24 protein KW - Replication KW - Nucleotide sequence KW - Transcription KW - Digestion KW - Promoters KW - RNA KW - Human immunodeficiency virus 1 KW - Simian virus 40 KW - DNA KW - Syncytia KW - Actin KW - Ribozymes KW - V 22360:AIDS and HIV KW - W 30940:Products KW - N 14815:Nucleotide Sequence UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/19713262?accountid=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=Multitarget-ribozyme+directed+to+cleave+at+up+to+nine+highly+conserved+HIV-1+env+RNA+regions+inhibits+HIV-1+replication--potential+effectiveness+against+most+presently+sequenced+HIV-1+isolates.&rft.au=Chen%2C+C+J%3BBanerjea%2C+A+C%3BHarmison%2C+G+G%3BHaglund%2C+K%3BSchubert%2C+M&rft.aulast=Chen&rft.aufirst=C&rft.date=1992-09-11&rft.volume=20&rft.issue=17&rft.spage=4581&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 - Digestion; p24 protein; Promoters; RNA; Replication; Nucleotide sequence; DNA; Syncytia; Transcription; Actin; Ribozymes; Human immunodeficiency virus 1; Simian virus 40 ER - TY - JOUR T1 - Sequence of a rat TIS11 cDNA, an immediate early gene induced by growth factors and phorbol esters. AN - 73156957; 1511903 AB - We report here the nucleotide sequence of a rat TIS11 cDNA, an immediate early gene, induced by nerve growth factor and epidermal growth factor, by 12-O-tetradecanoyl phorbol-13-acetate, and other stimuli in PC12 pheochromocytoma cells. The deduced protein consists of 320 amino acid residues with two tandem repeats of a putative Zn(2+)-finger motif. JF - Gene AU - Kaneda, N AU - Oshima, M AU - Chung, S Y AU - Guroff, G AD - Section on Growth Factors, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/09/10/ PY - 1992 DA - 1992 Sep 10 SP - 289 EP - 291 VL - 118 IS - 2 SN - 0378-1119, 0378-1119 KW - DNA-Binding Proteins KW - 0 KW - Growth Substances KW - Immediate-Early Proteins KW - Proteins KW - RNA, Messenger KW - Tristetraprolin KW - Zfp36 protein, rat KW - DNA KW - 9007-49-2 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Rats KW - Animals KW - Base Sequence KW - Tumor Cells, Cultured KW - DNA -- genetics KW - Molecular Sequence Data KW - Amino Acid Sequence KW - RNA, Messenger -- genetics KW - Proteins -- chemistry KW - Zinc Fingers -- genetics KW - Growth Substances -- pharmacology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Gene Expression Regulation -- drug effects KW - Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73156957?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gene&rft.atitle=Sequence+of+a+rat+TIS11+cDNA%2C+an+immediate+early+gene+induced+by+growth+factors+and+phorbol+esters.&rft.au=Kaneda%2C+N%3BOshima%2C+M%3BChung%2C+S+Y%3BGuroff%2C+G&rft.aulast=Kaneda&rft.aufirst=N&rft.date=1992-09-10&rft.volume=118&rft.issue=2&rft.spage=289&rft.isbn=&rft.btitle=&rft.title=Gene&rft.issn=03781119&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-30 N1 - Date created - 1992-09-30 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - X63369; GENBANK; M74892; M79310; M74891; S43293; S43295; S43286; M90357; S43297; M79309 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The study of markers of biological effect in cancer prevention research trials. AN - 73185104; 1521908 AB - Biological markers may provide a valuable tool for the development of cancer prevention agents, for monitoring patient compliance to a selected intervention, or for further defining the carcinogenic process. This discussion focuses on markers of biological effect and the rationale for their use in cancer prevention trials. Recent studies with biological markers are investigating their incorporation into phase-I, -II, and -III chemoprevention clinical trial designs. Their use in clinical studies is expected to increase the number of agents that may be evaluated and to provide valuable information on the biological effectiveness of agents, doses, and schedules. Markers may also provide information to help in selecting high-risk groups for prevention research, and to indicate the pathways inhibited and the stage of carcinogenesis affected. Such information may prove of crucial importance in strengthening the rationale for long-term trials and other ancillary research. Biomarker research for colon carcinogenesis is discussed, including examples of a number of recent trials that may influence future progress in this area of prevention research. A crucial step in this process is marker validation as an aspect of major prospective observational and intervention studies where cancer incidence is the endpoint. We cannot be fully confident of markers as intermediate endpoints until the evidence from clinical trials is sufficiently strong to support major public health initiatives for prevention. JF - International journal of cancer AU - Greenwald, P AU - Witkin, K M AU - Malone, W F AU - Byar, D P AU - Freedman, L S AU - Stern, H R AD - Division of Cancer Prevention and Control, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/09/09/ PY - 1992 DA - 1992 Sep 09 SP - 189 EP - 196 VL - 52 IS - 2 SN - 0020-7136, 0020-7136 KW - Antineoplastic Agents KW - 0 KW - Biomarkers, Tumor KW - Index Medicus KW - Sensitivity and Specificity KW - Drug Evaluation KW - Colonic Neoplasms -- genetics KW - Patient Compliance KW - Colon -- pathology KW - Cell Transformation, Neoplastic -- chemistry KW - Risk Factors KW - Humans KW - Prognosis KW - Clinical Trials as Topic KW - Intestinal Mucosa -- pathology KW - Research KW - Antineoplastic Agents -- therapeutic use KW - Precancerous Conditions -- chemistry KW - Biomarkers, Tumor -- analysis KW - Neoplasms -- prevention & control KW - Precancerous Conditions -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73185104?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+study+of+markers+of+biological+effect+in+cancer+prevention+research+trials.&rft.au=Greenwald%2C+P%3BWitkin%2C+K+M%3BMalone%2C+W+F%3BByar%2C+D+P%3BFreedman%2C+L+S%3BStern%2C+H+R&rft.aulast=Greenwald&rft.aufirst=P&rft.date=1992-09-09&rft.volume=52&rft.issue=2&rft.spage=189&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 - 1992-10-13 N1 - Date created - 1992-10-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prescription drug diversion control and medical practice. AN - 73131286; 1507377 AB - Concern about the role of prescription drug diversion in drug abuse has led to demands for more stringent regulation and for better ways to detect prescription drug diversion. Advances in technology now allow point-of-sale computer systems to report prescriptions filled by pharmacies to state agencies rapidly and possibly more economically. However, the advantages of more comprehensive control systems must be balanced against their possible effects on medical practice and patient care. Our limited knowledge about prescription drug diversion and the impact of diversion control systems on medical practice is summarized. Needed research is outlined together with the components of a diversion control program that balances reducing drug diversion with minimizing adverse effects on medical practice and patient care. We stress the need for broadly defined practice parameters and peer review by medical experts thoroughly familiar with the complexities of medical practice. JF - JAMA AU - Cooper, J R AU - Czechowicz, D J AU - Petersen, R C AU - Molinari, S P AD - National Institute on Drug Abuse, Rockville, MD. Y1 - 1992/09/09/ PY - 1992 DA - 1992 Sep 09 SP - 1306 EP - 1310 VL - 268 IS - 10 SN - 0098-7484, 0098-7484 KW - Abridged Index Medicus KW - Index Medicus KW - United States KW - Humans KW - Health Services Research KW - Databases, Factual KW - Online Systems KW - Practice Management, Medical KW - Drug Utilization KW - Drug and Narcotic Control -- legislation & jurisprudence KW - Drug Prescriptions KW - Substance-Related Disorders -- prevention & control KW - Clinical Pharmacy Information Systems -- legislation & jurisprudence UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73131286?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Prescription+drug+diversion+control+and+medical+practice.&rft.au=Cooper%2C+J+R%3BCzechowicz%2C+D+J%3BPetersen%2C+R+C%3BMolinari%2C+S+P&rft.aulast=Cooper&rft.aufirst=J&rft.date=1992-09-09&rft.volume=268&rft.issue=10&rft.spage=1306&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-22 N1 - Date created - 1992-09-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Functional expression of renal organic anion transport in Xenopus laevis oocytes. AN - 73387559; 1281263 AB - Secretion of organic anions by the kidney plays a critical role in the elimination of toxic agents from the body. Recent findings in isolated membranes and intact tissue have demonstrated the participation of multiple transport proteins in this process. As a first step toward molecular characterization of these proteins through expression cloning, the studies reported below demonstrate functional expression of both fumarate- and lithium-sensitive glutarate and probenecid-sensitive p-aminohippurate transport in Xenopus oocytes injected with rat kidney poly(A)+ RNA. Maximal increase in substrate uptake over buffer-injected controls was reached by 5 days after mRNA injection. Expression of size-fractionated mRNA indicated that the active species with respect to both transport activities were in the range of 1.8 to 3.5 kb. JF - Molecular and cellular biochemistry AU - Wolff, N A AU - Philpot, R M AU - Miller, D S AU - Pritchard, J B AD - Laboratory of Cellular and Molecular Pharmacology, NIH/National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992/09/08/ PY - 1992 DA - 1992 Sep 08 SP - 35 EP - 41 VL - 114 IS - 1-2 SN - 0300-8177, 0300-8177 KW - Anions KW - 0 KW - Glutarates KW - Ion Channels KW - RNA, Messenger KW - p-Aminohippuric Acid KW - Y79XT83BJ9 KW - Index Medicus KW - Rats KW - Xenopus laevis KW - Animals KW - Glutarates -- metabolism KW - Biological Transport KW - p-Aminohippuric Acid -- metabolism KW - Microinjections KW - RNA, Messenger -- genetics KW - Oocytes -- metabolism KW - Kidney -- physiology KW - Anions -- metabolism KW - Ion Channels -- genetics KW - Ion Channels -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73387559?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+biochemistry&rft.atitle=Functional+expression+of+renal+organic+anion+transport+in+Xenopus+laevis+oocytes.&rft.au=Wolff%2C+N+A%3BPhilpot%2C+R+M%3BMiller%2C+D+S%3BPritchard%2C+J+B&rft.aulast=Wolff&rft.aufirst=N&rft.date=1992-09-08&rft.volume=114&rft.issue=1-2&rft.spage=35&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 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 - A leucine----proline mutation in the H1 subdomain of keratin 1 causes epidermolytic hyperkeratosis. AN - 73152605; 1381288 AB - Epidermolytic hyperkeratosis is an autosomal dominant disorder affecting the structural integrity of the suprabasal layers of human epidermis. We have recently documented in one family linkage of the disease phenotype to the cluster of type II keratins. We have now identified a leucine----proline amino acid substitution in the conserved H1 subdomain of keratin 1 that is present only in affected family members. Using a quantitative assay and electron microscopy with synthetic peptides, we show that, whereas the wild-type H1 peptide rapidly disassembles preformed keratin filaments in vitro, the mutant peptide does this far less efficiently. Therefore the mutation in keratin 1 is likely to cause defective keratin filaments and hence a defective cytoskeleton in the epidermal cells in vivo. JF - Cell AU - Chipev, C C AU - Korge, B P AU - Markova, N AU - Bale, S J AU - DiGiovanna, J J AU - Compton, J G AU - Steinert, P M AD - Skin Biology Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/09/04/ PY - 1992 DA - 1992 Sep 04 SP - 821 EP - 828 VL - 70 IS - 5 SN - 0092-8674, 0092-8674 KW - Keratins KW - 68238-35-7 KW - Proline KW - 9DLQ4CIU6V KW - Leucine KW - GMW67QNF9C KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Base Sequence KW - Intermediate Filaments -- chemistry KW - Humans KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Keratins -- genetics KW - Ichthyosiform Erythroderma, Congenital -- pathology KW - Ichthyosiform Erythroderma, Congenital -- etiology KW - Ichthyosiform Erythroderma, Congenital -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73152605?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+leucine----proline+mutation+in+the+H1+subdomain+of+keratin+1+causes+epidermolytic+hyperkeratosis.&rft.au=Chipev%2C+C+C%3BKorge%2C+B+P%3BMarkova%2C+N%3BBale%2C+S+J%3BDiGiovanna%2C+J+J%3BCompton%2C+J+G%3BSteinert%2C+P+M&rft.aulast=Chipev&rft.aufirst=C&rft.date=1992-09-04&rft.volume=70&rft.issue=5&rft.spage=821&rft.isbn=&rft.btitle=&rft.title=Cell&rft.issn=00928674&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-07 N1 - Date created - 1992-10-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Predicting responses of nonlinear neurons in monkey striate cortex to complex patterns. AN - 85233499; pmid-1527596 AB - The overwhelming majority of neurons in primate visual cortex are nonlinear. For those cells, the techniques of linear system analysis, used with some success to model retinal ganglion cells and striate simple cells, are of limited applicability. As a start toward understanding the properties of nonlinear visual neurons, we have recorded responses of striate complex cells to hundreds of images, including both simple stimuli (bars and sinusoids) as well as complex stimuli (random textures and 3-D shaded surfaces). The latter set tended to give the strongest response. We created a neural network model for each neuron using an iterative optimization algorithm. The recorded responses to some stimulus patterns (the training set) were used to create the model, while responses to other patterns were reserved for testing the networks. The networks predicted recorded responses to training set patterns with a median correlation of 0.95. They were able to predict responses to test stimuli not in the training set with a correlation of 0.78 overall, and a correlation of 0.65 for complex stimuli considered alone. Thus, they were able to capture much of the input/output transfer function of the neurons, even for complex patterns. Examining connection strengths within each network, different parts of the network appeared to handle information at different spatial scales. To gain further insights, the network models were inverted to construct "optimal" stimuli for each cell, and their receptive fields were mapped with high-resolution spots. The receptive field properties of complex cells could not be reduced to any simpler mathematical formulation than the network models themselves. JF - The Journal of Neuroscience AU - Lehky, S R AU - Sejnowski, T J AU - Desimone, R AD - Laboratory of Neuropsychology, National Institute of Mental Health, Bethesda, Maryland 20892. PY - 1992 SP - 3568 EP - 3581 VL - 12 IS - 9 SN - 0270-6474, 0270-6474 KW - Visual Cortex KW - Photic Stimulation KW - Neural Networks (Computer) KW - Neurons KW - Animal KW - Support, Non-U.S. Gov't KW - Forecasting KW - Macaca mulatta KW - Female KW - Nerve Net KW - Visual Perception UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85233499?accountid=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=Predicting+responses+of+nonlinear+neurons+in+monkey+striate+cortex+to+complex+patterns.&rft.au=Lehky%2C+S+R%3BSejnowski%2C+T+J%3BDesimone%2C+R&rft.aulast=Lehky&rft.aufirst=S&rft.date=1992-09-01&rft.volume=12&rft.issue=9&rft.spage=3568&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 - Dissociations among memory measures in memory-impaired subjects: evidence for a processing account of memory. AN - 85216382; pmid-1453972 AB - Deficits in conceptual transfer on both implicit and explicit memory tests were obtained for memory-impaired temporal lobe epileptic (TLE) subjects in three studies. In Experiment 1, in which a generate-read paradigm was employed, memory-impaired TLEs failed to show normal generation effects on conceptually driven tests of semantic cued recall and general knowledge questions, although their data-driven memory as measured by word-fragment completion and graphemic cued recall tasks was normal. In Experiment 2, memory-impaired patients having left temporal lobe seizure foci were tested on these four tasks and compared with nonimpaired TLEs having right temporal foci. The left TLEs showed deficits on conceptually driven tasks and normal memory for data-driven tests. These findings were extended in Experiment 3, in which left TLE patients failed to show any benefit from blocked study, as compared with random study, on category production and semantic cued-recall tests, although right TLEs and normal controls showed blocking effects on both tasks. These findings may be accommodated by a processing framework of memory in which memory-impaired patients are characterized as having deficits in conceptual, but not in data-driven, processing capabilities. JF - Memory and Cognition AU - Blaxton, T A AD - National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892. PY - 1992 SP - 549 EP - 562 VL - 20 IS - 5 SN - 0090-502X, 0090-502X KW - Wechsler Scales KW - Human KW - Adult KW - Word Association Tests KW - Neuropsychological Tests KW - Research Design KW - Female KW - Male KW - Memory Disorders UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85216382?accountid=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=Memory+and+Cognition&rft.atitle=Dissociations+among+memory+measures+in+memory-impaired+subjects%3A+evidence+for+a+processing+account+of+memory.&rft.au=Blaxton%2C+T+A&rft.aulast=Blaxton&rft.aufirst=T&rft.date=1992-09-01&rft.volume=20&rft.issue=5&rft.spage=549&rft.isbn=&rft.btitle=&rft.title=Memory+and+Cognition&rft.issn=0090502X&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Cyclic cortical reorganization during early childhood. AN - 85209883; pmid-1389121 AB - EEG coherence was computed from 8 left and 8 right intrahemispheric electrode pairs from 253 children ranging in mean age from 6 months to 7 years. The first derivative of mean coherence was computed in order to study growth spurts or rapid changes in mean coherence over the early childhood period. Growth spurts in EEG coherence were approximately 6 months to 1 year in duration and involved a cyclical process composed of a sequential lengthening of intracortical connections in the left hemisphere and a sequential contraction of intracortical connections in the right hemisphere. Each growth spurt cycle had a period of approximately 2 to 4 years and involved both a rostral-caudal expansion and contraction as well as a lateral-to-medial rotation. Data support the view that the functions of the left and right hemisphere are established early in human development through complementary developmental sequences and that these sequences appear to recapitulate differences in adult hemispheric function. JF - Brain and Cognition AU - Thatcher, R W AD - Clinical Neuroscience Program, National Institutes of Health, National Institutes of Neurological Disorders and Stroke, Bethesda, MD 20892. PY - 1992 SP - 24 EP - 50 VL - 20 IS - 1 SN - 0278-2626, 0278-2626 KW - Synapses KW - Age Factors KW - Sex Factors KW - Human KW - Electroencephalography KW - Infant, Newborn KW - Child KW - Child, Preschool KW - Cerebral Cortex KW - Frontal Lobe KW - Infant KW - Neural Pathways KW - Child Development KW - Models, Neurological KW - Laterality KW - Male KW - Female UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85209883?accountid=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+Cognition&rft.atitle=Cyclic+cortical+reorganization+during+early+childhood.&rft.au=Thatcher%2C+R+W&rft.aulast=Thatcher&rft.aufirst=R&rft.date=1992-09-01&rft.volume=20&rft.issue=1&rft.spage=24&rft.isbn=&rft.btitle=&rft.title=Brain+and+Cognition&rft.issn=02782626&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Clinical, pathologic, and biochemical features of a cholesterol lipidosis accompanied by hyperlipidemia and xanthomas. AN - 85161384; pmid-1513468 AB - We describe the unique clinical and histopathologic features of a child with biochemical and immunocytochemical features of Niemann-Pick disease type C (NPC). Clinically, she was found to have multiple xanthomas of the upper aerodigestive tract with dysphagia and expressive language delay, splenomegaly, bony infarcts, and type IIb hyperlipidemia. Neurologic examination was otherwise normal. Microscopy revealed foam cells in her bone marrow, liver, tongue, tonsils, glottis, and in normal-appearing peritonsillar mucosa. Lipid analysis of a liver biopsy specimen showed a small increase in phospholipids, a twofold increase in sphingomyelin, a fivefold increase in cholesterol, and a marked (25-fold) increase in bis(monoacylglycerol) phosphate. Lysosomal acid hydrolase activities in cultured skin fibroblasts were nondiagnostic. Biochemical and immunocytochemical studies of cultured fibroblasts demonstrated lysosomal accumulation of unesterified LDL-derived cholesterol as well as delayed induction of homeostatic responses to endogenous cholesterol consistent with a diagnosis of NPC. Based upon these observations, we speculate that this patient could have a new phenotypic expression of NPC or represents a new cholesterol lipidosis biochemically resembling NPC. The chance occurrence of two separate lipid disorders seems less likely. JF - Neurology AU - Filling-Katz, M R AU - Miller, S P AU - Merrick, H F AU - Travis, W D AU - Gregg, R E AU - Tsokos, M AU - Comly, M AU - Kaneski, C R AU - Mackie, S AU - Lebovics, R S AD - Laboratory of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892. PY - 1992 SP - 1768 EP - 1774 VL - 42 IS - 9 SN - 0028-3878, 0028-3878 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85161384?accountid=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=Clinical%2C+pathologic%2C+and+biochemical+features+of+a+cholesterol+lipidosis+accompanied+by+hyperlipidemia+and+xanthomas.&rft.au=Filling-Katz%2C+M+R%3BMiller%2C+S+P%3BMerrick%2C+H+F%3BTravis%2C+W+D%3BGregg%2C+R+E%3BTsokos%2C+M%3BComly%2C+M%3BKaneski%2C+C+R%3BMackie%2C+S%3BLebovics%2C+R+S&rft.aulast=Filling-Katz&rft.aufirst=M&rft.date=1992-09-01&rft.volume=42&rft.issue=9&rft.spage=1768&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 - Selective amplification and partial sequencing of cDNAs encoding G protein alpha subunits from cochlear tissues. AN - 85156007; pmid-1429253 AB - An approach utilizing the polymerase chain reaction (PCR) was devised to clone members of a family of cDNAs encoding the alpha subunit of G proteins in the cochlea. RNA was extracted from the whole cochlea of the mouse and from the organ of Corti or the lateral wall of the cochlea microdissected from the guinea pig cochlea. The RNA was reverse-transcribed to cDNA which was selectively amplified by PCR using degenerate primers corresponding to two conserved regions of the G protein coding sequence. PCR products were cloned into a plasmid for sequencing. The following seven cDNA clones of particular interest were obtained: three clones putatively coding for part of the alpha-subunit of a stimulatory G protein (Gs), one clone putatively coding for part of the alpha-subunit of an inhibitory G protein (Gi) and three clones putatively coding for part of the alpha-subunit of a transducin (Gi)-like protein. Possible functions in the cochlea of putative G proteins with alpha-subunits partly encoded by these cDNA clones are briefly discussed and future studies are suggested. JF - Hearing Research AU - Tachibana, M AU - Wilcox, E AU - Yokotani, N AU - Schneider, M AU - Fex, J AD - Laboratory of Molecular Biology, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, Maryland 20892. PY - 1992 SP - 82 EP - 88 VL - 62 IS - 1 SN - 0378-5955, 0378-5955 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85156007?accountid=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=Hearing+Research&rft.atitle=Selective+amplification+and+partial+sequencing+of+cDNAs+encoding+G+protein+alpha+subunits+from+cochlear+tissues.&rft.au=Tachibana%2C+M%3BWilcox%2C+E%3BYokotani%2C+N%3BSchneider%2C+M%3BFex%2C+J&rft.aulast=Tachibana&rft.aufirst=M&rft.date=1992-09-01&rft.volume=62&rft.issue=1&rft.spage=82&rft.isbn=&rft.btitle=&rft.title=Hearing+Research&rft.issn=03785955&rft_id=info:doi/ LA - English DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Construction of a cDNA library from microdissected guinea pig organ of Corti. AN - 85155700; pmid-1358871 AB - Poly (A) RNA was isolated from microdissected guinea pig organ of Corti and converted into cDNA with RNase H- murine leukemia virus reverse transcriptase. After size fractionation, the cDNA was directionally ligated into the vector pSPORT 1 and the plasmids were transformed into DH10B E. coli via electroporation. The library was found to have 3.35 x 10(6) independent colonies with ten percent of the colonies lacking an insert. After checking 33 randomly selected colonies for inserts, the average insert size was 1218 base pairs, ranging from 3300 base pairs to 400 base pairs. The library was screened with a beta-actin oligonucleotide probe and 1.4% of the colonies contained an insert hybridizing to the probe. JF - Hearing Research AU - Wilcox, E R AU - Fex, J AD - Laboratory of Molecular Biology, National Institute on Deafness and Other Communication Disorders, NIH, Bethesda, Maryland 20892. PY - 1992 SP - 124 EP - 126 VL - 62 IS - 1 SN - 0378-5955, 0378-5955 KW - Oligonucleotide Probes KW - RNA, Messenger KW - Animals KW - Poly A KW - Base Sequence KW - Guinea Pigs KW - Actins KW - DNA KW - Molecular Sequence Data KW - Organ of Corti KW - Plasmids KW - Gene Library UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85155700?accountid=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=Hearing+Research&rft.atitle=Construction+of+a+cDNA+library+from+microdissected+guinea+pig+organ+of+Corti.&rft.au=Wilcox%2C+E+R%3BFex%2C+J&rft.aulast=Wilcox&rft.aufirst=E&rft.date=1992-09-01&rft.volume=62&rft.issue=1&rft.spage=124&rft.isbn=&rft.btitle=&rft.title=Hearing+Research&rft.issn=03785955&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - CONF T1 - The role of biological markers in epidemiological research: future directions. AN - 73583747; 1363834 JF - Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology AU - Iwamoto, K AU - Obrams, G I AU - Schottenfeld, D Y1 - 1992 PY - 1992 DA - 1992 SP - 519 EP - 522 VL - 1 IS - 6 KW - Biomarkers KW - 0 KW - Carcinogens KW - Hormones KW - Index Medicus KW - Smoking KW - Hormones -- analysis KW - Disease Susceptibility KW - Humans KW - Forecasting KW - Carcinogens -- analysis KW - Diet KW - Neoplasms -- chemistry KW - Biomarkers -- analysis KW - Neoplasms -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73583747?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&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=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=The+role+of+biological+markers+in+epidemiological+research%3A+future+directions.&rft.au=Iwamoto%2C+K%3BObrams%2C+G+I%3BSchottenfeld%2C+D&rft.aulast=Iwamoto&rft.aufirst=K&rft.date=1992-09-01&rft.volume=1&rft.issue=6&rft.spage=519&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 - 1993-06-17 N1 - Date created - 1993-06-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Allelic frequency of a p53 polymorphism in human lung cancer. AN - 73522303; 1302561 AB - p53 is a tumor suppressor gene that is mutated in diverse tumor types. Here we report the frequencies of common polymorphic variants at codon 72 of the p53 gene in germline DNA of lung cancer cases and controls as determined by a polymerase chain reaction strategy. The observed allelic distribution was found to be significantly different between African-Americans and Caucasians in this U.S. population. The frequency of polymorphic variants was similar in lung cancer cases and controls after adjustment for race. However, among lung cancer patients the proline variant at codon 72 was in excess in adenocarcinoma patients by comparison with other histologies. JF - Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology AU - Weston, A AU - Perrin, L S AU - Forrester, K AU - Hoover, R N AU - Trump, B F AU - Harris, C C AU - Caporaso, N E AD - Laboratory of Human Carcinogenesis, National Cancer Institute, NIH, Bethesda 20892. PY - 1992 SP - 481 EP - 483 VL - 1 IS - 6 SN - 1055-9965, 1055-9965 KW - Codon KW - 0 KW - DNA, Neoplasm KW - Arginine KW - 94ZLA3W45F KW - Proline KW - 9DLQ4CIU6V KW - Index Medicus KW - Codon -- genetics KW - Homozygote KW - Humans KW - Adenocarcinoma -- genetics KW - European Continental Ancestry Group -- genetics KW - Lung Diseases, Obstructive -- genetics KW - Proline -- genetics KW - Exons -- genetics KW - Genotype KW - African Continental Ancestry Group -- genetics KW - Arginine -- genetics KW - Heterozygote KW - Case-Control Studies KW - DNA, Neoplasm -- genetics KW - Middle Aged KW - Carcinoma -- genetics KW - Alleles KW - Gene Frequency KW - Polymorphism, Genetic KW - Genes, p53 -- genetics KW - Lung Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73522303?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Allelic+frequency+of+a+p53+polymorphism+in+human+lung+cancer.&rft.au=Weston%2C+A%3BPerrin%2C+L+S%3BForrester%2C+K%3BHoover%2C+R+N%3BTrump%2C+B+F%3BHarris%2C+C+C%3BCaporaso%2C+N+E&rft.aulast=Weston&rft.aufirst=A&rft.date=1992-09-01&rft.volume=1&rft.issue=6&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 - 1993-06-17 N1 - Date created - 1993-06-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The effects of a non-competitive NMDA receptor antagonist, MK-801, on behavioral hyperalgesia and dorsal horn neuronal activity in rats with unilateral inflammation. AN - 73384771; 1454389 AB - The involvement of NMDA receptors in rats with peripheral inflammation and hyperalgesia was evaluated by administration of the non-competitive NMDA receptor antagonist, MK-801. Inflammation and hyperalgesia was induced by intradermal injection of complete Freund's adjuvant (CFA) or carrageenan into the left hind paw. The latency of paw withdrawal from a thermal stimulus was used as a measure of hyperalgesia in awake rats. MK-801 (1.6 mg/kg, i.p., or 31.5 micrograms, intrathecal) significantly attenuated thermal hyperalgesia and reduced its duration in comparison to saline-injected rats (P less than 0.05). The receptive field size of nociceptive-specific and wide-dynamic-range neurons in the superficial and deep spinal dorsal horn recorded 24 h after injection of CFA was significantly reduced to 73 +/- 6% (P less than 0.05, n = 8) and 74 +/- 4% (P less than 0.05, n = 8) of control values, respectively, by a cumulative dose of 3 mg/kg of MK-801 (i.v.). MK-801 (2 mg/kg) prevented the expansion of the receptive fields of dorsal horn neurons recorded 5 +/- 0.4 h (n = 5) after intradermal injection of CFA as compared to saline-injected rats (P less than 0.05). MK-801 had no significant effect on receptive field size of dorsal horn neurons in rats without CFA-induced inflammation but blocked a transient expansion of the receptive fields induced by 1 Hz, C-fiber intensity electrical stimulation of the sciatic nerve. The background activity and noxious heat-evoked response of dorsal horn neurons in rats with CFA-induced inflammation were primarily inhibited and noxious pinch-evoked activity was both facilitated and inhibited by the administration of MK-801. These results support the hypothesis that NMDA receptors are involved in the dorsal horn neuronal plasticity and behavioral hyperalgesia that follows peripheral tissue inflammation. JF - Pain AU - Ren, K AU - Hylden, J L AU - Williams, G M AU - Ruda, M A AU - Dubner, R AD - Neurobiology and Anesthesiology Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 331 EP - 344 VL - 50 IS - 3 SN - 0304-3959, 0304-3959 KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - Freund's Adjuvant KW - 9007-81-2 KW - Index Medicus KW - Rats KW - Animals KW - Neurons -- drug effects KW - Neurons -- physiology KW - Pain KW - Physical Stimulation KW - Electric Stimulation KW - Male KW - Behavior, Animal -- drug effects KW - Hyperalgesia -- physiopathology KW - Spinal Cord -- drug effects KW - Myelitis -- chemically induced KW - Spinal Cord -- pathology KW - Myelitis -- physiopathology KW - Myelitis -- pathology KW - Dizocilpine Maleate -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73384771?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pain&rft.atitle=The+effects+of+a+non-competitive+NMDA+receptor+antagonist%2C+MK-801%2C+on+behavioral+hyperalgesia+and+dorsal+horn+neuronal+activity+in+rats+with+unilateral+inflammation.&rft.au=Ren%2C+K%3BHylden%2C+J+L%3BWilliams%2C+G+M%3BRuda%2C+M+A%3BDubner%2C+R&rft.aulast=Ren&rft.aufirst=K&rft.date=1992-09-01&rft.volume=50&rft.issue=3&rft.spage=331&rft.isbn=&rft.btitle=&rft.title=Pain&rft.issn=03043959&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-01-06 N1 - Date created - 1993-01-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential expression of carboxyl terminal derivatives of amyloid precursor protein among cell lines. AN - 73357065; 1453480 AB - Understanding the pathway for amyloid percursor protein (APP) catabolism has become an important line of investigation. APP is a ubiquitous membrane bound protein that is rapidly cleaved at the membrane, yielding a secreted protein identical to protease nexin II and an internalized 11.5 kDa 100 residue C terminal derivative (CTD). The levels of CTDs in a variety of cell lines have been examined and were found to differ. Cell types associated with the pathology of Alzheimer's disease (AD), such as olfactory neuroblasts (ON) and cortical vascular endothelial cells, have higher levels of CTDs than lymphoblasts and melanoma cells. The mechanism of CTD catabolism appears to involve the lysosome because blockade of lysosomal but not endosomal or mitochondrial function results in increased levels of CTDs. Under these conditions, production of larger, amyloidogenic CTDs is also seen. In cells possessing higher levels of CTDs we find that the mechanism for production of amyloidogenic CTDs may involve the internalization of intact full-length APP. Thus, inhibition of the lysosomal system appears capable of generating amyloidogenic peptides. The amount of amyloidogenic peptides appears to vary among cell lines. Such variation may shed light on why amyloid accumulates around specific cell types such as vascular endothelial cells, neurons, and glia. Finally, disfunction of the lysosomal system may play a role in the pathogenesis of Alzheimer's disease. JF - Journal of neuroscience research AU - Wolozin, B AU - Bacic, M AU - Merrill, M J AU - Lesch, K P AU - Chen, C AU - Lebovics, R S AU - Sunderland, T AD - Laboratory of Clinical Science, NIMH, Bethesda, MD 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 163 EP - 169 VL - 33 IS - 1 SN - 0360-4012, 0360-4012 KW - Amyloid beta-Protein Precursor KW - 0 KW - Antimetabolites KW - Chloroquine KW - 886U3H6UFF KW - Monensin KW - 906O0YJ6ZP KW - Index Medicus KW - Antimetabolites -- pharmacology KW - Immunoblotting KW - Humans KW - Chloroquine -- metabolism KW - Monensin -- pharmacology KW - Lysosomes -- metabolism KW - Lysosomes -- drug effects KW - Alzheimer Disease -- metabolism KW - Immunohistochemistry KW - Cell Line KW - Alzheimer Disease -- pathology KW - Neurons -- metabolism KW - Neurons -- drug effects KW - Amyloid beta-Protein Precursor -- biosynthesis KW - Neurons -- ultrastructure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73357065?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Differential+expression+of+carboxyl+terminal+derivatives+of+amyloid+precursor+protein+among+cell+lines.&rft.au=Wolozin%2C+B%3BBacic%2C+M%3BMerrill%2C+M+J%3BLesch%2C+K+P%3BChen%2C+C%3BLebovics%2C+R+S%3BSunderland%2C+T&rft.aulast=Wolozin&rft.aufirst=B&rft.date=1992-09-01&rft.volume=33&rft.issue=1&rft.spage=163&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 - 1993-01-06 N1 - Date created - 1993-01-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The use of stable isotopes to identify reactive metabolites and target macromolecules associated with toxicities of halogenated hydrocarbon compounds. AN - 73338804; 1441605 AB - 1. Halogenated compounds, such as the inhalation anaesthetics, halothane and enflurane, and the chemicals chloroform, carbon tetrachloride, and bromotrichloromethane can cause hepatotoxicity, nephrotoxicity, and inactivation of cytochromes P-450. Each of these toxicities is mediated by reactive metabolites. 2. Stable isotopes of hydrogen, carbon, chlorine and oxygen have been used in conjunction with mass spectrometry and n.m.r. spectrometry to identify the structures of these metabolites, to elucidate the mechanisms of their formation, and to characterize the structures of their macromolecular adducts. 3. In a number of cases, oxidative pathways of metabolism to toxic metabolites have been defined by kinetic deuterium isotope effects. 4. Recently, we have found that the trichloromethyl radical metabolite of bromotrichloromethane can activate myoglobin by causing the covalent cross-linking of haem to protein. The structure of a haem-myoglobin adduct has been defined by the use of stable isotope studies. JF - Xenobiotica; the fate of foreign compounds in biological systems AU - Osawa, Y AU - Highet, R J AU - Pohl, L R AD - Laboratory of Chemical Pharmacology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. PY - 1992 SP - 1147 EP - 1156 VL - 22 IS - 9-10 SN - 0049-8254, 0049-8254 KW - Carbon Isotopes KW - 0 KW - Hydrocarbons, Halogenated KW - Isotopes KW - Macromolecular Substances KW - Oxygen Isotopes KW - Chlorine KW - 4R7X1O2820 KW - Deuterium KW - AR09D82C7G KW - Index Medicus KW - Oxidation-Reduction KW - Animals KW - Kinetics KW - Hydrocarbons, Halogenated -- toxicity KW - Hydrocarbons, Halogenated -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73338804?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+use+of+stable+isotopes+to+identify+reactive+metabolites+and+target+macromolecules+associated+with+toxicities+of+halogenated+hydrocarbon+compounds.&rft.au=Osawa%2C+Y%3BHighet%2C+R+J%3BPohl%2C+L+R&rft.aulast=Osawa&rft.aufirst=Y&rft.date=1992-09-01&rft.volume=22&rft.issue=9-10&rft.spage=1147&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 - 1992-12-23 N1 - Date created - 1992-12-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Massive intrahepatic hemorrhage following routine liver biopsy in a patient with rheumatoid arthritis treated with methotrexate. AN - 73328953; 1433018 AB - Massive intrahepatic hemorrhage occurred in a patient with rheumatoid arthritis (RA) after a routine liver biopsy done to assess possible methotrexate (MTX) hepatotoxicity. Major complications of liver biopsy occur about once in every 600 biopsies, and mortality from liver biopsy has been reported. Life threatening hepatic toxicity occurs rarely during low dose MTX administration, and it is unclear whether routine liver biopsies identify patients at high risk for these complications. Until the relative risks of liver biopsy and serious MTX liver toxicity are better defined, the use of routine liver biopsies should be recommended only after careful consideration of potential procedural complications in patients with RA treated with MTX. JF - The Journal of rheumatology AU - Cash, J M AU - Swain, M AU - Di Bisceglie, A M AU - Wilder, R L AU - Crofford, L J AD - Arthritis and Rheumatism Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 1466 EP - 1468 VL - 19 IS - 9 SN - 0315-162X, 0315-162X KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - Liver -- pathology KW - Dose-Response Relationship, Drug KW - Humans KW - Chemical and Drug Induced Liver Injury KW - Adult KW - Female KW - Arthritis, Rheumatoid -- drug therapy KW - Methotrexate -- adverse effects KW - Liver Diseases -- pathology KW - Methotrexate -- therapeutic use KW - Liver Diseases -- etiology KW - Biopsy -- adverse effects KW - Hemorrhage -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73328953?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+rheumatology&rft.atitle=Massive+intrahepatic+hemorrhage+following+routine+liver+biopsy+in+a+patient+with+rheumatoid+arthritis+treated+with+methotrexate.&rft.au=Cash%2C+J+M%3BSwain%2C+M%3BDi+Bisceglie%2C+A+M%3BWilder%2C+R+L%3BCrofford%2C+L+J&rft.aulast=Cash&rft.aufirst=J&rft.date=1992-09-01&rft.volume=19&rft.issue=9&rft.spage=1466&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+rheumatology&rft.issn=0315162X&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 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Identification of individual benzo[c]phenanthrene dihydrodiol epoxide-DNA adducts by the 32P-postlabeling assay. AN - 73328254; 1446010 AB - Purine deoxyribonucleoside 3'-phosphates were reacted separately with the four configurational isomers of benzo[c]phenanthrene 3,4-dihydrodiol 1,2-epoxide. Products resulting from the cis and trans opening of the epoxide ring by the exocyclic amino groups of deoxyadenosine and deoxyguanosine 3'-phosphates were separated by high-pressure liquid chromatography and identified by comparison of the observed circular dichroism spectra with the known spectra for the corresponding nucleoside adducts. The 16 structurally identified benzo[c]phenanthrene-purine deoxyribonucleoside 3'-phosphate adducts were then separately postlabeled according to the Randerath method, and the positions of the individual bisphosphates were mapped by thin-layer chromatography. Chromatographic conditions were developed that allowed separation of the four adducts for 3 of the 4 dihydrodiol epoxide isomers. JF - Chemical research in toxicology AU - Canella, K A AU - Peltonen, K AU - Yagi, H AU - Jerina, D M AU - Dipple, A AD - Chemistry of Carcinogenesis Laboratory, NCI-Frederick Cancer Research and Development Center, Maryland 21702. PY - 1992 SP - 685 EP - 690 VL - 5 IS - 5 SN - 0893-228X, 0893-228X KW - Epoxy Compounds KW - 0 KW - Mutagens KW - Phenanthrenes KW - benzo(c)phenanthrene 3,4-dihydrodiol KW - 73093-19-3 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Stereoisomerism KW - Circular Dichroism KW - Chromatography, Thin Layer KW - Chromatography, High Pressure Liquid KW - Epoxy Compounds -- chemistry KW - DNA -- chemistry KW - Phenanthrenes -- chemistry KW - Mutagens -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73328254?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Identification+of+individual+benzo%5Bc%5Dphenanthrene+dihydrodiol+epoxide-DNA+adducts+by+the+32P-postlabeling+assay.&rft.au=Canella%2C+K+A%3BPeltonen%2C+K%3BYagi%2C+H%3BJerina%2C+D+M%3BDipple%2C+A&rft.aulast=Canella&rft.aufirst=K&rft.date=1992-09-01&rft.volume=5&rft.issue=5&rft.spage=685&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 - 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 - A method for increasing the yield of properly folded recombinant fusion proteins: single-chain immunotoxins from renaturation of bacterial inclusion bodies. AN - 73314306; 1332541 AB - Many proteins produced in Escherichia coli accumulate in inclusion bodies. We have systematically evaluated the parameters that affect the refolding and renaturation of enzymatically active molecules from bacterial inclusion bodies containing a recombinant single-chain immunotoxin, B3(Fv)-PE38KDEL. This recombinant molecule is composed of the variable domains of monoclonal antibody B3 (B3(Fv)) fused to a truncated mutant form of Pseudomonas exotoxin A (PE38KDEL). This immunotoxin kills carcinoma cells in vitro, causes tumor regression in animal tumor models, and is being developed as an anti-cancer therapeutic agent (Brinkmann et al., 1991, Proc. Natl. Acad. Sci. USA 88, 8616-8620). Like many other recombinant proteins, B3(Fv)-PE38KDEL is produced in E. coli in inclusion bodies and must be denatured and refolded to become active. This requires correct folding, formation of native disulfide bonds, and the association of different domains. All these steps are strongly dependent on the renaturation conditions used. Optimum conditions of refolding were obtained by the addition of reduced and oxidized thiol reagents to promote disulfide bond formation and the addition of a labilizing agent such as L-arginine. Furthermore, the necessity to reactivate proteins at low protein concentrations due to its tendency to aggregate at high concentrations was overcome by a step-by-step addition of denatured and reduced protein into the refolding solution. This approach should be useful for the production of active forms of other recombinant proteins. JF - Analytical biochemistry AU - Buchner, J AU - Pastan, I AU - Brinkmann, U AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 263 EP - 270 VL - 205 IS - 2 SN - 0003-2697, 0003-2697 KW - Antibodies, Monoclonal KW - 0 KW - Bacterial Toxins KW - Exotoxins 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 - Index Medicus KW - Escherichia coli -- metabolism KW - Temperature KW - Protein Denaturation KW - Neoplasms -- immunology KW - Immunotoxins -- chemistry KW - Pseudomonas aeruginosa -- metabolism KW - Recombinant Fusion Proteins -- isolation & purification KW - Bacterial Toxins -- chemistry KW - Immunotoxins -- isolation & purification KW - Exotoxins -- chemistry KW - Inclusion Bodies -- chemistry KW - Recombinant Fusion Proteins -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73314306?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Analytical+biochemistry&rft.atitle=A+method+for+increasing+the+yield+of+properly+folded+recombinant+fusion+proteins%3A+single-chain+immunotoxins+from+renaturation+of+bacterial+inclusion+bodies.&rft.au=Buchner%2C+J%3BPastan%2C+I%3BBrinkmann%2C+U&rft.aulast=Buchner&rft.aufirst=J&rft.date=1992-09-01&rft.volume=205&rft.issue=2&rft.spage=263&rft.isbn=&rft.btitle=&rft.title=Analytical+biochemistry&rft.issn=00032697&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-01 N1 - Date created - 1992-12-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Toxicity and carcinogenicity of hydroquinone in F344/N rats and B6C3F1 mice. AN - 73308757; 1365401 AB - Toxicology and carcinogenesis studies were conducted by administering hydroquinone (more than 99% pure) by gavage to groups of F344/N rats and B6C3F1 mice of each sex for 14 days, 13 wk or 2 yr. 14-day studies were conducted by administering hydroquinone in corn oil to rats at doses ranging from 63 to 1000 mg/kg body weight and to mice at doses ranging from 31 to 500 mg/kg, 5 days/wk. In the 13-wk studies, doses for rats and mice ranged from 25 to 400 mg/kg. At those doses showing some indication of toxicity in the 14-day and 13-wk studies, the central nervous system, forestomach and liver were identified as target organs in both species and renal toxicity was observed in rats. Based on these results, 2-yr studies were conducted by administering 0, 25 or 50 mg hydroquinone/kg in deionized water by gavage to groups of 65 rats of each sex, 5 days/wk. Groups of 65 mice of each sex were given 0, 50 or 100 mg/kg on the same schedule. 10 rats and 10 mice from each group were killed and evaluated after 15 months. Mean body weights of high-dose male rats and high-dose mice were approx. 5-14% lower than those of controls during the second half of the study. No differences in survival were observed between dosed and control groups of rats or mice. Nearly all male rats and most female rats in all vehicle control and exposed groups had nephropathy, which was judged to be more severe in high-dose male rats. Hyperplasia of the renal pelvic transitional epithelium and renal cortical cysts were increased in male rats. Tubular cell hyperplasia of the kidney was seen in two high-dose male rats, and renal tubular adenomas were seen in 4/55 low-dose and 8/55 high-dose male rats; none was seen in vehicle controls or in female rats. Mononuclear cell leukaemia in female rats occurred with increased incidences in the dosed groups (vehicle control, 9/55; low dose, 15/55; high dose, 22/55). Compound-related lesions observed in the liver of high-dose male mice included anisokaryosis, syncytial alteration and basophilic foci. The incidences of hepatocellular neoplasms, primarily adenomas, were increased in dosed female mice (3/55; 16/55; 13/55). Follicular cell hyperplasia of the thyroid gland was increased in dosed mice.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association AU - Kari, F W AU - Bucher, J AU - Eustis, S L AU - Haseman, J K AU - Huff, J E AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 737 EP - 747 VL - 30 IS - 9 SN - 0278-6915, 0278-6915 KW - Hydroquinones KW - 0 KW - Corn Oil KW - 8001-30-7 KW - hydroquinone KW - XV74C1N1AE KW - Index Medicus KW - Seizures -- chemically induced KW - Administration, Oral KW - Thyroid Neoplasms -- chemically induced KW - Animals KW - Kidney -- pathology KW - Sex Factors KW - Dose-Response Relationship, Drug KW - Kidney -- drug effects KW - Mice KW - Tremor -- chemically induced KW - Stomach -- drug effects KW - Epithelium -- drug effects KW - Rats KW - Stomach -- pathology KW - Rats, Inbred F344 KW - Hyperplasia KW - Liver -- drug effects KW - Epithelium -- pathology KW - Female KW - Male KW - Leukemia, Myeloid -- chemically induced KW - Kidney Neoplasms -- chemically induced KW - Liver Neoplasms, Experimental -- chemically induced KW - Hydroquinones -- administration & dosage KW - Hydroquinones -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73308757?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Toxicity+and+carcinogenicity+of+hydroquinone+in+F344%2FN+rats+and+B6C3F1+mice.&rft.au=Kari%2C+F+W%3BBucher%2C+J%3BEustis%2C+S+L%3BHaseman%2C+J+K%3BHuff%2C+J+E&rft.aulast=Kari&rft.aufirst=F&rft.date=1992-09-01&rft.volume=30&rft.issue=9&rft.spage=737&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 - 1992-12-01 N1 - Date created - 1992-12-01 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Food Chem Toxicol. 1994 Sep;32(9):863-7 [7927084] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Risk for affective disorder and alcohol and other drug abuse in the relatives of affectively ill adoptees. AN - 73304104; 1430667 AB - We investigated the risk for substance abuse in the biological relatives of adoptees with affective illness, controlling for potential confounds, and additionally assessed risk by probands' and relatives' gender. Our sample consisted of 67 index adoptees with affective illness, matched control adoptees, and their biological and adoptive relatives. Both affective illness and substance abuse were more common in the biological relatives of affectively ill adoptees than in controls' relatives. Affective illness was more common than substance abuse among female index biological relatives, with the opposite pattern observed among male relatives. JF - Journal of affective disorders AU - Ingraham, L J AU - Wender, P H AD - Laboratory of Psychology and Psychopathology, NIMH, Bethesda, MD 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 45 EP - 51 VL - 26 IS - 1 SN - 0165-0327, 0165-0327 KW - Index Medicus KW - Risk Factors KW - Models, Genetic KW - Humans KW - Adult KW - Middle Aged KW - Male KW - Female KW - Depressive Disorder -- psychology KW - Child of Impaired Parents -- psychology KW - Bipolar Disorder -- genetics KW - Adoption -- psychology KW - Depressive Disorder -- genetics KW - Bipolar Disorder -- psychology KW - Substance-Related Disorders -- psychology KW - Alcoholism -- genetics KW - Alcoholism -- psychology KW - Substance-Related Disorders -- genetics KW - Social Environment UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73304104?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+affective+disorders&rft.atitle=Risk+for+affective+disorder+and+alcohol+and+other+drug+abuse+in+the+relatives+of+affectively+ill+adoptees.&rft.au=Ingraham%2C+L+J%3BWender%2C+P+H&rft.aulast=Ingraham&rft.aufirst=L&rft.date=1992-09-01&rft.volume=26&rft.issue=1&rft.spage=45&rft.isbn=&rft.btitle=&rft.title=Journal+of+affective+disorders&rft.issn=01650327&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-12-03 N1 - Date created - 1992-12-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Selective stimulation of Ca2+ flux in cells by maitotoxin. AN - 73275947; 1330638 AB - Maitotoxin elicits a dose-dependent stimulation of 45Ca2+ influx in glioma C6, pheochromocytoma PC12, insulinoma HIT and human blood cells, while having no effect in liposomes. In HIT cells maitotoxin also elicited influx of 86Rb+ greater than 22Na+ greater than 54Mn2+, but the stimulation was far less than for 45Ca2+. Stimulation of 45Ca2+ influx was blocked by Ni2+, Co2+, Cd2+ and Mn2+, and markedly reduced by Ba2+. Divalent cations, in particular Ca2+, Ba2+, Mn2+ and Cd2+, enhanced influx of the monovalent cations 22Na+ and 86Rb+. JF - European journal of pharmacology AU - Murata, M AU - Gusovsky, F AU - Yasumoto, T AU - Daly, J W AD - Laboratory of Bioorganic Chemistry, NIDDK, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/09/01/ PY - 1992 DA - 1992 Sep 01 SP - 43 EP - 49 VL - 227 IS - 1 SN - 0014-2999, 0014-2999 KW - Calcium Channels KW - 0 KW - Calcium Radioisotopes KW - Cations KW - Liposomes KW - Marine Toxins KW - Oxocins KW - Radioisotopes KW - Rubidium Radioisotopes KW - Sodium Radioisotopes KW - Manganese KW - 42Z2K6ZL8P KW - Chlorine KW - 4R7X1O2820 KW - maitotoxin KW - 9P59GES78D KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Manganese -- metabolism KW - Dose-Response Relationship, Drug KW - Liposomes -- metabolism KW - Chlorine -- metabolism KW - Rats KW - Tumor Cells, Cultured KW - Calcium Channels -- drug effects KW - Cricetinae KW - Marine Toxins -- pharmacology KW - Calcium -- metabolism KW - Calcium -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73275947?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Selective+stimulation+of+Ca2%2B+flux+in+cells+by+maitotoxin.&rft.au=Murata%2C+M%3BGusovsky%2C+F%3BYasumoto%2C+T%3BDaly%2C+J+W&rft.aulast=Murata&rft.aufirst=M&rft.date=1992-09-01&rft.volume=227&rft.issue=1&rft.spage=43&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 - 1992-12-04 N1 - Date created - 1992-12-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of dose, strain, and dosing vehicle on methacrylonitrile disposition in rats and identification of a novel-exhaled metabolite. AN - 73271090; 1358567 AB - Methacrylonitrile (MAN), an aliphatic nitrile used in the production of plastics and elastomers, is structurally related to the known animal carcinogen, acrylonitrile. Although MAN has potential to cause significant toxicity, minimal information is available on its toxicity or fate. Current studies were designed to investigate the biological fate of [2-14C]MAN in male F344 rats. Following gavage administration of 115, 11.5, or 1.15 mg MAN/kg in water, male F344 rats were placed in glass metabolism cages and urine, expired air, and feces were collected. Rats were sacrificed at various times, and the concentration of MAN-derived radioactivity in tissues was determined. MAN was rapidly absorbed from the gastrointestinal tract and distributed to all major tissues. After gavage administration of 1.15-115 mg/kg, [2-14C]MAN is primarily eliminated in the expired air. Sixty to 70% of the low and medium doses were exhaled as 14CO2 in 72 hr compared with 25% of the highest dose. Whereas 40% of the high dose was expired as organic volatiles in 72 hr, only 9-12% of the low and medium doses were exhaled as such. It is therefore apparent that saturation of MAN metabolism occurs at the high dose. HPLC analysis of expired organic volatiles from MAN-treated rats showed that it contained two components that were identified as unchanged MAN and acetone. The MAN:acetone ratio was directly proportional to dose and decreased as a function of time. Urinary excretion accounted for 20-30% of all MAN doses within 72 hr after dosing. Investigating the effect of dosing vehicle on MAN disposition in rats revealed that administration of 115 mg MAN/kg in oil resulted in the death of rats within 24 hr after treatment. Furthermore, monitoring the fate of MAN in these rats before death showed that a significantly higher percentage of the dose was eliminated in urine and expired air. Analysis of this expired air also revealed that significantly more acetone and less unchanged MAN were exhaled by these animals. It is apparent that administration of MAN to F344 rats in oil resulted in slower absorption, decreased elimination of unchanged MAN, and increased metabolism to acetone and/or decreased degradation of acetone to CO2. The combination of these effects of an oil vehicle may have contributed to the death of rats by MAN. Comparison of the metabolism and disposition of MAN in F344 and Sprague-Dawley rats showed minor differences between the two strains.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Drug metabolism and disposition: the biological fate of chemicals AU - Ghanayem, B I AU - Sanchez, I M AU - Burka, L T AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. PY - 1992 SP - 643 EP - 652 VL - 20 IS - 5 SN - 0090-9556, 0090-9556 KW - Methacrylates KW - 0 KW - Nitriles KW - Pharmaceutical Vehicles KW - methacrylonitrile KW - 04S4K38612 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Sprague-Dawley KW - Rats, Inbred F344 KW - Dose-Response Relationship, Drug KW - Tissue Distribution KW - Species Specificity KW - Male 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/73271090?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Effects+of+dose%2C+strain%2C+and+dosing+vehicle+on+methacrylonitrile+disposition+in+rats+and+identification+of+a+novel-exhaled+metabolite.&rft.au=Ghanayem%2C+B+I%3BSanchez%2C+I+M%3BBurka%2C+L+T&rft.aulast=Ghanayem&rft.aufirst=B&rft.date=1992-09-01&rft.volume=20&rft.issue=5&rft.spage=643&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 - 1992-12-23 N1 - Date created - 1992-12-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vivo binding of [125I]RTI-55 to dopamine transporters: pharmacology and regional distribution with autoradiography. AN - 73256901; 1411962 AB - Previous studies have demonstrated that para-substituted WIN 35,065-2 analogs of cocaine show high binding affinity for dopamine uptake sites both in vitro and in vivo, and inhibit DA uptake in vitro. These analogs also produce potent cocaine-like behavioral effects in various procedures. The purpose of the present studies was to evaluate the iodinated WIN 35,065-2 analog [125I]RTI-55 as an in vivo ligand for the DA transporter. Following intravenous injection in mice, [125I]RTI-55 showed highest accumulation in areas with high densities of dopamine uptake sites. Light microscopic autoradiography was used to examine binding with higher resolution. Displacement studies demonstrated that [125I]RTI-55 binding in dopamine containing regions, striatum and olfactory tubercles, was saturable and inhibited by other cocaine analogs. GBR 12909 and WIN 35,428 significantly inhibited [125I]RTI-55 binding in striatum, while paroxetine significantly inhibited hypothalamic binding but had little effect in striatum. The latter finding suggests that [125I]RTI-55 also binds to the serotonin transporter. Haloperidol had no effect on [125I]RTI-55 binding in any brain region measured. In addition, treatment of animals with the dopamine neurotoxin MPTP caused significant reductions in striatal [125I]RTI-55 binding. The results of these studies indicate that [125I]RTI-55 binds primarily to the dopamine transporter in the mouse striatum in vivo. JF - Synapse (New York, N.Y.) AU - Cline, E J AU - Scheffel, U AU - Boja, J W AU - Mitchell, W M AU - Carroll, F I AU - Abraham, P AU - Lewin, A H AU - Kuhar, M J AD - Neuroscience Branch, Addiction Research Center, National Institute on Drug Abuse, Baltimore, Maryland 21224. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 37 EP - 46 VL - 12 IS - 1 SN - 0887-4476, 0887-4476 KW - Carrier Proteins KW - 0 KW - Dopamine Plasma Membrane Transport Proteins KW - Iodine Radioisotopes KW - Membrane Glycoproteins KW - Membrane Transport Proteins KW - Nerve Tissue Proteins KW - 2beta-carbomethoxy-3beta-(4-iodophenyl)tropane KW - 4H1Z7121WS KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Mice, Inbred Strains KW - Animals KW - Kinetics KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- pharmacology KW - Organ Specificity KW - Mice KW - Autoradiography KW - Male KW - Cocaine -- analogs & derivatives KW - Carrier Proteins -- metabolism KW - Brain -- drug effects KW - Nerve Tissue Proteins -- metabolism KW - Brain -- metabolism KW - Cocaine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73256901?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+vivo+binding+of+%5B125I%5DRTI-55+to+dopamine+transporters%3A+pharmacology+and+regional+distribution+with+autoradiography.&rft.au=Cline%2C+E+J%3BScheffel%2C+U%3BBoja%2C+J+W%3BMitchell%2C+W+M%3BCarroll%2C+F+I%3BAbraham%2C+P%3BLewin%2C+A+H%3BKuhar%2C+M+J&rft.aulast=Cline&rft.aufirst=E&rft.date=1992-09-01&rft.volume=12&rft.issue=1&rft.spage=37&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 - 1992-11-12 N1 - Date created - 1992-11-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cirrhosis mortality and occupation. AN - 73246640; 1405639 AB - Cirrhosis, the ninth leading cause of death in the United States, has been associated with abusive alcohol consumption patterns. Since the workplace serves as a major exposure variable for alcohol consumption over a significant portion of the lifecourse, and since heavy drinking has been shown to differ by type of occupation, this study examines the relationship between type of occupation and cirrhosis mortality. The California Occupational Mortality Study data set (1979 to 1981) provided the information on primary occupation and liver cirrhosis mortality. Crude and sex-specific mortality rates were calculated based on information from a 20% sample of the 1980 California census (included in the data set). Ninety-five percent confidence intervals were calculated around all rates to determine if any were significantly different from rates for the entire state. The findings uphold the view that an association exists between occupation and cirrhosis mortality. The highest mortality rates were found among persons with blue-collar type jobs (e.g., construction laborers and machinists) or jobs where alcohol was easily available (e.g., bartenders and waitresses). Future research needs to specify the factors associated with occupation that may promote the chronic heavy drinking that leads to cirrhosis. JF - Journal of studies on alcohol AU - Harford, T C AU - Brooks, S D AD - Division of Biometry and Epidemiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20857. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 463 EP - 468 VL - 53 IS - 5 SN - 0096-882X, 0096-882X KW - Index Medicus KW - United States KW - California KW - Occupational Health KW - Sex Factors KW - Humans KW - Adult KW - Middle Aged KW - Occupations -- classification KW - Alcoholism -- complications KW - Male KW - Female KW - Occupational Exposure KW - Liver Cirrhosis -- etiology KW - Liver Cirrhosis -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73246640?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cirrhosis+mortality+and+occupation.&rft.au=Harford%2C+T+C%3BBrooks%2C+S+D&rft.aulast=Harford&rft.aufirst=T&rft.date=1992-09-01&rft.volume=53&rft.issue=5&rft.spage=463&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 - 1992-11-04 N1 - Date created - 1992-11-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of ibuprofen and pentoxifylline on the cardiovascular response of normal humans to endotoxin. AN - 73239755; 1400057 AB - Endotoxin is a major mediator of the life-threatening cardiovascular dysfunction that characterizes Gram-negative sepsis. In animal models of endotoxemia, pretreatment with ibuprofen or pentoxifylline attenuates some of these cardiovascular changes. To evaluate the effects of these agents on the human cardiovascular response to endotoxemia, hemodynamic variables were measured serially in 24 normal subjects who were given intravenous endotoxin. The subjects were randomized to receive oral ibuprofen (n = 9), pentoxifylline (n = 10), or no medication before endotoxin administration (n = 5). The subjects were volume loaded 3-5 h after endotoxin administration, and hemodynamic measurements were reassessed. Core temperature after endotoxin alone or endotoxin-pentoxifylline approached a maximum at 3 h (greater than or equal to 38.6 degrees C), while the endotoxin-ibuprofen group remained afebrile. At 3 and 5 h, all three groups had significant increases in heart rate, cardiac index, oxygen delivery, and oxygen consumption, while systemic vascular resistance index decreased significantly from baseline. The oxygen extraction ratio remained unchanged. After volume loading, the left ventricular ejection fraction and left ventricular end-diastolic and end-systolic volume indexes did not differ among the groups. The hyperdynamic cardiovascular response to endotoxin in humans occurs in the absence of fever and is not significantly ameliorated by oral cyclooxygenase or phosphodiesterase inhibition. JF - Journal of applied physiology (Bethesda, Md. : 1985) AU - Martich, G D AU - Parker, M M AU - Cunnion, R E AU - Suffredini, A F AD - Critical Care Medicine Department, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 925 EP - 931 VL - 73 IS - 3 SN - 8750-7587, 8750-7587 KW - Endotoxins KW - 0 KW - Tumor Necrosis Factor-alpha KW - Pentoxifylline KW - SD6QCT3TSU KW - Ibuprofen KW - WK2XYI10QM KW - Index Medicus KW - Ventricular Function, Left -- drug effects KW - Hemodynamics -- drug effects KW - Hemodynamics -- physiology KW - Oxygen Consumption -- drug effects KW - Humans KW - Shock, Septic -- etiology KW - Ventricular Function, Left -- physiology KW - Cardiovascular Physiological Phenomena KW - Adult KW - Shock, Septic -- physiopathology KW - Tumor Necrosis Factor-alpha -- metabolism KW - Female KW - Male KW - Shock, Septic -- prevention & control KW - Pentoxifylline -- pharmacology KW - Cardiovascular System -- drug effects KW - Ibuprofen -- pharmacology KW - Endotoxins -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73239755?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+of+aflatoxin+B1-induced+mutations+in+a+plasmid+replicated+in+xeroderma+pigmentosum+and+DNA+repair+proficient+human+cells.&rft.au=Levy%2C+D+D%3BGroopman%2C+J+D%3BLim%2C+S+E%3BSeidman%2C+M+M%3BKraemer%2C+K+H&rft.aulast=Levy&rft.aufirst=D&rft.date=1992-10-15&rft.volume=52&rft.issue=20&rft.spage=5668&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 - 1992-11-23 N1 - Date created - 1992-11-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The incidence of illicit drug use in the United States, 1962-1989. AN - 73221566; 1392556 AB - Epidemiological descriptions of drug abuse in the US in the last three decades have generally not included data on the patterns and trends in the incidence of illicit drug use (i.e. new users). In this paper, estimates of illicit drug use incidence are presented, based on retrospective data from the National Household Survey on Drug Abuse. Incidence of marijuana use began increasing in the 1960s and reached a peak in 1973, after which a continuing decline was seen. Cocaine use incidence began to increase in the late 1960s and reached a peak in 1982, then declined. JF - British journal of addiction AU - Gfroerer, J AU - Brodsky, M AD - National Institute on Drug Abuse, Division of Epidemiology and Prevention Research, Rockville, Maryland 20857. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 1345 EP - 1351 VL - 87 IS - 9 SN - 0952-0481, 0952-0481 KW - Street Drugs KW - 0 KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - United States KW - Cross-Sectional Studies KW - Heroin Dependence -- epidemiology KW - Humans KW - Adult KW - Retrospective Studies KW - Incidence KW - Marijuana Abuse -- epidemiology KW - Adolescent KW - Male KW - Female KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73221566?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+addiction&rft.atitle=The+incidence+of+illicit+drug+use+in+the+United+States%2C+1962-1989.&rft.au=Gfroerer%2C+J%3BBrodsky%2C+M&rft.aulast=Gfroerer&rft.aufirst=J&rft.date=1992-09-01&rft.volume=87&rft.issue=9&rft.spage=1345&rft.isbn=&rft.btitle=&rft.title=British+journal+of+addiction&rft.issn=09520481&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-04 N1 - Date created - 1992-11-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prenatal diethylstilbestrol exposure and performance on college entrance examinations. AN - 73218353; 1398561 AB - The fetal rodent brain is permanently altered by exposure to sex hormones. Long-term effects of prenatal sex hormones on the human brain are far less clear. In order to explore such effects, we studied a measure of cognitive function among young adults who had been exposed in utero to a powerful synthetic estrogen. In a randomized clinical trial conducted at the University of Chicago in 1950-1952, 1646 pregnant women were randomly assigned to receive either high doses of diethylstilbestrol or placebo. Women in this study gave birth to 1653 liveborn infants, of whom 1603 (820 sons and 783 daughters) survived to their fifteenth birthday. College entrance examination scores were obtained for 42% of these offspring. No differences in test performance were seen among exposed daughters. Among sons, test scores were marginally higher among the exposed, probably due to chance. JF - Hormones and behavior AU - Wilcox, A J AU - Maxey, J AU - Herbst, A L AD - Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 433 EP - 439 VL - 26 IS - 3 SN - 0018-506X, 0018-506X KW - Diethylstilbestrol KW - 731DCA35BT KW - Index Medicus KW - Double-Blind Method KW - Cognition -- drug effects KW - Humans KW - Adult KW - Male KW - Female KW - Pregnancy KW - Aptitude KW - Intelligence -- drug effects KW - Brain -- drug effects KW - Diethylstilbestrol -- pharmacology KW - Prenatal Exposure Delayed Effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73218353?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hormones+and+behavior&rft.atitle=Prenatal+diethylstilbestrol+exposure+and+performance+on+college+entrance+examinations.&rft.au=Wilcox%2C+A+J%3BMaxey%2C+J%3BHerbst%2C+A+L&rft.aulast=Wilcox&rft.aufirst=A&rft.date=1992-09-01&rft.volume=26&rft.issue=3&rft.spage=433&rft.isbn=&rft.btitle=&rft.title=Hormones+and+behavior&rft.issn=0018506X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-04 N1 - Date created - 1992-11-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - SV40 small t deletion mutants preferentially transform mononuclear phagocytes and B lymphocytes in vivo. AN - 73208951; 1529547 AB - Hamsters injected intracardiacally with wild-type SV40 developed diverse tumors, with no one type predominating. However, hamsters injected with small t deletion mutants of SV40 uniformly developed true histiocytic or B-cell lymphomas, both of which arise from rapidly dividing cell populations, with very few tumors of other types. Our results are consistent with in vitro studies which suggest a requirement for the small t function in SV40 transformation of nondividing cells. JF - Virology AU - Cicala, C AU - Pompetti, F AU - Nguyen, P AU - Dixon, K AU - Levine, A S AU - Carbone, M AD - Section on Viruses and Cellular Biology, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 475 EP - 479 VL - 190 IS - 1 SN - 0042-6822, 0042-6822 KW - Antigens, Polyomavirus Transforming KW - 0 KW - Index Medicus KW - Animals KW - Lymphoma, B-Cell -- microbiology KW - Lymphoma, Large B-Cell, Diffuse -- pathology KW - Osteosarcoma -- pathology KW - Lymphoma, B-Cell -- pathology KW - Lymphoma, Large B-Cell, Diffuse -- microbiology KW - Mesothelioma -- pathology KW - Mesocricetus KW - Lymphoma -- pathology KW - Mutagenesis KW - Cricetinae KW - B-Lymphocytes -- microbiology KW - Phagocytes -- microbiology KW - Antigens, Polyomavirus Transforming -- genetics KW - Cell Transformation, Viral UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73208951?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=SV40+small+t+deletion+mutants+preferentially+transform+mononuclear+phagocytes+and+B+lymphocytes+in+vivo.&rft.au=Cicala%2C+C%3BPompetti%2C+F%3BNguyen%2C+P%3BDixon%2C+K%3BLevine%2C+A+S%3BCarbone%2C+M&rft.aulast=Cicala&rft.aufirst=C&rft.date=1992-09-01&rft.volume=190&rft.issue=1&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 - 1992-10-16 N1 - Date created - 1992-10-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Progressive atypia in spontaneous and N-nitrosodiethylamine-induced hepatocellular adenomas of C3H/HeNCr mice. AN - 73206609; 1394837 AB - The progression of hepatocellular adenomas to carcinomas has been less well documented in mice than in rats. We studied progression of spontaneous and chemically induced hepatocellular adenomas in male C3H/HeNCr mice by image analysis. Spontaneous lesions in 15, 18 and 21 month old untreated male C3H/HeNCr mice and experimentally induced lesions were examined. Experimental group 1 received a single i.p. injection of N-nitrosodiethylamine (DEN) (5 mg/kg body wt) at 15 days of age. Groups 2 and 3 were injected a second time with DEN at 15 or 20 weeks of age (75 mg/kg body wt), with interim sacrifices at 11, 16 and 34 weeks after the second DEN injection. Atypia in adenomas were classified into four grades according to cell size, tinctorial changes, cellular pleomorphism and trabecular pattern. At earlier stages of the neoplastic process (11 or 16 weeks after the second DEN dose), most adenomas were well-differentiated lesions with no atypia or focal grade 1 or 2 atypia. At later stages (34 weeks after the second DEN dose), a large proportion of hepatocellular tumors were classified as adenoma with grade 3 atypia or carcinoma. The proportion of carcinomas in mice treated with a second dose of DEN at 20 weeks of age was significantly higher than in mice treated with a single dose of DEN or in mice given a second dose of DEN at 15 weeks. A positive correlation was found between increase in the size of lesions and increased atypia in both spontaneous and DEN-induced lesions and with age for spontaneous tumors. These results support the hypothesis that mouse hepatocellular adenomas are truly neoplastic lesions in different stages of progression toward malignancy. JF - Carcinogenesis AU - Jang, J J AU - Weghorst, C M AU - Henneman, J R AU - Devor, D E AU - Ward, J M AD - Tumor Pathology and Pathogenesis Section, National Cancer Institute, Frederick, MD 21702-1201. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 1541 EP - 1547 VL - 13 IS - 9 SN - 0143-3334, 0143-3334 KW - Diethylnitrosamine KW - 3IQ78TTX1A KW - Index Medicus KW - Body Weight KW - Animals KW - Liver -- pathology KW - Aging KW - Mice, Inbred C3H KW - Mice KW - Organ Size KW - Male KW - Female KW - Diethylnitrosamine -- toxicity KW - Liver Neoplasms, Experimental -- pathology KW - Liver Neoplasms, Experimental -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73206609?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Progressive+atypia+in+spontaneous+and+N-nitrosodiethylamine-induced+hepatocellular+adenomas+of+C3H%2FHeNCr+mice.&rft.au=Jang%2C+J+J%3BWeghorst%2C+C+M%3BHenneman%2C+J+R%3BDevor%2C+D+E%3BWard%2C+J+M&rft.aulast=Jang&rft.aufirst=J&rft.date=1992-09-01&rft.volume=13&rft.issue=9&rft.spage=1541&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-29 N1 - Date created - 1992-10-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human cytochromes P450: problems and prospects. AN - 73200886; 1529480 AB - Cytochromes P450 are a superfamily of haem-containing monooxygenases. In mammals, two general classes of P450s exist: six families involved in steroid and bile acid biosynthetic pathways of metabolism; four families containing numerous individual P450s, mainly responsible for metabolism of foreign compounds. Many of the latter P450s, particularly those in the CYP2 family, exhibit a large degree of inter- and intra-species variability in regulation and catalytic activities. From a practical standpoint, these variabilities suggest the need for careful characterization of P450 catalytic activities and determination of P450 expression levels in humans. Human P450-based in vitro systems are being developed to evaluate drug and carcinogen metabolism. JF - Trends in pharmacological sciences AU - Gonzalez, F J AD - National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 346 EP - 352 VL - 13 IS - 9 SN - 0165-6147, 0165-6147 KW - Bile Acids and Salts KW - 0 KW - Carcinogens KW - Steroids KW - Xenobiotics KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Biotransformation KW - Humans KW - Bile Acids and Salts -- metabolism KW - Steroids -- metabolism KW - Catalysis KW - Xenobiotics -- metabolism KW - Carcinogens -- pharmacokinetics 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/73200886?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Human+cytochromes+P450%3A+problems+and+prospects.&rft.au=Gonzalez%2C+F+J&rft.aulast=Gonzalez&rft.aufirst=F&rft.date=1992-09-01&rft.volume=13&rft.issue=9&rft.spage=346&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 - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Thymocyte injury after in vitro chemical exposure: potential mechanisms for thymic atrophy. AN - 73197012; 1527729 AB - In addition to hepatic injury, thymic atrophy is a common observation in rodent subchronic toxicity studies. We have examined representative chemicals which produce thymic atrophy in rodents for their ability to cause direct thymocyte injury because the mechanism(s) responsible for these effects have not been determined. Although a number of the compounds examined failed to have any observable direct effect on thymocytes, others either inhibited lymphocyte proliferation or initiated cell death. In the latter group, thymocyte death was always preceded by increases in intracellular Ca++ and involved, to varying degrees, necrotic and apoptotic events. Apoptosis, as evidenced by cellular DNA cleavage into multiples of 180-200-base pair oligonucleotides and partial cell protection by cycloheximide treatment, was most evident after treatment with acetaldehyde or dibutyltin dichloride. A number of compounds that produce thymic atrophy also inhibited T lymphocyte proliferation without evidence of cell death. Considering that many of the compounds tested failed to produce any evidence of direct thymocyte injury (i.e., necrosis, apoptosis or inhibition of cell proliferation), indirect mechanisms may also be involved in thymic atrophy and may target prothymocytes in the bone marrow, after normal homing patterns or injure the thymic epithelium. Thus, it appears that a variety of mechanisms may be responsible for chemical-induced thymic atrophy and/or injury. JF - The Journal of pharmacology and experimental therapeutics AU - Comment, C E AU - Blaylock, B L AU - Germolec, D R AU - Pollock, P L AU - Kouchi, Y AU - Brown, H W AU - Rosenthal, G J AU - Luster, M I AD - Systems Toxicity Branch, National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 1267 EP - 1273 VL - 262 IS - 3 SN - 0022-3565, 0022-3565 KW - Index Medicus KW - Rats KW - Atrophy -- chemically induced KW - Animals KW - Rats, Inbred F344 KW - Cell Survival -- drug effects KW - Liver -- drug effects KW - Cells, Cultured KW - Cell Division -- drug effects KW - Mice KW - Female KW - Thymus Gland -- ultrastructure KW - Drug-Related Side Effects and Adverse Reactions KW - Thymus Gland -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73197012?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Thymocyte+injury+after+in+vitro+chemical+exposure%3A+potential+mechanisms+for+thymic+atrophy.&rft.au=Comment%2C+C+E%3BBlaylock%2C+B+L%3BGermolec%2C+D+R%3BPollock%2C+P+L%3BKouchi%2C+Y%3BBrown%2C+H+W%3BRosenthal%2C+G+J%3BLuster%2C+M+I&rft.aulast=Comment&rft.aufirst=C&rft.date=1992-09-01&rft.volume=262&rft.issue=3&rft.spage=1267&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 - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - 5-Fluorouracil (5-FU) and leucovorin in platinum-refractory advanced stage ovarian carcinoma. AN - 73195989; 1526510 AB - Twenty-nine patients with recurrent advanced stage ovarian cancer were treated with 5-fluorouracil (5-FU) and leucovorin by intravenous bolus on 5 consecutive days, repeated every 3 weeks. Twenty-one of these patients had experienced disease progression while receiving a cisplatin- or carboplatin-based regimen. There were 2 clinical complete responders and 1 partial responder to therapy (10% response rate; 95% confidence interval, 2 to 27%) and 11 individuals who experienced stable disease for periods ranging from 5 to 27 months. Of 204 cycles of therapy administered, 9 cycles were associated with hospitalization. These occurred in the more heavily pretreated members of the cohort. 5-FU and leucovorin appear to have activity in platinum-refractory ovarian cancer and form a well-tolerated regimen in most patients. JF - Gynecologic oncology AU - Reed, E AU - Jacob, J AU - Ozols, R F AU - Young, R C AU - Allegra, C AD - National Institute of Health, National Cancer Institute, Medicine Branch, Rockville, Maryland 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 326 EP - 329 VL - 46 IS - 3 SN - 0090-8258, 0090-8258 KW - Platinum KW - 49DFR088MY KW - Carboplatin KW - BG3F62OND5 KW - Leucovorin KW - Q573I9DVLP KW - Fluorouracil KW - U3P01618RT KW - Index Medicus KW - Fluorouracil -- administration & dosage KW - Drug Administration Schedule KW - Neoplasm Staging KW - Leucovorin -- administration & dosage KW - Humans KW - Platinum -- therapeutic use KW - Adult KW - Drug Resistance KW - Aged KW - Middle Aged KW - Carboplatin -- therapeutic use KW - Female KW - Remission Induction KW - Ovarian Neoplasms -- pathology KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Ovarian Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73195989?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gynecologic+oncology&rft.atitle=5-Fluorouracil+%285-FU%29+and+leucovorin+in+platinum-refractory+advanced+stage+ovarian+carcinoma.&rft.au=Reed%2C+E%3BJacob%2C+J%3BOzols%2C+R+F%3BYoung%2C+R+C%3BAllegra%2C+C&rft.aulast=Reed&rft.aufirst=E&rft.date=1992-09-01&rft.volume=46&rft.issue=3&rft.spage=326&rft.isbn=&rft.btitle=&rft.title=Gynecologic+oncology&rft.issn=00908258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-20 N1 - Date created - 1992-10-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Functional subsensitivity of 5-hydroxytryptamine1C or alpha 2 adrenergic heteroreceptors mediating clonidine-induced growth hormone release in the Fawn-Hooded rat strain relative to the Wistar rat strain. AN - 73187202; 1356149 AB - Administration of various doses of clonidine increased plasma growth hormone levels. Pretreatment with the alpha 2 adrenergic antagonists, yohimbine and 1-(2-pyrimidyl)piperazine, completely blocked clonidine's effect on growth hormone levels. Pretreatment with the 5-hydroxytryptamine3 (5-HT3) receptor antagonist, MDL-72222, the 5-HT1A/5-HT2 antagonist, spiperone, and the mixed beta adrenergic/5-HT1B antagonists, l-propranolol and CGP361A, did not attenuate clonidine-induced increases in growth hormone levels. In contrast, pretreatment with the non-selective 5-HT1/2 antagonist, metergoline, and the 5-HT1C/5-HT2-selective antagonist, mesulergine, reduced clonidine-induced increases in growth hormone levels 81 to 87% without affecting clonidine-induced decreases in locomotor activity. Two other 5-HT1C/5-HT2 antagonists, ritanserin and mianserin, also attenuated (47%) clonidine-induced increases in growth hormone levels. Pretreatment with the noradrenergic neurotoxin, DSP4, did not block clonidine's effect on growth hormone levels. Clonidine administration decreased locomotor activity in both the Fawn-Hooded and the Wistar rat strains to the same extent. On the other hand, clonidine administration failed to increase growth hormone levels in the Fawn-Hooded rat strain. These findings suggest that clonidine stimulates growth hormone secretion by activation of alpha 2 adrenergic heteroreceptors present on 5-HT nerve terminals which, in turn, enhance 5-HT activity via stimulation of postsynaptic 5-HT1C receptors to promote growth hormone releasing factor. Furthermore, either 5-HT1C receptors or alpha 2 adrenergic heteroreceptors or both are functionally sub-sensitive in the Fawn-Hooded rat strain relative to the Wistar rat strain. JF - The Journal of pharmacology and experimental therapeutics AU - Aulakh, C S AU - Hill, J L AU - Lesch, K P AU - Murphy, D L AD - Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, Maryland. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 1038 EP - 1043 VL - 262 IS - 3 SN - 0022-3565, 0022-3565 KW - Adrenergic alpha-Antagonists KW - 0 KW - Receptors, Serotonin KW - Serotonin Antagonists KW - Growth Hormone KW - 9002-72-6 KW - Clonidine KW - MN3L5RMN02 KW - Index Medicus KW - Receptors, Serotonin -- drug effects KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Drug Interactions KW - Dose-Response Relationship, Drug KW - Motor Activity -- drug effects KW - Species Specificity KW - Male KW - Adrenergic alpha-Antagonists -- pharmacology KW - Serotonin Antagonists -- pharmacology KW - Growth Hormone -- blood KW - Clonidine -- pharmacology KW - Growth Hormone -- secretion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73187202?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Functional+subsensitivity+of+5-hydroxytryptamine1C+or+alpha+2+adrenergic+heteroreceptors+mediating+clonidine-induced+growth+hormone+release+in+the+Fawn-Hooded+rat+strain+relative+to+the+Wistar+rat+strain.&rft.au=Aulakh%2C+C+S%3BHill%2C+J+L%3BLesch%2C+K+P%3BMurphy%2C+D+L&rft.aulast=Aulakh&rft.aufirst=C&rft.date=1992-09-01&rft.volume=262&rft.issue=3&rft.spage=1038&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 - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pathophysiological and pharmacological mechanisms of acute cocaine toxicity in conscious rats. AN - 73184124; 1527734 AB - In conscious rats, continuous i.v. infusion of cocaine (2 mg/kg/min) produced a marked increase in blood pressure, an initial moderate increase followed by a decrease in heart rate, tonic-clonic convulsions and, finally, a lethal episode of status epilepticus. No change in rectal temperature was observed. Infusion of cocaine methiodide (2 mg/kg/min), a quaternary derivative of cocaine, also produced a lethal episode of status epilepticus, but it was 6 times less potent than cocaine on a molar basis. In pentobarbital-anesthetized, spontaneously breathing rats, cocaine produced death by respiratory failure. Artificial ventilation of pentobarbital-anesthetized rats elevated the lethal dose of cocaine by 15-fold and these animals died of marked hypotension. In conscious rats, pretreatment with dl-, d- or l-propranolol or the alpha 2-selective adrenoceptor antagonist yohimbine enhanced the convulsive and lethal effects of cocaine. In contrast, the alpha 2-selective adrenoceptor agonist clonidine or the alpha 1-selective adrenoceptor antagonist prazosin attenuated these effects. Yohimbine antagonized the protective effect of clonidine. The nonselective alpha adrenoceptor antagonist phentolamine, the autonomic ganglionic blocker chlorisondamine and various calcium channel blockers had no effect on the convulsive or lethal doses of cocaine. The pressor response to cocaine was attenuated by calcium channel blockers, clonidine, phentolamine and dl- or l-propranolol, but not by d-propranolol. The pressor response to cocaine was abolished by chlorisondamine, reversed to a depressor response by prazosin and enhanced by yohimbine. The initial tachycardiac response to cocaine was reversed to bradycardia by dl- and l-propranolol, prazosin, yohimbine or high doses of the calcium channel blockers, but was unaffected by phentolamine, d-propranolol, clonidine or chlorisondamine. These results indicate that in spontaneously breathing animals, acute i.v. infusions of lethal doses of cocaine produce death primarily by central effects, namely by status epilepticus in conscious rats and by respiratory arrest in pentobarbital-anesthetized rats. In artificially ventilated, pentobarbital-anesthetized rats, however, cocaine produces death by effects on the cardiovascular system. In conscious rats, endogenous alpha 1 adrenoceptors exert a deleterious influence on cocaine-induced convulsive and lethal effects, whereas alpha 2 adrenoceptors provide protective influence. Propranolol appears to enhance cocaine-induced acute lethality through a mechanism independent of beta adrenoceptors. Calcium channel blockers appear ineffective in antagonizing cocaine's lethality. JF - The Journal of pharmacology and experimental therapeutics AU - Tella, S R AU - Korupolu, G R AU - Schindler, C W AU - Goldberg, S R AD - Behavioral Pharmacology and Genetics Section, National Institute on Drug Abuse Addiction Research Center, Baltimore, Maryland. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 936 EP - 946 VL - 262 IS - 3 SN - 0022-3565, 0022-3565 KW - Calcium Channel Blockers KW - 0 KW - Cocaine KW - I5Y540LHVR KW - Chlorisondamine KW - JD3M24F66I KW - Index Medicus KW - Seizures -- chemically induced KW - Respiratory Insufficiency -- chemically induced KW - Rats, Inbred Strains KW - Rats KW - Chlorisondamine -- pharmacology KW - Animals KW - Drug Interactions KW - Infusions, Intravenous KW - Body Temperature -- drug effects KW - Seizures -- physiopathology KW - Body Weight -- drug effects KW - Respiratory Insufficiency -- physiopathology KW - Male KW - Hemodynamics -- drug effects KW - Calcium Channel Blockers -- pharmacology KW - Cocaine -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73184124?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Pathophysiological+and+pharmacological+mechanisms+of+acute+cocaine+toxicity+in+conscious+rats.&rft.au=Tella%2C+S+R%3BKorupolu%2C+G+R%3BSchindler%2C+C+W%3BGoldberg%2C+S+R&rft.aulast=Tella&rft.aufirst=S&rft.date=1992-09-01&rft.volume=262&rft.issue=3&rft.spage=936&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 - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Autoantibodies against the amino-terminal cadherin-like binding domain of pemphigus vulgaris antigen are pathogenic. AN - 73182104; 1522242 AB - Complementary DNA cloning of the 130-kD pemphigus vulgaris (PV) autoantigen (PVA) has indicated that it is a member of the cadherin family of Ca(2+)-dependent cell adhesion molecules. By homology with typical cadherins, PVA has five extracellular domains (EC1 through EC5). To localize immunogenic domains and to determine whether antibodies against them might be pathogenic, we produced beta-galactosidase fusion proteins with cDNA encoding different portions of the extracellular domains of PVA (EC1-2, EC3-5, and each individual domain). Immunoblot analysis of these fusion proteins with 23 PV patients' sera demonstrated that major immunogenic regions of PVA are located on the EC1, EC2, and EC4 domains. IgG was affinity-purified from PV sera on fusion proteins representing the amino (EC1-2) and carboxy (EC3-5) terminus of the extracellular PVA, and injected into neonatal mice. PV IgG affinity-purified on the EC1-2 fusion protein caused suprabasilar acantholysis, the typical histological finding of PV, but IgG affinity-purified on the EC3-5 fusion protein or beta-galactosidase alone did not. These results indicate that at least one pathogenic epitope, which is sufficient to cause suprabasilar acantholysis in neonatal mice, is located on the amino-terminal region of PVA, an area thought to be important in cadherin homophilic adhesion. JF - The Journal of clinical investigation AU - Amagai, M AU - Karpati, S AU - Prussick, R AU - Klaus-Kovtun, V AU - Stanley, J R AD - Dermatology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 919 EP - 926 VL - 90 IS - 3 SN - 0021-9738, 0021-9738 KW - Autoantibodies KW - 0 KW - Autoantigens KW - Cadherins KW - Immunoglobulin G KW - Peptide Fragments KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Immunoglobulin G -- isolation & purification KW - Molecular Sequence Data KW - Mice KW - Amino Acid Sequence KW - Mice, Inbred BALB C KW - Cell Adhesion KW - Autoantigens -- immunology KW - Pemphigus -- immunology KW - Cadherins -- immunology KW - Autoantibodies -- toxicity KW - Peptide Fragments -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73182104?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Autoantibodies+against+the+amino-terminal+cadherin-like+binding+domain+of+pemphigus+vulgaris+antigen+are+pathogenic.&rft.au=Amagai%2C+M%3BKarpati%2C+S%3BPrussick%2C+R%3BKlaus-Kovtun%2C+V%3BStanley%2C+J+R&rft.aulast=Amagai&rft.aufirst=M&rft.date=1992-09-01&rft.volume=90&rft.issue=3&rft.spage=919&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 - 1992-10-13 N1 - Date created - 1992-10-13 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Cell Biol. 1988 Mar;106(3):873-81 [2831236] Cell. 1991 Nov 29;67(5):869-77 [1720352] EMBO J. 1987 Dec 1;6(12):3647-53 [3501370] J Invest Dermatol. 1985 Jan;84(1):41-6 [3965577] Curr Opin Cell Biol. 1991 Oct;3(5):854-61 [1931086] J Cell Biol. 1991 Apr;113(2):381-91 [2010468] Proc Natl Acad Sci U S A. 1991 May 15;88(10):4476-80 [2034686] J Invest Dermatol. 1990 Mar;94(3):327-31 [2307852] Dev Biol. 1990 May;139(1):227-9 [2328837] J Neurochem. 1990 Sep;55(3):805-12 [2384753] J Clin Invest. 1989 May;83(5):1443-8 [2651476] J Cell Biol. 1989 Oct;109(4 Pt 1):1787-94 [2793940] J Clin Invest. 1988 Mar;81(3):807-12 [3343340] EMBO J. 1987 Dec 1;6(12):3655-61 [3428270] Nature. 1987 Sep 24-30;329(6137):341-3 [3498123] J Immunol. 1986 Feb 15;136(4):1227-30 [3511144] J Cell Biol. 1986 Mar;102(3):1109-17 [3512579] J Clin Invest. 1984 Aug;74(2):313-20 [6378972] J Exp Med. 1983 Jan 1;157(1):259-72 [6681540] N Engl J Med. 1982 May 20;306(20):1189-96 [7040962] Arch Dermatol Res. 1977 Oct 27;260(1):1-6 [337911] Proc Natl Acad Sci U S A. 1979 Sep;76(9):4350-4 [388439] Proc Natl Acad Sci U S A. 1991 Jun 1;88(11):4796-800 [1711210] J Cell Sci. 1991 Aug;99 ( Pt 4):809-21 [1770008] Science. 1991 Mar 22;251(5000):1451-5 [2006419] Annu Rev Biochem. 1990;59:237-52 [2197976] Cell. 1990 Apr 6;61(1):147-55 [2317870] J Exp Med. 1987 Jun 1;165(6):1719-24 [2438368] Science. 1989 Aug 11;245(4918):631-5 [2762814] J Exp Med. 1984 Nov 1;160(5):1509-18 [6491602] J Invest Dermatol. 1981 Aug;77(2):240-3 [7024426] Int J Dermatol. 1979 May;18(4):271-81 [378879] Biochem Biophys Res Commun. 1990 Dec 31;173(3):1224-30 [1702628] Eur J Cell Biol. 1990 Oct;53(1):1-12 [1706270] Proc Natl Acad Sci U S A. 1987 May;84(9):2808-12 [3472238] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A parkinsonian syndrome induced in the goldfish by the neurotoxin MPTP. AN - 73181231; 1521741 AB - Parkinson's disease has been modeled in humans, lower primates, and to a lesser extent in some other vertebrates by administration of the potent neurotoxin MPTP (1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine). The MPTP model has thus drawn considerable attention as a system to search for anti-Parkinson's disease drugs, although the cost and scarcity of primates has limited extensive applications. We now report that a parkinsonian syndrome can be elicited in the common goldfish (Carassius auratus) by a single dose of MPTP. The syndrome is characterized by profound bradykinesia (slow movement), the full extent of which is reached 3 days after MPTP administration. The reduction in movement is paralleled by loss of dopamine and norepinephrine from the forebrain and midbrain and in other brain regions as well. The toxic oxidative product of MPTP, MPP+, is also accumulated predominantly in forebrain and midbrain, and pretreatment with the monoamine oxidase blocker tranylcypromine substantially reduces accumulation of the toxic metabolite. A barely perceptible coarseness in balance adjustment also occurs in treated animals. The MPTP-treated goldfish recover normal movement and normal brain monoamine levels within 10-13 days after administration of the drug. We interpret these and other data to indicate that MPTP can induce a Parkinson's disease-like syndrome in the goldfish that is similar in many aspects to the syndrome induced by MPTP in humans and other primates. This remarkable parallel may permit the goldfish to supplement expensive and scarce primates for the purpose of searching and screening neuroprotective drugs with specific relevance to Parkinson's disease. JF - FASEB journal : official publication of the Federation of American Societies for Experimental Biology AU - Pollard, H B AU - Dhariwal, K AU - Adeyemo, O M AU - Markey, C J AU - Caohuy, H AU - Levine, M AU - Markey, S AU - Youdim, M B AD - Laboratory of Cell Biology and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 3108 EP - 3116 VL - 6 IS - 12 SN - 0892-6638, 0892-6638 KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Monoamine Oxidase KW - EC 1.4.3.4 KW - Dopamine KW - VTD58H1Z2X KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Brain -- enzymology KW - Animals KW - Norepinephrine -- metabolism KW - Brain -- pathology KW - Brain -- drug effects KW - Goldfish KW - Dopamine -- metabolism KW - Disease Models, Animal KW - Locomotion -- drug effects KW - Monoamine Oxidase -- metabolism KW - Parkinson Disease, Secondary -- metabolism KW - Parkinson Disease, Secondary -- chemically induced KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73181231?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FASEB+journal+%3A+official+publication+of+the+Federation+of+American+Societies+for+Experimental+Biology&rft.atitle=A+parkinsonian+syndrome+induced+in+the+goldfish+by+the+neurotoxin+MPTP.&rft.au=Pollard%2C+H+B%3BDhariwal%2C+K%3BAdeyemo%2C+O+M%3BMarkey%2C+C+J%3BCaohuy%2C+H%3BLevine%2C+M%3BMarkey%2C+S%3BYoudim%2C+M+B&rft.aulast=Pollard&rft.aufirst=H&rft.date=1992-09-01&rft.volume=6&rft.issue=12&rft.spage=3108&rft.isbn=&rft.btitle=&rft.title=FASEB+journal+%3A+official+publication+of+the+Federation+of+American+Societies+for+Experimental+Biology&rft.issn=08926638&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-15 N1 - Date created - 1992-10-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Brain vascular endothelial cells express JC virus large tumor antigen in immunocompetent and cyclophosphamide-treated hamsters. AN - 73179319; 1325648 AB - When injected intracerebrally into newborn hamsters, the human polyomavirus JC virus (JCV) establishes a nonproductive infection resulting in brain tumor formation. Using immunostaining methods to detect the JCV regulatory protein, large tumor antigen (T antigen), we have now demonstrated JCV infection of brain vascular endothelial cells (EC) in infected hamsters. JCV T antigen was detected in lectin-labeled EC as well as in von Willebrand factor-expressing EC in both cyclophosphamide-treated and nonimmunosuppressed hamster brains 16, 21, and 31 days after birth. Cyclophosphamide-treated hamsters exhibited a greater number of JCV-infected EC, whereas T-antigen expression in nonvascular cells was not affected. The influence of cyclophosphamide was most pronounced in the cerebellum where increased numbers of JCV-infected EC were located predominantly at the internal granular layer-white matter junction, also a prominent location for T-antigen-expressing neoplastic foci. The hamster model demonstrates in vivo infection of EC by a human polyomavirus and directs interest toward the role of these cells in human JCV infection. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Ressetar, H G AU - Webster, H D AU - Stoner, G L AD - Laboratory of Experimental Neuropathology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/09/01/ PY - 1992 DA - 1992 Sep 01 SP - 8170 EP - 8174 VL - 89 IS - 17 SN - 0027-8424, 0027-8424 KW - Antigens, Polyomavirus Transforming KW - 0 KW - von Willebrand Factor KW - Cyclophosphamide KW - 8N3DW7272P KW - Index Medicus KW - Animals KW - von Willebrand Factor -- metabolism KW - Cerebellum -- microbiology KW - Mesocricetus KW - Immunoenzyme Techniques KW - Cricetinae KW - Blood-Brain Barrier KW - JC Virus -- immunology KW - Tumor Virus Infections -- immunology KW - Antigens, Polyomavirus Transforming -- metabolism KW - Endothelium, Vascular -- microbiology KW - Endothelium, Vascular -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73179319?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Brain+vascular+endothelial+cells+express+JC+virus+large+tumor+antigen+in+immunocompetent+and+cyclophosphamide-treated+hamsters.&rft.au=Ressetar%2C+H+G%3BWebster%2C+H+D%3BStoner%2C+G+L&rft.aulast=Ressetar&rft.aufirst=H&rft.date=1992-09-01&rft.volume=89&rft.issue=17&rft.spage=8170&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 - 1992-10-07 N1 - Date created - 1992-10-07 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Infect Immun. 1981 Jul;33(1):319-21 [7196387] Infect Immun. 1981 Jul;33(1):297-303 [7263066] J Gen Virol. 1979 Jan;42(1):49-57 [215712] Infect Immun. 1979 Nov;26(2):705-13 [397932] Lab Invest. 1990 Mar;62(3):287-96 [1690314] Lab Invest. 1986 Sep;55(3):328-36 [3018360] Coll Relat Res. 1986 Oct;6(4):333-49 [3028708] J Immunol. 1986 Jul 1;137(1):245-54 [3086451] Ann Intern Med. 1987 Jul;107(1):78-87 [3296901] Histochem J. 1987 Apr;19(4):225-34 [3597137] Biochemistry. 1985 Sep 24;24(20):5480-6 [4074709] Am J Pathol. 1972 Jul;68(1):15-22 [4342991] J Infect Dis. 1973 Apr;127(4):467-70 [4571704] Br J Exp Pathol. 1970 Aug;51(4):434-9 [4991966] J Exp Med. 1972 Aug 1;136(2):261-76 [5043412] J Comp Neurol. 1970 Jan;138(1):31-47 [5412719] J Cell Biol. 1967 Jul;34(1):207-17 [6033532] EMBO J. 1984 Jul;3(7):1485-91 [6204863] J Comput Assist Tomogr. 1980 Jun;4(3):285-90 [6246149] Blood. 1980 Jun;55(6):1056-9 [6769518] Transplant Proc. 1981 Mar;13(1 Pt 1):262-6 [7022837] Cancer Res. 1977 Mar;37(3):718-20 [189911] Science. 1978 Sep 29;201(4362):1246-9 [211583] Microvasc Res. 1977 Jul;14(1):53-65 [895546] J Neuroimmunol. 1988 Sep;19(3):223-36 [2842376] Acta Pathol Jpn. 1986 Jun;36(6):815-25 [3020865] Acta Neuropathol. 1988;77(2):175-81 [3227814] J Immunol. 1986 Aug 15;137(4):1270-4 [3525675] J Exp Med. 1971 Feb 1;133(2):275-88 [4332371] Science. 1973 Aug 17;181(4100):674-6 [4353360] J Clin Invest. 1973 Nov;52(11):2757-64 [4583980] Brain Res. 1969 Oct;15(2):532-6 [5344385] Nature. 1968 Oct 26;220(5165):399-401 [5684888] J Clin Microbiol. 1980 Feb;11(2):178-83 [6244330] Clin Exp Immunol. 1983 Aug;53(2):289-96 [6309442] Am J Surg Pathol. 1980 Jun;4(3):273-6 [6772042] Cell. 1976 Dec;9(4 PT 2):685-93 [189941] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Radiation therapy of acromegaly. AN - 73171083; 1521519 AB - Conventional megavoltage irradiation of GH-secreting tumors has predictable effects on tumor mass, GH, and pituitary function. 1. Further growth of the tumor is prevented in more than 99% of patients, with only a fraction of a percent of patients requiring subsequent surgery for tumor mass effects. 2. GH falls predictably with time. By 2 years GH falls by about 50% from the baseline level, and by 5 years by about 75% from the baseline level. The initial GH elevation and the size and erosive features of the sella turcica do not affect the percent decrease in GH from the baseline elevation. 3. With prolonged follow-up, further decrease in GH is seen at 10 and 15 years, with the fraction of surviving patients achieving GH levels less than 5 ng/mL approaching 90% after 15 years in our experience. Gender, previous surgery, and hyperprolactinemia do not seem to affect the response to treatment. Patients with initial GH greater than 100 ng/mL are significantly less likely to achieve GH values less than 5 ng/mL during long-term follow-up. 4. Hypopituitarism is a predictable outcome of treatment, is delayed, and may be more likely in patients who have had surgery prior to irradiation. There is no evidence that this complication is more common in patients with acromegaly than in patients with other pituitary adenomas receiving similar treatment. 5. Vision loss due to megavoltage irradiation--using modern techniques and limiting the total dose to 4680 rad given in 25 fractions over 35 days, with individual fractions not exceeding 180 rad--is extremely rare. The reported cases have occurred almost entirely in patients who have received larger doses or higher fractional doses. The theory that patients with acromegaly are prone to radiation-induced injury to the CNS and optic nerves and chiasm because of small vessel disease is not supported by a review of the reported cases. 6. Brain necrosis and secondary neoplasms induced by irradiation are extremely rare. 7. Although anecdotal evidence raises the question of changes in intellectual function following irradiation, this has not been studied in adults receiving pituitary irradiation. JF - Endocrinology and metabolism clinics of North America AU - Eastman, R C AU - Gorden, P AU - Glatstein, E AU - Roth, J AD - Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 693 EP - 712 VL - 21 IS - 3 SN - 0889-8529, 0889-8529 KW - Growth Hormone KW - 9002-72-6 KW - Index Medicus KW - Adenoma -- radiotherapy KW - Pituitary Neoplasms -- pathology KW - Humans KW - Pituitary Neoplasms -- radiotherapy KW - Adenoma -- pathology KW - Radiation Injuries KW - Growth Hormone -- secretion KW - Acromegaly -- pathology KW - Acromegaly -- radiotherapy KW - Acromegaly -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73171083?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+and+metabolism+clinics+of+North+America&rft.atitle=Radiation+therapy+of+acromegaly.&rft.au=Eastman%2C+R+C%3BGorden%2C+P%3BGlatstein%2C+E%3BRoth%2C+J&rft.aulast=Eastman&rft.aufirst=R&rft.date=1992-09-01&rft.volume=21&rft.issue=3&rft.spage=693&rft.isbn=&rft.btitle=&rft.title=Endocrinology+and+metabolism+clinics+of+North+America&rft.issn=08898529&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-13 N1 - Date created - 1992-10-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Genetic vulnerability to drug abuse. The D2 dopamine receptor Taq I B1 restriction fragment length polymorphism appears more frequently in polysubstance abusers. AN - 73170326; 1355337 AB - Alcoholics are more likely than nonalcoholics to display the Taq I A1 restriction fragment length polymorphism of the D2 dopamine receptor gene, according to four of six studies that examined alcoholics and controls. The current study examines whether the association observed in alcoholism might extend to other addictive substances by examining D2 dopamine receptor Taq I A and B restriction fragment length polymorphisms in polysubstance users and controls free of significant substance use. We hypothesized a stronger association for the B1 restriction fragment length polymorphism since it lies closer to dopamine receptor protein coding and 5' regulatory regions. Heavy polysubstance users and subjects with DSM-III-R psychoactive substance use diagnoses displayed significantly higher Taq I B1 frequencies than control subjects; Taq I A1 results for these comparisons were less robust. These results are consistent with a role for a D2 dopamine receptor gene variant marked by these restriction fragment length polymorphisms in enhanced substance abuse vulnerability. JF - Archives of general psychiatry AU - Smith, S S AU - O'Hara, B F AU - Persico, A M AU - Gorelick, D A AU - Newlin, D B AU - Vlahov, D AU - Solomon, L AU - Pickens, R AU - Uhl, G R AD - Addiction Research Center, National Institute on Drug Abuse, Bethesda, Md. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 723 EP - 727 VL - 49 IS - 9 SN - 0003-990X, 0003-990X KW - Genetic Markers KW - 0 KW - Receptors, Dopamine KW - Abridged Index Medicus KW - Index Medicus KW - Alleles KW - Humans KW - Alcoholism -- genetics KW - Male KW - Female KW - Polymorphism, Restriction Fragment Length KW - Receptors, Dopamine -- genetics KW - Substance-Related Disorders -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73170326?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Genetic+vulnerability+to+drug+abuse.+The+D2+dopamine+receptor+Taq+I+B1+restriction+fragment+length+polymorphism+appears+more+frequently+in+polysubstance+abusers.&rft.au=Smith%2C+S+S%3BO%27Hara%2C+B+F%3BPersico%2C+A+M%3BGorelick%2C+D+A%3BNewlin%2C+D+B%3BVlahov%2C+D%3BSolomon%2C+L%3BPickens%2C+R%3BUhl%2C+G+R&rft.aulast=Smith&rft.aufirst=S&rft.date=1992-09-01&rft.volume=49&rft.issue=9&rft.spage=723&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 - 1992-09-28 N1 - Date created - 1992-09-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transforming growth factor-alpha in human hepatocellular carcinoma and coexpression with hepatitis B surface antigen in adjacent liver. AN - 73167964; 1325266 AB - Hepatitis B virus (HBV) infection is closely associated with the development of hepatocellular carcinoma (HCC) in many patients, but the mechanisms by which HBV contributes to HCC are not known. Transforming growth factor-alpha (TGF-alpha), a regulator of growth and regeneration in rat liver that can be found in high levels in some human cancers, theoretically could play such an intermediate role in the development of HCC. The expression of TGF-alpha and its relation to the HBV antigens were evaluated in human HCC and adjacent nontumorous livers from 33 patients from the United States and China using immunoperoxidase staining of paraffin-embedded sections. TGF-alpha was detected in HCC from 27 of 33 (82%) patients; the frequencies were similar in patients from the United States and China. TGF-alpha was detected in HCC more frequently in patients whose adjacent nontumorous livers had detectable hepatitis B surface antigen (HBsAg) and/or hepatitis B core antigen (HBcAg) than in those whose adjacent livers lacked HBsAg and HBcAg. Detection of TGF-alpha was not affected by tumor size, histologic type, or grade. TGF-alpha was detected in adjacent nontumorous livers from 31 of 33 patients (94%). Coexpression at a high intensity of TGF-alpha and HBsAg in the same hepatocytes could be demonstrated by specific staining of consecutively cut sections for 17 of 33 patients (52%). TGF-alpha is expressed at a high level in 82% of human HCC. Localization of HBsAg within the same hepatocytes as TGF-alpha suggests a possible interaction between HBV and TGF-alpha during hepatocarcinogenesis in humans. Stimulation of TGF-alpha expression could be part of a chain of events by which HBV contributes to the development of HCC in some patients. JF - Cancer AU - Hsia, C C AU - Axiotis, C A AU - Di Bisceglie, A M AU - Tabor, E AD - Biological Carcinogenesis Program, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/09/01/ PY - 1992 DA - 1992 Sep 01 SP - 1049 EP - 1056 VL - 70 IS - 5 SN - 0008-543X, 0008-543X KW - Hepatitis B Surface Antigens KW - 0 KW - Transforming Growth Factor alpha KW - Abridged Index Medicus KW - Index Medicus KW - Sensitivity and Specificity KW - Hepatitis B virus KW - Humans KW - Aged KW - Cell Differentiation KW - Hepatitis B -- complications KW - China -- epidemiology KW - Adult KW - Middle Aged KW - United States -- epidemiology KW - Immunohistochemistry KW - Female KW - Male KW - Liver Neoplasms -- pathology KW - Liver -- immunology KW - Hepatitis B Surface Antigens -- analysis KW - Transforming Growth Factor alpha -- physiology KW - Liver Neoplasms -- chemistry KW - Carcinoma, Hepatocellular -- pathology KW - Liver -- metabolism KW - Carcinoma, Hepatocellular -- chemistry KW - Transforming Growth Factor alpha -- analysis KW - Liver -- chemistry KW - Carcinoma, Hepatocellular -- immunology KW - Liver Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73167964?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Transforming+growth+factor-alpha+in+human+hepatocellular+carcinoma+and+coexpression+with+hepatitis+B+surface+antigen+in+adjacent+liver.&rft.au=Hsia%2C+C+C%3BAxiotis%2C+C+A%3BDi+Bisceglie%2C+A+M%3BTabor%2C+E&rft.aulast=Hsia&rft.aufirst=C&rft.date=1992-09-01&rft.volume=70&rft.issue=5&rft.spage=1049&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-07 N1 - Date created - 1992-10-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interferon gamma induces the expression of human immunodeficiency virus in persistently infected promonocytic cells (U1) and redirects the production of virions to intracytoplasmic vacuoles in phorbol myristate acetate-differentiated U1 cells. AN - 73163476; 1512539 AB - Interferon gamma (IFN-gamma), a lymphokine that exerts multiple immunoregulatory effects, has been found to be elevated in the plasma, cerebrospinal fluid, and lymph nodes of human immunodeficiency virus (HIV)-infected individuals and has shown variable effects on HIV replication in acutely infected cells. In the present study, we have demonstrated that IFN-gamma is a potent modulator of HIV expression in persistently infected U1 promonocytic cells in which virus production is characterized by a constitutive state of relative latency. Direct stimulation of U1 cells with IFN-gamma (10-1,000 U/ml) activated HIV expression, as measured by reverse transcriptase (RT) activity in the culture supernatant and increased levels of cell-associated viral protein and mRNAs. These effects on virus expression were not accounted for by the induction of endogenous TNF-alpha secretion, as previously described in U1 cells stimulated with phorbol myristate acetate (PMA). At the ultrastructural level, the stimulatory activity of IFN-gamma was correlated with HIV particle production in intracytoplasmic vacuoles along with the differentiation of U1 into macrophage-like cells. Furthermore, costimulation of U1 cells with IFN-gamma and PMA significantly increased the accumulation of vacuole-associated HIV concomitant with decreasing membrane-associated particles and RT activity production, as compared with cells stimulated with PMA alone. No evidence of spontaneous secretion of intracellular vacuole-associated virus was obtained by kinetic analysis of the RT activity released in the supernatants throughout the culture period unless cells were deliberately disrupted. These findings suggest that vacuole-associated virions likely represent a relatively stable intracellular reservoir of HIV, as previously described in primary macrophages infected in vitro or in infected macrophages in the brains of patients with acquired immune deficiency syndrome. The reduced levels of RT activity observed in the culture supernatants of U1 cells stimulated with PMA in the presence of IFN-gamma were not indicative of a suppressive effect of IFN-gamma on PMA-induced expression of HIV proteins and mRNAs, either directly or mediated by the release of IFN-alpha/beta. This study suggests that IFN-gamma may play an important role as an inducer of HIV expression in infected mononuclear phagocytes. JF - The Journal of experimental medicine AU - Biswas, P AU - Poli, G AU - Kinter, A L AU - Justement, J S AU - Stanley, S K AU - Maury, W J AU - Bressler, P AU - Orenstein, J M AU - Fauci, A S AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/09/01/ PY - 1992 DA - 1992 Sep 01 SP - 739 EP - 750 VL - 176 IS - 3 SN - 0022-1007, 0022-1007 KW - Interferon-gamma KW - 82115-62-6 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - AIDS/HIV KW - Kinetics KW - Humans KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Cell Differentiation KW - Microscopy, Electron KW - Virion -- growth & development KW - Up-Regulation KW - Virus Activation KW - Cell Line KW - HIV -- growth & development KW - Monocytes -- cytology KW - Monocytes -- drug effects KW - Monocytes -- microbiology KW - Interferon-gamma -- physiology KW - Vacuoles -- microbiology KW - HIV -- ultrastructure KW - Monocytes -- ultrastructure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73163476?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Interferon+gamma+induces+the+expression+of+human+immunodeficiency+virus+in+persistently+infected+promonocytic+cells+%28U1%29+and+redirects+the+production+of+virions+to+intracytoplasmic+vacuoles+in+phorbol+myristate+acetate-differentiated+U1+cells.&rft.au=Biswas%2C+P%3BPoli%2C+G%3BKinter%2C+A+L%3BJustement%2C+J+S%3BStanley%2C+S+K%3BMaury%2C+W+J%3BBressler%2C+P%3BOrenstein%2C+J+M%3BFauci%2C+A+S&rft.aulast=Biswas&rft.aufirst=P&rft.date=1992-09-01&rft.volume=176&rft.issue=3&rft.spage=739&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 - 1992-09-30 N1 - Date created - 1992-09-30 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Science. 1988 Sep 23;241(4873):1673-5 [3047875] J Immunol. 1988 Jan 1;140(1):120-4 [3121735] J Virol. 1988 Aug;62(8):2578-86 [3260631] J Immunol. 1985 Mar;134(3):1503-7 [3918102] N Engl J Med. 1985 Dec 12;313(24):1504-10 [3934537] J Leukoc Biol. 1991 Jun;49(6):566-78 [1673992] FASEB J. 1991 Jul;5(10):2382-90 [1676689] Leuk Res. 1990;14(11-12):1027-33 [1704084] Exp Cell Res. 1991 Mar;193(1):20-6 [1825297] Neurology. 1991 Jan;41(1):69-74 [1898675] Leuk Res. 1991;15(5):327-39 [1904515] J Immunol. 1991 Nov 1;147(9):2922-7 [1918999] J Immunol. 1990 Jun 15;144(12):4628-32 [1972163] FASEB J. 1991 Jul;5(10):2391-7 [2065887] J Clin Invest. 1990 Jul;86(1):148-59 [2114424] J Interferon Res. 1990 Dec;10(6):599-603 [2128302] Semin Oncol. 1990 Dec;17(6 Suppl 9):38-46 [2148026] Immunol Today. 1990 Jun;11(6):217-23 [2191685] Proc Natl Acad Sci U S A. 1990 Jan;87(2):782-5 [2300561] Clin Exp Immunol. 1985 Oct;62(1):128-35 [2415279] J Interferon Res. 1986 Apr;6(2):143-52 [2425014] Annu Rev Biochem. 1987;56:727-77 [2441659] Science. 1988 Nov 11;242(4880):919-22 [2460922] Science. 1989 May 5;244(4904):575-7 [2470148] Proc Natl Acad Sci U S A. 1989 Jan;86(2):675-9 [2492110] Science. 1989 Jul 21;245(4915):305-8 [2665081] Blood. 1986 Jul;68(1):281-4 [3013342] Science. 1986 Jul 11;233(4760):215-9 [3014648] Onkologie. 1986 Jun;9(3):163-6 [3018647] AIDS Res Hum Retroviruses. 1987 Summer;3(2):125-33 [3113463] AIDS Res Hum Retroviruses. 1988 Aug;4(4):287-94 [3144996] J Exp Med. 1988 Apr 1;167(4):1428-41 [3258626] Hum Pathol. 1988 Mar;19(3):350-61 [3346011] N Engl J Med. 1984 Apr 5;310(14):883-9 [6422299] AIDS Res Hum Retroviruses. 1992 Feb;8(2):199-207 [1371692] Proc Natl Acad Sci U S A. 1991 Nov 1;88(21):9838-42 [1682922] J Virol. 1991 Jul;65(7):3968-71 [1710293] J Leukoc Biol. 1991 Mar;49(3):294-301 [1847718] Clin Exp Immunol. 1991 Jul;85(1):143-50 [1906383] J Infect Dis. 1991 Dec;164(6):1051-7 [1955708] Pharmacol Ther. 1990;45(1):137-51 [2105509] Biochem Pharmacol. 1990 Oct 1;40(7):1433-9 [2121146] J Exp Pathol. 1990;5(3):127-32 [2128842] J Exp Med. 1990 Jul 1;172(1):151-8 [2193094] Cell. 1990 Jun 29;61(7):1271-6 [2364429] Proc Natl Acad Sci U S A. 1986 Nov;83(22):8734-8 [2430298] J Immunol. 1988 Feb 15;140(4):1117-22 [2449497] J Exp Med. 1989 Mar 1;169(3):1137-51 [2466937] N Engl J Med. 1985 Jul 11;313(2):79-84 [2582258] Proc Natl Acad Sci U S A. 1989 Aug;86(15):5974-8 [2762307] Science. 1986 Sep 5;233(4768):1089-93 [3016903] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inter-relationships between quinolinic acid, neuroactive kynurenines, neopterin and beta 2-microglobulin in cerebrospinal fluid and serum of HIV-1-infected patients. AN - 73159494; 1387655 AB - Quinolinic acid (QUIN) is an neurotoxic N-methyl-D-aspartate receptor agonist and an L-tryptophan metabolite of the kynurenine pathway. Increased concentrations of QUIN occur in both cerebrospinal fluid (CSF) and blood of patients infected with human immunodeficiency virus (HIV)-1, particularly those with neurologic disturbances. In the present study of HIV-1 infected patients in Walter Reed stages 4, 5 and 6, reductions in L-tryptophan accompanied proportional increases in L-kynurenine and QUIN in both serum and CSF. Further, close inter-correlations exist between QUIN kynurenic acid and L-kynurenine with both beta 2-microglobulin and neopterin in CSF and serum. These correlations support the hypotheses that the kynurenine pathway is activated in association with inflammation and induction of indoleamine-2,3-dioxygenase. There were no relationships between CSF QUIN, L-kynurenine or kynurenic acid with the ratio of serum:CSF albumin concentrations, which indicates that the increases in CSF QUIN, L-kynurenine or kynurenic acid were not dependent on a breakdown of the blood-brain barrier. Kynurenic acid is also a kynurenine pathway metabolite that can attenuate the excitotoxic effects of QUIN when present in higher molar concentrations. While CSF kynurenic acid levels were increased in HIV-1-infected patients, the magnitude of the increases were smaller than those of QUIN and the molar concentrations of kynurenic acid were consistently lower than QUIN by at least one order of magnitude. We conclude that immune activation increases the levels of neuroactive kynurenines within the central nervous system of HIV-1-infected patients secondary to activation of indoleamine-2,3-dioxygenase. JF - Journal of neuroimmunology AU - Heyes, M P AU - Brew, B J AU - Saito, K AU - Quearry, B J AU - Price, R W AU - Lee, K AU - Bhalla, R B AU - Der, M AU - Markey, S P AD - Section on Analytical Biochemistry, NIMH, NIH, Bethesda, MD 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 71 EP - 80 VL - 40 IS - 1 SN - 0165-5728, 0165-5728 KW - Neurotoxins KW - 0 KW - Quinolinic Acids KW - beta 2-Microglobulin KW - Biopterin KW - 22150-76-1 KW - Serotonin KW - 333DO1RDJY KW - Kynurenine KW - 343-65-7 KW - Neopterin KW - 670-65-5 KW - Quinolinic Acid KW - F6F0HK1URN KW - Index Medicus KW - AIDS/HIV KW - AIDS Dementia Complex -- metabolism KW - Serotonin -- cerebrospinal fluid KW - Humans KW - Serotonin -- blood KW - Nervous System Physiological Phenomena KW - AIDS Dementia Complex -- psychology KW - Blood-Brain Barrier KW - Quinolinic Acids -- blood KW - beta 2-Microglobulin -- metabolism KW - Biopterin -- cerebrospinal fluid KW - HIV-1 KW - Biopterin -- analogs & derivatives KW - Kynurenine -- blood KW - Kynurenine -- cerebrospinal fluid KW - Kynurenine -- physiology KW - Acquired Immunodeficiency Syndrome -- blood KW - Biopterin -- blood KW - beta 2-Microglobulin -- cerebrospinal fluid KW - Quinolinic Acids -- cerebrospinal fluid KW - Acquired Immunodeficiency Syndrome -- cerebrospinal fluid UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73159494?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+neuroimmunology&rft.atitle=Inter-relationships+between+quinolinic+acid%2C+neuroactive+kynurenines%2C+neopterin+and+beta+2-microglobulin+in+cerebrospinal+fluid+and+serum+of+HIV-1-infected+patients.&rft.au=Heyes%2C+M+P%3BBrew%2C+B+J%3BSaito%2C+K%3BQuearry%2C+B+J%3BPrice%2C+R+W%3BLee%2C+K%3BBhalla%2C+R+B%3BDer%2C+M%3BMarkey%2C+S+P&rft.aulast=Heyes&rft.aufirst=M&rft.date=1992-09-01&rft.volume=40&rft.issue=1&rft.spage=71&rft.isbn=&rft.btitle=&rft.title=Journal+of+neuroimmunology&rft.issn=01655728&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-08 N1 - Date created - 1992-10-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - GGT to GTT transversions in codon 12 of the K-ras oncogene in rat renal sarcomas induced with nickel subsulfide or nickel subsulfide/iron are consistent with oxidative damage to DNA. AN - 73159492; 1511440 AB - Nickel is a toxic, mutagenic, and carcinogenic metal of significant occupational and environmental concern. Although several cellular targets of nickel have been identified, considerable evidence suggests that it can act indirectly upon DNA by inducing the formation of oxidized purines or pyrimidines that constitute promutagenic lesions. In this study, we examined nickel subsulfide (Ni3S2)- or Ni3S2/iron-induced renal sarcomas in F344 rats for the presence of transforming mutations in the K-ras oncogene. Selective oligonucleotide hybridization analysis of K-ras gene sequences amplified by polymerase chain reaction revealed that 1 of 12 primary tumors induced with Ni3S2 and 7 of 9 primary tumors induced with Ni3S2/iron contained exclusively GGT to GTT activating mutations in codon 12. These mutations are consistent with the known ability of nickel, in the presence of an oxidizing agent, to catalyze formation of 8-hydroxydeoxyguanosine, which in turn promotes misincorporation of dATP opposite the oxidized guanine residue. The presence of GGT to GTT transversions was confirmed by direct sequencing of the polymerase chain reaction products. Sequencing also revealed that there were no transforming mutations in codons 13 or 59-61. Additionally, a direct correlation between shortened tumor latency and the presence of activating ras mutations was noted. These results show that, in rat kidney, Ni3S2 can induce transforming mutations that are consistent with the ability of nickel to produce oxidative lesions and that iron, which exacerbates the extent of cellular oxidative damage, can enhance the frequency of these transforming mutations. JF - Cancer research AU - Higinbotham, K G AU - Rice, J M AU - Diwan, B A AU - Kasprzak, K S AU - Reed, C D AU - Perantoni, A O AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick, Maryland 21702-1201. Y1 - 1992/09/01/ PY - 1992 DA - 1992 Sep 01 SP - 4747 EP - 4751 VL - 52 IS - 17 SN - 0008-5472, 0008-5472 KW - Codon KW - 0 KW - Oligodeoxyribonucleotides KW - nickel subsulfide KW - 12035-72-2 KW - Nickel KW - 7OV03QG267 KW - DNA KW - 9007-49-2 KW - Iron KW - E1UOL152H7 KW - Proto-Oncogene Proteins p21(ras) KW - EC 3.6.5.2 KW - Index Medicus KW - Rats KW - Oxidation-Reduction KW - Animals KW - Rats, Inbred F344 KW - Base Sequence KW - Oligodeoxyribonucleotides -- chemistry KW - Molecular Sequence Data KW - DNA -- chemistry KW - Kidney Neoplasms -- genetics KW - Genes, ras KW - Sarcoma, Experimental -- chemically induced KW - Kidney Neoplasms -- chemically induced KW - DNA Damage KW - Iron -- chemistry KW - Nickel -- toxicity KW - Sarcoma, Experimental -- genetics KW - Iron -- toxicity KW - Nickel -- chemistry KW - Proto-Oncogene Proteins p21(ras) -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73159492?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=GGT+to+GTT+transversions+in+codon+12+of+the+K-ras+oncogene+in+rat+renal+sarcomas+induced+with+nickel+subsulfide+or+nickel+subsulfide%2Firon+are+consistent+with+oxidative+damage+to+DNA.&rft.au=Higinbotham%2C+K+G%3BRice%2C+J+M%3BDiwan%2C+B+A%3BKasprzak%2C+K+S%3BReed%2C+C+D%3BPerantoni%2C+A+O&rft.aulast=Higinbotham&rft.aufirst=K&rft.date=1992-09-01&rft.volume=52&rft.issue=17&rft.spage=4747&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 - 1992-09-29 N1 - Date created - 1992-09-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - 95-kilodalton B-Raf serine/threonine kinase: identification of the protein and its major autophosphorylation site. AN - 73157874; 1508179 AB - B-Raf, a member of the Raf family of serine/threonine kinases, is expressed primarily in the brain and in the nervous system. In this study, the biochemical properties of the B-Raf protein were investigated in nerve growth factor (NGF)-responsive cell lines and in brain tissues. B-Raf was identified by using phosphopeptide mapping analysis and cDNA analysis as a 95-kDa protein which is primarily localized in the cytosol. NGF rapidly stimulated both serine and threonine phosphorylation in vivo and autophosphorylation activity in vitro of the B-Raf protein. In PC12 cells, B-Raf autokinase activity was induced by both differentiation factors and mitogens, with maximal activity observed after 5 min of factor addition. B-Raf kinase activity was also observed following NGF treatment of SH-SY5Y neuroblastoma cells and in adult mouse brain and hippocampus. Induction of B-Raf kinase activity in NGF-treated PC12 cells required expression of kinase-active trk receptors. Exogenous substrates or a peptide containing the autophosphorylation site became phosphorylated when added to immune complex kinase assays and reduced the in vitro autophosphorylation activity of B-Raf, suggesting that in vitro autophosphorylation sites and exogenous substrates compete for active sites of the B-Raf kinase. Finally, the major in vitro autophosphorylation site of B-Raf was identified as threonine 372 in the conserved region 2 domain. A threonine residue is present at similar positions in all three mammalian Raf family members and may represent a regulatory site for these proteins. JF - Molecular and cellular biology AU - Stephens, R M AU - Sithanandam, G AU - Copeland, T D AU - Kaplan, D R AU - Rapp, U R AU - Morrison, D K AD - Molecular Mechanisms of Carcinogenesis Laboratory, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 3733 EP - 3742 VL - 12 IS - 9 SN - 0270-7306, 0270-7306 KW - Nerve Growth Factors KW - 0 KW - Proto-Oncogene Proteins KW - Protein Kinases KW - EC 2.7.- KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Proto-Oncogene Proteins c-raf KW - EC 2.7.11.1 KW - Index Medicus KW - Brain -- enzymology KW - Animals KW - Blotting, Western KW - Phosphorylation KW - Peptide Mapping KW - Enzyme Activation KW - Molecular Sequence Data KW - Nerve Growth Factors -- physiology KW - Mice KW - Amino Acid Sequence KW - Protein-Tyrosine Kinases -- metabolism KW - PC12 Cells KW - Protein Kinases -- metabolism KW - Proto-Oncogene Proteins -- chemistry KW - Proto-Oncogene Proteins -- metabolism KW - Protein Kinases -- genetics KW - Proto-Oncogene Proteins -- genetics KW - Protein Kinases -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73157874?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=95-kilodalton+B-Raf+serine%2Fthreonine+kinase%3A+identification+of+the+protein+and+its+major+autophosphorylation+site.&rft.au=Stephens%2C+R+M%3BSithanandam%2C+G%3BCopeland%2C+T+D%3BKaplan%2C+D+R%3BRapp%2C+U+R%3BMorrison%2C+D+K&rft.aulast=Stephens&rft.aufirst=R&rft.date=1992-09-01&rft.volume=12&rft.issue=9&rft.spage=3733&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 - 1992-09-23 N1 - Date created - 1992-09-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cell. 1991 May 17;65(4):663-75 [2032290] Cold Spring Harb Symp Quant Biol. 1985;50:253-62 [3938363] Mol Cell Biol. 1990 Jun;10(6):2503-12 [2188091] Methods Enzymol. 1990;182:194-203 [2314237] Science. 1986 Apr 25;232(4749):485-7 [2421409] Proc Natl Acad Sci U S A. 1989 Dec;86(24):10128-32 [2602361] Mol Cell Biol. 1989 Feb;9(2):639-47 [2710120] Nucleic Acids Res. 1988 Dec 9;16(23):11057-74 [2905047] J Cell Biol. 1986 Mar;102(3):830-43 [3005338] Nucleic Acids Res. 1987 Jan 26;15(2):595-609 [3029685] Mol Cell Biol. 1988 Jun;8(6):2651-4 [3043188] Proc Natl Acad Sci U S A. 1988 Jul;85(13):4691-5 [3133658] EMBO J. 1988 Oct;7(10):3053-60 [3181128] Science. 1987 Nov 6;238(4828):797-9 [3672127] J Neurosci. 1986 Aug;6(8):2155-62 [3746405] J Neurosci Res. 1982;8(2-3):375-91 [6296415] Proc Natl Acad Sci U S A. 1976 Jul;73(7):2424-8 [1065897] Cell. 1991 Sep 6;66(5):961-6 [1653650] J Biol Chem. 1991 Jan 25;266(3):1359-62 [1703147] Nature. 1991 Mar 14;350(6314):158-60 [1706478] J Biol Chem. 1991 Oct 25;266(30):19908-16 [1718957] Cell. 1991 Apr 5;65(1):189-97 [1849459] Nature. 1991 Apr 25;350(6320):678-83 [1850821] Brain Res. 1991 May 3;547(2):309-14 [1884206] Methods Enzymol. 1991;201:110-49 [1943760] Mol Cell Biol. 1991 Feb;11(2):913-9 [1990291] Nature. 1991 Jan 31;349(6308):426-8 [1992343] Exp Brain Res. 1991;84(2):403-10 [2065747] Eur J Biochem. 1990 Nov 13;193(3):661-9 [2174361] Mol Cell Biol. 1990 Jul;10(7):3828-33 [2192265] Oncogene. 1990 Dec;5(12):1775-80 [2284096] J Biol Chem. 1990 Sep 15;265(26):15471-80 [2394735] Cell. 1989 Aug 25;58(4):649-57 [2475255] Cell. 1989 Sep 22;58(6):1121-33 [2550144] J Gen Virol. 1977 Jul;36(1):59-74 [886304] Oncogene. 1990 Mar;5(3):345-51 [1690378] Eur J Biochem. 1989 Jul 15;183(1):227-33 [2666134] J Biol Chem. 1989 May 25;264(15):8646-52 [2785993] Virology. 1985 Oct 15;146(1):78-89 [2994296] Proc Natl Acad Sci U S A. 1991 Jul 1;88(13):5650-4 [1712104] J Biol Chem. 1991 Dec 15;266(35):23753-60 [1748651] Science. 1991 Apr 26;252(5005):554-8 [1850549] Genes Dev. 1991 Sep;5(9):1553-67 [1884998] Methods Enzymol. 1991;201:149-52 [1943761] Nucleic Acids Res. 1986 Jan 24;14(2):1009-15 [3003687] Cell. 1986 Nov 21;47(4):545-54 [3022937] EMBO J. 1986 Dec 20;5(13):3441-7 [3030727] Proc Natl Acad Sci U S A. 1987 Apr;84(7):1819-23 [3031652] Cell. 1988 Apr 8;53(1):37-43 [3127059] J Biol Chem. 1988 Nov 5;263(31):15853-6 [3141398] Nucleic Acids Res. 1987 Oct 26;15(20):8125-48 [3313277] Proc Natl Acad Sci U S A. 1986 Apr;83(8):2353-7 [3458200] Science. 1987 Dec 18;238(4834):1726-8 [3686012] Nature. 1985 Feb 14-20;313(6003):545-51 [3918274] Cancer Cells. 1990 Dec;2(12):377-82 [2150916] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cross-talk between excitatory and inhibitory amino acids in the regulation of luteinizing hormone-releasing hormone secretion. AN - 73151890; 1354606 AB - Inhibitory (IAA) and excitatory amino acid (EAA) neurotransmitters appear to play an important role in regulating reproductive functions. L-Glutamic acid (GLU), the major representative of the EAA system, stimulates LHRH release from arcuate nucleus-median eminence (AN-ME) fragments in vitro. Several studies have provided evidence for considering gamma-aminobutyric acid (GABA), a major IAA neurotransmitter, as another regulator of LHRH secretion. Recent reports have indicated that a cross-talk between GABA and GLU participates in the regulation of synaptic transmission in the brain. In concert with this notion, we present evidence indicating that this cross-talk between GABA and GLU appears to be also involved in neuroendocrinological paradigms. In this respect, bicuculline, a GABA-A receptor antagonist, blocked GLU-evoked LHRH secretion from AN-ME fragments in vitro without affecting basal LHRH release. In addition, activation of GABA-A receptors by muscimol (MUS) stimulated basal LHRH secretion. Interestingly, when MUS and GLU were added together to the incubation medium, an additive, stimulatory effect was observed. These observations clearly indicate that a GABAergic mechanism participates, via GABA-A receptors, in GLU-induced LHRH secretion from terminals of the ME. Furthermore, GABA-B receptors appear to negatively modulate the effects of GLU. Activation of GABA-B receptors by baclofen (BAC) blocked GLU-induced LHRH secretion, while phaclofen, a GABA-B receptor antagonist, reversed this effect. In summary, our data provide evidence for a cross-talk between EAA and IAA systems in the regulation of LHRH release, and, therefore, in the control of gonadal function. JF - Endocrinology AU - Donoso, A O AU - López, F J AU - Negro-Vilar, A AD - Reproductive Neuroendocrinology Section, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 1559 EP - 1561 VL - 131 IS - 3 SN - 0013-7227, 0013-7227 KW - Excitatory Amino Acid Antagonists KW - 0 KW - GABA-A Receptor Antagonists KW - Glutamates KW - Receptors, GABA-A KW - phaclofen KW - 108351-35-5 KW - Muscimol KW - 2763-96-4 KW - Gonadotropin-Releasing Hormone KW - 33515-09-2 KW - Glutamic Acid KW - 3KX376GY7L KW - gamma-Aminobutyric Acid KW - 56-12-2 KW - Baclofen KW - H789N3FKE8 KW - Bicuculline KW - Y37615DVKC KW - Abridged Index Medicus KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Drug Interactions KW - Receptors, GABA-A -- physiology KW - In Vitro Techniques KW - Baclofen -- analogs & derivatives KW - Male KW - Baclofen -- pharmacology KW - Bicuculline -- pharmacology KW - Median Eminence -- secretion KW - Glutamates -- pharmacology KW - Arcuate Nucleus of Hypothalamus -- drug effects KW - gamma-Aminobutyric Acid -- pharmacology KW - Arcuate Nucleus of Hypothalamus -- secretion KW - Gonadotropin-Releasing Hormone -- secretion KW - Muscimol -- pharmacology KW - Median Eminence -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73151890?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cross-talk+between+excitatory+and+inhibitory+amino+acids+in+the+regulation+of+luteinizing+hormone-releasing+hormone+secretion.&rft.au=Donoso%2C+A+O%3BL%C3%B3pez%2C+F+J%3BNegro-Vilar%2C+A&rft.aulast=Donoso&rft.aufirst=A&rft.date=1992-09-01&rft.volume=131&rft.issue=3&rft.spage=1559&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=00137227&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-22 N1 - Date created - 1992-09-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effect of ICRF-187 on the pulmonary damage induced by hyperoxia in the rat. AN - 73148320; 1519241 AB - Histological and ultrastructural studies were made of the lungs of rats that were exposed to 100% oxygen for 60 h and were treated with either normal saline or with ICRF-187, a bis-diketopiperazine derivative of EDTA that has the capacity to chelate iron. This metal is thought to be needed to catalyze the formation of toxic oxygen free radicals. ICRF-187 (20 mg/kg) was given intraperitoneally at approximately 12 h intervals (5 doses) during the 60 h exposure. Seven of the ten saline-treated rats exposed to oxygen died prior to the end of the study whereas only one of the 10 rats in the ICRF-187-treated group died. This difference in mortality is found to be statistically significant (P less than 0.05). All saline-treated rats showed light and electron microscopic evidence of pulmonary damage. ICRF-187 attenuated the morphologic alterations observed by light microscopy (intra-alveolar edema, inflammatory exudates and bronchiolar epithelial cell swelling and hyperplasia; P less than 0.05). In addition, electron microscopic evaluation revealed that capillary thrombi, endothelial cell alterations and alveolar epithelial cell damage also were less severe in ICRF-187-treated rats. It is concluded that ICRF-187 may provide a new and useful approach for the prevention of hyperoxia-induced pulmonary damage. JF - Toxicology AU - Fukuda, Y AU - Herman, E H AU - Ferrans, V J AD - Pathology Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 185 EP - 202 VL - 74 IS - 2-3 SN - 0300-483X, 0300-483X KW - Free Radicals KW - 0 KW - Razoxane KW - 5AR83PR647 KW - Iron KW - E1UOL152H7 KW - Oxygen KW - S88TT14065 KW - Index Medicus KW - Space life sciences KW - Rats, Inbred Strains KW - Rats KW - Injections, Intraperitoneal KW - Animals KW - Chelation Therapy KW - Microscopy, Electron KW - Male KW - Razoxane -- pharmacology KW - Razoxane -- administration & dosage KW - Oxygen -- toxicity KW - Lung -- drug effects KW - Lung -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73148320?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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&rft.atitle=Effect+of+ICRF-187+on+the+pulmonary+damage+induced+by+hyperoxia+in+the+rat.&rft.au=Fukuda%2C+Y%3BHerman%2C+E+H%3BFerrans%2C+V+J&rft.aulast=Fukuda&rft.aufirst=Y&rft.date=1992-09-01&rft.volume=74&rft.issue=2-3&rft.spage=185&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=0300483X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-08 N1 - Date created - 1992-10-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vitro and in vivo suppression of interleukin-2-activated killer cell activity by chimeric proteins between interleukin-2 and Pseudomonas exotoxin. AN - 73148168; 1511480 AB - The biological effects of IL-2 are mediated through high (complex of alpha and beta chain) or intermediate (beta chain) affinity IL-2 receptors. Previously, chimeric proteins composed of IL-2 and Pseudomonas exotoxin (IL-2-PE) were shown to be specifically cytotoxic to cells bearing IL-2 receptors. It has also been shown that IL-2-PE chimeric proteins can abrogate T cell-mediated immune response in vitro. In the current study, we have investigated the effects of IL-2-PE on LAK activity both in vivo and in vitro. We administered either IL-2-PE40 (comprised of IL-2 and 40-kDa portion of PE) or IL-2-PE66 (comprised of IL-2 and 66-kDa molecule of PE) to normal C57BL/6 mice for 3 or 8 days and LAK activity was assessed in various organs of mice. We found that IL-2-PE40 generated LAK activity in various compartments of mice and the level of activity was slightly lower than that observed with an equivalent amount of recombinant (r) IL-2 alone. However, IL-2-PE66 failed to generate LAK activity which would have been induced due to an equivalent concentration of rIL-2. IL-2-PE66 also did not induce LAK activity from the splenocytes during in vitro culture while IL-2-PE40 generated good LAK activity. An equivalent amount of IL-2 also generated potent LAK activity. The suppression of LAK activity by IL-2-PE66 was also evident in cells preactivated with IL-2; however, this inhibition was partial. The suppressive activity of IL-2-PE66 was shown to be mediated through IL-2 receptor interactions as excess amounts of rIL-2 were able to abrogate its effect. Both IL-2 toxins were equivalently cytotoxic to IL-2 receptor-bearing HUT 102 cells and both were able to compete from high and intermediate affinity IL-2 receptors. Taken together, our data indicate that IL-2-PE66 is highly cytotoxic to LAK cells while IL-2-PE40 is less cytotoxic. Thus, data from our study and from other published reports indicate that IL-2-PE66 is more potent immunosuppressive agent than IL-2-PE40. JF - Cellular immunology AU - Puri, R K AU - FitzGerald, D AU - Leland, P AU - Kozak, R W AU - Pastan, I AD - Laboratory of Cellular Immunology, Food and Drug Administration, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 324 EP - 334 VL - 143 IS - 2 SN - 0008-8749, 0008-8749 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - Interleukin-2 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 - Recombinant Fusion Proteins -- metabolism KW - Lymphocyte Activation -- drug effects KW - Animals KW - Receptors, Interleukin-2 -- metabolism KW - In Vitro Techniques KW - Mice, Inbred C57BL KW - Immunity, Cellular -- drug effects KW - Mice KW - Recombinant Fusion Proteins -- toxicity KW - Female KW - Interleukin-2 -- antagonists & inhibitors KW - Interleukin-2 -- metabolism KW - Killer Cells, Lymphokine-Activated -- immunology KW - Killer Cells, Lymphokine-Activated -- drug effects KW - Exotoxins -- toxicity KW - Exotoxins -- chemistry KW - Cytotoxicity, Immunologic -- drug effects KW - Interleukin-2 -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73148168?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=In+vitro+and+in+vivo+suppression+of+interleukin-2-activated+killer+cell+activity+by+chimeric+proteins+between+interleukin-2+and+Pseudomonas+exotoxin.&rft.au=Puri%2C+R+K%3BFitzGerald%2C+D%3BLeland%2C+P%3BKozak%2C+R+W%3BPastan%2C+I&rft.aulast=Puri&rft.aufirst=R&rft.date=1992-09-01&rft.volume=143&rft.issue=2&rft.spage=324&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 - 1992-10-01 N1 - Date created - 1992-10-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evidence for IFN-gamma as a mediator of the lethality of endotoxin and tumor necrosis factor-alpha. AN - 73130231; 1506688 AB - Current evidence indicates that endogenously produced peptide cytokines, most notably TNF-alpha and IL-1, mediate the lethality of experimental endotoxemia. Because circulating serum levels of IFN-gamma can be detected soon after TNF-alpha and IL-1 in response to endotoxin, we investigated the role of IFN-gamma in endotoxin and TNF-alpha lethality. Specific neutralizing antibodies to murine TNF-alpha (anti-TNF-alpha Ab) or murine IFN gamma (anti-IFN-gamma Ab) produced in our laboratory protected mice against the lethality of Escherichia coli endotoxin (LPS) administered 6 h later. Serum IFN-gamma levels 2 h after i.v. LPS were lower in mice treated with anti-TNF-alpha Ab compared to mice that received nonimmune IgG (median less than 2.5 vs 3.0 U/ml, P2 less than 0.05). In contrast, serum TNF-alpha levels 1 h after i.v. LPS peaked more than fourfold higher in mice treated with anti-IFN-gamma Ab compared to controls (median greater than 6400 vs 1405 pg/ml, p2 less than 0.05). Doses of TNF-alpha (300 micrograms/kg) and IFN-gamma (50,000 U) which were well tolerated when given individually were synergistically lethal in combination (0% lethality vs 100% lethality, P2 less than 0.001), and were associated with higher serum levels of IL-6 than with either cytokine alone. Anti-IFN-gamma Ab provided complete protection against exogenous human rTNF-alpha at the LD100 dose (1400 micrograms/kg, p2 less than 0.001), and in fact prevented lethality at doses four- to fivefold greater than the LD100 human rTNF-alpha (up to 6000 micrograms/kg). We conclude that IFN-gamma is synergistic with TNF-alpha, is essential for the lethality of LPS and TNF-alpha, and may have modulating effects on the negative control of serum levels of TNF-alpha after LPS in mice. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Doherty, G M AU - Lange, J R AU - Langstein, H N AU - Alexander, H R AU - Buresh, C M AU - Norton, J A AD - Surgical Metabolism Section, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/09/01/ PY - 1992 DA - 1992 Sep 01 SP - 1666 EP - 1670 VL - 149 IS - 5 SN - 0022-1767, 0022-1767 KW - Antibodies KW - 0 KW - Endotoxins KW - Interleukin-6 KW - Lipopolysaccharides KW - Tumor Necrosis Factor-alpha KW - Interferon-gamma KW - 82115-62-6 KW - Abridged Index Medicus KW - Index Medicus KW - Interleukin-6 -- blood KW - Antibodies -- immunology KW - Animals KW - Mice, Inbred C3H KW - Rabbits KW - Mice KW - Female KW - Tumor Necrosis Factor-alpha -- toxicity KW - Tumor Necrosis Factor-alpha -- analysis KW - Lipopolysaccharides -- toxicity KW - Interferon-gamma -- physiology KW - Interferon-gamma -- blood KW - Endotoxins -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73130231?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Angiogenin+is+a+cytotoxic%2C+tRNA-specific+ribonuclease+in+the+RNase+A+superfamily.&rft.au=Saxena%2C+S+K%3BRybak%2C+S+M%3BDavey%2C+R+T%3BYoule%2C+R+J%3BAckerman%2C+E+J&rft.aulast=Saxena&rft.aufirst=S&rft.date=1992-10-25&rft.volume=267&rft.issue=30&rft.spage=21982&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 - 1992-09-22 N1 - Date created - 1992-09-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - CONF T1 - Multistage carcinogenesis: the Twenty-Second International Symposium of the Princess Takamatsu Cancer Research Fund. AN - 73128225; 1511448 JF - Cancer research AU - Harris, C C AU - Hirohashi, S AU - Ito, N AU - Pitot, H C AU - Sugimura, T AU - Terada, M AU - Yokota, J Y1 - 1992/09/01/ PY - 1992 DA - 1992 Sep 01 SP - 4837 EP - 4840 VL - 52 IS - 17 KW - DNA, Neoplasm KW - 0 KW - Index Medicus KW - Neoplasm Invasiveness KW - Animals KW - Humans KW - Neoplasm Metastasis KW - DNA, Neoplasm -- genetics KW - Cell Differentiation KW - Cell Division KW - Neoplasms -- pathology KW - Neoplasms -- genetics KW - Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73128225?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&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=Cancer+research&rft.atitle=Multistage+carcinogenesis%3A+the+Twenty-Second+International+Symposium+of+the+Princess+Takamatsu+Cancer+Research+Fund.&rft.au=Harris%2C+C+C%3BHirohashi%2C+S%3BIto%2C+N%3BPitot%2C+H+C%3BSugimura%2C+T%3BTerada%2C+M%3BYokota%2C+J&rft.aulast=Harris&rft.aufirst=C&rft.date=1992-09-01&rft.volume=52&rft.issue=17&rft.spage=4837&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 - 1992-09-29 N1 - Date created - 1992-09-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential isoprenylation of carboxy-terminal mutants of an inhibitory G-protein alpha-subunit: neither farnesylation nor geranylgeranylation is sufficient for membrane attachment. AN - 73124507; 1510988 AB - To determine the effect of protein isoprenylation with farnesyl vs geranylgeranyl groups on membrane association in vivo, COS cells were transfected with cDNAs encoding the wild-type G-protein alpha i1 (WT) subunit, the soluble nonmyristoylated G-protein alpha i1 glycine to alanine mutant (GA), a double mutant in which the carboxy-terminal residues CGLF of GA were mutated to CVLS (GA-CVLS), and a double mutant in which the carboxy terminus of GA was mutated to CALL (GA-CALL). As opposed to the WT and GA proteins, the GA-CVLS and GA-CALL proteins were not pertussis toxin substrates nor were they recognized by antibodies that recognize the nonmutated alpha i1 carboxy terminus. Only the GA-CVLS and GA-CALL proteins incorporated [3H]mevalonate in the form of a farnesyl and a geranylgeranyl moiety, respectively. Subcellular localization, as assessed by immunoblotting and immunoprecipitation, revealed that the WT protein localizes almost exclusively to the membrane fraction, whereas the GA, GA-CVLS, and GA-CALL proteins localize predominantly to the soluble fraction. The soluble GA-CVLS and GA-CALL proteins were not carboxyl methylated, but the small amount localized to the membrane was partially carboxyl methylated. These results indicate that neither farnesylation nor geranylgeranylation is sufficient alone to lead to membrane association. JF - Biochemistry AU - Butrynski, J E AU - Jones, T L AU - Backlund, P S AU - Spiegel, A M AD - Molecular Pathophysiology Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1992/09/01/ PY - 1992 DA - 1992 Sep 01 SP - 8030 EP - 8035 VL - 31 IS - 34 SN - 0006-2960, 0006-2960 KW - Macromolecular Substances KW - 0 KW - Polyisoprenyl Phosphates KW - Sesquiterpenes KW - geranylgeranyl pyrophosphate KW - 6699-20-3 KW - farnesyl pyrophosphate KW - 79W6B01D07 KW - DNA KW - 9007-49-2 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Mevalonic Acid KW - S5UOB36OCZ KW - Index Medicus KW - Animals KW - Protein Processing, Post-Translational KW - Amino Acid Sequence KW - Chromatography, High Pressure Liquid KW - Rats KW - Mutagenesis, Site-Directed KW - Transfection KW - DNA -- genetics KW - Mevalonic Acid -- metabolism KW - Molecular Sequence Data KW - DNA -- chemistry KW - Immunosorbent Techniques KW - Methylation KW - Cell Line KW - Polyisoprenyl Phosphates -- metabolism KW - GTP-Binding Proteins -- metabolism KW - GTP-Binding Proteins -- chemistry KW - Cell Membrane -- metabolism KW - GTP-Binding Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73124507?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Differential+isoprenylation+of+carboxy-terminal+mutants+of+an+inhibitory+G-protein+alpha-subunit%3A+neither+farnesylation+nor+geranylgeranylation+is+sufficient+for+membrane+attachment.&rft.au=Butrynski%2C+J+E%3BJones%2C+T+L%3BBacklund%2C+P+S%3BSpiegel%2C+A+M&rft.aulast=Butrynski&rft.aufirst=J&rft.date=1992-09-01&rft.volume=31&rft.issue=34&rft.spage=8030&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-30 N1 - Date created - 1992-09-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Predictors of smoking cessation and relapse in older adults. AN - 73124350; 1503170 AB - We examined longitudinal changes in smoking behavior among older adults in three community cohorts of the Established Populations for Epidemiologic Studies of the Elderly. Smoking prevalence declined from 15% at baseline to 9% during 6 years of follow-up. Annual smoking cessation and relapse rates were 10% and less than 1%, respectively. Interval diagnosis of myocardial infarction, stroke, or cancer increased subsequent smoking cessation but not relapse. Although smoking cessation around diagnosis is increased, primary prevention could yield greater benefits. JF - American journal of public health AU - Salive, M E AU - Cornoni-Huntley, J AU - LaCroix, A Z AU - Ostfeld, A M AU - Wallace, R B AU - Hennekens, C H AD - Epidemiology, Demography and Biometry Program, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 1268 EP - 1271 VL - 82 IS - 9 SN - 0090-0036, 0090-0036 KW - Abridged Index Medicus KW - Index Medicus KW - Aged, 80 and over KW - Risk Factors KW - Humans KW - Aged KW - United States -- epidemiology KW - Recurrence KW - Male KW - Female KW - Prevalence KW - Tobacco Use Disorder -- epidemiology KW - Smoking Cessation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73124350?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Predictors+of+smoking+cessation+and+relapse+in+older+adults.&rft.au=Salive%2C+M+E%3BCornoni-Huntley%2C+J%3BLaCroix%2C+A+Z%3BOstfeld%2C+A+M%3BWallace%2C+R+B%3BHennekens%2C+C+H&rft.aulast=Salive&rft.aufirst=M&rft.date=1992-09-01&rft.volume=82&rft.issue=9&rft.spage=1268&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 - 1992-09-17 N1 - Date created - 1992-09-17 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Psychoactive Drugs. 1989 Jul-Sep;21(3):293-8 [2809895] Am J Public Health. 1983 Apr;73(4):446-50 [6829829] N Engl J Med. 1988 Nov 24;319(21):1365-9 [3185646] JAMA. 1984 Nov 23-30;252(20):2831-4 [6492363] Am J Public Health. 1977 Oct;67(10):921-30 [911003] N Engl J Med. 1991 Jun 6;324(23):1619-25 [2030718] Am Fam Physician. 1990 Oct;42(4):1017-26 [2220510] Am Fam Physician. 1990 Oct;42(4):959-60, 962, 965 [2220522] Prev Med. 1990 Sep;19(5):552-61 [2235922] J Clin Epidemiol. 1990;43(12):1399-405 [2254778] JAMA. 1990 May 23-30;263(20):2760-5 [2271019] Am J Prev Med. 1990 Mar-Apr;6(2):61-70 [2363951] Prev Med. 1990 May;19(3):335-45 [2377595] J Natl Cancer Inst. 1990 Sep 5;82(17):1402-6 [2388290] Am J Public Health. 1989 Feb;79(2):144-51 [2913831] Am J Public Health. 1987 Oct;77(10):1301-5 [3631364] J Natl Cancer Inst. 1983 Sep;71(3):473-9 [6577223] Erratum In: Am J Public Health 1992 Nov;82(11):1489 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ras controls coupling of growth factor receptors and protein kinase C in the membrane to Raf-1 and B-Raf protein serine kinases in the cytosol. AN - 73122215; 1386920 AB - A dominant negative mutant of Ras, M17 Ras, was used to study the role of Ras in receptor coupling of Raf-1 and B-Raf protein serine/threonine kinases (PSKs). We found that mutant Ras blocks serum- and 12-O-tetradecanoyl phorbol 13-acetate-induced activation of Raf-1 kinase in NIH3T3 cells and Raf-1 as well as B-Raf PSK stimulation by nerve growth factor (NGF) in PC12 pheochromocytoma cells. Mitogen stimulation of Raf kinase was measured by determination of Raf hyperphosphorylation and activity towards exogenous substrates and both of these events were inhibited in cells expressing M17 Ras. In contrast, tyrosine phosphorylation of a direct substrate of activated tyrosine kinase receptors, phospholipase C-gamma 1 (PLC-gamma 1), was unaffected. These data indicate that tyrosine phosphorylation of PLC-gamma 1 is not sufficient for growth induction in NIH3T3 cells and that Ras mediates signal transfer from activated membrane receptors to Raf kinases in the cytosol. As activated Raf induced differentiation in PC12 cells expressing M17 Ras we conclude that Raf kinase activation may be sufficient to account for this aspect of NGF function. JF - Oncogene AU - Troppmair, J AU - Bruder, J T AU - App, H AU - Cai, H AU - Liptak, L AU - Szeberényi, J AU - Cooper, G M AU - Rapp, U R AD - Viral Pathology Section, National Cancer Institute, Frederick, Maryland 21702-1201. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 1867 EP - 1873 VL - 7 IS - 9 SN - 0950-9232, 0950-9232 KW - Nerve Growth Factors KW - 0 KW - Proto-Oncogene Proteins KW - Dexamethasone KW - 7S5I7G3JQL KW - Protein Kinases KW - EC 2.7.- KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Receptor, Epidermal Growth Factor KW - Receptor, Macrophage Colony-Stimulating Factor KW - Protein-Serine-Threonine Kinases KW - EC 2.7.11.1 KW - Proto-Oncogene Proteins c-raf KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - 3T3 Cells KW - Animals KW - Cytosol -- metabolism KW - Nerve Growth Factors -- pharmacology KW - Dexamethasone -- pharmacology KW - Receptor, Macrophage Colony-Stimulating Factor -- physiology KW - Receptor, Epidermal Growth Factor -- physiology KW - Amino Acid Sequence KW - Mice KW - Protein-Tyrosine Kinases -- metabolism KW - Phosphorylation KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Blood Physiological Phenomena KW - Genes, ras KW - Protein Kinases -- physiology KW - Protein Kinase C -- physiology KW - Proto-Oncogene Proteins -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73122215?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Ras+controls+coupling+of+growth+factor+receptors+and+protein+kinase+C+in+the+membrane+to+Raf-1+and+B-Raf+protein+serine+kinases+in+the+cytosol.&rft.au=Troppmair%2C+J%3BBruder%2C+J+T%3BApp%2C+H%3BCai%2C+H%3BLiptak%2C+L%3BSzeber%C3%A9nyi%2C+J%3BCooper%2C+G+M%3BRapp%2C+U+R&rft.aulast=Troppmair&rft.aufirst=J&rft.date=1992-09-01&rft.volume=7&rft.issue=9&rft.spage=1867&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=09509232&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-15 N1 - Date created - 1992-09-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Purification of immature cores of mouse mammary tumor virus and immunolocalization of protein domains. AN - 73121252; 1380097 AB - The immature capsids of the mouse mammary tumor virus (MMTV), known as intracytoplasmic A particles, have been isolated from murine L1210 leukemia cells. The diameter of the isolated particles was 80 nm as determined by negative staining. Two polypeptides of 77 and 110 kDa were found to be their major polypeptide components, in agreement with the expected sizes of the Gag and Gag-Pro precursor polypeptides of the mature MMTV proteins. Both polypeptides were recognized by antibodies directed toward the matrix (p10) and capsid (p27) proteins of MMTV. Immunogold labeling of p10 on isolated A particles, visualized by negative staining, showed that this protein is located at the surface of the immature capsids, whereas p27 can be detected only in broken or disrupted particles, suggesting that it has an internal location. These observations were confirmed by immunolabeling of both proteins on thin sections of A particle-producing cells. In addition, the viral protease had a more internal position than p27. Since the sequential order of the viral proteins in the Gag precursor is p10-pp21-p27-p14 and that in Gag-Pro is p10-pp21-p27-p30-protease, our results demonstrate the radial organization of the polypeptide precursors forming the intracytoplasmic A particles. JF - Journal of virology AU - Menéndez-Arias, L AU - Risco, C AU - Pinto da Silva, P AU - Oroszlan, S AD - Laboratory of Molecular Virology and Carcinogenesis, NCI-Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 5615 EP - 5620 VL - 66 IS - 9 SN - 0022-538X, 0022-538X KW - Antigens, Viral KW - 0 KW - Epitopes KW - Viral Core Proteins KW - Dexamethasone KW - 7S5I7G3JQL KW - Index Medicus KW - Animals KW - Tumor Cells, Cultured KW - Virus Replication -- drug effects KW - Dexamethasone -- pharmacology KW - Antigens, Viral -- immunology KW - Molecular Sequence Data KW - Mice KW - Amino Acid Sequence KW - Immunohistochemistry KW - Leukemia L1210 KW - Capsid -- isolation & purification KW - Viral Core Proteins -- immunology KW - Capsid -- ultrastructure KW - Viral Core Proteins -- ultrastructure KW - Mammary Tumor Virus, Mouse -- immunology KW - Viral Core Proteins -- isolation & purification KW - Mammary Tumor Virus, Mouse -- ultrastructure KW - Capsid -- immunology KW - Mammary Tumor Virus, Mouse -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73121252?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Purification+of+immature+cores+of+mouse+mammary+tumor+virus+and+immunolocalization+of+protein+domains.&rft.au=Men%C3%A9ndez-Arias%2C+L%3BRisco%2C+C%3BPinto+da+Silva%2C+P%3BOroszlan%2C+S&rft.aulast=Men%C3%A9ndez-Arias&rft.aufirst=L&rft.date=1992-09-01&rft.volume=66&rft.issue=9&rft.spage=5615&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 - 1992-09-16 N1 - Date created - 1992-09-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Virology. 1977 Feb;76(2):835-50 [65829] Virology. 1977 Aug;81(1):91-106 [196403] Proc Natl Acad Sci U S A. 1978 Mar;75(3):1404-8 [206897] Anal Biochem. 1976 May 7;72:248-54 [942051] J Virol. 1990 Oct;64(10):5076-92 [1697912] Cell. 1990 Oct 5;63(1):77-86 [2170021] Proc Natl Acad Sci U S A. 1987 Oct;84(20):7041-5 [2823251] Proc Natl Acad Sci U S A. 1987 Jun;84(12):4298-302 [3035577] Virology. 1972 Jul;49(1):61-78 [4114180] J Virol. 1973 Apr;11(4):575-84 [4349496] Proc Natl Acad Sci U S A. 1981 Jun;78(6):3403-7 [6167985] J Virol. 1983 May;46(2):355-61 [6302307] Virology. 1977 Mar;77(1):135-48 [65834] J Gen Virol. 1978 Oct;41(1):193-200 [81268] Virology. 1978 Mar;85(1):157-67 [205999] Proc Natl Acad Sci U S A. 1979 Sep;76(9):4350-4 [388439] Proc Natl Acad Sci U S A. 1977 Aug;74(8):3446-50 [410020] J Biol Chem. 1992 Jun 5;267(16):11392-8 [1375941] EMBO J. 1991 Mar;10(3):535-46 [1705884] J Virol. 1989 Jun;63(6):2543-9 [2542570] Infect Immun. 1989 Sep;57(9):2878-85 [2668192] J Virol. 1987 Feb;61(2):480-90 [3027377] Virology. 1987 Jan;156(1):171-6 [3643678] Cancer Res. 1986 Nov;46(11):5851-7 [3756926] Appl Microbiol. 1974 Dec;28(6):1040-6 [4141598] Science. 1974 Apr 12;184(4133):158-60 [4361099] Virology. 1981 Feb;109(1):201-4 [6258309] Virology. 1981 Dec;115(2):262-71 [6274085] Science. 1978 Jan 13;199(4325):183-6 [202022] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The precore gene of the woodchuck hepatitis virus genome is not essential for viral replication in the natural host. AN - 73115351; 1501300 AB - A number of naturally occurring hepatitis B virus mutants that cannot synthesize the virus precore protein have been identified. Such mutants have been associated with more severe forms of hepatitis, including fulminant hepatitis. The most common mutation observed is a substitution of G to A in the distal precore gene that converts a codon specifying Trp (TGG) to a termination codon (TAG). Using oligonucleotide-directed mutagenesis, we have produced the same point mutation in the precore gene of an infectious clone of woodchuck hepatitis virus (WHV). Transfection of mutant WHV DNA into the livers of adult woodchucks resulted in replication of the mutant in three of three susceptible animals. Levels of virus replication and transient elevations in liver enzymes in serum were similar to those of adult animals infected with wild-type WHV. Virions, found to possess mutant precore genes by polymerase chain reaction amplification and DNA sequencing, were recovered from the serum of one of the animals and inoculated subcutaneously into neonatal woodchucks. They produced infection in all five animals studied. The level of virus replication in neonatal animals infected with this mutant virus was comparable to that found in neonatal woodchucks infected with wild-type WHV, but none of five woodchucks infected with the precore mutant virus as neonates became chronic virus carriers. It was concluded that the precore gene of the WHV genome is not essential for virus replication in the natural host but may be important for chronic infection. JF - Journal of virology AU - Chen, H S AU - Kew, M C 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, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/09// PY - 1992 DA - September 1992 SP - 5682 EP - 5684 VL - 66 IS - 9 SN - 0022-538X, 0022-538X KW - Protein Precursors KW - 0 KW - Viral Core Proteins KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Animals KW - Base Sequence KW - Protein Precursors -- metabolism KW - Protein Precursors -- genetics KW - Molecular Sequence Data KW - Carrier State KW - Animals, Newborn -- microbiology KW - Liver -- microbiology KW - Virus Replication KW - Marmota -- microbiology KW - Hepatitis, Animal -- metabolism KW - Hepatitis, Animal -- microbiology KW - Viral Core Proteins -- genetics KW - Hepadnaviridae -- physiology KW - Hepadnaviridae -- genetics KW - Viral Core Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73115351?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+precore+gene+of+the+woodchuck+hepatitis+virus+genome+is+not+essential+for+viral+replication+in+the+natural+host.&rft.au=Chen%2C+H+S%3BKew%2C+M+C%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=1992-09-01&rft.volume=66&rft.issue=9&rft.spage=5682&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 - 1992-09-16 N1 - Date created - 1992-09-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Virology. 1991 Apr;181(2):733-7 [2014646] Proc Natl Acad Sci U S A. 1990 Dec;87(23):9329-32 [2251274] Cancer Detect Prev. 1989;14(2):227-9 [2695243] Lab Anim Sci. 1985 Aug;35(4):376-81 [2864472] Proc Natl Acad Sci U S A. 1989 Mar;86(6):1846-9 [2928306] Proc Natl Acad Sci U S A. 1986 Mar;83(6):1578-82 [3006057] Proc Natl Acad Sci U S A. 1987 Feb;84(3):866-70 [3468514] J Hepatol. 1991;13 Suppl 4:S68-73 [1668333] Proc Natl Acad Sci U S A. 1991 May 15;88(10):4186-90 [2034663] J Virol. 1990 Mar;64(3):1298-303 [2304145] Hepatology. 1989 Feb;9(2):322-7 [2643549] J Clin Microbiol. 1989 Sep;27(9):1930-3 [2778059] Nucleic Acids Res. 1989 Feb 11;17(3):1266 [2922271] J Infect Dis. 1985 Jun;151(6):1081-92 [2987366] Nucleic Acids Res. 1986 Dec 22;14(24):9679-98 [3027659] J Virol. 1987 Oct;61(10):3322-5 [3041052] J Virol. 1987 Dec;61(12):3701-9 [3682059] N Engl J Med. 1991 Jun 13;324(24):1699-704 [2034246] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Quisqualic acid-induced neurotoxicity is protected by NMDA and non-NMDA receptor antagonists. AN - 73291299; 1359473 AB - Quisqualic acid-mediated excitotoxicity has been attributed essentially to the activation of non-N-methyl-D-aspartate (non-NMDA) receptors. In the present study we demonstrate the possible involvement of both NMDA and non-NMDA receptors in quisqualic acid-induced toxicity in mouse brain slices, in vitro. Incubation of mouse brain sagittal slices with various concentrations of quisqualic acid resulted in significant increase in the leakage of lactate dehydrogenase and potassium from the slices into the medium. Prior incubation of mouse brain slices with NMDA (MK-801 or AP7) or non-NMDA receptor antagonists (GDEE or quinoxalinediones) protected against quisqualic acid-mediated toxicity. Slices prepared from animals pretreated in vivo with MK-801 (5 mg/kg b.wt.) were also resistant to the toxic effects of quisqualic acid, indicating the possible involvement of NMDA receptors in quisqualic acid toxicity. JF - Neuroscience letters AU - Pai, K S AU - Ravindranath, V AD - Department of Neurochemistry, National Institute of Mental Health and Neuroscience, Bangalore, India. Y1 - 1992/08/31/ PY - 1992 DA - 1992 Aug 31 SP - 177 EP - 180 VL - 143 IS - 1-2 SN - 0304-3940, 0304-3940 KW - Amino Acids KW - 0 KW - Excitatory Amino Acid Antagonists KW - Glutamates KW - Quinoxalines KW - Receptors, AMPA KW - Receptors, Glutamate KW - Receptors, Kainic Acid KW - Receptors, N-Methyl-D-Aspartate KW - 2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline KW - 118876-58-7 KW - Glutamic Acid KW - 3KX376GY7L KW - FG 9041 KW - 62T278S1MX KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - 6-Cyano-7-nitroquinoxaline-2,3-dione KW - 6OTE87SCCW KW - 2-Amino-5-phosphonovalerate KW - 76726-92-6 KW - Quisqualic Acid KW - 8OC22C1B99 KW - L-Lactate Dehydrogenase KW - EC 1.1.1.27 KW - 2-amino-7-phosphonoheptanoic acid KW - P34K80CUSM KW - Potassium KW - RWP5GA015D KW - Index Medicus KW - Animals KW - Brain -- drug effects KW - L-Lactate Dehydrogenase -- analysis KW - Receptors, Glutamate -- physiology KW - Mice KW - Dizocilpine Maleate -- pharmacology KW - Ion Channel Gating -- drug effects KW - Glutamates -- pharmacology KW - Amino Acids -- pharmacology KW - Potassium -- analysis KW - Quinoxalines -- pharmacology KW - Receptors, N-Methyl-D-Aspartate -- physiology KW - 2-Amino-5-phosphonovalerate -- analogs & derivatives KW - Receptors, N-Methyl-D-Aspartate -- antagonists & inhibitors KW - Quisqualic Acid -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73291299?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+letters&rft.atitle=Quisqualic+acid-induced+neurotoxicity+is+protected+by+NMDA+and+non-NMDA+receptor+antagonists.&rft.au=Pai%2C+K+S%3BRavindranath%2C+V&rft.aulast=Pai&rft.aufirst=K&rft.date=1992-08-31&rft.volume=143&rft.issue=1-2&rft.spage=177&rft.isbn=&rft.btitle=&rft.title=Neuroscience+letters&rft.issn=03043940&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 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Okadaic acid is a potent inducer of AP-1, NF-kappa B, and tumor necrosis factor-alpha in human B lymphocytes. AN - 73181754; 1520341 AB - Treatment of human B lymphocytes with an optimal concentration of okadaic acid, an inhibitor of phosphatases 1 and 2A, resulted in the induction of the transcription factor, AP-1 and a marked increase in NF-kappa B levels. In contrast, no effect on the levels of the octamer binding proteins, Oct-1 or Oct-2, were found. Since both AP-1 and NF-kappa B have been reported to be important in the induction of the tumor necrosis factor-alpha (TNF-alpha) gene we examined the effects of okadaic acid on TNF-alpha mRNA levels. Treatment with okadaic acid resulted in a striking increase in TNF-alpha mRNA transcripts within 1 h of stimulation and large amounts of TNF-alpha were released into the culture media. Although okadaic acid provides a potent inductive signal for AP-1 and NF-kappa B it did not induce either B cell proliferation or immunoglobulin secretion. JF - Biochemical and biophysical research communications AU - Rieckmann, P AU - Thévenin, C AU - Kehrl, J H AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/08/31/ PY - 1992 DA - 1992 Aug 31 SP - 51 EP - 57 VL - 187 IS - 1 SN - 0006-291X, 0006-291X KW - c-fos KW - c-jun KW - Ethers, Cyclic KW - 0 KW - Immunoglobulins KW - NF-kappa B KW - Proto-Oncogene Proteins c-jun KW - RNA, Messenger KW - Tumor Necrosis Factor-alpha KW - Okadaic Acid KW - 1W21G5Q4N2 KW - Cycloheximide KW - 98600C0908 KW - Index Medicus KW - RNA, Messenger -- metabolism KW - Cells, Cultured KW - Immunoglobulins -- metabolism KW - Humans KW - Cycloheximide -- pharmacology KW - Genes, fos -- genetics KW - Genes, jun -- genetics KW - Cell Division KW - B-Lymphocytes -- drug effects KW - NF-kappa B -- biosynthesis KW - Tumor Necrosis Factor-alpha -- biosynthesis KW - Proto-Oncogene Proteins c-jun -- biosynthesis KW - Ethers, Cyclic -- pharmacology KW - B-Lymphocytes -- metabolism KW - Tumor Necrosis Factor-alpha -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73181754?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Okadaic+acid+is+a+potent+inducer+of+AP-1%2C+NF-kappa+B%2C+and+tumor+necrosis+factor-alpha+in+human+B+lymphocytes.&rft.au=Rieckmann%2C+P%3BTh%C3%A9venin%2C+C%3BKehrl%2C+J+H&rft.aulast=Rieckmann&rft.aufirst=P&rft.date=1992-08-31&rft.volume=187&rft.issue=1&rft.spage=51&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 - 1992-10-07 N1 - Date created - 1992-10-07 N1 - Date revised - 2017-01-13 N1 - Gene symbol - c-fos; c-jun N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The met proto-oncogene receptor and lumen formation. AN - 73164819; 1387731 AB - The met proto-oncogene product (Met) and its ligand, hepatocyte growth factor/scatter factor (HGF/SF), have been implicated in cell mitogenic response, cell motility, and the promotion of the ordered spatial arrangement of tissue. By means of confocal laser-scanning microscopy, it was shown that Met is expressed in cells bordering lumen-like structures that resemble ducts in the human mammary cell line T47D. In human breast tissue biopsies, Met staining was intense in normal cells bordering mammary ducts but was reduced in adjacent tumor tissue. Met staining in lumen-forming organs colocalizes with staining of antibody to phosphotyrosine, which suggests that the Met receptor and its substrates may be activated in lumen structures or ducts. HGF/SF treatment of human epithelial carcinoma cell lines resulted in the formation of lumen-like structures in vitro. Reduced expression of Met could be related to the extent of tumor cell differentiation. JF - Science (New York, N.Y.) AU - Tsarfaty, I AU - Resau, J H AU - Rulong, S AU - Keydar, I AU - Faletto, D L AU - Vande Woude, G F AD - ABL-Basic Research Program, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, MD 21702. Y1 - 1992/08/28/ PY - 1992 DA - 1992 Aug 28 SP - 1258 EP - 1261 VL - 257 IS - 5074 SN - 0036-8075, 0036-8075 KW - Growth Substances KW - 0 KW - Proto-Oncogene Proteins KW - Hepatocyte Growth Factor KW - 67256-21-7 KW - Proto-Oncogene Proteins c-met KW - EC 2.7.10.1 KW - Index Medicus KW - Adenocarcinoma -- metabolism KW - Animals KW - Dose-Response Relationship, Drug KW - Humans KW - Digestive System -- metabolism KW - Breast Neoplasms -- metabolism KW - Cell Differentiation -- genetics KW - Mice KW - Mice, Inbred BALB C KW - Colonic Neoplasms -- chemically induced KW - Chromosomes, Human, Pair 7 KW - Adenocarcinoma -- pathology KW - Microscopy, Fluorescence KW - Breast Neoplasms -- pathology KW - Colonic Neoplasms -- metabolism KW - Microscopy, Immunoelectron KW - Colonic Neoplasms -- pathology KW - Growth Substances -- pharmacology KW - Growth Substances -- physiology KW - Proto-Oncogene Proteins -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73164819?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+met+proto-oncogene+receptor+and+lumen+formation.&rft.au=Tsarfaty%2C+I%3BResau%2C+J+H%3BRulong%2C+S%3BKeydar%2C+I%3BFaletto%2C+D+L%3BVande+Woude%2C+G+F&rft.aulast=Tsarfaty&rft.aufirst=I&rft.date=1992-08-28&rft.volume=257&rft.issue=5074&rft.spage=1258&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 - 1992-10-06 N1 - Date created - 1992-10-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The intrathecal administration of excitatory amino acid receptor antagonists selectively attenuated carrageenan-induced behavioral hyperalgesia in rats. AN - 73307682; 1358641 AB - A single unilateral injection of carrageenan (4.5-6.0 mg in 0.15-0.20 ml saline) into the rat hindpaw induced behavioral hyperalgesia as evidenced by a significant reduction in hindpaw withdrawal latency to a noxious thermal stimulus. The involvement of N-methyl-D-aspartate (NMDA) receptors in this model of hyperalgesia was examined by intrathecal administration of the selective excitatory amino acid (EAA) receptor antagonists: (+/-)-2-amino-5-phosphonopentanoic acid (AP-5), (+/-)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP), ketamine hydrochloride (ketamine), 7-chlorokynurenic acid (7-Cl kynurenic acid), and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). The effects of dizocilpine maleate (MK-801) were studied under the same conditions and published previously (Ren et al., 1992) and the data are presented for comparison. While the withdrawal latencies of the non-injected paws and of the paws of naive rats were not significantly affected by application of the EAA receptor antagonists at doses tested, the paw withdrawal latencies of the carrageenan-injected paws were elevated dose dependently. The rank order of potency of these agents to reduce hyperalgesia was: MK-801 greater than or equal to AP-5 greater than or equal to CPP = 7-Cl kynurenic acid = ketamine much greater than CNQX greater than 0. In contrast, intrathecal injection of the opioid receptor agonists, [D-Ala2,MePhe4,Gly-ol5]enkephalin (DAMGO, mu-selective) and [D-Pen2,D-Pen5] enkephalin (DPDPE, delta-selective), produced antinociception in both injected and non-injected paws. DAMGO was much more potent, while DPDPE was less potent, than MK-801.(ABSTRACT TRUNCATED AT 250 WORDS) JF - European journal of pharmacology AU - Ren, K AU - Williams, G M AU - Hylden, J L AU - Ruda, M A AU - Dubner, R AD - Neurobiology and Anesthesiology Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/08/25/ PY - 1992 DA - 1992 Aug 25 SP - 235 EP - 243 VL - 219 IS - 2 SN - 0014-2999, 0014-2999 KW - Analgesics KW - 0 KW - Enkephalins KW - Piperazines KW - Quinoxalines KW - Receptors, N-Methyl-D-Aspartate KW - Enkephalin, Ala(2)-MePhe(4)-Gly(5)- KW - 100929-53-1 KW - Ketamine KW - 690G0D6V8H KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - 6-Cyano-7-nitroquinoxaline-2,3-dione KW - 6OTE87SCCW KW - 2-amino-5-phosphopentanoic acid KW - 76326-31-3 KW - Enkephalin, D-Penicillamine (2,5)- KW - 88373-73-3 KW - Carrageenan KW - 9000-07-1 KW - 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid KW - 98Y1I8ZD4M KW - Kynurenic Acid KW - H030S2S85J KW - Valine KW - HG18B9YRS7 KW - 7-chlorokynurenic acid KW - S7936QON2K KW - Index Medicus KW - Animals KW - Analysis of Variance KW - Inflammation -- physiopathology KW - Analgesics -- pharmacology KW - Valine -- pharmacology KW - Piperazines -- pharmacology KW - Kynurenic Acid -- pharmacology KW - Ketamine -- pharmacology KW - Dizocilpine Maleate -- pharmacology KW - Rats KW - Behavior, Animal -- drug effects KW - Rats, Sprague-Dawley KW - Carrageenan -- toxicity KW - Enkephalins -- pharmacology KW - Injections, Spinal KW - Valine -- analogs & derivatives KW - Kynurenic Acid -- analogs & derivatives KW - Quinoxalines -- pharmacology KW - Male KW - Receptors, N-Methyl-D-Aspartate -- physiology KW - Receptors, N-Methyl-D-Aspartate -- antagonists & inhibitors KW - Hyperalgesia -- chemically induced KW - Hyperalgesia -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73307682?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+intrathecal+administration+of+excitatory+amino+acid+receptor+antagonists+selectively+attenuated+carrageenan-induced+behavioral+hyperalgesia+in+rats.&rft.au=Ren%2C+K%3BWilliams%2C+G+M%3BHylden%2C+J+L%3BRuda%2C+M+A%3BDubner%2C+R&rft.aulast=Ren&rft.aufirst=K&rft.date=1992-08-25&rft.volume=219&rft.issue=2&rft.spage=235&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 - 1992-12-07 N1 - Date created - 1992-12-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pertussis toxin-catalyzed ADP-ribosylation of G(o) alpha with mutations at the carboxyl terminus. AN - 73166043; 1510959 AB - The guanine nucleotide-binding protein G(o alpha) has been implicated in the regulation of Ca2+ channels in neural tissues. Covalent modification of G(o alpha) by pertussis toxin-catalyzed ADP-ribosylation of a cysteine (position 351) four amino acids from the carboxyl terminus decouples G(o alpha) from receptor. To define the structural requirements for ADP-ribosylation, preparations of recombinant G(o alpha) with mutations within the five amino acids at the carboxyl terminus were evaluated for their ability to serve as pertussis toxin substrates. As expected, the mutant in which cysteine 351 was replaced by glycine (C351G) was not a toxin substrate. Other inactive mutants were G352D and L353 delta/Y354 delta. Mutations that had no significant effect on toxin-catalyzed ADP-ribosylation included G350D, G350R, Y354 delta, and L353V/Y354 delta. Less active mutants were L353G/Y354 delta, L353A/Y354 delta, and L353G. ADP-ribosylation of the active mutants, like that of wild-type G(o alpha), was enhanced by the beta gamma subunits of bovine transducin. It appears that three of the four terminal amino acids critically influence pertussis toxin-catalyzed ADP-ribosylation of G(o alpha). JF - Biochemistry AU - Avigan, J AU - Murtagh, J J AU - Stevens, L A AU - Angus, C W 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 - 1992/08/25/ PY - 1992 DA - 1992 Aug 25 SP - 7736 EP - 7740 VL - 31 IS - 33 SN - 0006-2960, 0006-2960 KW - Macromolecular Substances KW - 0 KW - Oligodeoxyribonucleotides KW - Recombinant Proteins KW - Virulence Factors, Bordetella KW - NAD KW - 0U46U6E8UK KW - Adenosine Diphosphate Ribose KW - 20762-30-5 KW - Pertussis Toxin KW - EC 2.4.2.31 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Transducin KW - EC 3.6.5.1 KW - Index Medicus KW - Retina -- metabolism KW - Animals KW - Escherichia coli -- genetics KW - Cloning, Molecular KW - Recombinant Proteins -- isolation & purification KW - Base Sequence KW - Cattle KW - Recombinant Proteins -- metabolism KW - Genetic Vectors KW - Restriction Mapping KW - Polymerase Chain Reaction -- methods KW - Molecular Sequence Data KW - Transducin -- isolation & purification KW - Substrate Specificity KW - Transducin -- metabolism KW - Mutagenesis, Site-Directed KW - Virulence Factors, Bordetella -- pharmacology KW - NAD -- metabolism KW - Virulence Factors, Bordetella -- metabolism KW - GTP-Binding Proteins -- metabolism KW - GTP-Binding Proteins -- isolation & purification KW - Adenosine Diphosphate Ribose -- metabolism KW - GTP-Binding Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73166043?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Pertussis+toxin-catalyzed+ADP-ribosylation+of+G%28o%29+alpha+with+mutations+at+the+carboxyl+terminus.&rft.au=Avigan%2C+J%3BMurtagh%2C+J+J%3BStevens%2C+L+A%3BAngus%2C+C+W%3BMoss%2C+J%3BVaughan%2C+M&rft.aulast=Avigan&rft.aufirst=J&rft.date=1992-08-25&rft.volume=31&rft.issue=33&rft.spage=7736&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-29 N1 - Date created - 1992-09-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Five PDGF B amino acid substitutions convert PDGF A to a PDGF B-like transforming molecule. AN - 73155190; 1380958 AB - We used site-directed mutagenesis to determine the minimum number of PDGF B residues needed to convert PDGF A to a potently transforming PDGF B-like molecule. Substitution of two PDGF B subdomains, 106-115 and 135-144, were found to be critical. These substitutions were sufficient to broaden the ability of PDGF A to activate beta as well as alpha platelet-derived growth factor (PDGF) receptors and increase its transforming efficiency to that of PDGF B. Within subdomain I, either PDGF B residues Arg-109 and Asn-115 or Arg-109, Leu-110, and Arg-113, in combination with subdomain II PDGF B residues Asn-136, Arg-137, and Arg-142 were identified as being essential. Those mutants with transforming ability comparable with PDGF B showed significantly lower efficiencies of beta receptor triggering. Thus, our studies identify a small number of PDGF B amino acids indispensable for beta PDGF receptor interaction and suggest that a low level of beta PDGF receptor activation is sufficient to dramatically increase PDGF transforming efficiency in NIH 3T3 cells. JF - The Journal of biological chemistry AU - LaRochelle, W J AU - Pierce, J H AU - May-Siroff, M AU - Giese, N AU - Aaronson, S A AD - Laboratory of Cellular and Molecular Biology, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/08/25/ PY - 1992 DA - 1992 Aug 25 SP - 17074 EP - 17077 VL - 267 IS - 24 SN - 0021-9258, 0021-9258 KW - Macromolecular Substances KW - 0 KW - Platelet-Derived Growth Factor KW - Receptors, Cell Surface KW - Recombinant Proteins KW - Phosphotyrosine KW - 21820-51-9 KW - Tyrosine KW - 42HK56048U KW - Receptors, Platelet-Derived Growth Factor KW - EC 2.7.10.1 KW - Index Medicus KW - 3T3 Cells KW - Animals KW - Recombinant Proteins -- pharmacology KW - Humans KW - Amino Acid Sequence KW - Mice KW - Tyrosine -- analysis KW - Mutagenesis, Site-Directed KW - Receptors, Cell Surface -- metabolism KW - Transfection KW - Recombinant Proteins -- metabolism KW - Molecular Sequence Data KW - Tyrosine -- analogs & derivatives KW - DNA Replication KW - Receptors, Cell Surface -- drug effects KW - Platelet-Derived Growth Factor -- pharmacology KW - Platelet-Derived Growth Factor -- genetics KW - Platelet-Derived Growth Factor -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73155190?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Five+PDGF+B+amino+acid+substitutions+convert+PDGF+A+to+a+PDGF+B-like+transforming+molecule.&rft.au=LaRochelle%2C+W+J%3BPierce%2C+J+H%3BMay-Siroff%2C+M%3BGiese%2C+N%3BAaronson%2C+S+A&rft.aulast=LaRochelle&rft.aufirst=W&rft.date=1992-08-25&rft.volume=267&rft.issue=24&rft.spage=17074&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 - 1992-09-25 N1 - Date created - 1992-09-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Molecular species analysis of a product of phospholipase D activation. Phosphatidylethanol is formed from phosphatidylcholine in phorbol ester- and bradykinin-stimulated PC12 cells. AN - 73135136; 1512226 AB - Tumor-promoting phorbol esters or calcium-mobilizing receptor ligands stimulate phosphatidylcholine breakdown and in many cells this is accompanied by phospholipase D (PLD) activation. We tested whether or not a direct relationship exists between these two phenomena. Pheochromocytoma (PC12) cells were stimulated with the phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate or with the calcium-mobilizing receptor ligand bradykinin in media containing 1% ethanol. The fatty acid composition of the molecular species of phosphatidylethanol (PEt), a product of PLD activation, formed in stimulated cells was compared with the molecular species of endogenous phospholipids isolated from unstimulated PC12 cells. PEt was isolated and analyzed by fast atom bombardment-mass spectrometry (FAB-MS) in the negative ion mode. Fatty acid composition and headgroup structure of the major PEt molecular ions were confirmed by linked scan analysis. Phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, and phosphatidylinositol were isolated from unstimulated cells and converted into phosphatidic acids using PLD. Mass spectra of the respective phosphatidic acids were obtained by fast atom bombardment-mass spectrometry as described above. The molecular species of PEt formed in 12-O-tetradecanoylphorbol-13-acetate- and bradykinin-stimulated PC12 cell were identical to those of phosphatidylcholine isolated from untreated cells. JF - The Journal of biological chemistry AU - Holbrook, P G AU - Pannell, L K AU - Murata, Y 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 - 1992/08/25/ PY - 1992 DA - 1992 Aug 25 SP - 16834 EP - 16840 VL - 267 IS - 24 SN - 0021-9258, 0021-9258 KW - Glycerophospholipids KW - 0 KW - Oleic Acids KW - Phosphatidic Acids KW - Phosphatidylcholines KW - Phospholipids KW - phosphatidylethanol KW - Oleic Acid KW - 2UMI9U37CP KW - Phospholipase D KW - EC 3.1.4.4 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Bradykinin KW - S8TIM42R2W KW - Index Medicus KW - Mass Spectrometry KW - Animals KW - Phospholipids -- isolation & purification KW - Oleic Acids -- metabolism KW - Kinetics KW - Phospholipids -- metabolism KW - PC12 Cells KW - Phospholipase D -- metabolism KW - Phosphatidic Acids -- metabolism KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Phosphatidylcholines -- metabolism KW - Bradykinin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73135136?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+addiction&rft.atitle=Dying+to+be+equal%3A+women%2C+alcohol%2C+and+cardiovascular+disease.&rft.au=Hanna%2C+E%3BDufour%2C+M+C%3BElliott%2C+S%3BStinson%2C+F%3BHarford%2C+T+C&rft.aulast=Hanna&rft.aufirst=E&rft.date=1992-11-01&rft.volume=87&rft.issue=11&rft.spage=1593&rft.isbn=&rft.btitle=&rft.title=British+journal+of+addiction&rft.issn=09520481&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-25 N1 - Date created - 1992-09-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Electrophysiological properties of early postnatal rat septal neurons in short-term culture. AN - 73243942; 1327409 AB - Electrophysiological properties of septal neurons dissociated from PN1-PN7 rats were examined between 1 and 5 days in vitro (DIV) with whole-cell patch-clamp recording. The neurons had RMPs in the range -40 to -80 mV, resistances 0.5-1.5 G omega, and 50-90 mV action potentials. By 2-3 DIV, most neurons were spontaneously active, with some cells exhibiting rhythmic firing patterns. Depolarizations from -80 mV holding potential elicited TTX-sensitive inward Na+ currents, and transient and sustained outward K+ currents. Pharmacological dissection of the outward currents in PN6/7 neurons suggest the presence of multiple types of K+ currents (IA, IC, IK). L-type Ca2+ currents were observed in all PN6/7 neurons examined but were not always detectable in PN1/2 neurons. All PN1/2 and PN6/7 neurons were sensitive to glutamate and GABA but did not respond to ACh or NE applications. Responses to GABA were excitatory i.e., characteristic of immature neurons. Comparison of the results obtained in this study with the properties of adult neurons characterized in vivo or in brain slice preparations in vitro, suggest that septal neurons from PN1-PN7 rats are still in the process of differentiation of their mature electrical and chemosensitive membrane properties. JF - Brain research AU - Suszkiw, J B AU - Schaffner, A E AU - Barker, J L AD - Laboratory of Neurophysiology, NINDS, NIH, Bethesda, MD 20892. Y1 - 1992/08/21/ PY - 1992 DA - 1992 Aug 21 SP - 246 EP - 254 VL - 588 IS - 2 SN - 0006-8993, 0006-8993 KW - Potassium Channels KW - 0 KW - Sodium Channels KW - Tetrodotoxin KW - 4368-28-9 KW - gamma-Aminobutyric Acid KW - 56-12-2 KW - Guanosine Triphosphate KW - 86-01-1 KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Index Medicus KW - Rats KW - Animals KW - Rats, Sprague-Dawley KW - Cells, Cultured KW - gamma-Aminobutyric Acid -- physiology KW - Membrane Potentials -- drug effects KW - Electrophysiology KW - Tetrodotoxin -- pharmacology KW - Potassium Channels -- drug effects KW - Sodium Channels -- drug effects KW - Immunohistochemistry KW - Guanosine Triphosphate -- pharmacology KW - Adenosine Triphosphate -- pharmacology KW - Brain -- cytology KW - Neurons -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73243942?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Electrophysiological+properties+of+early+postnatal+rat+septal+neurons+in+short-term+culture.&rft.au=Suszkiw%2C+J+B%3BSchaffner%2C+A+E%3BBarker%2C+J+L&rft.aulast=Suszkiw&rft.aufirst=J&rft.date=1992-08-21&rft.volume=588&rft.issue=2&rft.spage=246&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 - 1992-11-13 N1 - Date created - 1992-11-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The origin of plagues: old and new. AN - 73154288; 1509258 AB - Viruses and bacteria emerge in new and old forms to cause disease epidemics. Some microorganisms recur when changing life-styles (including increased international travel) offer new opportunities; others arise from new genetic variations. These various epidemics connect the future with the past, offering lessons for guarding the health of generations to come--lessons learned from diseases such as tuberculosis, toxic shock syndrome, Lyme disease, streptococcal infection, influenza, and acquired immunodeficiency syndrome (AIDS). The public must be vigilant to the possibility of new epidemics, learn more about the biology and epidemiology of microbes, and strengthen systems of surveillance and detection. JF - Science (New York, N.Y.) AU - Krause, R M AD - Fogarty International Center for Advanced Study in the Health Sciences, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/08/21/ PY - 1992 DA - 1992 Aug 21 SP - 1073 EP - 1078 VL - 257 IS - 5073 SN - 0036-8075, 0036-8075 KW - Index Medicus KW - AIDS/HIV KW - Genes, Bacterial KW - Acquired Immunodeficiency Syndrome -- epidemiology KW - Bacterial Infections -- microbiology KW - Bacterial Infections -- epidemiology KW - Humans KW - Molecular Sequence Data KW - Genes, Viral KW - Virus Diseases -- microbiology KW - Virus Diseases -- epidemiology KW - Disease Outbreaks UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73154288?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+origin+of+plagues%3A+old+and+new.&rft.au=Krause%2C+R+M&rft.aulast=Krause&rft.aufirst=R&rft.date=1992-08-21&rft.volume=257&rft.issue=5073&rft.spage=1073&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 - 1992-09-23 N1 - Date created - 1992-09-23 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M95929; GENBANK N1 - SuppNotes - Comment In: Science. 1992 Aug 21;257(5073):1021 [1509248] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cigarette smoking and other risk factors for progression of precancerous stomach lesions. AN - 73086594; 1640486 AB - Stomach cancer is generally thought to evolve through a series of gastric mucosal changes, but the determinants of the precancerous lesions are not well understood. Our purpose was to assess risk factors for intestinal metaplasia and gastric dysplasia arising from chronic atrophic gastritis in a general population at high risk for stomach cancer. A population-based gastroscopic screening of more than 3000 residents was conducted in a county in China with one of the world's highest rates of stomach cancer. Information on the lifestyle and other characteristics of the participants was obtained by interview, and responses were compared between those in whom the most advanced gastric lesion was dysplasia or intestinal metaplasia versus those with chronic atrophic gastritis. Cigarette smoking was found to nearly double the risk of transition to dysplasia and to be a mild risk factor for intestinal metaplasia. Smoking accounted almost entirely for the 55% higher prevalence of dysplasia among men than among women. Risk of transition to dysplasia had a weak association with several dietary factors and was increased among those participants with a family history of stomach cancer and with blood type A. The findings provide strong evidence for a role of tobacco consumption and offer clues to other environmental and genetic factors involved in the process of gastric carcinogenesis. JF - Journal of the National Cancer Institute AU - Kneller, R W AU - You, W C AU - Chang, Y S AU - Liu, W D AU - Zhang, L AU - Zhao, L AU - Xu, G W AU - Fraumeni, J F AU - Blot, W J AD - Division of Cancer Etiology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/08/19/ PY - 1992 DA - 1992 Aug 19 SP - 1261 EP - 1266 VL - 84 IS - 16 SN - 0027-8874, 0027-8874 KW - Index Medicus KW - Life Style KW - Intestines -- pathology KW - Logistic Models KW - Risk Factors KW - Metaplasia -- complications KW - Humans KW - Gastritis, Atrophic -- complications KW - Adult KW - Middle Aged KW - Male KW - Female KW - Prevalence KW - Precancerous Conditions -- etiology KW - Smoking -- adverse effects KW - Stomach Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73086594?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cigarette+smoking+and+other+risk+factors+for+progression+of+precancerous+stomach+lesions.&rft.au=Kneller%2C+R+W%3BYou%2C+W+C%3BChang%2C+Y+S%3BLiu%2C+W+D%3BZhang%2C+L%3BZhao%2C+L%3BXu%2C+G+W%3BFraumeni%2C+J+F%3BBlot%2C+W+J&rft.aulast=Kneller&rft.aufirst=R&rft.date=1992-08-19&rft.volume=84&rft.issue=16&rft.spage=1261&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 - 1992-09-01 N1 - Date created - 1992-09-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phosphorylation stimulates the transcriptional activity of the human beta 1 thyroid hormone nuclear receptor. AN - 73122312; 1502193 AB - The role of phosphorylation on the gene activation activity of the human beta 1 thyroid hormone nuclear receptor (h-TR beta 1) was examined. h-TR beta 1 was found to be a phosphoprotein when expressed in COS-1 cells, with serine, threonine, and tyrosine (85:10:5) as the phosphorylation sites. Okadaic acid (a potent inhibitor of phosphatases 1 and 2A) at 0.1, 0.25, and 0.5 microM increased the phosphorylation of h-TR beta 1 by 3-, 7-, and 11-fold, respectively. The increase in phosphorylation was accompanied by a concomitant increase in phosphorylation was accompanied by a concomitant increase in receptor-mediated transcription in transient transfection assays. h-TR beta 1 purified from Escherichia coli was phosphorylated in vitro by the endogenous kinase from cellular extracts. Serine, threonine, and tyrosine were phosphorylated in a similar ratio to that found in COS-1 cells. The in vitro phosphorylation was stimulated by okadaic acid. Phosphorylation did not affect the binding of h-TR beta 1 to 3,3',5-triiodo-L-thyronine. However, phosphorylation of h-TR beta 1 resulted in an increase of its binding to DNA and conferred on it the ability to bind to nuclear accessory proteins. The results indicate that phosphorylation plays an important role in the transcriptional activity of h-TR beta 1. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Lin, K H AU - Ashizawa, K AU - Cheng, S Y AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/08/15/ PY - 1992 DA - 1992 Aug 15 SP - 7737 EP - 7741 VL - 89 IS - 16 SN - 0027-8424, 0027-8424 KW - DNA-Binding Proteins KW - 0 KW - Ethers, Cyclic KW - Phosphates KW - Receptors, Thyroid Hormone KW - Okadaic Acid KW - 1W21G5Q4N2 KW - Vanadates KW - 3WHH0066W5 KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Methionine KW - AE28F7PNPL KW - Protein Kinase C KW - EC 2.7.11.13 KW - Index Medicus KW - Animals KW - HeLa Cells KW - Vanadates -- pharmacology KW - Humans KW - Methionine -- metabolism KW - Ethers, Cyclic -- pharmacology KW - Phosphates -- metabolism KW - Protein Kinase C -- antagonists & inhibitors KW - Phosphorylation KW - Transfection KW - Genetic Vectors KW - Kinetics KW - Adenosine Triphosphate -- metabolism KW - Cell Line KW - Cell Nucleus -- metabolism KW - Receptors, Thyroid Hormone -- metabolism KW - Receptors, Thyroid Hormone -- genetics KW - Transcription, Genetic KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73122312?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Phosphorylation+stimulates+the+transcriptional+activity+of+the+human+beta+1+thyroid+hormone+nuclear+receptor.&rft.au=Heineman%2C+E+F%3BOlsen%2C+J+H%3BPottern%2C+L+M%3BGomez%2C+M%3BRaffn%2C+E%3BBlair%2C+A&rft.aulast=Heineman&rft.aufirst=E&rft.date=1992-11-01&rft.volume=3&rft.issue=6&rft.spage=555&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 - 1992-09-15 N1 - Date created - 1992-09-15 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: EMBO J. 1988 Aug;7(8):2425-33 [2903825] Nature. 1986 Dec 18-31;324(6098):641-6 [2879243] Cell. 1988 Jul 29;54(3):313-23 [3396073] Cell. 1981 Jun;24(3):741-52 [6166387] Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] Cell. 1991 Jun 28;65(7):1267-79 [1648451] Mol Endocrinol. 1991 Sep;5(9):1215-28 [1663212] Mol Endocrinol. 1991 Jan;5(1):94-9 [1850112] Mol Endocrinol. 1991 Apr;5(4):485-92 [1922081] Endocrinology. 1991 May;128(5):2601-9 [1708338] FASEB J. 1991 Jun;5(9):2243-9 [1860615] J Biol Chem. 1990 Apr 5;265(10):5403-8 [2108136] Cell. 1990 Oct 5;63(1):155-65 [2170018] Cell. 1990 Feb 9;60(3):375-86 [2302733] EMBO J. 1986 Nov;5(11):2867-72 [2431901] Oncogene. 1989 Oct;4(10):1247-54 [2552374] J Virol. 1988 Apr;62(4):1258-65 [2831386] Proc Natl Acad Sci U S A. 1988 Jul;85(14):5031-5 [2899322] Cell. 1988 Sep 9;54(6):855-64 [3044613] Endocrinology. 1987 Jun;120(6):2591-6 [3569145] Methods Enzymol. 1983;99:387-402 [6196603] Cell. 1991 Jun 28;65(7):1255-66 [1648450] J Biol Chem. 1990 Feb 15;265(5):2500-4 [1968058] Nature. 1990 Apr 12;344(6267):678-82 [2157987] J Biol Chem. 1990 Mar 25;265(9):5161-5 [2180960] Cell. 1990 Jun 29;61(7):1161-4 [2194664] J Biol Chem. 1990 Sep 25;265(27):16548-55 [2398063] Genes Dev. 1989 May;3(5):620-7 [2545525] Biochem Biophys Res Commun. 1989 Oct 16;164(1):238-44 [2553014] Mol Endocrinol. 1989 Dec;3(12):1996-2004 [2628734] Gene. 1986;45(1):107-11 [3023200] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression of the cystic fibrosis transmembrane conductance regulator gene can be regulated by protein kinase C. AN - 73118297; 1379589 AB - Epithelial cells utilize at least two types of apical Cl- channels, the cAMP-activated cystic fibrosis transmembrane conductance regulator (CFTR) and the Ca2+/calmodulin-dependent Cl- channel. While phorbal ester (PMA) activates only CFTR-dependent Cl- secretion and the Ca2+ ionophore A23187 only the Ca2+/calmodulin-dependent Cl- secretion, PMA and A23187 share the ability to down-regulate expression of the CFTR gene at the transcriptional level. Since both PMA and A23187 can activate protein kinases, we hypothesized that protein kinase pathways may be involved in the regulation of CFTR gene expression. Exposure of HT-29 human colon carcinoma cells to the protein kinase C activator SC9 down-regulated CFTR mRNA levels in a dose-dependent fashion, similar to that seen with PMA. The reduction in CFTR transcript levels by SC9 and PMA was blocked by H7, an inhibitor of protein kinases. In a similar fashion, the down-regulation of CFTR transcript levels by A23187 was blocked by H7 as well as staurosporine, another protein kinase inhibitor. Interestingly, both H7 and staurosporine themselves increased CFTR mRNA levels. Quantification of CFTR gene transcription rate showed a reduction by SC9 (similar to that with PMA and A23187) that was prevented by H7 and that H7 by itself increased CFTR transcription. Together, these observations suggest that protein kinase pathways, likely including protein kinase C, are involved in the regulation of CFTR gene expression, with activation or inhibition of protein kinase activity down-regulating or up-regulating CFTR gene expression, respectively. JF - The Journal of biological chemistry AU - Bargon, J AU - Trapnell, B C AU - Yoshimura, K AU - Dalemans, W AU - Pavirani, A AU - Lecocq, J P AU - Crystal, R G AD - Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/08/15/ PY - 1992 DA - 1992 Aug 15 SP - 16056 EP - 16060 VL - 267 IS - 23 SN - 0021-9258, 0021-9258 KW - CFTR protein, human KW - 0 KW - Isoquinolines KW - Membrane Proteins KW - Piperazines KW - RNA, Messenger KW - Sulfonamides KW - N-(6-phenylhexyl)-5-chloro-1-naphthalenesulfonamide KW - 102649-78-5 KW - Cystic Fibrosis Transmembrane Conductance Regulator KW - 126880-72-6 KW - Calcimycin KW - 37H9VM9WZL KW - 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine KW - 84477-87-2 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Isoquinolines -- pharmacology KW - Sulfonamides -- pharmacology KW - Enzyme Activation KW - Kinetics KW - Humans KW - Calcimycin -- pharmacology KW - Piperazines -- pharmacology KW - Colonic Neoplasms KW - Cell Line KW - Protein Kinase C -- metabolism KW - Gene Expression Regulation, Neoplastic KW - Protein Kinase C -- antagonists & inhibitors KW - Transcription, Genetic -- drug effects KW - RNA, Messenger -- metabolism KW - Cystic Fibrosis -- genetics KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Membrane Proteins -- genetics KW - RNA, Messenger -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73118297?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+the+cystic+fibrosis+transmembrane+conductance+regulator+gene+can+be+regulated+by+protein+kinase+C.&rft.au=Bargon%2C+J%3BTrapnell%2C+B+C%3BYoshimura%2C+K%3BDalemans%2C+W%3BPavirani%2C+A%3BLecocq%2C+J+P%3BCrystal%2C+R+G&rft.aulast=Bargon&rft.aufirst=J&rft.date=1992-08-15&rft.volume=267&rft.issue=23&rft.spage=16056&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 - 1992-09-10 N1 - Date created - 1992-09-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dopamine transporter site-directed mutations differentially alter substrate transport and cocaine binding. AN - 73116806; 1502198 AB - Polar amino acids lying within three hydrophobic regions of the dopamine transporter (DAT) are analogous to those important for ligand recognition by catecholamine receptors. Possible functional significance of these amino acids was examined by expressing DAT cDNAs mutated in these polar residues. Replacement of aspartate at position 79 with alanine, glycine, or glutamate dramatically reduced uptake of [3H]dopamine and the tritium-labeled Parkinsonism-inducing neurotoxin 1-methyl-4-phenylpyridinium (MPP+) and reduced the mutants' affinity for the tritium-labeled cocaine analog (-)-2 beta-carbomethoxy-3 beta-(4-fluorophenyl)tropane (CFT) without affecting Bmax. Replacement of the serine residues at positions 356 and 359 in the seventh hydrophobic region by alanine or glycine caused reductions in [3H]dopamine and [3H]MPP+ uptake, whereas [3H]CFT binding was less affected. Substitution of two serines in the eighth hydrophobic region yielded wild-type values for [3H]dopamine and [3H]MPP+ uptake and [3H]CFT binding. These results demonstrate that aspartate and serine residues lying within the first and seventh hydrophobic putative transmembrane regions are crucial for DAT function and provide identification of residues differentially important for cocaine binding and for dopamine uptake. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Kitayama, S AU - Shimada, S AU - Xu, H AU - Markham, L AU - Donovan, D M AU - Uhl, G R AD - Laboratory of Molecular Neurobiology, Addiction Research Center/National Institute on Drug Abuse, Baltimore, MD. Y1 - 1992/08/15/ PY - 1992 DA - 1992 Aug 15 SP - 7782 EP - 7785 VL - 89 IS - 16 SN - 0027-8424, 0027-8424 KW - Carrier Proteins KW - 0 KW - Dopamine Plasma Membrane Transport Proteins KW - Membrane Glycoproteins KW - Membrane Transport Proteins KW - Nerve Tissue Proteins KW - DNA KW - 9007-49-2 KW - Cocaine KW - I5Y540LHVR KW - 1-Methyl-4-phenylpyridinium KW - R865A5OY8J KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Animals KW - Models, Structural KW - Transfection KW - Kinetics KW - DNA -- genetics KW - Binding, Competitive KW - Molecular Sequence Data KW - Biological Transport KW - Amino Acid Sequence KW - 1-Methyl-4-phenylpyridinium -- metabolism KW - Cell Membrane -- metabolism KW - Cell Line KW - Protein Conformation KW - Mutagenesis, Site-Directed KW - Carrier Proteins -- metabolism KW - Carrier Proteins -- genetics KW - Dopamine -- metabolism KW - Cocaine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73116806?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Dopamine+transporter+site-directed+mutations+differentially+alter+substrate+transport+and+cocaine+binding.&rft.au=Kitayama%2C+S%3BShimada%2C+S%3BXu%2C+H%3BMarkham%2C+L%3BDonovan%2C+D+M%3BUhl%2C+G+R&rft.aulast=Kitayama&rft.aufirst=S&rft.date=1992-08-15&rft.volume=89&rft.issue=16&rft.spage=7782&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 - 1992-09-15 N1 - Date created - 1992-09-15 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 1992 Jan 5;267(1):649-52 [1370453] J Mol Biol. 1984 May 5;175(1):75-81 [6427470] Curr Opin Neurobiol. 1991 Jun;1(1):84-90 [1688010] Mol Pharmacol. 1991 Jun;39(6):733-9 [1828858] Brain Res Mol Brain Res. 1991 Feb;9(3):271-6 [1851530] Nature. 1991 Nov 7;354(6348):66-70 [1944572] Science. 1991 Oct 25;254(5031):576-8 [1948034] Science. 1991 Oct 25;254(5031):578-9 [1948035] Science. 1991 Oct 25;254(5031):579-80 [1948036] Science. 1990 Sep 14;249(4974):1303-6 [1975955] J Med Chem. 1991 Mar;34(3):883-6 [2002468] Nature. 1991 Mar 28;350(6316):350-4 [2008212] Prog Neurobiol. 1990;34(5):387-400 [2192393] Life Sci. 1990;46(9):635-45 [2308472] FASEB J. 1989 May;3(7):1825-32 [2541037] Science. 1987 Sep 4;237(4819):1219-23 [2820058] Neurology. 1986 Feb;36(2):250-8 [3080696] Methods Enzymol. 1987;154:367-82 [3323813] Biochem Pharmacol. 1986 Apr 1;35(7):1123-9 [3964292] Br J Pharmacol. 1971 Apr;41(4):571-91 [4397129] Mol Pharmacol. 1991 Aug;40(2):168-79 [1678850] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Monoclonal antibody MRK16 reverses the multidrug resistance of multidrug-resistant transgenic mice. AN - 73080394; 1353705 AB - Using multidrug-resistant (MDR)-transgenic mice, whose bone marrow cells express the human MDR1 gene at a level approximately equal to that found in many human cancers, we determined the efficacy of human-specific anti-P-glycoprotein monoclonal antibody MRK16 in overcoming multidrug resistance in an intact animal. MRK16 alone (2 mg) did not significantly affect the WBC counts of the MDR-transgenic mice, but MRK16, as well as the F(ab')2 fragments of MRK16, led to a dose-dependent circumvention of bone marrow resistance against daunomycin, doxorubicin, vincristine, vinblastine, etoposide, and taxol. This sensitizing effect could not be enhanced by combining MRK16 with low molecular weight chemosensitizing agents such as verapamil, quinine, quinidine, or cyclosporin A. We also investigated the concept of specifically targeting and killing multidrug-resistant cells by using MRK16 coupled to Pseudomonas exotoxin (PE). MRK16-PE resulted in a dose-dependent killing of bone marrow cells in MDR-transgenic mice, whereas no bone marrow toxicity was observed in normal control mice. Administration of excess MRK16 prior to injection of MRK16-PE successfully blocked the effect of MRK16-PE. MOPC-PE, a non-MDR-related control monoclonal antibody conjugate, did not target and kill multidrug-resistant bone marrow cells in MDR-transgenic mice. Thus, these immunological approaches to reversing multidrug resistance appear to be both specific and effective. JF - Cancer research AU - Mickisch, G H AU - Pai, L H AU - Gottesman, M M AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/08/15/ PY - 1992 DA - 1992 Aug 15 SP - 4427 EP - 4432 VL - 52 IS - 16 SN - 0008-5472, 0008-5472 KW - MDR1 KW - Alkaloids KW - 0 KW - Antibodies, Monoclonal KW - Immunotoxins KW - Vincristine KW - 5J49Q6B70F KW - Vinblastine KW - 5V9KLZ54CY KW - Etoposide KW - 6PLQ3CP4P3 KW - Doxorubicin KW - 80168379AG KW - Paclitaxel KW - P88XT4IS4D KW - Daunorubicin KW - ZS7284E0ZP KW - Index Medicus KW - Etoposide -- pharmacology KW - Vinblastine -- pharmacology KW - Animals KW - Drug Screening Assays, Antitumor KW - Vincristine -- pharmacology KW - Mice KW - Mice, Transgenic KW - Leukocyte Count KW - Daunorubicin -- pharmacology KW - Doxorubicin -- pharmacology KW - Alkaloids -- pharmacology KW - Pseudomonas aeruginosa KW - Drug Resistance -- genetics KW - Immunotoxins -- therapeutic use KW - Antibodies, Monoclonal -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73080394?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Monoclonal+antibody+MRK16+reverses+the+multidrug+resistance+of+multidrug-resistant+transgenic+mice.&rft.au=Mickisch%2C+G+H%3BPai%2C+L+H%3BGottesman%2C+M+M%3BPastan%2C+I&rft.aulast=Mickisch&rft.aufirst=G&rft.date=1992-08-15&rft.volume=52&rft.issue=16&rft.spage=4427&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 - 1992-09-10 N1 - Date created - 1992-09-10 N1 - Date revised - 2017-01-13 N1 - Gene symbol - MDR1 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A proteolytically sensitive region common to several rat liver cytochromes P450: effect of cleavage on substrate binding. AN - 73096720; 1643049 AB - Limited proteolysis of rat liver microsomes was used to probe the topography and structure of cytochrome P450 bound to the endoplasmic reticulum. Three cytochromes P450 from two families were examined. Monoclonal antibodies to cytochrome P450 forms 1A1, 2B1, and 2E1 were used to immunopurify these proteolyzed cytochromes P450 from microsomes from rats treated with 3-methylcholanthrene, phenobarbital, and acetone, respectively. Electrophoretic and immunoblot analysis of tryptic fragments revealed a highly sensitive cleavage site in all three cytochromes P450. N-Terminal sequencing was performed on the fragments after transfer onto poly(vinylidene difluoride) membranes and showed that this preferential cleavage site is at amino acid position 298 of P450 1A1, position 277 of P450 2B1, and position 278 of P450 2E1. Multiple sequence alignment revealed that these positions are at the amino terminal of a highly conserved region of these cytochromes P450. The important functional role implied by primary sequence conservation along with the proteolytic sensitivity at its amino terminal suggests that this region is a protein domain. Comparison with the known structure of the bacterial cytochrome P450cam predicts that this proteolytically sensitive site is within an interhelical turn region connected to the distal helix that partially encompasses the heme-containing active site. Substrate binding to the cleaved cytochromes P450 was examined in order to determine whether the newly added conformational freedom near the cleavage site functionally altered these cytochromes P450. Cleavage of P450 2B1 abolished benzphetamine binding, which indicates that the cleavage site contains an important structural determinant for binding this substrate. However, cleavage did not affect benzo[a]pyrene binding to P450 1A1. JF - Biochemistry AU - Tsokos, D C AU - Omata, Y AU - Robinson, R C AU - Krutzsch, H C AU - Gelboin, H V AU - Friedman, F K AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/08/11/ PY - 1992 DA - 1992 Aug 11 SP - 7155 EP - 7159 VL - 31 IS - 31 SN - 0006-2960, 0006-2960 KW - Benzo(a)pyrene KW - 3417WMA06D KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Blotting, Western KW - Sequence Alignment KW - Electrophoresis, Polyacrylamide Gel KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Hydrolysis KW - Male KW - Benzo(a)pyrene -- metabolism KW - Microsomes, Liver -- enzymology KW - Cytochrome P-450 Enzyme System -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73096720?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+proteolytically+sensitive+region+common+to+several+rat+liver+cytochromes+P450%3A+effect+of+cleavage+on+substrate+binding.&rft.au=Tsokos%2C+D+C%3BOmata%2C+Y%3BRobinson%2C+R+C%3BKrutzsch%2C+H+C%3BGelboin%2C+H+V%3BFriedman%2C+F+K&rft.aulast=Tsokos&rft.aufirst=D&rft.date=1992-08-11&rft.volume=31&rft.issue=31&rft.spage=7155&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-10 N1 - Date created - 1992-09-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Microglial-produced nitric oxide and reactive nitrogen oxides mediate neuronal cell death. AN - 73190737; 1381982 AB - The role of inflammatory cytokines in the pathogenesis of neurological diseases is not well understood. The neurotoxic effects of cytokines could be mediated by immunostimulation of glial cells to produce toxic concentrations of nitric oxide (NO) and reactive nitrogen oxides. Cultured microglia and meningeal fibroblasts, but not Type 1 astrocytes, were induced by lipopolysaccharides and cytokines to synthesize NO and reactive nitrogen oxides from L-arginine. In co-cultures of immunostimulated microglia and cerebellar granule neurons, neurotoxicity was blocked by an inhibitor of NO synthase, NG-nitroarginine, and by oxyhemoglobin, which inactivates NO. Microglial-induced neurotoxicity was also partially attenuated by the N-methyl-D-aspartate (NMDA) receptor antagonists, MK-801 and 2-amino-5-phosphovalerate (APV). Superoxide dismutase, which stabilizes NO through inactivation of superoxide anion, augmented microglial-mediated neurotoxicity either alone or in combination with MK-801 or APV. Hence, immunostimulated microglia mediate neurotoxicity by NO, reactive nitrogen oxides, superoxide anion and NMDA-like substances. These findings suggest a novel role for microglial-produced NO and reactive nitrogen oxides as a neurotoxic agent in neurodegenerative disease states. JF - Brain research AU - Boje, K M AU - Arora, P K AD - Laboratory of Neuroscience, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/08/07/ PY - 1992 DA - 1992 Aug 07 SP - 250 EP - 256 VL - 587 IS - 2 SN - 0006-8993, 0006-8993 KW - Cytokines KW - 0 KW - Nitrites KW - Nitrogen Oxides KW - Receptors, N-Methyl-D-Aspartate 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 - Animals KW - Cell Death -- physiology KW - Amino Acid Oxidoreductases -- metabolism KW - Cytokines -- pharmacology KW - Nitrites -- metabolism KW - Immunization KW - Pregnancy KW - Cerebellum -- metabolism KW - Rats, Inbred Strains KW - Rats KW - Receptors, N-Methyl-D-Aspartate -- physiology KW - Cells, Cultured KW - Receptors, N-Methyl-D-Aspartate -- antagonists & inhibitors KW - Arginine -- physiology KW - Immunohistochemistry KW - Female KW - Neuroglia -- metabolism KW - Nitrogen Oxides -- metabolism KW - Nitric Oxide -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73190737?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Microglial-produced+nitric+oxide+and+reactive+nitrogen+oxides+mediate+neuronal+cell+death.&rft.au=Boje%2C+K+M%3BArora%2C+P+K&rft.aulast=Boje&rft.aufirst=K&rft.date=1992-08-07&rft.volume=587&rft.issue=2&rft.spage=250&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 - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of myelin basic protein thyroid hormone response element and its function in the context of native and heterologous promoter. AN - 73097304; 1379237 AB - In this report we have characterized further the myelin basic protein (MBP) gene thyroid hormone response element (TRE) by functional and binding analysis. Mutation and deletion experiments revealed that this TRE, confined to the sequences -184 to -167 of the MBP promoter, is able to function as a classical regulatory element in the context of the native and a heterologous promoter. It is comprised of two regions, containing a motif that is highly conserved among other TREs: AGGACA, arranged as an inverted palindrome. Any mutation within the footprinted region impaired receptor binding and function. Moreover, the deletion of sequences outside of the receptor footprinted region (MBP-TRE-18) resulted in a higher triiodothyronine responsiveness and a concomitant increase in receptor-dependent, hormone-independent repression. Results of transfection assays showed that both receptors alpha and beta elicit indistinguishable triiodothyronine responses when the MBP-TRE functions as a regulator of a heterologous promoter activity. However, a preferential beta receptor transactivation was observed when the MBP-TRE was placed in the context of its native promoter. JF - The Journal of biological chemistry AU - Farsetti, A AU - Desvergne, B AU - Hallenbeck, P AU - Robbins, J AU - Nikodem, V M AD - Genetics and Biochemistry Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/08/05/ PY - 1992 DA - 1992 Aug 05 SP - 15784 EP - 15788 VL - 267 IS - 22 SN - 0021-9258, 0021-9258 KW - Macromolecular Substances KW - 0 KW - Myelin Basic Protein KW - Oligodeoxyribonucleotides KW - Receptors, Thyroid Hormone KW - Recombinant Proteins KW - Triiodothyronine KW - 06LU7C9H1V KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Thymidine Kinase KW - EC 2.7.1.21 KW - Index Medicus KW - 3T3 Cells KW - Animals KW - Thymidine Kinase -- metabolism KW - Mice KW - Plasmids KW - Chloramphenicol O-Acetyltransferase -- metabolism KW - Mutagenesis, Site-Directed KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Base Sequence KW - Transfection KW - Recombinant Proteins -- metabolism KW - Kinetics KW - Binding, Competitive KW - Molecular Sequence Data KW - Thymidine Kinase -- genetics KW - Promoter Regions, Genetic KW - Triiodothyronine -- pharmacology KW - Myelin Basic Protein -- genetics KW - Receptors, Thyroid Hormone -- metabolism KW - Genes, Regulator UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73097304?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+myelin+basic+protein+thyroid+hormone+response+element+and+its+function+in+the+context+of+native+and+heterologous+promoter.&rft.au=Farsetti%2C+A%3BDesvergne%2C+B%3BHallenbeck%2C+P%3BRobbins%2C+J%3BNikodem%2C+V+M&rft.aulast=Farsetti&rft.aufirst=A&rft.date=1992-08-05&rft.volume=267&rft.issue=22&rft.spage=15784&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 - 1992-08-28 N1 - Date created - 1992-08-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Fusions of anthrax toxin lethal factor to the ADP-ribosylation domain of Pseudomonas exotoxin A are potent cytotoxins which are translocated to the cytosol of mammalian cells. AN - 73089346; 1639793 AB - The lethal factor (LF) and edema factor (EF) components of anthrax toxin are toxic to animal cells only if internalized by interaction with the protective antigen (PA) component. PA binds to a cell surface receptor and is proteolytically cleaved to expose a binding site for LF and EF. To study how LF and EF are internalized and trafficked within cells, LF was fused to the translocation and ADP-ribosylation domains (domains II and III, respectively) of Pseudomonas exotoxin A. LF fusion proteins containing Pseudomonas exotoxin A domains II and III were less toxic than those containing only domain III. Fusion proteins with a functional endoplasmic reticulum retention sequence, REDLK, at the carboxyl terminus of domain III were less toxic than those with a nonfunctional sequence, LDER. The most potent fusion protein, FP33, had an EC50 = 2 pM on Chinese hamster ovary cells, exceeding that of native Pseudomonas exotoxin A (EC50 = 420 pM). Toxicity of all the fusion proteins required the presence of PA and was blocked by monensin. These data suggest that LF and LF fusion proteins are efficiently translocated from acidified endosomes directly to the cytosol without trafficking through other organelles, as is required for Pseudomonas exotoxin A. This system provides a potential vehicle for importing diverse proteins into the cytosol of mammalian cells. JF - The Journal of biological chemistry AU - Arora, N AU - Klimpel, K R AU - Singh, Y AU - Leppla, S H AD - Laboratory of Microbial Ecology, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/08/05/ PY - 1992 DA - 1992 Aug 05 SP - 15542 EP - 15548 VL - 267 IS - 22 SN - 0021-9258, 0021-9258 KW - Antigens, Bacterial KW - 0 KW - Bacterial Toxins KW - Exotoxins KW - Protein Synthesis Inhibitors KW - Recombinant Fusion Proteins KW - Virulence Factors KW - anthrax toxin 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 - Index Medicus KW - Animals KW - Cytosol -- metabolism KW - Genes, Bacterial KW - Pseudomonas aeruginosa -- genetics KW - Dose-Response Relationship, Drug KW - Escherichia coli -- genetics KW - Mice KW - Plasmids KW - Adenosine Diphosphate Ribose -- metabolism KW - Binding Sites KW - Cloning, Molecular KW - Recombinant Fusion Proteins -- metabolism KW - Bacillus anthracis -- genetics KW - Kinetics KW - Restriction Mapping KW - Recombinant Fusion Proteins -- pharmacology KW - CHO Cells KW - Cricetinae KW - Macrophages -- cytology KW - Exotoxins -- genetics KW - Exotoxins -- pharmacology KW - Bacterial Toxins -- pharmacology KW - Macrophages -- drug effects KW - Bacterial Toxins -- genetics KW - Bacterial Toxins -- metabolism KW - Cell Survival -- drug effects KW - Protein Synthesis Inhibitors -- pharmacology KW - Exotoxins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73089346?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Fusions+of+anthrax+toxin+lethal+factor+to+the+ADP-ribosylation+domain+of+Pseudomonas+exotoxin+A+are+potent+cytotoxins+which+are+translocated+to+the+cytosol+of+mammalian+cells.&rft.au=Arora%2C+N%3BKlimpel%2C+K+R%3BSingh%2C+Y%3BLeppla%2C+S+H&rft.aulast=Arora&rft.aufirst=N&rft.date=1992-08-05&rft.volume=267&rft.issue=22&rft.spage=15542&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 - 1992-08-28 N1 - Date created - 1992-08-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of focal transcranial magnetic stimulation on simple reaction time to acoustic, visual and somatosensory stimuli. AN - 85228695; pmid-1393501 AB - In a simple reaction time (RT) paradigm, magnetic stimulation of different intensities was delivered over different scalp positions and at variable delays before (negative) or after (positive) the go-signal. Magnetic stimulation shortened RT to different go-signals (auditory, visual and somatosensory stimuli) by approximately 30 ms when delivered over the motor cortex contralateral to the responding arm at intensities below motor threshold. This effect was maximal at a delay of approximately +10 ms. A similar effect was found with suprathreshold stimulation to the ipsilateral motor cortex. Magnetic stimulation over other scalp areas did not affect RT regardless of the delay. No differences were found between the effects on elbow flexion and thumb abduction. The shortening of RT was not associated with changes in the timing development of premovement excitability increase in the motor cortex. We conclude that magnetic stimulation shortens RT by inducing an earlier initiation of this excitability increase. JF - Brain AU - Pascual-Leone, A AU - Valls-Solé J AU - Wassermann, E M AU - Brasil-Neto, J AU - Cohen, L G AU - Hallett, M AD - Human Cortical Physiology Unit, National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 1045 EP - 1059 VL - 115 ( Pt 4) SN - 0006-8950, 0006-8950 KW - Motor Cortex KW - Human KW - Adult KW - Electromyography KW - Support, Non-U.S. Gov't KW - Movement KW - Evoked Potentials, Somatosensory KW - Male KW - Female KW - Reaction Time KW - Photic Stimulation KW - Magnetics KW - Acoustic Stimulation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85228695?accountid=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&rft.atitle=Effects+of+focal+transcranial+magnetic+stimulation+on+simple+reaction+time+to+acoustic%2C+visual+and+somatosensory+stimuli.&rft.au=Pascual-Leone%2C+A%3BValls-Sol%C3%A9+J%3BWassermann%2C+E+M%3BBrasil-Neto%2C+J%3BCohen%2C+L+G%3BHallett%2C+M&rft.aulast=Pascual-Leone&rft.aufirst=A&rft.date=1992-08-01&rft.volume=115+%28+Pt+4%29&rft.issue=&rft.spage=1045&rft.isbn=&rft.btitle=&rft.title=Brain&rft.issn=00068950&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Rational immunotherapy with ribonuclease chimeras. An approach toward humanizing immunotoxins. AN - 75516262; 1285324 AB - Members of the pancreatic ribonuclease (RNase) family have diverse activities toward RNA that could cause them to function during host defense and physiological cell death pathways. This activity could be harnessed by coupling RNases to cell binding ligands for the purpose of engineering them into cell-type specific cytotoxins. Therefore, the cytotoxic potential of RNase was explored by linking bovine pancreatic ribonuclease A via a disulfide bond to human transferrin or antibodies to the transferrin receptor. The RNase hybrid proteins were cytotoxic to K562 human erythroleukemia cells in vitro with an IC50 around 10(-7) M, whereas > 10(-4) M of native RNase was required to inhibit protein synthesis. Cytotoxicity required both components of the conjugate since excess transferrin or ribonuclease inhibitors added to the medium protected the cells from the transferrin-RNase toxicity. Importantly, the RNase conjugates were found to have potent antitumor effects in vivo. Chimeric RNase fusion proteins were also developed. F(ab')2-like antibody-enzyme fusions were prepared by linking the gene for human RNase to a chimeric antitransferrin receptor heavy chain gene. The antibody enzyme fusion gene was introduced into a transfectoma that secreted the chimeric light chain of the same antibody, and cell lines were cloned that synthesized and secreted the antibody-enzyme fusion protein of the expected size at a concentration of 1-5 ng/mL. Culture supernatants from clones secreting the fusion protein caused inhibition of growth and protein synthesis toward K562 cells that express the human transferrin receptor but not toward a nonhuman derived cell line. Since human ribonucleases coupled to antibodies also exhibited receptor mediated toxicities, a new approach to selective cell killing is provided. This may allow the development of new therapeutics for cancer treatment that exhibit less systemic toxicity and, importantly, less immunogenicity than the currently employed ligand-toxin conjugates. JF - Cell biophysics AU - Rybak, S M AU - Hoogenboom, H R AU - Newton, D L AU - Raus, J C AU - Youle, R J AD - Surgical Neurology Branch, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, MD 20892. PY - 1992 SP - 121 EP - 138 VL - 21 IS - 1-3 SN - 0163-4992, 0163-4992 KW - Immunotoxins KW - 0 KW - DNA KW - 9007-49-2 KW - Ribonucleases KW - EC 3.1.- KW - Index Medicus KW - Base Sequence KW - Humans KW - DNA -- genetics KW - Molecular Sequence Data KW - DNA -- analysis KW - Amino Acid Sequence KW - Chimera KW - Immunotherapy KW - Ribonucleases -- therapeutic use KW - Immunotoxins -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75516262?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+biophysics&rft.atitle=Rational+immunotherapy+with+ribonuclease+chimeras.+An+approach+toward+humanizing+immunotoxins.&rft.au=Rybak%2C+S+M%3BHoogenboom%2C+H+R%3BNewton%2C+D+L%3BRaus%2C+J+C%3BYoule%2C+R+J&rft.aulast=Rybak&rft.aufirst=S&rft.date=1992-08-01&rft.volume=21&rft.issue=1-3&rft.spage=121&rft.isbn=&rft.btitle=&rft.title=Cell+biophysics&rft.issn=01634992&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 - 2017-01-17 ER - TY - JOUR T1 - Effective regional therapy of experimental cancer with paralesional administration of tumour necrosis factor-alpha + interferon-gamma. AN - 75510141; 1341263 AB - Systemically administered tumour necrosis factor (TNF) has anti-tumour effects in animal tumour models but its clinical application is limited by severe toxicity. Interferon-gamma(IFN-gamma) has been shown to augment the anti-tumour effect of TNF. We evaluated the effect of paralesional (p.I.) injections of TNF plus IFN-gamma in a murine tumour model and compared the toxicity and anti-tumour effect with that seen with systemic administration. C57BL6 mice with 10-day subcutaneous MCA sarcomas were treated with daily p.I. injections of recombinant huTNF +/- IFN-gamma for 5 days. Optimal mean survival and 30-day cure rate was seen with doses of 5 micrograms TNF-alpha + 5000 U IFN-gamma (P 5 micrograms TNF had initial complete necrosis of tumour with a variable degree of surrounding tissue necrosis, with rapid regrowth of tumour seen in some animals. Although treatment-related mortality was similar between i.v. and p.I. therapy, there was a higher percentage of animals cured with p.I. injections with overall cure rates in treated animals at 30 days of 17% vs. 72% (i.v. vs. p.I., P < 0.01) and 13% vs. 67% (P < 0.04) in a repeat study. 2+ clinical applications. JF - Surgical oncology AU - Thom, A K AU - Fraker, D L AU - Taubenberger, J K AU - Norton, J A AD - Surgical Metabolism Section, National Cancer Institute, National Institutes of Health, Bethesda, MD. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 291 EP - 298 VL - 1 IS - 4 SN - 0960-7404, 0960-7404 KW - Recombinant Proteins KW - 0 KW - Tumor Necrosis Factor-alpha KW - Methylcholanthrene KW - 56-49-5 KW - Interferon-gamma KW - 82115-62-6 KW - Index Medicus KW - Neoplasm Transplantation KW - Drug Screening Assays, Antitumor KW - Animals KW - Injections, Intralesional KW - Random Allocation KW - Mice, Inbred C57BL KW - Mice KW - Drug Synergism KW - Female KW - Remission Induction KW - Tumor Necrosis Factor-alpha -- toxicity KW - Sarcoma, Experimental -- therapy KW - Tumor Necrosis Factor-alpha -- administration & dosage KW - Sarcoma, Experimental -- chemically induced KW - Interferon-gamma -- toxicity KW - Interferon-gamma -- administration & dosage KW - Sarcoma, Experimental -- pathology KW - Sarcoma, Experimental -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75510141?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Effective+regional+therapy+of+experimental+cancer+with+paralesional+administration+of+tumour+necrosis+factor-alpha+%2B+interferon-gamma.&rft.au=Thom%2C+A+K%3BFraker%2C+D+L%3BTaubenberger%2C+J+K%3BNorton%2C+J+A&rft.aulast=Thom&rft.aufirst=A&rft.date=1992-08-01&rft.volume=1&rft.issue=4&rft.spage=291&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 - 1994-01-13 N1 - Date created - 1994-01-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phase I/II studies of the toxicity and immunogenicity of recombinant gp160 and p24 vaccines in HIV-infected individuals. AN - 73410622; 1466952 JF - AIDS research and human retroviruses AU - Zunich, K M AU - Lane, H C AU - Davey, R T AU - Falloon, J AU - Polis, M AU - Kovacs, J A AU - Masur, H AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 1335 VL - 8 IS - 8 SN - 0889-2229, 0889-2229 KW - AIDS Vaccines KW - 0 KW - Gene Products, env KW - HIV Core Protein p24 KW - HIV Envelope Protein gp160 KW - Protein Precursors KW - Recombinant Proteins KW - Vaccines, Synthetic KW - Index Medicus KW - AIDS/HIV KW - Recombinant Proteins -- toxicity KW - Humans KW - Recombinant Proteins -- immunology KW - Recombinant Proteins -- therapeutic use KW - Recombinant Proteins -- administration & dosage KW - Vaccines, Synthetic -- toxicity KW - AIDS Vaccines -- administration & dosage KW - AIDS Vaccines -- therapeutic use KW - AIDS Vaccines -- immunology KW - Vaccines, Synthetic -- therapeutic use KW - Gene Products, env -- therapeutic use KW - Gene Products, env -- toxicity KW - HIV Core Protein p24 -- toxicity KW - Protein Precursors -- toxicity KW - Protein Precursors -- immunology KW - HIV Infections -- immunology KW - HIV Infections -- therapy KW - Vaccines, Synthetic -- immunology KW - HIV Core Protein p24 -- therapeutic use KW - Immunotherapy, Active KW - Gene Products, env -- immunology KW - Protein Precursors -- therapeutic use KW - HIV Core Protein p24 -- immunology KW - AIDS Vaccines -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73410622?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Phase+I%2FII+studies+of+the+toxicity+and+immunogenicity+of+recombinant+gp160+and+p24+vaccines+in+HIV-infected+individuals.&rft.au=Zunich%2C+K+M%3BLane%2C+H+C%3BDavey%2C+R+T%3BFalloon%2C+J%3BPolis%2C+M%3BKovacs%2C+J+A%3BMasur%2C+H&rft.aulast=Zunich&rft.aufirst=K&rft.date=1992-08-01&rft.volume=8&rft.issue=8&rft.spage=1335&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 - 1993-01-28 N1 - Date created - 1993-01-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Humoral immune responses to homologous envelope peptides in vaccinees and lab workers infected with HIV. AN - 73399852; 1466954 JF - AIDS research and human retroviruses AU - Pincus, S H AU - Messer, K AD - NIAID, Rocky Mountain Laboratories, Hamilton, MT 59840. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 1347 VL - 8 IS - 8 SN - 0889-2229, 0889-2229 KW - AIDS Vaccines KW - 0 KW - Gene Products, env KW - HIV Antibodies KW - HIV Antigens KW - Peptide Fragments KW - Index Medicus KW - AIDS/HIV KW - Humans KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Gene Products, env -- chemistry KW - HIV -- immunology KW - HIV Antibodies -- immunology KW - HIV Infections -- immunology KW - Gene Products, env -- immunology KW - HIV Antigens -- chemistry KW - Laboratory Infection -- immunology KW - HIV Antigens -- immunology KW - Vaccination KW - Peptide Fragments -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73399852?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Humoral+immune+responses+to+homologous+envelope+peptides+in+vaccinees+and+lab+workers+infected+with+HIV.&rft.au=Pincus%2C+S+H%3BMesser%2C+K&rft.aulast=Pincus&rft.aufirst=S&rft.date=1992-08-01&rft.volume=8&rft.issue=8&rft.spage=1347&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 - 1993-01-28 N1 - Date created - 1993-01-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - HLA phenotype is a factor in determining rate of disease progression and outcome in HIV-1-infected individuals. AN - 73386616; 1361351 AB - HLA allele frequencies were examined for possible association(s) with the rate of disease progression and with the disease outcome (AIDS diagnosis) in a population of HIV-1-infected individuals. Certain alleles were associated with the relative rate of CD4+ T-cell decline. Association of particular alleles with several disease outcomes associated with infection was also observed. It is important to keep these two aspects (disease progression, AIDS diagnosis) separate when studying HLA in the HIV-1-infected population. Alleles that may play a role in the rate of virus speed by effecting the immune response may be different from those found to be associated with a particular disease. We feel that the only truly informative data, in this regard, can be generated from a relative precise determination of the time of infection (to study disease progression) and adequate numbers of individuals with specific diseases to study specific disease association. If such data can be generated we will have a much better understanding of the pathogenetic process(es) of HIV-1 infection. JF - AIDS research and human retroviruses AU - Mann, D L AU - Carrington, M AU - O'Donnell, M AU - Miller, T AU - Goedert, J AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick, MD 21702-1201. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 1345 EP - 1346 VL - 8 IS - 8 SN - 0889-2229, 0889-2229 KW - HLA Antigens KW - 0 KW - Index Medicus KW - AIDS/HIV KW - Phenotype KW - Alleles KW - Humans KW - Disease Susceptibility -- immunology KW - Genetic Predisposition to Disease KW - Male KW - Leukocyte Count KW - CD4-Positive T-Lymphocytes KW - HIV Infections -- immunology KW - HIV Infections -- genetics KW - HLA Antigens -- analysis KW - HIV-1 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73386616?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=HLA+phenotype+is+a+factor+in+determining+rate+of+disease+progression+and+outcome+in+HIV-1-infected+individuals.&rft.au=Mann%2C+D+L%3BCarrington%2C+M%3BO%27Donnell%2C+M%3BMiller%2C+T%3BGoedert%2C+J&rft.aulast=Mann&rft.aufirst=D&rft.date=1992-08-01&rft.volume=8&rft.issue=8&rft.spage=1345&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 - 1993-01-28 N1 - Date created - 1993-01-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Clues to cancer etiology from studies of farmers. AN - 73261434; 1411362 AB - This article summarizes cancer risks among farmers to clarify the magnitude of the problem and to suggest directions for future research. Significant excesses occurred for Hodgkin's disease, multiple myeloma, leukemia, skin melanomas, and cancers of the lip, stomach, and prostate. Nonsignificant increases in risk were also noted for non-Hodgkin's lymphoma and cancers of connective tissue and brain. These excesses occurred against a background of substantial deficits among farmers for total mortality and mortality from many specific diseases. The tumors vary in frequency, histology, and prognosis and do not fall into any obvious grouping. Two commonalities may be important. Several of the tumors excessive among farmers appear to be rising in the general population and are excessive among patients with naturally occurring or medically induced immunodeficiencies. Therefore epidemiologic studies on specific exposures among farmers may help explain the rising trend of certain cancers in developed countries and provide clues to mechanisms of action for environmental carcinogens. JF - Scandinavian journal of work, environment & health AU - Blair, A AU - Zahm, S H AU - Pearce, N E AU - Heineman, E F AU - Fraumeni, J F AD - Epidemiology and Biostatistics Program, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 209 EP - 215 VL - 18 IS - 4 SN - 0355-3140, 0355-3140 KW - Carcinogens, Environmental KW - 0 KW - Index Medicus KW - Risk KW - Carcinogens, Environmental -- adverse effects KW - Humans KW - Male KW - Female KW - Cause of Death KW - Occupational Exposure KW - Agricultural Workers' Diseases -- mortality KW - Neoplasms -- mortality KW - Agricultural Workers' Diseases -- etiology KW - Cross-Cultural Comparison KW - Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73261434?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Clues+to+cancer+etiology+from+studies+of+farmers.&rft.au=Blair%2C+A%3BZahm%2C+S+H%3BPearce%2C+N+E%3BHeineman%2C+E+F%3BFraumeni%2C+J+F&rft.aulast=Blair&rft.aufirst=A&rft.date=1992-08-01&rft.volume=18&rft.issue=4&rft.spage=209&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 - 1992-11-04 N1 - Date created - 1992-11-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modulation of thioacetamide-induced hepatocellular necrosis by prostaglandins is associated with novel histologic changes. AN - 73250900; 1406079 AB - Cytoprotective effects of the prostaglandins 16,16-dimethyl PGE2 (dmPGE2) and PGF2 alpha tromethamine (PGF2 alpha) were evaluated in the rat model of acute hepatocellular necrosis induced by thioacetamide (TAA). dmPGE2 (100 micrograms/kg SC 8 hourly) did not induce a significant increase in survival when started after the onset of TAA-induced fulminant hepatic failure. However, priming with dmPGE2 (100 micrograms/kg SC 30 min before TAA) reduced TAA-induced elevations in serum ALT (684 +/- 68 (SEM) vs 274 +/- 135 IU/1, p less than 0.01). This phenomenon did not occur if dmPGE2 was administered after TAA or by the IP route. Modulation of TAA-induced centrizonal hepatocellular necrosis by dmPGE2 was associated with a striking increase in centrizonal ballooning of hepatocytes (p less than 0.01), and, as assessed by stereology, less hepatocellular necrosis and degenerative changes. PGF2 alpha, which in contrast to dmPGE2 does not act via cAMP, had no effect on TAA-induced changes in serum ALT or hepatic histology. These findings suggest that dmPGE2 decreases hepatocellular necrosis by activating surface membrane adenylate cyclase and consequently stimulating cAMP. Ballooning of hepatocytes could occur secondary to these membrane events and appears to be a marker of dmPGE2-induced cytoprotection in this model. JF - Liver AU - Bergasa, N V AU - Borque, M J AU - Wahl, L M AU - Rabin, L AU - Jones, E A AD - Liver Diseases Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 168 EP - 174 VL - 12 IS - 4 Pt 1 SN - 0106-9543, 0106-9543 KW - Thioacetamide KW - 075T165X8M KW - Dinoprost KW - B7IN85G1HY KW - dinoprost tromethamine KW - CT6BBQ5A68 KW - Alanine Transaminase KW - EC 2.6.1.2 KW - 16,16-Dimethylprostaglandin E2 KW - M790V82VAC KW - Index Medicus KW - Rats KW - Animals KW - Rats, Sprague-Dawley KW - Necrosis KW - Alanine Transaminase -- blood KW - Male KW - Hepatic Encephalopathy -- drug therapy KW - Liver -- pathology KW - Liver -- drug effects KW - Dinoprost -- therapeutic use KW - Dinoprost -- analogs & derivatives KW - Hepatic Encephalopathy -- pathology KW - 16,16-Dimethylprostaglandin E2 -- therapeutic use KW - Hepatic Encephalopathy -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73250900?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Liver&rft.atitle=Modulation+of+thioacetamide-induced+hepatocellular+necrosis+by+prostaglandins+is+associated+with+novel+histologic+changes.&rft.au=Bergasa%2C+N+V%3BBorque%2C+M+J%3BWahl%2C+L+M%3BRabin%2C+L%3BJones%2C+E+A&rft.aulast=Bergasa&rft.aufirst=N&rft.date=1992-08-01&rft.volume=12&rft.issue=4+Pt+1&rft.spage=168&rft.isbn=&rft.btitle=&rft.title=Liver&rft.issn=01069543&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-11-13 N1 - Date created - 1992-11-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cerebrospinal fluid and serum levels of neuron-specific enolase in patients with schizophrenia. AN - 73250717; 1357702 AB - Some patients with schizophrenia appear to have brain abnormalities, including enlarged third and lateral ventricles and reduced volumes of temporal lobe structures. These abnormalities could be attributed to a developmental abnormality or a neurodegenerative process. Neuron-specific enolase (NSE), a protein that is found primarily in neurons and neuroendocrine cells, has been used as an index of neuronal damage or degeneration. Levels of NSE in cerebrospinal fluid (CSF) and serum from 50 patients with acute and chronic schizophrenia were compared with those in normal and neurological control subjects. A double-antibody, solid phase iodinated radioimmunoassay was used to determine NSE levels. There was no evidence of elevated levels in patients with schizophrenia, whereas control subjects with neurological illnesses had increased levels of NSE in CSF. Because NSE is rapidly cleared from CSF, however, elevated levels could have been missed. Unmedicated patients tended to have lower levels than medicated patients. JF - Psychiatry research AU - Egan, M F AU - el-Mallakh, R S AU - Suddath, R L AU - Lohr, J B AU - Bracha, H S AU - Wyatt, R J AD - Neuropsychiatry Branch, National Institute of Mental Health, Washington, DC. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 187 EP - 195 VL - 43 IS - 2 SN - 0165-1781, 0165-1781 KW - Antipsychotic Agents KW - 0 KW - Phosphopyruvate Hydratase KW - EC 4.2.1.11 KW - Index Medicus KW - Magnetic Resonance Imaging KW - Psychiatric Status Rating Scales KW - Humans KW - Brain -- pathology KW - Adult KW - Tomography, X-Ray Computed KW - Chronic Disease KW - Antipsychotic Agents -- adverse effects KW - Male KW - Female KW - Neurocognitive Disorders -- diagnosis KW - Neurocognitive Disorders -- cerebrospinal fluid KW - Neurocognitive Disorders -- psychology KW - Schizophrenia -- diagnosis KW - Blood-Brain Barrier -- physiology KW - Schizophrenic Psychology KW - Schizophrenia -- drug therapy KW - Neurocognitive Disorders -- drug therapy KW - Schizophrenia -- cerebrospinal fluid KW - Phosphopyruvate Hydratase -- cerebrospinal fluid UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73250717?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cerebrospinal+fluid+and+serum+levels+of+neuron-specific+enolase+in+patients+with+schizophrenia.&rft.au=Egan%2C+M+F%3Bel-Mallakh%2C+R+S%3BSuddath%2C+R+L%3BLohr%2C+J+B%3BBracha%2C+H+S%3BWyatt%2C+R+J&rft.aulast=Egan&rft.aufirst=M&rft.date=1992-08-01&rft.volume=43&rft.issue=2&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 - 1992-11-23 N1 - Date created - 1992-11-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutagenesis induced by bacterial UmuDC proteins and their plasmid homologues. AN - 73236097; 1406263 AB - The popular image of a world full of pollutants mutating DNA is only partly true since there are relatively few agents which can subtly and directly change base coding; for example, some alkylating agents alter guanine so that it pairs like adenine. Many more mutagens are less subtle and simply destroy coding altogether rather than changing it. Such mutagens include ultraviolet light, X-rays, DNA cross-linkers and other agents which make DNA breaks or large adducts. In Escherichia coli, mutagenesis by these agents occurs during a DNA repair process which increases cell survival but with an inherent possibility of changing the original sequence. Such mutagenic DNA repair is, in part, encoded by the E. coli umuDC operon. This article reviews the structure, function, regulation and evolution of the umuDC operon and similar genes found both in other species and on naturally occurring plasmids. JF - Molecular microbiology AU - Woodgate, R AU - Sedgwick, S G AD - Section on Viruses and Cellular Biology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 2213 EP - 2218 VL - 6 IS - 16 SN - 0950-382X, 0950-382X KW - umu KW - Bacterial Proteins KW - 0 KW - Escherichia coli Proteins KW - DNA-Directed DNA Polymerase KW - EC 2.7.7.7 KW - UmuD protein, E coli KW - Index Medicus KW - Phenotype KW - DNA Repair KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Bacterial Proteins -- genetics KW - Escherichia coli -- genetics KW - Plasmids KW - Mutagenesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73236097?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mutagenesis+induced+by+bacterial+UmuDC+proteins+and+their+plasmid+homologues.&rft.au=Woodgate%2C+R%3BSedgwick%2C+S+G&rft.aulast=Woodgate&rft.aufirst=R&rft.date=1992-08-01&rft.volume=6&rft.issue=16&rft.spage=2213&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 - 1992-10-29 N1 - Date created - 1992-10-29 N1 - Date revised - 2017-01-13 N1 - Gene symbol - umu N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - D2 or not D2? AN - 73207241; 1326905 JF - Alcoholism, clinical and experimental research AU - Karp, R W AD - Division of Basic Research, National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20857. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 786 EP - 787 VL - 16 IS - 4 SN - 0145-6008, 0145-6008 KW - Receptors, Dopamine KW - 0 KW - Receptors, Dopamine D2 KW - Index Medicus KW - Rats KW - Liver Cirrhosis, Alcoholic -- genetics KW - Animals KW - Liver Cirrhosis, Alcoholic -- physiopathology KW - Synaptic Transmission -- genetics KW - Risk Factors KW - Humans KW - Synaptic Transmission -- physiology KW - Receptors, Dopamine -- physiology KW - Alleles KW - Receptors, Dopamine -- genetics KW - Alcoholism -- physiopathology KW - Alcoholism -- genetics KW - Alcoholism -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73207241?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=D2+or+not+D2%3F&rft.au=Karp%2C+R+W&rft.aulast=Karp&rft.aufirst=R&rft.date=1992-08-01&rft.volume=16&rft.issue=4&rft.spage=786&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 - 1992-10-20 N1 - Date created - 1992-10-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Synergy of carbamazepine and valproic acid in affective illness: case report and review of the literature. AN - 73188824; 1527232 AB - Carbamazepine and valproic acid are anticonvulsants with mood-stabilizing properties. Basic and clinical research suggest that these medications used together may have synergistic anticonvulsant effects. Psychotropic synergy of the combination has yet to be explored systematically. We present the case of a patient with rapid-cycling bipolar disorder studied under double-blind conditions whose hypomanias and depressions were refractory to either carbamazepine or valproic acid alone, but responded dramatically to the combination. The superior response to the combination appeared to be due to pharmacodynamic rather than pharmacokinetic effects. The clinical and theoretical aspects of the use of carbamazepine and valproic acid in combination are discussed. JF - Journal of clinical psychopharmacology AU - Ketter, T A AU - Pazzaglia, P J AU - Post, R M AD - Biological Psychiatry Branch, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 276 EP - 281 VL - 12 IS - 4 SN - 0271-0749, 0271-0749 KW - Carbamazepine KW - 33CM23913M KW - Valproic Acid KW - 614OI1Z5WI KW - Index Medicus KW - Drug Therapy, Combination KW - Double-Blind Method KW - Humans KW - Middle Aged KW - Drug Synergism KW - Male KW - Bipolar Disorder -- drug therapy KW - Carbamazepine -- therapeutic use KW - Valproic Acid -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73188824?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Synergy+of+carbamazepine+and+valproic+acid+in+affective+illness%3A+case+report+and+review+of+the+literature.&rft.au=Ketter%2C+T+A%3BPazzaglia%2C+P+J%3BPost%2C+R+M&rft.aulast=Ketter&rft.aufirst=T&rft.date=1992-08-01&rft.volume=12&rft.issue=4&rft.spage=276&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 - 1992-10-22 N1 - Date created - 1992-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Variability in alkaloid profiles in neotropical poison frogs (Dendrobatidae): genetic versus environmental determinants. AN - 73187408; 1523680 AB - Dendrobatid frogs produce a diverse set of alkaloids, whose profiles appear characteristic of frogs of each species or, in the case of variable species, of each population. In the case of one widespread species, Dendrobates auratus, alkaloid profiles in extracts of skin are markedly different in three populations, one from a Pacific island, Isla Taboga, Panama, one from central mountains in Panama, and the third from the Caribbean coast in Costa Rica. The first contains three major classes of dendrobatid alkaloids, the histrionicotoxins, the pumiliotoxin-A class and the decahydroquinolines. The second contains mainly histrionicotoxins, pumiliotoxin-A class alkaloids and one indolizidine. The third contains histrionicotoxins, a homopumiliotoxin, one decahydroquinoline, and a variety of indolizidines, quinolizidines and pyrrolizidines. Frogs from Isla Taboga or a nearby island were introduced into the Manoa Valley, Oahu, Hawaii, in 1932. Remarkably, although alkaloids of the pumiliotoxin-A class and one decahydroquinoline are still major constituents in skin extracts of Hawaiian frogs descended from the 1932 founding population, histrionicotoxins are absent and a novel tricyclic alkaloid is present. Offspring of wild-caught parents from Hawaii, Panama or Costa Rica raised in indoor terrariums on a diet of crickets and fruit flies do not contain detectable amounts of skin alkaloids. Offspring raised in large outside terrariums in Hawaii and fed mainly wild-caught termites and fruit flies do contain the same profile of alkaloids as their wild-caught parents in Hawaii, but at reduced levels. The genetic, environmental and dietary determinants of alkaloid profiles in dendrobatid frogs remain obscure, in particular the underlying cause for total absence in terrarium-reared frogs. JF - Toxicon : official journal of the International Society on Toxinology AU - Daly, J W AU - Secunda, S I AU - Garraffo, H M AU - Spande, T F AU - Wisnieski, A AU - Nishihira, C AU - Cover, J F AD - Laboratory of Bioorganic Chemistry, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 887 EP - 898 VL - 30 IS - 8 SN - 0041-0101, 0041-0101 KW - Alkaloids KW - 0 KW - Poisons KW - Index Medicus KW - Panama KW - Ecology KW - Skin -- chemistry KW - Animals KW - Costa Rica KW - Hawaii KW - Diet KW - Ranidae -- metabolism KW - Alkaloids -- chemistry KW - Poisons -- chemistry KW - Genetics, Population KW - Alkaloids -- isolation & purification KW - Poisons -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73187408?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicon+%3A+official+journal+of+the+International+Society+on+Toxinology&rft.atitle=Variability+in+alkaloid+profiles+in+neotropical+poison+frogs+%28Dendrobatidae%29%3A+genetic+versus+environmental+determinants.&rft.au=Daly%2C+J+W%3BSecunda%2C+S+I%3BGarraffo%2C+H+M%3BSpande%2C+T+F%3BWisnieski%2C+A%3BNishihira%2C+C%3BCover%2C+J+F&rft.aulast=Daly&rft.aufirst=J&rft.date=1992-08-01&rft.volume=30&rft.issue=8&rft.spage=887&rft.isbn=&rft.btitle=&rft.title=Toxicon+%3A+official+journal+of+the+International+Society+on+Toxinology&rft.issn=00410101&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-09 N1 - Date created - 1992-10-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Angiotensin AT2 receptors regulate cerebral blood flow in rats. AN - 73171003; 1520859 AB - LARGE cerebral arteries have been reported to contain angiotensin receptors that are exclusively of the AT2 subtype. We measured the effect of the AT2 receptor selective ligand PD 123319 on cerebral blood flow (CBF) in rats, using laser-doppler flowmetry. PD 123319 (1-10 mg kg-1) dose-dependently inhibited the increase in CBF, when the blood pressure was increased by a norepinephrine infusion. However, PD 123319 did not alter baseline CBF at normal blood pressures. Therefore PD 123319 appears to interfere with the autoregulatory mechanisms of CBF. The participation of AT2 receptors in the regulation of CBF confirms a physiological role for this receptor subtype, and may give clues for future treatment of various cerebrovascular disorders. JF - Neuroreport AU - Strömberg, C AU - Näveri, L AU - Saavedra, J M AD - Section on Pharmacology, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 703 EP - 704 VL - 3 IS - 8 SN - 0959-4965, 0959-4965 KW - Angiotensin Receptor Antagonists KW - 0 KW - Imidazoles KW - Pyridines KW - Receptors, Angiotensin KW - Angiotensin II KW - 11128-99-7 KW - PD 123319 KW - 130663-39-7 KW - Sodium Chloride KW - 451W47IQ8X KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Hypertension -- chemically induced KW - Imidazoles -- pharmacology KW - Hypertension -- physiopathology KW - Dose-Response Relationship, Drug KW - Hypertension -- prevention & control KW - Pyridines -- pharmacology KW - Male KW - Angiotensin II -- metabolism KW - Receptors, Angiotensin -- physiology KW - Norepinephrine -- pharmacology KW - Cerebrovascular Circulation -- physiology KW - Cerebrovascular Circulation -- drug effects KW - Blood Pressure -- drug effects KW - Angiotensin II -- pharmacology KW - Receptors, Angiotensin -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73171003?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroreport&rft.atitle=Angiotensin+AT2+receptors+regulate+cerebral+blood+flow+in+rats.&rft.au=Str%C3%B6mberg%2C+C%3BN%C3%A4veri%2C+L%3BSaavedra%2C+J+M&rft.aulast=Str%C3%B6mberg&rft.aufirst=C&rft.date=1992-08-01&rft.volume=3&rft.issue=8&rft.spage=703&rft.isbn=&rft.btitle=&rft.title=Neuroreport&rft.issn=09594965&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-15 N1 - Date created - 1992-10-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - An examination of the association between maximum-tolerated dose and carcinogenicity in 326 long-term studies in rats and mice. AN - 73153376; 1516777 AB - The association between rodent carcinogenicity and maximum-tolerated dose (MTD) was evaluated in 326 long-term carcinogenicity studies in mice and rats. Others investigating this association have focused primarily on positive studies, but our investigation considered all experimental outcomes. We found that chemicals with low MTDs were somewhat more likely to be rodent carcinogens than chemicals with high MTDs, but this association was limited primarily to gavage studies. Overall, the MTD was not a reliable predictor of whether or not a chemical would be a rodent carcinogen. Our investigation confirms that comparisons of carcinogenic potencies based only on positive studies may result in artifactually elevated estimates of the underlying association between chemical toxicity and rodent carcinogenicity and thus may also inflate the estimated interspecies correlation in carcinogenic response. Nevertheless, the results of our study are consistent with the frequently cited 75% concordance in carcinogenicity outcome between rats and mice. This concordance is quite high, particularly since 80% is approximately the maximum level of observable interspecies concordance achievable for a set of chemicals with relatively low carcinogenic potency, because of the variability in observed tumor responses that can induce false negative or false positive outcomes in either of the two species. Thus, the underlying qualitative interspecies correlation in carcinogenic response between rats and mice may be greater than is commonly recognized. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Haseman, J K AU - Seilkop, S K AD - Division of Biometry and Risk Assessment, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 207 EP - 213 VL - 19 IS - 2 SN - 0272-0590, 0272-0590 KW - Carcinogens KW - 0 KW - Index Medicus KW - Rats KW - Animals KW - Dose-Response Relationship, Drug KW - Carcinogenicity Tests KW - Mice KW - Species Specificity KW - Male KW - Female KW - Carcinogens -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73153376?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=An+examination+of+the+association+between+maximum-tolerated+dose+and+carcinogenicity+in+326+long-term+studies+in+rats+and+mice.&rft.au=Haseman%2C+J+K%3BSeilkop%2C+S+K&rft.aulast=Haseman&rft.aufirst=J&rft.date=1992-08-01&rft.volume=19&rft.issue=2&rft.spage=207&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 - 1992-10-02 N1 - Date created - 1992-10-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - N-methyl-D-aspartate exposure blocks glutamate toxicity in cultured cerebellar granule cells. AN - 73146442; 1355259 AB - Exposure of cultured cerebellar granule cells to glutamate results in a concentration-dependent (EC50 = 22.7 +/- 0.4 microM) and delayed (24-72 hr) neurotoxicity, which is blocked by the specific N-methyl-D-aspartate (NMDA) receptor antagonists 2-amino-5-phosphovalerate and MK-801 but is unaffected by the non-NMDA receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione and 6,7-dinitroquinoxaline-2,3-dione. Although glutamate toxicity in these cells is mediated by the NMDA subtype of glutamate receptor, pretreatment of cerebellar granule cells with subtoxic concentrations of NMDA markedly antagonizes the neurotoxic actions of glutamate, with an IC50 of 55 +/- 4 microM. The neuroprotective effect of NMDA requires a preincubation time of approximately 120 min to be fully manifested and does not require the presence of NMDA during glutamate exposure. These data demonstrate that NMDA receptors mediate both neurotoxicity and neuroprotection in cerebellar granule cells. Among four glutamate receptor agonists tested (NMDA, quisqualate, ibotenate, and kainate), only NMDA was able to provide a robust neuroprotection against glutamate toxicity. Quisqualate was neither neurotoxic nor neuroprotective, whereas ibotenate, which was nontoxic by itself, induced a small degree of neuroprotection. In contrast, kainate, which was neurotoxic to cerebellar granule cells, also provided considerable neuroprotection against glutamate toxicity. Because preincubation of cerebellar granule cells with NMDA fails to alter NMDA receptor-mediated phosphoinositide hydrolysis or the specific binding of [3H]MK-801 to NMDA receptors, it appears that the neuroprotective effects of NMDA are not due to NMDA receptor desensitization. JF - Molecular pharmacology AU - Chuang, D M AU - Gao, X M AU - Paul, S M AD - Section on Molecular Neurobiology, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 210 EP - 216 VL - 42 IS - 2 SN - 0026-895X, 0026-895X KW - Culture Media KW - 0 KW - Excitatory Amino Acid Antagonists KW - Glutamates KW - Receptors, Glutamate KW - Receptors, N-Methyl-D-Aspartate KW - Receptors, Neurotransmitter KW - Tritium KW - 10028-17-8 KW - Ibotenic Acid KW - 2552-55-8 KW - Aspartic Acid KW - 30KYC7MIAI KW - Glutamic Acid KW - 3KX376GY7L KW - Ouabain KW - 5ACL011P69 KW - N-Methylaspartate KW - 6384-92-5 KW - Quisqualic Acid KW - 8OC22C1B99 KW - Magnesium KW - I38ZP9992A KW - Glucose KW - IY9XDZ35W2 KW - Kainic Acid KW - SIV03811UC KW - Index Medicus KW - Sensitivity and Specificity KW - Animals KW - Neurons -- drug effects KW - Receptors, Neurotransmitter -- drug effects KW - Cytoplasmic Granules -- metabolism KW - Ibotenic Acid -- pharmacology KW - Aspartic Acid -- pharmacokinetics KW - Rats KW - Receptors, Neurotransmitter -- physiology KW - Receptors, N-Methyl-D-Aspartate -- physiology KW - Receptors, N-Methyl-D-Aspartate -- drug effects KW - Magnesium -- pharmacology KW - Cytoplasmic Granules -- drug effects KW - Ouabain -- metabolism KW - Kainic Acid -- pharmacology KW - Neurons -- metabolism KW - Quisqualic Acid -- pharmacology KW - Rats, Inbred Strains KW - Glucose -- pharmacology KW - Cells, Cultured KW - Cerebellum -- cytology KW - N-Methylaspartate -- pharmacology KW - Glutamates -- metabolism KW - Cerebellum -- drug effects KW - Glutamates -- toxicity KW - Cerebellum -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73146442?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=N-methyl-D-aspartate+exposure+blocks+glutamate+toxicity+in+cultured+cerebellar+granule+cells.&rft.au=Chuang%2C+D+M%3BGao%2C+X+M%3BPaul%2C+S+M&rft.aulast=Chuang&rft.aufirst=D&rft.date=1992-08-01&rft.volume=42&rft.issue=2&rft.spage=210&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 - 1992-09-30 N1 - Date created - 1992-09-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Early onset of drinking as a risk factor for lifetime alcohol-related problems. AN - 73144518; 1511233 AB - Heavy drinking among students has been a major public health concern over the past decade. A nationally representative 1988 survey on drinking practices and related problems examined the effect of age of of onset of drinking on lifetime alcohol-related problems. Prevalence estimates were obtained for major demographic subgroups of the population. Results and implications are discussed in the context of minimum legal drinking age. JF - British journal of addiction AU - Chou, S P AU - Pickering, R P AD - National Institute on Alcohol Abuse and Alcoholism, Division of Biometry and Epidemiology, Rockville, MD 20857. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 1199 EP - 1204 VL - 87 IS - 8 SN - 0952-0481, 0952-0481 KW - Index Medicus KW - Cross-Sectional Studies KW - Risk 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 - Alcohol Drinking -- psychology KW - Personality Development KW - Alcohol Drinking -- epidemiology KW - Alcoholism -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73144518?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+addiction&rft.atitle=Early+onset+of+drinking+as+a+risk+factor+for+lifetime+alcohol-related+problems.&rft.au=Chou%2C+S+P%3BPickering%2C+R+P&rft.aulast=Chou&rft.aufirst=S&rft.date=1992-08-01&rft.volume=87&rft.issue=8&rft.spage=1199&rft.isbn=&rft.btitle=&rft.title=British+journal+of+addiction&rft.issn=09520481&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-01 N1 - Date created - 1992-10-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Enhanced hydroxyl radical generation by 2'-methyl analog of MPTP: suppression by clorgyline and deprenyl. AN - 73138445; 1323883 AB - Sodium salicylate was infused through a microdialysis probe placed in the striatum of anesthetized rats in order to assay the formation of hydroxyl radical (.OH) in the extracellular fluid in vivo. In addition to causing sustained dopamine release, intrastriatal infusion of the 2'-methyl analog of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (2'CH3-MPTP) increased the formation of 2,3-dihydroxybenzoic acid (2,3-DHBA), the nonenzymatic .OH adduct of salicylate in the brain dialysate. Inhibition of monoamine oxidase (MAO) by clorgyline and deprenyl completely blocked the formation of 2,3-DHBA and the sustained dopamine overflow induced by 2'-CH3-MPTP. The results indicate that the enhanced formation of cytotoxic .OH by 2'-CH3-MPTP is suppressed by MAO inhibitors. These data support the hypothesis that the protective effect of MAO inhibitors on the neurotoxicity induced by MPTP analogues may be due not only to the inhibition of MPTP metabolism by MAO but also the blockade of the formation of .OH free radicals. An enhanced generation of cytotoxic .OH free radicals in the striatum which in turn leads to oxidant damage may be relevant to the development of parkinsonism-like changes in animals produced by MPTP analogues. JF - Synapse (New York, N.Y.) AU - Chiueh, C C AU - Huang, S J AU - Murphy, D L AD - Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 346 EP - 348 VL - 11 IS - 4 SN - 0887-4476, 0887-4476 KW - Free Radicals KW - 0 KW - Hydroxides KW - 1-methyl-4-(2'-methylphenyl)-1,2,3,6-tetrahydropyridine KW - 102417-86-7 KW - Selegiline KW - 2K1V7GP655 KW - Hydroxyl Radical KW - 3352-57-6 KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Clorgyline KW - LYJ16FZU9Q KW - Index Medicus KW - Rats KW - Animals KW - Dialysis KW - Selegiline -- pharmacology KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- analogs & derivatives KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- metabolism KW - Clorgyline -- pharmacology KW - Hydroxides -- metabolism KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- antagonists & inhibitors KW - Hydroxides -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73138445?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Enhanced+hydroxyl+radical+generation+by+2%27-methyl+analog+of+MPTP%3A+suppression+by+clorgyline+and+deprenyl.&rft.au=Chiueh%2C+C+C%3BHuang%2C+S+J%3BMurphy%2C+D+L&rft.aulast=Chiueh&rft.aufirst=C&rft.date=1992-08-01&rft.volume=11&rft.issue=4&rft.spage=346&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 - 1992-09-14 N1 - Date created - 1992-09-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Development of renal toxicity in F344 rats gavaged with mercuric chloride for 2 weeks, or 2, 4, 6, 15, and 24 months. AN - 73127496; 1354752 AB - Both sexes of F344 rats were gavaged with maximal tolerated doses of mercuric chloride for periods from 2 wk to up to 2 yr to investigate chronic nephrotoxicity and potential carcinogenicity. The toxicity of mercuric chloride was excessive after 2 wk of exposure to doses ranging from 1.25 to 20 mg/kg, compromising renal function by selectively destroying cells of the proximal tubules, and eliciting marked elevations in urinary biomarker enzymes diagnostic for acute renal tubule necrosis. In the 2-wk studies, urinary alkaline phosphatase and aspartate amino-transferase were most sensitive to renal mercury toxicity among a panel of six enzymes, exhibiting twofold increases above controls at the 5.0 mg/kg dose, before changes in the other enzymes occurred. Urinary lactate dehydrogenase was the most responsive enzyme, with up to 11-fold increases in activity above controls. In response to mercuric chloride exposure of 5.0 mg/kg for 2-6 mo, the greatest and most persistent increases in elevation of urinary enzyme activities were exhibited by alkaline phosphatase and gamma-glutamyl transferase, which increased two-to threefold above controls. At this interval, the maximal severity of the renal lesions in both sexes of rats was graded as minimal to mild. Beyond 6 mo none of the urinary enzymes measured in this study was adequate as biomarkers of nephrotoxicity, although the severity of the renal lesions had progressed. Mercury accumulated in a dose-related fashion primarily in the kidney, and to a lesser extent in the liver. The severity of the renal lesions was increased by continued exposure to mercuric chloride, as tissue concentrations of mercury rose in proportion to dose. Mercuric chloride treatment for 2 yr clearly exacerbated the severity of the spontaneous nephrotoxicity prevalent in aging F344 rats. The excessive mortality that occurred in the male rats was probably due to a combination of these factors. No renal tumors were detected in rats, possibly because the potential for their development was reduced; however, direct tissue contact with mercury induced squamous-cell papillomas of the forestomach in both sexes. JF - Journal of toxicology and environmental health AU - Dieter, M P AU - Boorman, G A AU - Jameson, C W AU - Eustis, S L AU - Uraih, L C AD - National Institutes of Health, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 319 EP - 340 VL - 36 IS - 4 SN - 0098-4108, 0098-4108 KW - Mercuric Chloride KW - 53GH7MZT1R KW - gamma-Glutamyltransferase KW - EC 2.3.2.2 KW - Aspartate Aminotransferases KW - EC 2.6.1.1 KW - Alkaline Phosphatase KW - EC 3.1.3.1 KW - Acid Phosphatase KW - EC 3.1.3.2 KW - Leucyl Aminopeptidase KW - EC 3.4.11.1 KW - Mercury KW - FXS1BY2PGL KW - Index Medicus KW - Aspartate Aminotransferases -- urine KW - Animals KW - Alkaline Phosphatase -- urine KW - Dose-Response Relationship, Drug KW - Brain Chemistry KW - Mercury -- analysis KW - Kidney -- drug effects KW - Tissue Distribution KW - Kidney -- chemistry KW - Liver -- chemistry KW - Drug Administration Routes KW - Acid Phosphatase -- urine KW - Rats KW - Rats, Inbred F344 KW - Leucyl Aminopeptidase -- urine KW - Body Weight -- drug effects KW - Hyperparathyroidism -- chemically induced KW - Time Factors KW - gamma-Glutamyltransferase -- urine KW - Male KW - Female KW - Organ Size -- drug effects KW - Kidney -- anatomy & histology KW - Mercuric Chloride -- pharmacokinetics KW - Kidney Diseases -- metabolism KW - Kidney Diseases -- enzymology KW - Mercuric Chloride -- toxicity KW - Kidney Diseases -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73127496?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Development+of+renal+toxicity+in+F344+rats+gavaged+with+mercuric+chloride+for+2+weeks%2C+or+2%2C+4%2C+6%2C+15%2C+and+24+months.&rft.au=Dieter%2C+M+P%3BBoorman%2C+G+A%3BJameson%2C+C+W%3BEustis%2C+S+L%3BUraih%2C+L+C&rft.aulast=Dieter&rft.aufirst=M&rft.date=1992-08-01&rft.volume=36&rft.issue=4&rft.spage=319&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 - 1992-09-22 N1 - Date created - 1992-09-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Structure, expression, and regulation of the major noncollagenous matrix proteins of bone. AN - 73113156; 1499220 AB - The noncollagenous proteins (NCPs) that predominate the bone matrix have recently been the focus of intense investigation because of their potential influence on cell attachment, Ca2+ and hydroxyapatite binding, and the mineralization of bone tissue. With the advent of molecular biology, all of the major NCPs of bone have been cloned and their amino acid sequences completely determined. While each of the proteins has distinct structural properties, some proteins appear to be part of gene families. Examples include the small proteoglycans, decorin and biglycan, as well as the gamma carboxyglutamic acid proteins, such as matrix gla protein and osteocalcin (bone gla protein). Some of the NCPs that are clearly not members of any known gene family still share several common characteristics. One such example of this "convergent evolution" is bone sialoprotein and osteopontin. Both are highly posttranslationally modified glycoproteins that share the cell attachment amino acid sequence RGD (arginine-glycine-aspartic acid), which facilitates the attachment of bone cells in vitro, yet they are clearly not related genetically. Using cDNAs and antisera as probes, the precise temporal localization of NCP expression has been determined, and it has been shown that NCPs are produced in skeletal, and in most cases, nonskeletal tissue as well. This observation implies that the functions of the NCPs are not necessarily limited to bone tissue. Many of the promoters for these genes have been isolated and functional domains determined by a combination of chloramphenicol acetyltransferase assay, gel shift, and footprint analyses. The most extensively studied promoter in the NCP category is osteocalcin, whose sensitivity to 1,25-dihydroxycholecalciferol has been delineated in detail. Future studies on the individual and cooperative activities of the NCPs in bone are likely to involve site-directed mutagenesis of cloned DNA and a combination of in vitro and in vivo functional analyses. JF - Clinical orthopaedics and related research AU - Young, M F AU - Kerr, J M AU - Ibaraki, K AU - Heegaard, A M AU - Robey, P G AD - Bone Research Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 275 EP - 294 IS - 281 SN - 0009-921X, 0009-921X KW - BGN protein, human KW - 0 KW - Biglycan KW - Calcium-Binding Proteins KW - DCN protein, human KW - Decorin KW - Extracellular Matrix Proteins KW - Glycoproteins KW - IBSP protein, human KW - Integrin-Binding Sialoprotein KW - Osteonectin KW - Phosphoproteins KW - Platelet Membrane Glycoproteins KW - Proteins KW - Proteoglycans KW - SPP1 protein, human KW - Sialoglycoproteins KW - Thrombospondins KW - bone acidic glycoprotein-75, human KW - matrix Gla protein KW - Osteocalcin KW - 104982-03-8 KW - Osteopontin KW - 106441-73-0 KW - Abridged Index Medicus KW - Index Medicus KW - Space life sciences KW - Phosphoproteins -- genetics KW - Sialoglycoproteins -- genetics KW - Humans KW - Phosphoproteins -- physiology KW - Proteoglycans -- physiology KW - Platelet Membrane Glycoproteins -- genetics KW - Osteocalcin -- physiology KW - Glycoproteins -- genetics KW - Sialoglycoproteins -- physiology KW - Platelet Membrane Glycoproteins -- physiology KW - Proteoglycans -- genetics KW - Osteocalcin -- genetics KW - Genetic Techniques KW - Osteonectin -- genetics KW - Calcium-Binding Proteins -- physiology KW - Calcium-Binding Proteins -- genetics KW - Osteonectin -- physiology KW - Glycoproteins -- physiology KW - Proteins -- chemistry KW - Gene Expression KW - Proteins -- genetics KW - Proteins -- physiology KW - Bone Matrix -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73113156?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+orthopaedics+and+related+research&rft.atitle=Structure%2C+expression%2C+and+regulation+of+the+major+noncollagenous+matrix+proteins+of+bone.&rft.au=Young%2C+M+F%3BKerr%2C+J+M%3BIbaraki%2C+K%3BHeegaard%2C+A+M%3BRobey%2C+P+G&rft.aulast=Young&rft.aufirst=M&rft.date=1992-08-01&rft.volume=&rft.issue=281&rft.spage=275&rft.isbn=&rft.btitle=&rft.title=Clinical+orthopaedics+and+related+research&rft.issn=0009921X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-14 N1 - Date created - 1992-09-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Classical conditioning and protein kinase C activation regulate the same single potassium channel in Hermissenda crassicornis photoreceptors. AN - 73112041; 1496012 AB - The patch-clamp technique was used to study the effects of classical conditioning and protein kinase C (PKC) activation on K+ channels of identified neurons in the snail Hermissenda crassicornis. Here we present evidence that classical conditioning and PKC activation similarly modify the same K+ channel. K+ channels were recorded in cells from animals with different training experience. The 64-pS K+ channel appeared with significantly lower frequency in the conditioned group compared to the frequencies in control animals (naive and unpaired). In addition, when present, the 64-pS channel exhibited a lower percentage of open time and an increased interval between opening bursts in cells from conditioned animals. The 42-pS K+ channel was observed with about the same frequency in all three groups, and its percentage of open time was invariant, regardless of the animal's experience. Incubation of the photoreceptor with the PKC activator phorbol 12,13-dibutyrate (PDBu) led to a profound decrease in the percentage of open time of the 64-pS K+ channel, from 35.7% in the control group to 2.5% in the PDBu-treated group. The inactive phorbol 4 alpha-phorbol 12-myristate 13-acetate had no effect. The use of the PKC inhibitor H-7 significantly blocked the phorbol effect. Inside-out patches obtained from phorbol preincubated cells likewise showed the same effect of PDBu on K+ channels, but the effect was not observed when phorbol was added after the cell-free patches were obtained from nontreated cells. By contrast, the percentage of open time of the 42-pS K+ channel remained unchanged after phorbol treatment. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Etcheberrigaray, R AU - Matzel, L D AU - Lederhendler, I I AU - Alkon, D L AD - Neural Systems Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/08/01/ PY - 1992 DA - 1992 Aug 01 SP - 7184 EP - 7188 VL - 89 IS - 15 SN - 0027-8424, 0027-8424 KW - Isoquinolines KW - 0 KW - Piperazines KW - Potassium Channels KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine KW - 84477-87-2 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Isoquinolines -- pharmacology KW - Animals KW - Enzyme Activation KW - In Vitro Techniques KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Membrane Potentials -- drug effects KW - Piperazines -- pharmacology KW - Phorbol 12,13-Dibutyrate -- pharmacology KW - Protein Kinase C -- metabolism KW - Protein Kinase C -- antagonists & inhibitors KW - Conditioning, Classical -- physiology KW - Snails -- physiology KW - Potassium Channels -- physiology KW - Photoreceptor Cells -- physiology KW - Potassium Channels -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73112041?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Classical+conditioning+and+protein+kinase+C+activation+regulate+the+same+single+potassium+channel+in+Hermissenda+crassicornis+photoreceptors.&rft.au=Etcheberrigaray%2C+R%3BMatzel%2C+L+D%3BLederhendler%2C+I+I%3BAlkon%2C+D+L&rft.aulast=Etcheberrigaray&rft.aufirst=R&rft.date=1992-08-01&rft.volume=89&rft.issue=15&rft.spage=7184&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 - 1992-09-04 N1 - Date created - 1992-09-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: FEBS Lett. 1990 Jul 2;267(1):25-8 [1694792] Science. 1982 Feb 5;215(4533):693-5 [7058334] J Neurophysiol. 1991 Apr;65(4):796-807 [2051204] Behav Neural Biol. 1990 Sep;54(2):131-45 [2241759] Biochem Biophys Res Commun. 1986 Feb 13;134(3):1215-22 [2418836] Neurosci Lett. 1987 Jul 9;78(1):101-6 [2441331] Biochim Biophys Acta. 1988 Sep 1;943(3):419-27 [2458133] J Neurosci. 1988 Nov;8(11):4069-78 [2846795] Proc Natl Acad Sci U S A. 1985 Apr;82(8):2538-42 [3157991] Science. 1984 Nov 30;226(4678):1037-45 [6093258] Pflugers Arch. 1981 Aug;391(2):85-100 [6270629] FEBS Lett. 1991 Feb 25;279(2):256-60 [1900473] J Exp Biol. 1991 Mar;156:619-23 [2051138] J Neurosci. 1990 May;10(5):1699-706 [2159060] J Neurosci. 1990 Jul;10(7):2300-7 [2376776] Nature. 1986 Jan 16-22;319(6050):220-3 [2418358] Science. 1987 Jan 16;235(4786):345-8 [2432663] J Neurochem. 1988 Sep;51(3):903-17 [2457656] J Neurophysiol. 1989 May;61(5):971-81 [2542473] Behav Brain Res. 1989 Oct 1;35(1):75-80 [2803546] Biophys J. 1988 Nov;54(5):955-60 [2853980] J Neurosci. 1986 May;6(5):1325-31 [3711982] Behav Neural Biol. 1985 Sep;44(2):278-300 [4062781] J Exp Biol. 1984 Sep;112:95-112 [6150967] Erratum In: Proc Natl Acad Sci U S A 1992 Nov 15;89(22):11107 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Monoclonal antibody C242-Pseudomonas exotoxin A. A specific and potent immunotoxin with antitumor activity on a human colon cancer xenograft in nude mice. AN - 73110894; 1644913 AB - Two immunotoxins were constructed by chemically coupling the monoclonal antibody C242 to Pseudomonas exotoxin A (PE) or a modified form, NlysPE40, that lacks the cell binding domain of PE. Monoclonal antibody C242 recognizes a specific sialylated carbohydrate epitope on a high molecular weight membrane glycoprotein present on cells of human colon, pancreatic, and cervical cancers. C242-PE and C242-NlysPE40 were very cytotoxic for cells expressing this antigen with 50% inhibition of protein synthesis occurring on Colo205 cells at 0.2 ng/ml (0.9 pM) for C242-PE and 6.0 ng/ml (31 pM) for C242-NlysPE40. The two immunotoxins also exhibited a strong antitumor effect on a human colon cancer xenograft grown in nude mice. The specificity and potency of these two C242 immunotoxins warrant their further development for the treatment of cancer. JF - The Journal of clinical investigation AU - Debinski, W AU - Karlsson, B AU - Lindholm, L AU - Siegall, C B AU - Willingham, M C AU - FitzGerald, D AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 405 EP - 411 VL - 90 IS - 2 SN - 0021-9738, 0021-9738 KW - Antibodies, Monoclonal KW - 0 KW - Antibodies, Neoplasm KW - Antigens, Tumor-Associated, Carbohydrate KW - Bacterial Toxins KW - Exotoxins KW - Immunotoxins KW - Neoplasm Proteins KW - Oligodeoxyribonucleotides 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 - Animals KW - Neoplasm Proteins -- biosynthesis KW - Humans KW - Immunotherapy KW - Adenocarcinoma -- therapy KW - Amino Acid Sequence KW - Mice KW - Mice, Nude KW - Antibody Affinity KW - Neoplasm Transplantation KW - Base Sequence KW - Tumor Cells, Cultured KW - Oligodeoxyribonucleotides -- chemistry KW - In Vitro Techniques KW - Molecular Sequence Data KW - Transplantation, Heterologous KW - Immunotoxins -- chemistry KW - Exotoxins -- administration & dosage KW - Colonic Neoplasms -- therapy KW - Antigens, Tumor-Associated, Carbohydrate -- immunology KW - Exotoxins -- toxicity KW - Antibodies, Neoplasm -- administration & dosage KW - Antibodies, Monoclonal -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73110894?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Monoclonal+antibody+C242-Pseudomonas+exotoxin+A.+A+specific+and+potent+immunotoxin+with+antitumor+activity+on+a+human+colon+cancer+xenograft+in+nude+mice.&rft.au=Debinski%2C+W%3BKarlsson%2C+B%3BLindholm%2C+L%3BSiegall%2C+C+B%3BWillingham%2C+M+C%3BFitzGerald%2C+D%3BPastan%2C+I&rft.aulast=Debinski&rft.aufirst=W&rft.date=1992-08-01&rft.volume=90&rft.issue=2&rft.spage=405&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 - 1992-09-09 N1 - Date created - 1992-09-09 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Br J Cancer. 1989 Dec;60(6):845-51 [2557879] Biochemistry. 1973 Aug 14;12(17):3266-73 [4581787] Proc Natl Acad Sci U S A. 1991 Apr 15;88(8):3358-62 [2014255] Cancer Res. 1991 Mar 1;51(5):1529-36 [1997194] Cancer Res. 1990 Dec 15;50(24):7750-3 [2253218] J Biol Chem. 1989 Aug 25;264(24):14256-61 [2503515] Proc Natl Acad Sci U S A. 1986 Mar;83(5):1320-4 [3006045] Peptides. 1986 Mar-Apr;7(2):241-6 [2942845] J Biol Chem. 1988 Jul 5;263(19):9470-5 [3132465] Cell. 1987 Jan 16;48(1):129-36 [3098436] Proc Natl Acad Sci U S A. 1989 Nov;86(21):8545-9 [2510169] J Biol Chem. 1989 Sep 15;264(26):15157-60 [2504717] Cancer Res. 1989 Jul 1;49(13):3562-7 [2499420] Proc Natl Acad Sci U S A. 1988 May;85(9):2939-43 [3283735] Science. 1987 Nov 20;238(4830):1098-104 [3317828] Acta Pathol Microbiol Immunol Scand A. 1987 Jul;95(4):177-83 [3303832] Cell. 1986 Dec 5;47(5):641-8 [3536124] J Immunol Methods. 1984 Aug 3;72(1):77-89 [6086763] Proc Natl Acad Sci U S A. 1978 Jul;75(7):3405-9 [80012] Eur J Biochem. 1979 Nov;101(2):395-9 [574817] Arch Biochem Biophys. 1959 May;82(1):70-7 [13650640] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of a tyrosine kinase activity associated with the high-affinity interleukin 2 receptor complex. AN - 73110564; 1497623 AB - The IL-2 receptor complex is minimally composed of two genetically unrelated subunits of relative molecular masses 55 and 75 kDa respectively. Structural information deduced from the cDNA sequences of either subunit have not revealed significant information as to the basis of the mechanisms of IL-2 receptor signal transduction. Nevertheless, IL-2 stimulates the activation of one or more tyrosine kinases requiring the functional participation of the p75 member of the receptor complex. Here we have developed the methods to isolate the receptor complex with an associated tyrosine protein kinase. Extracts of membrane glycoproteins from activated normal human T lymphocytes and cell lines demonstrated catalytic activation of tyrosine kinase activity when stimulated with IL-2. Purification of the receptor complex with biotinylated IL-2 revealed the presence of two dominant phosphotyrosyl-proteins of approximate molecular masses 58 and 97 kDa. Denaturation gel electrophoresis followed by renaturation of proteins associated with the IL-2 receptor complex demonstrated that the 97 kDa protein had catalytic autophosphorylation activity. The results indicate that the 58 and 97 kDa phosphotyrosyl-proteins can be found to co-precipitate with the IL-2 receptor complex and that the 97 kDa protein was demonstrated to have protein kinase activity. The association of such kinases with receptors devoid of catalytic structure may represent a unique paradigm of growth-factor receptor mechanisms. JF - The Biochemical journal AU - Garcia, G G AU - Evans, G A AU - Michiel, D F AU - Farrar, W L AD - Biological Carcinogenesis and Development Program, NCI-Frederick Cancer Research and Development Center, MD 21702-1201. Y1 - 1992/08/01/ PY - 1992 DA - 1992 Aug 01 SP - 851 EP - 856 VL - 285 ( Pt 3) SN - 0264-6021, 0264-6021 KW - Interleukin-2 KW - 0 KW - Phosphoproteins KW - Receptors, Interleukin-2 KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Index Medicus KW - Interleukin-2 -- pharmacology KW - Phosphorylation KW - Enzyme Activation KW - Humans KW - Phosphoproteins -- analysis KW - Electrophoresis, Gel, Two-Dimensional KW - Chemical Precipitation KW - T-Lymphocytes -- enzymology KW - Molecular Weight KW - Cell Line KW - Phosphoproteins -- metabolism KW - Receptors, Interleukin-2 -- metabolism KW - Receptors, Interleukin-2 -- isolation & purification KW - Protein-Tyrosine Kinases -- isolation & purification KW - Protein-Tyrosine Kinases -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73110564?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Characterization+of+a+tyrosine+kinase+activity+associated+with+the+high-affinity+interleukin+2+receptor+complex.&rft.au=Garcia%2C+G+G%3BEvans%2C+G+A%3BMichiel%2C+D+F%3BFarrar%2C+W+L&rft.aulast=Garcia&rft.aufirst=G&rft.date=1992-08-01&rft.volume=285+%28+Pt+3%29&rft.issue=&rft.spage=851&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 - 1992-09-10 N1 - Date created - 1992-09-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Science. 1991 Jun 14;252(5012):1523-8 [2047859] Mol Cell Biol. 1991 Jan;11(1):568-72 [1986248] Cell. 1990 Apr 20;61(2):203-12 [2158859] Proc Natl Acad Sci U S A. 1990 Jan;87(1):11-5 [2296573] Cell. 1990 Mar 23;60(6):941-51 [2317865] J Immunol Methods. 1988 May 9;109(2):277-85 [2452204] J Immunol. 1989 Oct 15;143(8):2530-3 [2477446] Cell. 1989 Sep 22;58(6):1023-4 [2550142] Biochem Biophys Res Commun. 1989 Oct 31;164(2):788-95 [2554900] J Biol Chem. 1989 Dec 5;264(34):20723-9 [2555369] Cell. 1989 Dec 1;59(5):837-45 [2590941] J Immunol Methods. 1989 Aug 15;122(1):33-41 [2668418] Science. 1989 May 5;244(4904):551-6 [2785715] J Biol Chem. 1989 Jul 25;264(21):12562-7 [2787319] J Immunol. 1989 Aug 1;143(3):870-6 [2787350] J Biol Chem. 1988 May 25;263(15):6956-9 [3259228] Nature. 1984 Oct 18-24;311(5987):626-31 [6090948] Cell. 1990 Aug 10;62(3):481-92 [1696179] Cytokine. 1991 Sep;3(5):428-38 [1751780] EMBO J. 1991 Feb;10(2):317-25 [1825055] J Exp Med. 1990 Mar 1;171(3):637-44 [2106566] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A signature element distinguishes sibling and independent mutations in a shuttle vector plasmid. AN - 73108549; 1644298 AB - We have developed a new shuttle vector plasmid for studying mutagenesis in mammalian cells that permits proof of independence of identical mutations. Mutations occur more frequently at some sites in a gene than in others, and in a collection of mutant plasmids from a single transfection of mammalian cells the same mutation may appear several times. However, those arising from independent events cannot be distinguished from siblings of an initial event. The new vector system (pSP189) is a population of plasmids, each of which contains an 8-bp 'signature sequence'. This sequence confers a unique identification tag to each plasmid and allows individual members to be identified by a distinctive signature. The plasmid also carries the Escherichia coli bacterial supF gene as a marker for mutagenesis, as well as sequences which support replication in primate (including human) cells and E. coli. We have used the pSP189 system to generate a UV-induced spectrum of mutations in supF following replication in a single plate of human DNA-repair-deficient cells (xeroderma pigmentosum, complementation group A). With the signature sequence, we were able to determine whether identical mutations derived from the transfection were of independent or sibling origin. There were eight identical mutations at the strongest hotspot, all of which had different signature sequences. Only one of these events would have been reported in previous experiments. This plasmid reduces the effort required to generate a spectrum of mutations caused by a DNA-damaging agent and allows a more accurate assessment of mutational hotspot intensity. JF - Gene AU - Parris, C N AU - Seidman, M M AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/08/01/ PY - 1992 DA - 1992 Aug 01 SP - 1 EP - 5 VL - 117 IS - 1 SN - 0378-1119, 0378-1119 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Ultraviolet Rays KW - Base Sequence KW - Humans KW - Molecular Sequence Data KW - Cell Line, Transformed KW - Genetic Vectors -- radiation effects KW - Xeroderma Pigmentosum -- genetics KW - Plasmids -- radiation effects KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73108549?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gene&rft.atitle=A+signature+element+distinguishes+sibling+and+independent+mutations+in+a+shuttle+vector+plasmid.&rft.au=Parris%2C+C+N%3BSeidman%2C+M+M&rft.aulast=Parris&rft.aufirst=C&rft.date=1992-08-01&rft.volume=117&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Gene&rft.issn=03781119&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-08 N1 - Date created - 1992-09-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Poliovirus induces indoleamine-2,3-dioxygenase and quinolinic acid synthesis in macaque brain. AN - 73108020; 1322853 AB - Accumulation of the neurotoxin quinolinic acid within the brain occurs in a broad spectrum of patients with inflammatory neurologic disease and may be of neuropathologic significance. The production of quinolinic acid was postulated to reflect local induction of indoleamine 2,3-dioxygenase by cytokines in reactive cells and inflammatory cell infiltrates within the central nervous system. To test this hypothesis, macaques received an intraspinal injection of poliovirus as a model of localized inflammatory neurologic disease. Seventeen days later, spinal cord indoleamine 2,3-dioxygenase activity and quinolinic acid concentrations in spinal cord and cerebrospinal fluid were both increased in proportion to the degree of inflammatory responses and neurologic damage in the spinal cord, as well as the severity of motor paralysis. The absolute concentrations of quinolinic acid achieved in spinal cord and cerebrospinal fluid exceeded levels reported to kill spinal cord neurons in vitro. Smaller increases in indoleamine 2,3-dioxygenase activity and quinolinic acid concentrations also occurred in parietal cortex, a poliovirus target area. In frontal cortex, which is not a target for poliovirus, indoleamine 2,3-dioxygenase was not affected. A monoclonal antibody to human indoleamine 2,3-dioxygenase was used to visualize indoleamine 2,3-dioxygenase predominantly in grey matter of poliovirus-infected spinal cord, in conjunction with local inflammatory lesions. Macrophage/monocytes in vitro synthesized [13C6]quinolinic acid from [13C6]L-tryptophan, particularly when stimulated by interferon-gamma. Spinal cord slices from poliovirus-inoculated macaques in vitro also converted [13C6]L-tryptophan to [13C6]quinolinic acid. We conclude that local synthesis of quinolinic acid from L-tryptophan within the central nervous system follows the induction of indoleamine-2,3-dioxygenase, particularly within macrophage/microglia. In view of this link between immune stimulation and the synthesis of neurotoxic amounts of quinolinic acid, we propose that attenuation of local inflammation, strategies to reduce the synthesis of neuroactive kynurenine pathway metabolites, or drugs that interfere with the neurotoxicity of quinolinic acid offer new approaches to therapy in inflammatory neurologic disease. JF - FASEB journal : official publication of the Federation of American Societies for Experimental Biology AU - Heyes, M P AU - Saito, K AU - Jacobowitz, D AU - Markey, S P AU - Takikawa, O AU - Vickers, J H AD - Section on Analytical Biochemistry, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 2977 EP - 2989 VL - 6 IS - 11 SN - 0892-6638, 0892-6638 KW - Quinolinic Acids KW - 0 KW - Interferon-gamma KW - 82115-62-6 KW - Tryptophan KW - 8DUH1N11BX KW - Tryptophan Oxygenase KW - EC 1.13.11.11 KW - Quinolinic Acid KW - F6F0HK1URN KW - Index Medicus KW - Animals KW - Macaca KW - Interferon-gamma -- pharmacology KW - Enzyme Induction KW - Tryptophan -- metabolism KW - Immunohistochemistry KW - Poliovirus KW - Tryptophan Oxygenase -- biosynthesis KW - Poliomyelitis -- metabolism KW - Quinolinic Acids -- metabolism KW - Brain -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73108020?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FASEB+journal+%3A+official+publication+of+the+Federation+of+American+Societies+for+Experimental+Biology&rft.atitle=Poliovirus+induces+indoleamine-2%2C3-dioxygenase+and+quinolinic+acid+synthesis+in+macaque+brain.&rft.au=Heyes%2C+M+P%3BSaito%2C+K%3BJacobowitz%2C+D%3BMarkey%2C+S+P%3BTakikawa%2C+O%3BVickers%2C+J+H&rft.aulast=Heyes&rft.aufirst=M&rft.date=1992-08-01&rft.volume=6&rft.issue=11&rft.spage=2977&rft.isbn=&rft.btitle=&rft.title=FASEB+journal+%3A+official+publication+of+the+Federation+of+American+Societies+for+Experimental+Biology&rft.issn=08926638&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-09 N1 - Date created - 1992-09-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Gene- and strand-specific damage and repair in Chinese hamster ovary cells treated with 4-nitroquinoline 1-oxide. AN - 73102084; 1638532 AB - 4-Nitroquinoline 1-oxide (4NQO) is a model chemical carcinogen that has often been referred to as a UV mimetic agent. Previous studies have indicated that UV-induced pyrimidine dimers are repaired preferentially and strand-specifically in actively transcribing genes. In the current study we have examined the gene-specific and strand-specific repair of 4NQO in Chinese hamster ovary B-11 cells treated with 2.5 microM 4NQO. The methodology used for detecting adducts involved the treatment of DNA from 4NQO-exposed cells with uvrABC excinuclease, which incises DNA at adduct sites, followed by denaturing gel electrophoresis of DNA, Southern hybridization, and probing for the sequence of interest. We examined the active and inactive coding regions of the DHFR gene, the active adenine phosphoribosyltransferase gene, relatively inactive c-fos oncogene, and the mitochondrial genome for 4NQO adducts. Initial 4NQO adduct levels found in these genes varied from 1.10 to 1.52 adducts/10 kilobases. Little difference in repair was found between active coding and inactive regions of the DHFR gene, or between DHFR, adenine phosphoribosyltransferase, and c-fos genes, which are transcribed at different levels. Approximately 71% of 4NQO adducts were repaired within 24 h in all gene sequences examined. During this same time period, approximately 51% of adducts were repaired from the genome overall, as determined by comparing the removal of bound radiolabeled 4NQO to total DNA. The results indicate that 4NQO adducts, unlike UV light-induced cyclobutane pyrimidine dimers (UV dimers), are not preferentially repaired in transcriptionally active genes. However, there may be regions of the genome that are not repaired with the same efficiency as the specific genes examined here. In addition, little to no difference was observed in the repair of 4NQO adducts in the transcribed and nontranscribed strands of the DHFR gene, a finding which is also in contrast to results with UV dimers. Interestingly, 4NQO adducts, unlike UV dimers, were removed from the mitochondrial genome, suggesting that repair of select lesions occurs in this organelle. Thus, there appear to be some differences in the repair pathways operating for 4NQO adducts and UV dimers, particularly with respect to gene- and strand-specific DNA repair. JF - Cancer research AU - Snyderwine, E G AU - Bohr, V A AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1992/08/01/ PY - 1992 DA - 1992 Aug 01 SP - 4183 EP - 4189 VL - 52 IS - 15 SN - 0008-5472, 0008-5472 KW - APRT KW - DHFR KW - c-fos KW - DNA Probes KW - 0 KW - DNA, Mitochondrial KW - Escherichia coli Proteins KW - 4-Nitroquinoline-1-oxide KW - 56-57-5 KW - DNA KW - 9007-49-2 KW - Tetrahydrofolate Dehydrogenase KW - EC 1.5.1.3 KW - Adenine Phosphoribosyltransferase KW - EC 2.4.2.7 KW - Endodeoxyribonucleases KW - EC 3.1.- KW - endodeoxyribonuclease uvrABC KW - EC 3.1.25.- KW - Index Medicus KW - Animals KW - Ultraviolet Rays KW - Transcription, Genetic -- drug effects KW - DNA -- drug effects KW - DNA, Mitochondrial -- drug effects KW - Transfection KW - Blotting, Southern KW - DNA -- genetics KW - Genes -- drug effects KW - Restriction Mapping KW - CHO Cells KW - Cricetinae KW - DNA, Mitochondrial -- genetics KW - 4-Nitroquinoline-1-oxide -- pharmacology KW - DNA Repair KW - DNA Damage KW - Adenine Phosphoribosyltransferase -- genetics KW - Endodeoxyribonucleases -- metabolism KW - Genes, fos -- drug effects KW - Tetrahydrofolate Dehydrogenase -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73102084?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Gene-+and+strand-specific+damage+and+repair+in+Chinese+hamster+ovary+cells+treated+with+4-nitroquinoline+1-oxide.&rft.au=Snyderwine%2C+E+G%3BBohr%2C+V+A&rft.aulast=Snyderwine&rft.aufirst=E&rft.date=1992-08-01&rft.volume=52&rft.issue=15&rft.spage=4183&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 - 1992-08-28 N1 - Date created - 1992-08-28 N1 - Date revised - 2017-01-13 N1 - Gene symbol - APRT; DHFR; c-fos N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Abnormal structure and expression of the p53 gene in human ovarian carcinoma cell lines. AN - 73100534; 1638534 AB - In an effort to analyze molecular mechanisms of human ovarian carcinogenesis, we studied the structure and expression of the p53 gene in different cell lines established from human ovarian carcinomas. In all six lines (PA-1, Caov-3 and -4, OVCAR-3, SK-OV-3, and Kuramochi), p53 abnormalities were detected. In the SK-OV-3 cell line, Southern analysis suggested the presence of sequence deletions/rearrangements in at least one allele of the p53 gene, and transcripts were not detectable by either Northern or polymerase chain reaction analysis. Sequence analysis of the entire coding region of the p53 gene revealed point mutations resulting in codon changes of a highly conserved region of the protein in four cell lines, Caov-3 and -4, OVCAR-3, and Kuramochi. In the Caov-3 cell line, the point mutation resulted in chain termination at codon 136. Quantitation of p53 protein by immunoprecipitation analysis revealed a 6-fold higher than control cell level in PA-1. By contrast, p53 protein was not detectable in lines Caov-3 and SK-OV-3. We conclude that altered levels of p53 gene expression and/or mutant forms of the p53 gene product are associated with all human ovarian cancer cells tested. JF - Cancer research AU - Yaginuma, Y AU - Westphal, H AD - Laboratory of Mammalian Genes and Development, National Institute of Child Health and Human Development, NIH, Bethesda, Maryland 20892. Y1 - 1992/08/01/ PY - 1992 DA - 1992 Aug 01 SP - 4196 EP - 4199 VL - 52 IS - 15 SN - 0008-5472, 0008-5472 KW - p53 KW - DNA, Neoplasm KW - 0 KW - Oligodeoxyribonucleotides KW - RNA, Messenger KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Placenta -- chemistry KW - Humans KW - Gene Expression KW - RNA, Messenger -- genetics KW - DNA, Neoplasm -- isolation & purification KW - Pregnancy KW - Cloning, Molecular KW - DNA -- isolation & purification KW - Promoter Regions, Genetic KW - Base Sequence KW - Blotting, Southern KW - Polymerase Chain Reaction -- methods KW - DNA -- genetics KW - Molecular Sequence Data KW - DNA, Neoplasm -- genetics KW - RNA, Messenger -- isolation & purification KW - Cell Line KW - Female KW - Genes, p53 KW - Ovarian Neoplasms -- genetics KW - Transcription, Genetic KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73100534?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Abnormal+structure+and+expression+of+the+p53+gene+in+human+ovarian+carcinoma+cell+lines.&rft.au=Yaginuma%2C+Y%3BWestphal%2C+H&rft.aulast=Yaginuma&rft.aufirst=Y&rft.date=1992-08-01&rft.volume=52&rft.issue=15&rft.spage=4196&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 - 1992-08-28 N1 - Date created - 1992-08-28 N1 - Date revised - 2017-01-13 N1 - Gene symbol - p53 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Endothelial leukocyte adhesion molecule-1 in endotoxin-induced uveitis. AN - 73099851; 1379217 AB - Expression of endothelial leukocyte adhesion molecule-1 (ELAM-1) on endothelial cells leads to the attachment of polymorphonuclear leukocytes. The sequential expression of ELAM-1 and major histocompatibility complex (MHC) class II antigen was examined in the eyes of 59 Lewis rats with endotoxin-induced uveitis (EIU) after the injection of Salmonella typhimurium endotoxin. The eyes were enucleated at 2-hr intervals. Hematoxylin and eosin-stained paraffin-embedded sections and immunohistochemically stained cryostat sections were graded by two masked observers. The MHC class II antigen was expressed on cells in the iris and ciliary body 4 hr after injection of endotoxin and on the corneal endothelium, 8 hr postinjection. It was found that ELAM-1 was expressed first on cells of the ciliary body and iris 10 hr after the injection of endotoxin and on the corneal endothelium, 22 hr postinjection. Clinical and histopathologic disease developed 16 hr postinjection. Adherence of polymorphonuclear cells to the corneal endothelium was observed at the time of ELAM-1 expression. In conclusion, expression of ELAM-1 on ocular tissue occurred in EIU and appeared to promote polymorphonuclear cell accumulation in the anterior segment of the eye. JF - Investigative ophthalmology & visual science AU - Whitcup, S M AU - Wakefield, D AU - Li, Q AU - Nussenblatt, R B AU - Chan, C C AD - Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 2626 EP - 2630 VL - 33 IS - 9 SN - 0146-0404, 0146-0404 KW - Antibodies, Monoclonal KW - 0 KW - Bacterial Toxins KW - Cell Adhesion Molecules KW - E-Selectin KW - Endotoxins KW - Enterotoxins KW - Histocompatibility Antigens Class II KW - Membrane Glycoproteins KW - Receptors, Immunologic KW - salmonella toxin KW - Index Medicus KW - Animals KW - Rats, Inbred Lew KW - Endothelium, Corneal -- metabolism KW - Endothelium, Corneal -- immunology KW - Rats KW - Neutrophils -- metabolism KW - Histocompatibility Antigens Class II -- metabolism KW - Receptors, Immunologic -- metabolism KW - Anterior Eye Segment -- metabolism KW - Salmonella KW - Immunoenzyme Techniques KW - Female KW - Cell Adhesion KW - Uveitis, Anterior -- chemically induced KW - Uveitis, Anterior -- immunology KW - Cell Adhesion Molecules -- metabolism KW - Uveitis, Anterior -- metabolism KW - Membrane Glycoproteins -- immunology KW - Membrane Glycoproteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73099851?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Endothelial+leukocyte+adhesion+molecule-1+in+endotoxin-induced+uveitis.&rft.au=Whitcup%2C+S+M%3BWakefield%2C+D%3BLi%2C+Q%3BNussenblatt%2C+R+B%3BChan%2C+C+C&rft.aulast=Whitcup&rft.aufirst=S&rft.date=1992-08-01&rft.volume=33&rft.issue=9&rft.spage=2626&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 - 1992-08-31 N1 - Date created - 1992-08-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Induction of colony-stimulating factor receptor expression on hematopoietic progenitor cells: proposed mechanism for growth factor synergism. AN - 73097375; 1379087 AB - In many cells systems, the cellular interaction between two or more humoral factors leads to a synergistic response in terms of cellular growth and function. In particular, the growth and differentiation of hematopoietic progenitor cells involves numerous synergistic interactions between colony-stimulating factors (CSFs) that individually stimulate hematopoiesis (granulocyte-CSF, granulocyte-macrophage-CSF, and interleukin-3 [IL-3]), as well as between these factors and other cytokines that individually have no proliferative effect on progenitor cell growth (IL-1 and IL-6). The present study investigated whether hematopoietic growth factor (HGF) synergy could be mediated by upregulation of CSF receptors. Synergistic effects on bone marrow (BM) progenitor cell colony formation, regardless of the combination of factors used, were consistently preceded by increased CSF receptor expression on highly enriched BM progenitor cells, but not on unfractionated BM cells. Induction of CSF receptors preceded detectable differentiation and did not require cell division because nocodazole, an inhibitor of mitosis, blocked CSF-mediated cell proliferation, but not receptor upregulation. Furthermore, combinations of cytokines that did not synergize also failed to affect the level of CSF receptors on BM progenitors. These results have led us to propose a model for HGF synergy whereby one mechanism of action the investigated synergistic cytokines might be the ability to induce increased expression of CSF receptors. JF - Blood AU - Jacobsen, S E AU - Ruscetti, F W AU - Dubois, C M AU - Wine, J AU - Keller, J R AD - Laboratory of Molecular Immunoregulation, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702-1201. Y1 - 1992/08/01/ PY - 1992 DA - 1992 Aug 01 SP - 678 EP - 687 VL - 80 IS - 3 SN - 0006-4971, 0006-4971 KW - Growth Substances KW - 0 KW - Interleukin-1 KW - Interleukin-3 KW - Interleukin-6 KW - Iodine Radioisotopes KW - Receptors, Colony-Stimulating Factor KW - Recombinant Proteins KW - Granulocyte Colony-Stimulating Factor KW - 143011-72-7 KW - Granulocyte-Macrophage Colony-Stimulating Factor KW - 83869-56-1 KW - Thymidine KW - VC2W18DGKR KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Interleukin-1 -- pharmacology KW - Recombinant Proteins -- pharmacology KW - Bone Marrow -- physiology KW - Interleukin-3 -- pharmacology KW - Cell Division -- drug effects KW - Mice KW - Interleukin-6 -- pharmacology KW - Radioligand Assay KW - Mice, Inbred BALB C KW - Autoradiography KW - Granulocyte Colony-Stimulating Factor -- pharmacology KW - Granulocyte-Macrophage Colony-Stimulating Factor -- pharmacology KW - DNA Replication -- drug effects KW - Thymidine -- metabolism KW - Bone Marrow Cells KW - Granulocyte Colony-Stimulating Factor -- metabolism KW - Recombinant Proteins -- metabolism KW - Kinetics KW - Drug Synergism KW - Granulocyte-Macrophage Colony-Stimulating Factor -- metabolism KW - Receptors, Colony-Stimulating Factor -- biosynthesis KW - Growth Substances -- pharmacology KW - Receptors, Colony-Stimulating Factor -- metabolism KW - Hematopoietic Stem Cells -- physiology KW - Hematopoietic Stem Cells -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73097375?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Induction+of+colony-stimulating+factor+receptor+expression+on+hematopoietic+progenitor+cells%3A+proposed+mechanism+for+growth+factor+synergism.&rft.au=Jacobsen%2C+S+E%3BRuscetti%2C+F+W%3BDubois%2C+C+M%3BWine%2C+J%3BKeller%2C+J+R&rft.aulast=Jacobsen&rft.aufirst=S&rft.date=1992-08-01&rft.volume=80&rft.issue=3&rft.spage=678&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=00064971&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-31 N1 - Date created - 1992-08-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interferon-gamma gene expression in human B-cell lines: induction by interleukin-2, protein kinase C activators, and possible effect of hypomethylation on gene regulation. AN - 73092329; 1322203 AB - Human interferon-gamma (IFN-gamma) is an important immunomodulatory protein produced predominantly by T cells and large granular lymphocytes (LGLs). Whereas large amounts of data have been accumulated regarding IFN gamma gene expression in these two cell types, little information about IFN gamma expression in other cell types exists. In this study, we have analyzed the production of IFN gamma by the Epstein-Barr virus (EBV)-positive B-cell line, JLP(c), derived from a patient with Burkitt's lymphoma, and another human B-cell line, PA682BM-1, which was derived from an acquired immunodeficiency syndrome patient. Southern blot analysis indicates the presence of an Ig heavy chain gene rearrangement, but no rearrangement of the T-cell receptor beta chain gene or IFN gamma gene in these B-cell lines. Both cell lines were found to express surface IgD and other B-cell surface markers, thus confirming their B-cell lineage. Analysis for surface Ig, cytoplasmic Ig, and secreted Ig indicates that the two cell lines are in relatively early stages of the B-cell differentiation pathway. We now report that PA682BM-1 can be triggered by the protein kinase C (PKC) activators, phorbol 12-myristate 13-acetate (PMA) and (-)Indolactam-v, to secrete IFN gamma, whereas JLP(c) cells spontaneously produce low levels of IFN gamma that can be enhanced by PKC activators and interleukin-2 (IL-2). After activation of the cell lines with IL-2, (-)Indolactam-v, and PMA, increases in cytoplasmic messenger RNAs (mRNAs) of IFN gamma and the IL-2 receptor chains were also observed. The induction of IFN gamma mRNA and protein by IL-2 was completely blocked by a monoclonal antibody to IL-2 receptor p75 (beta chain), but not by the monoclonal antibody to p55 (alpha chain). Analysis of IFN gamma genomic DNA indicates that the gene is not amplified, but that hypomethylation in the 5' noncoding region of the IFN gamma gene has occurred in the B-cell line from the Burkitt's lymphoma patient that spontaneously produces IFN gamma. This finding suggests that the methylation state of the promoter region may play an important role in the control of IFN gamma gene expression in B cells. JF - Blood AU - Pang, Y AU - Norihisa, Y AU - Benjamin, D AU - Kantor, R R AU - Young, H A AD - Laboratory of Experimental Immunology, BRMP, NCI-FCRDC, Frederick, MD 21702-1201. Y1 - 1992/08/01/ PY - 1992 DA - 1992 Aug 01 SP - 724 EP - 732 VL - 80 IS - 3 SN - 0006-4971, 0006-4971 KW - Antigens, Surface KW - 0 KW - Carcinogens KW - DNA, Neoplasm KW - Immunoglobulin Heavy Chains KW - Indoles KW - Interleukin-1 KW - Interleukin-2 KW - Interleukin-6 KW - Lactams KW - Recombinant Proteins KW - Interleukin-4 KW - 207137-56-2 KW - Interferon-gamma KW - 82115-62-6 KW - indolactam V KW - 8CIY9O1323 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Gene Expression -- drug effects KW - Carcinogens -- pharmacology KW - Acquired Immunodeficiency Syndrome -- complications KW - Burkitt Lymphoma -- etiology KW - Interleukin-1 -- pharmacology KW - Humans KW - Burkitt Lymphoma -- genetics KW - Genes, Immunoglobulin KW - Interleukin-6 -- pharmacology KW - Immunoglobulin Heavy Chains -- genetics KW - Blotting, Southern KW - Flow Cytometry KW - Antigens, Surface -- analysis KW - Recombinant Proteins -- pharmacology KW - Enzyme Activation KW - Interleukin-4 -- pharmacology KW - Gene Rearrangement KW - Gene Rearrangement, beta-Chain T-Cell Antigen Receptor KW - B-Lymphocytes -- immunology KW - Burkitt Lymphoma -- immunology KW - Gene Expression Regulation, Neoplastic -- drug effects KW - Lactams -- pharmacology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Indoles -- pharmacology KW - Methylation KW - Cell Line KW - Protein Kinase C -- metabolism KW - Interleukin-2 -- pharmacology KW - Interferon-gamma -- genetics KW - DNA, Neoplasm -- genetics KW - DNA, Neoplasm -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73092329?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Interferon-gamma+gene+expression+in+human+B-cell+lines%3A+induction+by+interleukin-2%2C+protein+kinase+C+activators%2C+and+possible+effect+of+hypomethylation+on+gene+regulation.&rft.au=Pang%2C+Y%3BNorihisa%2C+Y%3BBenjamin%2C+D%3BKantor%2C+R+R%3BYoung%2C+H+A&rft.aulast=Pang&rft.aufirst=Y&rft.date=1992-08-01&rft.volume=80&rft.issue=3&rft.spage=724&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=00064971&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-31 N1 - Date created - 1992-08-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Methotrexate pharmacokinetics following administration of recombinant carboxypeptidase-G2 in rhesus monkeys. AN - 73092099; 1634927 AB - Carboxypeptidase-G2 (CPDG2) is a bacterial enzyme that rapidly hydrolyzes methotrexate (MTX) into inactive metabolites. As an alternative form of rescue after high-dose MTX (HDMTX), CPDG2 has more potential advantages than standard leucovorin (LV) rescue. In this study, the plasma pharmacokinetics of MTX with and without CPDG2 were evaluated in adult rhesus monkeys. The plasma pharmacokinetics of MTX were determined in groups of animals that had received a 300-mg/m2 loading dose of MTX followed by a 60-mg/m2/h infusion during an 18-hour period. One group received CPDG2 at the end of the infusion, and the other group served as a control. Two additional animals with high titers of anti-CPDG2 antibody also were studied. During infusion, the steady-state MTX plasma concentration was 11.3 +/- 4.8 mumol/L. Without CPDG2, the postinfusion plasma MTX concentration remained above 0.1 mumol/L for more than 6 hours. After the administration of 50 U/kg of CPDG2, plasma MTX concentrations decreased to nontoxic levels (less than 0.05 mumol/L) within 30 minutes. The initial half-life (t1/2 alpha) of MTX decreased from 5.8 +/- 2.1 minutes to 0.7 +/- 0.02 minutes after enzyme administration. The postinfusion area under the plasma concentration time curve of MTX was 301 +/- 171 mumol/L/min without CPDG2 compared with 19.6 +/- 6.1 mumol/L/min with CPDG2. The immunogenicity studies performed indicated that although animals developed anti-CPDG2 antibodies, none of them manifested allergic symptoms. The effectiveness of CPDG2 was diminished but not eliminated in animals with high titers of anti-CPDG2 antibody. CPDG2 is capable of rapidly decreasing plasma MTX concentrations to nontoxic levels. The administration of CPDG2 seems safe, well tolerated, and it may be useful as an alternative to LV rescue. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Adamson, P C AU - Balis, F M AU - McCully, C L AU - Godwin, K S AU - Poplack, D G AD - Pediatric Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 1359 EP - 1364 VL - 10 IS - 8 SN - 0732-183X, 0732-183X KW - Recombinant Proteins KW - 0 KW - gamma-Glutamyl Hydrolase KW - EC 3.4.19.9 KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - Animals KW - Feasibility Studies KW - Drug Interactions KW - Recombinant Proteins -- pharmacology KW - Recombinant Proteins -- immunology KW - Recombinant Proteins -- pharmacokinetics KW - Antibody Formation KW - Macaca mulatta KW - Male KW - Methotrexate -- pharmacokinetics KW - gamma-Glutamyl Hydrolase -- pharmacology KW - gamma-Glutamyl Hydrolase -- pharmacokinetics KW - gamma-Glutamyl Hydrolase -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73092099?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Methotrexate+pharmacokinetics+following+administration+of+recombinant+carboxypeptidase-G2+in+rhesus+monkeys.&rft.au=Adamson%2C+P+C%3BBalis%2C+F+M%3BMcCully%2C+C+L%3BGodwin%2C+K+S%3BPoplack%2C+D+G&rft.aulast=Adamson&rft.aufirst=P&rft.date=1992-08-01&rft.volume=10&rft.issue=8&rft.spage=1359&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 - 1992-08-25 N1 - Date created - 1992-08-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Gonadotropin-releasing hormone-induced calcium signaling in clonal pituitary gonadotrophs. AN - 73090225; 1379169 AB - In agonist-stimulated clonal pituitary gonadotrophs (alpha T3-1 cells), cytoplasmic calcium ([Ca2+]i) exhibited rapid and prominent peak increases, followed by lower, but sustained, elevations for up to 15 min. The [Ca2+]i response to GnRH was rapidly inhibited by prior addition of a potent GnRH antagonist. In the absence of extracellular Ca2+ the initial peak [Ca2+]i response was only slightly decreased, but the prolonged increase in [Ca2+]i was abolished, indicating that the peak is derived largely from intracellular calcium mobilization and the sustained phase from Ca2+ influx. Application of the endoplasmic reticulum Ca(2+)-ATPase blocker thapsigargin caused progressive and dose-dependent elevation of [Ca2+]i and decreased the peak amplitude of the GnRH-induced Ca2+ response. On the other hand, addition of dihydropyridine calcium channel antagonists before or after GnRH treatment prevented or terminated the plateau phase, respectively, consistent with entry of Ca2+ through L-type voltage-sensitive Ca2+ channels (VSCC) as the major Ca2+ influx pathway during GnRH action. The presence of L-type VSCC in alpha T3-1 cells was further indicated by the ability of elevated extracellular K+ levels and the dihydropyridine calcium channel agonist Bay K 8644 to elevate [Ca2+]i in an extracellular calcium-dependent manner. These actions of depolarization and Bay K 8644 were inhibited by nifedipine, with an IC50 of 10 nM. High extracellular K(+)- and GnRH-induced Ca2+ entry was also attenuated by phorbol esters and permeant diacylglycerols, indicating that protein kinase-C exerts inhibitory modulation of VSCC activity. In contrast to normal pituitary gonadotrophs, in which GnRH induces a frequency-modulated oscillatory [Ca2+]i response, single alpha T3-1 cells exhibited a nonoscillatory amplitude-modulated signal during agonist stimulation. The [Ca2+]i responses observed in alpha T3-1 gonadotrophs indicate that the immortalized cells retain functional GnRH receptors and their coupling to the Ca2+ signaling pathway. Ca2+ influx through L-type channels maintains the plateau phase of the [Ca2+]i response during agonist stimulation and is inhibited by activation of protein kinase-C. JF - Endocrinology AU - Merelli, F AU - Stojilković, S S AU - Iida, T AU - Krsmanovic, L Z AU - Zheng, L AU - Mellon, P L AU - Catt, K J AD - Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 925 EP - 932 VL - 131 IS - 2 SN - 0013-7227, 0013-7227 KW - Calcium Channel Blockers KW - 0 KW - Calcium Channels KW - Dihydropyridines KW - Terpenes KW - Gonadotropin-Releasing Hormone KW - 33515-09-2 KW - Ionomycin KW - 56092-81-0 KW - Thapsigargin KW - 67526-95-8 KW - 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester KW - 71145-03-4 KW - Calcium-Transporting ATPases KW - EC 3.6.3.8 KW - Nifedipine KW - I9ZF7L6G2L KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Potassium KW - RWP5GA015D KW - Calcium KW - SY7Q814VUP KW - Abridged Index Medicus KW - Index Medicus KW - Nifedipine -- pharmacology KW - Endoplasmic Reticulum -- enzymology KW - Dihydropyridines -- pharmacology KW - Calcium Channels -- metabolism KW - Calcium Channel Blockers -- pharmacology KW - 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester -- pharmacology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Potassium -- pharmacology KW - Ionomycin -- pharmacology KW - Calcium-Transporting ATPases -- antagonists & inhibitors KW - Terpenes -- pharmacology KW - Cell Line KW - Calcium -- metabolism KW - Signal Transduction -- drug effects KW - Gonadotropin-Releasing Hormone -- antagonists & inhibitors KW - Calcium -- pharmacology KW - Pituitary Gland -- metabolism KW - Gonadotropin-Releasing Hormone -- pharmacology KW - Pituitary Gland -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73090225?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Gonadotropin-releasing+hormone-induced+calcium+signaling+in+clonal+pituitary+gonadotrophs.&rft.au=Merelli%2C+F%3BStojilkovi%C4%87%2C+S+S%3BIida%2C+T%3BKrsmanovic%2C+L+Z%3BZheng%2C+L%3BMellon%2C+P+L%3BCatt%2C+K+J&rft.aulast=Merelli&rft.aufirst=F&rft.date=1992-08-01&rft.volume=131&rft.issue=2&rft.spage=925&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=00137227&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-02 N1 - Date created - 1992-09-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Identification of a stage selector element in the human gamma-globin gene promoter that fosters preferential interaction with the 5' HS2 enhancer when in competition with the beta-promoter. AN - 73084165; 1639067 AB - The erythroid-specific enhancer within hypersensitivity site 2 (HS2) of the human beta-globin locus control region is required for high level globin gene expression. We investigated interaction between HS2 and the gamma- and beta-promoters using reporter constructs in transient assays in human erythroleukemia (K562) cells. The beta-promoter, usually silent in K562 cells, was activated by HS2. This activity was abolished when a gamma-promoter was linked in cis. Analysis of truncation mutants suggested that sequences conveying the competitive advantage of the gamma-promoter for HS2 included those between positions -53 and -35 relative to the transcriptional start site. This sequence, when used to replace the corresponding region of the beta-promoter, increased beta-promoter activity 10-fold when linked to HS2. The modified beta-promoter was also capable of competing with a gamma-promoter modified internally in the -53 to -35 region, when the two promoters were linked to HS2 in a single plasmid. The corresponding sequences from the Galago gamma-promoter, a species which lacks fetal gamma-gene expression, were inactive in analogous assays. We have identified and partially purified a nuclear protein found in human (fetal stage) erythroleukemia cells, but present in much lower concentration in murine (adult stage) erythroleukemia cells, that binds the -53 to -35 sequence of the gamma-promoter. We speculate that this region of the gamma-promoter functions as a stage selector element in the regulation of hemoglobin switching in humans. JF - The EMBO journal AU - Jane, S M AU - Ney, P A AU - Vanin, E F AU - Gumucio, D L AU - Nienhuis, A W AD - National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 2961 EP - 2969 VL - 11 IS - 8 SN - 0261-4189, 0261-4189 KW - Recombinant Fusion Proteins KW - 0 KW - Globins KW - 9004-22-2 KW - Luciferases KW - EC 1.13.12.- KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Index Medicus KW - Animals KW - Humans KW - Luciferases -- metabolism KW - Gene Expression KW - Mice KW - Chloramphenicol O-Acetyltransferase -- metabolism KW - Binding Sites KW - Recombinant Fusion Proteins -- metabolism KW - Mutagenesis, Site-Directed KW - Gene Expression Regulation, Neoplastic KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Base Sequence KW - Leukemia, Experimental KW - Transfection KW - Kinetics KW - Restriction Mapping KW - Binding, Competitive KW - Molecular Sequence Data KW - Leukemia, Myelogenous, Chronic, BCR-ABL Positive KW - Cell Nucleus -- physiology KW - Luciferases -- genetics KW - Cell Line KW - Promoter Regions, Genetic KW - Enhancer Elements, Genetic KW - Globins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73084165?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Identification+of+a+stage+selector+element+in+the+human+gamma-globin+gene+promoter+that+fosters+preferential+interaction+with+the+5%27+HS2+enhancer+when+in+competition+with+the+beta-promoter.&rft.au=Jane%2C+S+M%3BNey%2C+P+A%3BVanin%2C+E+F%3BGumucio%2C+D+L%3BNienhuis%2C+A+W&rft.aulast=Jane&rft.aufirst=S&rft.date=1992-08-01&rft.volume=11&rft.issue=8&rft.spage=2961&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 - 1992-08-28 N1 - Date created - 1992-08-28 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nature. 1979 Jul 12;280(5718):164-5 [95354] Cell. 1984 Jul;37(3):889-901 [6540146] Anal Biochem. 1976 May 7;72:248-54 [942051] Genes Dev. 1989 Mar;3(3):314-23 [2721958] Proc Natl Acad Sci U S A. 1989 Apr;86(8):2554-8 [2704733] Proc Natl Acad Sci U S A. 1989 Sep;86(18):7033-7 [2476809] Cell. 1988 Oct 7;55(1):17-26 [3167976] Proc Natl Acad Sci U S A. 1988 Sep;85(17):6267-71 [3166139] Genes Dev. 1989 Dec;3(12A):1860-73 [2620826] Genes Dev. 1989 Dec;3(12A):1845-59 [2620825] Proc Natl Acad Sci U S A. 1986 Jun;83(12):4312-6 [3459175] Cell. 1986 Jul 4;46(1):89-94 [3719696] J Clin Invest. 1987 Aug;80(2):374-80 [3611352] Mol Cell Biol. 1987 Jan;7(1):398-402 [3561396] Proc Natl Acad Sci U S A. 1987 Jul;84(14):4786-90 [3474625] Proc Natl Acad Sci U S A. 1985 Oct;82(19):6384-8 [3879975] EMBO J. 1985 Jul;4(7):1715-23 [2992937] Nature. 1986 Feb 20-26;319(6055):685-9 [3951540] Mol Cell Biol. 1987 Nov;7(11):4024-9 [2828925] Cell. 1987 Dec 24;51(6):975-85 [3690667] J Biol Chem. 1987 Dec 15;262(35):17051-7 [2445753] Nature. 1985 Mar 28-Apr 3;314(6009):377-80 [3982505] Mol Cell Biol. 1987 Feb;7(2):725-37 [3821727] Biochemistry. 1987 Nov 17;26(23):7234-8 [3322397] Proc Natl Acad Sci U S A. 1984 Nov;81(22):7161-5 [6438633] Blood. 1991 Sep 1;78(5):1355-63 [1878596] Genes Dev. 1991 Aug;5(8):1387-94 [1714415] Blood. 1991 Oct 1;78(7):1853-63 [1912570] Nature. 1991 Mar 21;350(6315):252-4 [1706482] Nucleic Acids Res. 1990 Sep 25;18(18):5465-72 [2216720] Nature. 1990 Dec 20-27;348(6303):749-52 [2175398] Nucleic Acids Res. 1989 Jan 11;17(1):37-54 [2911469] J Mol Biol. 1988 Sep 20;203(2):439-55 [3199442] Cell. 1989 Mar 24;56(6):969-77 [2924354] Genes Dev. 1988 Jul;2(7):863-73 [3209071] Nature. 1989 Mar 23;338(6213):352-5 [2922063] Genes Dev. 1990 Jun;4(6):993-1006 [2116990] Mol Cell Biol. 1990 Mar;10(3):1116-25 [2304460] Nature. 1990 Mar 22;344(6264):309-13 [2314472] Genes Dev. 1990 Mar;4(3):380-9 [1692558] Nature. 1990 Jan 4;343(6253):92-6 [2104960] Proc Natl Acad Sci U S A. 1990 Jan;87(2):668-72 [2300555] Proc Natl Acad Sci U S A. 1980 Jun;77(6):3509-13 [6932034] Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] Nucleic Acids Res. 1983 Mar 11;11(5):1475-89 [6828386] Methods Enzymol. 1980;65(1):499-560 [6246368] Nucleic Acids Res. 1981 Dec 11;9(23):6505-25 [6275366] Blood. 1975 Mar;45(3):321-34 [163658] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Specific antibody to the thyrotropin receptor identifies multiple receptor forms in membranes of cells transfected with wild-type receptor complementary deoxyribonucleic acid: characterization of their relevance to receptor synthesis, processing, structure, and function. AN - 73083816; 1639025 AB - An antibody to a peptide of the TSH receptor, residues 352-366 which are not present in gonadotropin receptors, specifically identifies three major forms of the receptor on Western blots of detergent-solubilized membrane preparations from Cos-7 cells transfected with full-length rat and human TSH receptor cDNA: 230, 180, and 95-100 kilodaltons (kDa), based on simultaneously run protein standards. The 95- to 100-kDa protein is absent in cells transfected with a mutant receptor with no signal peptide and is sensitive to endoglycosidase-F. Its size is consistent with the sum of amino acids predicted from its cDNA sequence (84 kDa after subtracting the signal peptide) plus its carbohydrate content (14 kDa estimated from glycosylation mutants). It alone is absent in two deletion mutants that have lost TSH binding and activity after transfection: M1 missing residues 37-121 and M2 missing residues 110-307. It, thus, appears to be the processed glycosylated functional receptor on the cell surface. The 230-kDa protein is a nonprocessed form of the receptor, as evidenced by its insensitivity to endoglycosidase-F and its continued presence in cells transfected with a mutant receptor with no signal peptide. It is the primary form identified in rat FRTL-5 thyroid cells that have a functioning TSH receptor; it is not present in rat FRT thyroid cells with no functioning TSH receptor or receptor RNA. It appears, therefore, to be a early synthetic form of the functional TSH receptor. The 180-kDa protein is endoglycosidase-F sensitive and appears to be a processed intermediate between the 230-kDa early synthetic form and the 95- to 100-kDa functional receptor, rather than a dimer of the latter. Thus, with decreases in size appropriate to a receptor monomer, it remains present in membranes from the M1 and M2 deletion mutants that contain the 230-kDa protein but are missing the 95- to 100-kDa receptor form in association with lost TSH binding and activity after transfection. Minor receptor forms (54 kDa in rat receptor transfectants, 54 and 48 kDa in human receptor transfectants) appear to be degraded forms of the processed and glycosylated 95- to 100-kDa receptor. The presence or absence of reducing agents in the detergent solubilization mixture does not change the pattern or amount of the receptor forms recognized by the antibody, including the 54-kDa form; however, boiling does.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Endocrinology AU - Ban, T AU - Kosugi, S AU - Kohn, L D AD - Cell Regulation Section, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 815 EP - 829 VL - 131 IS - 2 SN - 0013-7227, 0013-7227 KW - Antibodies KW - 0 KW - Detergents KW - Receptors, Thyrotropin KW - DNA KW - 9007-49-2 KW - Mannosyl-Glycoprotein Endo-beta-N-Acetylglucosaminidase KW - EC 3.2.1.96 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Antibodies -- immunology KW - Humans KW - Amino Acid Sequence KW - Glycosylation KW - Molecular Weight KW - Structure-Activity Relationship KW - Rats KW - Oxidation-Reduction KW - Mutagenesis, Site-Directed KW - Antibody Specificity KW - Hot Temperature KW - Blotting, Western KW - Mannosyl-Glycoprotein Endo-beta-N-Acetylglucosaminidase -- metabolism KW - Molecular Sequence Data KW - Receptors, Thyrotropin -- chemistry KW - Receptors, Thyrotropin -- physiology KW - Transfection KW - DNA -- genetics KW - Cell Membrane -- chemistry KW - Receptors, Thyrotropin -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73083816?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Specific+antibody+to+the+thyrotropin+receptor+identifies+multiple+receptor+forms+in+membranes+of+cells+transfected+with+wild-type+receptor+complementary+deoxyribonucleic+acid%3A+characterization+of+their+relevance+to+receptor+synthesis%2C+processing%2C+structure%2C+and+function.&rft.au=Ban%2C+T%3BKosugi%2C+S%3BKohn%2C+L+D&rft.aulast=Ban&rft.aufirst=T&rft.date=1992-08-01&rft.volume=131&rft.issue=2&rft.spage=815&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=00137227&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-02 N1 - Date created - 1992-09-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ultraviolet mutagenesis in human lymphocytes: the effect of cellular transformation. AN - 73074994; 1322318 AB - We have assessed the role of cellular transformation in ultraviolet (uv)-induced mutagenic events in human cells. To maintain uniformity of genetic background and to eliminate the effect of DNA repair, primary nontransformed lymphocytes (T-cells) and Epstein-Barr virus-transformed lymphocytes (B-cells) from one patient (XP12Be) with the DNA repair-deficient disorder xeroderma pigmentosum (group A) were transfected with the mutagenesis shuttle vector pZ189. Parallel control experiments were performed with primary, nontransformed lymphocytes from a normal individual and with a repair-proficient Epstein-Barr virus-transformed lymphocyte line (KR6058). pZ189 was treated with uv and introduced into the four cell lines by electroporation. Plasmid survival and mutations inactivating the marker supF suppressor tRNA gene in the recovered pZ189 were scored by transforming an indicator strain of Escherichia coli. Plasmid survival was reduced and mutation frequency elevated equally with both XP-A cell lines compared to both normal cell lines. Base sequence analysis of more than 250 independent plasmids showed that while the G:C----A:T base substitution mutation was found in at least 60% of plasmids with single or tandem mutations with all four cell lines, the frequency with the transformed XP-A (93%) cells was significantly higher (P less than 0.01) than that with the nontransformed XP-A cells (77%). In addition, with the transformed XP-A cells, there were significantly fewer plasmids with transversions and with mutations at a transversion hotspot (base pair 134) than with plasmids recovered from nontransformed XP-A cells. Interleukin-2 and phytohemagglutinin (used to maintain growth of the nontransformed lymphocytes) treatment of transformed XP12Be cells did not change overall plasmid survival or mutation frequency, but increased the transversion frequency and induced a mutational hotspot (at base pair 159), while another mutational hotspot (at base pair 123) disappeared. Thus we have demonstrated that in repair-deficient human cells, cellular transformation, while not affecting overall postuv plasmid survival and mutation frequency, does increase the susceptibility to G:C----A:T transition mutations, a type of mutation associated with uv-induced neoplasia. JF - Experimental cell research AU - Parris, C N AU - Kraemer, K H AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 462 EP - 469 VL - 201 IS - 2 SN - 0014-4827, 0014-4827 KW - Interleukin-2 KW - 0 KW - Phytohemagglutinins KW - Index Medicus KW - Interleukin-2 -- pharmacology KW - Ultraviolet Rays KW - Base Sequence KW - Transfection KW - Humans KW - Genetic Vectors KW - Molecular Sequence Data KW - Mutation KW - Herpesvirus 4, Human KW - Cell Line KW - Mutagenesis KW - Lymphocytes -- pathology KW - Xeroderma Pigmentosum -- physiopathology KW - Lymphocytes -- radiation effects KW - Lymphocytes -- drug effects KW - Cell Transformation, Viral UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73074994?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+cell+research&rft.atitle=Ultraviolet+mutagenesis+in+human+lymphocytes%3A+the+effect+of+cellular+transformation.&rft.au=Parris%2C+C+N%3BKraemer%2C+K+H&rft.aulast=Parris&rft.aufirst=C&rft.date=1992-08-01&rft.volume=201&rft.issue=2&rft.spage=462&rft.isbn=&rft.btitle=&rft.title=Experimental+cell+research&rft.issn=00144827&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-03 N1 - Date created - 1992-09-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Synthesis, characterization, and some immunological properties of conjugates composed of the detoxified lipopolysaccharide of Vibrio cholerae O1 serotype Inaba bound to cholera toxin. AN - 73072829; 1639490 AB - Protection against cholera has been correlated with the level of serum vibriocidal antibodies. The specificity of these vibriocidal antibodies was mostly to the lipopolysaccharide (LPS). We synthesized conjugates of detoxified LPS with cholera toxin (CT) and other proteins in order to elicit serum LPS antibodies with vibriocidal activity. Treatment with hydrazine (deacylated LPS) reduced the endotoxic properties of the LPS to clinically acceptable levels and resulted in a molecule larger and more antigenic than the saccharide produced by acid hydrolysis. More immunogenic conjugates resulted from multipoint compared with single-point attachment of the deacylated LPS to the protein. The conjugates containing CT had low levels of pyrogen and no toxic activity upon Chinese hamster ovary cells and elicited booster responses of vibriocidal and CT antibodies when injected subcutaneously as saline solutions into mice; the vibriocidal titers were similar to those elicited by comparable doses of cellular vaccines. We suggest how serum vibriocidal antibodies might prevent cholera. JF - Infection and immunity AU - Gupta, R K AU - Szu, S C AU - Finkelstein, R A AU - Robbins, J B AD - Laboratory of Developmental and Molecular Immunity, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 3201 EP - 3208 VL - 60 IS - 8 SN - 0019-9567, 0019-9567 KW - Antibodies, Bacterial KW - 0 KW - Cholera Vaccines KW - Lipopolysaccharides KW - Vaccines, Synthetic KW - Cholera Toxin KW - 9012-63-9 KW - Index Medicus KW - Animals KW - Antibodies, Bacterial -- analysis KW - Antibodies, Bacterial -- immunology KW - Rabbits KW - Mice KW - Mice, Inbred BALB C KW - Female KW - Cholera Toxin -- immunology KW - Lipopolysaccharides -- immunology KW - Cholera Vaccines -- immunology KW - Vibrio cholerae -- immunology KW - Vaccines, Synthetic -- immunology KW - Lipopolysaccharides -- toxicity KW - Cholera Toxin -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73072829?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+and+immunity&rft.atitle=Synthesis%2C+characterization%2C+and+some+immunological+properties+of+conjugates+composed+of+the+detoxified+lipopolysaccharide+of+Vibrio+cholerae+O1+serotype+Inaba+bound+to+cholera+toxin.&rft.au=Gupta%2C+R+K%3BSzu%2C+S+C%3BFinkelstein%2C+R+A%3BRobbins%2C+J+B&rft.aulast=Gupta&rft.aufirst=R&rft.date=1992-08-01&rft.volume=60&rft.issue=8&rft.spage=3201&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 completed - 1992-08-28 N1 - Date created - 1992-08-28 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Vaccine. 1990 Oct;8(5):469-72 [2251873] J Immunol. 1970 Aug;105(2):431-41 [5433700] Infect Immun. 1991 Mar;59(3):977-82 [1705246] Infect Immun. 1991 Nov;59(11):4266-70 [1937784] Infect Immun. 1986 Aug;53(2):272-7 [2426198] Bull Johns Hopkins Hosp. 1965 Mar;116:152-60 [14280312] Am J Public Health Nations Health. 1954 Dec;44(12):1572-9 [13207484] Biochem J. 1952 Jan;50(3):298-303 [14915949] J Infect Dis. 1991 Aug;164(2):407-11 [1856488] Infect Immun. 1991 Dec;59(12):4450-8 [1937803] J Infect Dis. 1991 Jun;163(6):1235-42 [2037789] J Clin Microbiol. 1986 Aug;24(2):203-9 [3528211] Infect Immun. 1987 May;55(5):1116-20 [3552989] J Biol Stand. 1986 Jan;14(1):25-33 [2420803] J Immunol. 1986 Aug 15;137(4):1181-6 [3016088] Infect Immun. 1986 Nov;54(2):448-55 [3095243] J Infect Dis. 1988 Aug;158(2):301-11 [3042872] Infect Immun. 1988 Jan;56(1):142-8 [2447017] Infect Immun. 1989 Dec;57(12):3823-7 [2807549] J Med Microbiol. 1987 Feb;23(1):9-18 [3820275] J Bacteriol. 1985 Feb;161(2):795-8 [3968044] J Infect Dis. 1990 May;161(5):821-32 [2182727] Lancet. 1990 Feb 3;335(8684):270-3 [1967730] Infect Immun. 1990 Apr;58(4):1030-7 [2108085] Infect Immun. 1990 Jul;58(7):2352-60 [1694826] Infect Immun. 1990 Jul;58(7):2309-12 [2365462] Adv Exp Med Biol. 1990;256:189-97 [2327294] Carbohydr Res. 1982 Mar 1;100:341-9 [7083255] J Immunol. 1984 Jun;132(6):2736-41 [6233359] Infect Immun. 1984 Feb;43(2):515-22 [6693169] Infect Immun. 1979 Nov;26(2):528-33 [546785] Biochim Biophys Acta. 1979 May 1;584(2):346-52 [86366] J Infect Dis. 1977 Aug;136 Suppl:S105-12 [197173] Immunochemistry. 1978 Sep;15(9):611-4 [738758] Lancet. 1973 Jun 2;1(7814):1232-5 [4122575] J Infect Dis. 1974 Oct;130(4):325-33 [4443613] Infect Immun. 1976 Mar;13(3):735-40 [1270131] Eur J Biochem. 1974 Oct 2;48(2):319-23 [4375034] J Infect Dis. 1972 Oct;126(4):401-7 [4627648] J Infect Dis. 1972 Jul;126(1):41-7 [5038023] J Infect Dis. 1970 May;121(5):505-13 [4986889] J Infect Dis. 1971 Aug;124(2):223-6 [4942061] J Infect Dis. 1971 Oct;124(4):359-66 [5143844] Proc Natl Acad Sci U S A. 1991 Mar 1;88(5):1641-5 [2000374] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Bipartite signal for read-through suppression in murine leukemia virus mRNA: an eight-nucleotide purine-rich sequence immediately downstream of the gag termination codon followed by an RNA pseudoknot. AN - 73058503; 1629968 AB - The pol gene of murine leukemia virus and other mammalian type C retroviruses is expressed by read-through suppression of an in-frame UAG codon which separates the gag and pol coding regions. In this study, we have analyzed the sequence requirements for read-through suppression by placing different portions of wild-type and mutant viral sequences from the gag-pol junction between reporter genes and testing transcripts of these constructs for suppression in reticulocyte lysates. We find that the read-through signal is contained within the first 57 nucleotides on the 3' side of the UAG codon. Our results indicate that the identities of six conserved bases in the eight-nucleotide, purine-rich sequence immediately downstream of the UAG codon are critical for suppression, as is the existence of a pseudoknot structure spanning the next 49 nucleotides. Thus, read-through suppression depends on a complex, bipartite signal in the mRNA. JF - Journal of virology AU - Feng, Y X AU - Yuan, H AU - Rein, A AU - Levin, J G AD - Laboratory of Molecular Virology and Carcinogenesis, NCI-Frederick Cancer Research and Development Center, Maryland 21702. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 5127 EP - 5132 VL - 66 IS - 8 SN - 0022-538X, 0022-538X KW - gag KW - pol KW - Codon KW - 0 KW - Fusion Proteins, gag-pol KW - RNA, Messenger KW - RNA, Viral KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Animals KW - Base Sequence KW - Codon -- genetics KW - Reticulocytes -- metabolism KW - Molecular Sequence Data KW - Fusion Proteins, gag-pol -- genetics KW - Transcription, Genetic KW - Nucleic Acid Conformation KW - Signal Transduction KW - Genes, pol KW - Cloning, Molecular KW - Terminator Regions, Genetic KW - Suppression, Genetic KW - Moloney murine leukemia virus -- genetics KW - RNA, Viral -- genetics KW - RNA, Messenger -- genetics KW - Genes, gag UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73058503?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Bipartite+signal+for+read-through+suppression+in+murine+leukemia+virus+mRNA%3A+an+eight-nucleotide+purine-rich+sequence+immediately+downstream+of+the+gag+termination+codon+followed+by+an+RNA+pseudoknot.&rft.au=Feng%2C+Y+X%3BYuan%2C+H%3BRein%2C+A%3BLevin%2C+J+G&rft.aulast=Feng&rft.aufirst=Y&rft.date=1992-08-01&rft.volume=66&rft.issue=8&rft.spage=5127&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 - 1992-08-14 N1 - Date created - 1992-08-14 N1 - Date revised - 2017-01-13 N1 - Gene symbol - gag; pol N1 - SuppNotes - Cited By: Cell. 1989 May 19;57(4):537-47 [2720781] J Virol. 1989 May;63(5):2405-10 [2784837] Nucleic Acids Res. 1985 Mar 11;13(5):1717-31 [4000943] Trends Biochem Sci. 1990 Apr;15(4):143-7 [1692647] J Virol. 1990 Jun;64(6):2642-52 [2186174] Virus Genes. 1990 Jul;4(2):121-36 [2402881] Virology. 1984 Apr 15;134(1):196-207 [6200992] J Virol. 1984 Jan;49(1):214-22 [6197537] Nature. 1981 Oct 15-21;293(5833):543-8 [6169994] Virology. 1977 May 1;78(1):11-34 [67705] Cell. 1978 Jan;13(1):189-99 [202399] EMBO J. 1984 Feb;3(2):351-6 [16453503] J Biol Chem. 1991 Sep 5;266(25):16257-60 [1832153] J Virol. 1984 Feb;49(2):471-8 [6319746] J Virol. 1980 May;34(2):464-73 [7373716] Nature. 1991 Sep 19;353(6341):273-6 [1832744] Proc Natl Acad Sci U S A. 1990 Nov;87(22):8860-3 [2247457] Proc Natl Acad Sci U S A. 1992 Jan 15;89(2):713-7 [1309954] Adv Virus Res. 1992;41:193-239 [1575083] J Mol Biol. 1991 Aug 20;220(4):889-902 [1880803] Proc Natl Acad Sci U S A. 1991 Aug 15;88(16):6991-5 [1871115] Virology. 1991 Jul;183(1):313-9 [2053284] J Mol Biol. 1991 Mar 20;218(2):365-73 [2010914] Proc Natl Acad Sci U S A. 1991 Jan 1;88(1):174-8 [1986362] J Virol. 1988 Oct;62(10):3574-80 [2843660] Cell. 1988 Nov 4;55(3):447-58 [2846182] Cell. 1989 Jul 14;58(1):9-12 [2473840] J Virol. 1986 Oct;60(1):267-74 [2427747] Nucleic Acids Res. 1989 Aug 11;17(15):5933-45 [2549503] J Virol. 1989 Jun;63(6):2870-3 [2542597] Proc Natl Acad Sci U S A. 1985 Mar;82(6):1618-22 [3885215] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interaction of the human papillomavirus type 16 E6 oncoprotein with wild-type and mutant human p53 proteins. AN - 73053400; 1321290 AB - The E6 oncoproteins encoded by the cancer-associated human papillomaviruses (HPVs) can associate with and promote the degradation of wild-type p53 in vitro. To gain further insight into this process, the ability of HPV-16 E6 to complex with and promote the degradation of mutant forms of p53 was studied. A correlation between binding and the targeted degradation of p53 was established. Mutant p53 proteins that bound HPV-16 E6 were targeted for degradation, whereas those that did not complex HPV-16 E6 were not degraded. Since the HPV-16 E6-promoted degradation involves the ubiquitin-dependent proteolysis pathway, specific mutations were made in the amino terminus of p53 to examine whether the E6 targeted degradation involved the N-end rule pathway. No requirement for destabilizing amino acids at the N terminus of p53 was found, nor was evidence found that HPV-16 E6 could provide this determinant in trans, indicating that the N-terminal rule pathway is not involved in the E6-promoted degradation of p53. JF - Journal of virology AU - Scheffner, M AU - Takahashi, T AU - Huibregtse, J M AU - Minna, J D AU - Howley, P M AD - Laboratory of Tumor Virus Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 5100 EP - 5105 VL - 66 IS - 8 SN - 0022-538X, 0022-538X KW - E6 protein, Human papillomavirus type 16 KW - 0 KW - Oligodeoxyribonucleotides KW - Oncogene Proteins, Viral KW - Repressor Proteins KW - Tumor Suppressor Protein p53 KW - Index Medicus KW - Protein Biosynthesis KW - Polymerase Chain Reaction KW - Animals KW - Humans KW - Reticulocytes -- metabolism KW - Papillomaviridae -- metabolism KW - Rabbits KW - Papillomaviridae -- genetics KW - Amino Acid Sequence KW - Binding Sites KW - Mutagenesis, Site-Directed KW - Oncogene Proteins, Viral -- genetics KW - Tumor Suppressor Protein p53 -- genetics KW - Tumor Suppressor Protein p53 -- metabolism KW - Oncogene Proteins, Viral -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73053400?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Interaction+of+the+human+papillomavirus+type+16+E6+oncoprotein+with+wild-type+and+mutant+human+p53+proteins.&rft.au=Scheffner%2C+M%3BTakahashi%2C+T%3BHuibregtse%2C+J+M%3BMinna%2C+J+D%3BHowley%2C+P+M&rft.aulast=Scheffner&rft.aufirst=M&rft.date=1992-08-01&rft.volume=66&rft.issue=8&rft.spage=5100&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 - 1992-08-14 N1 - Date created - 1992-08-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nature. 1979 Mar 15;278(5701):261-3 [218111] Mol Cell Biol. 1981 Feb;1(2):101-10 [6100960] Oncogene. 1991 May;6(5):873-5 [1646990] Proc Natl Acad Sci U S A. 1991 Jul 1;88(13):5523-7 [1648218] Mol Carcinog. 1991;4(3):171-5 [1648361] J Virol. 1991 Dec;65(12):6671-6 [1658367] EMBO J. 1991 Dec;10(13):4129-35 [1661671] EMBO J. 1990 May;9(5):1595-602 [1691710] J Virol. 1991 Jan;65(1):292-8 [1845889] Nature. 1991 Jan 10;349(6305):132-8 [1846030] Proc Natl Acad Sci U S A. 1991 Jan 1;88(1):139-43 [1846034] Lancet. 1990 May 19;335(8699):1171-4 [1971033] Oncogene. 1990 Oct;5(10):1603-10 [1979160] Cell. 1991 May 31;65(5):765-74 [2040013] Cell. 1990 May 18;61(4):697-708 [2111732] Oncogene. 1990 Jul;5(7):945-52 [2142762] J Virol. 1990 Mar;64(3):1353-6 [2154613] Cell. 1990 Dec 21;63(6):1129-36 [2175676] New Biol. 1990 Mar;2(3):227-34 [2177651] EMBO J. 1988 Jun;7(6):1815-20 [2458921] J Biol Chem. 1989 Oct 5;264(28):16700-12 [2506181] J Virol. 1989 Mar;63(3):1247-55 [2536832] J Virol. 1989 Mar;63(3):1465-9 [2536847] EMBO J. 1989 Dec 1;8(12):3905-10 [2555178] Med Microbiol Immunol. 1987;176(5):245-56 [2821369] Cell. 1988 May 20;53(4):539-47 [2836062] Cell. 1988 Jul 15;54(2):275-83 [2839300] Nature. 1988 Jul 14;334(6178):124-9 [2968522] Proc Natl Acad Sci U S A. 1986 Jul;83(13):4680-4 [3014503] J Virol. 1987 Apr;61(4):962-71 [3029430] Cell. 1984 Aug;38(1):119-26 [6088057] Cell. 1982 Feb;28(2):387-94 [6277513] Mol Cell Biol. 1983 Dec;3(12):2143-50 [6318085] Nature. 1991 Jun 6;351(6326):453-6 [2046748] J Virol. 1990 Feb;64(2):723-30 [2153238] Nature. 1990 Jul 19;346(6281):287-91 [2165217] Science. 1990 Oct 5;250(4977):113-6 [2218501] J Virol. 1989 Oct;63(10):4417-21 [2476573] J Virol. 1989 Feb;63(2):965-9 [2536119] Science. 1989 Feb 17;243(4893):934-7 [2537532] EMBO J. 1989 Dec 20;8(13):4099-105 [2556261] Virology. 1988 Jul;165(1):321-5 [2838969] Oncogene Res. 1988 Sep;3(2):167-75 [2852339] Nature. 1985 Mar 7-13;314(6006):111-4 [2983228] J Biol Chem. 1988 Feb 25;263(6):2693-8 [3343227] Cell. 1979 May;17(1):43-52 [222475] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutational analysis of the core, spacer, and initiator regions of vaccinia virus intermediate-class promoters. AN - 73053187; 1629951 AB - Activation of vaccinia virus late gene transcription is dependent on DNA replication and the expression of three genes: A1L, A2L, and G8R (J. G. Keck, C. J. Baldick, Jr., and B. Moss, Cell 61:801-809, 1990). To fully characterize the promoter elements of these trans-activator genes, we prepared more than 140 plasmid vectors containing natural and mutated DNA segments ligated to the Escherichia coli lacZ or chloramphenicol acetyltransferase reporter gene. Expression of the reporter genes occurred when the plasmids were transfected into vaccinia virus-infected cells and was enhanced when DNA replication was prevented, indicating that the A1L, A2L, and G8R promoters belong to the intermediate regulatory class. Deletional mutagenesis demonstrated that the regulatory elements of all three promoters extended between 20 and 30 nucleotides upstream of their RNA start sites. Single-base substitutions of the G8R promoter revealed two critical elements located from -26 to -13 (the core element) and -1 to +3 (the initiator element). Mutations in these regions drastically affected expression, as determined by beta-galactosidase and mRNA analyses. Additional mutations defined the TAAA sequence as the critical initiator element. The length, but not the nucleotide sequence, of the segment between the core and initiator regions was crucial. The requirement for the spacer to be 10 or 11 nucleotides was consistent with a single turn of a double helix. The A1L and A2L promoters resembled the G8R promoter, and mutations in the conserved bases had the predicted effects on expression. We concluded that the three intermediate promoters are composed of a 14-bp A+T-rich core sequence separated by one turn of the double helix from the TAAA initiator element. JF - Journal of virology AU - Baldick, C J AU - Keck, J G AU - Moss, B AD - Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 4710 EP - 4719 VL - 66 IS - 8 SN - 0022-538X, 0022-538X KW - A1L KW - A2L KW - G8R KW - DNA, Ribosomal KW - 0 KW - Oligodeoxyribonucleotides KW - RNA, Viral KW - Trans-Activators KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Base Sequence KW - Transfection KW - Humans KW - Restriction Mapping KW - Polymerase Chain Reaction -- methods KW - Molecular Sequence Data KW - Transcription, Genetic KW - RNA, Viral -- isolation & purification KW - RNA, Viral -- genetics KW - DNA Replication KW - Cell Line KW - Cloning, Molecular KW - Vaccinia virus -- genetics KW - Promoter Regions, Genetic KW - Trans-Activators -- genetics KW - Genes, Viral KW - DNA, Ribosomal -- genetics KW - Genes, Regulator UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73053187?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+core%2C+spacer%2C+and+initiator+regions+of+vaccinia+virus+intermediate-class+promoters.&rft.au=Baldick%2C+C+J%3BKeck%2C+J+G%3BMoss%2C+B&rft.aulast=Baldick&rft.aufirst=C&rft.date=1992-08-01&rft.volume=66&rft.issue=8&rft.spage=4710&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 - 1992-08-14 N1 - Date created - 1992-08-14 N1 - Date revised - 2017-01-13 N1 - Gene symbol - A1L; A2L; G8R N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1989 Aug;86(16):6126-30 [2548200] J Virol. 1989 Oct;63(10):4224-33 [2476568] Virology. 1987 May;158(1):206-10 [3472413] Anal Biochem. 1987 Apr;162(1):156-9 [2440339] EMBO J. 1986 Aug;5(8):1951-7 [3019674] Proc Natl Acad Sci U S A. 1985 Jan;82(1):19-23 [3855541] EMBO J. 1987 Dec 1;6(12):3787-94 [2828037] J Virol. 1988 Jun;62(6):1889-97 [2835495] EMBO J. 1988 Nov;7(11):3487-92 [2850166] EMBO J. 1986 May;5(5):1071-6 [3013615] J Virol. 1986 Nov;60(2):436-49 [3021979] Nucleic Acids Res. 1986 Apr 11;14(7):3003-16 [3008103] J Virol. 1989 Jan;63(1):226-32 [2462059] J Mol Biol. 1989 Dec 20;210(4):771-84 [2515287] J Mol Biol. 1989 Dec 20;210(4):749-69 [2515286] J Virol. 1988 Jan;62(1):297-304 [3334746] Anal Biochem. 1986 Feb 1;152(2):232-8 [3516005] Proc Natl Acad Sci U S A. 1987 Sep;84(17):6069-73 [3476927] Cell. 1987 Jul 17;50(2):163-9 [3594569] J Virol. 1987 Jan;61(1):75-80 [3783825] J Virol. 1985 Apr;54(1):30-7 [3973982] J Virol. 1990 Jun;64(6):3019-24 [2335825] Proc Natl Acad Sci U S A. 1990 Feb;87(4):1536-40 [1968253] Annu Rev Biochem. 1990;59:661-88 [2197987] Cell. 1990 Jun 1;61(5):801-9 [2344616] J Biol Chem. 1991 Aug 15;266(23):15539-44 [1869571] EMBO J. 1991 Sep;10(9):2553-8 [1651230] J Biol Chem. 1991 Jan 25;266(3):1355-8 [1988424] Cell. 1991 Apr 5;65(1):105-13 [2013091] J Virol. 1991 Jul;65(7):3715-20 [2041091] J Virol. 1990 Dec;64(12):6063-9 [2243387] J Biol Chem. 1988 May 5;263(13):6220-5 [2834368] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A block in full-length transcript maturation in cells nonpermissive for B19 parvovirus. AN - 73049885; 1385833 AB - Vertebrate parvoviruses share a similar genomic organization, with the capsid proteins encoded by genes on the right side and nonstructural proteins encoded by genes on the left side. The temporal and cell-specific appearances of these two types of gene products are regulated by a variety of genetic mechanisms. Rodent parvovirus structural proteins, for example, are encoded by a separate promoter which is positively regulated by nonstructural-gene products. In contrast, for the human B19 parvovirus, the analogous structural-gene promoter is nonfunctional, and both left- and right-side transcripts originate from a single promoter and are highly processed. Using a combination of sensitive RNA analyses of wild-type and mutant templates, we have found that the relative abundance of these alternatively processed transcripts appears to be governed by unique postinitiation events. In permissive cells, the steady-state level of right-side structural-gene transcripts predominates over that of left-side nonstructural-gene transcripts. In nonpermissive cells transfected with the B19 virus genome, nonstructural-gene transcripts predominate. Removal of 3' processing signals located in the middle of the viral genome increases transcription of the far right side. Disruption of a polyadenylation signal in this region makes readthrough of full-length right-side transcripts possible. These results suggest that the abundance of B19 virus RNAs is determined by active 3' processing and is coupled to DNA template replication. JF - Journal of virology AU - Liu, J M AU - Green, S W AU - Shimada, T AU - Young, N S AD - Clinical Hematology Branch, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 4686 EP - 4692 VL - 66 IS - 8 SN - 0022-538X, 0022-538X KW - Capsid Proteins KW - 0 KW - DNA, Viral KW - Oligodeoxyribonucleotides KW - Oligonucleotides, Antisense KW - RNA, Viral KW - Viral Core Proteins KW - Viral Nonstructural Proteins KW - Index Medicus KW - Animals KW - Blotting, Northern KW - HeLa Cells KW - Humans KW - Transcription, Genetic KW - Mutagenesis, Site-Directed KW - Promoter Regions, Genetic KW - Base Sequence KW - Transfection KW - Restriction Mapping KW - Polymerase Chain Reaction -- methods KW - Molecular Sequence Data KW - Templates, Genetic KW - Cell Line KW - Parvoviridae -- genetics KW - Capsid -- genetics KW - Viral Core Proteins -- genetics KW - RNA, Viral -- genetics KW - Parvoviridae -- physiology KW - DNA, Viral -- genetics KW - DNA Replication UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73049885?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+block+in+full-length+transcript+maturation+in+cells+nonpermissive+for+B19+parvovirus.&rft.au=Liu%2C+J+M%3BGreen%2C+S+W%3BShimada%2C+T%3BYoung%2C+N+S&rft.aulast=Liu&rft.aufirst=J&rft.date=1992-08-01&rft.volume=66&rft.issue=8&rft.spage=4686&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 - 1992-08-14 N1 - Date created - 1992-08-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Blood. 1990 Nov 15;76(10):1997-2004 [2146978] Virology. 1991 Jul;183(1):133-42 [2053277] J Biol Chem. 1989 Jun 15;264(17):10057-64 [2722860] Virology. 1989 Oct;172(2):659-64 [2800343] Semin Hematol. 1988 Apr;25(2):159-72 [2838911] J Clin Invest. 1987 May;79(5):1486-92 [3033026] Blood. 1987 Aug;70(2):384-91 [3038211] Science. 1987 Jun 5;236(4806):1237-45 [3296191] J Gen Virol. 1987 Mar;68 ( Pt 3):601-14 [3546593] J Virol. 1986 Jun;58(3):921-36 [3701931] J Virol. 1984 Oct;52(1):266-76 [6090703] Cell. 1981 Dec;27(2 Pt 1):279-88 [6277501] Cell. 1982 Aug;30(1):173-83 [6290076] Cell. 1980 Jun;20(2):293-301 [6771018] Cell. 1980 Jun;20(2):303-12 [6771019] Nature. 1981 Mar 12;290(5802):113-8 [7207591] Cell. 1978 Jul;14(3):725-31 [210957] Virology. 1991 Nov;185(1):39-47 [1926783] Virology. 1991 May;182(1):361-4 [2024472] J Virol. 1990 Jan;64(1):387-96 [2293668] J Virol. 1989 Jun;63(6):2422-6 [2657097] Gene. 1989 Apr 15;77(1):51-9 [2744487] J Virol. 1988 Aug;62(8):2884-9 [2969055] N Engl J Med. 1987 Jul 30;317(5):287-94 [3037373] Adv Virus Res. 1987;33:91-174 [3296697] J Virol. 1987 Aug;61(8):2395-406 [3599180] Science. 1986 Aug 22;233(4766):883-6 [3738514] Nature. 1982 Jul 15;298(5871):240-4 [6283379] J Virol. 1983 Jun;46(3):937-43 [6602221] Cell. 1980 Jun;20(2):313-9 [6771020] Blood. 1992 Jan 1;79(1):18-24 [1728307] Genes Dev. 1991 Feb;5(2):244-53 [1995416] Blood. 1990 Feb 1;75(3):603-10 [2404522] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ultraviolet light irradiation increases cellular diacylglycerol and induces translocation of diacylglycerol kinase in murine keratinocytes. AN - 73048760; 1321202 AB - Cellular lipid metabolism can provide a variety of mediators of signal transduction, including diacylglycerols and inositol phosphates. These factors may be involved in the control of epidermal differentiation and proliferation because they are modulated by extracellular calcium, which also regulates the maturation phenotype of cultured keratinocytes. The effect of non-cytotoxic exposures to ultraviolet light on lipid metabolism was studied in cultured murine keratinocytes. Ultraviolet treatment of cultured murine keratinocytes growing in 0.05 mM Ca++ did not significantly change the total amount of [3H]inositol phosphates at 0.5, 8 or 24 h post-irradiation. Irradiated cells responded to an increase from 0.05 mM Ca++ to 1.4 mM Ca++ medium with increased formation of inositol phosphates suggesting irradiation did not alter the normal inositol lipid turnover in response to the Ca++ signal for terminal differentiation. Irradiation (20-120 J/m2 of UVB) induced a dose-dependent increase in the cellular level of diacylglycerols as measured at 24 h post-irradiation, without changing the turnover of other phospholipids including phosphatidylcholine and phosphatidylethanolamine. The increased cellular levels of diacylglycerols following ultraviolet exposure were accompanied by changes in the activity of diacylglycerol kinase (DAG-kinase). The cytosolic DAG-kinase activity was decreased whereas the DAG-kinase activity in the membrane fraction was increased. These results suggest that ultraviolet irradiation increases the level of diacylglycerols via changes in de novo metabolism through a DAG-kinase pathway. Elevated diacylglycerol may influence signal-transduction pathways mediated by cellular lipids and contribute to some keratinocyte responses to ultraviolet light. JF - The Journal of investigative dermatology AU - Punnonen, K AU - Yuspa, S H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 221 EP - 226 VL - 99 IS - 2 SN - 0022-202X, 0022-202X KW - Diglycerides KW - 0 KW - Membrane Lipids KW - Phospholipids KW - Phosphotransferases KW - EC 2.7.- KW - Diacylglycerol Kinase KW - EC 2.7.1.107 KW - Index Medicus KW - Translocation, Genetic -- radiation effects KW - Animals KW - Cells, Cultured KW - Phospholipids -- analysis KW - Mice KW - Diglycerides -- analysis KW - Chromatography, Thin Layer KW - Signal Transduction -- radiation effects KW - Phosphotransferases -- genetics KW - Ultraviolet Rays KW - Membrane Lipids -- radiation effects KW - Keratinocytes -- chemistry KW - Keratinocytes -- enzymology KW - Membrane Lipids -- metabolism KW - Keratinocytes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73048760?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Ultraviolet+light+irradiation+increases+cellular+diacylglycerol+and+induces+translocation+of+diacylglycerol+kinase+in+murine+keratinocytes.&rft.au=Punnonen%2C+K%3BYuspa%2C+S+H&rft.aulast=Punnonen&rft.aufirst=K&rft.date=1992-08-01&rft.volume=99&rft.issue=2&rft.spage=221&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 - 1992-08-20 N1 - Date created - 1992-08-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Basis for receptor specificity of nonecotropic murine leukemia virus surface glycoprotein gp70SU. AN - 73043934; 1321266 AB - Murine leukemia viruses (MuLVs) initiate infection of NIH 3T3 cells by binding of the viral envelope (Env) protein to a cell surface receptor. Interference assays have shown that MuLVs can be divided into four groups, each using a distinct receptor: ecotropic, polytropic, amphotropic, and 10A1. In this study, we have attempted to map the determinants within viral Env proteins by constructing chimeric env genes. Chimeras were made in all six pairwise combinations between Moloney MCF (a polytropic MuLV), amphotropic MuLV, and 10A1, using a conserved EcoRI site in the middle of the Env coding region. The receptor specificity of each chimera was determined by using an interference assay. We found that amphotropic receptor specificity of each chimera was determined by using an interference assay. We found that amphotropic receptor specificity seems to map to the N-terminal portion of surface glycoprotein gp70SU. The difference between amphotropic and 10A1 receptor specificity can be attributed to one or more of only six amino acid differences in this region. Nearly all other cases showed evidence of interaction between Env domains in the generation of receptor specificity. Thus, a chimera composed exclusively of MCF and amphotropic sequences was found to exhibit 10A1 receptor specificity. None of the chimeras were able to infect cells by using the MCF receptor; however, two chimeras containing the C-terminal portion of MCF gp70SU could bind to this receptor, while they were able to infect cells via the amphotropic receptor. This result raises the possibility that receptor binding maps to the C-terminal portion of MCF gp70SU but requires MCF N-terminal sequences for a functional interaction with the MCF receptor. JF - Journal of virology AU - Ott, D AU - Rein, A AD - Laboratory of Molecular Virology and Carcinogenesis, NCI-Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1992/08// PY - 1992 DA - August 1992 SP - 4632 EP - 4638 VL - 66 IS - 8 SN - 0022-538X, 0022-538X KW - Receptors, Virus KW - 0 KW - Retroviridae Proteins, Oncogenic KW - Viral Envelope Proteins KW - Index Medicus KW - Animals KW - 3T3 Cells KW - Chimera KW - Sequence Homology, Nucleic Acid KW - Molecular Sequence Data KW - CHO Cells KW - Mice KW - Amino Acid Sequence KW - Cricetinae KW - Leukemia Virus, Murine -- physiology KW - Retroviridae Proteins, Oncogenic -- genetics KW - Receptors, Virus -- physiology KW - Leukemia Virus, Murine -- genetics KW - Viral Envelope Proteins -- metabolism KW - Retroviridae Proteins, Oncogenic -- metabolism KW - Viral Envelope Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73043934?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Basis+for+receptor+specificity+of+nonecotropic+murine+leukemia+virus+surface+glycoprotein+gp70SU.&rft.au=Ott%2C+D%3BRein%2C+A&rft.aulast=Ott&rft.aufirst=D&rft.date=1992-08-01&rft.volume=66&rft.issue=8&rft.spage=4632&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 - 1992-08-14 N1 - Date created - 1992-08-14 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M33470; GENBANK; M55596; M33469; M55597 N1 - SuppNotes - Cited By: Virology. 1991 Aug;183(2):545-54 [1853560] Virology. 1984 Jul 15;136(1):144-52 [6330990] J Virol. 1989 Jan;63(1):273-80 [2535733] Cell. 1986 May 9;45(3):365-74 [3009025] Virology. 1986 Jul 30;152(2):343-54 [3014723] Virology. 1966 Aug;29(4):642-53 [4287699] J Virol. 1980 Mar;33(3):983-92 [6154154] J Virol. 1984 Feb;49(2):452-8 [6198530] J Virol. 1981 Sep;39(3):777-91 [6270351] J Virol. 1983 Jan;45(1):1-9 [6296423] J Virol. 1982 Oct;44(1):19-31 [7143566] J Virol. 1992 Mar;66(3):1468-75 [1310758] J Virol. 1990 Feb;64(2):757-66 [2153240] J Virol. 1985 Jan;53(1):32-9 [2981357] Proc Natl Acad Sci U S A. 1988 Nov;85(22):8420-4 [3141927] Virology. 1973 Apr;52(2):456-67 [4705382] Nature. 1981 Oct 15-21;293(5833):543-8 [6169994] Virology. 1982 Jul 15;120(1):251-7 [6285602] J Virol. 1991 Aug;65(8):4026-32 [2072445] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mechanistic aspects of signaling through Ras in NIH 3T3 cells. AN - 73101039; 1496380 AB - Serum and growth factors can increase the proportion of Ras in the active guanosine triphosphate (GTP)-bound form. Growth factors might stimulate guanine nucleotide exchange or decrease the activity of the guanosine triphosphatase-activating proteins GAP and neurofibromin (NF1). In NIH 3T3 cells that overexpress the mutant Ras protein His116, which releases bound guanine nucleotide at a constitutively high rate and retains sensitivity to GAP and NF1, the proportion of GTP bound to the His116 protein was not altered by serum or platelet-derived growth factor. However, these mitogens increased the proportion of Ras in the GTP-bound form in cells that overexpressed control Ras proteins with a normal intrinsic rate of guanine nucleotide release. The amount of GTP-bound His116 or control Ras proteins was higher in cells at low density than in cells at high density, which have more GAP-like activity. The lower proportion of GTP-bound Ras in NIH 3T3 cells at high density may result from increased GAP-like activity. By contrast, serum and platelet-derived growth factors appear to stimulate guanine nucleotide exchange. JF - Science (New York, N.Y.) AU - Zhang, K AU - Papageorge, A G AU - Lowy, D R AD - Laboratory of Cellular Oncology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/07/31/ PY - 1992 DA - 1992 Jul 31 SP - 671 EP - 674 VL - 257 IS - 5070 SN - 0036-8075, 0036-8075 KW - c-ras KW - GTPase-Activating Proteins KW - 0 KW - Growth Substances KW - Neurofibromin 1 KW - Platelet-Derived Growth Factor KW - Proteins KW - ras GTPase-Activating Proteins KW - Histidine KW - 4QD397987E KW - Guanosine Triphosphate KW - 86-01-1 KW - Methionine KW - AE28F7PNPL KW - Proto-Oncogene Proteins p21(ras) KW - EC 3.6.5.2 KW - Index Medicus KW - 3T3 Cells KW - Animals KW - Platelet-Derived Growth Factor -- pharmacology KW - Gene Expression KW - Mice KW - Mutagenesis KW - Proteins -- pharmacology KW - Blood KW - Cell Line, Transformed KW - Proto-Oncogene Proteins p21(ras) -- metabolism KW - Growth Substances -- pharmacology KW - Genes, ras -- physiology KW - Signal Transduction -- genetics KW - Proto-Oncogene Proteins p21(ras) -- chemistry KW - Fibroblasts -- metabolism KW - Proto-Oncogene Proteins p21(ras) -- genetics KW - Guanosine Triphosphate -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73101039?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mechanistic+aspects+of+signaling+through+Ras+in+NIH+3T3+cells.&rft.au=Zhang%2C+K%3BPapageorge%2C+A+G%3BLowy%2C+D+R&rft.aulast=Zhang&rft.aufirst=K&rft.date=1992-07-31&rft.volume=257&rft.issue=5070&rft.spage=671&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 - 1992-09-04 N1 - Date created - 1992-09-04 N1 - Date revised - 2017-01-13 N1 - Gene symbol - c-ras N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inhibition of protein phosphatases blocks myogenesis by first altering MyoD binding activity. AN - 73081346; 1321827 AB - To examine the role of protein phosphatases in skeletal muscle differentiation, C2C12 myoblasts were treated with okadaic acid, a potent in vitro inhibitor of protein phosphatases 1 and 2A which regulate various cellular events in intact cells. We now show that okadaic acid treatment of the mouse myoblast C2C12 cell line reversibly altered the morphology of the cells and blocked differentiation. At a molecular level, it extinguished expression of the myogenic determination genes, MyoD1 and myogenin, but induced the expression of an inhibitor of differentiation, Id. Analysis of the MyoD1 promoter showed that inhibition of MyoD1 expression by okadaic acid occurs at the transcriptional level. These changes occur 10-20 h after okadaic acid treatment. However, within 1 h of treatment the ability of muscle extracts to support a specific MyoD-dependent gel mobility shift using a MyoD DNA binding site is lost. These data suggest that protein phosphatases play an important role during myogenic differentiation. JF - The Journal of biological chemistry AU - Kim, S J AU - Kim, K Y AU - Tapscott, S J AU - Winokur, T S AU - Park, K AU - Fujiki, H AU - Weintraub, H AU - Roberts, A B AD - Laboratory of Chemoprevention, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/07/25/ PY - 1992 DA - 1992 Jul 25 SP - 15140 EP - 15145 VL - 267 IS - 21 SN - 0021-9258, 0021-9258 KW - DNA-Binding Proteins KW - 0 KW - Ethers, Cyclic KW - Muscle Proteins KW - MyoD Protein KW - RNA, Messenger KW - Okadaic Acid KW - 1W21G5Q4N2 KW - DNA KW - 9007-49-2 KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Phosphoprotein Phosphatases KW - EC 3.1.3.16 KW - Index Medicus KW - Animals KW - DNA -- metabolism KW - Cell Differentiation KW - Mice KW - Ethers, Cyclic -- pharmacology KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Promoter Regions, Genetic KW - Base Sequence KW - RNA, Messenger -- metabolism KW - Transfection KW - Molecular Sequence Data KW - Muscles -- enzymology KW - Cell Line KW - Muscles -- drug effects KW - Phosphoprotein Phosphatases -- antagonists & inhibitors KW - Muscle Proteins -- metabolism KW - Muscle Proteins -- genetics KW - Muscle Development KW - DNA-Binding Proteins -- genetics KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73081346?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Inhibition+of+protein+phosphatases+blocks+myogenesis+by+first+altering+MyoD+binding+activity.&rft.au=Kim%2C+S+J%3BKim%2C+K+Y%3BTapscott%2C+S+J%3BWinokur%2C+T+S%3BPark%2C+K%3BFujiki%2C+H%3BWeintraub%2C+H%3BRoberts%2C+A+B&rft.aulast=Kim&rft.aufirst=S&rft.date=1992-07-25&rft.volume=267&rft.issue=21&rft.spage=15140&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 - 1992-08-26 N1 - Date created - 1992-08-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evidence for GTP-binding protein involvement in the tyrosine phosphorylation of the T cell receptor zeta chain. AN - 73077685; 1386076 AB - The zeta subunit of the T cell receptor (TCR) is a prominent substrate for a TCR-activated tyrosine kinase. Tyrosine phosphorylation of the zeta subunit in response to antibody-mediated receptor cross-linking was synergized in permeabilized T cells by either of two non-hydrolyzable GTP analogues, guanosine 5'-[gamma-thio]triphosphate (GTP gamma S) or guanosine 5'-[beta, gamma-imido]triphosphate Gpp(NH)p. ATP analogues did not significantly affect antibody-induced tyrosine phosphorylation. Unlike the GTP analogues, the GDP analogue guanosine 5'-[beta-thio]diphosphate (GDP beta S) did not enhance phosphorylation of zeta. The effect induced by the GTP analogues required TCR occupancy and was independent of protein kinase C. Taken together these observations implicate a GTP-binding protein in the modulation of TCR-induced tyrosine phosphorylation. JF - The Journal of biological chemistry AU - Cenciarelli, C AU - Hohman, R J AU - Atkinson, T P AU - Gusovsky, F AU - Weissman, A M AD - Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/07/25/ PY - 1992 DA - 1992 Jul 25 SP - 14527 EP - 14530 VL - 267 IS - 21 SN - 0021-9258, 0021-9258 KW - Receptors, Antigen, T-Cell, gamma-delta KW - 0 KW - Thionucleotides KW - Guanosine Diphosphate KW - 146-91-8 KW - 6-thioguanosine 5'-diphosphate KW - 16541-19-8 KW - Guanylyl Imidodiphosphate KW - 34273-04-6 KW - Guanosine 5'-O-(3-Thiotriphosphate) KW - 37589-80-3 KW - Tyrosine KW - 42HK56048U KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Guanylyl Imidodiphosphate -- metabolism KW - Blotting, Western KW - Tumor Cells, Cultured KW - Phosphorylation KW - Guanosine Diphosphate -- metabolism KW - Electrophoresis, Polyacrylamide Gel KW - Guanosine Diphosphate -- analogs & derivatives KW - Thionucleotides -- metabolism KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Guanosine 5'-O-(3-Thiotriphosphate) -- metabolism KW - Mice KW - GTP-Binding Proteins -- physiology KW - Tyrosine -- metabolism KW - Receptors, Antigen, T-Cell, gamma-delta -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73077685?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Evidence+for+GTP-binding+protein+involvement+in+the+tyrosine+phosphorylation+of+the+T+cell+receptor+zeta+chain.&rft.au=Cenciarelli%2C+C%3BHohman%2C+R+J%3BAtkinson%2C+T+P%3BGusovsky%2C+F%3BWeissman%2C+A+M&rft.aulast=Cenciarelli&rft.aufirst=C&rft.date=1992-07-25&rft.volume=267&rft.issue=21&rft.spage=14527&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 - 1992-08-26 N1 - Date created - 1992-08-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Identification of cis-regulatory elements in the myelin proteolipid protein (PLP) gene. AN - 73074474; 1378839 AB - Regulatory elements of the proteolipid protein (PLP) gene were identified physically by footprinting and gel mobility shift assays and functionally by transfecting glial cell lines with PLP-chloramphenicol acetyltransferase chimeric genes. In both human and rat glial cells, only several hundred base pairs of upstream sequence were sufficient for high level activity of the human PLP promoter. This region contains five sites that contact nuclear proteins in vitro. More distal recognition sites may exist, as regions upstream of -524 displayed silencing activity indicative of a negative regulatory element. A series of site directed mutations revealed one essential positive element (ATGGA at -118) which is found in other genes encoding myelin proteins. Our combined biochemical and functional analyses indicate that the key cis sites for maximal tissue-specific expression of PLP in cultured glial cells are clustered near the promoter. Within this cluster are several conserved motifs that may coordinate the regulation of myelin-specific genes. JF - The Journal of biological chemistry AU - Berndt, J A AU - Kim, J G AU - Hudson, L D AD - Laboratory of Viral and Molecular Pathogenesis, National Institute of Neurologic Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/07/25/ PY - 1992 DA - 1992 Jul 25 SP - 14730 EP - 14737 VL - 267 IS - 21 SN - 0021-9258, 0021-9258 KW - PLP KW - Myelin Proteins KW - 0 KW - Myelin Proteolipid Protein KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Index Medicus KW - Neuroglia -- cytology KW - Animals KW - HeLa Cells KW - Humans KW - Gene Expression KW - DNA Fingerprinting KW - Rats KW - Neuroglia -- metabolism KW - Mutagenesis, Site-Directed KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Promoter Regions, Genetic KW - Base Sequence KW - Chimera KW - Transfection KW - Cells, Cultured KW - Molecular Sequence Data KW - Methylation KW - Regulatory Sequences, Nucleic Acid KW - Myelin Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73074474?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+cis-regulatory+elements+in+the+myelin+proteolipid+protein+%28PLP%29+gene.&rft.au=Berndt%2C+J+A%3BKim%2C+J+G%3BHudson%2C+L+D&rft.aulast=Berndt&rft.aufirst=J&rft.date=1992-07-25&rft.volume=267&rft.issue=21&rft.spage=14730&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 - 1992-08-26 N1 - Date created - 1992-08-26 N1 - Date revised - 2017-01-13 N1 - Gene symbol - PLP N1 - Genetic sequence - M93105; GENBANK; M86615; M86618; M86619; M86616; M86617; X62322; M63383; M95057; M86620 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modulation of P-glycoprotein phosphorylation and drug transport by sodium butyrate. AN - 73081851; 1352990 AB - P-Glycoprotein (Pgp) expression in cell lines derived from tumors arising from cells which normally express Pgp can be increased by sodium butyrate and other differentiating agents. Although the Pgp level increased 25-fold after sodium butyrate treatment in SW620 human colon carcinoma cells, the intracellular accumulation of vinblastine, adriamycin, and actinomycin D increased rather than decreased. In contrast, colchicine showed the expected decrease in accumulation, as a result of increased efflux. Likewise, treatment of a Pgp-expressing multidrug-resistant SW620 subline with sodium butyrate resulted in active interference with Pgp function. This effect was partially reversed by phorbol esters with a resulting decrease in the accumulation of vinblastine, adriamycin, and actinomycin D. Sodium butyrate, while increasing Pgp levels, inhibited the phosphorylation of Pgp. Time course studies revealed a tight relationship between decreased Pgp phosphorylation and increased vinblastine accumulation after sodium butyrate treatment. Either treatment with phorbol esters or withdrawal of sodium butyrate increased Pgp phosphorylation while decreasing vinblastine accumulation. These studies suggest that the specificity of Pgp transport can be modulated by phosphorylation and that vinblastine, adriamycin, or actinomycin D transport, but not that of colchicine, is diminished after dephosphorylation by sodium butyrate. JF - Biochemistry AU - Bates, S E AU - Currier, S J AU - Alvarez, M AU - Fojo, A T AD - Medicine Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/07/21/ PY - 1992 DA - 1992 Jul 21 SP - 6366 EP - 6372 VL - 31 IS - 28 SN - 0006-2960, 0006-2960 KW - Butyrates KW - 0 KW - Membrane Glycoproteins KW - P-Glycoprotein KW - Phorbol Esters KW - Phosphoproteins KW - Butyric Acid KW - 107-92-6 KW - Dactinomycin KW - 1CC1JFE158 KW - Vinblastine KW - 5V9KLZ54CY KW - Doxorubicin KW - 80168379AG KW - Colchicine KW - SML2Y3J35T KW - Index Medicus KW - Vinblastine -- metabolism KW - Humans KW - Biological Transport -- drug effects KW - Colchicine -- metabolism KW - Phorbol Esters -- pharmacology KW - Dactinomycin -- metabolism KW - Doxorubicin -- metabolism KW - Phosphorylation KW - In Vitro Techniques KW - Cell Line KW - Phosphoproteins -- metabolism KW - Butyrates -- pharmacology KW - Drug Resistance KW - Membrane Glycoproteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73081851?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Modulation+of+P-glycoprotein+phosphorylation+and+drug+transport+by+sodium+butyrate.&rft.au=Bates%2C+S+E%3BCurrier%2C+S+J%3BAlvarez%2C+M%3BFojo%2C+A+T&rft.aulast=Bates&rft.aufirst=S&rft.date=1992-07-21&rft.volume=31&rft.issue=28&rft.spage=6366&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-25 N1 - Date created - 1992-08-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Methionine enkephalin accumulates in plasma but not in brain or cerebrospinal fluid of rats with acute toxic hepatitis. AN - 73325900; 1436641 AB - In order to determine whether acute toxic hepatitis in the rat is associated with an accumulation of methionine enkephalin in plasma and increased blood-to-brain transfer of methionine enkephalin, immunoreactive methionine enkephalin levels were determined by radioimmunoassay in plasma, cerebrospinal fluid and whole brain samples from rats with thioacetamide induced acute toxic hepatitis. Thioacetamide treatment was associated with an 8.7-fold increase in plasma immunoreactive methionine enkephalin levels (P less than or equal to 0.005) 24 h after treatment. However, this marked elevation in plasma immunoreactive methionine enkephalin levels was not associated with an increase in whole brain or cerebrospinal fluid immunoreactive methionine enkephalin levels. These data suggest that increased plasma-to-brain transfer of methionine enkephalin does not occur in this model of acute toxic hepatitis. JF - Neuroscience letters AU - Swain, M G AU - Heyes, M P AU - Vergalla, J AU - Jones, E A AD - Liver Diseases Section, NIDDK, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/07/20/ PY - 1992 DA - 1992 Jul 20 SP - 243 EP - 246 VL - 141 IS - 2 SN - 0304-3940, 0304-3940 KW - Thioacetamide KW - 075T165X8M KW - Enkephalin, Methionine KW - 58569-55-4 KW - Index Medicus KW - Rats KW - Acute Disease KW - Animals KW - Rats, Sprague-Dawley KW - Liver -- pathology KW - Liver -- drug effects KW - Thioacetamide -- pharmacology KW - Male KW - Enkephalin, Methionine -- blood KW - Chemical and Drug Induced Liver Injury -- blood KW - Enkephalin, Methionine -- cerebrospinal fluid KW - Chemical and Drug Induced Liver Injury -- cerebrospinal fluid KW - Enkephalin, Methionine -- metabolism KW - Brain -- metabolism KW - Chemical and Drug Induced Liver Injury -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73325900?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+letters&rft.atitle=Methionine+enkephalin+accumulates+in+plasma+but+not+in+brain+or+cerebrospinal+fluid+of+rats+with+acute+toxic+hepatitis.&rft.au=Swain%2C+M+G%3BHeyes%2C+M+P%3BVergalla%2C+J%3BJones%2C+E+A&rft.aulast=Swain&rft.aufirst=M&rft.date=1992-07-20&rft.volume=141&rft.issue=2&rft.spage=243&rft.isbn=&rft.btitle=&rft.title=Neuroscience+letters&rft.issn=03043940&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 - N-methyl-D-aspartate receptor-mediated neuroprotection in cerebellar granule cells requires new RNA and protein synthesis. AN - 73070281; 1385875 AB - Cerebellar granule cells are susceptible to the excitotoxin glutamate, which acts at N-methyl-D-aspartate (NMDA) receptors, as well as the neurotoxin 1-methyl-4-phenylpyridinium ion (MPP+), the active cytotoxic metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Paradoxically, preincubation of cultured cerebellar granule cells with low concentrations of NMDA or glutamate markedly antagonizes the neurotoxicity resulting from subsequent exposure to toxic concentrations of either MPP+ or glutamate. The neuroprotective effects of NMDA and glutamate against MPP+ toxicity are observed at agonist concentrations as low as 1 microM, are blocked by specific NMDA receptor antagonists, and require at least 30 min to develop fully. Moreover, NMDA receptor-mediated neuroprotection is prevented by the RNA synthesis inhibitor actinomycin D or the protein synthesis inhibitor cycloheximide. Thus, in cerebellar granule cells activation of NMDA receptors by glutamate can result in either neurotoxicity or neuroprotection, depending on the apparent degree of receptor stimulation. NMDA receptor-mediated neuroprotection requires new RNA and protein synthesis and therefore appears to be mediated by the expression of a neuroprotective protein(s). These data demonstrate the presence of an active NMDA receptor-mediated and transcriptionally directed neuroprotective mechanism in cerebellar granule cells. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Marini, A M AU - Paul, S M AD - Section on Molecular Pharmacology, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1992/07/15/ PY - 1992 DA - 1992 Jul 15 SP - 6555 EP - 6559 VL - 89 IS - 14 SN - 0027-8424, 0027-8424 KW - Glutamates KW - 0 KW - Nerve Tissue Proteins KW - Receptors, N-Methyl-D-Aspartate KW - N-Methylaspartate KW - 6384-92-5 KW - 1-Methyl-4-phenylpyridinium KW - R865A5OY8J KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Cell Survival -- drug effects KW - 1-Methyl-4-phenylpyridinium -- toxicity KW - Dose-Response Relationship, Drug KW - Cells, Cultured KW - In Vitro Techniques KW - N-Methylaspartate -- toxicity KW - Gene Expression KW - Glutamates -- toxicity KW - Time Factors KW - Nerve Tissue Proteins -- physiology KW - Receptors, N-Methyl-D-Aspartate -- physiology KW - Cerebellum -- cytology KW - Receptors, N-Methyl-D-Aspartate -- drug effects KW - Cerebellum -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73070281?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=N-methyl-D-aspartate+receptor-mediated+neuroprotection+in+cerebellar+granule+cells+requires+new+RNA+and+protein+synthesis.&rft.au=Marini%2C+A+M%3BPaul%2C+S+M&rft.aulast=Marini&rft.aufirst=A&rft.date=1992-07-15&rft.volume=89&rft.issue=14&rft.spage=6555&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 - 1992-08-18 N1 - Date created - 1992-08-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: FASEB J. 1990 Jul;4(10):2789-97 [2165013] Nature. 1991 Jan 31;349(6308):414-8 [1846943] Neurosci Lett. 1989 Apr 24;99(1-2):113-8 [2568605] Neurosci Lett. 1988 Aug 15;91(1):47-52 [2845308] Annu Rev Neurosci. 1988;11:81-96 [3129982] J Neurosci. 1988 Jun;8(6):2153-63 [3385492] J Neurosci. 1988 Jun;8(6):2164-71 [3385493] Brain Res. 1984 Jan 2;290(1):77-86 [6140986] Nature. 1976 Sep 16;263(5574):244-6 [8731] Biochem Biophys Res Commun. 1991 Dec 31;181(3):1442-8 [1764096] Proc Natl Acad Sci U S A. 1990 Feb;87(3):1193-7 [2153974] Neuroscience. 1990;37(1):251-8 [2173814] J Neurosci. 1989 Oct;9(10):3665-72 [2571685] Neuron. 1988 Oct;1(8):623-34 [2908446] Science. 1988 Jun 3;240(4857):1328-31 [3131879] Proc Natl Acad Sci U S A. 1982 Dec;79(24):7919-23 [6130529] J Biol Chem. 1951 Nov;193(1):265-75 [14907713] Eur J Pharmacol. 1991 Feb 26;194(1):131-2 [1676372] J Neurochem. 1990 May;54(5):1509-16 [1691274] J Pharmacol Exp Ther. 1991 Jan;256(1):402-11 [1846423] Brain Res. 1988 Jun 7;451(1-2):205-12 [2472189] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Antitumor activity and immune responses induced by a recombinant carcinoembryonic antigen-vaccinia virus vaccine. AN - 73043914; 1619682 AB - Human carcinoembryonic antigen (CEA) is a 180-kd glycoprotein expressed in human colorectal, gastric, pancreatic, breast, and non-small-cell lung carcinomas. Previous studies have demonstrated enhanced immune responses to other antigens presented with vaccinia virus proteins via a recombinant vaccinia virus construct. In addition, we have developed a recombinant CEA-vaccinia virus construct, designated rV(WR)-CEA, and have demonstrated humoral anti-CEA responses in mice after immunization with that virus. The goals of this study were (a) to construct a recombinant CEA-vaccinia vaccine in a less virulent vaccinia strain that is potentially safe and effective for treatment of patients whose tumors express CEA and (b) to evaluate the ability of the recombinant CEA-vaccinia vaccine to prevent and reverse tumor growth in mice and to elicit cell-mediated and humoral anti-CEA immune responses. Using the New York City strain of vaccinia virus, which is used in smallpox vaccination and is more attenuated for humans than rV(WR), we derived a recombinant CEA-vaccinia construct, designated rV(NYC)-CEA. The ability of this construct to induce antitumor immunity was evaluated in mice receiving subcutaneous injections of murine colon adenocarcinoma cells expressing the human CEA gene. Administration of rV(NYC)-CEA in mice induced strong anti-CEA antibody responses, as well as CEA-specific cell-mediated responses, including delayed-type hypersensitivity, lymphoproliferative, and cytotoxic responses. Vaccination of mice with the rV(NYC)-CEA rendered them resistant to the growth of subsequently transplanted CEA-expressing tumors. Moreover, when mice were vaccinated 7 days after tumor cell injection, tumor growth was either greatly reduced or eliminated. No toxic effects were observed in any of the mice. These studies demonstrate that antitumor activity can be induced with the use of a recombinant CEA-vaccinia virus construct derived from an attenuated vaccinia strain, and they reveal the range of cell-mediated and humoral responses induced by this recombinant vaccine. JF - Journal of the National Cancer Institute AU - Kantor, J AU - Irvine, K AU - Abrams, S AU - Kaufman, H AU - DiPietro, J AU - Schlom, J AD - Laboratory of Tumor Immunology and Biology, National Cancer Institute, Bethesda, Md 20892. Y1 - 1992/07/15/ PY - 1992 DA - 1992 Jul 15 SP - 1084 EP - 1091 VL - 84 IS - 14 SN - 0027-8874, 0027-8874 KW - Antibodies, Neoplasm KW - 0 KW - Carcinoembryonic Antigen KW - Vaccines, Synthetic KW - Index Medicus KW - Animals KW - Humans KW - Antibodies, Neoplasm -- immunology KW - T-Lymphocytes, Cytotoxic -- immunology KW - Mice KW - Immunity, Cellular -- immunology KW - Cytotoxicity, Immunologic -- immunology KW - Vaccination KW - Hypersensitivity, Delayed -- immunology KW - Neoplasm Transplantation KW - Blotting, Western KW - Tumor Cells, Cultured KW - Lymphocyte Activation -- immunology KW - Antibody Formation -- immunology KW - Mice, Inbred C57BL KW - T-Lymphocytes -- immunology KW - Female KW - Vaccinia virus -- immunology KW - Carcinoembryonic Antigen -- immunology KW - Vaccines, Synthetic -- immunology KW - Vaccines, Synthetic -- administration & dosage KW - Adenocarcinoma -- immunology KW - Adenocarcinoma -- prevention & control KW - Colonic Neoplasms -- prevention & control KW - Colonic Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73043914?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Antitumor+activity+and+immune+responses+induced+by+a+recombinant+carcinoembryonic+antigen-vaccinia+virus+vaccine.&rft.au=Kantor%2C+J%3BIrvine%2C+K%3BAbrams%2C+S%3BKaufman%2C+H%3BDiPietro%2C+J%3BSchlom%2C+J&rft.aulast=Kantor&rft.aufirst=J&rft.date=1992-07-15&rft.volume=84&rft.issue=14&rft.spage=1084&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 - 1992-08-03 N1 - Date created - 1992-08-03 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: J Natl Cancer Inst. 1992 Jul 15;84(14):1059-61 [1619675] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Parity and primary liver cancer among young women. AN - 73024073; 1619686 JF - Journal of the National Cancer Institute AU - Hsing, A W AU - McLaughlin, J K AU - Hoover, R N 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 - 1992/07/15/ PY - 1992 DA - 1992 Jul 15 SP - 1118 EP - 1119 VL - 84 IS - 14 SN - 0027-8874, 0027-8874 KW - Contraceptives, Oral KW - 0 KW - Index Medicus KW - Population KW - United States KW - Fertility KW - Research Methodology KW - Metabolic Effects KW - Estrogens--changes KW - Population Dynamics KW - Physiology KW - Contraceptive Methods--side effects KW - Oral Contraceptives--side effects KW - Hormones KW - Developed Countries KW - Liver Neoplasms KW - Demographic Factors KW - Diseases KW - Family Planning KW - Parity KW - North America KW - Americas KW - Endocrine System KW - Studies KW - Methodological Studies KW - Matched Groups KW - Pregnancy KW - Case Control Studies KW - Northern America KW - Neoplasms KW - Control Groups KW - Contraception KW - Reproduction KW - Fertility Measurements KW - Biology KW - Contraceptives, Oral -- adverse effects KW - Risk Factors KW - Humans KW - Adult KW - Case-Control Studies KW - Middle Aged KW - Female KW - Liver Neoplasms -- chemically induced KW - Liver Neoplasms -- epidemiology KW - Liver Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73024073?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Parity+and+primary+liver+cancer+among+young+women.&rft.au=Hsing%2C+A+W%3BMcLaughlin%2C+J+K%3BHoover%2C+R+N%3BCo+Chien%2C+H+T%3BBlot%2C+W+J%3BFraumeni%2C+J+F&rft.aulast=Hsing&rft.aufirst=A&rft.date=1992-07-15&rft.volume=84&rft.issue=14&rft.spage=1118&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 - 1992-08-03 N1 - Date created - 1992-08-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutagenesis of T cell antigen receptor zeta chain tyrosine residues. Effects on tyrosine phosphorylation and lymphokine production. AN - 73051315; 1535630 AB - Occupancy of the T cell antigen receptor triggers a complex set of events that culminate in cellular activation. It is clear that tyrosine kinases play important roles in this process. The zeta subunit of the T cell antigen receptor is a 16-kDa transmembrane structure that exists primarily as a disulfide-linked homodimer. On receptor activation, a subset of zeta molecules undergo tyrosine phosphorylation. To evaluate this process and the role of zeta phosphorylation in T cell activation, site-specific mutagenesis of the intracytoplasmic tyrosines of zeta has been carried out. Analysis of cells expressing these mutant zeta subunits demonstrated that multiple tyrosines underwent phosphorylation in response to receptor engagement, and that the four most carboxyl tyrosines were most crucial to this process. Despite abnormalities in phosphorylation induced by the mutations, lymphokine production in these transfectants was unaffected. Hence, although zeta is a prominent substrate for a receptor-activated tyrosine kinase, neither the mutation of individual tyrosines nor the alteration of the phosphorylation state of the molecule substantively affected the coupling of T cell receptor activation to lymphokine production. These findings raise questions regarding the role of zeta phosphorylation in T cell activation. JF - The Journal of biological chemistry AU - Frank, S J AU - Cenciarelli, C AU - Niklinska, B B AU - Letourneur, F AU - Ashwell, J D AU - Weissman, A M AD - Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/07/05/ PY - 1992 DA - 1992 Jul 05 SP - 13656 EP - 13660 VL - 267 IS - 19 SN - 0021-9258, 0021-9258 KW - Interleukin-2 KW - 0 KW - Receptors, Antigen, T-Cell, gamma-delta KW - Tyrosine KW - 42HK56048U KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Lymphocyte Activation KW - Animals KW - Hybridomas KW - Phosphorylation KW - Transfection KW - Mice KW - Precipitin Tests KW - T-Lymphocytes -- immunology KW - Mutagenesis, Site-Directed KW - Receptors, Antigen, T-Cell, gamma-delta -- genetics KW - Interleukin-2 -- biosynthesis KW - Tyrosine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73051315?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mutagenesis+of+T+cell+antigen+receptor+zeta+chain+tyrosine+residues.+Effects+on+tyrosine+phosphorylation+and+lymphokine+production.&rft.au=Frank%2C+S+J%3BCenciarelli%2C+C%3BNiklinska%2C+B+B%3BLetourneur%2C+F%3BAshwell%2C+J+D%3BWeissman%2C+A+M&rft.aulast=Frank&rft.aufirst=S&rft.date=1992-07-05&rft.volume=267&rft.issue=19&rft.spage=13656&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 - 1992-08-05 N1 - Date created - 1992-08-05 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: J Biol Chem 1992 Sep 25;267(27):19752 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Physiological abnormalities in hereditary hyperekplexia. AN - 85273721; pmid-1642471 AB - Five patients from a kindred with hereditary hyperekplexia had physiological testing. The surface-recorded electromyographic pattern of audiogenic muscle jerks was identical to that of the normal acoustic startle reflex. Testing at graded stimulus intensities indicated an increase in the gain of the acoustic startle reflex. Nose-tap stimuli resulted in short-latency generalized electromyographic bursts that were similar to the R1 component of the blink reflex. Electrical stimulation of peripheral nerves elicited a pattern of generalized muscle jerks that was similar to that of the acoustic startle reflex. Somatosensory evoked potentials, brainstem auditory evoked potentials, and cortical auditory evoked potentials were normal. The primary physiological abnormality in hereditary hyperekplexia is widespread elevated gain of vestigial withdrawal reflexes in the brainstem and possibly the spinal cord, most likely resulting from increased excitability of reticular neurons. JF - Annals of Neurology AU - Matsumoto, J AU - Fuhr, P AU - Nigro, M AU - Hallett, M AD - Human Motor Control Section, Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. PY - 1992 SP - 41 EP - 50 VL - 32 IS - 1 SN - 0364-5134, 0364-5134 KW - Reference Values KW - Spinal Cord KW - Startle Reaction KW - Human KW - Electromyography KW - Child KW - Sensation KW - Child, Preschool KW - Infant KW - Needles KW - Movement Disorders KW - Adult KW - Neural Conduction KW - Middle Age KW - Acoustic Stimulation KW - Reflex KW - Adolescent KW - Time Factors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85273721?accountid=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=Annals+of+Neurology&rft.atitle=Physiological+abnormalities+in+hereditary+hyperekplexia.&rft.au=Matsumoto%2C+J%3BFuhr%2C+P%3BNigro%2C+M%3BHallett%2C+M&rft.aulast=Matsumoto&rft.aufirst=J&rft.date=1992-07-01&rft.volume=32&rft.issue=1&rft.spage=41&rft.isbn=&rft.btitle=&rft.title=Annals+of+Neurology&rft.issn=03645134&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Ethanol dependence and withdrawal selectively alter localized cerebral glucose utilization. AN - 85231841; pmid-1515942 AB - The 2-deoxyglucose technique was used to determine local cerebral glucose utilization (LCGU) in over 50 brain regions of rats physically dependent upon ethanol and compared to those of acutely intoxicated and those undergoing an overt ethanol-withdrawal syndrome. Dependent-intoxicated rats (average blood ethanol concentration 64 mM) had decreased LCGU in 13/54 regions, including those associated with the limbic system, cerebellum, and motor system. The ethanol withdrawal syndrome was associated with 17/50 gray regions showing an increase, including regions involved with motor function, auditory system, and mammillary bodies-anterior thalamus-cingulate cortex pathway. The most pronounced differences between these groups occurred in regions associated with motor function, cerebellar function, anterior thalamus, and median raphe. Comparisons between dependent-intoxicated and acutely intoxicated rats (average blood ethanol concentration 66 mM) revealed that acute intoxication was associated with a relatively greater reduction in LCGU in regions involved with sensory-related functions, mammillary bodies, and median raphe. With the development of dependence, adaptation occurred in these regions except for inferior colliculus and median raphe. Dependence was also associated with a relative decrease in LCGU in white matter, limbic system, and extrapyramidal motor system. JF - Brain Research AU - Eckardt, M J AU - Campbell, G A AU - Marietta, C A AU - Majchrowicz, E AU - Rawlings, R R AU - Weight, F F AD - Laboratory of Clinical Studies, DICBR, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892. PY - 1992 SP - 244 EP - 250 VL - 584 IS - 1-2 SN - 0006-8993, 0006-8993 KW - Rats KW - Rats, Inbred Strains KW - Substance Withdrawal Syndrome KW - Brain Chemistry KW - Animal KW - Glucose KW - Substance-Related Disorders KW - Deoxyglucose KW - Autoradiography KW - Male KW - Ethanol UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85231841?accountid=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+Research&rft.atitle=Ethanol+dependence+and+withdrawal+selectively+alter+localized+cerebral+glucose+utilization.&rft.au=Eckardt%2C+M+J%3BCampbell%2C+G+A%3BMarietta%2C+C+A%3BMajchrowicz%2C+E%3BRawlings%2C+R+R%3BWeight%2C+F+F&rft.aulast=Eckardt&rft.aufirst=M&rft.date=1992-07-01&rft.volume=584&rft.issue=1-2&rft.spage=244&rft.isbn=&rft.btitle=&rft.title=Brain+Research&rft.issn=00068993&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Intensive therapy with cisplatin, interleukin-2 and interferon-alpha-2a in patients with metastatic melanoma. A phase II Study. AN - 75541645; 1343617 AB - Based upon their individual clinical activity and combined effects in animal models or in vitro, we wished to evaluate a regimen of cisplatin, interferon-alpha, and IL-2 in patients with metastatic melanoma. Phase II pilot study. Referral-based US Government clinical research unit. Nine patients with metastatic malignant melanoma. Cisplatin 75-100 mg/m2 was administered intravenously over 30 minutes on days 1 and 8. Interferon-alpha 2a 5 Mu/m2 body surface area (BSA) was given subcutaneously for 4 days beginning 1 day before each dose of cisplatin. Beginning on day 15 and day 22, IL-2 was administered by intravenous continuous infusion at 3 Mu/m2 BSA/d for 96 hours and by daily intravenous bolus concurrent with daily subcutaneous doses of interferon-alpha 2a. Antitumor response and toxicities. The study was stopped due to renal and hematopoietic toxicity and severe, delayed nausea and vomiting associated with the cisplatin-interferon treatment. Three of 9 patients achieved a partial response (duration 2.5, 4, 14+ months), and an additional patient had a 50% reduction in measurable tumor volume before undergoing resection of residual disease. Overall response rate was 45%. This regimen was associated with excessive toxicity, and the lack of complete responses in a patient cohort with favorable characteristics for response (good performance status, predominance of skin and lymph node metastatic sites) suggests that it had no advantage over less toxic treatment regimens. National Cancer Institute/Cancer Therapy Evaluation Program T89-0137. JF - The Online journal of current clinical trials AU - Sznol, M AU - Steis, R G AU - Smith, J W AU - Janik, J E AU - Sharfman, W H AU - Urba, W J AU - Fenton, R G AU - Creekmore, S P AU - Beveridge, J AU - Longo, D L AD - Clinical Research Branch, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland 21701. Y1 - 1992/07/01/ PY - 1992 DA - 1992 Jul 01 VL - Doc No 9 KW - Interferon-alpha KW - 0 KW - Interleukin-2 KW - Recombinant Proteins KW - interferon alfa-2a KW - 47RRR83SK7 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Nausea -- chemically induced KW - Combined Modality Therapy KW - Humans KW - Vomiting -- chemically induced KW - Adult KW - Aged KW - Middle Aged KW - Male KW - Female KW - Cisplatin -- therapeutic use KW - Interleukin-2 -- adverse effects KW - Interferon-alpha -- therapeutic use KW - Interferon-alpha -- adverse effects KW - Melanoma -- secondary KW - Interleukin-2 -- therapeutic use KW - Melanoma -- therapy KW - Cisplatin -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/75541645?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Intensive+therapy+with+cisplatin%2C+interleukin-2+and+interferon-alpha-2a+in+patients+with+metastatic+melanoma.+A+phase+II+Study.&rft.au=Sznol%2C+M%3BSteis%2C+R+G%3BSmith%2C+J+W%3BJanik%2C+J+E%3BSharfman%2C+W+H%3BUrba%2C+W+J%3BFenton%2C+R+G%3BCreekmore%2C+S+P%3BBeveridge%2C+J%3BLongo%2C+D+L&rft.aulast=Sznol&rft.aufirst=M&rft.date=1992-07-01&rft.volume=Doc+No+9&rft.issue=&rft.spage=%5B3841+words%3B+32+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 - 2017-01-17 ER - TY - JOUR T1 - Alkylation of DNA by 1,3-dialkyl-3-acyltriazenes: correlation of biological activity with chemical behavior. AN - 73218601; 1391620 AB - The reactions of calf thymus DNA with four 1,3-dialkyl-3-acyltriazenes were studied alone or in the presence of pig liver esterase in pH 7.4 phosphate buffer for varying lengths of time. The best alkylating agent in the absence of esterase was determined to be 1,3-dimethyl-3-carbethoxytriazene (DMC), followed in order by 1-(2-hydroxyethyl)-3-methyl-3-carbethoxytriazene (HMC), 1-(2-hydroxyethyl)-3-methyl-3-acetyltriazene (HMA), and 1-(2- chloroethyl)-3-methyl-3-carbethoxytriazene (CMC). This order is the same as that for the rate of decomposition of the various acyltriazenes in pH 7.5 phosphate buffer. The extent of calf thymus DNA alkylation by CMC was found to be dependent on both the reaction buffer and the ionic strength of the medium. Alkylation by CMC alone in low ionic strength glycine buffer produced large quantities of 7-(2-chloroethyl)guanine and 7-(2-hydroxyethyl)guanine. The products of DNA alkylation observed at neutral pH are consistent with N(2)-N(3) heterolysis of the triazene, resulting in the N(1) alkyldiazonium ion as the sole alkylating species. In the presence of esterase, CMC showed an enhanced rate of product formation. Furthermore, the product distribution shifted dramatically from mainly hydroxyethylation to predominantly methylation. CMC is postulated to undergo initial enzymatic deacylation, leading to two different alkyldiazonium ions which competitively alkylate DNA. HMC, on the other hand, was little affected by the esterase. The enzyme-catalyzed reaction showed a small increase in methylation and a smaller decrease in hydroxyethylation.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Chemical research in toxicology AU - Kroeger-Koepke, M B AU - Michejda, C J AU - Smith, R H AD - Molecular Aspects of Drug Design Section, NCI-Frederick Cancer Research and Development Center, Maryland 21702. PY - 1992 SP - 541 EP - 547 VL - 5 IS - 4 SN - 0893-228X, 0893-228X KW - Alkylating Agents KW - 0 KW - Triazenes KW - DNA KW - 9007-49-2 KW - Esterases KW - EC 3.1.- KW - Index Medicus KW - Animals KW - Cattle KW - Esterases -- metabolism KW - Kinetics KW - Catalysis KW - Triazenes -- metabolism KW - Alkylating Agents -- metabolism KW - DNA -- metabolism KW - Triazenes -- chemistry KW - DNA -- chemistry KW - Alkylating Agents -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73218601?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Alkylation+of+DNA+by+1%2C3-dialkyl-3-acyltriazenes%3A+correlation+of+biological+activity+with+chemical+behavior.&rft.au=Kroeger-Koepke%2C+M+B%3BMichejda%2C+C+J%3BSmith%2C+R+H&rft.aulast=Kroeger-Koepke&rft.aufirst=M&rft.date=1992-07-01&rft.volume=5&rft.issue=4&rft.spage=541&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 - 1992-11-04 N1 - Date created - 1992-11-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - CONF T1 - Agricultural chemical utilization and human health. AN - 73218240; 1396466 AB - The public is justifiably concerned about the human health effects of agricultural chemicals. The many gaps in information about the mechanisms of toxic action, human exposures, and the nature and extent of human health effects are large. Very few older pesticides, in particular, have been tested for human health effects. Workers who produce, harvest, store, transport, process, and prepare food and fibers are exposed to many chemicals that are potentially hazardous and that are used in agriculture. The occupational health of these workers has not been adequately studied, and protective efforts have sometimes been minimal. Valid and accurate risk assessment is best based on sound information about how chemicals, in this case agricultural chemicals, are involved in toxic events--their mechanisms of action. These health effects include tumor promotion, chronic and acute neurotoxicity, immunotoxicity, and reproductive and developmental toxicity. Another key part of risk assessment is exposure assessment. Fundamental studies of the toxicology of target organisms and nontarget organisms exposed to agricultural chemicals are needed to discover and develop better solutions to the problems of agricultural pest control, including better formulations, optimal application rates and public education in safety and alternative agricultural practices. The large number of pesticides that have never been adequately tested for effects on human health is particularly worrisome in light of emerging information about delayed nervous system effects. JF - Environmental health perspectives AU - Mushak, E W AU - Piver, W T Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 269 EP - 274 VL - 97 KW - Agrochemicals KW - 0 KW - Biomarkers KW - Index Medicus KW - Research -- education KW - Humans KW - Research Design KW - Health Status Indicators KW - Environmental Exposure -- adverse effects KW - Agrochemicals -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73218240?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&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=Agricultural+chemical+utilization+and+human+health.&rft.au=Mushak%2C+E+W%3BPiver%2C+W+T&rft.aulast=Mushak&rft.aufirst=E&rft.date=1992-07-01&rft.volume=97&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 - 1992-10-26 N1 - Date created - 1992-10-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modeling cyanide release from nitriles: prediction of cytochrome P450 mediated acute nitrile toxicity. AN - 73214882; 1391621 AB - A mechanism-based model for prediction of acute nitrile toxicity was developed using octanol-water partition coefficients (log P) and estimated rates of alpha-hydrogen atom abstraction as variables. Relative rates of hydrogen atom abstraction were derived from differences in heats of formation for ground-state and radical geometries and radical ionization potentials. Calculated energies of activation for all potential sites of oxidation for a given nitrile were used to estimate partitioning of metabolites among multiple oxidative pathways. logP and the resulting corrected rate constants for alpha-carbon oxidation were effective variables in an acute toxicity model of structurally diverse nitriles. The pharmacokinetics of substrate disposition is discussed in the context of multiple metabolic pathways. Structure-toxicity relationships are also discussed. JF - Chemical research in toxicology AU - Grogan, J AU - DeVito, S C AU - Pearlman, R S AU - Korzekwa, K R AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. PY - 1992 SP - 548 EP - 552 VL - 5 IS - 4 SN - 0893-228X, 0893-228X KW - Cyanides KW - 0 KW - Nitriles KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Thermodynamics KW - Cytochrome P-450 Enzyme System -- metabolism KW - Models, Chemical KW - Cyanides -- metabolism KW - Nitriles -- metabolism KW - Nitriles -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73214882?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Modeling+cyanide+release+from+nitriles%3A+prediction+of+cytochrome+P450+mediated+acute+nitrile+toxicity.&rft.au=Grogan%2C+J%3BDeVito%2C+S+C%3BPearlman%2C+R+S%3BKorzekwa%2C+K+R&rft.aulast=Grogan&rft.aufirst=J&rft.date=1992-07-01&rft.volume=5&rft.issue=4&rft.spage=548&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 - 1992-11-04 N1 - Date created - 1992-11-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cancer risk following exposure to Thorotrast: overview in relation to a case report. AN - 73185726; 1522013 AB - Radioactive measurements and histopathologic findings are described in a patient administered Thorotrast, a radiographic contrast agent, 36 y prior to death and compared with cancer risks noted in epidemiologic studies. This person [designated as U.S. Uranium Registry (USUR) Case 1001] had prearranged for donation of her body to the USUR and the National Cancer Institute for study. Elevated levels of radioactivity were noted in those organs in which excess cancers have been reported in epidemiologic surveys of Thorotrast-exposed subjects. Hepatic tissue in USUR Case 1001 was estimated to have received an average lifetime absorbed dose of 16.2 Gy, based on radiochemical analyses, consistent with the high risks for liver tumors reported in all studied populations. Thorotrast was present throughout the bone marrow of USUR Case 1001, who died secondary to complications of refractory anemia with excess blasts (RAEB). Elevated risks for acute myeloid leukemia have been noted in Thorotrast patients, and more recently, cases of RAEB and RAEB in transformation have been reported. The thorium decay series includes the bone-seeking radionuclides 224Ra and 228Ra, which have been associated with high risks for osteosarcomas, although the association between Thorotrast and bone cancer is not as convincing. The skeleton of USUR Case 1001, however, contained significant levels of radioactivity. Other tissues evaluated in USUR Case 1001 included lung, eye, kidney, and breast, which did not contain elevated levels of radioactivity. JF - Health physics AU - Travis, L B AU - Kathren, R L AU - Boice, J D AD - Radiation Epidemiology Branch, National Cancer Institute, National Institutes of Health, U.S. Department of Health and Human Services, Rockville, MD 20852. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 89 EP - 97 VL - 63 IS - 1 SN - 0017-9078, 0017-9078 KW - Contrast Media KW - 0 KW - Thorium Dioxide KW - 9XA7X17UQC KW - Index Medicus KW - Risk KW - Humans KW - Leukemia, Radiation-Induced -- etiology KW - Aged KW - Leukemia, Myeloid -- etiology KW - Liver Neoplasms -- etiology KW - Time Factors KW - Female KW - Contrast Media -- adverse effects KW - Thorium Dioxide -- adverse effects KW - Neoplasms, Radiation-Induced -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73185726?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+physics&rft.atitle=Cancer+risk+following+exposure+to+Thorotrast%3A+overview+in+relation+to+a+case+report.&rft.au=Travis%2C+L+B%3BKathren%2C+R+L%3BBoice%2C+J+D&rft.aulast=Travis&rft.aufirst=L&rft.date=1992-07-01&rft.volume=63&rft.issue=1&rft.spage=89&rft.isbn=&rft.btitle=&rft.title=Health+physics&rft.issn=00179078&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-15 N1 - Date created - 1992-10-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Amphibian tumors: a comparison of anurans and urodeles. AN - 73181722; 1520844 AB - Anuran and urodele amphibians develop spontaneous neoplasms in all major organ systems with the integumentary system a frequent target. Anurans and urodeles have spontaneous viral-associated tumors, the biological behavior of which is temperature-related. Anurans seem to have a greater frequency of spontaneous neoplasms than do urodeles and respond to chemical carcinogens in a manner analogous to mammalian species. Urodeles have greater cell regenerative capabilities than do anurans and paradoxically, are more refractory than anurans or mammalian species to chemical carcinogens in their proliferating regenerative blastema. JF - In vivo (Athens, Greece) AU - Anver, M R AD - PRI/DynCorp, Inc., National Cancer Institute, Frederick Cancer Research and Development Center, Maryland 21702-1201. PY - 1992 SP - 435 EP - 437 VL - 6 IS - 4 SN - 0258-851X, 0258-851X KW - Carcinogens KW - 0 KW - Index Medicus KW - Animals KW - Species Specificity KW - Neoplasms -- veterinary KW - Urodela KW - Neoplasms -- pathology KW - Neoplasms -- chemically induced KW - Neoplasms -- epidemiology KW - Anura UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73181722?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Amphibian+tumors%3A+a+comparison+of+anurans+and+urodeles.&rft.au=Anver%2C+M+R&rft.aulast=Anver&rft.aufirst=M&rft.date=1992-07-01&rft.volume=6&rft.issue=4&rft.spage=435&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 - 1992-10-15 N1 - Date created - 1992-10-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - External gamma-ray counting of selected tissues from a Thorotrast patient. AN - 73179141; 1522008 AB - Results of gamma-ray measurements of selected tissues from a patient who was injected with Thorotrast almost 36 y ago are reported. The purposes of this study were: 1) to determine the relative tissue distribution and activities of specific radionuclides in the 232Th decay chain, specifically 228Ra (as measured by 228Ac), 212Pb, and 224Ra (measured directly and as measured by 212Pb), and 2) to evaluate the level of radioactive disequilibrium among the daughter products. The spleen and liver had the highest concentrations of radioactivity. Bone also appears to be a long-term sink for 232Th daughter products based on estimates from a small portion of one rib. Larynx and esophagus contained measurable activity, which may have been due to their proximity to the "Thorotrastoma." Radioactivity in the remaining measured tissues were low, as expected. Secular equilibrium could be demonstrated in bone, pancreas, larynx, esophagus, and breast. Significant disequilibrium was observed for spleen, liver, kidney, and red blood cells. Radioactivity measurements reported here will be useful in estimating radiation doses to selected tissues. Such dose estimates are valuable in refining current risk estimates (e.g., liver) and in identifying tissues at risk for further epidemiologic studies. These results, while consistent with other published studies, should be interpreted with caution since measurements were made on only one patient. JF - Health physics AU - Mays, C W AU - Aamodt, R L AU - Inn, K G AU - Brown, D R AU - Greenberg, R R AU - Iyengar, V G AU - Schima, F J AU - Slaback, L S AU - Tracy, J W AU - Lynch, T P AD - National Cancer Institute, National Institutes of Health, Rockville, MD 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 33 EP - 40 VL - 63 IS - 1 SN - 0017-9078, 0017-9078 KW - Contrast Media KW - 0 KW - Thorium Dioxide KW - 9XA7X17UQC KW - Index Medicus KW - Spleen -- metabolism KW - Humans KW - Liver -- metabolism KW - Aged KW - Tissue Distribution KW - Radioactivity KW - Bone and Bones -- metabolism KW - Time Factors KW - Female KW - Thorium Dioxide -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73179141?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+physics&rft.atitle=External+gamma-ray+counting+of+selected+tissues+from+a+Thorotrast+patient.&rft.au=Mays%2C+C+W%3BAamodt%2C+R+L%3BInn%2C+K+G%3BBrown%2C+D+R%3BGreenberg%2C+R+R%3BIyengar%2C+V+G%3BSchima%2C+F+J%3BSlaback%2C+L+S%3BTracy%2C+J+W%3BLynch%2C+T+P&rft.aulast=Mays&rft.aufirst=C&rft.date=1992-07-01&rft.volume=63&rft.issue=1&rft.spage=33&rft.isbn=&rft.btitle=&rft.title=Health+physics&rft.issn=00179078&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-15 N1 - Date created - 1992-10-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comprehensive evaluation of a Thorotrast patient: an overview. AN - 73174256; 1522002 AB - For several decades, thousands of people received Thorotrast during the course of angiography and other radiologic procedures. Eventually, as the hazards of this radioactive, radiographic contrast agent became apparent, research was initiated to further evaluate its associated adverse effects. In 1988 and 1989, Charles W. Mays, together with colleagues at a variety of sites, developed a detailed protocol for the comprehensive postmortem evaluation of one subject who had been administered Thorotrast 36 y previously. This case represents the first holistic approach to the analysis of Thorotrast in a whole body, simultaneously assembling clinical and autopsy findings with dosimetric, radiochemical, autoradiographic, and molecular evaluations. JF - Health physics AU - Travis, L B AU - Kathren, R L AU - Mays, D AU - Mays, C W AD - Epidemiology and Biostatistics Program, National Cancer Institute, National Institutes of Health, Rockville, MD 20852. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 10 EP - 12 VL - 63 IS - 1 SN - 0017-9078, 0017-9078 KW - Contrast Media KW - 0 KW - Thorium Dioxide KW - 9XA7X17UQC KW - Index Medicus KW - Humans KW - Aged KW - Tissue Distribution KW - Time Factors KW - Female KW - Contrast Media -- adverse effects KW - Thorium Dioxide -- pharmacokinetics KW - Contrast Media -- pharmacokinetics KW - Thorium Dioxide -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73174256?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+physics&rft.atitle=Comprehensive+evaluation+of+a+Thorotrast+patient%3A+an+overview.&rft.au=Travis%2C+L+B%3BKathren%2C+R+L%3BMays%2C+D%3BMays%2C+C+W&rft.aulast=Travis&rft.aufirst=L&rft.date=1992-07-01&rft.volume=63&rft.issue=1&rft.spage=10&rft.isbn=&rft.btitle=&rft.title=Health+physics&rft.issn=00179078&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-15 N1 - Date created - 1992-10-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Possible roles for nitric oxide in AIDS and associated pathology. AN - 73168170; 1513271 AB - The endogenous free radical, nitric oxide (NO), plays a neurotransmitter-like role in vascular endothelium, a second-messenger role in N-methyl-D-aspartate (NMDA)-responsive neurons in the central nervous system (CNS), a neurotoxic role after its release from these neurons, and a cytotoxic role after its release by macrophages. NO also derives from exogenous sources, such as the nitrite inhalants, amyl, butyl and isobutyl nitrite. There is evidence that abuse of nitrite inhalants can affect immunomodulation, and epidemiological studies suggest that such abuse may be a cofactor in the pathogenesis of acquired immunodeficiency syndrome (AIDS). Hitherto, however, the potential role of NO in such pathogenesis has not been examined. This paper presents some current evidence that implicates both endogenous and exogenous sources of NO in AIDS and associated pathology. JF - Medical hypotheses AU - Morgan, M J AU - Kimes, A S AU - London, E D AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 189 EP - 193 VL - 38 IS - 3 SN - 0306-9877, 0306-9877 KW - Free Radicals KW - 0 KW - Neurotoxins KW - Nitrites KW - Nitric Oxide KW - 31C4KY9ESH KW - Index Medicus KW - AIDS/HIV KW - Nitrites -- adverse effects KW - Humans KW - Pneumonia, Pneumocystis -- etiology KW - Homosexuality KW - Neurotoxins -- adverse effects KW - Administration, Inhalation KW - Male KW - Sarcoma, Kaposi -- etiology KW - Acquired Immunodeficiency Syndrome -- pathology KW - Acquired Immunodeficiency Syndrome -- complications KW - Nitric Oxide -- metabolism KW - Acquired Immunodeficiency Syndrome -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73168170?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Medical+hypotheses&rft.atitle=Possible+roles+for+nitric+oxide+in+AIDS+and+associated+pathology.&rft.au=Morgan%2C+M+J%3BKimes%2C+A+S%3BLondon%2C+E+D&rft.aulast=Morgan&rft.aufirst=M&rft.date=1992-07-01&rft.volume=38&rft.issue=3&rft.spage=189&rft.isbn=&rft.btitle=&rft.title=Medical+hypotheses&rft.issn=03069877&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-25 N1 - Date created - 1992-09-25 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Med Hypotheses 1993 Feb;40(2):142 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Primary chemotherapy for locally advanced uterine cervical carcinoma. AN - 73155117; 1514836 AB - From September 1985 to May 1991, thirty consecutive patients with locally advanced cervical carcinoma stage IB-II (FIGO) with high risk factors of local treatment failure were treated with Epirubicin and Cisplatinum combination as primary chemotherapy. Twenty-five patients were evaluated for response, operability and survival. This combination chemotherapy could induce remarkable clinical complete response of 68% (17/25) and partial response of 28% (7/25), but only 18 patients were permitted for surgery, therefore operability rate was 72% (18/25). Pathological examination revealed complete response at 24% (6/25) and partial response was 48% (12/25) due to the presence of residual tumor at the cervix and dissected lymph nodes. The average number of lymph node dissected was II (range 0-26), which have been usually found in stage IIB-III patients. This combination chemotherapy did not allow to complicate surgery in these circumstances. Toxicities were mild except only leukopenia which was moderate to severe degree (WHO, grading). No death related to treatment has been found. The median time of follow up was 19 months (range 4-72), 24 patients still living, 22 without disease and 2 with diseases at the cervix and bone. The result of pilot study has suggested a beneficial role of primary chemotherapy in this type of malignancy. However, these data require further confirmation and longer follow up before a definite conclusion can be made regarding cure rate and prolong disease free-survival in locally-advanced uterine cervical carcinoma. JF - Gan to kagaku ryoho. Cancer & chemotherapy AU - Cheirsilpa, A AU - Kosiyatrakul, T AU - Benjachai, W AU - Tangkrutt, S AU - Puriphat, S AD - Division of Medical Oncology, National Cancer Institute, Bangkok, Thailand. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 1224 EP - 1232 VL - 19 IS - 8 Suppl SN - 0385-0684, 0385-0684 KW - Antiemetics KW - 0 KW - Epirubicin KW - 3Z8479ZZ5X KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Drug Administration Schedule KW - Humans KW - Vomiting -- chemically induced KW - Aged KW - Epirubicin -- adverse effects KW - Cisplatin -- administration & dosage KW - Nausea -- chemically induced KW - Antiemetics -- administration & dosage KW - Survival Rate KW - Adult KW - Middle Aged KW - Follow-Up Studies KW - Cisplatin -- adverse effects KW - Epirubicin -- administration & dosage KW - Female KW - Alopecia -- chemically induced KW - Uterine Cervical Neoplasms -- drug therapy KW - Uterine Cervical Neoplasms -- mortality KW - Carcinoma, Squamous Cell -- mortality KW - Adenocarcinoma -- mortality KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Adenocarcinoma -- drug therapy KW - Carcinoma, Squamous Cell -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73155117?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gan+to+kagaku+ryoho.+Cancer+%26+chemotherapy&rft.atitle=Primary+chemotherapy+for+locally+advanced+uterine+cervical+carcinoma.&rft.au=Cheirsilpa%2C+A%3BKosiyatrakul%2C+T%3BBenjachai%2C+W%3BTangkrutt%2C+S%3BPuriphat%2C+S&rft.aulast=Cheirsilpa&rft.aufirst=A&rft.date=1992-07-01&rft.volume=19&rft.issue=8+Suppl&rft.spage=1224&rft.isbn=&rft.btitle=&rft.title=Gan+to+kagaku+ryoho.+Cancer+%26+chemotherapy&rft.issn=03850684&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-29 N1 - Date created - 1992-09-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Sympathoadrenal contribution to plasma dopa (3,4-dihydroxyphenylalanine) in rats. AN - 73146295; 1325324 AB - 1. To determine the sources of dopa (3,4-dihydroxyphenylalanine) in plasma, we measured regional arteriovenous differences, tissue concentrations and urinary excretion of dopa during systemic intravenous infusions of I-[3H]dopa into anaesthetized intact rats and rats pretreated with the sympathetic neurotoxin, 6-hydroxydopamine. 2. In intact rats, large arteriovenous increments in plasma dopa concentrations were noted in the femoral (47%) and adrenal (141%) beds, with a small arterial-portal venous increment (11%), whereas in the kidney there was a substantial (47%) arteriovenous decrement in plasma dopa levels. Skeletal muscle appeared to be a major source of dopa in arterial plasma. 3. Treatment with 6-hydroxydopamine abolished the afferent-efferent increment of plasma dopa concentrations in the femoral bed. The arteriovenous decrement of plasma dopa concentrations in the kidney was preserved, and the arteriovenous increment in the adrenal bed was decreased by about half. Arterial plasma dopa levels fell by 41%. 4. Regional extraction percentages of I-[3H]dopa were used to estimate the clearances and rates of appearance (spillovers) of dopa in plasma. Dopa spillover was detected in the femoral, renal, splanchnic and adrenal beds, with skeletal muscle accounting for about 44% and the kidneys accounting for about 18% of dopa in arterial plasma. Whereas chemical sympathectomy decreased the femoral and renal spillover of dopa by 90% or more, arterial dopa levels and estimated dopa spillover into arterial plasma were decreased by only about 45%. 5. The kidneys accounted for 22% of dopa clearance from arterial plasma. From the renal extraction of I-[3H]dopa and the urinary excretion of [3H]dopamine, it was estimated that 77% of dopa removed in the kidneys was excreted as dopamine in intact animals and 69% was excreted as dopamine in sympathectomized animals. Conversely, about 80% of urinary endogenous dopamine was derived from plasma dopa, regardless of 6-hydroxydopamine treatment. 6. The results indicate that endogenous dopa in arterial plasma is derived substantially but not exclusively from sympathetic nerve endings that are destroyed by 6-hydroxydopamine, especially in skeletal muscle and the kidneys. Regional dopa spillover therefore probably reflects regional catecholamine biosynthesis. In rats, urinary dopamine is derived mainly from renal decarboxylation of circulating dopa. JF - Clinical science (London, England : 1979) AU - Grossman, E AU - Hoffman, A AU - Armando, I AU - Abassi, Z AU - Kopin, I J AU - Goldstein, D S AD - Hypertension-Endocrine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 65 EP - 74 VL - 83 IS - 1 SN - 0143-5221, 0143-5221 KW - Dihydroxyphenylalanine KW - 63-84-3 KW - Oxidopamine KW - 8HW4YBZ748 KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Kidney -- metabolism KW - Arteries KW - Muscles -- metabolism KW - Sympathectomy, Chemical KW - Femoral Artery KW - Dopamine -- urine KW - Male KW - Adrenal Glands -- metabolism KW - Dihydroxyphenylalanine -- biosynthesis KW - Sympathetic Nervous System -- metabolism KW - Dihydroxyphenylalanine -- blood KW - Adrenal Glands -- blood supply UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73146295?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+science+%28London%2C+England+%3A+1979%29&rft.atitle=Sympathoadrenal+contribution+to+plasma+dopa+%283%2C4-dihydroxyphenylalanine%29+in+rats.&rft.au=Grossman%2C+E%3BHoffman%2C+A%3BArmando%2C+I%3BAbassi%2C+Z%3BKopin%2C+I+J%3BGoldstein%2C+D+S&rft.aulast=Grossman&rft.aufirst=E&rft.date=1992-07-01&rft.volume=83&rft.issue=1&rft.spage=65&rft.isbn=&rft.btitle=&rft.title=Clinical+science+%28London%2C+England+%3A+1979%29&rft.issn=01435221&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-06 N1 - Date created - 1992-10-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Systemically administered antifungal agents. A review of their clinical pharmacology and therapeutic applications. AN - 73116016; 1379913 AB - Systemic antifungal agents express great diversity in their pharmacokinetic profiles, mechanisms of action, and toxicities. Understanding the diverse pharmacokinetic properties of systemic antifungals is critical to their appropriate application. Amphotericin B, drug of choice for most invasive mycoses, has unique pharmacokinetic properties, binding initially to serum lipoproteins and redistributing from blood to tissues. Dosing recommendations are based on the specific infection and the status of the host. Lipid formulations of amphotericin B may be able to attenuate some of its toxicities. Flucytosine is a water-soluble, fluorinated pyrimidine that possesses excellent bioavailability. It is administered only in combination with amphotericin B because of frequent development of secondary drug resistance, and is associated with dose-dependent bone marrow suppression. The antifungal azoles are relatively well tolerated, have broad spectrum antifungal activity, and are fungistatic in vitro. Ketoconazole and itraconazole are highly bound to plasma proteins, are extensively metabolised by the liver, and are relatively insoluble in aqueous solution. By comparison, fluconazole is only weakly bound to serum proteins, is relatively stable to metabolic conversion, and is water soluble. Fluconazole penetrates the cerebrospinal fluid well and is approved for primary and suppressive therapy of cryptococcal meningitis in AIDS patients. The echinocandins have a narrow spectrum of antifungal activity, being effective only against Candida spp. JF - Drugs AU - Lyman, C A AU - Walsh, T J AD - Pediatric Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 9 EP - 35 VL - 44 IS - 1 SN - 0012-6667, 0012-6667 KW - Antifungal Agents KW - 0 KW - Azoles KW - Drugs, Investigational KW - Amphotericin B KW - 7XU7A7DROE KW - Flucytosine KW - D83282DT06 KW - Index Medicus KW - AIDS/HIV KW - Drugs, Investigational -- therapeutic use KW - Drugs, Investigational -- pharmacokinetics KW - Flucytosine -- pharmacology KW - Drugs, Investigational -- pharmacology KW - Azoles -- therapeutic use KW - Azoles -- pharmacology KW - Humans KW - Drug Resistance, Microbial KW - Amphotericin B -- pharmacology KW - Amphotericin B -- therapeutic use KW - Flucytosine -- therapeutic use KW - Antifungal Agents -- pharmacokinetics KW - Antifungal Agents -- pharmacology KW - Mycoses -- drug therapy KW - Fungi -- drug effects KW - Antifungal Agents -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73116016?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Drugs&rft.atitle=Systemically+administered+antifungal+agents.+A+review+of+their+clinical+pharmacology+and+therapeutic+applications.&rft.au=Lyman%2C+C+A%3BWalsh%2C+T+J&rft.aulast=Lyman&rft.aufirst=C&rft.date=1992-07-01&rft.volume=44&rft.issue=1&rft.spage=9&rft.isbn=&rft.btitle=&rft.title=Drugs&rft.issn=00126667&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-17 N1 - Date created - 1992-09-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Photodynamic therapy for thoracic malignancies. AN - 73105962; 1386470 AB - Photodynamic therapy (PDT) is an experimental form of cancer therapy which employs photoactivation of a sensitizing chemical by light of a given wavelength via the production of toxic oxygen species. PDT causes local destruction of cancer, and relies on a therapeutic index between normal and malignant tissue since the latter seems to selectively retain the sensitizer. PDT has both direct tumoricidal effects as well as indirect effects on tumor vasculature causing an early hemorrhagic necrosis of tissue. The treatment has been used for the treatment of endobronchial obstruction by primary and metastatic tumors. Most recently, trials are being performed to evaluate this therapy as a surgical adjunct in the treatment of pleural malignancies such as mesothelioma. JF - Seminars in surgical oncology AU - Pass, H I AU - Pogrebniak, H AD - Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. PY - 1992 SP - 217 EP - 225 VL - 8 IS - 4 SN - 8756-0437, 8756-0437 KW - Antineoplastic Agents KW - 0 KW - Deuteroporphyrins KW - Hematoporphyrins KW - hydroxyethylvinyldeuteroporphyrin KW - 82647-38-9 KW - Dihematoporphyrin Ether KW - 97067-70-4 KW - Index Medicus KW - Humans KW - Hematoporphyrins -- therapeutic use KW - Laser Therapy KW - Antineoplastic Agents -- therapeutic use KW - Deuteroporphyrins -- therapeutic use KW - Lung Neoplasms -- diagnosis KW - Hematoporphyrin Photoradiation KW - Lung Neoplasms -- drug therapy KW - Pleural Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73105962?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+surgical+oncology&rft.atitle=Photodynamic+therapy+for+thoracic+malignancies.&rft.au=Pass%2C+H+I%3BPogrebniak%2C+H&rft.aulast=Pass&rft.aufirst=H&rft.date=1992-07-01&rft.volume=8&rft.issue=4&rft.spage=217&rft.isbn=&rft.btitle=&rft.title=Seminars+in+surgical+oncology&rft.issn=87560437&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-28 N1 - Date created - 1992-08-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A pilot study of suramin in the treatment of progressive refractory follicular lymphomas. AN - 73103852; 1498080 AB - Ten patients with progressive follicular lymphomas (seven with follicular mixed lymphomas, three with follicular, small cleaved cell lymphomas) with clinical indications for systemic therapy received parenteral suramin. Each had failed from one to six prior chemotherapeutic regimens and three had in addition received prior radiation therapy. All had measurable disease and nine of the ten had documented bone marrow involvement at the start of therapy. Suramin was administered at an initial infusion rate of 350 mg/m2/day, which was then modified on the basis of subsequent weekly plasma suramin concentrations in order to reach a final plasma concentrations of 250-350 micrograms/ml. Treatment cycles were repeated at eight week intervals. Nine of ten patients are evaluable for response. Five of nine evaluable patients achieved a partial remission as defined by a greater than 50% decrease in the sum of the product of all measurable lesions. Sites of response include: Peripheral (five patients) and central (four patients) adenopathy, disappearance of biopsy-proven skin involvement (one patient), malignant pleural effusions (one patient) and shrinkage of an enlarged spleen (two patients). Disappearance of B symptoms occurred in the one responder with these symptoms. Response duration varied from 3 to 9 months (mean 5.6 months) with time to subsequent systemic therapy varying from 5 to 12 months (mean 8 months). Drug related toxicity included the development of polyradiculopathy (one case), liver function abnormalities (three cases), thrombocytopenia (five cases), vortex keratopathy (two cases) and bacterial infection (two cases). We conclude that suramin has significant activity against follicular lymphomas refractory to standard chemotherapy and that its precise role in the treatment of lymphoproliferative neoplasms in general warrants further investigation. JF - Annals of oncology : official journal of the European Society for Medical Oncology AU - La Rocca, R V AU - Cooper, M R AU - Stein, C A AU - Kohler, D AU - Uhrich, M AU - Weinberger, E AU - Myers, C E AD - Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 571 EP - 573 VL - 3 IS - 7 SN - 0923-7534, 0923-7534 KW - Suramin KW - 6032D45BEM KW - Index Medicus KW - Humans KW - Adult KW - Pilot Projects KW - Suramin -- adverse effects KW - Lymphoma, Follicular -- drug therapy KW - Suramin -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73103852?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+oncology+%3A+official+journal+of+the+European+Society+for+Medical+Oncology&rft.atitle=A+pilot+study+of+suramin+in+the+treatment+of+progressive+refractory+follicular+lymphomas.&rft.au=La+Rocca%2C+R+V%3BCooper%2C+M+R%3BStein%2C+C+A%3BKohler%2C+D%3BUhrich%2C+M%3BWeinberger%2C+E%3BMyers%2C+C+E&rft.aulast=La+Rocca&rft.aufirst=R&rft.date=1992-07-01&rft.volume=3&rft.issue=7&rft.spage=571&rft.isbn=&rft.btitle=&rft.title=Annals+of+oncology+%3A+official+journal+of+the+European+Society+for+Medical+Oncology&rft.issn=09237534&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-11 N1 - Date created - 1992-09-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of DNA repair in malignant neoplastic transformation of human mammary epithelial cells in culture. AN - 73100507; 1638679 AB - Epithelial cells derived from normal human mammary tissue were examined for capacity to repair radiation-induced chromatin DNA damage. Repair capacity was estimated by quantifying chromatid aberrations in metaphase cells arrested 0.5-1.5 h after X-irradiation during G2. The parental cells at passage 12 had 19 chromatid breaks and 16 gaps per 100 metaphase cells, representing efficient repair. Of two continuous cell lines, derived after benzo[a]pyrene treatment, A1 maintained the efficient repair phenotype through passage 50, while a subline of A1 developed the repair-deficient phenotype characterized by a 3- to 5-fold higher frequency of chromatid breaks or gaps. This line was transformed to tumorigenic cells by HaMSV and SV40 T antigen. The second continuous line B5 and derivatives had 102-165 chromatid breaks and 87-134 gaps per 100 metaphases (deficient repair phenotype). This line was transformed to tumorigenic cells by KiMSV. As reported previously for human epidermal keratinocytes, acquisition of this repair-deficient phenotype appears to be an early requisite step in the malignant neoplastic transformation of human cells in culture. JF - Carcinogenesis AU - Sanford, K K AU - Price, F M AU - Rhim, J S AU - Stampfer, M R AU - Parshad, R AD - Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 1137 EP - 1141 VL - 13 IS - 7 SN - 0143-3334, 0143-3334 KW - Chromatin KW - 0 KW - Index Medicus KW - G2 Phase -- radiation effects KW - Chromatin -- radiation effects KW - Epithelial Cells KW - Cells, Cultured KW - Humans KW - Epithelium -- physiology KW - Adult KW - Metaphase KW - Epithelium -- radiation effects KW - Female KW - Breast -- radiation effects KW - DNA Repair KW - DNA Damage KW - Cell Transformation, Neoplastic -- radiation effects KW - Breast -- cytology KW - Chromosome Aberrations KW - Breast -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73100507?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Role+of+DNA+repair+in+malignant+neoplastic+transformation+of+human+mammary+epithelial+cells+in+culture.&rft.au=Sanford%2C+K+K%3BPrice%2C+F+M%3BRhim%2C+J+S%3BStampfer%2C+M+R%3BParshad%2C+R&rft.aulast=Sanford&rft.aufirst=K&rft.date=1992-07-01&rft.volume=13&rft.issue=7&rft.spage=1137&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-28 N1 - Date created - 1992-08-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of lymphocytes infiltrating human breast cancer: specific immune reactivity detected by measuring cytokine secretion. AN - 73096897; 1637779 AB - Primary breast cancers from 19 patients and draining lymph nodes from nine of them (seven containing metastatic tumor) were used in growing tumor-infiltrating lymphocytes (TIL) in culture. TIL were studied for proliferation, phenotype, cytotoxicity, and the ability to secrete cytokines in response to autologous tumor. Lymphocytes from primary breast tumors proliferated in 15 of 19 cultures, a median of 6.7 x 10(3)-fold in 65 days. For eight of nine patients, lymphocytes derived from draining lymph nodes proliferated in culture, a median of 110-fold in 49 days. Breast TIL became predominantly CD4+ cells over time in culture and were 73% CD4+ and 21% CD8+ (means) at 63 days (median). Lymph node lymphocytes were 63% CD4+ at 51 days. TIL were poorly lytic in 4-hour 51Cr release assays. Lysis of autologous tumor occurred in only one of 12 breast TIL and one of nine lymph node cultures. This lysis was low (15% at effector:target = 40:1) and was nonspecific (non-major-histocompatibility-complex restricted). Cytokine secretion was tested by co-culturing TIL with autologous or allogeneic tumors for 24 hours. Cytokines were measured in culture supernatants by enzyme-linked immunosorbent assay or radioimmunoassay. TIL from three of 11 patients specifically secreted granulocyte macrophage-colony-stimulating factor, tumor necrosis factor-alpha and interferon-gamma when stimulated by autologous tumor and not by a panel of four to five allogeneic breast cancers. Cytokine secretion has made possible the identification of lymphocytes infiltrating breast cancers with specific immune reactivity. This finding will guide the development of new immunotherapies for patients with breast cancer. JF - Journal of immunotherapy : official journal of the Society for Biological Therapy AU - Schwartzentruber, D J AU - Solomon, D AU - Rosenberg, S A AU - Topalian, S L AD - Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 1 EP - 12 VL - 12 IS - 1 SN - 1053-8550, 1053-8550 KW - Cytokines KW - 0 KW - HLA Antigens KW - HLA-D Antigens KW - Histocompatibility Antigens Class I KW - Index Medicus KW - HLA-D Antigens -- analysis KW - Tumor Cells, Cultured KW - Lymphatic Metastasis KW - Cells, Cultured KW - Cell Division -- immunology KW - Humans KW - HLA Antigens -- immunology KW - Cytotoxicity Tests, Immunologic KW - Histocompatibility Antigens Class I -- analysis KW - Immunophenotyping KW - Immunohistochemistry KW - Female KW - Breast Neoplasms -- immunology KW - Lymphocytes, Tumor-Infiltrating -- secretion KW - Lymphocytes, Tumor-Infiltrating -- immunology KW - Breast Neoplasms -- pathology KW - Cytokines -- secretion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73096897?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Characterization+of+lymphocytes+infiltrating+human+breast+cancer%3A+specific+immune+reactivity+detected+by+measuring+cytokine+secretion.&rft.au=Schwartzentruber%2C+D+J%3BSolomon%2C+D%3BRosenberg%2C+S+A%3BTopalian%2C+S+L&rft.aulast=Schwartzentruber&rft.aufirst=D&rft.date=1992-07-01&rft.volume=12&rft.issue=1&rft.spage=1&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 - 1992-08-31 N1 - Date created - 1992-08-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A role for behavioral sensitization in uncontrolled ethanol intake. AN - 73090560; 1637498 AB - The processes that underlie the transition from controlled to uncontrolled consumption of ethanol are unknown. Behavioral sensitization is proposed as one of these processes and occurs with repeated administration of psychomotor stimulants whereby both behavioral and neurochemical responses to the drugs are progressively enhanced. Because ethanol shares some actions in common with these drugs, chronic exposure to ethanol may intensify its reinforcing properties. The effect of ethanol on several behavioral models suggests that behavioral sensitization may develop especially in the presence of environmental cues. Thus, a research opportunity exists to study factors that contribute to an increasing probability of progressively higher ethanol consumption. Knowledge of these factors will lead to a better understanding of why some people drink uncontrollably. JF - Alcohol (Fayetteville, N.Y.) AU - Hunt, W A AU - Lands, W E AD - Division of Basic Research, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20857. PY - 1992 SP - 327 EP - 328 VL - 9 IS - 4 SN - 0741-8329, 0741-8329 KW - Index Medicus KW - Environment KW - Animals KW - Humans KW - Alcoholism -- physiopathology KW - Behavior -- physiology KW - Alcohol Drinking KW - Alcoholism -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73090560?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+%28Fayetteville%2C+N.Y.%29&rft.atitle=A+role+for+behavioral+sensitization+in+uncontrolled+ethanol+intake.&rft.au=Hunt%2C+W+A%3BLands%2C+W+E&rft.aulast=Hunt&rft.aufirst=W&rft.date=1992-07-01&rft.volume=9&rft.issue=4&rft.spage=327&rft.isbn=&rft.btitle=&rft.title=Alcohol+%28Fayetteville%2C+N.Y.%29&rft.issn=07418329&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-03 N1 - Date created - 1992-09-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chemical modification and irreversible inhibition of striatal A2a adenosine receptors. AN - 73089495; 1635550 AB - The ligand recognition site of A2a-adenosine receptors in rabbit striatal membranes was probed using non-site-directed labeling reagents and specific affinity labels. Exposure of membranes to diethylpyrocarbonate at a concentration of 2.5 mM, followed by washing, was found to inhibit the binding of [3H]CGS 21680 and [3H]xanthine amine congener to A2a receptors, by 86 and 30%, respectively. Protection from diethylpyrocarbonate inactivation by an adenosine receptor agonist, 5'-N-ethylcarboxamidoadenosine, and an antagonist, theophylline, suggested the presence of two histidyl residues on the receptor, one associated with agonist binding and the other with antagonist binding. Binding of [3H]CGS 21680 or [3H]xanthine amine congener was partially restored after incubation with 250 mM hydroxylamine, further supporting histidine as the modification site. Preincubation with disulfide-reactive reagents, dithiothreitol or sodium dithionite, at greater than 5 mM inhibited radioligand binding, indicating the presence of essential disulfide bridges in A2a receptors, whereas the concentration of mercaptoethanol required to inhibit binding was greater than 50 mM. A number of isothiocyanate-bearing affinity labels derived from the A2a-selective agonist 2-[(2-aminoethylamino) carbonylethylphenylethylamino]-5'-N- ethylcarboxamidoadenosine (APEC) were synthesized and found to inhibit A2a receptor binding in rabbit and bovine striatal membranes. Binding to rabbit A1 receptors was not inhibited. Preincubation with the affinity label 4-isothiocyanatophenylaminothiocarbonyl-APEC (100 nM) diminished the Bmax for [3H]CGS 21680 binding by 71%, and the Kd was unaffected, suggesting a direct modification of the ligand binding site. Reversal of 4-isothiocyanatophenylaminothiocarbonyl-APEC inhibition of [3H]CGS 21680 binding with hydroxylamine suggested that the site of modification by the isothiocyanate is a cysteine residue. A bromoacetyl derivative of APEC was ineffective as an affinity label at submicromolar concentrations. JF - Molecular pharmacology AU - Jacobson, K A AU - Stiles, G L AU - Ji, X D AD - Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 123 EP - 133 VL - 42 IS - 1 SN - 0026-895X, 0026-895X KW - Affinity Labels KW - 0 KW - Hydroxylamines KW - Phenethylamines KW - Purinergic Antagonists KW - Receptors, Purinergic KW - Xanthines KW - 2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine KW - 120225-54-9 KW - Hydroxylamine KW - 2FP81O2L9Z KW - Adenosine-5'-(N-ethylcarboxamide) KW - 35920-39-9 KW - 8-(4-((2-aminoethyl)aminocarbonylmethyloxy)phenyl)-1,3-dipropylxanthine KW - 96865-92-8 KW - Theophylline KW - C137DTR5RG KW - Adenosine KW - K72T3FS567 KW - Diethyl Pyrocarbonate KW - LMR3LZG146 KW - Index Medicus KW - Animals KW - Adenosine -- analogs & derivatives KW - Xanthines -- metabolism KW - Rabbits KW - Amino Acid Sequence KW - Radioligand Assay KW - Receptors, Purinergic -- drug effects KW - Receptors, Purinergic -- metabolism KW - Phenethylamines -- metabolism KW - Adenosine -- pharmacology KW - Theophylline -- pharmacology KW - Diethyl Pyrocarbonate -- pharmacology KW - Molecular Sequence Data KW - Receptors, Purinergic -- chemistry KW - Hydroxylamines -- pharmacology KW - Drug Antagonism KW - Adenosine -- metabolism KW - Corpus Striatum -- metabolism KW - Corpus Striatum -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73089495?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Chemical+modification+and+irreversible+inhibition+of+striatal+A2a+adenosine+receptors.&rft.au=Jacobson%2C+K+A%3BStiles%2C+G+L%3BJi%2C+X+D&rft.aulast=Jacobson&rft.aufirst=K&rft.date=1992-07-01&rft.volume=42&rft.issue=1&rft.spage=123&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 - 1992-08-21 N1 - Date created - 1992-08-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Pharmacol Exp Ther. 1991 Oct;259(1):286-94 [1920121] Biochem Pharmacol. 1990 Aug 15;40(4):835-42 [2143656] Methods Enzymol. 1977;47:431-42 [22021] Mol Pharmacol. 1992 Feb;41(2):352-9 [1311411] Med Res Rev. 1992 Sep;12(5):423-71 [1513184] Neurochem Int. 1991;18(2):207-13 [20504695] Mol Pharmacol. 1988 Dec;34(6):724-8 [3200248] J Biol Chem. 1988 Nov 25;263(33):17522-6 [3182861] FEBS Lett. 1985 May 6;184(1):30-5 [2985445] Naunyn Schmiedebergs Arch Pharmacol. 1988 Jan;337(1):64-8 [2835689] Proc Natl Acad Sci U S A. 1989 Sep;86(17):6572-6 [2771944] J Med Chem. 1989 May;32(5):1043-51 [2709373] J Pharmacol Exp Ther. 1989 Dec;251(3):888-93 [2600819] J Mol Recognit. 1989 Dec;2(4):170-8 [2561548] Science. 1989 May 5;244(4904):569-72 [2541503] Physiol Rev. 1990 Jul;70(3):761-845 [2194223] Mol Pharmacol. 1991 Jul;40(1):1-7 [1857334] Bioconjug Chem. 1991 Mar-Apr;2(2):77-88 [1868116] Mol Pharmacol. 1991 Feb;39(2):130-5 [1899902] Mol Pharmacol. 1991 Nov;40(5):639-47 [1944235] Biochem Pharmacol. 1991 Mar 1;41(5):735-42 [1998528] FEBS Lett. 1990 Oct 29;273(1-2):6-10 [2121544] Biochem Biophys Res Commun. 1990 Dec 31;173(3):1169-78 [2125216] J Clin Invest. 1990 Apr;85(4):1150-7 [2156895] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Parkinsonism-inducing neurotoxin MPP+: uptake and toxicity in nonneuronal COS cells expressing dopamine transporter cDNA. AN - 73084197; 1642464 AB - Expression of a cloned dopamine transporter complementary DNA in COS cells allows these primate kidney cells to accumulate the parkinsonism-inducing neurotoxin metabolite MPP+ (1-methyl-4-phenylpyridinium) avidly, and MPP+ toxicity results. By documenting that the dopamine transporter can confer MPP+ sensitivity to nonneural cells, these results highlight the key role that this transporter could play in mechanisms underlying parkinsonism. JF - Annals of neurology AU - Kitayama, S AU - Shimada, S AU - Uhl, G R AD - Laboratory of Molecular Neurobiology, Addiction Research Center/National Institute on Drug Abuse, Johns Hopkins University School of Medicine, Baltimore, MD. 21224. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 109 EP - 111 VL - 32 IS - 1 SN - 0364-5134, 0364-5134 KW - Carrier Proteins KW - 0 KW - Dopamine Plasma Membrane Transport Proteins KW - Membrane Glycoproteins KW - Membrane Transport Proteins KW - Nerve Tissue Proteins KW - Neurotoxins KW - DNA KW - 9007-49-2 KW - 1-Methyl-4-phenylpyridinium KW - R865A5OY8J KW - Index Medicus KW - Animals KW - Neurotoxins -- pharmacokinetics KW - Neurotoxins -- poisoning KW - Nerve Tissue Proteins -- genetics KW - Cell Line KW - Parkinson Disease, Secondary -- chemically induced KW - Kidney -- metabolism KW - 1-Methyl-4-phenylpyridinium -- pharmacokinetics KW - DNA -- metabolism KW - Carrier Proteins -- genetics KW - 1-Methyl-4-phenylpyridinium -- poisoning KW - Kidney -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73084197?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Parkinsonism-inducing+neurotoxin+MPP%2B%3A+uptake+and+toxicity+in+nonneuronal+COS+cells+expressing+dopamine+transporter+cDNA.&rft.au=Kitayama%2C+S%3BShimada%2C+S%3BUhl%2C+G+R&rft.aulast=Kitayama&rft.aufirst=S&rft.date=1992-07-01&rft.volume=32&rft.issue=1&rft.spage=109&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 - 1992-09-01 N1 - Date created - 1992-09-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Drug abuse related emergency room episodes in the United States. AN - 73079165; 1643400 AB - Drug-related hospital emergency room cases provide one measure of the morbidity associated with drug abuse. Over time, they indicate if problems associated with particular drugs are increasing or decreasing. These trends may be influenced by a number of factors including increased prevalence of use, increased dosages, increased potency, increased frequency of use, the aging of drug addicts, the use of more dangerous routes of administration, and the combined use of two or more drugs. The primary source of this information in the United States is the Drug Abuse Warning Network (DAWN). This paper will present statistics on the drug-related emergencies reported to the DAWN system for 1989 and 1990. In addition to numbers of drug-related emergencies, this paper includes the population based rates for drug-related emergencies in 1990. JF - British journal of addiction AU - Kopstein, A AD - Division of Epidemiology and Prevention Research, National Institute on Drug Abuse, Rockville, Maryland 20852. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 1071 EP - 1075 VL - 87 IS - 7 SN - 0952-0481, 0952-0481 KW - Psychotropic Drugs KW - 0 KW - Street Drugs KW - Index Medicus KW - Cross-Sectional Studies KW - Humans KW - Adult KW - Incidence KW - Middle Aged KW - Child KW - Adolescent KW - United States -- epidemiology KW - Male KW - Female KW - Street Drugs -- adverse effects KW - Substance-Related Disorders -- complications KW - Emergency Service, Hospital -- utilization KW - Psychotropic Drugs -- adverse effects KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73079165?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+addiction&rft.atitle=Drug+abuse+related+emergency+room+episodes+in+the+United+States.&rft.au=Kopstein%2C+A&rft.aulast=Kopstein&rft.aufirst=A&rft.date=1992-07-01&rft.volume=87&rft.issue=7&rft.spage=1071&rft.isbn=&rft.btitle=&rft.title=British+journal+of+addiction&rft.issn=09520481&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-09-10 N1 - Date created - 1992-09-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Addiction. 1993 Feb;88(2):281-3 [8292181] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phthalate ester effects on rat Sertoli cell function in vitro: effects of phthalate side chain and age of animal. AN - 73077105; 1321518 AB - Mono(2-ethylhexyl) phthalate (MEHP), the active metabolite of the testicular toxicant di(2-ethylhexyl) phthalate, inhibits FSH-stimulated rat Sertoli cell cAMP accumulation, stimulates basal lactate production, and decreases intracellular ATP levels in vitro. Dibutyl phthalate and dipentyl phthalate but not diethyldimethyl or dipropyl are also age-dependent testicular toxicants in vivo. We therefore examined the effect of animal age and phthalate monoester on the Sertoli cell FSH-stimulated cAMP accumulation, lactate secretion, and ATP levels in order to determine if these effects are part of the mechanism of action of phthalate esters in vivo. MEHP, monobutyl and monopentyl phthalates but not the monoethyl, monomethyl, or monopropyl phthalates inhibited FSH-stimulated cAMP accumulation, a segregation which matches the in vivo toxicity potential of these agents. MEHP and monopentyl, but not monobutyl phthalates, also stimulated Sertoli cell lactate secretion. The effect of the active phthalates on FSH-stimulated cAMP accumulation and lactate secretion is not dependent on age of animal over a range of 13-80 days, suggesting that the age-related toxicity in vivo may be related to differences in metabolism and disposition rather than tissue sensitivity. Since the ED50 of MEHP inhibition of cAMP accumulation and lactate secretion is similar, these two effects may be related to a common initial effect of the active phthalates. Inhibition of intracellular ATP levels is specific for MEHP and is lost with age (greater than 28 days of age) and thus is not likely to be an essential part of the in vivo mechanism of action of phthalate diesters. JF - Toxicology and applied pharmacology AU - Heindel, J J AU - Powell, C J AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 116 EP - 123 VL - 115 IS - 1 SN - 0041-008X, 0041-008X KW - Lactates KW - 0 KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Follicle Stimulating Hormone KW - 9002-68-0 KW - Diethylhexyl Phthalate KW - C42K0PH13C KW - Cyclic AMP KW - E0399OZS9N KW - mono-(2-ethylhexyl)phthalate KW - FU2EWB60RT KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Lactates -- metabolism KW - Cells, Cultured KW - Adenosine Triphosphate -- metabolism KW - Cyclic AMP -- metabolism KW - Follicle Stimulating Hormone -- pharmacology KW - Male KW - Sertoli Cells -- secretion KW - Sertoli Cells -- drug effects KW - Sertoli Cells -- cytology KW - Diethylhexyl Phthalate -- toxicity KW - Aging KW - Diethylhexyl Phthalate -- chemistry KW - Diethylhexyl Phthalate -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73077105?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Phthalate+ester+effects+on+rat+Sertoli+cell+function+in+vitro%3A+effects+of+phthalate+side+chain+and+age+of+animal.&rft.au=Heindel%2C+J+J%3BPowell%2C+C+J&rft.aulast=Heindel&rft.aufirst=J&rft.date=1992-07-01&rft.volume=115&rft.issue=1&rft.spage=116&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 - 1992-08-18 N1 - Date created - 1992-08-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Drug treatment of canine acral lick. An animal model of obsessive-compulsive disorder. AN - 73063547; 1385694 AB - Canine acral lick dermatitis is a naturally occurring disorder in which excessive licking of paws or flank can produce ulcers and infection that require medical treatment. Forty-two dogs with severe chronic canine acral lick dermatitis were treated in three double-blind crossover comparisons of clomipramine hydrochloride/desipramine hydrochloride, fluoxetine hydrochloride/fenfluramine hydrochloride, and sertraline hydrochloride/placebo. The serotonin uptake blocking drugs were clinically effective, while the other drugs were not. Based on phenomenology and pharmacological response, we propose canine acral lick dermatitis as an animal model of obsessive-compulsive disorder. JF - Archives of general psychiatry AU - Rapoport, J L AU - Ryland, D H AU - Kriete, M AD - Child Psychiatry Branch, National Institute of Mental Health, Bethesda, Md. 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 517 EP - 521 VL - 49 IS - 7 SN - 0003-990X, 0003-990X KW - Neurotransmitter Uptake Inhibitors KW - 0 KW - Fluoxetine KW - 01K63SUP8D KW - Fenfluramine KW - 2DS058H2CF KW - Serotonin KW - 333DO1RDJY KW - 1-Naphthylamine KW - 9753I242R5 KW - Clomipramine KW - NUV44L116D KW - Sertraline KW - QUC7NX6WMB KW - Desipramine KW - TG537D343B KW - Abridged Index Medicus KW - Index Medicus KW - Ulcer -- drug therapy KW - Animals KW - Double-Blind Method KW - Humans KW - Fenfluramine -- therapeutic use KW - Clomipramine -- therapeutic use KW - 1-Naphthylamine -- analogs & derivatives KW - Ulcer -- veterinary KW - Desipramine -- therapeutic use KW - Dogs KW - Fluoxetine -- therapeutic use KW - Follow-Up Studies KW - 1-Naphthylamine -- therapeutic use KW - Obsessive-Compulsive Disorder -- physiopathology KW - Serotonin -- physiology KW - Dermatitis -- veterinary KW - Obsessive-Compulsive Disorder -- drug therapy KW - Grooming -- drug effects KW - Grooming -- physiology KW - Dog Diseases -- drug therapy KW - Disease Models, Animal KW - Neurotransmitter Uptake Inhibitors -- therapeutic use KW - Dermatitis -- drug therapy KW - Dog Diseases -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73063547?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Drug+treatment+of+canine+acral+lick.+An+animal+model+of+obsessive-compulsive+disorder.&rft.au=Rapoport%2C+J+L%3BRyland%2C+D+H%3BKriete%2C+M&rft.aulast=Rapoport&rft.aufirst=J&rft.date=1992-07-01&rft.volume=49&rft.issue=7&rft.spage=517&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 - 1992-08-12 N1 - Date created - 1992-08-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Selective interaction of beta 2- and alpha 2-adrenergic receptors with stimulatory and inhibitory guanine nucleotide-binding proteins. AN - 73063101; 1321955 AB - In Chinese hamster ovary cells expressing recombinant beta 2-adrenergic receptors, isoproterenol enhanced cholera toxin-catalyzed ADP-ribosylation of the large form of G5 alpha. The effect was stereoselectively blocked by the enantiomers of propranolol, indicating receptor mediation. The ADP-ribosylated form of Gs alpha-subunit was resolved into a triplet in gradient gels. beta 2-Adrenergic receptors increased both the labelling and the apparent mass of the slower migrating forms of large Gs alpha, as determined by autoradiography and immunoblotting, suggesting that Gs alpha, can incorporate more than one ADP-ribose per molecule. In cells coexpressing similar amounts of beta 2-adrenergic, alpha 2-adrenergic, and m1 muscarinic receptors, beta 2 receptors stimulated the ADP-ribosylation of only large Gs and alpha 2 receptors that of only Gi; muscarinic receptors had no apparent effect. Thus, in native membranes there appears to be a selectivity for the interaction between adrenergic receptor subtypes and Gs alpha or Gi alpha subunits. JF - Molecular pharmacology AU - Ogino, Y AU - Fraser, C M AU - Costa, T AD - Laboratory of Theoretical and Physical Biology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 6 EP - 9 VL - 42 IS - 1 SN - 0026-895X, 0026-895X KW - Receptors, Adrenergic, alpha KW - 0 KW - Receptors, Adrenergic, beta KW - Recombinant Proteins 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 - Isoproterenol KW - L628TT009W KW - Index Medicus KW - Animals KW - Blotting, Western KW - Recombinant Proteins -- metabolism KW - Electrophoresis, Polyacrylamide Gel KW - Humans KW - Cholera Toxin -- pharmacology KW - CHO Cells KW - Autoradiography KW - Adenosine Diphosphate Ribose -- metabolism KW - Isoproterenol -- pharmacology KW - Cricetinae KW - Receptors, Adrenergic, beta -- metabolism KW - GTP-Binding Proteins -- metabolism KW - Receptors, Adrenergic, alpha -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73063101?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Selective+interaction+of+beta+2-+and+alpha+2-adrenergic+receptors+with+stimulatory+and+inhibitory+guanine+nucleotide-binding+proteins.&rft.au=Ogino%2C+Y%3BFraser%2C+C+M%3BCosta%2C+T&rft.aulast=Ogino&rft.aufirst=Y&rft.date=1992-07-01&rft.volume=42&rft.issue=1&rft.spage=6&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 - 1992-08-21 N1 - Date created - 1992-08-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Recombinant anti-erbB2 immunotoxins containing Pseudomonas exotoxin. AN - 73055343; 1352878 AB - Immunotoxins were made using five different murine monoclonal antibodies to the human erbB2 gene product and LysPE40, a 40-kDa recombinant form of Pseudomonas exotoxin (PE) lacking its cell-binding domain. All five conjugates were specifically cytotoxic to cancer cell lines overexpressing erbB2 protein. The most active conjugate was e23-LysPE40, generated by chemical crosslinking of anti-erbB2 monoclonal antibody e23 to LysPE40. In addition, a recombinant immunotoxin, e23(Fv)PE40, was constructed that consists of the light-chain variable domain of e23 connected through a peptide linker to its heavy-chain variable domain, which in turn is fused to PE40. The recombinant protein was made in Escherichia coli, purified to near homogeneity, and shown to selectively kill cells expressing the erbB2 protooncogene. To improve the cytotoxic activity of e23(Fv)PE40, PE40 was replaced with a variant, PE38KDEL, in which the carboxyl end of PE is changed from Arg-Glu-Asp-Leu-Lys to Lys-Asp-Glu-Leu and amino acids 365-380 of PE are deleted. The e23(Fv)PE38KDEL protein inhibits the growth of tumors formed by the human gastric cancer cell line N87 in immunodeficient mice. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Batra, J K AU - Kasprzyk, P G AU - Bird, R E AU - Pastan, I AU - King, C R AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/07/01/ PY - 1992 DA - 1992 Jul 01 SP - 5867 EP - 5871 VL - 89 IS - 13 SN - 0027-8424, 0027-8424 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - Immunotoxins KW - Oligodeoxyribonucleotides KW - Proto-Oncogene Proteins KW - Receptors, Cell Surface 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 - Receptor, ErbB-2 KW - EC 2.7.10.1 KW - Index Medicus KW - Animals KW - Antibody-Dependent Cell Cytotoxicity KW - Immunotherapy KW - Amino Acid Sequence KW - Mice KW - Mice, Nude KW - Recombinant Fusion Proteins -- toxicity KW - Structure-Activity Relationship KW - Neoplasm Transplantation KW - Cytotoxicity, Immunologic KW - Base Sequence KW - Tumor Cells, Cultured KW - Oligodeoxyribonucleotides -- chemistry KW - In Vitro Techniques KW - Stomach Neoplasms -- therapy KW - Molecular Sequence Data KW - Bacterial Toxins -- chemistry KW - Bacterial Toxins -- toxicity KW - Pseudomonas aeruginosa KW - Immunotoxins -- chemistry KW - Receptors, Cell Surface -- immunology KW - Proto-Oncogene Proteins -- immunology KW - Exotoxins -- toxicity KW - Exotoxins -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73055343?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Recombinant+anti-erbB2+immunotoxins+containing+Pseudomonas+exotoxin.&rft.au=Batra%2C+J+K%3BKasprzyk%2C+P+G%3BBird%2C+R+E%3BPastan%2C+I%3BKing%2C+C+R&rft.aulast=Batra&rft.aufirst=J&rft.date=1992-07-01&rft.volume=89&rft.issue=13&rft.spage=5867&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 - 1992-08-14 N1 - Date created - 1992-08-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Science. 1991 Nov 22;254(5035):1173-7 [1683495] Nature. 1970 Aug 15;227(5259):680-5 [5432063] Mol Cell Biol. 1991 Apr;11(4):2200-5 [2005905] Proc Natl Acad Sci U S A. 1990 Feb;87(3):1066-70 [2105495] Nature. 1989 Jun 1;339(6223):394-7 [2498664] J Biol Chem. 1989 Aug 25;264(24):14256-61 [2503515] Br J Cancer. 1988 Oct;58(4):453-7 [2849975] Science. 1987 Jul 10;237(4811):178-82 [2885917] Proc Natl Acad Sci U S A. 1987 Oct;84(20):7159-63 [2890160] EMBO J. 1987 Mar;6(3):605-10 [3034598] J Biol Chem. 1988 Jul 5;263(19):9470-5 [3132465] Cancer Res. 1987 Nov 15;47(22):6123-5 [3664511] Science. 1987 Jan 9;235(4785):177-82 [3798106] Cancer Res. 1992 May 15;52(10):2771-6 [1349849] Proc Natl Acad Sci U S A. 1991 Oct 1;88(19):8616-20 [1924323] Proc Natl Acad Sci U S A. 1991 Apr 15;88(8):3358-62 [2014255] Science. 1989 May 12;244(4905):707-12 [2470152] Proc Natl Acad Sci U S A. 1989 Nov;86(21):8545-9 [2510169] Lancet. 1986 Apr 5;1(8484):765-7 [2870269] Science. 1985 Sep 6;229(4717):974-6 [2992089] Cell. 1987 Jan 16;48(1):129-36 [3098436] Science. 1987 Nov 20;238(4830):1098-104 [3317828] J Biol Chem. 1991 Sep 15;266(26):17376-81 [1910044] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Adaptive control with feedback strategies for suramin dosing. AN - 73052884; 1623689 AB - Suramin, a drug used in the treatment of parasitic diseases, is currently being evaluated in clinical trials as an antineoplastic agent. The use of therapeutic drug monitoring and adaptive control with feedback in clinical trials of suramin was initially motivated by an association between acute neurologic toxicity and plasma suramin concentrations in excess of 350 micrograms/ml. We have prospectively examined the performance of both two- and three-compartment population pharmacokinetic models in controlling plasma suramin concentrations and have found that a three-compartment model best describes this drug. No correlation was found between the clearance of suramin and creatinine clearance, as had been previously hypothesized. The low systemic clearance of suramin and the number of parameters required to describe the three-compartment model suggest the need for a bayesian approach to the estimation of individual pharmacokinetics. JF - Clinical pharmacology and therapeutics AU - Cooper, M R AU - Lieberman, R AU - La Rocca, R V AU - Gernt, P R AU - Weinberger, M S AU - Headlee, D J AU - Kohler, D R AU - Goldspiel, B R AU - Peck, C C AU - Myers, C E AD - Clinical Pharmacology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 11 EP - 23 VL - 52 IS - 1 SN - 0009-9236, 0009-9236 KW - Antineoplastic Agents KW - 0 KW - Suramin KW - 6032D45BEM KW - Creatinine KW - AYI8EX34EU KW - Abridged Index Medicus KW - Index Medicus KW - Software KW - Prospective Studies KW - Infusions, Intravenous KW - Humans KW - Bayes Theorem KW - Nervous System Diseases -- blood KW - Creatinine -- pharmacokinetics KW - Nervous System Diseases -- chemically induced KW - Models, Biological KW - Drug Monitoring -- methods KW - Suramin -- adverse effects KW - Antineoplastic Agents -- administration & dosage KW - Adrenal Gland Neoplasms -- blood KW - Suramin -- pharmacokinetics KW - Suramin -- administration & dosage KW - Adrenal Gland Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73052884?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Adaptive+control+with+feedback+strategies+for+suramin+dosing.&rft.au=Cooper%2C+M+R%3BLieberman%2C+R%3BLa+Rocca%2C+R+V%3BGernt%2C+P+R%3BWeinberger%2C+M+S%3BHeadlee%2C+D+J%3BKohler%2C+D+R%3BGoldspiel%2C+B+R%3BPeck%2C+C+C%3BMyers%2C+C+E&rft.aulast=Cooper&rft.aufirst=M&rft.date=1992-07-01&rft.volume=52&rft.issue=1&rft.spage=11&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 - 1992-08-10 N1 - Date created - 1992-08-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Population-based monitoring of an urban HIV/AIDS epidemic. Magnitude and trends in the District of Columbia. AN - 73046291; 1619741 AB - To assess the extent of the human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS) epidemic in the District of Columbia and demonstrate an approach to monitoring HIV infection and projecting AIDS incidence at a community level. Backcalculation methods to reconstruct HIV incidence from AIDS incidence in subgroups. Results were compared with directly measured HIV seroprevalence in selected sentinel populations: childbearing women, civilian applicants for military service, and hospital patients admitted for conditions unrelated to HIV infection. Between the start of the epidemic in 1980 and January 1, 1991, one in 57 District of Columbia men aged 20 to 64 years was diagnosed with AIDS. Unlike the plateau projected for the nation, AIDS incidence for the District of Columbia was projected to increase by 34% between 1990 and 1994. Models of HIV infection incidence suggested two broad epidemic waves of approximately equal size. The first occurred in men who have sex with men and peaked during the period from 1982 through 1983. The second began in the mid-1980s in injecting drug users and heterosexuals. We estimated that among District of Columbia residents aged 20 to 64 years, 0.3% of white women, 2.9% of white men, 1.6% of black women, and 4.9% of black men were living with HIV infection as of January 1, 1991. These estimates are broadly consistent with survey data: among black childbearing women in their 20s, HIV prevalence doubled to 2% between the fall of 1989 and the spring of 1991; from military applicant data, we estimated that over 5% of black men born from 1951 through 1967 were HIV-positive; in the sentinel hospital, HIV prevalence rates among male patients aged 25 to 34 years were 11.3% in white men and 16.9% in black men. Backcalculation and surveys yielded quantitatively consistent estimates of HIV prevalence. Many injecting drug users and heterosexuals in the District of Columbia were infected after January 1, 1986. Similar monitoring of the epidemic in other localities is needed to focus efforts to reduce the incidence of HIV transmission. JF - JAMA AU - Rosenberg, P S AU - Levy, M E AU - Brundage, J F AU - Petersen, L R AU - Karon, J M AU - Fears, T R AU - Gardner, L I AU - Gail, M H AU - Goedert, J J AU - Blattner, W A AD - Epidemiologic Methods Section, National Cancer Institute, Rockville, Md 20892. PY - 1992 SP - 495 EP - 503 VL - 268 IS - 4 SN - 0098-7484, 0098-7484 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - HIV Seroprevalence -- trends KW - Humans KW - Models, Statistical KW - Pregnancy KW - Population Surveillance KW - Military Personnel KW - Adult KW - District of Columbia -- epidemiology KW - Incidence KW - Middle Aged KW - Substance Abuse, Intravenous -- complications KW - African Continental Ancestry Group KW - Female KW - Male KW - Acquired Immunodeficiency Syndrome -- ethnology KW - Acquired Immunodeficiency Syndrome -- epidemiology KW - Urban Health -- statistics & numerical data KW - HIV Infections -- ethnology KW - Disease Outbreaks KW - HIV Infections -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73046291?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Population-based+monitoring+of+an+urban+HIV%2FAIDS+epidemic.+Magnitude+and+trends+in+the+District+of+Columbia.&rft.au=Rosenberg%2C+P+S%3BLevy%2C+M+E%3BBrundage%2C+J+F%3BPetersen%2C+L+R%3BKaron%2C+J+M%3BFears%2C+T+R%3BGardner%2C+L+I%3BGail%2C+M+H%3BGoedert%2C+J+J%3BBlattner%2C+W+A&rft.aulast=Rosenberg&rft.aufirst=P&rft.date=1992-07-01&rft.volume=268&rft.issue=4&rft.spage=495&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-31 N1 - Date created - 1992-07-31 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: JAMA. 1993 Jan 27;269(4):472-3 [8481178] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Disruption of a silencer domain by a retrotransposon. AN - 73044117; 1321064 AB - A galactose-inducible Ty element carrying the HIS3 gene has been used as an insertional mutagen to generate alpha-factor resistant mutants. This collection of Ty-induced mutations includes insertions into the gene for the alpha-factor receptor (STE2), several nonspecific STE genes, and mutations that lead to the expression of the normally silent HML alpha locus. The hml alpha "on" mutations fall into two classes, those that disrupt trans-acting regulators involved in silencing HML alpha and a novel class of mutations that activate HML alpha by insertion at that locus. The hml alpha::Ty "on" mutations illustrate the unusual ability of these retrotransposons to activate genes by overcoming gene silencing mechanisms. The hml alpha::Ty "on" mutations include examples of multimeric Ty arrays. Single Ty and solo delta insertion derivatives of these Ty multimers restore the ability of the silencing mechanism to repress HML alpha. JF - Genetics AU - Mastrangelo, M F AU - Weinstock, K G AU - Shafer, B K AU - Hedge, A M AU - Garfinkel, D J AU - Strathern, J N AD - Laboratory of Eukaryotic Gene Expression, NCI-Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 519 EP - 529 VL - 131 IS - 3 SN - 0016-6731, 0016-6731 KW - HIS3 KW - HML&agr; KW - MAR KW - MAT KW - SIR KW - STE KW - DNA Transposable Elements KW - 0 KW - Peptides KW - Receptors, Cell Surface KW - Receptors, Mating Factor KW - Receptors, Peptide KW - Transcription Factors KW - Mating Factor KW - 61194-02-3 KW - Index Medicus KW - Saccharomyces cerevisiae -- genetics KW - Phenotype KW - Genes, Fungal KW - Blotting, Southern KW - Electrophoresis, Gel, Pulsed-Field KW - Receptors, Cell Surface -- genetics KW - Mutagenesis, Insertional KW - Gene Expression Regulation, Fungal KW - Regulatory Sequences, Nucleic Acid KW - Peptides -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73044117?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Disruption+of+a+silencer+domain+by+a+retrotransposon.&rft.au=Mastrangelo%2C+M+F%3BWeinstock%2C+K+G%3BShafer%2C+B+K%3BHedge%2C+A+M%3BGarfinkel%2C+D+J%3BStrathern%2C+J+N&rft.aulast=Mastrangelo&rft.aufirst=M&rft.date=1992-07-01&rft.volume=131&rft.issue=3&rft.spage=519&rft.isbn=&rft.btitle=&rft.title=Genetics&rft.issn=00166731&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-18 N1 - Date created - 1992-08-18 N1 - Date revised - 2017-01-13 N1 - Gene symbol - HIS3; HML&agr;; MAR; MAT; SIR; STE N1 - SuppNotes - Cited By: Cell. 1989 Nov 17;59(4):637-47 [2684414] Cell. 1990 Feb 23;60(4):649-64 [2406028] Proc Natl Acad Sci U S A. 1988 Apr;85(7):2120-4 [3281162] Cell. 1987 Dec 4;51(5):721-32 [3315231] Methods Enzymol. 1987;154:164-75 [3323810] J Mol Biol. 1984 Oct 5;178(4):815-34 [6092645] Nature. 1981 Jan 22;289(5795):239-44 [6256655] Cell. 1982 Nov;31(1):183-92 [6297747] Cold Spring Harb Symp Quant Biol. 1983;47 Pt 2:989-98 [6345082] J Mol Biol. 1984 Jul 5;176(3):307-31 [6379190] Cell. 1981 Nov;27(1 Pt 2):15-23 [7034964] Genetics. 1979 Sep;93(1):13-35 [16118901] Genetics. 1977 Mar;85(3):395-405 [17248736] Genetics. 1979 Dec;93(4):877-901 [397913] Proc Natl Acad Sci U S A. 1991 Nov 1;88(21):9392-6 [1946350] Genes Dev. 1991 Apr;5(4):605-15 [2010086] Nature. 1989 Dec 14;342(6251):749-57 [2513489] EMBO J. 1989 Jul;8(7):2067-75 [2551674] Mol Cell Biol. 1989 Nov;9(11):4621-30 [2689860] Cell. 1985 Mar;40(3):491-500 [2982495] Mol Cell Biol. 1988 Jan;8(1):210-25 [3275867] Genetics. 1987 May;116(1):9-22 [3297920] Mol Cell Biol. 1987 Oct;7(10):3713-22 [3316986] Cell. 1985 May;41(1):41-8 [3888409] Mol Cell Biol. 1985 Aug;5(8):1878-86 [3915783] Cell. 1982 Sep;30(2):567-78 [6215985] Nature. 1981 Jan 22;289(5795):244-50 [6256656] Cell. 1981 Aug;25(2):517-24 [6269749] Methods Enzymol. 1983;101:202-11 [6310324] Genetics. 1983 Jun;104(2):219-34 [6345265] J Cell Biol. 1980 Jun;85(3):811-22 [6993497] J Mol Biol. 1981 Apr 15;147(3):357-72 [7031257] Mol Cell Biol. 1982 Jan;2(1):11-20 [7050665] EMBO J. 1985 Oct;4(10):2643-8 [16453635] Genetics. 1976 Jun;83(2):245-58 [17248712] Genetics. 1979 Sep;93(1):37-50 [17248968] Cell. 1979 Oct;18(2):309-19 [387260] Mol Cell Biol. 1991 Feb;11(2):1069-79 [1990267] Genetics. 1988 Sep;120(1):95-108 [2851484] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Skeletal hyperostosis in patients receiving chronic, very-low-dose isotretinoin. AN - 73043576; 1626958 AB - We conducted a prospective roentgenographic survey of patients participating in a randomized, placebo-controlled, multicenter clinical trial that evaluated the effectiveness of chronic, very-low-dose (approximately 0.14 mg/kg per day for 3 years) isotretinoin in preventing the subsequent occurrences of new basal cell carcinoma in patients with previous basal cell carcinoma. To assess potential skeletal changes, a sample of 269 patients from among a total of 981 enrollees were randomly selected for comparative roentgenographic review. Baseline and 36-month roentgenograms of the cervical and thoracic spine of each patient were read side by side by a radiologist, masked to treatment group, who noted both the presence and extent of abnormalities at each vertebral level at baseline and the progression of existing or occurrence of new abnormalities at previously unaffected levels at 36 months. In comparison with the placebo group, significantly more patients in the isotretinoin group exhibited progression of existing hyperostotic abnormalities (40% vs 18%; P less than .001) and new hyperostotic involvement at previously unaffected vertebral levels (8% vs 1%; P = .015). Our findings indicate that chronic, very-low-dose isotretinoin can induce hyperostotic axial skeletal changes similar to those reported in patients taking higher doses. JF - Archives of dermatology AU - Tangrea, J A AU - Kilcoyne, R F AU - Taylor, P R AU - Helsel, W E AU - Adrianza, M E AU - Hartman, A M AU - Edwards, B K AU - Peck, G L AD - Division of Cancer Prevention and Control, National Cancer Institute, National Institutes of Health, Bethesda, Md. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 921 EP - 925 VL - 128 IS - 7 SN - 0003-987X, 0003-987X KW - Isotretinoin KW - EH28UP18IF KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Thoracic Vertebrae -- diagnostic imaging KW - Aged KW - Skin Neoplasms -- prevention & control KW - Neoplasm Recurrence, Local -- prevention & control KW - Carcinoma, Basal Cell -- prevention & control KW - Prospective Studies KW - Cervical Vertebrae -- diagnostic imaging KW - Adult KW - Middle Aged KW - Radiography KW - Female KW - Male KW - Isotretinoin -- administration & dosage KW - Hyperostosis, Diffuse Idiopathic Skeletal -- diagnostic imaging KW - Isotretinoin -- adverse effects KW - Hyperostosis, Diffuse Idiopathic Skeletal -- chemically induced KW - Isotretinoin -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73043576?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+dermatology&rft.atitle=Skeletal+hyperostosis+in+patients+receiving+chronic%2C+very-low-dose+isotretinoin.&rft.au=Tangrea%2C+J+A%3BKilcoyne%2C+R+F%3BTaylor%2C+P+R%3BHelsel%2C+W+E%3BAdrianza%2C+M+E%3BHartman%2C+A+M%3BEdwards%2C+B+K%3BPeck%2C+G+L&rft.aulast=Tangrea&rft.aufirst=J&rft.date=1992-07-01&rft.volume=128&rft.issue=7&rft.spage=921&rft.isbn=&rft.btitle=&rft.title=Archives+of+dermatology&rft.issn=0003987X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-13 N1 - Date created - 1992-08-13 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Arch Dermatol. 1992 Dec;128(12):1650 [1308126] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Soft tissue sarcoma and tobacco use: data from a prospective cohort study of United States veterans. AN - 73041322; 1617125 AB - A report of an increased risk of soft tissue sarcoma (STS) among users of smokeless tobacco led us to evaluate this association and the role of other types of tobacco in a prospective cohort mortality-study of United States veterans. A total of 248,046 veterans provided tobacco-use histories on a mail questionnaire in 1954 or 1957. Data on subsequent tobacco use were not collected. By 1980, 119 deaths from STS had occurred among the cohort members. Veterans who had ever chewed tobacco or used snuff had a nonsignificant 40 percent excess of STS (95 percent confidence interval [CI] = 0.8-2.6; 21 deaths) in comparison with veterans who had never used any tobacco products. Risk was limited to former users (relative risk [RR] = 1.5) with no excess seen among current users (RR = 0.9). Frequent former users had higher risk (RR = 1.9) than infrequent users (RR = 1.3). Risk was slightly higher in persons who started using smokeless tobacco at younger ages, but did not increase with duration of use or with late age at cessation of use. Most veterans who used chewing tobacco or snuff also used some other form of tobacco. No STS deaths occurred among the 2,308 veterans who used smokeless tobacco only. An unexpected finding of the study was the significant excess of STS deaths among cigarette smokers (RR = 1.8, CI = 1.1-2.9). Risk was higher among ex-smokers (RR = 2.2) than among current smokers (RR = 1.5) and was not related to number of cigarettes per day, age started smoking, duration, or pack-years.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Cancer causes & control : CCC AU - Zahm, S H AU - Heineman, E F AU - Vaught, J B AD - Occupational Studies Section, National Cancer Institute, Rockville, MD 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 371 EP - 376 VL - 3 IS - 4 SN - 0957-5243, 0957-5243 KW - Index Medicus KW - Prospective Studies KW - Aged, 80 and over KW - Risk Factors KW - Humans KW - Cohort Studies KW - Adult KW - Smoking -- adverse effects KW - Aged KW - Middle Aged KW - United States -- epidemiology KW - Veterans KW - Plants, Toxic KW - Mouth Neoplasms -- mortality KW - Soft Tissue Neoplasms -- mortality KW - Sarcoma -- mortality KW - Pharyngeal Neoplasms -- etiology KW - Mouth Neoplasms -- etiology KW - Tobacco, Smokeless -- adverse effects KW - Soft Tissue Neoplasms -- etiology KW - Pharyngeal Neoplasms -- mortality KW - Sarcoma -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73041322?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Soft+tissue+sarcoma+and+tobacco+use%3A+data+from+a+prospective+cohort+study+of+United+States+veterans.&rft.au=Zahm%2C+S+H%3BHeineman%2C+E+F%3BVaught%2C+J+B&rft.aulast=Zahm&rft.aufirst=S&rft.date=1992-07-01&rft.volume=3&rft.issue=4&rft.spage=371&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 - 1992-08-04 N1 - Date created - 1992-08-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Reduced mRNA levels for the multidrug-resistance genes in cAMP-dependent protein kinase mutant cell lines. AN - 73041049; 1352302 AB - We have previously shown that in Chinese hamster ovary (CHO) cells, a mutant cell line with a defective regulatory subunit (RI) for the cAMP-dependent protein kinase (Abraham et al: Mol. Cell. Biol., 7:3098-3106, 1987), and a transfectant cell line expressing the same mutant kinase, showed increased sensitivity to a number of drugs that are known to be substrates for the multidrug transporter (P-glycoprotein). In the current study we have investigated the mechanism by which cAMP-dependent protein kinase controls drug resistance. We report here that the sensitivity of the kinase defective CHO cell lines to multiple drugs results from decreased RNA levels for the multidrug-resistance gene. Similar results were obtained with mouse Y1 adrenal cells. Wild-type Y1 cells had high levels of P-glycoprotein due to expression of both the mdr1b and mdr2 genes, whereas the cAMP-dependent protein kinase mutant Kin 8 cells had decreased RNA levels for these genes. A Kin 8 transfectant with restored cAMP-dependent protein kinase activity recovered mdr expression, indicating a cause and effect relationship between the protein kinase mutations and mdr expression. No changes in nuclear run-off assays could be detected, suggesting a non-transcriptional mechanism of regulation. Wild-type Y1 cells are more drug sensitive despite having higher levels of P-glycoprotein than the mutant cells. This paradoxical result may be explained by the higher rate of synthesis of steroids by the wild-type Y1 cells, which appear to be inhibitors of P-glycoprotein transport activity. JF - Journal of cellular physiology AU - Chin, K V AU - Chauhan, S S AU - Abraham, I AU - Sampson, K E AU - Krolczyk, A J AU - Wong, M AU - Schimmer, B AU - Pastan, I AU - Gottesman, M M AD - Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 87 EP - 94 VL - 152 IS - 1 SN - 0021-9541, 0021-9541 KW - mdr KW - Cytotoxins KW - 0 KW - Membrane Glycoproteins KW - P-Glycoprotein KW - RNA, Messenger KW - Steroids KW - Verapamil KW - CJ0O37KU29 KW - Cyclic AMP KW - E0399OZS9N KW - Protein Kinases KW - EC 2.7.- KW - Quinidine KW - ITX08688JL KW - Colchicine KW - SML2Y3J35T KW - Index Medicus KW - Animals KW - Cricetulus KW - Transcription, Genetic KW - Mice KW - Cytotoxins -- pharmacology KW - Verapamil -- pharmacology KW - Precipitin Tests KW - Polymerase Chain Reaction KW - Base Sequence KW - Colchicine -- pharmacology KW - Transfection KW - Cells, Cultured KW - Molecular Sequence Data KW - Quinidine -- pharmacology KW - Female KW - Steroids -- metabolism KW - Cricetinae KW - Ovary -- chemistry KW - Adrenal Glands -- metabolism KW - Adrenal Glands -- cytology KW - RNA, Messenger -- analysis KW - RNA, Messenger -- genetics KW - Ovary -- metabolism KW - RNA, Messenger -- metabolism KW - Ovary -- cytology KW - Cyclic AMP -- pharmacology KW - Protein Kinases -- genetics KW - Mutation -- genetics KW - Adrenal Glands -- chemistry KW - Membrane Glycoproteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73041049?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Reduced+mRNA+levels+for+the+multidrug-resistance+genes+in+cAMP-dependent+protein+kinase+mutant+cell+lines.&rft.au=Chin%2C+K+V%3BChauhan%2C+S+S%3BAbraham%2C+I%3BSampson%2C+K+E%3BKrolczyk%2C+A+J%3BWong%2C+M%3BSchimmer%2C+B%3BPastan%2C+I%3BGottesman%2C+M+M&rft.aulast=Chin&rft.aufirst=K&rft.date=1992-07-01&rft.volume=152&rft.issue=1&rft.spage=87&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 - 1992-08-04 N1 - Date created - 1992-08-04 N1 - Date revised - 2017-01-13 N1 - Gene symbol - mdr N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Elevated level of nuclear protein kinase C in multidrug-resistant MCF-7 human breast carcinoma cells. AN - 73039706; 1617646 AB - Previous studies have demonstrated elevated levels of protein kinase C (PKC) activity in multidrug-resistant human breast carcinoma MCF-7/ADR cells compared to control drug-sensitive MCF-7/WT cells (R.L. Fine, J. Patel, and B.A. Chabner, Proc. Natl. Acad. Sci. USA, 85:582-586, 1988). In our present studies, immunohistochemical localization analysis using a polyclonal PKC antibody recognizing the alpha, beta, and gamma subtypes of PKC demonstrates that immunoreactivity is enhanced in MCF-7/ADR cells, with pronounced staining noted in the nuclear region. Other studies with purified nuclei isolated from MCF-7/ADR cells also show a marked increase in the intensity of immunostaining for PKC when compared to nuclei prepared from control MCF-7/WT cells. Western blot analysis of proteins extracted from purified nuclear preparations further establishes an increase in PKC enzyme protein associated with the nuclear fraction of MCF-7/ADR cells. Subcellular fractionation studies also indicate that MCF-7/ADR cells have 4-8 times higher nuclear PKC activity compared to that of control MCF-7/WT cells. MCF-7/ADR cells also possess 3-5-fold elevated cytosolic PKC activity, while a less than 2-fold increase is found in PKC activity associated with the plasma membrane fraction of MCF-7/ADR cells. Examination of these extracts with PKC isotype-specific antisera, as well as by DEAE-cellulose chromatography, reveals that nuclei prepared from MCF-7/ADR cells contain markedly elevated amounts of a slightly altered form of PKC alpha. These results suggest that elevated levels of a modified form of PKC alpha at the nucleus may play a role in modulating nuclear events to promote the development of multidrug resistance in MCF-7 cells. JF - Cancer research AU - Lee, S A AU - Karaszkiewicz, J W AU - Anderson, W B AD - Laboratory of Cellular Oncology, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1992/07/01/ PY - 1992 DA - 1992 Jul 01 SP - 3750 EP - 3759 VL - 52 IS - 13 SN - 0008-5472, 0008-5472 KW - Doxorubicin KW - 80168379AG KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Blotting, Western KW - Tumor Cells, Cultured KW - Doxorubicin -- pharmacology KW - Chromatography, DEAE-Cellulose KW - Humans KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Amino Acid Sequence KW - Immunohistochemistry KW - Female KW - Protein Kinase C -- analysis KW - Cell Nucleus -- enzymology KW - Breast Neoplasms -- pathology KW - Drug Resistance KW - Breast Neoplasms -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73039706?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Elevated+level+of+nuclear+protein+kinase+C+in+multidrug-resistant+MCF-7+human+breast+carcinoma+cells.&rft.au=Lee%2C+S+A%3BKaraszkiewicz%2C+J+W%3BAnderson%2C+W+B&rft.aulast=Lee&rft.aufirst=S&rft.date=1992-07-01&rft.volume=52&rft.issue=13&rft.spage=3750&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 - 1992-08-04 N1 - Date created - 1992-08-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The effect of acculturation on drinking attitudes among Japanese in Japan and Japanese Americans in Hawaii and California. AN - 73034768; 1619931 AB - Data from a joint Japan-U.S. collaborative study were examined to determine the relationship of acculturation to drinking attitudes among Japanese in Japan and Japanese Americans in Hawaii and California. Drinking attitudes (i.e., self-reported acceptable or appropriate levels of drinking) among ethnic groups differed significantly for the nine situations studied: (1) at a bar with friends, (2) at a party at someone else's house, (3) as a parent, spending time with small children, (4) during working hours, (5) visiting in-laws, (6) with friends at home, (7) with friends after work, (8) with people at sports events and (9) before driving a car. Factor analysis was used to determine the differences in drinking attitudes among these ethnic groups. Japanese and Japanese Americans differentiated drinking situations into different categories. The major difference between the two groups was that the Japanese associated spending time with small children with a situation appropriate for drinking, such as being with friends at home, whereas Japanese Americans associated spending time with small children with a situation inappropriate for drinking, such as before driving. JF - Journal of studies on alcohol AU - Tsunoda, T AU - Parrish, K M AU - Higuchi, S AU - Stinson, F S AU - Kono, H AU - Ogata, M AU - Harford, T C AD - National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20857. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 369 EP - 377 VL - 53 IS - 4 SN - 0096-882X, 0096-882X KW - Index Medicus KW - California KW - Alcoholic Intoxication -- psychology KW - Humans KW - Adult KW - Social Values KW - Hawaii KW - Aged KW - Middle Aged KW - Adolescent KW - Male KW - Japan KW - Female KW - Asian Americans -- psychology KW - Acculturation KW - Cross-Cultural Comparison KW - Alcohol Drinking -- psychology KW - Attitude KW - Social Environment UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73034768?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+effect+of+acculturation+on+drinking+attitudes+among+Japanese+in+Japan+and+Japanese+Americans+in+Hawaii+and+California.&rft.au=Tsunoda%2C+T%3BParrish%2C+K+M%3BHiguchi%2C+S%3BStinson%2C+F+S%3BKono%2C+H%3BOgata%2C+M%3BHarford%2C+T+C&rft.aulast=Tsunoda&rft.aufirst=T&rft.date=1992-07-01&rft.volume=53&rft.issue=4&rft.spage=369&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 - 1992-07-31 N1 - Date created - 1992-07-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cloning of the outer membrane high-affinity Fe(III)-pyochelin receptor of Pseudomonas aeruginosa. AN - 73031911; 1320609 AB - Pseudomonas aeruginosa produces the phenolic siderophore pyochelin under iron-limiting conditions. In this study, an Fe(III)-pyochelin transport-negative (Fpt-) strain, IA613, was isolated and characterized. 55Fe(III)-pyochelin transport assays determined that no Fe(III)-pyochelin associated with the Fpt- IA613 cells while a significant amount associated with KCN-poisoned Fpt+ cells. A P. aeruginosa genomic library was constructed in the IncP cosmid pLAFR1. The genomic library was mobilized into IA613, and a recombinant cosmid, pCC41, which complemented the Fpt- phenotype of IA613, was isolated. pCC41 contained a 28-kb insert of P. aeruginosa DNA, and the Fpt(-)-complementing region was localized to a 3.6-kb BamHI-EcoRI fragment by deletion and subcloning of the insert. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis of IA613 revealed that it lacked a 75-kDa outer membrane protein present in Fpt+ strains. IA613 strains bearing plasmid pRML303, which carries the 3.6-kb BamHI-EcoRI fragment of pCC41, expressed the 75-kDa outer membrane protein and demonstrated a 55Fe(III)-pyochelin transport phenotype identical to that of a wild-type Fpt+ strain. Minicell analysis demonstrated that the 3.6-kb BamHI-EcoRI fragment of pCC41 encoded a protein of approximately 75 kDa. The results presented here and in a previous report (D. E. Heinrichs, L. Young, and K. Poole, Infect. Immun. 59:3680-3684, 1991) lead to the conclusion that the 75-kDa outer membrane protein is the high-affinity receptor for Fe(III)-pyochelin in P. aeruginosa. JF - Journal of bacteriology AU - Ankenbauer, R G AD - Laboratory of Microbial Structure and Function, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, Hamilton, Montana 59840. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 4401 EP - 4409 VL - 174 IS - 13 SN - 0021-9193, 0021-9193 KW - Bacterial Outer Membrane Proteins KW - 0 KW - DNA, Bacterial KW - FPTA protein, Pseudomonas KW - Iron Chelating Agents KW - Phenols KW - Receptors, Cell Surface KW - Recombinant Proteins KW - Thiazoles KW - pyochelin KW - 69772-54-9 KW - Iron KW - E1UOL152H7 KW - Index Medicus KW - Electrophoresis, Polyacrylamide Gel KW - DNA, Bacterial -- isolation & purification KW - Escherichia coli -- genetics KW - Plasmids KW - Molecular Weight KW - Cloning, Molecular KW - Phenotype KW - Recombinant Proteins -- isolation & purification KW - Recombinant Proteins -- metabolism KW - DNA, Bacterial -- genetics KW - Kinetics KW - Restriction Mapping KW - Iron Chelating Agents -- metabolism KW - Cell Membrane -- metabolism KW - Receptors, Cell Surface -- metabolism KW - Receptors, Cell Surface -- isolation & purification KW - Pseudomonas aeruginosa -- metabolism KW - Pseudomonas aeruginosa -- genetics KW - Bacterial Outer Membrane Proteins -- genetics KW - Phenols -- metabolism KW - Bacterial Outer Membrane Proteins -- isolation & purification KW - Bacterial Outer Membrane Proteins -- metabolism KW - Receptors, Cell Surface -- genetics KW - Iron -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73031911?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cloning+of+the+outer+membrane+high-affinity+Fe%28III%29-pyochelin+receptor+of+Pseudomonas+aeruginosa.&rft.au=Ankenbauer%2C+R+G&rft.aulast=Ankenbauer&rft.aufirst=R&rft.date=1992-07-01&rft.volume=174&rft.issue=13&rft.spage=4401&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 - 1992-08-07 N1 - Date created - 1992-08-07 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Bacteriol. 1979 Jan;137(1):357-64 [104968] Infect Immun. 1982 Apr;36(1):17-23 [6804387] J Bacteriol. 1979 Dec;140(3):902-10 [118160] Proc Natl Acad Sci U S A. 1979 Apr;76(4):1648-52 [377280] J Bacteriol. 1976 Sep;127(3):1370-5 [783142] Mol Microbiol. 1991 Mar;5(3):647-55 [1646376] J Clin Invest. 1990 Oct;86(4):1030-7 [2170442] Microbiol Rev. 1989 Dec;53(4):517-30 [2531838] Gene. 1988 Oct 15;70(1):191-7 [2853689] J Clin Microbiol. 1986 Mar;23(3):560-2 [2937804] J Bacteriol. 1987 Aug;169(8):3638-46 [2956250] Infect Immun. 1986 Mar;51(3):896-900 [3081447] Infect Immun. 1987 Sep;55(9):2021-5 [3114141] J Bacteriol. 1988 Nov;170(11):5364-7 [3141387] Antibiot Chemother (1971). 1985;36:1-12 [3159335] Microb Pathog. 1988 Sep;5(3):197-205 [3216778] Biotechniques. 1988 Oct;6(9):839, 841-3 [3273192] J Gen Microbiol. 1966 May;43(2):159-271 [5963505] Infect Immun. 1983 May;40(2):665-9 [6302002] J Bacteriol. 1984 Jun;158(3):1115-21 [6427188] J Bacteriol. 1980 Jan;141(1):199-204 [6766439] Proc Natl Acad Sci U S A. 1981 Jul;78(7):4256-60 [6794030] J Bacteriol. 1982 Aug;151(2):783-7 [6807961] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7347-51 [7012838] J Bacteriol. 1978 Oct;136(1):381-90 [101518] Infect Immun. 1979 Dec;26(3):925-32 [160892] FEBS Lett. 1975 Oct 15;58(1):254-8 [773686] Infect Immun. 1991 Oct;59(10):3680-4 [1910015] Biotechniques. 1990 Nov;9(5):565-6, 568 [2268423] Plasmid. 1989 Mar;21(2):99-112 [2740456] Infect Immun. 1986 Jun;52(3):885-91 [2940187] J Bacteriol. 1987 Jul;169(7):3365-8 [3036785] J Bacteriol. 1988 Nov;170(11):5344-51 [3141386] Infect Immun. 1985 Apr;48(1):130-8 [3156815] Infect Immun. 1985 Jul;49(1):132-40 [3159677] J Bacteriol. 1974 May;118(2):442-53 [4208134] Gene. 1982 Jun;18(3):289-96 [6290332] Biochemistry. 1984 Oct 9;23(21):5076-80 [6437446] J Bacteriol. 1980 May;142(2):581-7 [6769903] J Bacteriol. 1979 Apr;138(1):193-200 [108250] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cytogenetic studies of mice exposed to styrene by inhalation. AN - 73026204; 1377343 AB - The data for the in vivo genotoxicity of styrene (STY) are equivocal. To evaluate the clastogenicity and sister-chromatid exchange (SCE)-inducing potential of STY in vivo under carefully controlled conditions, B6C3F1 female mice were exposed by inhalation for 6 h/day for 14 consecutive days to either 0, 125, 250 or 500 ppm STY. One day after the final exposure, peripheral blood, spleen, and lungs were removed and cells were cultured for the analysis of micronucleus (MN) induction using the cytochalasin B-block method, chromosome breakage, and SCE induction. Peripheral blood smears were also made for scoring MN in erythrocytes. There was a significant concentration-related elevation of SCE frequency in lymphocytes from the spleen and the peripheral blood as well as in cells from the lung. However, no statistically significant concentration-related increases were found in the frequency of chromosome aberrations in the cultured splenocytes or lung cells, and no significant increases in MN frequencies were observed in binucleated splenocytes or normochromatic erythrocytes in peripheral blood smears. JF - Mutation research AU - Kligerman, A D AU - Allen, J W AU - Bryant, M F AU - Campbell, J A AU - Collins, B W AU - Doerr, C L AU - Erexson, G L AU - Kwanyuen, P AU - Morgan, D L AD - U.S. Environmental Protection Agency, National Institute of Environmental Health Sciences, Research Triangle Park, NC. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 35 EP - 43 VL - 280 IS - 1 SN - 0027-5107, 0027-5107 KW - Styrenes KW - 0 KW - Cytochalasin B KW - 3CHI920QS7 KW - Styrene KW - 44LJ2U959V KW - Index Medicus KW - Animals KW - Mutagenicity Tests KW - Micronucleus Tests KW - Sister Chromatid Exchange KW - Cytochalasin B -- pharmacology KW - Mice KW - Administration, Inhalation KW - Female KW - Styrenes -- administration & dosage KW - Chromosome Aberrations KW - Styrenes -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73026204?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cytogenetic+studies+of+mice+exposed+to+styrene+by+inhalation.&rft.au=Kligerman%2C+A+D%3BAllen%2C+J+W%3BBryant%2C+M+F%3BCampbell%2C+J+A%3BCollins%2C+B+W%3BDoerr%2C+C+L%3BErexson%2C+G+L%3BKwanyuen%2C+P%3BMorgan%2C+D+L&rft.aulast=Kligerman&rft.aufirst=A&rft.date=1992-07-01&rft.volume=280&rft.issue=1&rft.spage=35&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 - 1992-07-28 N1 - Date created - 1992-07-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Delayed L-phenylalanine infusion allows for simultaneous kinetic analysis and improved evaluation of specific-to-nonspecific fluorine-18-dopa uptake in brain. AN - 73025645; 1613582 AB - The accumulation of 3-O-methyl-6-[18F]fluoro-L-DOPA (18F-30M-DOPA) in the brain from the circulation is responsible for most of the nonspecific background during 18F-DOPA positron emission tomography scanning. To increase the sensitivity of 18F-DOPA for imaging presynaptic dopamine systems, we took advantage of 18F-30M-DOPA's rapid clearance from the brain (T1/2 approximately 15-20 min). The infusion of the unlabeled amino acid L-phenylalanine, starting 75 min after 18F-DOPA administration, prevents 18F-30M-DOPA entrance into the brain through competition at the large amino acid transport system of the blood brain barrier. This method produces high specific-to-nonspecific contrast images of 18F accumulation beginning 15-30 min after onset of amino acid infusion and better sensitivity to small changes in 18F-DOPA uptake while still allowing for kinetic analysis of the data in the early time points. Kinetic and anatomical data were found to be strongly correlated. JF - Journal of nuclear medicine : official publication, Society of Nuclear Medicine AU - Doudet, D J AU - McLellan, C A AU - Aigner, T G AU - Wyatt, R J AU - Cohen, R M AD - Section on Clinical Brain Imaging, LCM, NIMH, IRP Bethesda, Maryland. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 1383 EP - 1389 VL - 33 IS - 7 SN - 0161-5505, 0161-5505 KW - 3-O-methyl-6-fluoro-dopa KW - 107257-16-9 KW - fluorodopa F 18 KW - 2C598205QX KW - Phenylalanine KW - 47E5O17Y3R KW - Dihydroxyphenylalanine KW - 63-84-3 KW - Carbidopa KW - MNX7R8C5VO KW - Index Medicus KW - Corpus Striatum -- diagnostic imaging KW - Animals KW - Cerebral Cortex -- drug effects KW - Cerebral Cortex -- metabolism KW - Carbidopa -- pharmacology KW - Corpus Striatum -- metabolism KW - Tomography, Emission-Computed KW - Corpus Striatum -- drug effects KW - Macaca mulatta KW - Time Factors KW - Cerebral Cortex -- diagnostic imaging KW - MPTP Poisoning KW - Brain -- drug effects KW - Dihydroxyphenylalanine -- metabolism KW - Brain -- metabolism KW - Phenylalanine -- administration & dosage KW - Brain -- diagnostic imaging KW - Dihydroxyphenylalanine -- pharmacokinetics KW - Dihydroxyphenylalanine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73025645?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+nuclear+medicine+%3A+official+publication%2C+Society+of+Nuclear+Medicine&rft.atitle=Delayed+L-phenylalanine+infusion+allows+for+simultaneous+kinetic+analysis+and+improved+evaluation+of+specific-to-nonspecific+fluorine-18-dopa+uptake+in+brain.&rft.au=Doudet%2C+D+J%3BMcLellan%2C+C+A%3BAigner%2C+T+G%3BWyatt%2C+R+J%3BCohen%2C+R+M&rft.aulast=Doudet&rft.aufirst=D&rft.date=1992-07-01&rft.volume=33&rft.issue=7&rft.spage=1383&rft.isbn=&rft.btitle=&rft.title=Journal+of+nuclear+medicine+%3A+official+publication%2C+Society+of+Nuclear+Medicine&rft.issn=01615505&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-28 N1 - Date created - 1992-07-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - L-histidinol: preclinical therapeutic studies in combination with antitumor agents and pharmacokinetic studies in mice. AN - 73016518; 1617631 AB - Therapeutic studies were conducted with L-histidinol, in combination with cyclophosphamide, bischloroethylnitrosourea, 5-fluorouracil, phenylalanine mustard, or cis-platinum(II)diammine dichloride, in several transplantable tumors in mice. These tumor types included murine L1210 P388 leukemias, M5076 sarcoma, mammary 16/C adenocarcinoma, human LOX melanoma, and colon HT-29 adenocarcinoma. Therapeutic benefits of adding L-histidinol to a regimen, compared to the regimen alone, were marginal. Pharmacokinetic studies indicated a rapid clearance of L-histidinol following a bolus dose (250 mg/kg i.p.), peak plasma concentration of 200 micrograms/ml (1.4 mM), and beta phase t1/2 of 12.6 min. Maximum tolerable plasma steady state concentrations with a 24-h infusion (2000 mg/kg/24 h) were no greater than 25 micrograms/ml (0.18 mM). JF - Cancer research AU - Zaharko, D AU - Plowman, J AU - Waud, W AU - Dykes, D AU - Malspeis, L AD - Pharmacology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1992/07/01/ PY - 1992 DA - 1992 Jul 01 SP - 3604 EP - 3609 VL - 52 IS - 13 SN - 0008-5472, 0008-5472 KW - Histidinol KW - 501-28-0 KW - Cyclophosphamide KW - 8N3DW7272P KW - Cisplatin KW - Q20Q21Q62J KW - Carmustine KW - U68WG3173Y KW - Index Medicus KW - Neoplasm Transplantation KW - Cyclophosphamide -- administration & dosage KW - Animals KW - Leukemia P388 -- drug therapy KW - Humans KW - Mice, Inbred C57BL KW - Mice, Inbred C3H KW - Transplantation, Heterologous KW - Mice KW - Leukemia L1210 -- drug therapy KW - Carmustine -- administration & dosage KW - Cisplatin -- administration & dosage KW - Histidinol -- administration & dosage KW - Neoplasms, Experimental -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Histidinol -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73016518?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=L-histidinol%3A+preclinical+therapeutic+studies+in+combination+with+antitumor+agents+and+pharmacokinetic+studies+in+mice.&rft.au=Zaharko%2C+D%3BPlowman%2C+J%3BWaud%2C+W%3BDykes%2C+D%3BMalspeis%2C+L&rft.aulast=Zaharko&rft.aufirst=D&rft.date=1992-07-01&rft.volume=52&rft.issue=13&rft.spage=3604&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 - 1992-08-04 N1 - Date created - 1992-08-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Somatostatin content increases following norepinephrine depletion in frontal cortex of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated mice. AN - 73013837; 1351925 AB - The effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on somatostatin (SS)-containing neurons were examined by measuring dopamine, norepinephrine (NE), SS, and SS mRNA in striatum and frontal cortex of C57/B16 mice at various times following treatment with MPTP-HCl (96 mg/kg i.p.). MPTP caused a 70% depletion of dopamine in striatum by 1 day and a 40% depletion of NE in frontal cortex within 3 days. SS content was increased in frontal cortex 4 days later, but not in striatum; there were no changes in SS mRNA. Maprotiline, a specific NE-uptake blocker, prevented both the depletion of NE and the increase of SS in frontal cortex due to MPTP administration. These results support the possibility that NE can regulate SS in frontal cortex and are discussed in terms of the decrease of SS seen in parkinsonian patients with dementia. JF - Journal of neurochemistry AU - Mitsuo, K AU - Schwartz, J P AD - Clinical Neuroscience Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 267 EP - 272 VL - 59 IS - 1 SN - 0022-3042, 0022-3042 KW - RNA, Messenger KW - 0 KW - Maprotiline KW - 2U1W68TROF KW - Somatostatin KW - 51110-01-1 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 - Maprotiline -- pharmacology KW - RNA, Messenger -- metabolism KW - Mice, Inbred C57BL KW - Dopamine -- metabolism KW - Mice KW - Male KW - Somatostatin -- genetics KW - Norepinephrine -- metabolism KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- pharmacology KW - Frontal Lobe -- metabolism KW - Somatostatin -- metabolism KW - Norepinephrine -- deficiency UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73013837?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Somatostatin+content+increases+following+norepinephrine+depletion+in+frontal+cortex+of+1-methyl-4-phenyl-1%2C2%2C3%2C6-tetrahydropyridine-treated+mice.&rft.au=Mitsuo%2C+K%3BSchwartz%2C+J+P&rft.aulast=Mitsuo&rft.aufirst=K&rft.date=1992-07-01&rft.volume=59&rft.issue=1&rft.spage=267&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 - 1992-07-24 N1 - Date created - 1992-07-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vivo evidence that lithium inactivates Gi modulation of adenylate cyclase in brain. AN - 73013616; 1319465 AB - In vivo microdialysis of cyclic AMP from prefrontal cortex complemented by ex vivo measures was used to investigate the possibility that lithium produces functional changes in G proteins that could account for its effects on adenylate cyclase activity. Four weeks of lithium administration (serum lithium concentration of 0.85 +/- 0.05 mM; n = 11) significantly increased the basal cyclic AMP content in dialysate from prefrontal cortex of anesthetized rats. Forskolin infused through the probe increased dialysate cyclic AMP, but the magnitude of this increase was unaffected by chronic lithium administration. Inactivation of the inhibitory guanine nucleotide binding protein Gi with pertussis toxin increased dialysate cyclic AMP in control rats, as did stimulation with cholera toxin (which activates the stimulatory guanine nucleotide binding protein Gs). The effect of pertussis toxin was abolished following chronic lithium, whereas the increase in cyclic AMP after cholera toxin was enhanced. In vitro pertussis toxin-catalyzed ADP ribosylation of alpha i (and alpha o) was increased by 20% in prefrontal cortex from lithium-treated rats, but the alpha i and alpha s contents (as determined by immunoblot) as well as the cholera toxin-catalyzed ADP ribosylation of alpha s were unchanged. Taken together, these results suggest that chronic lithium administration may interfere with the dissociation of Gi into its active components and thereby remove a tonic inhibitory influence on adenylate cyclase, with resultant enhanced basal and cholera toxin-stimulated adenylate cyclase activity. JF - Journal of neurochemistry AU - Masana, M I AU - Bitran, J A AU - Hsiao, J K AU - Potter, W Z AD - Section on Clinical Pharmacology, Experimental Therapeutics Branch, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 200 EP - 205 VL - 59 IS - 1 SN - 0022-3042, 0022-3042 KW - Adenylate Cyclase Toxin KW - 0 KW - Virulence Factors, Bordetella KW - Colforsin KW - 1F7A44V6OU KW - Cholera Toxin KW - 9012-63-9 KW - Lithium KW - 9FN79X2M3F KW - Cyclic AMP KW - E0399OZS9N KW - Pertussis Toxin KW - EC 2.4.2.31 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Adenylyl Cyclases KW - EC 4.6.1.1 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Virulence Factors, Bordetella -- pharmacology KW - Animals KW - Colforsin -- pharmacology KW - Cyclic AMP -- metabolism KW - Cholera Toxin -- pharmacology KW - Male KW - Dialysis -- methods KW - Brain -- enzymology KW - GTP-Binding Proteins -- antagonists & inhibitors KW - Adenylyl Cyclases -- metabolism KW - GTP-Binding Proteins -- physiology KW - Lithium -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73013616?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=In+vivo+evidence+that+lithium+inactivates+Gi+modulation+of+adenylate+cyclase+in+brain.&rft.au=Masana%2C+M+I%3BBitran%2C+J+A%3BHsiao%2C+J+K%3BPotter%2C+W+Z&rft.aulast=Masana&rft.aufirst=M&rft.date=1992-07-01&rft.volume=59&rft.issue=1&rft.spage=200&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 - 1992-07-24 N1 - Date created - 1992-07-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Use of hair coloring products and the risk of lymphoma, multiple myeloma, and chronic lymphocytic leukemia. AN - 73012297; 1609918 AB - Hair coloring products are widely used and contain components that are mutagenic and carcinogenic. An association between occupational exposure to hair coloring products and hematopoietic cancers has been reported, but the risk for these cancers among users has not been carefully evaluated. We conducted a population-based, case-control study with telephone interviews from 385 with telephone interviews from 385 non-Hodgkin's lymphoma cases, 70 Hodgkin's disease cases, 72 multiple myeloma cases, 56 chronic lymphocytic leukemia cases, and 1432 controls. Among women, use was associated with odds ratios of 1.5 for non-Hodgkin's lymphoma, 1.7 for Hodgkin's disease, 1.8 for multiple myeloma, and 1.0 for chronic lymphocytic leukemia. Risk was higher for permanent hair coloring products than for semi- or nonpermanent products, particularly for dark colors. Long duration and early age of first use tended to increase risk, but the patterns were inconsistent. Use was much less common in men and did not significantly increase risk. The use of hair coloring products appears to increase the risk of non-Hodgkin's lymphoma. Multiple myeloma and Hodgkin's disease were also associated, although based on far fewer subjects. If these results represent a causal association, use of hair coloring products would account for 35% of non-Hodgkin's lymphoma cases in exposed women and 20% in all women. JF - American journal of public health AU - Zahm, S H AU - Weisenburger, D D AU - Babbitt, P A AU - Saal, R C AU - Vaught, J B AU - Blair, A AD - Occupational Studies Section, National Cancer Institute, Rockville, MD 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 990 EP - 997 VL - 82 IS - 7 SN - 0090-0036, 0090-0036 KW - Hair Dyes KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Causality KW - Odds Ratio KW - Age Factors KW - Humans KW - Nebraska -- epidemiology KW - Registries KW - Health Status Indicators KW - Logistic Models KW - Adult KW - Case-Control Studies KW - Incidence KW - Interviews as Topic KW - Middle Aged KW - Time Factors KW - Female KW - Male KW - Multiple Myeloma -- chemically induced KW - Lymphoma -- epidemiology KW - Leukemia, Lymphocytic, Chronic, B-Cell -- epidemiology KW - Lymphoma -- classification KW - Hair Dyes -- classification KW - Multiple Myeloma -- epidemiology KW - Leukemia, Lymphocytic, Chronic, B-Cell -- chemically induced KW - Lymphoma -- chemically induced KW - Hair Dyes -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73012297?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Use+of+hair+coloring+products+and+the+risk+of+lymphoma%2C+multiple+myeloma%2C+and+chronic+lymphocytic+leukemia.&rft.au=Zahm%2C+S+H%3BWeisenburger%2C+D+D%3BBabbitt%2C+P+A%3BSaal%2C+R+C%3BVaught%2C+J+B%3BBlair%2C+A&rft.aulast=Zahm&rft.aufirst=S&rft.date=1992-07-01&rft.volume=82&rft.issue=7&rft.spage=990&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 - 1992-07-23 N1 - Date created - 1992-07-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Lancet. 1979 Sep 8;2(8141):536 [90265] Lancet. 1979 Nov 17;2(8151):1070-1 [91802] Curr Probl Dermatol. 1978;7:196-204 [752455] Br J Cancer. 1977 Oct;36(4):467-78 [588414] J Natl Cancer Inst. 1977 Nov;59(5):1423-5 [909104] J Natl Cancer Inst. 1979 Feb;62(2):277-83 [283264] Epidemiology. 1990 Sep;1(5):349-56 [2078610] Mod Pathol. 1988 Jan;1(1):29-34 [3266335] Am J Public Health. 1988 May;78(5):570-1 [3354743] Am J Pathol. 1987 Apr;127(1):1-8 [3494405] Int J Epidemiol. 1989 Mar;18(1):283 [2722380] Drug Chem Toxicol. 1984;7(6):573-86 [6534733] Cancer Res. 1987 Jun 1;47(11):2978-81 [3567914] Int J Epidemiol. 1985 Dec;14(4):549-54 [4086141] Pathol Annu. 1990;25 Pt 1:99-115 [2404252] Lancet. 1990 Aug 25;336(8713):474-81 [1974997] Eur J Cancer. 1990 Apr;26(4):500-8 [2141517] Am J Epidemiol. 1990 Oct;132(4):746-8 [2403115] J Clin Epidemiol. 1990;43(1):87-91 [2319285] J Natl Cancer Inst. 1984 May;72(5):1051-7 [6585583] J Natl Cancer Inst. 1983 Mar;70(3):443-6 [6572734] Am J Ind Med. 1984;6(2):97-102 [6465143] Br J Cancer. 1983 Dec;48(6):853-7 [6652026] Am J Epidemiol. 1983 Jan;117(1):76-85 [6823955] J Natl Cancer Inst. 1981 Mar;66(3):591-602 [6937712] J Natl Cancer Inst. 1980 Oct;65(4):735-8 [6932526] Am J Ind Med. 1982;3(2):169-71 [7137173] Am J Epidemiol. 1981 Apr;113(4):464-73 [7211828] Br J Cancer. 1981 Feb;43(2):236-9 [7470387] Lancet. 1979 Nov 17;2(8151):1070 [91801] Lancet. 1979 Jun 30;1(8131):1390-3 [87844] Comment In: Am J Public Health. 1993 Apr;83(4):598-9 [8460749] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Presentation of three different viral peptides, HTLV-1 Tax, HCMV gB, and influenza virus M1, is determined by common structural features of the HLA-A2.1 molecule. AN - 73010626; 1607654 AB - To determine whether similar or dissimilar molecular features of class I molecules are involved in the presentation of structurally distinct peptides, we have investigated the influence of different pockets of the HLA-A2.1 molecule on the presentation of three different viral peptides. HTLV-I Tax peptide 12-19, HCMV gB 619-628, and influenza M1 58-66 are minimal peptides that induce HLA-A2.1-restricted noncross-reactive CTL. A detailed analysis of the structural features of HLA-A2.1 that are involved in peptide presentation was undertaken using a panel of 11 HLA-A2 mutants with single amino acid substitutions within pockets present in the peptide binding site. Nine of the 11 mutants affected presentation of each of the three peptides, whereas the other two mutants had negative effects on presentation of only two of these viral peptides. These results indicate that common structural features in HLA-A2 determine the binding of different peptides, and help to provide a plausible explanation for how structurally diverse peptides bind to HLA-A2. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Utz, U AU - Koenig, S AU - Coligan, J E AU - Biddison, W E AD - Molecular Immunology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health (NIH), Bethesda, MD 20892. Y1 - 1992/07/01/ PY - 1992 DA - 1992 Jul 01 SP - 214 EP - 221 VL - 149 IS - 1 SN - 0022-1767, 0022-1767 KW - Antigens, Viral KW - 0 KW - Gene Products, tax KW - HLA-A2 Antigen KW - M-protein, influenza virus KW - M1 protein, Influenza A virus KW - Peptides KW - Viral Envelope Proteins KW - Viral Matrix Proteins KW - glycoprotein B, Simplexvirus KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Mutagenesis, Site-Directed KW - Cytotoxicity, Immunologic KW - Viral Envelope Proteins -- immunology KW - Humans KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Gene Products, tax -- immunology KW - Viral Matrix Proteins -- immunology KW - Structure-Activity Relationship KW - Binding Sites KW - Antigens, Viral -- metabolism KW - Peptides -- immunology KW - Human T-lymphotropic virus 1 -- immunology KW - Antigen-Presenting Cells -- immunology KW - HLA-A2 Antigen -- metabolism KW - HLA-A2 Antigen -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73010626?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Presentation+of+three+different+viral+peptides%2C+HTLV-1+Tax%2C+HCMV+gB%2C+and+influenza+virus+M1%2C+is+determined+by+common+structural+features+of+the+HLA-A2.1+molecule.&rft.au=Utz%2C+U%3BKoenig%2C+S%3BColigan%2C+J+E%3BBiddison%2C+W+E&rft.aulast=Utz&rft.aufirst=U&rft.date=1992-07-01&rft.volume=149&rft.issue=1&rft.spage=214&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 - 1992-07-21 N1 - Date created - 1992-07-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phase I study of taxol and granulocyte colony-stimulating factor in patients with refractory ovarian cancer. AN - 73010258; 1376773 AB - To increase the taxol dose beyond the current standard dose intensity of 175 mg/m2 per 21 days in patients with refractory ovarian cancer. Fifteen patients who had platinum-refractory or recurrent advanced-stage ovarian cancer were treated with taxol in a phase I trial and were given granulocyte-colony stimulating factor (G-CSF). Taxol was administered at doses of 170, 200, 250, and 300 mg/m2 every 3 weeks. G-CSF was given as a daily subcutaneous injection that started 24 hours after the completion of the taxol infusion. Four patients required either taxol dose reduction or delay. The dose-limiting toxicity (DLT) was peripheral neuropathy, and it occurred at 300 mg/m2. This toxicity was manifested clinically as a stocking-and-glove sensory disturbance that primarily affected proprioception, and was associated with objective changes on nerve conduction studies in affected individuals. Mucositis was rarely observed. Substantial myelosuppression was observed, but was not dose-limiting. Five of 14 assessable patients experienced an objective response to therapy, with another five individuals who experienced a 30% to 45% reduction in tumor mass. Taxol can be safely administered in doses up to 250 mg/m2 with G-CSF support, which may make it possible to study taxol dose intensification. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Sarosy, G AU - Kohn, E AU - Stone, D A AU - Rothenberg, M AU - Jacob, J AU - Adamo, D O AU - Ognibene, F P AU - Cunnion, R E AU - Reed, E AD - Medicine Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 1165 EP - 1170 VL - 10 IS - 7 SN - 0732-183X, 0732-183X KW - Alkaloids KW - 0 KW - Antineoplastic Agents, Phytogenic KW - Granulocyte Colony-Stimulating Factor KW - 143011-72-7 KW - Paclitaxel KW - P88XT4IS4D KW - Index Medicus KW - Drug Evaluation KW - Humans KW - Carcinoma -- drug therapy KW - Adult KW - Treatment Outcome KW - Aged KW - Middle Aged KW - Female KW - Granulocyte Colony-Stimulating Factor -- therapeutic use KW - Bone Marrow Diseases -- prevention & control KW - Bone Marrow Diseases -- chemically induced KW - Antineoplastic Agents, Phytogenic -- adverse effects KW - Alkaloids -- adverse effects KW - Antineoplastic Agents, Phytogenic -- administration & dosage KW - Ovarian Neoplasms -- drug therapy KW - Alkaloids -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73010258?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+taxol+and+granulocyte+colony-stimulating+factor+in+patients+with+refractory+ovarian+cancer.&rft.au=Sarosy%2C+G%3BKohn%2C+E%3BStone%2C+D+A%3BRothenberg%2C+M%3BJacob%2C+J%3BAdamo%2C+D+O%3BOgnibene%2C+F+P%3BCunnion%2C+R+E%3BReed%2C+E&rft.aulast=Sarosy&rft.aufirst=G&rft.date=1992-07-01&rft.volume=10&rft.issue=7&rft.spage=1165&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 - 1992-07-23 N1 - Date created - 1992-07-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Elevation of interleukin-6 in response to a chronic inflammatory stimulus in mice: inhibition by indomethacin. AN - 73006999; 1611085 AB - Intraperitoneal (i.p.) injection of a mineral oil such as pristane induces a chronic inflammatory response in mice. This is characterized by a large influx of macrophages and other inflammatory cells into the peritoneal cavity for months after injection of the oil. By using the B9 cell bioassay, it was found that injection of pristane caused a marked and prolonged elevation of interleukin-6 (IL-6) levels in the peritoneal cavities of the mice. IL-6 was undetectable (less than 15 U/mL) in the peritoneal fluids of unprimed mice and during the first week after injecting pristane. From 4 to 20 weeks, the concentration of IL-6 increased to an apparent plateau with concentrations ranging from 200 to 2,000 U/mL. Increasing the dose of pristane did not substantially increase the peritoneal levels of IL-6 established at 20 weeks after pristane treatment. At later times (by day 250), the level decreased to 263 +/- 217 U/mL. However, mice that developed plasma cell tumors around day 300 showed high levels of IL-6 in the ascites fluid (650 to 2,400 U/mL). Serum levels of IL-6 were also elevated in pristane-primed mice but were substantially lower than those found in the peritoneal cavity. Chronic administration of the nonsteroidal anti-inflammatory drug indomethacin decreased the levels of IL-6 by 75% to 80%. Experiments performed in vitro showed that pristane-elicited macrophages secreted low levels of IL-6 constitutively and high levels of IL-6 in the presence of lipopolysaccharide. Both IL-6 and prostaglandin E2 production were inhibited by addition of indomethacin to macrophage cultures in vitro. Treatment of mice with pristane may provide a model system for studying the inflammatory pathways that control IL-6 levels in vivo. The relevance of these results to elucidation of the role of IL-6 in plasma cell tumorigenesis is discussed. JF - Blood AU - Shacter, E AU - Arzadon, G K AU - Williams, J AD - Laboratory of Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/07/01/ PY - 1992 DA - 1992 Jul 01 SP - 194 EP - 202 VL - 80 IS - 1 SN - 0006-4971, 0006-4971 KW - Interleukin-6 KW - 0 KW - Lipopolysaccharides KW - Terpenes KW - pristane KW - 26HZV48DT1 KW - Dinoprostone KW - K7Q1JQR04M KW - Indomethacin KW - XXE1CET956 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Peritoneal Cavity -- cytology KW - Lipopolysaccharides -- administration & dosage KW - Terpenes -- administration & dosage KW - Dinoprostone -- biosynthesis KW - Dose-Response Relationship, Drug KW - Mice KW - Ascitic Fluid -- metabolism KW - Mice, Inbred BALB C KW - Time Factors KW - Interleukin-6 -- metabolism KW - Inflammation -- metabolism KW - Indomethacin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73006999?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Elevation+of+interleukin-6+in+response+to+a+chronic+inflammatory+stimulus+in+mice%3A+inhibition+by+indomethacin.&rft.au=Shacter%2C+E%3BArzadon%2C+G+K%3BWilliams%2C+J&rft.aulast=Shacter&rft.aufirst=E&rft.date=1992-07-01&rft.volume=80&rft.issue=1&rft.spage=194&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=00064971&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-29 N1 - Date created - 1992-07-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Hematopoietic stem cell depletion by restorative growth factor regimens during repeated high-dose cyclophosphamide therapy. AN - 73002362; 1377055 AB - We studied the effects of six cycles of repeated cyclophosphamide (CTX) therapy followed by restorative therapy with either granulocyte-macrophage colony-stimulating factor (GM-CSF) or G-CSF on the hematopoietic stem cell compartment. Stem cell function was assessed by serially transferring bone marrow cells from CTX-CSF-treated mice into lethally irradiated recipient mice. Bone marrow cells from mice that initially received either G-CSF or GM-CSF after CTX therapy more rapidly lost the ability to repopulate the recipient lymphoid organs, showed a dramatic loss of hematopoietic progenitors, a more rapid loss of CFU-S capacity, and a 40% to 50% reduction in marrow repopulating ability (MRA). Interleukin-1 (IL-1) appeared to have little effect on the CTX-treated mice when used alone. However, when administered before the CTX-CSF regimen, IL-1 prevented the stem cell depletion as determined by CFU-C, CFU-S, and MRA through the serial transplantation procedures. These results support the hypothesis that repeated treatments with myelosuppressive drugs followed by stimulation with the CSFs may induce damage to the host stem cell compartment, and further suggest that pretreatment with IL-1 before CTX therapy may prevent this stem cell damage. JF - Blood AU - Hornung, R L AU - Longo, D L AD - Biological Carcinogenesis & Development Program, Program Resources, Inc/DynCorp, National Cancer Institute-Frederick Cancer Research & Development Center 21702-1201. Y1 - 1992/07/01/ PY - 1992 DA - 1992 Jul 01 SP - 77 EP - 83 VL - 80 IS - 1 SN - 0006-4971, 0006-4971 KW - Antigens, Ly KW - 0 KW - Interleukin-1 KW - Granulocyte Colony-Stimulating Factor KW - 143011-72-7 KW - Granulocyte-Macrophage Colony-Stimulating Factor KW - 83869-56-1 KW - Cyclophosphamide KW - 8N3DW7272P KW - Abridged Index Medicus KW - Index Medicus KW - Bone Marrow Cells KW - Animals KW - Dose-Response Relationship, Drug KW - Antigens, Ly -- analysis KW - Mice, Inbred C57BL KW - Mice KW - Time Factors KW - Bone Marrow -- drug effects KW - Radiation Chimera KW - Female KW - Bone Marrow Transplantation KW - Granulocyte-Macrophage Colony-Stimulating Factor -- administration & dosage KW - Cyclophosphamide -- administration & dosage KW - Interleukin-1 -- administration & dosage KW - Hematopoiesis -- drug effects KW - Granulocyte Colony-Stimulating Factor -- administration & dosage KW - Hematopoietic Stem Cells -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73002362?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Hematopoietic+stem+cell+depletion+by+restorative+growth+factor+regimens+during+repeated+high-dose+cyclophosphamide+therapy.&rft.au=Hornung%2C+R+L%3BLongo%2C+D+L&rft.aulast=Hornung&rft.aufirst=R&rft.date=1992-07-01&rft.volume=80&rft.issue=1&rft.spage=77&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=00064971&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-29 N1 - Date created - 1992-07-29 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Blood. 1992 Jul 1;80(1):3-7 [1377052] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression of the murine homologue of the cell cycle control protein p34cdc2 in T lymphocytes. AN - 72999757; 1637418 AB - The mammalian homologue of the cdc2 gene of the fission yeast Schizosaccharomyces pombe encodes a p34cdc2 cyclin-dependent kinase that regulates the cell cycle of a wide variety of cell types. Resting murine T lymphocytes contained no detectable p34cdc2 protein, histone kinase activity, or specific mRNA for the cdc2 gene. Activation of the T cells by immobilized anti-CD3 resulted in the expression of specific mRNA late in the G1 phase of the cell cycle, and p34cdc2 protein was detectable at or near G1/S. At this point in the cell cycle, the protein was phosphorylated at tyrosine and displayed no H1 histone kinase activity. As the cells progressed through the cycle, the amount of specific mRNA and p34cdc2 increased, and H1 histone kinase activity was detectable when the cells were blocked at G2/M by nocodazole. The activation of T cells by phorbol dibutyrate induced the expression of IL-2R but failed to induce the synthesis of IL-2 or the expression of cdc2-specific mRNA. Under these conditions, the activated cells failed to enter the S phase of the cell cycle. Because the presence of IL-2 added exogenously during activation by phorbol dibutyrate resulted in the expression of cdc2-specific mRNA and progression through the cell cycle, either IL-2 or the interaction with IL-2R may be involved in the expression of cdc2 and regulation of the G1/S transition. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Kim, Y H AU - Proust, J J AU - Buchholz, M J AU - Chrest, F J AU - Nordin, A A AD - Clinical Immunology Section, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224. Y1 - 1992/07/01/ PY - 1992 DA - 1992 Jul 01 SP - 17 EP - 23 VL - 149 IS - 1 SN - 0022-1767, 0022-1767 KW - Proto-Oncogene Proteins KW - 0 KW - Proto-Oncogene Proteins c-myb KW - RNA, Messenger KW - Receptors, Interleukin-2 KW - Receptors, Transferrin KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Protein Kinases KW - EC 2.7.- KW - CDC2 Protein Kinase KW - EC 2.7.11.22 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Genes, myc KW - Gene Expression KW - Amino Acid Sequence KW - Mice KW - RNA, Messenger -- genetics KW - Receptors, Interleukin-2 -- genetics KW - Phorbol 12,13-Dibutyrate -- pharmacology KW - Protein Kinases -- metabolism KW - Blotting, Western KW - Cells, Cultured KW - Receptors, Transferrin -- genetics KW - In Vitro Techniques KW - Mice, Inbred C57BL KW - Molecular Sequence Data KW - Proto-Oncogene Proteins -- genetics KW - Lymphocyte Activation KW - CDC2 Protein Kinase -- genetics KW - T-Lymphocytes -- physiology KW - Cell Cycle UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72999757?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Expression+of+the+murine+homologue+of+the+cell+cycle+control+protein+p34cdc2+in+T+lymphocytes.&rft.au=Kim%2C+Y+H%3BProust%2C+J+J%3BBuchholz%2C+M+J%3BChrest%2C+F+J%3BNordin%2C+A+A&rft.aulast=Kim&rft.aufirst=Y&rft.date=1992-07-01&rft.volume=149&rft.issue=1&rft.spage=17&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 - 1992-07-21 N1 - Date created - 1992-07-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of ultraviolet radiation on murine epidermal Langerhans cells: doses of ultraviolet radiation that modulate ICAM-1 (CD54) expression and inhibit Langerhans cell function cause delayed cytotoxicity in vitro. AN - 72994537; 1351507 AB - Low doses (100 J/m2) of ultraviolet B (UVB) radiation from sunlamp fluorescent FS20 tubes inhibit the ability of freshly isolated murine epidermal Langerhans cells (LC) to support anti-CD3 MoAb-induced T-cell mitogenesis and selectively inhibit the upregulation of ICAM-1 expression by LC without causing appreciable cytotoxicity in short-term (less than or equal to 24 h) incubations (J Immunol 146:3347-3355, 1991). In the present study, epidermal cells (EC) were exposed to UVB radiation or were sham-irradiated and cultured for 24, 48, or 72 h when LC were recovered, enumerated, and assayed for simultaneous expression of I-A antigens and ICAM-1 by flow cytometry. UVB-irradiated LC that had been cultured for 24 h exhibited levels of I-A antigens comparable to those on unirradiated LC but expressed substantially less ICAM-1. After 48 and 72 h, cultured UVB-irradiated LC expressed somewhat lower levels of I-A antigens and markedly less ICAM-1 than unirradiated controls. Although similar numbers of LC were recovered from cultures initiated with UVB-irradiated and unirradiated epidermal cells after 24 h, far fewer identifiable LC were recovered from cultures seeded with irradiated cells at 48 and 72 h (approximately 50 and approximately 10% of control, respectively). The effect of UVB radiation on the survival of LC in vitro was not reversible with exogenous TNF alpha (125 U/ml) alone or granulocyte/macrophage colony-stimulating factor (5 ng/ml) and IL-1 (50 U/ml) in combination, although these cytokines had modest effects on the expression of I-A antigens and ICAM-1 by cultured UVB-irradiated LC. Results of survival studies performed with enriched LC preparations demonstrated that UVB radiation was clearly cytotoxic for LC and did not merely downregulate surface expression of I-A antigens or alter LC buoyant density. Exposure of LC to radiation from blacklight fluorescent (UVA) tubes (0.25 J/cm2) in the presence of 8-methoxypsoralen (1 micrograms/ml; PUVA) or monochromatic UVC radiation (20 J/m2) also inhibited LC accessory cell function. Results of survival studies performed with EC that had been exposed to PUVA or UVC radiation before culture were similar to those of studies performed with UVB-irradiated cells, although PUVA- and UVC-induced LC cytotoxicity was much more pronounced 48 h after culture initiation than UVB-induced cytotoxicity. UVA radiation alone augmented LC recovery at 24 and 48 h, but did not influence I-A antigen or ICAM-1 expression.(ABSTRACT TRUNCATED AT 400 WORDS) JF - The Journal of investigative dermatology AU - Tang, A AU - Udey, M C AD - Dermatology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 83 EP - 89 VL - 99 IS - 1 SN - 0022-202X, 0022-202X KW - Cell Adhesion Molecules KW - 0 KW - Cytokines KW - Histocompatibility Antigens Class II KW - Intercellular Adhesion Molecule-1 KW - 126547-89-5 KW - Index Medicus KW - Animals KW - Cell Adhesion Molecules -- genetics KW - Cytokines -- pharmacology KW - PUVA Therapy KW - Mice KW - Dose-Response Relationship, Radiation KW - Mice, Inbred BALB C KW - Gene Expression Regulation -- radiation effects KW - Cell Survival -- drug effects KW - Antigen-Presenting Cells -- physiology KW - Histocompatibility Antigens Class II -- physiology KW - Antigen-Presenting Cells -- radiation effects KW - Cell Survival -- radiation effects KW - Female KW - Langerhans Cells -- radiation effects KW - Ultraviolet Rays KW - Langerhans Cells -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72994537?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Effects+of+ultraviolet+radiation+on+murine+epidermal+Langerhans+cells%3A+doses+of+ultraviolet+radiation+that+modulate+ICAM-1+%28CD54%29+expression+and+inhibit+Langerhans+cell+function+cause+delayed+cytotoxicity+in+vitro.&rft.au=Tang%2C+A%3BUdey%2C+M+C&rft.aulast=Tang&rft.aufirst=A&rft.date=1992-07-01&rft.volume=99&rft.issue=1&rft.spage=83&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 - 1992-07-22 N1 - Date created - 1992-07-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Statistical methods for short-term tests in genetic toxicology: the first fifteen years. AN - 72993418; 1376440 AB - Short-term tests (STTs) for detecting and assessing genotoxic or mutagenic effects have catalyzed the development of biostatistical methods for more than one decade. Most notably, the Ames Salmonella/microsome assay created statistical methodology with a range of applications going beyond genotoxicity. Early approaches with parametric statistical methods appeared to be insufficient and have been replaced by non-parametric ones requiring less restrictive distributional assumptions. There have also been successful attempts to use biomathematical models for establishing dose-response relationships. Overdispersion has been recognized as a major problem for the evaluation of mutagenic count data and methods to cope with it have became available. A theory of generalized linear modelling is emerging to combine dose-response modeling with much less restrictive distributional assumptions, while allowing the inclusion of concomitant factors arising from the experimental conditions. The methodological survey below reviews the present state of this development and is intended to promote further research into biostatistical issues and methods of analysis. Appropriate methods for the design and analysis of STTs are discussed. The progress for the Ames assay was only partially transmitted to the analysis of the large number of other short-term assays. Several such assays are reviewed with respect to their present state of statistical evaluation. JF - Mutation research AU - Edler, L AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1992/07// PY - 1992 DA - July 1992 SP - 11 EP - 33 VL - 277 IS - 1 SN - 0027-5107, 0027-5107 KW - Index Medicus KW - Animals KW - Models, Genetic KW - Models, Statistical KW - Mutagenicity Tests KW - Statistics as Topic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72993418?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Statistical+methods+for+short-term+tests+in+genetic+toxicology%3A+the+first+fifteen+years.&rft.au=Edler%2C+L&rft.aulast=Edler&rft.aufirst=L&rft.date=1992-07-01&rft.volume=277&rft.issue=1&rft.spage=11&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 - 1992-07-16 N1 - Date created - 1992-07-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - NMDA receptors: role in ethanol withdrawal seizures. AN - 73068719; 1321581 JF - Annals of the New York Academy of Sciences AU - Hoffman, P L AU - Grant, K A AU - Snell, L D AU - Reinlib, L AU - Iorio, K AU - Tabakoff, B AD - Laboratory of Physiologic and Pharmacologic Studies, National Institute on Alcohol Abuse and Alcoholism Rockville, Maryland 20852. Y1 - 1992/06/28/ PY - 1992 DA - 1992 Jun 28 SP - 52 EP - 60 VL - 654 SN - 0077-8923, 0077-8923 KW - Receptors, GABA-A KW - 0 KW - Receptors, N-Methyl-D-Aspartate KW - Index Medicus KW - Animals KW - Receptors, GABA-A -- physiology KW - Humans KW - Receptors, N-Methyl-D-Aspartate -- physiology KW - Substance Withdrawal Syndrome -- physiopathology KW - Seizures -- physiopathology KW - Alcoholism -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73068719?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=NMDA+receptors%3A+role+in+ethanol+withdrawal+seizures.&rft.au=Hoffman%2C+P+L%3BGrant%2C+K+A%3BSnell%2C+L+D%3BReinlib%2C+L%3BIorio%2C+K%3BTabakoff%2C+B&rft.aulast=Hoffman&rft.aufirst=P&rft.date=1992-06-28&rft.volume=654&rft.issue=&rft.spage=52&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 - 1992-08-17 N1 - Date created - 1992-08-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Conditioned sensitization to the psychomotor stimulant cocaine. AN - 73067394; 1632592 JF - Annals of the New York Academy of Sciences AU - Post, R M AU - Weiss, S R AU - Fontana, D AU - Pert, A AD - Biological Psychiatry Branch, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1992/06/28/ PY - 1992 DA - 1992 Jun 28 SP - 386 EP - 399 VL - 654 SN - 0077-8923, 0077-8923 KW - Cocaine KW - I5Y540LHVR KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Substance-Related Disorders -- physiopathology KW - Animals KW - Humans KW - Dopamine -- metabolism KW - Substance-Related Disorders -- psychology KW - Conditioning (Psychology) KW - Brain -- drug effects KW - Motor Activity -- drug effects KW - Cocaine -- pharmacology KW - Cocaine -- administration & dosage KW - Brain -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73067394?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Conditioned+sensitization+to+the+psychomotor+stimulant+cocaine.&rft.au=Post%2C+R+M%3BWeiss%2C+S+R%3BFontana%2C+D%3BPert%2C+A&rft.aulast=Post&rft.aufirst=R&rft.date=1992-06-28&rft.volume=654&rft.issue=&rft.spage=386&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 - 1992-08-17 N1 - Date created - 1992-08-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The role of solvent viscosity in the dynamics of protein conformational changes. AN - 73016715; 1615323 AB - Nanosecond lasers were used to measure the rate of conformational changes in myoglobin after ligand dissociation at ambient temperatures. At low solvent viscosities the rate is independent of viscosity, but at high viscosities it depends on approximately the inverse first power of the viscosity. Kramers theory for unimolecular rate processes can be used to explain this result if the friction term is modified to include protein as well as solvent friction. The theory and experiment suggest that the dominant factor in markedly reducing the rate of conformational changes in myoglobin at low temperatures (less than 200 K) is the very high viscosity (greater than 10(7) centipoise) of the glycerol-water solvent. That is, at low temperatures conformational substates may not be "frozen" so much as "stuck." JF - Science (New York, N.Y.) AU - Ansari, A AU - Jones, C M AU - Henry, E R AU - Hofrichter, J AU - Eaton, W A AD - Laboratory of Chemical Physics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/06/26/ PY - 1992 DA - 1992 Jun 26 SP - 1796 EP - 1798 VL - 256 IS - 5065 SN - 0036-8075, 0036-8075 KW - Myoglobin KW - 0 KW - Solvents KW - Carbon Monoxide KW - 7U1EE4V452 KW - Index Medicus KW - Hot Temperature KW - Viscosity KW - Spectrophotometry, Atomic KW - Lasers KW - Protein Conformation KW - Myoglobin -- chemistry KW - Solvents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73016715?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+role+of+solvent+viscosity+in+the+dynamics+of+protein+conformational+changes.&rft.au=Ansari%2C+A%3BJones%2C+C+M%3BHenry%2C+E+R%3BHofrichter%2C+J%3BEaton%2C+W+A&rft.aulast=Ansari&rft.aufirst=A&rft.date=1992-06-26&rft.volume=256&rft.issue=5065&rft.spage=1796&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 - 1992-07-24 N1 - Date created - 1992-07-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Risk of leukemia after chemotherapy and radiation treatment for breast cancer. AN - 72966855; 1594016 AB - Few studies have evaluated the late effects of adjuvant chemotherapy for breast cancer. Moreover, the relation between the risk of leukemia and the amount of drug given and the interaction of chemotherapy with radiotherapy have not been described in detail. We conducted a case-control study in a cohort of 82,700 women given a diagnosis of breast cancer from 1973 to 1985 in five areas of the United States. Detailed information about therapy was obtained for 90 patients with leukemia and 264 matched controls. The dose of radiation to the active marrow was estimated from individual radiotherapy records (mean dose, 7.5 Gy). The risk of acute nonlymphocytic leukemia was significantly increased after regional radiotherapy alone (relative risk, 2.4), alkylating agents alone (relative risk, 10.0), and combined radiation and drug therapy (relative risk, 17.4). Dose-dependent risks were observed after radiotherapy and treatment with melphalan and cyclophosphamide. Melphalan was 10 times more leukemogenic than cyclophosphamide (relative risk, 31.4 vs. 3.1). There was little increase in the risk associated with total cyclophosphamide doses of less than 20,000 mg. Although leukemia occurs in few patients with breast cancer, significantly elevated risks were linked to treatments with regional radiation and alkylating agents. Melphalan is a more potent leukemogen than cyclophosphamide or radiotherapy. Low risks were associated with the levels of cyclophosphamide in common use today. Systemic drug therapy combined with radiotherapy that delivers high doses to the marrow appears to enhance the risk of leukemia. JF - The New England journal of medicine AU - Curtis, R E AU - Boice, J D AU - Stovall, M AU - Bernstein, L AU - Greenberg, R S AU - Flannery, J T AU - Schwartz, A G AU - Weyer, P AU - Moloney, W C AU - Hoover, R N AD - Radiation Epidemiology Branch, National Cancer Institute, Bethesda, Md. 20892. Y1 - 1992/06/25/ PY - 1992 DA - 1992 Jun 25 SP - 1745 EP - 1751 VL - 326 IS - 26 SN - 0028-4793, 0028-4793 KW - Alkylating Agents KW - 0 KW - Cyclophosphamide KW - 8N3DW7272P KW - Melphalan KW - Q41OR9510P KW - Abridged Index Medicus KW - Index Medicus KW - Dose-Response Relationship, Drug KW - Humans KW - Leukemia, Radiation-Induced -- etiology KW - Aged KW - Combined Modality Therapy -- adverse effects KW - Dose-Response Relationship, Radiation KW - Radiotherapy -- adverse effects KW - Cyclophosphamide -- adverse effects KW - Risk KW - Radiotherapy Dosage KW - Leukemia, Myeloid, Acute -- etiology KW - Melphalan -- adverse effects KW - Case-Control Studies KW - Middle Aged KW - Alkylating Agents -- adverse effects KW - Myelodysplastic Syndromes -- etiology KW - Female KW - Breast Neoplasms -- drug therapy KW - Breast Neoplasms -- therapy KW - Leukemia -- etiology KW - Breast Neoplasms -- radiotherapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72966855?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+role+of+breakfast+and+a+mid-morning+snack+on+the+ability+of+children+to+concentrate+at+school&rft.au=Benton%2C+David%3BJarvis%2C+Megan&rft.aulast=Benton&rft.aufirst=David&rft.date=2007-02-01&rft.volume=90&rft.issue=2-3&rft.spage=382&rft.isbn=&rft.btitle=&rft.title=Physiology+%26+Behavior&rft.issn=00319384&rft_id=info:doi/10.1016%2Fj.physbeh.2006.09.029 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-26 N1 - Date created - 1992-06-26 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: N Engl J Med. 1992 Jun 25;326(26):1774-5 [1594020] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dolastatin 15, a potent antimitotic depsipeptide derived from Dolabella auricularia. Interaction with tubulin and effects of cellular microtubules. AN - 73070523; 1632820 AB - Dolastatin 15, a seven-subunit depsipeptide derived from Dolabella auricularia, is a potent antimitotic agent structurally related to the antitubulin agent dolastatin 10, a five-subunit peptide obtained from the same organism. We have compared dolastatin 15 with dolastatin 10 for its effects on cells grown in culture and on biochemical properties of tubulin. The IC50 values for cell growth were obtained for dolastatin 15 with L1210 murine leukemia cells, human Burkitt lymphoma cells, and Chinese hamster ovary (CHO) cells (3, 3, and 5 nM with the three cell lines, respectively). For dolastatin 10, IC50 values of 0.4 and 0.5 nM were obtained with the L1210 and CHO cells, respectively. At toxic concentrations dolastatin 15 caused the leukemia and lymphoma cells to arrest in mitosis. In the CHO cells both dolastatin 15 and dolastatin 10 caused moderate loss of microtubules at the IC50 values and complete disappearance of microtubules at concentrations 10-fold higher. Despite its potency and the loss of microtubules in treated cells, the interaction of dolastatin 15 with tubulin in vitro was weak. Its IC50 value for inhibition of glutamate-induced polymerization of tubulin was 23 microM, as compared to values of 1.2 microM for dolastatin 10 and 1.5 microM for vinblastine. Dolastatin 10 noncompetitively inhibits the binding of vincristine to tubulin, inhibits nucleotide exchange, stabilizes the colchicine binding activity of tubulin, and inhibits tubulin-dependent GTP hydrolysis (Bai et al., Biochem Pharmacol 39: 1941-1949, 1990; Bai et al. J Biol Chem 265: 17141-17149, 1990). Only the latter reaction was inhibited by dolastatin 15. Nevertheless, its structural similarity to dolastatin 10 indicates that dolastatin 15 may bind weakly in the "vinca domain" of tubulin (a region of the protein we postulate to be physically close to but not identical with the specific binding site of vinca alkaloids and maytansinoids), presumably in the same site as dolastatin 10 (the "peptide site"). JF - Biochemical pharmacology AU - Bai, R AU - Friedman, S J AU - Pettit, G R AU - Hamel, E AD - Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/06/23/ PY - 1992 DA - 1992 Jun 23 SP - 2637 EP - 2645 VL - 43 IS - 12 SN - 0006-2952, 0006-2952 KW - Antineoplastic Agents KW - 0 KW - Depsipeptides KW - Glutamates KW - Microtubule-Associated Proteins KW - Oligopeptides KW - Tubulin KW - dolastatin 10 KW - 110417-88-4 KW - dolastatin 15 KW - 123884-00-4 KW - Vinblastine KW - 5V9KLZ54CY KW - Guanosine Triphosphate KW - 86-01-1 KW - Index Medicus KW - Vinblastine -- pharmacology KW - Cell Line -- ultrastructure KW - Animals KW - Mitotic Index -- drug effects KW - Microtubule-Associated Proteins -- pharmacology KW - Glutamates -- pharmacology KW - Cell Line -- drug effects KW - Molecular Sequence Data KW - Cell Line -- cytology KW - Amino Acid Sequence KW - Guanosine Triphosphate -- metabolism KW - Binding Sites KW - Tubulin -- chemistry KW - Mollusca -- chemistry KW - Antineoplastic Agents -- isolation & purification KW - Tubulin -- metabolism KW - Oligopeptides -- isolation & purification KW - Antineoplastic Agents -- chemical synthesis KW - Oligopeptides -- pharmacology KW - Microtubules -- drug effects KW - Oligopeptides -- chemical synthesis KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73070523?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Dolastatin+15%2C+a+potent+antimitotic+depsipeptide+derived+from+Dolabella+auricularia.+Interaction+with+tubulin+and+effects+of+cellular+microtubules.&rft.au=Bai%2C+R%3BFriedman%2C+S+J%3BPettit%2C+G+R%3BHamel%2C+E&rft.aulast=Bai&rft.aufirst=R&rft.date=1992-06-23&rft.volume=43&rft.issue=12&rft.spage=2637&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 - 1992-08-14 N1 - Date created - 1992-08-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Frequent expression of the tumor antigen CAK1 in squamous-cell carcinomas. AN - 72977283; 1351045 AB - K1 is a murine monoclonal antibody (MAb) derived from a hybridoma generated by the fusion of splenocytes of BALB/c mice immunized with a human ovarian tumor cell line, OVCAR-3. This antibody reacts strongly with epithelial ovarian tumors and mesotheliomas. The antigen recognized by MAb K1, designated CAK1, has recently been characterized as a 40-kDa protein probably anchored to the cell surface by glycosyl-phosphatidylinositol. Using immunoperoxidase histochemical methods, we examined 37 squamous-cell carcinoma (SqCC) samples from cervix, lung, esophagus and other origins, and 12 normal squamous epithelia of the cervix and esophagus for their reactivity with MAb K1. Of the SqCC specimens, 81% showed K1 reactivity with variable intensity, but none of 12 normal tissue samples of squamous epithelia did so. Two patterns of CAK1 expression in tumor samples were found, i.e., a heterogeneous pattern with strong intensity, and a homogeneous pattern with weak intensity. Three carcinomas in situ of the larynx, vulva and esophagus were moderately positive with K1, suggesting that CAK1 antigen may occur in the early stage of carcinogenesis of SqCC. The expression of CAK1 was also compared with expression of CA125, HER-2/neu, p53 and P-glycoprotein, and MAb K1 was found to react most consistently with SqCC. Since K1 reacts with a majority of cervical and esophageal carcinomas but has no detectable reactivity in normal epithelia of the cervix uteri and esophagus, MAb K1 could be of value as a reagent to help distinguish between normal and neoplastic cells on sections as well as in cytological samples. JF - International journal of cancer AU - Chang, K AU - Pastan, I AU - Willingham, M C AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/06/19/ PY - 1992 DA - 1992 Jun 19 SP - 548 EP - 554 VL - 51 IS - 4 SN - 0020-7136, 0020-7136 KW - Antigens, Neoplasm KW - 0 KW - Butanols KW - Membrane Glycoproteins KW - Oncogene Proteins, Viral KW - P-Glycoprotein KW - Tumor Suppressor Protein p53 KW - 1-Butanol KW - 8PJ61P6TS3 KW - Receptor, ErbB-2 KW - EC 2.7.10.1 KW - Phosphoric Diester Hydrolases KW - EC 3.1.4.- KW - Phosphoinositide Phospholipase C KW - EC 3.1.4.11 KW - Index Medicus KW - Tumor Suppressor Protein p53 -- analysis KW - Humans KW - Oncogene Proteins, Viral -- analysis KW - Membrane Glycoproteins -- analysis KW - Epithelium -- immunology KW - Female KW - Carcinoma, Squamous Cell -- immunology KW - Mouth Neoplasms -- immunology KW - Lung Neoplasms -- immunology KW - Antigens, Neoplasm -- analysis KW - Uterine Cervical Neoplasms -- immunology KW - Esophageal Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72977283?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Frequent+expression+of+the+tumor+antigen+CAK1+in+squamous-cell+carcinomas.&rft.au=Chang%2C+K%3BPastan%2C+I%3BWillingham%2C+M+C&rft.aulast=Chang&rft.aufirst=K&rft.date=1992-06-19&rft.volume=51&rft.issue=4&rft.spage=548&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 - 1992-07-13 N1 - Date created - 1992-07-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pilot study of interleukin-2 and lymphokine-activated killer cells combined with immunomodulatory doses of chemotherapy and sequenced with interferon alfa-2a in patients with metastatic melanoma and renal cell carcinoma. AN - 73052862; 1629914 AB - Experiments in animal tumor models suggest that the antitumor effects of interleukin-2 (IL-2) or IL-2 in combination with lymphokine-activated killer (LAK) cells can be enhanced by chemotherapy agents such as cyclophosphamide or doxorubicin or by the biologic agent interferon alpha. We determined the toxicity and clinical response rate of an IL-2-LAK cell regimen modified by the addition of moderate, immunomodulatory doses of chemotherapy and sequenced with interferon alfa-2a (IFN alpha-2a) in patients with metastatic melanoma and renal cell carcinoma. IL-2 (3-6 million units/m2 per day) was administered by continuous infusion on days 0-5 and days 11-16. LAK cells were infused on days 11 and 12 or on days 11, 12, and 14. Low doses of cyclophosphamide (300 mg/m2) and doxorubicin (25 mg/m2) were given on day 9 before the LAK cell infusions. Following the IL-2-LAK cell infusion, IFN alpha-2a (12 million units/m2) was administered for a total of nine doses to complete a cycle of treatment. A total of 89 patients were enrolled in the study. For each histology, there were eight partial responses in 40 assessable patients, for an overall response rate of 20% (90% confidence interval = 10%-33%). The median response duration was 5 months, although two patients with renal cell carcinoma and one patient with metastatic melanoma had almost complete disappearance of tumor and are still responding after 26+, 22+, and 26+ months, respectively. Toxic effects were severe in patients receiving the highest dose of IL-2 administered in this study and similar to those reported with other high-dose IL-2-LAK cell regimens. Although toxic effects were completely reversible in most patients, there were four treatment-related deaths. This regimen is active in patients with metastatic melanoma and renal cell carcinoma and produces meaningful responses in a small percentage of these patients; however, it is not clear whether cyclophosphamide, doxorubicin, and IFN alpha-2a as used in this protocol appreciably augmented the antitumor activity of the IL-2-LAK cell regimen. JF - Journal of the National Cancer Institute AU - Sznol, M AU - Clark, J W AU - Smith, J W AU - Steis, R G AU - Urba, W J AU - Rubinstein, L V AU - VanderMolen, L A AU - Janik, J AU - Sharfman, W H AU - Fenton, R G AD - Division of Cancer Treatment, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/06/17/ PY - 1992 DA - 1992 Jun 17 SP - 929 EP - 937 VL - 84 IS - 12 SN - 0027-8874, 0027-8874 KW - Interferon-alpha KW - 0 KW - Interleukin-2 KW - Recombinant Proteins KW - interferon alfa-2a KW - 47RRR83SK7 KW - Doxorubicin KW - 80168379AG KW - Cyclophosphamide KW - 8N3DW7272P KW - Index Medicus KW - Cyclophosphamide -- administration & dosage KW - Doxorubicin -- adverse effects KW - Drug Administration Schedule KW - Infusions, Intravenous KW - Humans KW - Immunotherapy KW - Aged KW - Heart -- drug effects KW - Pilot Projects KW - Doxorubicin -- administration & dosage KW - Cyclophosphamide -- adverse effects KW - Immune System -- drug effects KW - Adult KW - Lung -- drug effects KW - Middle Aged KW - Male KW - Female KW - Kidney Neoplasms -- therapy KW - Interleukin-2 -- adverse effects KW - Interferon-alpha -- therapeutic use KW - Interferon-alpha -- adverse effects KW - Carcinoma, Renal Cell -- therapy KW - Interleukin-2 -- therapeutic use KW - Melanoma -- therapy KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Killer Cells, Lymphokine-Activated -- transplantation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73052862?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Pilot+study+of+interleukin-2+and+lymphokine-activated+killer+cells+combined+with+immunomodulatory+doses+of+chemotherapy+and+sequenced+with+interferon+alfa-2a+in+patients+with+metastatic+melanoma+and+renal+cell+carcinoma.&rft.au=Sznol%2C+M%3BClark%2C+J+W%3BSmith%2C+J+W%3BSteis%2C+R+G%3BUrba%2C+W+J%3BRubinstein%2C+L+V%3BVanderMolen%2C+L+A%3BJanik%2C+J%3BSharfman%2C+W+H%3BFenton%2C+R+G&rft.aulast=Sznol&rft.aufirst=M&rft.date=1992-06-17&rft.volume=84&rft.issue=12&rft.spage=929&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 - 1992-08-17 N1 - Date created - 1992-08-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A1 adenosine-receptor antagonists activate chloride efflux from cystic fibrosis cells. AN - 73015578; 1376923 AB - A1 adenosine-receptor-antagonist drugs such as 8-cyclopentyl-1,3-dipropylxanthine (CPX) and xanthine amine congener (XAC) are found to activate the efflux of 36Cl- from CFPAC cells. These cells are a pancreatic adenocarcinoma cell line derived from a cystic fibrosis (CF) patient homozygous for the common mutation, deletion of Phe-508. The active concentrations for these compounds are in the low nanomolar range, consistent with action on A1 adenosine receptors. In addition, drug action can be blocked by exogenous agonists such as 2-chloroadenosine and also can be antagonized by removal of endogenous agonists by treatment with adenosine deaminase. Cells lacking the CF genotype and phenotype, such as HT-29 and T84 colon carcinoma cell lines, appear to be resistant to activation of chloride efflux by either drug. CFPAC cells transfected with the CF transmembrane regulator gene, CFTR, are also resistant to activation by CPX. We conclude that, since these antagonists are of relatively low toxicity and appear to act somewhat selectively, they might be considered as promising therapeutic candidates for CF. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Eidelman, O AU - Guay-Broder, C AU - van Galen, P J AU - Jacobson, K A AU - Fox, C AU - Turner, R J AU - Cabantchik, Z I AU - Pollard, H B AD - Clinical Investigations and Patient Care Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/06/15/ PY - 1992 DA - 1992 Jun 15 SP - 5562 EP - 5566 VL - 89 IS - 12 SN - 0027-8424, 0027-8424 KW - CFTR protein, human KW - 0 KW - Chlorides KW - Membrane Proteins KW - Purinergic Antagonists KW - Xanthines KW - Cystic Fibrosis Transmembrane Conductance Regulator KW - 126880-72-6 KW - 2-Chloroadenosine KW - 146-77-0 KW - 1,3-dipropyl-8-cyclopentylxanthine KW - 9PTP4FOI9E KW - Adenosine KW - K72T3FS567 KW - Index Medicus KW - Chromosome Deletion KW - Humans KW - Pancreatic Neoplasms KW - Membrane Proteins -- genetics KW - Phenotype KW - Genotype KW - Kinetics KW - 2-Chloroadenosine -- pharmacology KW - Adenocarcinoma KW - Colonic Neoplasms KW - Mutation KW - Cell Line KW - Adenosine -- pharmacology KW - Cystic Fibrosis -- genetics KW - Adenosine -- analogs & derivatives KW - Cystic Fibrosis -- physiopathology KW - Chlorides -- metabolism KW - Xanthines -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73015578?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A1+adenosine-receptor+antagonists+activate+chloride+efflux+from+cystic+fibrosis+cells.&rft.au=Eidelman%2C+O%3BGuay-Broder%2C+C%3Bvan+Galen%2C+P+J%3BJacobson%2C+K+A%3BFox%2C+C%3BTurner%2C+R+J%3BCabantchik%2C+Z+I%3BPollard%2C+H+B&rft.aulast=Eidelman&rft.aufirst=O&rft.date=1992-06-15&rft.volume=89&rft.issue=12&rft.spage=5562&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 - 1992-07-21 N1 - Date created - 1992-07-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Neurosci Lett. 1989 Apr 24;99(1-2):107-12 [2748004] Science. 1989 Sep 8;245(4922):1073-80 [2570460] J Clin Invest. 1986 Feb;77(2):348-54 [3003156] Proc Natl Acad Sci U S A. 1985 Sep;82(18):6167-71 [3862125] Am J Physiol. 1982 Feb;242(2):G116-23 [6121487] J Clin Invest. 1984 Sep;74(3):929-35 [6206092] Science. 1983 Sep 9;221(4615):1067-70 [6308769] Nature. 1983 Feb 3;301(5899):421-2 [6823316] N Engl J Med. 1983 May 19;308(20):1185-9 [6843595] Proc Natl Acad Sci U S A. 1990 May;87(10):4012-6 [1692630] Nature. 1991 Dec 19-26;354(6354):526-8 [1722027] J Med Chem. 1992 Feb 7;35(3):407-22 [1738138] J Biol Chem. 1991 Jun 5;266(16):10319-23 [2037584] FASEB J. 1990 Jul;4(10):2709-17 [2197151] Am J Physiol. 1989 Jun;256(6 Pt 1):C1111-9 [2472065] Naunyn Schmiedebergs Arch Pharmacol. 1989 Aug;340(2):204-9 [2554151] Br J Pharmacol. 1989 Nov;98(3):1066-74 [2590769] J Clin Invest. 1985 Nov;76(5):1837-42 [2997291] Biochem Pharmacol. 1988 Oct 1;37(19):3653-61 [3178879] Biochem J. 1971 Mar;122(1):115-20 [4330960] Proc Natl Acad Sci U S A. 1981 May;78(5):3260-4 [6265942] Am J Physiol. 1984 Oct;247(4 Pt 2):R646-9 [6496713] J Clin Invest. 1983 May;71(5):1410-7 [6853720] J Clin Invest. 1992 Mar;89(3):834-41 [1311718] Proc Natl Acad Sci U S A. 1992 Mar 1;89(5):1539-43 [1371876] J Recept Res. 1992;12(2):149-69 [1583620] J Pharm Pharmacol. 1991 Feb;43(2):138-9 [1672902] FASEB J. 1990 Jul;4(10):2718-25 [1695593] Cell. 1990 Sep 21;62(6):1227-33 [1698126] Science. 1991 Dec 20;254(5039):1797-9 [1722350] J Clin Invest. 1991 Dec;88(6):1933-9 [1752953] N Engl J Med. 1991 Aug 22;325(8):533-8 [1857389] N Engl J Med. 1990 Apr 26;322(17):1189-94 [2157983] Science. 1989 Jun 16;244(4910):1353-6 [2472006] Science. 1989 Sep 8;245(4922):1066-73 [2475911] Am J Physiol. 1989 Jan;256(1 Pt 1):C197-203 [2536228] Science. 1989 Sep 8;245(4922):1059-65 [2772657] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interlocus V-J recombination measures genomic instability in agriculture workers at risk for lymphoid malignancies. AN - 73012001; 1608939 AB - V(D)J [variable-(diversity)-joining] rearrangements occur between, as well as within, immune receptor loci, resulting in the generation of hybrid antigen-receptor genes and the formation of a variety of lymphocyte-specific chromosomal aberrations. Such hybrid genes occur at a low frequency in the peripheral blood lymphocytes (PBL) of normal individuals but show a markedly increased incidence in the PBL of individuals with the autosomal recessive disease ataxia-telangiectasia. In this manuscript we demonstrate that the frequency of hybrid antigen-receptor genes is 10- to 20-fold increased in the PBL of an occupational group, agriculture workers, with related environmental exposures. Both ataxia-telangiectasia patients and this population of agriculture workers are at increased risk for lymphoid malignancy. This result suggests that the measurement of hybrid antigen receptor-genes in PBL may be a sensitive assay for a type of lymphocyte-specific genomic instability. As a corollary, this assay may identify populations at risk of developing common types of lymphoid malignancy. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Lipkowitz, S AU - Garry, V F AU - Kirsch, I R AD - National Cancer Institute-Navy Medical Oncology Branch, Bethesda Naval Hospital, MD 20889-5105. Y1 - 1992/06/15/ PY - 1992 DA - 1992 Jun 15 SP - 5301 EP - 5305 VL - 89 IS - 12 SN - 0027-8424, 0027-8424 KW - Immunoglobulin Joining Region KW - 0 KW - Immunoglobulin Variable Region KW - Oligodeoxyribonucleotides KW - Receptors, Antigen, T-Cell KW - DNA KW - 9007-49-2 KW - Index Medicus KW - DNA -- isolation & purification KW - Base Sequence KW - Risk Factors KW - Humans KW - Polymerase Chain Reaction -- methods KW - DNA -- genetics KW - Molecular Sequence Data KW - Immunoglobulin Variable Region -- genetics KW - Lymphoma -- etiology KW - Agricultural Workers' Diseases -- immunology KW - Lymphoma -- genetics KW - Agricultural Workers' Diseases -- genetics KW - Recombination, Genetic KW - Gene Rearrangement KW - Lymphoma -- immunology KW - Receptors, Antigen, T-Cell -- genetics KW - Chromosomes, Human, Pair 7 KW - Immunoglobulin Joining Region -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73012001?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Interlocus+V-J+recombination+measures+genomic+instability+in+agriculture+workers+at+risk+for+lymphoid+malignancies.&rft.au=Lipkowitz%2C+S%3BGarry%2C+V+F%3BKirsch%2C+I+R&rft.aulast=Lipkowitz&rft.aufirst=S&rft.date=1992-06-15&rft.volume=89&rft.issue=12&rft.spage=5301&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 - 1992-07-21 N1 - Date created - 1992-07-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: FASEB J. 1989 Oct;3(12):2344-59 [2676678] Cell. 1987 Jul 3;50(1):97-105 [3036367] Hum Genet. 1989 Nov;83(4):347-52 [2807275] Science. 1989 Oct 13;246(4927):251-5 [2799386] Cell. 1985 Dec;43(3 Pt 2):705-13 [3935328] Science. 1985 Sep 27;229(4720):1390-3 [3929382] Scand J Work Environ Health. 1985 Dec;11(6):397-407 [3912986] Proc Natl Acad Sci U S A. 1985 Dec;82(24):8624-8 [3866244] J Natl Cancer Inst. 1990 May 16;82(10):840-8 [2332902] J Exp Med. 1990 Aug 1;172(2):409-18 [1695665] Nature. 1983 Apr 14;302(5909):575-81 [6300689] Science. 1984 Jun 29;224(4656):1403-6 [6610211] Proc Natl Acad Sci U S A. 1983 Apr;80(7):1982-6 [6572957] J Genet Hum. 1981 Sep;29(3):235-47 [6950025] Mutat Res. 1980 Feb;69(2):369-74 [7360152] Nucleic Acids Res. 1976 Sep;3(9):2303-8 [987581] Cell. 1986 Apr 25;45(2):237-46 [2938743] Science. 1986 Oct 10;234(4773):197-200 [3092355] Annu Rev Immunol. 1986;4:339-68 [3085692] Adv Immunol. 1987;40:247-321 [3109221] Proc Natl Acad Sci U S A. 1989 Mar;86(6):2031-5 [2467296] Science. 1989 Sep 15;245(4923):1242-6 [2551037] Blood. 1989 Nov 1;74(6):2076-80 [2529926] Scand J Clin Lab Invest Suppl. 1968;97:77-89 [4179068] Nature. 1975 May 15;255(5505):241-5 [1143322] Epidemiology. 1990 Sep;1(5):349-56 [2078610] Science. 1990 Dec 7;250(4986):1426-9 [2255914] Cancer Res. 1990 Oct 15;50(20):6585-91 [2208120] Cancer Genet Cytogenet. 1987 May;26(1):95-104 [3470137] Annu Rev Immunol. 1987;5:253-77 [2885014] Cancer Genet Cytogenet. 1985 Sep;18(1):55-63 [3875398] Hum Genet. 1985;71(1):19-21 [4029952] JAMA. 1986 Sep 5;256(9):1141-7 [3801091] Nature. 1986 Apr 10-16;320(6062):549-51 [3008004] Blood. 1989 May 1;73(6):1402-15 [2653455] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Reduced susceptibility to HIV-1 infection of ethyl-methanesulfonate-treated CEM subclones correlates with a blockade in their protein kinase C signaling pathway. AN - 73011014; 1351090 AB - We have described the isolation of chemically induced CEM subclones that express CD4 receptors and bind soluble gp120, yet show a markedly reduced susceptibility to infection with HIV-1. Two subclones were found to have an abnormal response to the protein kinase C (PKC) activator PMA. PMA treatment induced CD3 and CD25 (IL-2R) receptors on the parental line and on other ethyl-methanesulfonate-derived subclones, but not on these two mutants. Direct assays of PKC activity were conducted. Total cellular PKC enzymatic activity was found to be normal in these subclones. PMA-induced CD4 down-modulation occurred normally. In addition, activation of c-raf kinase was normal. Since HIV-1 long terminal repeat contains two functional nuclear factor kB (NF-kB) regulatory elements, we studied the ability of PMA to induce NF-kB binding activity by different assays. Chloramphenicol acetyl transferase (CAT) assays using the HIV-1 (-139)long terminal repeat-CAT construct showed no PMA induction of CAT activity in these subclones (unlike the parental line and other subclones). Okadaic acid, an inhibitor of phosphatases 1 and 2A, did not overcome the defect in these subclones. Gel retardation assays, using a 32P-probe containing the HIV-1 NF-kB probe and nuclear extracts from PMA-treated cells, showed significantly reduced induction of nuclear NF-kB binding proteins in these two subclones compared with wild type CEM and a control subclone. Deoxycholate treatment of cytoplasmic extracts from these subclones released much reduced NF-kB binding proteins from their cytoplasmic pools. Thus, reduced levels of PKC-induced nuclear NF-kB activity in two T cell subclones did not affect their normal cell growth, but correlated with a pronounced reduction in their susceptibility to HIV-1 infection. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Hillman, K AU - Qian, J AU - Siegel, J N AU - Roderiquez, G AU - Blackburn, R AU - Manischewitz, J AU - Norcross, M AU - Golding, H AD - Division of Virology, Food and Drug Administration, National Institutes of Health, Bethesda, MD 20892. Y1 - 1992/06/15/ PY - 1992 DA - 1992 Jun 15 SP - 3991 EP - 3998 VL - 148 IS - 12 SN - 0022-1767, 0022-1767 KW - DNA-Binding Proteins KW - 0 KW - Ethers, Cyclic KW - NF-kappa B KW - Nuclear Proteins KW - Proto-Oncogene Proteins KW - Okadaic Acid KW - 1W21G5Q4N2 KW - Ethyl Methanesulfonate KW - 9H154DI0UP KW - Proto-Oncogene Proteins c-raf KW - EC 2.7.11.1 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Clone Cells KW - Humans KW - Proto-Oncogene Proteins -- metabolism KW - Gene Expression KW - Ethers, Cyclic -- pharmacology KW - HIV Long Terminal Repeat KW - Base Sequence KW - Ethyl Methanesulfonate -- pharmacology KW - Cells, Cultured KW - Cytoplasm -- metabolism KW - Cell Compartmentation KW - In Vitro Techniques KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Nuclear Proteins -- metabolism KW - Mutation KW - Signal Transduction KW - NF-kappa B -- metabolism KW - DNA-Binding Proteins -- metabolism KW - HIV Infections -- physiopathology KW - Protein Kinase C -- physiology KW - CD4-Positive T-Lymphocytes -- microbiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73011014?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Reduced+susceptibility+to+HIV-1+infection+of+ethyl-methanesulfonate-treated+CEM+subclones+correlates+with+a+blockade+in+their+protein+kinase+C+signaling+pathway.&rft.au=Hillman%2C+K%3BQian%2C+J%3BSiegel%2C+J+N%3BRoderiquez%2C+G%3BBlackburn%2C+R%3BManischewitz%2C+J%3BNorcross%2C+M%3BGolding%2C+H&rft.aulast=Hillman&rft.aufirst=K&rft.date=1992-06-15&rft.volume=148&rft.issue=12&rft.spage=3991&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 - 1992-07-10 N1 - Date created - 1992-07-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The carboxylesterase family exhibits C-terminal sequence diversity reflecting the presence or absence of endoplasmic-reticulum-retention sequences. AN - 73007465; 1606962 AB - Resident proteins of the endoplasmic reticulum lumen are continuously retrieved from an early Golgi compartment by a receptor-mediated mechanism. The sorting or retention sequence on the endoplasmic reticulum proteins is located at the C-terminus and was initially shown to be the tetrapeptide KDEL in mammalian cells and HDEL in Saccharomyces cerevisiae. The carboxylesterases are a large family of enzymes primarily localized to the lumen of the endoplasmic reticulum. Retention sequences in these proteins have been difficult to identify due to atypical and heterogeneous C-terminal sequences. Utilizing the polymerase chain reaction with degenerate primers, we have identified and characterized the C-termini of four members of the carboxylesterase family from rat liver. Three of the carboxylesterases sequences contained C-terminal sequences (HVEL, HNEL or HTEL) resembling the yeast sorting signal which were reported to be non-functional in mammalian cells. A fourth carboxylesterase contained a distinct C-terminal sequence, TEHT. A full-length esterase cDNA clone, terminating in the sequence HVEL, was isolated and was used to assess the retention capabilities of the various esterase C-terminal sequences. This esterase was retained in COS-1 cells, but was secreted when its C-terminal tetrapeptide, HVEL, was deleted. Addition of C-terminal sequences containing HNEL and HTEL resulted in efficient retention. However, the C-terminal sequence containing TEHT was not a functional retention signal. Both HDEL, the authentic yeast retention signal, and KDEL were efficient retention sequences for the esterase. These studies show that some members of the rat liver carboxylesterase family contain novel C-terminal retention sequences that resemble the yeast signal. At least one member of the family does not contain a C-terminal retention signal and probably represents a secretory form. JF - European journal of biochemistry AU - Medda, S AU - Proia, R L AD - Genetics and Biochemistry Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda 20892. Y1 - 1992/06/15/ PY - 1992 DA - 1992 Jun 15 SP - 801 EP - 806 VL - 206 IS - 3 SN - 0014-2956, 0014-2956 KW - DNA KW - 9007-49-2 KW - Carboxylic Ester Hydrolases KW - EC 3.1.1.- KW - Carboxylesterase KW - EC 3.1.1.1 KW - Index Medicus KW - Endoplasmic Reticulum -- enzymology KW - Animals KW - Liver -- enzymology KW - Sequence Homology, Nucleic Acid KW - Gene Expression KW - Amino Acid Sequence KW - Mutagenesis KW - Cloning, Molecular KW - Rats, Inbred Strains KW - Rats KW - Polymerase Chain Reaction KW - Base Sequence KW - Transfection KW - DNA -- genetics KW - Molecular Sequence Data KW - DNA -- chemistry KW - Immunosorbent Techniques KW - Cell Line KW - Carboxylic Ester Hydrolases -- chemistry KW - Carboxylic Ester Hydrolases -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/73007465?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+biochemistry&rft.atitle=The+carboxylesterase+family+exhibits+C-terminal+sequence+diversity+reflecting+the+presence+or+absence+of+endoplasmic-reticulum-retention+sequences.&rft.au=Medda%2C+S%3BProia%2C+R+L&rft.aulast=Medda&rft.aufirst=S&rft.date=1992-06-15&rft.volume=206&rft.issue=3&rft.spage=801&rft.isbn=&rft.btitle=&rft.title=European+journal+of+biochemistry&rft.issn=00142956&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-23 N1 - Date created - 1992-07-23 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M85175; GENBANK; M85174; X65181; M85177; X65296; X65180; M85176; X65295; X65294; X65179 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cell surface and intracellular functions for ricin galactose binding. AN - 72992490; 1601861 AB - The role of the two galactose binding sites of ricin B chain in ricin toxicity was evaluated by studying a series of ricin point mutants. Wild-type (WT) ricin and three ricin B chain point mutants having mutations in either 1) the first galactose binding domain (site 1 mutant, Met in place of Lys-40 and Gly in place of Asn-46), 2) the second galactose binding domain (site 2 mutant, Gly in place of Asn-255), or 3) both galactose binding domains (double site mutant containing all three amino acid replacements formerly stated) were expressed in Xenopus oocytes and then reassociated with recombinant ricin A chain. The different ricin B chains were mannosylated to the same extent. Cytotoxicity of these toxins was evaluated when cell entry was mediated either by galactose-containing receptors or through an alternate receptor, the mannose receptor of macrophages. WT ricin and each of the single domain mutants was able to kill Vero cells following uptake by galactose containing receptors. Lactose blocked the toxicity of each of these ricins. Site 1 and 2 mutants were 20-40 times less potent than WT ricin, and the double site mutant had no detectable cytotoxicity. WT ricin, the site 1 mutant, and the site 2 mutant also inhibited protein synthesis of mannose receptor-containing cells. Ricin can enter these cells through either a cell-surface galactose-containing receptor or through the mannose receptor. By including lactose in the cell medium, galactose-containing receptor-mediated uptake is blocked and cytotoxicity occurs solely via the mannose receptor. WT ricin, site 1, and site 2 mutants were cytotoxic to macrophages in the presence of lactose with the relative potency, WT greater than site 2 mutant greater than site 1 mutant. The double site mutant lacked cytotoxicity either in the absence or presence of lactose. Thus, even for mannose receptor-mediated toxicity of ricin, at least one galactose binding site remains necessary for cytotoxicity and two galactose binding sites further increases potency. These results are consistent with the model that the ricin B chain galactose binding activity plays a role not only in cell surface binding but also intracellularly for ricin cytotoxicity. JF - The Journal of biological chemistry AU - Newton, D L AU - Wales, R AU - Richardson, P T AU - Walbridge, S AU - Saxena, S K AU - Ackerman, E J AU - Roberts, L M AU - Lord, J M AU - Youle, R J AD - Biochemistry Section, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1992/06/15/ PY - 1992 DA - 1992 Jun 15 SP - 11917 EP - 11922 VL - 267 IS - 17 SN - 0021-9258, 0021-9258 KW - Lectins, C-Type KW - 0 KW - Mannose-Binding Lectins KW - Receptors, Cell Surface KW - Receptors, Immunologic KW - Receptors, Mitogen KW - Ricinus communis lectin receptor KW - mannose receptor KW - Ricin KW - 9009-86-3 KW - Mannose KW - PHA4727WTP KW - Galactose KW - X2RN3Q8DNE KW - Index Medicus KW - Bone Marrow Cells KW - Receptors, Immunologic -- drug effects KW - Animals KW - Peritoneal Cavity -- cytology KW - Cell Survival -- drug effects KW - Receptors, Immunologic -- metabolism KW - Vero Cells KW - Mannose -- metabolism KW - Macrophages -- drug effects KW - Mutation KW - Bone Marrow -- drug effects KW - Ricin -- genetics KW - Ricin -- toxicity KW - Ricin -- metabolism KW - Receptors, Mitogen -- metabolism KW - Galactose -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72992490?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+surface+and+intracellular+functions+for+ricin+galactose+binding.&rft.au=Newton%2C+D+L%3BWales%2C+R%3BRichardson%2C+P+T%3BWalbridge%2C+S%3BSaxena%2C+S+K%3BAckerman%2C+E+J%3BRoberts%2C+L+M%3BLord%2C+J+M%3BYoule%2C+R+J&rft.aulast=Newton&rft.aufirst=D&rft.date=1992-06-15&rft.volume=267&rft.issue=17&rft.spage=11917&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 - 1992-07-16 N1 - Date created - 1992-07-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Growth inhibition by cholera toxin of human lung carcinoma cell lines: correlation with GM1 ganglioside expression. AN - 72985515; 1375868 AB - The effect of cholera toxin (CT) on the growth of 12 small cell lung carcinoma (SCLC) and 15 non-small cell lung carcinoma (NSCLC) cell lines is presented. CT inhibited the growth of nine SCLC cell lines (concentration for 50% inhibition of growth, 27-700 ng/ml), all of which had abundant expression of GM1 ganglioside, the surface receptor for CT. CT-resistant SCLC all had greatly decreased GM1 expression. In contrast, CT inhibited the growth of only four of 15 NSCLC cell lines. Seven of the 11 CT-resistant NSCLC had levels of GM1 comparable to CT-sensitive NSCLC or SCLC. In a limited panel of cell lines, cyclic AMP (cAMP) agonists including forskolin, 8Br[cAMP], and dibutyryl[cAMP] did not consistently reproduce CT-mediated inhibition of cell growth, nor did these compounds overcome resistance of cells to the growth inhibitory effects of CT. Expression of the RI and RII regulatory subunits of cAMP-dependent protein kinase was similar in CT-resistant and CT-sensitive SCLC or NSCLC cell lines. In the presence of isobutylmethylxanthine, intracellular cAMP levels induced by CT in a CT-resistant, GM1(+) NSCLC cell line were comparable to those achieved in a CT-sensitive NSCLC cell line. We conclude that inhibition of lung carcinoma cell growth by CT in all cases requires expression of GM1, and in the case of SCLC cell lines the presence of GM1 is sufficient. In NSCLC cell lines, expression of GM1 is not sufficient for growth inhibition by CT. These findings imply refractoriness to growth inhibition by cAMP in GM1(+), CT-resistant NSCLC cell lines and the possibility of non-cAMP-related mechanisms for growth inhibition in CT-sensitive cell lines. JF - Cancer research AU - Kaur, G AU - Viallet, J AU - Laborda, J AU - Blair, O AU - Gazdar, A F AU - Minna, J D AU - Sausville, E A AD - Laboratory of Biological Chemistry, National Cancer Institute-Navy Medical Oncology Branch, Bethesda, Maryland 20892. Y1 - 1992/06/15/ PY - 1992 DA - 1992 Jun 15 SP - 3340 EP - 3346 VL - 52 IS - 12 SN - 0008-5472, 0008-5472 KW - G(M1) Ganglioside KW - 37758-47-7 KW - Cholera Toxin KW - 9012-63-9 KW - Cyclic AMP KW - E0399OZS9N KW - 1-Methyl-3-isobutylxanthine KW - TBT296U68M KW - Index Medicus KW - Drug Screening Assays, Antitumor KW - Cyclic AMP -- biosynthesis KW - Tumor Cells, Cultured KW - Humans KW - Cyclic AMP -- antagonists & inhibitors KW - Cell Division -- drug effects KW - 1-Methyl-3-isobutylxanthine -- pharmacology KW - Carcinoma, Small Cell -- pathology KW - G(M1) Ganglioside -- analysis KW - Carcinoma, Non-Small-Cell Lung -- metabolism KW - Lung Neoplasms -- chemistry KW - Carcinoma, Small Cell -- metabolism KW - Cholera Toxin -- pharmacology KW - Carcinoma, Non-Small-Cell Lung -- chemistry KW - Carcinoma, Small Cell -- chemistry KW - Lung Neoplasms -- pathology KW - Lung Neoplasms -- metabolism KW - Carcinoma, Non-Small-Cell Lung -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72985515?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Growth+inhibition+by+cholera+toxin+of+human+lung+carcinoma+cell+lines%3A+correlation+with+GM1+ganglioside+expression.&rft.au=Kaur%2C+G%3BViallet%2C+J%3BLaborda%2C+J%3BBlair%2C+O%3BGazdar%2C+A+F%3BMinna%2C+J+D%3BSausville%2C+E+A&rft.aulast=Kaur&rft.aufirst=G&rft.date=1992-06-15&rft.volume=52&rft.issue=12&rft.spage=3340&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 - 1992-07-06 N1 - Date created - 1992-07-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential immunohistochemical detection of amphiregulin and cripto in human normal colon and colorectal tumors. AN - 72983620; 1596904 AB - Thirty-six primary human colorectal tumors, 43 noninvolved colon samples that were adjacent to either carcinomas of adenomas, 22 adenomas, and nine normal colon specimens were immunohistochemically examined for the presence and localization of two epidermal growth factor-related peptides, amphiregulin (AR) and cripto. Within the primary tumors, 18 (50%) showed moderate levels of AR expression. Approximately 60% of the tubular and tubulovillous adenomas were positive for AR expression, whereas only 15% of the adjacent, noninvolved colon mucosa expressed AR. A greater proportion of well-differentiated tumors (71%) were positive for AR expression than were poorly differentiated tumors (18%). All of the nine normal colon specimens were positive. Consequently, AR expression appeared to be associated with both normal and malignant epithelial cells that were more differentiated. The distribution of cripto expression was different. Seventy-nine % of the colon tumors expressed cripto with a frequency of expression that was approximately equivalent between well-differentiated and poorly differentiated tumors. Approximately 86% of the tubulovillous adenomas, but only 43% of the tubular adenomas, were positive for cripto expression. In contrast, whereas AR was expressed in normal colon specimens, none of these tissues expressed cripto, and only 12% of the noninvolved normal colon samples adjacent to tumors or adenomas were positive for cripto. Cripto expression therefore appeared related to neoplasia. These data suggest that AR and cripto may be functioning as potential autocrine and/or paracrine growth factors in the colon and that the differential expression of cripto may serve as a potential tumor marker for colonic carcinogenesis. JF - Cancer research AU - Saeki, T AU - Stromberg, K AU - Qi, C F AU - Gullick, W J AU - Tahara, E AU - Normanno, N AU - Ciardiello, F AU - Kenney, N AU - Johnson, G R AU - Salomon, D S AD - Laboratory of Tumor Immunology and Biology, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1992/06/15/ PY - 1992 DA - 1992 Jun 15 SP - 3467 EP - 3473 VL - 52 IS - 12 SN - 0008-5472, 0008-5472 KW - AREG protein, human KW - 0 KW - Amphiregulin KW - Biomarkers, Tumor KW - EGF Family of Proteins KW - GPI-Linked Proteins KW - Glycoproteins KW - Growth Substances KW - Intercellular Signaling Peptides and Proteins KW - Membrane Glycoproteins KW - Neoplasm Proteins KW - RNA, Messenger KW - RNA, Neoplasm KW - TDGF1 protein, human KW - Epidermal Growth Factor KW - 62229-50-9 KW - Index Medicus KW - Phenotype KW - Adenoma -- chemistry KW - Tumor Cells, Cultured KW - Carcinoma -- chemistry KW - Humans KW - Colonic Polyps -- chemistry KW - Breast Neoplasms -- chemistry KW - Intestinal Mucosa -- chemistry KW - Immunoenzyme Techniques KW - Biomarkers, Tumor -- genetics KW - Growth Substances -- genetics KW - Glycoproteins -- analysis KW - RNA, Messenger -- analysis KW - RNA, Neoplasm -- analysis KW - Glycoproteins -- genetics KW - Colorectal Neoplasms -- chemistry KW - Neoplasm Proteins -- genetics KW - Biomarkers, Tumor -- analysis KW - Colon -- chemistry KW - Growth Substances -- analysis KW - Neoplasm Proteins -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72983620?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Tax+Journal&rft.atitle=Provincial+Budget+Roundup%2C+2002&rft.au=Deborah+L.+Ort*+and+David+B.+Perry**&rft.aulast=Deborah+L.+Ort*+and+David+B.+Perry**&rft.aufirst=&rft.date=2002-05-01&rft.volume=50&rft.issue=3&rft.spage=933&rft.isbn=&rft.btitle=&rft.title=Canadian+Tax+Journal&rft.issn=00085111&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-06 N1 - Date created - 1992-07-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dose-response relationships for chronic exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin in a rat tumor promotion model: quantification and immunolocalization of CYP1A1 and CYP1A2 in the liver. AN - 72982082; 1596902 AB - The mechanisms responsible for the braod spectrum of effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) are not entirely clear but seem to involve an initial interaction with the Ah receptor. A major uncertainty in risk assessment for TCDD is the lack of adequate dose-response relationships following chronic exposure to TCDD. Induction of cytochrome P-450 enzymes (CYP1A1 and CYP1A2) is one of the most sensitive responses to TCDD and its structural analogues. We have used a two-stage model for hepatocarcinogenesis in female Sprague-Dawley rats to evaluate dose-response relationships for induction of CYP1A1 and CYP1A2 in diethylnitrosamine-initiated as well as in noninitiated rats. After initiation with a single dose of diethylnitrosamine, TCDD was administered biweekly by p.o. gavage at doses equivalent to 3.5, 10.7, 35.7, and 125 ng/kg/day for 30 weeks. CYP1A1 and CYP1A2 concentrations were quantified in hepatic microsomes by radioimmunoassay and localized in hepatic tissue slices by immunohistochemical techniques. Radioimmunoassay data revealed a maximum induction of 200-fold for CYP1A1 and 10-fold for CYP1A2 and there were no statistically significant differences between initiated and noninitiated rats. Induction at the lowest dose (3.5 ng/kg/day) was 20-fold for CYP1A1 and 3-fold for CYP1A2. Mathematical analysis indicates that the best fit of the induction data are inconsistent with a threshold for this response. There was a linear relationship between administered dose and TCDD liver concentration over the entire dose range of the study. This indicates that induction of CYP1A2 does not significantly alter the distribution of TCDD in our chronic dosing regimen. Immunolocalization of CYP1A1 and CYP1A2 revealed the same localization and induction pattern for both isozymes in the cytoplasm of hepatocytes. However, the hepatic distribution pattern was not uniform with the most intense staining observed around central veins. These studies help to clarify dose-response relationships for dioxin-mediated effects and demonstrate different sensitivity of hepatocytes to the effects of TCDD. JF - Cancer research AU - Tritscher, A M AU - Goldstein, J A AU - Portier, C J AU - McCoy, Z AU - Clark, G C AU - Lucier, G W AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1992/06/15/ PY - 1992 DA - 1992 Jun 15 SP - 3436 EP - 3442 VL - 52 IS - 12 SN - 0008-5472, 0008-5472 KW - Isoenzymes KW - 0 KW - Polychlorinated Dibenzodioxins KW - Diethylnitrosamine KW - 3IQ78TTX1A KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Enzyme Induction -- drug effects KW - Dose-Response Relationship, Drug KW - Microsomes, Liver -- enzymology KW - Female KW - Cytochrome P-450 Enzyme System -- analysis KW - Isoenzymes -- analysis KW - Polychlorinated Dibenzodioxins -- analysis KW - Isoenzymes -- biosynthesis KW - Liver Neoplasms, Experimental -- enzymology KW - Liver Neoplasms, Experimental -- chemically induced KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Liver Neoplasms, Experimental -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72982082?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Dose-response+relationships+for+chronic+exposure+to+2%2C3%2C7%2C8-tetrachlorodibenzo-p-dioxin+in+a+rat+tumor+promotion+model%3A+quantification+and+immunolocalization+of+CYP1A1+and+CYP1A2+in+the+liver.&rft.au=Tritscher%2C+A+M%3BGoldstein%2C+J+A%3BPortier%2C+C+J%3BMcCoy%2C+Z%3BClark%2C+G+C%3BLucier%2C+G+W&rft.aulast=Tritscher&rft.aufirst=A&rft.date=1992-06-15&rft.volume=52&rft.issue=12&rft.spage=3436&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 - 1992-07-06 N1 - Date created - 1992-07-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR