TY - JOUR T1 - Whole-Word Training Therapy in a Stable Surface Alexic Patient: It Works AN - 85320370; llba-9204732 AB - An experimental therapy was developed to focus on whole-word reading. It was used with a surface alexic patient whose reading deficit had been stable for several years. The S practiced reading a list of words with ambiguous vowels. A control list of words with the same ambiguous vowels was not studied but was also tested. The S's reading of the studied words improved steadily over the training sessions. Performance on the control words varied considerably. It is concluded that impaired access to orthographic entries in the lexicon can be repaired with practice, but that generalization to similar words is more difficult to achieve. 1 Figure, 13 References. Adapted from the source document JF - Aphasiology AU - Friedman, Rhonda B AU - Robinson, Susan R AD - Cognitive Neuroscience Section NINDS/NIH, Bethesda MD 20892 Y1 - 1991/11// PY - 1991 DA - Nov 1991 SP - 521 EP - 527 VL - 5 IS - 6 SN - 0268-7038, 0268-7038 KW - whole-word reading therapy, surface alexic patient, training process KW - *Vowels (95650) KW - *Reading Processes (71150) KW - *Language Therapy (44400) KW - *Aphasia (03400) KW - *Ambiguity (01950) KW - article KW - 6410: language-pathological and normal; language-pathological and normal UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85320370?accountid=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=Aphasiology&rft.atitle=Whole-Word+Training+Therapy+in+a+Stable+Surface+Alexic+Patient%3A+It+Works&rft.au=Friedman%2C+Rhonda+B%3BRobinson%2C+Susan+R&rft.aulast=Friedman&rft.aufirst=Rhonda&rft.date=1991-11-01&rft.volume=5&rft.issue=6&rft.spage=521&rft.isbn=&rft.btitle=&rft.title=Aphasiology&rft.issn=02687038&rft_id=info:doi/ LA - English DB - ComDisDome N1 - Date revised - 2003-10-01 N1 - Last updated - 2014-06-17 N1 - CODEN - APHAEA N1 - SubjectsTermNotLitGenreText - *Aphasia (03400); *Language Therapy (44400); *Reading Processes (71150); *Vowels (95650); *Ambiguity (01950) ER - TY - JOUR T1 - Changing patterns of lung cancer incidence by histological type. AN - 72777333; 1845165 AB - Using data from five registries covering 7% of the U.S. population, we investigated lung carcinoma incidence trends from 1969-86 by histological type, sex, race, age, calendar time period, and cohort year of birth. Among white men, squamous cell carcinoma was the most frequent histological type, but by the mid-1980s the age-adjusted rates were decreasing while rates of adenocarcinoma and small (oat) cell carcinoma continued to rise. Among white women, adenocarcinoma was the most frequent type, followed by small cell carcinoma, with rates of all histological types rising over the entire study period. Similar time trends were seen among blacks. Rates for squamous cell carcinoma among both sexes and adenocarcinoma among men, however, were considerably higher for blacks than whites, whereas no racial disparity was seen for small cell carcinomas. Rates for each histological type were higher among men than women, although male-female sex ratios diminished over time. Age-specific rates varied considerably by cohort year of birth; incidence of squamous cell carcinoma among men increased steadily among those born from the late 1800s to the first quarter of this century before declining among those born thereafter. Cohort peaks were also reached, although about 10 to 20 years later, for small cell carcinoma and adenocarcinoma, suggesting an eventual reduction in incidence in these histological types as well. For each type, the peak incidence occurred earlier for men than women. These differing incidence patterns add to the evidence that the mechanisms of lung carcinogenesis may vary by histological type. JF - Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology AU - Devesa, S S AU - Shaw, G L AU - Blot, W J AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland 20892. PY - 1991 SP - 29 EP - 34 VL - 1 IS - 1 SN - 1055-9965, 1055-9965 KW - Index Medicus KW - Age Factors KW - Sex Factors KW - Humans KW - Continental Population Groups KW - Aged KW - Population Surveillance KW - Registries KW - Aged, 80 and over KW - Adult KW - Cohort Studies KW - Incidence KW - Middle Aged KW - United States -- epidemiology KW - Female KW - Male KW - Lung Neoplasms -- epidemiology KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72777333?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Changing+patterns+of+lung+cancer+incidence+by+histological+type.&rft.au=Devesa%2C+S+S%3BShaw%2C+G+L%3BBlot%2C+W+J&rft.aulast=Devesa&rft.aufirst=S&rft.date=1991-11-01&rft.volume=1&rft.issue=1&rft.spage=29&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 - 1993-07-08 N1 - Date created - 1993-07-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - [Exertion-induced low back pain: a case-control study of health service workers in a local health unit]. TT - Lombalgia da sforzo: studio caso-controllo tra i lavoratori dei servizi sanitari di una unità sanitaria locale. AN - 72704067; 1839429 AB - Data concerning all accidents with absence from work exceeding three days were analysed in a cohort of 5000 workers (all employees of a Local Health Unit). A total of 1062 accidents were recorded in the file from 1987 to 1989, 118 coded as "low-back injury". A case-control study design was used to detect the main causes of these accidents, using accidents coded as other than low-back injury as controls. The odds ratios and related confidence limits were calculated in order to assess the degree of association, taking account of potentially confounding factors. A significant relationship was observed between hospital wards and other health service departments rated as "high exposure" and low-back injury (OR high exposure versus low exposure = 2.13; 95% C.L. 1.06-4.29). Selection bias and its influence on the results is also discussed. JF - La Medicina del lavoro AU - Baldasseroni, A AU - Tartaglia, R AU - Biggeri, A AU - Carnevale, F AD - Servizio di Prevenzione, Igiene e Sicurezza nei Luoghi di Lavoro (SPISLL), Unità Sanitaria Locale 10/D, Firenze. PY - 1991 SP - 515 EP - 520 VL - 82 IS - 6 SN - 0025-7818, 0025-7818 KW - Index Medicus KW - Humans KW - Adult KW - Case-Control Studies KW - Adolescent KW - Male KW - Female KW - Back Pain -- etiology KW - Health Personnel KW - Occupational Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72704067?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=La+Medicina+del+lavoro&rft.atitle=%5BExertion-induced+low+back+pain%3A+a+case-control+study+of+health+service+workers+in+a+local+health+unit%5D.&rft.au=Baldasseroni%2C+A%3BTartaglia%2C+R%3BBiggeri%2C+A%3BCarnevale%2C+F&rft.aulast=Baldasseroni&rft.aufirst=A&rft.date=1991-11-01&rft.volume=82&rft.issue=6&rft.spage=515&rft.isbn=&rft.btitle=&rft.title=La+Medicina+del+lavoro&rft.issn=00257818&rft_id=info:doi/ LA - Italian DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-28 N1 - Date created - 1992-04-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Terephthalamidine: past and future. AN - 72700615; 1804802 AB - Terephthalamidine (NSC 57155) is one of 800 terephthalanilides and related compounds which were synthesized and tested preclinically in the late 1950's and early 1960's. Based upon their activity against murine leukemias, some of these agents were tested briefly in clinical trials at that time. Despite the observation of responses, the compounds were dropped because of severe and unusual neurotoxicity. More recently, terephthalamidine has been screened for antitumor activity and chosen for further clinical investigation by the NCI's Project for the Review of Old Drugs (P.R.O.D.) because of its novel structure and spectrum of preclinical activity. The current availability of a plasma assay for the drug permits further study of its clinical pharmacokinetics and pharmacodynamics and, perhaps, the development of improved scheduling strategies. JF - Investigational new drugs AU - Fisherman, J S AU - Cline, E M AU - Plowman, J AU - Quinn, F R AU - Hawkins, M J AD - Cancer Therapy Evaluation Program, National Cancer Institute, NIH, Bethesda MD. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 295 EP - 303 VL - 9 IS - 4 SN - 0167-6997, 0167-6997 KW - Antineoplastic Agents KW - 0 KW - Phthalimides KW - terephthalamidine KW - 15411-54-8 KW - Index Medicus KW - Molecular Structure KW - Animals KW - Forecasting KW - Phthalimides -- therapeutic use KW - Phthalimides -- pharmacology KW - Antineoplastic Agents -- therapeutic use KW - Antineoplastic Agents -- chemistry KW - Phthalimides -- chemistry KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72700615?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Investigational+new+drugs&rft.atitle=Terephthalamidine%3A+past+and+future.&rft.au=Fisherman%2C+J+S%3BCline%2C+E+M%3BPlowman%2C+J%3BQuinn%2C+F+R%3BHawkins%2C+M+J&rft.aulast=Fisherman&rft.aufirst=J&rft.date=1991-11-01&rft.volume=9&rft.issue=4&rft.spage=295&rft.isbn=&rft.btitle=&rft.title=Investigational+new+drugs&rft.issn=01676997&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-07 N1 - Date created - 1992-05-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inhibition of [3H]resiniferatoxin binding to rat dorsal root ganglion membranes as a novel approach in evaluating compounds with capsaicin-like activity. AN - 72697817; 1811172 AB - We have recently reported the specific binding of [3H]resiniferatoxin to sensory ganglion membranes; this binding appears to represent the postulated vanilloid (capsaicin) receptor. In the present report, we compare the structure/activity relations for binding to rat dorsal root ganglion membranes and for biological responses in the rat, using a series of vanilloids of the capsaicin (homovanilloyl-decylamide, homovanilloyl-dodecylamide, homovanilloyl-cyclododecylamide, homovanilloyl-hexadecylamide, homovanilloyl-piperidine and nonenoyl-homoveratrylamide) and resiniferatoxin (tinyatoxin, 12-deoxyphorbol 13-phenylacetate 20-homovanillate) classes. We find that all the tested biologically active vanilloids, but not the inactive structure analogs, compete for the [3H]resiniferatoxin binding sites in rat dorsal root ganglion membranes, and we conclude that the [3H]resiniferatoxin binding assay may provide an efficient approach for evaluating such compounds. We also provide evidence that the [3H]resiniferatoxin receptor is likely to recognize vanilloids which are inserted into the membranes; and that the apparent activity of capsaicinoids may be significantly influenced by factors other than equilibrium binding affinities. JF - Naunyn-Schmiedeberg's archives of pharmacology AU - Szallasi, A AU - Szolcsanyi, J AU - Szallasi, Z AU - Blumberg, P M AD - Molecular Mechanisms of Tumor Promotion Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 551 EP - 556 VL - 344 IS - 5 SN - 0028-1298, 0028-1298 KW - Diterpenes KW - 0 KW - resiniferatoxin KW - A5O6P1UL4I KW - Capsaicin KW - S07O44R1ZM KW - tinyatoxin KW - WN080Z1OL0 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Drug Interactions KW - Cell Membrane KW - Mice KW - Female KW - Structure-Activity Relationship KW - Binding Sites KW - Diterpenes -- toxicity KW - Ganglia, Spinal -- metabolism KW - Capsaicin -- metabolism KW - Capsaicin -- analogs & derivatives KW - Diterpenes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72697817?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Naunyn-Schmiedeberg%27s+archives+of+pharmacology&rft.atitle=Inhibition+of+%5B3H%5Dresiniferatoxin+binding+to+rat+dorsal+root+ganglion+membranes+as+a+novel+approach+in+evaluating+compounds+with+capsaicin-like+activity.&rft.au=Szallasi%2C+A%3BSzolcsanyi%2C+J%3BSzallasi%2C+Z%3BBlumberg%2C+P+M&rft.aulast=Szallasi&rft.aufirst=A&rft.date=1991-11-01&rft.volume=344&rft.issue=5&rft.spage=551&rft.isbn=&rft.btitle=&rft.title=Naunyn-Schmiedeberg%27s+archives+of+pharmacology&rft.issn=00281298&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-03 N1 - Date created - 1992-06-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Synthesis of homologous peptides using fragment condensation: analogs of an HIV proteinase substrate. AN - 72693693; 1802863 AB - Two protected peptides Boc-Val-Ser(Bzl)-Gln-Asn-Tyr(BrZ)OH and Boc-Val-Ser(Bzl)-Gln-Asn-Tyr(BrZ)-ProOH were synthesized on a resin substituted by 9-(hydroxymethyl)-2-fluoreneacetic acid. After cleavage with piperidine/DMF, desalting, and activation, these peptides were used for the synthesis of 11 analogs of an HIV proteinase nonapeptide substrate Val-Ser-Gln-Asn-Tyr-Pro-Ile-Val-Gln-NH2 using fragment condensation in solid phase. The fragment condensation was made in an ultrasonic bath. Using only 2 equivalents of the activated peptide in a DMF solution, this reaction was complete in 2 h. All nonapeptides were assayed as substrates for HIV-1 and HIV-2 proteinases. JF - International journal of peptide and protein research AU - Bláha, I AU - Nemec, J AU - Tözsér, J AU - Oroszlan, S AD - Laboratory of Molecular Virology and Carcinogenesis, PRI/DynCorp., NCI-Frederick Cancer Research and Development Center, MD. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 453 EP - 458 VL - 38 IS - 5 SN - 0367-8377, 0367-8377 KW - Oligopeptides KW - 0 KW - tert-butyloxycarbonyl-valyl-benzylseryl-glutaminyl-asparaginyl-(BrZ)tyrosine KW - 138865-76-6 KW - tert-butyloxycarbonyl-valyl-(benzyl)seryl-glutaminyl-asparaginyl-(BrZ)tyrosyl-proline KW - 138865-77-7 KW - HIV protease nonapeptide substrate KW - 61970-47-6 KW - Dimethylformamide KW - 8696NH0Y2X 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 Homology, Nucleic Acid KW - Dimethylformamide -- chemistry KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Substrate Specificity KW - Structure-Activity Relationship KW - Oligopeptides -- chemistry KW - Oligopeptides -- metabolism KW - HIV Protease -- metabolism KW - Oligopeptides -- chemical synthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72693693?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+peptide+and+protein+research&rft.atitle=Synthesis+of+homologous+peptides+using+fragment+condensation%3A+analogs+of+an+HIV+proteinase+substrate.&rft.au=Bl%C3%A1ha%2C+I%3BNemec%2C+J%3BT%C3%B6zs%C3%A9r%2C+J%3BOroszlan%2C+S&rft.aulast=Bl%C3%A1ha&rft.aufirst=I&rft.date=1991-11-01&rft.volume=38&rft.issue=5&rft.spage=453&rft.isbn=&rft.btitle=&rft.title=International+journal+of+peptide+and+protein+research&rft.issn=03678377&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-29 N1 - Date created - 1992-04-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The rat liver epithelial (RLE) cell protein database. AN - 72667631; 1794345 AB - Computer databases of rat liver epithelial (RLE) cellular polypeptides have been established using high resolution two-dimensional gel electrophoresis and computer-assisted analysis. Databases have been constructed utilizing both [35S]methionine- and [32P]orthophosphate-labeled as well as silver-stained polypeptides from normal RLE cells. The RLE database, which contains both qualitative and quantitative annotations, includes experiments with normal, chemically and oncogene transformed as well as spontaneously transformed cell lines. A total of 2537 [35S]methionine-labeled polypeptides from whole cell lysates (1920 acidic and 617 basic, separated in the first dimension using isoelectric focusing and nonequilibrium pH gradient electrophoresis, respectively) were analyzed and databases constructed using the Elsie 5 gel analysis system. To increase the "viewing window" and hence the usefulness of the RLE database, subcellular fractionation of whole cell preparations was performed and high resolution two-dimensional maps of the individual subcellular components were constructed. Databases representing 1229 cytosolic, 1539 acidic and 674 basic nuclear, 1746 membrane-associated, 415 mitochondrial, 773 in vitro translated and 350 phosphoproteins were established from these maps. The RLE databases contain the Elsie 5 identification number, protein name (if known), molecular weight and pI information, quantitative and spot shape data, and specific information regarding transformation-sensitive, growth-related (exponentially proliferating versus confluent) cell populations as well as those polypeptides modulated by specific growth factors. The RLE databases represent initial efforts toward the establishment of comprehensive databases of rat liver proteins and serve as a vital resource for on-going as well as future studies regarding the regulation of growth and differentiation as well as transformation of RLE cells. JF - Electrophoresis AU - Wirth, P J AU - Luo, L D AU - Fujimoto, Y AU - Bisgaard, H C AU - Olson, A D AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 931 EP - 954 VL - 12 IS - 11 SN - 0173-0835, 0173-0835 KW - Cytoskeletal Proteins KW - 0 KW - Index Medicus KW - Animals KW - Mitochondria, Liver -- chemistry KW - Subcellular Fractions -- chemistry KW - Cell Nucleus -- chemistry KW - Cytoskeletal Proteins -- chemistry KW - Rats KW - Rats, Inbred F344 KW - Epithelial Cells KW - Cells, Cultured KW - Electrophoresis, Gel, Two-Dimensional KW - Cell Membrane -- chemistry KW - Protein Biosynthesis -- genetics KW - Cytosol -- chemistry KW - Image Processing, Computer-Assisted KW - Epithelium -- chemistry KW - Female KW - Liver -- cytology KW - Databases, Factual KW - Liver -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72667631?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Electrophoresis&rft.atitle=The+rat+liver+epithelial+%28RLE%29+cell+protein+database.&rft.au=Wirth%2C+P+J%3BLuo%2C+L+D%3BFujimoto%2C+Y%3BBisgaard%2C+H+C%3BOlson%2C+A+D&rft.aulast=Wirth&rft.aufirst=P&rft.date=1991-11-01&rft.volume=12&rft.issue=11&rft.spage=931&rft.isbn=&rft.btitle=&rft.title=Electrophoresis&rft.issn=01730835&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-08 N1 - Date created - 1992-04-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - CD8 gamma delta cells: presence in the adult rat thymus and generation in vitro from CD4-/CD8- thymocytes in the presence of interleukin 2. AN - 72654071; 1838702 AB - Three to fifteen percent of peripheral T cells in adults express the recently described gamma delta T-cell antigen receptor (TcR) heterodimer. A small subpopulation of gamma delta cells express the CD8 accessory molecule. In this study, we analyzed the potential of highly purified CD4-/CD8-, double negative (DN) rat precursor thymocytes to give rise to gamma delta cells. We observed that in the presence of interleukin 2 (IL-2) and concanavalin A (ConA), both DN and CD8 cells expressing the gamma delta TcR were generated in vitro. We then examined the rat thymus for these cells and confirmed the presence of a previously undescribed CD8 TcR-alpha beta- subset in the rat thymus, expressing high levels of TcR-gamma and delta messages with no detectable TcR-alpha transcripts, similar to the cells generated in vitro in the presence of IL-2 and ConA. JF - Cytokine AU - Gotlieb, W H AU - Takacs, L AU - Finch, L R AU - Kopp, W AU - Weissman, A M AU - Durum, S K AD - Biological Carcinogenesis Development Program, Program Resources Inc., NCI-Frederick Cancer Research and Development Center, Frederick, MD. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 598 EP - 608 VL - 3 IS - 6 SN - 1043-4666, 1043-4666 KW - Antigens, CD4 KW - 0 KW - Antigens, CD8 KW - Interleukin-2 KW - RNA, Messenger KW - Receptors, Antigen, T-Cell, alpha-beta KW - Receptors, Antigen, T-Cell, gamma-delta KW - Concanavalin A KW - 11028-71-0 KW - Index Medicus KW - Rats KW - Animals KW - Antigens, CD4 -- analysis KW - Antigens, CD8 -- analysis KW - RNA, Messenger -- analysis KW - Receptors, Antigen, T-Cell, alpha-beta -- drug effects KW - Cells, Cultured -- drug effects KW - Cell Separation KW - Cell Differentiation -- drug effects KW - Rats, Inbred BUF KW - Concanavalin A -- pharmacology KW - Receptors, Antigen, T-Cell, gamma-delta -- drug effects KW - Thymus Gland -- immunology KW - Thymus Gland -- cytology KW - Interleukin-2 -- pharmacology KW - T-Lymphocyte Subsets -- drug effects KW - Receptors, Antigen, T-Cell, gamma-delta -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72654071?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cytokine&rft.atitle=CD8+gamma+delta+cells%3A+presence+in+the+adult+rat+thymus+and+generation+in+vitro+from+CD4-%2FCD8-+thymocytes+in+the+presence+of+interleukin+2.&rft.au=Gotlieb%2C+W+H%3BTakacs%2C+L%3BFinch%2C+L+R%3BKopp%2C+W%3BWeissman%2C+A+M%3BDurum%2C+S+K&rft.aulast=Gotlieb&rft.aufirst=W&rft.date=1991-11-01&rft.volume=3&rft.issue=6&rft.spage=598&rft.isbn=&rft.btitle=&rft.title=Cytokine&rft.issn=10434666&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-31 N1 - Date created - 1992-03-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Activation of cholera toxin and Escherichia coli heat-labile enterotoxins by ADP-ribosylation factors, a family of 20 kDa guanine nucleotide-binding proteins. AN - 72629376; 1779753 AB - Cholera toxin and Escherichia coli heat-labile enterotoxins are responsible, in part, for the symptomatology of cholera and traveller's diarrhoea, respectively. Effects of the toxins result from ADP-ribosylation of regulatory guanine nucleotide-binding (G) proteins; the ADP-ribosylated G protein is stabilized in an activated state, resulting in prolonged effects on its target. Toxin-catalysed ADP-ribosylation is stimulated in vitro by a family of guanine nucleotide-binding proteins, c. 20 kDa, termed ADP-ribosylation factors or ARFs. In the presence of GTP, but not GDP or adenine analogues, ARFs serve as allosteric activators of the toxin. The effects are amplified by certain phospholipids and detergents which promote guanine nucleotide binding. Six different mammalian ARF genes have been identified. They encode highly conserved, ubiquitous proteins of 175 to 181 amino acids, containing consensus domains responsible for guanine nucleotide binding. Differences in amino acid sequences are localized near the amino terminus and in the carboxy half of the protein. Although the physiological functions of ARFs have not been precisely defined, their immunological localization to the Golgi is consistent with a role in the regulated orderly movement of newly synthesized proteins from the endoplasmic reticulum, through the Golgi system to their ultimate destination. JF - Molecular microbiology 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 - 1991/11// PY - 1991 DA - November 1991 SP - 2621 EP - 2627 VL - 5 IS - 11 SN - 0950-382X, 0950-382X KW - ARF KW - ARF 1 KW - ARF 2 KW - ARF 4 KW - ARF 6 KW - Bacterial Proteins KW - 0 KW - Bacterial Toxins KW - Enterotoxins KW - Escherichia coli Proteins KW - Fungal Proteins KW - heat-labile enterotoxin, E coli KW - Adenosine Diphosphate Ribose KW - 20762-30-5 KW - Guanosine Triphosphate KW - 86-01-1 KW - Cholera Toxin KW - 9012-63-9 KW - Poly(ADP-ribose) Polymerases KW - EC 2.4.2.30 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - ADP-Ribosylation Factors KW - EC 3.6.5.2 KW - Index Medicus KW - Saccharomyces cerevisiae -- genetics KW - Animals KW - Genes KW - Sequence Homology, Nucleic Acid KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Fungal Proteins -- genetics KW - Mammals -- genetics KW - Guanosine Triphosphate -- metabolism KW - Escherichia coli -- metabolism KW - Bacterial Toxins -- metabolism KW - Enterotoxins -- metabolism KW - GTP-Binding Proteins -- metabolism KW - Bacterial Proteins -- metabolism KW - Vibrio cholerae -- metabolism KW - Adenosine Diphosphate Ribose -- metabolism KW - Poly(ADP-ribose) Polymerases -- metabolism KW - GTP-Binding Proteins -- genetics KW - Cholera Toxin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72629376?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Activation+of+cholera+toxin+and+Escherichia+coli+heat-labile+enterotoxins+by+ADP-ribosylation+factors%2C+a+family+of+20+kDa+guanine+nucleotide-binding+proteins.&rft.au=Moss%2C+J%3BVaughan%2C+M&rft.aulast=Moss&rft.aufirst=J&rft.date=1991-11-01&rft.volume=5&rft.issue=11&rft.spage=2621&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 - 1992-03-10 N1 - Date created - 1992-03-10 N1 - Date revised - 2017-01-13 N1 - Gene symbol - ARF; ARF 1; ARF 2; ARF 4; ARF 6 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The bovine chromogranin A gene: structural basis for hormone regulation and generation of biologically active peptides. AN - 72628232; 1779968 AB - The structure of the gene encoding bovine chromogranin-A has been determined by characterization of two isolated genomic clones. Chromogranin-A is encoded by eight exons, which organize the coding region into several distinct structural and functional domains. Exons 1-5 represent the highly conserved signal peptide and N-terminal domain, which are separated into regions corresponding to the signal peptide, N-terminal sequence, disulfide-bonded loop, and remainder of the conserved N-terminal domain. Exon 6 represents the variable domain and encodes a region that is identical to the novel chromogranin-A-derived peptide chromostatin. Exon 7 encodes the biologically active peptide pancreastatin as well as most of the conserved C-terminal domain, with the remainder found on exon 8. The mRNA sequence obtained from the gene contains five nucleotide differences from the consensus sequence of four reported bovine chromogranin-A cDNA clones. Two of the differences in the gene result in two amino acid changes in the region encoded by exon 6. The structural organization of the chromogranin-A gene resembles that of the chromogranin-B gene in the exons corresponding to the signal peptide, N-terminal sequence, disulfide loop, and C-terminal sequence.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Molecular endocrinology (Baltimore, Md.) AU - Iacangelo, A L AU - Grimes, M AU - Eiden, L E AD - Unit on Molecular and Cellular Neurobiology, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 1651 EP - 1660 VL - 5 IS - 11 SN - 0888-8809, 0888-8809 KW - Chromogranin A KW - 0 KW - Chromogranins KW - Oligodeoxyribonucleotides KW - RNA, Messenger KW - chromogranin A, mouse KW - Colforsin KW - 1F7A44V6OU KW - Dexamethasone KW - 7S5I7G3JQL KW - DNA KW - 9007-49-2 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Sequence Homology, Nucleic Acid KW - Dexamethasone -- pharmacology KW - Transcription, Genetic KW - Genomic Library KW - RNA, Messenger -- genetics KW - Colforsin -- pharmacology KW - Promoter Regions, Genetic KW - Blotting, Southern KW - Molecular Sequence Data KW - Gene Expression Regulation KW - Adrenal Medulla -- drug effects KW - Adrenal Medulla -- cytology KW - Amino Acid Sequence KW - Mice KW - Binding Sites KW - Cloning, Molecular KW - DNA -- isolation & purification KW - Cattle KW - Base Sequence KW - Cells, Cultured KW - Restriction Mapping KW - DNA -- genetics KW - Adrenal Medulla -- physiology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - TATA Box KW - Cell Line KW - Chromogranins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72628232?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+bovine+chromogranin+A+gene%3A+structural+basis+for+hormone+regulation+and+generation+of+biologically+active+peptides.&rft.au=Iacangelo%2C+A+L%3BGrimes%2C+M%3BEiden%2C+L+E&rft.aulast=Iacangelo&rft.aufirst=A&rft.date=1991-11-01&rft.volume=5&rft.issue=11&rft.spage=1651&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 - 1992-03-10 N1 - Date created - 1992-03-10 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - S79258; GENBANK; S79270; S79260; M64566; S79256; S79262; S79264; S79266; S79277; S79268 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Growth and branching morphogenesis of rat collecting duct anlagen in the absence of metanephrogenic mesenchyme. AN - 72627955; 1773916 AB - The growth and differentiation of the epithelium in many tissues is mediated by interactions with the adjacent mesenchyme, but the mechanisms responsible remain undefined. To identify the factors involved in the growth and branching morphogenesis of ureteric bud, which is the collecting duct anlagen, buds from 13-gestation-day rat embryos were separated from the metanephrogenic mesenchyme and explanted to culture dishes coated with gelled type I collagen in a defined medium. Under these conditions buds attached to the substrate and grew out without indication of cell senescence. When buds were instead suspended in gelled type I collagen, branching morphogenesis was observed despite the absence of mesenchyme although it was not as extensive as in vivo. Since growth occurred much more slowly in culture than expected, culture conditions were varied in attempts to accelerate the process. Despite extensive screening of matrices and growth factors, only epidermal and endothelial cell growth factors stimulated growth to a significant extent. Transforming growth factor-beta, on the other hand, was a potent inhibitor of growth. Homogenates from tumors that caricature metanephrogenic mesenchyme were highly mitogenic for bud cells and, thus, will be a source of material for characterizing regulatory factors involved in renal growth. These studies show that growth and branching morphogenesis of the ureteric bud can occur without direct cell-cell interactions with the metanephrogenic mesenchyme and that matrices and factors secreted by the mesenchyme may mediated these activities in vivo. JF - Differentiation; research in biological diversity AU - Perantoni, A O AU - Williams, C L AU - Lewellyn, A L AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick, MD 21702. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 107 EP - 113 VL - 48 IS - 2 SN - 0301-4681, 0301-4681 KW - Culture Media, Serum-Free KW - 0 KW - Endothelial Growth Factors KW - Transforming Growth Factor beta KW - Epidermal Growth Factor KW - 62229-50-9 KW - Collagen KW - 9007-34-5 KW - Index Medicus KW - Stem Cells -- drug effects KW - Endothelial Growth Factors -- pharmacology KW - Transforming Growth Factor beta -- pharmacology KW - Animals KW - Kidney Neoplasms -- pathology KW - Stem Cells -- physiology KW - Epidermal Growth Factor -- pharmacology KW - Rats KW - Rats, Inbred F344 KW - Stem Cells -- cytology KW - Tumor Cells, Cultured KW - Cell Differentiation -- physiology KW - Culture Media, Serum-Free -- pharmacology KW - Cell Differentiation -- drug effects KW - Female KW - Male KW - Kidney Tubules, Collecting -- cytology KW - Kidney Tubules, Collecting -- physiology KW - Morphogenesis -- physiology KW - Mesoderm -- physiology KW - Morphogenesis -- drug effects KW - Mesoderm -- cytology KW - Kidney Tubules, Collecting -- embryology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72627955?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Differentiation%3B+research+in+biological+diversity&rft.atitle=Growth+and+branching+morphogenesis+of+rat+collecting+duct+anlagen+in+the+absence+of+metanephrogenic+mesenchyme.&rft.au=Perantoni%2C+A+O%3BWilliams%2C+C+L%3BLewellyn%2C+A+L&rft.aulast=Perantoni&rft.aufirst=A&rft.date=1991-11-01&rft.volume=48&rft.issue=2&rft.spage=107&rft.isbn=&rft.btitle=&rft.title=Differentiation%3B+research+in+biological+diversity&rft.issn=03014681&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-03 N1 - Date created - 1992-03-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interleukin-1 alpha and tumor necrosis factor-alpha (TNF alpha) inhibit growth and induce TNF messenger RNA in MCF-7 human breast cancer cells. AN - 72615740; 1779975 AB - We studied the effects of interleukin-1 alpha (IL-1) and tumor necrosis factor-alpha (TNF), alone and in combination, on MCF-7 breast cancer cells to determine whether these cytokines alter cell growth, TNF gene expression, and TNF secretion. We found that IL-1 alone and TNF alone inhibited cell growth in a dose-dependent manner. Each cytokine arrested growth in the G0/G1 phase of the cell cycle, with maximum growth inhibition at 1000 U/ml (P less than 0.05) and 100 U/ml (P less than 0.01), respectively. However, the combination of these two cytokines did not result in greater growth inhibition or a greater percentage of cells arrested in the G0/G1 phase of the cell cycle compared with each cytokine alone. We examined the effect of exogenous IL-1 and TNF on TNF gene expression by Northern blot analysis. In the absence of any cytokine, these cells do not express TNF mRNA. Exposure to IL-1 (1000 U/ml) induced TNF mRNA at 3 h; however, mRNA levels diminished thereafter to barely detectable levels by 24 h. Exposure to TNF (1000 U/ml) also induced TNF mRNA at 3 h, but in contrast to IL-1, the level of enhanced expression persisted at these levels through 72 h of exposure. Secretion of TNF by these cells is induced by exogenous TNF, but not by IL-1. IL-1 and TNF in combination do not produce greater inhibition of growth, greater amounts of TNF mRNA at 3 h, or greater secretion of TNF than that produced by TNF alone.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Molecular endocrinology (Baltimore, Md.) AU - Sgagias, M K AU - Kasid, A AU - Danforth, D N AD - Surgery Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 1740 EP - 1747 VL - 5 IS - 11 SN - 0888-8809, 0888-8809 KW - DNA, Neoplasm KW - 0 KW - Interleukin-1 KW - RNA, Messenger KW - Recombinant Proteins KW - Tumor Necrosis Factor-alpha KW - Index Medicus KW - Drug Interactions KW - Recombinant Proteins -- pharmacology KW - Blotting, Northern KW - Dose-Response Relationship, Drug KW - Kinetics KW - Humans KW - Breast Neoplasms KW - DNA, Neoplasm -- analysis KW - Female KW - Cell Line KW - Cell Cycle -- drug effects KW - Interleukin-1 -- pharmacology KW - RNA, Messenger -- metabolism KW - Tumor Necrosis Factor-alpha -- pharmacology KW - RNA, Messenger -- drug effects KW - Cell Division -- drug effects KW - RNA, Messenger -- genetics KW - Tumor Necrosis Factor-alpha -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72615740?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Interleukin-1+alpha+and+tumor+necrosis+factor-alpha+%28TNF+alpha%29+inhibit+growth+and+induce+TNF+messenger+RNA+in+MCF-7+human+breast+cancer+cells.&rft.au=Sgagias%2C+M+K%3BKasid%2C+A%3BDanforth%2C+D+N&rft.aulast=Sgagias&rft.aufirst=M&rft.date=1991-11-01&rft.volume=5&rft.issue=11&rft.spage=1740&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 - 1992-03-10 N1 - Date created - 1992-03-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Mol Endocrinol 1992 Apr;6(4):620 N1 - Last updated - 2017-01-17 ER - TY - CONF T1 - Symposium on indirect mechanisms of immune modulation. AN - 72608703; 1685714 JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Sanders, V M AU - Fuchs, B A AU - Pruett, S B AU - Kerkvliet, N I AU - Kaminski, N E Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 641 EP - 650 VL - 17 IS - 4 KW - Adjuvants, Immunologic KW - 0 KW - Xenobiotics KW - Index Medicus KW - Animals KW - Humans KW - Xenobiotics -- toxicity KW - Adjuvants, Immunologic -- pharmacology KW - Immunity -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72608703?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&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=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.atitle=Symposium+on+indirect+mechanisms+of+immune+modulation.&rft.au=Sanders%2C+V+M%3BFuchs%2C+B+A%3BPruett%2C+S+B%3BKerkvliet%2C+N+I%3BKaminski%2C+N+E&rft.aulast=Sanders&rft.aufirst=V&rft.date=1991-11-01&rft.volume=17&rft.issue=4&rft.spage=641&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 - 1992-03-06 N1 - Date created - 1992-03-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inorganic particles induce secretion of a macrophage homologue of platelet-derived growth factor in a density-and time-dependent manner in vitro. AN - 72608493; 1663030 AB - The inhalation of inorganic dust can lead to the development of interstitial pulmonary fibrosis, characterized by the accumulation of fibroblasts and connective tissue matrix in the lung interstitium. The fibrosis causes alterations in the architecture of the lung parenchyma, resulting in abnormal gas exchange and hypoxemia. In a rat model of asbestos exposure, inhaled fibers are deposited on alveolar duct bifurcations, followed by an accumulation of alveolar macrophages at the sites of dust deposition. The alveolar macrophage is thought to be a major mediator of the pulmonary inflammatory response to inhaled dust. Platelet-derived growth factor (PDGF) is a cytokine that has potent chemotactic and mitogenic effects on mesenchymal cells, such as fibroblasts and smooth muscle cells. We studied the secretion of an alveolar macrophage-derived homologue of PDGF in response to carbonyl iron spheres or chrysotile asbestos fibers in vitro. We demonstrate here that rat alveolar macrophages attached to a plastic substrate produce 69 +/- 79 picograms (pg) of PDGF per 10 million macrophages. This is similar to amounts recovered from human platelets. In contrast, macrophages exposed to iron spheres secrete 429 +/- 177 pg of PDGF/10(6) macrophages after 24 h in culture. Exposure to asbestos fibers increased the PDGF production to 628 +/- 213 pg/10(6) cells. PDGF secretion was influenced by the particles in a density- and time-dependent manner. We hypothesize that PDGF and other cytokines secreted by macrophages mediate the development of dust-induced lung disease. JF - Experimental lung research AU - Schapira, R M AU - Osornio-Vargas, A R AU - Brody, A R AD - Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. PY - 1991 SP - 1011 EP - 1024 VL - 17 IS - 6 SN - 0190-2148, 0190-2148 KW - Asbestos, Serpentine KW - 0 KW - Dust KW - Organometallic Compounds KW - Platelet-Derived Growth Factor KW - Asbestos KW - 1332-21-4 KW - Iron Carbonyl Compounds KW - 13463-40-6 KW - Index Medicus KW - Animals KW - Cell Count KW - Pulmonary Alveoli -- secretion KW - Pulmonary Alveoli -- cytology KW - Phagocytosis KW - Time Factors KW - Microscopy, Electron, Scanning KW - Macrophages -- secretion KW - Platelet-Derived Growth Factor -- secretion KW - Macrophages -- physiology KW - Macrophages -- ultrastructure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72608493?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+lung+research&rft.atitle=Inorganic+particles+induce+secretion+of+a+macrophage+homologue+of+platelet-derived+growth+factor+in+a+density-and+time-dependent+manner+in+vitro.&rft.au=Schapira%2C+R+M%3BOsornio-Vargas%2C+A+R%3BBrody%2C+A+R&rft.aulast=Schapira&rft.aufirst=R&rft.date=1991-11-01&rft.volume=17&rft.issue=6&rft.spage=1011&rft.isbn=&rft.btitle=&rft.title=Experimental+lung+research&rft.issn=01902148&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-27 N1 - Date created - 1992-02-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Radiation-induced chromatid aberrations in Cockayne syndrome and xeroderma pigmentosum group C fibroblasts in relation to cancer predisposition. AN - 72577332; 1756475 AB - We showed previously that the persistence of chromatid breaks and gaps after G2 phase irradiation with X-rays or near-UV visible light characterizes skin fibroblasts from individuals with cancer-prone genetic diseases. This abnormal response appears to result from deficient DNA repair during G2 and to be associated with cancer proneness. We have, therefore, compared the responses of cells from two genetic disorders, Cockayne syndrome (CS) and xeroderma pigmentosum complementation group C(XP-C), both of which exhibit cellular hypersensitivity to sunlight, but only one of which, XP, manifests a high rate of sunlight-induced cancer. CS cells, in contrast to XP cells, showed a normal G2 response to irradiation with either X-rays or near-UV visible light. However, CS cells showed a deficiency in repair of DNA damage inflicted by light during S and G1 phases of the cell cycle. The present results support the concept that deficient DNA repair during G2 phase plays a role in carcinogenesis. This deficient repair in the presence of DNA damage and continuous cell cycling from activation of proto-oncogenes or loss of suppressor genes may be necessary and sufficient for cancer development. JF - Cancer genetics and cytogenetics AU - Price, F M AU - Parshad, R AU - Tarone, R E AU - Sanford, K K AD - Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 1 EP - 10 VL - 57 IS - 1 SN - 0165-4608, 0165-4608 KW - Cytarabine KW - 04079A1RDZ KW - Index Medicus KW - Cytarabine -- pharmacology KW - Causality KW - X-Rays KW - DNA Repair KW - Cells, Cultured KW - Humans KW - In Vitro Techniques KW - Chromatids -- radiation effects KW - Chromosome Aberrations KW - Neoplasms -- genetics KW - Cockayne Syndrome -- genetics KW - Xeroderma Pigmentosum -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72577332?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+genetics+and+cytogenetics&rft.atitle=Radiation-induced+chromatid+aberrations+in+Cockayne+syndrome+and+xeroderma+pigmentosum+group+C+fibroblasts+in+relation+to+cancer+predisposition.&rft.au=Price%2C+F+M%3BParshad%2C+R%3BTarone%2C+R+E%3BSanford%2C+K+K&rft.aulast=Price&rft.aufirst=F&rft.date=1991-11-01&rft.volume=57&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Cancer+genetics+and+cytogenetics&rft.issn=01654608&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-04 N1 - Date created - 1992-02-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Gene-specific repair of DNA damage induced by UV irradiation and cancer chemotherapeutics. AN - 72571785; 1760244 AB - DNA repair processes are critically important in the prevention of carcinogenesis, and currently much research is directed toward elucidation of the biochemical mechanisms by which DNA repair occurs. Techniques have been developed for examining individual genes to quantitate the lesions induced by various chemotherapeutic agents and to measure the rate of gene-specific DNA repair. In mammalian cells, the DNA repair response exhibits intragenomic heterogeneity-active genes are preferentially repaired and the transcribed strand of DNA is repaired more rapidly than the nontranscribed strand. These studies have provided new insight into the molecular biology of DNA repair and a new perspective on the role of repair processes in cellular resistance to DNA damage and malignancy. Elucidation of the mechanisms by which gene-specific lesions are formed and repaired will be important if we are to understand the fundamental processes of malignancy. JF - Cancer cells (Cold Spring Harbor, N.Y. : 1989) AU - Link, C J AU - Burt, R K AU - Bohr, V A AD - Laboratory of Molecular Pharmacology, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 427 EP - 436 VL - 3 IS - 11 SN - 1042-2196, 1042-2196 KW - Antineoplastic Agents KW - 0 KW - Pyrimidine Dimers KW - Tetrahydrofolate Dehydrogenase KW - EC 1.5.1.3 KW - Index Medicus KW - Animals KW - Ultraviolet Rays KW - Pyrimidine Dimers -- metabolism KW - Humans KW - Drug Resistance KW - Tetrahydrofolate Dehydrogenase -- genetics KW - Genes KW - DNA Repair KW - DNA Damage KW - Antineoplastic Agents -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72571785?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+cells+%28Cold+Spring+Harbor%2C+N.Y.+%3A+1989%29&rft.atitle=Gene-specific+repair+of+DNA+damage+induced+by+UV+irradiation+and+cancer+chemotherapeutics.&rft.au=Link%2C+C+J%3BBurt%2C+R+K%3BBohr%2C+V+A&rft.aulast=Link&rft.aufirst=C&rft.date=1991-11-01&rft.volume=3&rft.issue=11&rft.spage=427&rft.isbn=&rft.btitle=&rft.title=Cancer+cells+%28Cold+Spring+Harbor%2C+N.Y.+%3A+1989%29&rft.issn=10422196&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-12 N1 - Date created - 1992-02-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Retinoids and their receptors in differentiation, embryogenesis, and neoplasia. AN - 72561655; 1661245 AB - The crucial role of retinoids in controlling differentiation processes has become evident from studies conducted in a variety of in vivo and in vitro systems. Most striking is the role of retinoic acid as a morphogenic substance in vertebrate limb development, but equally important is its role in the maintenance of epithelial integrity in most superficial linings of the body. The similarity of the mode of action of retinoids to that of the steroid and thyroid hormones has recently been demonstrated with the discovery of the nuclear receptors for retinoic acid, which belong to the steroid/thyroid hormone receptor superfamily. These receptors act as transcriptional activators by binding as heterodimers to specific nucleotide sequences in the response elements of target genes. Response elements for retinoic acid have so far been identified for the rat growth hormone and phosphoenolpyruvate carboxykinase, the mouse complement H and laminin B1, the human and mouse retinoic acid receptor beta, the human osteocalcin, and the human alcohol dehydrogenase genes. The retinoic acid response element (RARE) for the rat growth hormone gene is also a thyroid hormone response element (TRE), and the AP-1 binding site of the human osteocalcin promoter is also a vitamin D response element (VDRE) and a RARE. Both these elements are palindromic. Other RAREs have a direct repeat configuration of the half-site motif AGGTCA separated by five nucleotides (AGGTCA xxxxx AGGTCA). The direct repeat arrangement of the same core motif AGGTCA separated by three or four nucleotides becomes a VDRE or TRE, respectively. A point mutation has been identified in the RAR alpha gene of embryonal carcinoma cells resistant to retinoic acid. In addition to the three retinoic acid receptors (alpha, beta, gamma) belonging to the steroid/thyroid hormone receptor superfamily, a second class of retinoid receptors (RXR) alpha, beta, gamma has also been characterized and its relatedness to a gene, XR2C, of the locus ultraspiracle required for pattern formation in Drosophila has been established. That would suggest that both vertebrates and invertebrates may require similar transcriptional activators during morphogenesis. An RXRE has been identified in the CRBPII gene promoter and it contains five repeats of the canonical sequence AGGTCA separated by one nucleotide. The importance of retinoids, both as chemopreventive agents of tumorigenesis and potent differentiation inducers of neoplastic cells, can only be emphasized by the recent finding that the t(15;17) (q21- q11-22) translocation, specifically associated with acute promyelocytic leukemia, also causes translocation of the retinoic acid receptor alpha gene and its fusion with with a new locus, myl, of unknown function.(ABSTRACT TRUNCATED AT 250 WORDS) JF - FASEB journal : official publication of the Federation of American Societies for Experimental Biology AU - De Luca, L M AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 2924 EP - 2933 VL - 5 IS - 14 SN - 0892-6638, 0892-6638 KW - Carrier Proteins KW - 0 KW - Receptors, Retinoic Acid KW - Retinoids KW - Index Medicus KW - Animals KW - Base Sequence KW - Humans KW - Molecular Sequence Data KW - Embryonic and Fetal Development KW - Cell Differentiation KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72561655?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Retinoids+and+their+receptors+in+differentiation%2C+embryogenesis%2C+and+neoplasia.&rft.au=De+Luca%2C+L+M&rft.aulast=De+Luca&rft.aufirst=L&rft.date=1991-11-01&rft.volume=5&rft.issue=14&rft.spage=2924&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 - 1992-01-29 N1 - Date created - 1992-01-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression of transforming growth factor-beta 1 during chemical hepatocarcinogenesis in the rat. AN - 72556960; 1753701 AB - Cellular distribution of both transcripts and protein of transforming growth factor (TGF)-beta 1 was studied in preneoplastic nodules (6 cases) and primary hepatic carcinomas (16 hepatocellular carcinomas and 2 mixed tumors of hepatocellular carcinoma and cholangiocellular carcinoma) produced by Solt-Farber's protocol in rats using in situ hybridization and immunohistochemistry. The TGF-beta 1 transcripts were primarily observed in nonparenchymal cells, some of which were desmin-positive perisinusoidal cells, surrounding or within the preneoplastic nodules or carcinomas. The distribution of latent TGF-beta 1 protein was similar to the transcripts. However, mature TGF-beta 1, which was identified with CC-antibody, was only detected in nonparenchymal cells and connective tissue associated with carcinomas, but was not observed in preneoplastic nodules or in normal liver with the exception of the periportal space. There was no difference in TGF-beta 1 expression associated with tumor types or the differentiation status of primary hepatic carcinomas. The present study demonstrates that nonparenchymal cells, particularly desmin-positive perisinusoidal cells, are the principal source of TGF-beta 1 production during hepatocarcinogenesis. Furthermore, the data suggest that the close interaction between nonparenchymal cells and carcinoma cells may be necessary for the activation of latent TGF-beta 1. It is hypothesized that regulatory effects of TGF-beta 1 on growth of preneoplastic or carcinoma cells in the liver are exerted via paracrine mechanism. JF - Laboratory investigation; a journal of technical methods and pathology AU - Nakatsukasa, H AU - Evarts, R P AU - Hsia, C C AU - Marsden, E AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 511 EP - 517 VL - 65 IS - 5 SN - 0023-6837, 0023-6837 KW - Transforming Growth Factor beta KW - 0 KW - Index Medicus KW - Rats KW - Animals KW - Reference Values KW - Rats, Inbred F344 KW - Liver -- pathology KW - Liver -- metabolism KW - Precancerous Conditions -- metabolism KW - Nucleic Acid Hybridization KW - Immunohistochemistry KW - Liver Neoplasms -- pathology KW - Liver Neoplasms -- metabolism KW - Carcinoma -- pathology KW - Liver Neoplasms -- chemically induced KW - Carcinoma -- metabolism KW - Transforming Growth Factor beta -- metabolism KW - Carcinoma -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72556960?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+transforming+growth+factor-beta+1+during+chemical+hepatocarcinogenesis+in+the+rat.&rft.au=Nakatsukasa%2C+H%3BEvarts%2C+R+P%3BHsia%2C+C+C%3BMarsden%2C+E%3BThorgeirsson%2C+S+S&rft.aulast=Nakatsukasa&rft.aufirst=H&rft.date=1991-11-01&rft.volume=65&rft.issue=5&rft.spage=511&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 - 1992-01-30 N1 - Date created - 1992-01-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Suitability of Chinese oil well loggers for an epidemiologic study of the carcinogenic effects of neutrons. AN - 72552426; 1752747 AB - Neutron exposures to 191 well loggers at four oil fields in China were measured over a 3-mo period using CR-39 polycarbonate dosimeters. Doses (96% less than 0.02 mGy) were slightly lower than literature values for well loggers in North America, possibly because of differences in drilling activity. Because doses are so low, an epidemiologic study of cancer among Chinese well loggers is unlikely to be informative about the carcinogenicity of neutrons relative to sparsely ionizing radiation. JF - Health physics AU - Inskip, P D AU - Wang, Z Y AU - Fen, Y S AD - Radiation Epidemiology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 637 EP - 640 VL - 61 IS - 5 SN - 0017-9078, 0017-9078 KW - Petroleum KW - 0 KW - Index Medicus KW - Humans KW - China KW - Occupational Exposure KW - Neutrons KW - Occupational Health KW - Neoplasms, Radiation-Induced -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72552426?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Suitability+of+Chinese+oil+well+loggers+for+an+epidemiologic+study+of+the+carcinogenic+effects+of+neutrons.&rft.au=Inskip%2C+P+D%3BWang%2C+Z+Y%3BFen%2C+Y+S&rft.aulast=Inskip&rft.aufirst=P&rft.date=1991-11-01&rft.volume=61&rft.issue=5&rft.spage=637&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 - 1992-01-30 N1 - Date created - 1992-01-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of non-lytic cytolysin-membrane intermediates. AN - 72506500; 1961199 AB - In order to understand the nature of cytolysin-membrane interactions, the characteristics of stable, non-lytic cytolysin-target cell intermediates formed at low ionic strength, neutral pH, and at physiological ionic strength, pH 6.0, were examined. Protease treatment of cytolysin-RBC intermediates formed at low ionic strength inhibited subsequent hemolysis when the intermediates were exposed to physiological ionic strength and pH. Similarly, when such intermediates were treated with anti-granule and anti-cytolysin antibodies a significant dose-dependent inhibition of hemolysis was observed. These results suggested that in this non-lytic state the cytolysin molecule was exposed on the RBC surface. If low ionic strength or pH 6.0 generated intermediates were washed in 0.5 M NaCl, hemolytic activity was greatly reduced and cytolysin activity could be recovered from the medium. In addition to RBC, both murine (Yac-1 and Lettre ascites) and human (K562) tumor targets formed cytolysin-target cell intermediates at low ionic strength and at low pH. Multilamellar vesicles composed of either phosphatidylcholine, sphingomyelin or phosphatidylserine inhibited the binding of cytolysin to RBC at both low ionic strength and pH 6.0 indicating a lack of polar head group specificity for cytolysin binding. JF - Molecular immunology AU - Kuta, A E AU - Bashford, C L AU - Pasternak, C A AU - Reynolds, C W AU - Henkart, P A AD - Experimental Immunology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 1263 EP - 1270 VL - 28 IS - 11 SN - 0161-5890, 0161-5890 KW - Cytotoxins KW - 0 KW - Phosphatidylcholines KW - Phosphatidylserines KW - Sphingomyelins KW - Sodium Chloride KW - 451W47IQ8X KW - Chymotrypsin KW - EC 3.4.21.1 KW - Trypsin KW - EC 3.4.21.4 KW - Pronase KW - EC 3.4.24.- KW - Index Medicus KW - Rats KW - Hemolysis -- drug effects KW - Animals KW - Tumor Cells, Cultured KW - Sphingomyelins -- pharmacology KW - Phosphatidylserines -- pharmacology KW - Hydrogen-Ion Concentration KW - Humans KW - In Vitro Techniques KW - Pronase -- pharmacology KW - Mice KW - Chymotrypsin -- pharmacology KW - Trypsin -- pharmacology KW - Sodium Chloride -- pharmacology KW - Phosphatidylcholines -- pharmacology KW - Cytotoxins -- chemistry KW - Cell Membrane -- drug effects KW - Cytotoxins -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72506500?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+immunology&rft.atitle=Characterization+of+non-lytic+cytolysin-membrane+intermediates.&rft.au=Kuta%2C+A+E%3BBashford%2C+C+L%3BPasternak%2C+C+A%3BReynolds%2C+C+W%3BHenkart%2C+P+A&rft.aulast=Kuta&rft.aufirst=A&rft.date=1991-11-01&rft.volume=28&rft.issue=11&rft.spage=1263&rft.isbn=&rft.btitle=&rft.title=Molecular+immunology&rft.issn=01615890&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-08 N1 - Date created - 1992-01-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cardiac complications observed in elderly patients following 2'-deoxycoformycin therapy. AN - 72483835; 1951329 AB - Deoxycoformycin (dCF) is an investigational nucleoside with significant activity in hairy cell leukemia, cutaneous T-cell lymphoma, and chronic lymphocytic leukemia. During a 4-year period, 11 patients have experienced cardiac events as a complication of dCF therapy under NCI sponsorship. The cases are presented and recommendations for the administration of dCF to patients with pre-existing heart disease are made. JF - American journal of hematology AU - Grem, J L AU - King, S A AU - Chun, H G AU - Grever, M R AD - Clinical Oncology Program, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 245 EP - 247 VL - 38 IS - 3 SN - 0361-8609, 0361-8609 KW - Pentostatin KW - 395575MZO7 KW - Index Medicus KW - Arrhythmias, Cardiac -- chemically induced KW - Myocardial Infarction -- chemically induced KW - Humans KW - Electrocardiography KW - Chest Pain -- chemically induced KW - Aged KW - Middle Aged KW - Male KW - Female KW - Pentostatin -- adverse effects KW - Heart Diseases -- chemically induced KW - Heart Diseases -- physiopathology KW - Pentostatin -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72483835?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+hematology&rft.atitle=Cardiac+complications+observed+in+elderly+patients+following+2%27-deoxycoformycin+therapy.&rft.au=Grem%2C+J+L%3BKing%2C+S+A%3BChun%2C+H+G%3BGrever%2C+M+R&rft.aulast=Grem&rft.aufirst=J&rft.date=1991-11-01&rft.volume=38&rft.issue=3&rft.spage=245&rft.isbn=&rft.btitle=&rft.title=American+journal+of+hematology&rft.issn=03618609&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-27 N1 - Date created - 1991-11-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Levamisole: known effects on the immune system, clinical results, and future applications to the treatment of cancer. AN - 72462543; 1941064 AB - Levamisole has been used in a wide array of clinical research and treatment settings over the past two decades, ranging from such diseases as helminthic infestations to various autoimmune diseases. Numerous preclinical evaluations and clinical trials with levamisole in the cancer arena have been sponsored by the National Cancer Institute and other agencies worldwide with the hopes of demonstrating anticancer activity. Trials in advanced breast cancer, lung cancer, colorectal cancer, melanoma, and lymphoproliferative diseases have generally been negative or inconclusive. However, there is some indication that levamisole may be useful by itself as an adjuvant therapy for resected melanoma; recently it has been shown to be effective in combination with fluorouracil (5-FU) as adjuvant therapy for tumor-node-metastasis (TNM) stage III (Dukes' C) colon carcinoma. In the aggregate, the past 20 years of clinical experience with levamisole has resulted in as many questions as answers. However, further testing of the anticancer activity of levamisole can be expected in clinical research trials over the next few years. Hopefully, these future trials will include studies of the mechanisms of action of this agent. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Stevenson, H C AU - Green, I AU - Hamilton, J M AU - Calabro, B A AU - Parkinson, D R AD - Investigational Drug Branches, National Cancer Institute, National Institute of Health, Bethesda, MD 20892. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 2052 EP - 2066 VL - 9 IS - 11 SN - 0732-183X, 0732-183X KW - Levamisole KW - 2880D3468G KW - Index Medicus KW - Animals KW - Drug Interactions KW - Neoplasms, Experimental -- immunology KW - Humans KW - In Vitro Techniques KW - Forecasting KW - Neoplasms, Experimental -- drug therapy KW - Neoplasms -- drug therapy KW - Levamisole -- pharmacology KW - Immunity -- drug effects KW - Neoplasms -- immunology KW - Levamisole -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72462543?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Levamisole%3A+known+effects+on+the+immune+system%2C+clinical+results%2C+and+future+applications+to+the+treatment+of+cancer.&rft.au=Stevenson%2C+H+C%3BGreen%2C+I%3BHamilton%2C+J+M%3BCalabro%2C+B+A%3BParkinson%2C+D+R&rft.aulast=Stevenson&rft.aufirst=H&rft.date=1991-11-01&rft.volume=9&rft.issue=11&rft.spage=2052&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 - 1991-12-06 N1 - Date created - 1991-12-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transdermal estradiol with oral progestin: biological and clinical effects in younger and older postmenopausal women. AN - 72457288; 1834727 AB - The purpose of this study was to compare the biochemical and clinical effects of transdermal estrogen replacement therapy (tERT) in younger and older postmenopausal women. We treated 15 younger (less than 60 y) and 13 older (greater than or equal to 60 y) healthy postmenopausal women (45-72 y) with four successive 8-week regimens of tERT at doses of 0 to 150 micrograms/day, combined with cyclic oral medroxyprogesterone acetate (MPA). In both age groups, there were similar (p = .0001) dose-responsive increases in plasma estrogen levels and decreases in LH and FSH levels, although LH values were lower in older women both before and after tERT (p less than .02). The addition of MPA further suppressed LH and, to a lesser extent, FSH in both younger and older women. The ratio of estrogenized to nonestrogenized vaginal cells increased with tERT (p less than .007) in both age groups, but significant symptomatic improvement of vaginal irritation was noted only at the highest tERT dose. Adverse effects unrelated to age included short-term nausea in 4/28 women, and skin irritation at the patch sites in 20/28 women. Vaginal bleeding was of shorter duration, but breast tenderness was more common in older women. Further studies of long-term tERT effects in elderly women are indicated. JF - Journal of gerontology AU - Bellantoni, M F AU - Harman, S M AU - Cullins, V E AU - Engelhardt, S M AU - Blackman, M R AD - Laboratory of Clinical Physiology, National Institute on Aging. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - M216 EP - M222 VL - 46 IS - 6 SN - 0022-1422, 0022-1422 KW - Delayed-Action Preparations KW - 0 KW - Placebos KW - Estrone KW - 2DI9HA706A KW - Estradiol KW - 4TI98Z838E KW - Luteinizing Hormone KW - 9002-67-9 KW - Follicle Stimulating Hormone KW - 9002-68-0 KW - Medroxyprogesterone Acetate KW - C2QI4IOI2G KW - Medroxyprogesterone KW - HSU1C9YRES KW - Abridged Index Medicus KW - Index Medicus KW - Vagina -- drug effects KW - Administration, Oral KW - Administration, Cutaneous KW - Analysis of Variance KW - Double-Blind Method KW - Vagina -- pathology KW - Humans KW - Aged KW - Body Mass Index KW - Follicle Stimulating Hormone -- blood KW - Menstruation -- drug effects KW - Body Weight -- drug effects KW - Middle Aged KW - Luteinizing Hormone -- blood KW - Estrone -- blood KW - Female KW - Menopause -- physiology KW - Estrogen Replacement Therapy KW - Estradiol -- adverse effects KW - Aging -- physiology KW - Medroxyprogesterone -- adverse effects KW - Medroxyprogesterone -- administration & dosage KW - Estradiol -- blood KW - Estradiol -- administration & dosage KW - Menopause -- drug effects KW - Estradiol -- therapeutic use KW - Medroxyprogesterone -- analogs & derivatives KW - Medroxyprogesterone -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72457288?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+gerontology&rft.atitle=Transdermal+estradiol+with+oral+progestin%3A+biological+and+clinical+effects+in+younger+and+older+postmenopausal+women.&rft.au=Bellantoni%2C+M+F%3BHarman%2C+S+M%3BCullins%2C+V+E%3BEngelhardt%2C+S+M%3BBlackman%2C+M+R&rft.aulast=Bellantoni&rft.aufirst=M&rft.date=1991-11-01&rft.volume=46&rft.issue=6&rft.spage=M216&rft.isbn=&rft.btitle=&rft.title=Journal+of+gerontology&rft.issn=00221422&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-02 N1 - Date created - 1991-12-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Absorption of micronized progesterone from a nonliquefying vaginal cream. AN - 72449433; 1936339 AB - An improved delivery method to achieve sustained physiological P levels would be useful. Based on this single-dose pharmacokinetic study, micronized P prepared in a nonliquefying vaginal cream holds promise as a convenient method to achieve this goal with a single daily application. JF - Fertility and sterility AU - Kimzey, L M AU - Gumowski, J AU - Merriam, G R AU - Grimes, G J AU - Nelson, L M AD - Nursing Department, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 995 EP - 996 VL - 56 IS - 5 SN - 0015-0282, 0015-0282 KW - Vaginal Creams, Foams, and Jellies KW - 0 KW - Progesterone KW - 4G7DS2Q64Y KW - Index Medicus KW - Administration, Oral KW - Headache -- chemically induced KW - Sleep Stages KW - Humans KW - Adult KW - Absorption KW - Female KW - Progesterone -- adverse effects KW - Progesterone -- administration & dosage KW - Progesterone -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72449433?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fertility+and+sterility&rft.atitle=Absorption+of+micronized+progesterone+from+a+nonliquefying+vaginal+cream.&rft.au=Kimzey%2C+L+M%3BGumowski%2C+J%3BMerriam%2C+G+R%3BGrimes%2C+G+J%3BNelson%2C+L+M&rft.aulast=Kimzey&rft.aufirst=L&rft.date=1991-11-01&rft.volume=56&rft.issue=5&rft.spage=995&rft.isbn=&rft.btitle=&rft.title=Fertility+and+sterility&rft.issn=00150282&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-12 N1 - Date created - 1991-12-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Diethylstilbestrol stimulates persistent phosphatidylinositol lipid turnover by an estrogen receptor-mediated mechanism in immature mouse uterus. AN - 72446579; 1935776 AB - The effect of estrogen on phosphoinositide (PI) metabolism was evaluated in the immature mouse uterus, a tissue which undergoes estrogen-induced proliferation. Uteri isolated from untreated mice or from mice injected ip with diethylstilbestrol (DES) were incubated with [3H]myo-inositol and assessed for incorporation of label into PI lipids or inositol phosphate generation. DES administration elicited a rapid increase in [3H]myo-inositol incorporation, which persisted until at least 18 h post treatment. This effect could not be duplicated by incubation of uteri with DES in vitro, although [3H]myo-inositol incorporation in uteri removed from DES-treated mice remained elevated for 3 h of in vitro incubation. Stimulation of PI lipid metabolism by DES was blocked by ICI 164,384, a specific estrogen receptor antagonist. The effect of DES on PI metabolism consisted of a time-dependent increase in the specific activity of both phosphatidylinositol-4-phosphate and phosphatidylinositol-4,5-bisphosphate and a significant increase of inositol (1,4,5)-trisphosphate mass by 12 h post treatment. These changes occur before the onset of estrogen-induced DNA synthesis. The results indicate that estrogens rapidly modulate PI lipid turnover through an estrogen receptor-mediated mechanism. Since the metabolic products of PI lipids are important for signal transduction and cellular proliferation, altered metabolism of these lipids may play an integral role in estrogen-induced mitogenesis. JF - Endocrinology AU - Ignar-Trowbridge, D M AU - Hughes, A R AU - Putney, J W AU - McLachlan, J A AU - Korach, K S AD - Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 2423 EP - 2430 VL - 129 IS - 5 SN - 0013-7227, 0013-7227 KW - Estrogen Antagonists KW - 0 KW - Phosphatidylinositols KW - Polyunsaturated Alkamides KW - Receptors, Estrogen KW - Inositol KW - 4L6452S749 KW - Estradiol KW - 4TI98Z838E KW - Diethylstilbestrol KW - 731DCA35BT KW - ICI 164384 KW - 84LT43726C KW - Inositol 1,4,5-Trisphosphate KW - 85166-31-0 KW - Dienestrol KW - RRW32X4U1F KW - Abridged Index Medicus KW - Index Medicus KW - Estradiol -- analogs & derivatives KW - Mice, Inbred Strains KW - Animals KW - Dienestrol -- pharmacology KW - Estrogen Antagonists -- pharmacology KW - Dose-Response Relationship, Drug KW - Inositol 1,4,5-Trisphosphate -- analysis KW - Estradiol -- pharmacology KW - Mice KW - Inositol -- metabolism KW - Female KW - Uterus -- metabolism KW - Phosphatidylinositols -- metabolism KW - Diethylstilbestrol -- pharmacology KW - Receptors, Estrogen -- physiology KW - Lipid Metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72446579?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Diethylstilbestrol+stimulates+persistent+phosphatidylinositol+lipid+turnover+by+an+estrogen+receptor-mediated+mechanism+in+immature+mouse+uterus.&rft.au=Ignar-Trowbridge%2C+D+M%3BHughes%2C+A+R%3BPutney%2C+J+W%3BMcLachlan%2C+J+A%3BKorach%2C+K+S&rft.aulast=Ignar-Trowbridge&rft.aufirst=D&rft.date=1991-11-01&rft.volume=129&rft.issue=5&rft.spage=2423&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=00137227&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-02 N1 - Date created - 1991-12-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Acute and long-term effects on limb function of combined modality limb sparing therapy for extremity soft tissue sarcoma. AN - 72446476; 1938558 AB - A retrospective review is presented on 145 patients who underwent limb-sparing surgery and radiation therapy (with or without adjuvant chemotherapy) for their primary soft tissue sarcomas of the extremities on protocol between 1975 and 1986. The focus on our analysis was the acute and long term toxicity of treatment on limb function. The most common acute complication was skin reaction, occurring in 52 patients (36%). Long term (occurring after more than 1 year following all treatment) treatment complications in the extremity were as follows: bone fracture = 6%; contracture = 20%; pain requiring narcotics = 7%; edema greater than 2+ = 19%; moderate to severe decrease in range of motion = 32%; moderate to severe decrease in manual muscle strength = 20%; orthotic device required = 9%; cane or crutch required = 7%; chronic infection = 9%; and tissue induration = 57%. Three amputations for treatment complications were required. Inclusion of more than 50% of the joint in the radiation portal was associated with a higher frequency of contracture. High nominal standard dose (greater than 1760 rets, greater than 63 Gy at 1.8 Gy per fraction) resulted in more painful limbs as well as limbs with increased edema, decreased manual muscle strength, decreased range of motion, and skin telangiectasias. Edema was more often noted in patients with a longer radiation portal (greater than 35 cm), as was tissue induration. Chronic ulcer or infection was more frequently seen in patients with lower extremity tumors and when more than 75% of the extremity diameter was irradiated. Although chemotherapy given concurrent with radiation therapy was associated with a higher number of acute skin reactions, this did not appear to translate into increased long term morbidity. The percentage of patients ambulating without assistive devices and with mild or no pain was 84%. Careful attention to the techniques of radiation therapy may have a significant impact on minimizing acute and long term complications of limb sparing treatment for extremity soft tissue sarcoma. JF - International journal of radiation oncology, biology, physics AU - Stinson, S F AU - DeLaney, T F AU - Greenberg, J AU - Yang, J C AU - Lampert, M H AU - Hicks, J E AU - Venzon, D AU - White, D E AU - Rosenberg, S A AU - Glatstein, E J AD - Radiation Oncology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 1493 EP - 1499 VL - 21 IS - 6 SN - 0360-3016, 0360-3016 KW - Index Medicus KW - Infection -- etiology KW - Skin -- radiation effects KW - Skin -- drug effects KW - Combined Modality Therapy KW - Humans KW - Retrospective Studies KW - Contracture -- etiology KW - Follow-Up Studies KW - Radiation Injuries -- complications KW - Male KW - Female KW - Sarcoma -- physiopathology KW - Extremities -- radiation effects KW - Soft Tissue Neoplasms -- physiopathology KW - Soft Tissue Neoplasms -- therapy KW - Extremities -- physiopathology KW - Sarcoma -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72446476?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+radiation+oncology%2C+biology%2C+physics&rft.atitle=Acute+and+long-term+effects+on+limb+function+of+combined+modality+limb+sparing+therapy+for+extremity+soft+tissue+sarcoma.&rft.au=Stinson%2C+S+F%3BDeLaney%2C+T+F%3BGreenberg%2C+J%3BYang%2C+J+C%3BLampert%2C+M+H%3BHicks%2C+J+E%3BVenzon%2C+D%3BWhite%2C+D+E%3BRosenberg%2C+S+A%3BGlatstein%2C+E+J&rft.aulast=Stinson&rft.aufirst=S&rft.date=1991-11-01&rft.volume=21&rft.issue=6&rft.spage=1493&rft.isbn=&rft.btitle=&rft.title=International+journal+of+radiation+oncology%2C+biology%2C+physics&rft.issn=03603016&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-23 N1 - Date created - 1991-12-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Single-dose tumor necrosis factor protection against endotoxin-induced shock and tissue injury in rats. AN - 72443690; 1937748 AB - Tumor necrosis factor (TNF), a macrophage product released in response to endotoxin and other stimuli, has been shown to be a central mediator of endotoxin or septic shock. However, its highly conserved and wide-ranging physiological effects suggest that it may also be an essential cytokine in the host defense against acute bacterial infection or sepsis. A single nontoxic dose of human recombinant TNF administered intravenously 24 h prior to a lethal infusion of Escherichia coli lipopolysaccharide (LPS) completely prevented acute LPS-induced hypotension, ameliorated tissue injury in the lungs and liver, and improved survival in male Fisher 344 rats. The protective effects of TNF were dose dependent and required a 24-h pretreatment interval. After the infusion of LPS, animals in both groups (TNF-treated animals and saline-pretreated controls) initially appeared acutely ill and had a similar severe metabolic acidosis, indicating that TNF did not inactivate or prevent the toxic effects of LPS. Twelve hours after the administration of TNF, the gene for manganous superoxide dismutase, a mitochondrial enzyme which scavenges toxic reactive oxygen species and is induced during conditions which generate a free radical stress, was expressed in liver tissue, suggesting that the induction of manganous superoxide dismutase may be an important in vivo protective mechanism against cellular injury during lethal endotoxemia. JF - Infection and immunity AU - Alexander, H R AU - Doherty, G M AU - Block, M I AU - Kragel, P J AU - Jensen, J C AU - Langstein, H N AU - Walker, E AU - Norton, J A AD - Surgical Metabolism Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 3889 EP - 3894 VL - 59 IS - 11 SN - 0019-9567, 0019-9567 KW - Lipopolysaccharides KW - 0 KW - RNA, Messenger KW - Tumor Necrosis Factor-alpha KW - Superoxide Dismutase KW - EC 1.15.1.1 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Blotting, Northern KW - Gene Expression KW - Enzyme Induction KW - RNA, Messenger -- genetics KW - Time Factors KW - Shock, Septic -- pathology KW - Superoxide Dismutase -- genetics KW - Lipopolysaccharides -- toxicity KW - Shock, Septic -- physiopathology KW - Tumor Necrosis Factor-alpha -- therapeutic use KW - Shock, Septic -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72443690?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Single-dose+tumor+necrosis+factor+protection+against+endotoxin-induced+shock+and+tissue+injury+in+rats.&rft.au=Alexander%2C+H+R%3BDoherty%2C+G+M%3BBlock%2C+M+I%3BKragel%2C+P+J%3BJensen%2C+J+C%3BLangstein%2C+H+N%3BWalker%2C+E%3BNorton%2C+J+A&rft.aulast=Alexander&rft.aufirst=H&rft.date=1991-11-01&rft.volume=59&rft.issue=11&rft.spage=3889&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 - 1991-11-27 N1 - Date created - 1991-11-27 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Clin Invest. 1991 Jul;88(1):34-9 [2056127] Am J Physiol. 1990 Dec;259(6 Pt 1):L506-12 [2260678] Biochemistry. 1979 Nov 27;18(24):5294-9 [518835] Science. 1985 Apr 12;228(4696):149-54 [3856324] Science. 1985 Aug 30;229(4716):869-71 [3895437] Science. 1986 Oct 24;234(4775):470-4 [3764421] CRC Crit Rev Biochem. 1987;22(2):111-80 [3315461] Nature. 1987 Dec 17-23;330(6149):662-4 [3317066] J Exp Med. 1988 Jul 1;168(1):95-105 [3294337] Science. 1988 Nov 11;242(4880):941-4 [3263703] Biochem Biophys Res Commun. 1989 Jul 31;162(2):794-801 [2547375] Surgery. 1989 Aug;106(2):156-61; discussion 161-2 [2669193] Cell. 1989 Sep 8;58(5):923-31 [2476237] J Appl Physiol (1985). 1990 Mar;68(3):1211-9 [2341345] Cancer Res. 1990 Jul 1;50(13):3928-33 [2354441] J Exp Med. 1990 Aug 1;172(2):599-607 [2165128] Medicine (Baltimore). 1973 Jul;52(4):287-94 [4722658] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Gene specific DNA repair. AN - 72441711; 1934282 JF - Carcinogenesis AU - Bohr, V A AD - Laboratory of Molecular Pharmacology, National Cancer Institute, NIH, Bethesda, MD 20892. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 1983 EP - 1992 VL - 12 IS - 11 SN - 0143-3334, 0143-3334 KW - DHFR KW - c-myc KW - DNA KW - 9007-49-2 KW - Tetrahydrofolate Dehydrogenase KW - EC 1.5.1.3 KW - DNA Ligases KW - EC 6.5.1.- KW - Index Medicus KW - Animals KW - Drug Resistance -- genetics KW - Genes, myc KW - DNA Damage KW - Models, Genetic KW - Humans KW - DNA Ligases -- physiology KW - Mice KW - DNA -- radiation effects KW - Tetrahydrofolate Dehydrogenase -- genetics KW - DNA -- drug effects KW - Cricetinae KW - Genes KW - DNA Repair UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72441711?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Gene+specific+DNA+repair.&rft.au=Bohr%2C+V+A&rft.aulast=Bohr&rft.aufirst=V&rft.date=1991-11-01&rft.volume=12&rft.issue=11&rft.spage=1983&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-19 N1 - Date created - 1991-12-19 N1 - Date revised - 2017-01-13 N1 - Gene symbol - DHFR; c-myc N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Development of resistance to the growth inhibitory effects of transforming growth factor beta 1 during the spontaneous transformation of rat liver epithelial cells. AN - 72441670; 1718589 AB - The temporary maintenance of a rat liver epithelial cell population at confluence before passaging followed by periods of rapid proliferation resulted in the generation of spontaneous transformants after about 108 population doublings. The appearance of morphologically aberrant transformants correlated directly with an increased resistance of the population to the growth inhibitory effects of transforming growth factor beta 1 (TGF-beta 1). Clonal cell lines derived from the transformants were resistant to TGF-beta 1 dependent inhibition of DNA synthesis. These cell lines were also highly tumorigenic and aneuploid, with characteristic gross chromosomal abnormalities, and they expressed a number of phenotypic markers common to rat liver epithelial cells transformed by oncogenes or chemicals. In contrast, apparently normal looking cell lines cloned from the same population were nontumorigenic and near diploid, with few chromosomal abnormalities, and they were as sensitive to TGF-beta 1 as early passage normal rat liver epithelial cells. Morphologically normal late passage rat liver epithelial cells were sensitive to transformation by the DNA hypomethylating agent 5-aza-2-deoxycytidine, in contrast to earlier passage cells, and this transformation was accompanied by the development of resistance to the growth inhibitory effects of TGF-beta 1. These findings suggest that acquisition of resistance to the effects of growth inhibitors such as TGF-beta 1 is an important and possibly essential stage in the spontaneous transformation of rat liver epithelial cells. JF - Cancer research AU - Huggett, A C AU - Ellis, P A AU - Ford, C P AU - Hampton, L L AU - Rimoldi, D AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1991/11/01/ PY - 1991 DA - 1991 Nov 01 SP - 5929 EP - 5936 VL - 51 IS - 21 SN - 0008-5472, 0008-5472 KW - DNA Probes KW - 0 KW - RNA, Messenger KW - Transforming Growth Factor beta KW - Poly A KW - 24937-83-5 KW - RNA KW - 63231-63-0 KW - Index Medicus KW - Poly A -- isolation & purification KW - Clone Cells KW - Karyotyping KW - Animals KW - Blotting, Northern KW - Cell Division -- drug effects KW - DNA Replication -- drug effects KW - Epithelium -- drug effects KW - Rats KW - Oncogenes KW - Epithelial Cells KW - Restriction Mapping KW - RNA -- isolation & purification KW - Poly A -- genetics KW - Cell Line KW - RNA -- genetics KW - Transforming Growth Factor beta -- pharmacology KW - Drug Resistance -- physiology KW - Liver -- cytology KW - Liver -- drug effects KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72441670?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Development+of+resistance+to+the+growth+inhibitory+effects+of+transforming+growth+factor+beta+1+during+the+spontaneous+transformation+of+rat+liver+epithelial+cells.&rft.au=Huggett%2C+A+C%3BEllis%2C+P+A%3BFord%2C+C+P%3BHampton%2C+L+L%3BRimoldi%2C+D%3BThorgeirsson%2C+S+S&rft.aulast=Huggett&rft.aufirst=A&rft.date=1991-11-01&rft.volume=51&rft.issue=21&rft.spage=5929&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 - 1991-11-25 N1 - Date created - 1991-11-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Down-regulation of cdc2 in senescent human and hamster cells. AN - 72441423; 1933864 AB - Senescent cells fail to respond to serum-induced signals for DNA synthesis. Because a central role for the p34cdc2 protein kinase is postulated in control of the cell cycle, we examined the status of this kinase in senescent cells and other growth-arrested cells. In growing human and Syrian hamster fibroblasts, three 35S-labeled proteins of 34-36 kDa were immunoprecipitated with p34cdc2 antiserum. Only the two slower migrating forms were phosphorylated as determined by 32P labelling. In senescent cells, which failed to incorporate [3H]thymidine, no p34cdc2 protein was synthesized and very little or no cdc2 mRNA was observed. When maintained for 48 h in 0.5% serum, young cells also retained only marginal cdc2 expression. After stimulation of low serum-arrested cells by addition of 10% serum, a time-dependent increase of cdc2 mRNA was observed, whereas serum stimulation of senescent cells did not increase cdc2 mRNA. In contrast to senescent and low serum-arrested cells, cdc2 mRNA was expressed at normal levels in cells partially growth arrested by isoleucine deficiency in G1, by aphidicolin at G1-S, by etoposide in G2, or by Colcemid in the M phase of the cell cycle, indicating that cdc2 down-regulation does not always occur upon growth arrest. Following transfection of a plasmid containing the human CDC2 gene into hamster cells, expression of human cdc2 failed to overcome the block to DNA synthesis in senescent cells. Although p34cdc2 was synthesized in the transfected cells, the multiple phosphorylated forms of the proteins were not observed. Taken together, these data support the concept that a chain of events leads to senescence. While p34cdc2 kinase may be one of the critical elements, other cell cycle controls are also involved. JF - Cancer research AU - Richter, K H AU - Afshari, C A AU - Annab, L A AU - Burkhart, B A AU - Owen, R D AU - Boyd, J AU - Barrett, J C AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina 27709. Y1 - 1991/11/01/ PY - 1991 DA - 1991 Nov 01 SP - 6010 EP - 6013 VL - 51 IS - 21 SN - 0008-5472, 0008-5472 KW - Oligodeoxyribonucleotides KW - 0 KW - RNA, Messenger KW - CDC2 Protein Kinase KW - EC 2.7.11.22 KW - Index Medicus KW - Animals KW - Humans KW - RNA, Messenger -- genetics KW - Plasmids KW - Polymerase Chain Reaction KW - Base Sequence KW - Gene Expression Regulation, Enzymologic KW - Transfection KW - Cells, Cultured KW - Molecular Sequence Data KW - Cell Line KW - DNA Replication KW - Cricetinae KW - CDC2 Protein Kinase -- genetics KW - Cell Aging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72441423?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Down-regulation+of+cdc2+in+senescent+human+and+hamster+cells.&rft.au=Richter%2C+K+H%3BAfshari%2C+C+A%3BAnnab%2C+L+A%3BBurkhart%2C+B+A%3BOwen%2C+R+D%3BBoyd%2C+J%3BBarrett%2C+J+C&rft.aulast=Richter&rft.aufirst=K&rft.date=1991-11-01&rft.volume=51&rft.issue=21&rft.spage=6010&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 - 1991-11-25 N1 - Date created - 1991-11-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The anomalous biological activity of nitroso-2-oxopropyl compounds. AN - 72173030; 1933836 AB - The carcinogenic action of a set of N-nitroso compounds containing the 2-oxopropyl group was considered in relation to their metabolism and their activity as alkylating agents for DNA. In contrast with the great carcinogenic potency of methylnitrosourea and ethylnitrosourea, comparable with the corresponding dialkylnitrosamines, 2-oxopropylnitrosourea is a weak carcinogen with a limited range of target organs in rats and hamsters. 2-Oxopropylnitrosochloroethylurea was somewhat weaker than 2-oxopropylnitrosourea and similarly induced spleen hemangiosarcomas in hamsters, but few tumors of any kind in rats. The relatively much more potent carcinogenicity of nitrosobis-(2-oxopropyl)amine, nitroso-(2-hydroxypropyl) (2-oxopropyl) amine and methylnitroso-2-oxopropylamine suggests that the activity of an oxopropylating agent is not involved in carcinogenesis by nitroso-2-oxopropylamines. The nitrosamines are likely to undergo extensive metabolism to form proximate carcinogenic moieties, probably including the methyldiazonium ion, which are responsible for the induction of a broad range of tumors in rats and hamsters. These include tumors of the liver, pancreas ducts, lung and nasal mucosa in hamsters, and esophagus, liver, lung, thyroid, kidney, trachea, bladder and nasal mucosa in rats. JF - Cancer letters AU - Lijinsky, W AD - Laboratory of Chemical and Physical Carcinogenesis, ABL-Basic Research Program, NCI-Frederick Cancer Research and Development Center, MD 21701. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 121 EP - 127 VL - 60 IS - 2 SN - 0304-3835, 0304-3835 KW - Ketones KW - 0 KW - Nitroso Compounds KW - Nitrosourea Compounds KW - Propylamines KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Cricetinae KW - Nitrosourea Compounds -- pharmacology KW - Neoplasms, Experimental -- chemically induced KW - Propylamines -- pharmacology KW - Nitroso Compounds -- toxicity KW - Ketones -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72173030?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+anomalous+biological+activity+of+nitroso-2-oxopropyl+compounds.&rft.au=Lijinsky%2C+W&rft.aulast=Lijinsky&rft.aufirst=W&rft.date=1991-11-01&rft.volume=60&rft.issue=2&rft.spage=121&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 - 1991-12-02 N1 - Date created - 1991-12-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A randomized, controlled trial of foscarnet in the treatment of cytomegalovirus retinitis in patients with AIDS. AN - 72160637; 1656826 AB - To evaluate foscarnet sodium in treating cytomegalovirus retinitis in patients with AIDS. Twenty-four previously untreated persons with AIDS and cytomegalovirus retinitis who were at low risk for loss of their visual acuity. PATIENTS were randomly assigned to receive either no therapy (delayed treatment, control group) or immediate treatment with intravenous foscarnet at a dose of 60 mg/kg body weight three times a day for 3 weeks (induction regimen) followed by a maintenance regimen of 90 mg/kg once a day. PATIENTS were examined weekly until they reached the primary clinical end point, defined as progression of their retinitis border by 750 microns or the development of a new retinal lesion due to cytomegalovirus. Progression was evaluated using retinal photographs by masked readers. Secondary evaluations included changes in visual acuity, cytomegalovirus shedding in the blood and urine, serum levels of human immunodeficiency virus type 1 (HIV-1) p24 antigen, and total CD4 T lymphocyte counts. The mean time to progression of retinitis was 3.2 weeks in the control group (n = 11) compared with 13.3 weeks in the treatment group (n = 13) (P less than 0.001). Nine of 13 patients in the treatment group had positive blood cultures for cytomegalovirus at entry and all nine cleared their blood of cytomegalovirus by the end of the induction period (P = 0.004) compared with one of six patients in the control group. No reductions in p24 levels were seen in the control patients compared with a reduction of more than 50% in p24 levels for all four patients on treatment for whom follow-up levels were available. The main adverse effects of foscarnet treatment were seizures (2 of 13 patients), hypomagnesemia (9 of 13), hypocalcemia (11 of 13), and elevations in serum creatinine above 176.8 mumol/L (2.0 mg/dL) (3 of 13). The control patients received an average of 0.2 units of blood per week compared with an average of 0.6 units of blood per week for the patients on treatment. The administration of foscarnet decreases the rate of progression of cytomegalovirus retinitis in persons with AIDS. Its judicious use is likely to prevent loss of vision in these patients. In this study, however, there was little change in visual acuity in patients in either the immediate or delayed treatment group because only patients with non-sight-threatening disease were selected. JF - Annals of internal medicine AU - Palestine, A G AU - Polis, M A AU - De Smet, M D AU - Baird, B F AU - Falloon, J AU - Kovacs, J A AU - Davey, R T AU - Zurlo, J J AU - Zunich, K M AU - Davis, M AD - National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/11/01/ PY - 1991 DA - 1991 Nov 01 SP - 665 EP - 673 VL - 115 IS - 9 SN - 0003-4819, 0003-4819 KW - Antiviral Agents KW - 0 KW - Foscarnet KW - 364P9RVW4X KW - Phosphonoacetic Acid KW - N919E46723 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Humans KW - Adult KW - Middle Aged KW - Follow-Up Studies KW - Time Factors KW - Opportunistic Infections -- drug therapy KW - Visual Acuity KW - Cytomegalovirus Infections -- drug therapy KW - Antiviral Agents -- therapeutic use KW - Retinitis -- drug therapy KW - Acquired Immunodeficiency Syndrome -- complications KW - Phosphonoacetic Acid -- adverse effects KW - Cytomegalovirus Infections -- etiology KW - Retinitis -- physiopathology KW - Phosphonoacetic Acid -- analogs & derivatives KW - Eye Infections, Viral -- physiopathology KW - Retinitis -- microbiology KW - Phosphonoacetic Acid -- therapeutic use KW - Antiviral Agents -- adverse effects KW - Eye Infections, Viral -- etiology KW - Eye Infections, Viral -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72160637?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+internal+medicine&rft.atitle=A+randomized%2C+controlled+trial+of+foscarnet+in+the+treatment+of+cytomegalovirus+retinitis+in+patients+with+AIDS.&rft.au=Palestine%2C+A+G%3BPolis%2C+M+A%3BDe+Smet%2C+M+D%3BBaird%2C+B+F%3BFalloon%2C+J%3BKovacs%2C+J+A%3BDavey%2C+R+T%3BZurlo%2C+J+J%3BZunich%2C+K+M%3BDavis%2C+M&rft.aulast=Palestine&rft.aufirst=A&rft.date=1991-11-01&rft.volume=115&rft.issue=9&rft.spage=665&rft.isbn=&rft.btitle=&rft.title=Annals+of+internal+medicine&rft.issn=00034819&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-01 N1 - Date created - 1991-11-01 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Ann Intern Med. 1992 Apr 1;116(7):604-5 [1311907] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dopaminergic receptors linked to adenylate cyclase in human cerebromicrovascular endothelium. AN - 72140766; 1681036 AB - Cultured endothelium derived from three fractions of human cerebral microvessels was used to characterize dopamine (DA) receptors linked to adenylate cyclase activity. DA or D1 agonist, (+/-)-SKF-82958 hydrobromide, stimulated endothelial cyclic AMP formation in a dose-dependent manner. The selective D1 antagonist, (+/-)SCH-23390, inhibited in a dose-dependent manner the production of cyclic AMP induced by DA. The affinity for the D1 receptor appeared to be greater in endothelium derived from large and small microvessels than from capillaries. Cholera toxin ADP-ribosylation of Gs proteins abolished the DA stimulatory effect on endothelial adenylate cyclase, whereas pertussis toxin ADP-ribosylation enhanced the DA-inducible formation, indicating the presence of both D1 and D2 receptors. Agonists of alpha 1-adrenergic receptors (phenylephrine, 6-fluoronorepinephrine) or serotonin (5-HT), which stimulated the production of cyclic AMP, had no additive effect on DA-stimulated cyclic AMP formation. Incubation of these agents with DA produced the same or lower levels of cyclic AMP as compared to that formed by DA alone. The effect of alpha 1-adrenergic agonists or 5-HT on DA production of cyclic AMP was partially prevented by the D2 antagonist, S(-)-sulpiride, or ketanserin (5-HT2 greater than alpha 1 greater than H1 antagonists), respectively. These findings represent the first demonstration of D1- (stimulatory) and D2- (inhibitory) receptors linked to adenylate cyclase in microvascular endothelium derived from human brain. The data also indicate that dopaminergic receptors can interact with either alpha 1-adrenergic or or 5-HT receptors in endothelium on the adenylate cyclase level.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Journal of neurochemistry AU - Bacic, F AU - Uematsu, S AU - McCarron, R M AU - Spatz, M AD - Laboratory of Neuropathology and Neuroanatomical Sciences, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/11// PY - 1991 DA - November 1991 SP - 1774 EP - 1780 VL - 57 IS - 5 SN - 0022-3042, 0022-3042 KW - Adenylate Cyclase Toxin KW - 0 KW - Benzazepines KW - Dopamine Agents KW - Receptors, Dopamine KW - Receptors, Dopamine D1 KW - Receptors, Dopamine D2 KW - Virulence Factors, Bordetella KW - Phenylephrine KW - 1WS297W6MV KW - Serotonin KW - 333DO1RDJY KW - SK&F 82958 KW - 80751-65-1 KW - 6-fluoronorepinephrine KW - 86820-21-5 KW - Cholera Toxin KW - 9012-63-9 KW - Cyclic AMP KW - E0399OZS9N KW - Pertussis Toxin KW - EC 2.4.2.31 KW - Adenylyl Cyclases KW - EC 4.6.1.1 KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Serotonin -- pharmacology KW - Norepinephrine -- pharmacology KW - Humans KW - Cholera Toxin -- pharmacology KW - Capillaries KW - Virulence Factors, Bordetella -- pharmacology KW - Cells, Cultured KW - Kinetics KW - Cyclic AMP -- metabolism KW - Norepinephrine -- analogs & derivatives KW - Microcirculation KW - Phenylephrine -- pharmacology KW - Receptors, Dopamine -- drug effects KW - Receptors, Dopamine -- physiology KW - Benzazepines -- pharmacology KW - Endothelium, Vascular -- enzymology KW - Endothelium, Vascular -- drug effects KW - Dopamine Agents -- pharmacology KW - Adenylyl Cyclases -- metabolism KW - Cerebrovascular Circulation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72140766?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Dopaminergic+receptors+linked+to+adenylate+cyclase+in+human+cerebromicrovascular+endothelium.&rft.au=Bacic%2C+F%3BUematsu%2C+S%3BMcCarron%2C+R+M%3BSpatz%2C+M&rft.aulast=Bacic&rft.aufirst=F&rft.date=1991-11-01&rft.volume=57&rft.issue=5&rft.spage=1774&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 - 1991-11-15 N1 - Date created - 1991-11-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Waterborne Lead Affects Feeding Abilities and Neurotransmitter Levels of Juvenile Fathead Minnows AN - 19129753; 9204740 AB - Lead is rarely found in concentrations sufficient to cause immediate mortality in nature, due to complexation by carbonates and hydroxides. Therefore, even in aquatic systems that are heavily contaminated with lead, fish populations will generally be exposed to sublethal levels of 1 mg/L or less. Lead is a potent neurotoxin in vertebrates. Sublethal levels of lead can provoke a wide variety of behavioral changes in many species of higher and lower vertebrates. Fathead minnows (Pimephales promelas) were exposed for a total of 4 weeks to 0.5 or 1.0 mg/L lead, as lead acetate. After 14-day acclimation to flake food, separate groups were fed either 20 1-day, 2-day, or 7-day old Daphnia magna on alternate days for 14 days and tested for total time spent feeding, failed attempts and foraging distance. Time spend feeding on daphnids and number of miscues were significantly higher among lead-exposed groups than in control fish. Except for a high significance among fish exposed to 1.0 mg/L lead and feeding on the largest sized prey (7-day-olds), reaction distance showed no dose-response. After 4 weeks, body lead ranged from not detectable in the controls to 44.2 +/-2.5 mg/L in the 1.0 mg/L lead exposed groups. Examination of whole brain neurotransmitters indicated a significant increase in both serotonin and norepinephrine levels, but no change in dopamine in response to lead intoxication. (Mertz-PTT) JF - Aquatic Toxicology AQTODG, Vol. 21, No. 1/2, p 71-80, November 1991. 2 tab, 38 ref. NIEHS Grant ES 04184. AU - Weber, D N AU - Russo, A AU - Seale, D B AU - Spieler, R E AD - NIEHS Marine and Freshwater Biomedical Research Center University of Wisconsin-Milwaukee, Milwaukee, WI Y1 - 1991/11// PY - 1991 DA - Nov 1991 KW - Water Resources Abstracts KW - *Fish behavior KW - *Lead KW - *Minnows KW - *Sublethal effects KW - *Toxicity KW - *Toxicology KW - *Water pollution effects KW - Feeding rates KW - Fish physiology KW - Neurotransmitters KW - Water pollution KW - SW 3030:Effects of pollution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/19129753?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Awaterresources&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=&rft.atitle=Waterborne+Lead+Affects+Feeding+Abilities+and+Neurotransmitter+Levels+of+Juvenile+Fathead+Minnows&rft.au=Weber%2C+D+N%3BRusso%2C+A%3BSeale%2C+D+B%3BSpieler%2C+R+E&rft.aulast=Weber&rft.aufirst=D&rft.date=1991-11-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-14 ER - TY - JOUR T1 - Further characterization of a high affinity thyrotropin binding site on the rat thyrotropin receptor which is an epitope for blocking antibodies from idiopathic myxedema patients but not thyroid stimulating antibodies from Graves' patients. AN - 72491743; 1719963 AB - Cysteine 390 of the rat thyrotropin (TSH) receptor, when mutated to serine, results in a receptor with a reduced ability of TSH to bind and increase cAMP levels but a preserved ability of thyroid stimulating autoantibodies (TSAbs) from hyperthyroid Graves' patients to increase cAMP levels. The ability of receptor autoantibodies from hypothyroid patients with idiopathic myxedema to inhibit the TSAb activity which is preserved is, however, like TSH binding, significantly reduced. Cysteine 390, together with tyrosine 385, thus appears to be an important determinant in a high affinity TSH binding site which is an epitope for receptor autoantibodies which block TSH or TSAb action and cause hypothyroidism rather than TSAbs which increase cAMP levels and are associated with hyperthyroidism. Threonine 388 and aspartic acid 403 may contribute to this ligand interaction site. JF - Biochemical and biophysical research communications AU - Kosugi, S AU - Ban, T AU - Akamizu, T AU - Kohn, L D AD - Cell Regulation Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/10/31/ PY - 1991 DA - 1991 Oct 31 SP - 1118 EP - 1124 VL - 180 IS - 2 SN - 0006-291X, 0006-291X KW - Autoantibodies KW - 0 KW - Epitopes KW - Receptors, Thyrotropin KW - Thyrotropin KW - 9002-71-5 KW - Cyclic AMP KW - E0399OZS9N KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Animals KW - Transfection KW - Kinetics KW - Humans KW - Cyclic AMP -- pharmacology KW - Binding, Competitive KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Binding Sites, Antibody KW - Cell Line KW - Binding Sites KW - Receptors, Thyrotropin -- metabolism KW - Epitopes -- analysis KW - Receptors, Thyrotropin -- immunology KW - Myxedema -- immunology KW - Autoantibodies -- immunology KW - Thyrotropin -- metabolism KW - Graves Disease -- immunology KW - Receptors, Thyrotropin -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72491743?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Further+characterization+of+a+high+affinity+thyrotropin+binding+site+on+the+rat+thyrotropin+receptor+which+is+an+epitope+for+blocking+antibodies+from+idiopathic+myxedema+patients+but+not+thyroid+stimulating+antibodies+from+Graves%27+patients.&rft.au=Kosugi%2C+S%3BBan%2C+T%3BAkamizu%2C+T%3BKohn%2C+L+D&rft.aulast=Kosugi&rft.aufirst=S&rft.date=1991-10-31&rft.volume=180&rft.issue=2&rft.spage=1118&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 - 1991-12-02 N1 - Date created - 1991-12-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A proper amino terminus of diphtheria toxin is important for cytotoxicity. AN - 72486294; 1953725 AB - A series of deletions and substitutions were made at the 5' end of the gene fusion between the first 388 codons of diphtheria toxin (DT) and a cDNA encoding human IL2. The chimeric protein (DT388-IL2) was expressed and purified from E. coli and found to be very cytotoxic to a human T cell line, HUT 102, that expresses a large number of IL2 receptors. Deletion of the first five amino acids of DT resulted in a non-cytotoxic chimeric protein that had both ADP-ribosylation activity and IL2 receptor binding activity. Deletion of the first two amino acids of DT had little effect on cytotoxicity, while deletion of the first four amino acids or of two acidic residues at positions 3 and 4 greatly reduced cytotoxicity. Unexpectedly, a mutant containing a single leucine in place of the first two amino acids (gly, ala) was 2-3 fold more active. The amino terminus of DT may participate in the translocation of the A chain to the cytosol in a manner similar to Pseudomonas exotoxin (PE) in which a specific C-terminal sequence has been proposed to be involved in its cytotoxicity. JF - Biochemical and biophysical research communications AU - Chaudhary, V K AU - FitzGerald, D J AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/10/31/ PY - 1991 DA - 1991 Oct 31 SP - 545 EP - 551 VL - 180 IS - 2 SN - 0006-291X, 0006-291X KW - Diphtheria Toxin KW - 0 KW - Interleukin-2 KW - Receptors, Interleukin-2 KW - Recombinant Fusion Proteins KW - Adenosine Diphosphate Ribose KW - 20762-30-5 KW - Index Medicus KW - Chromosome Deletion KW - Humans KW - Recombinant Fusion Proteins -- isolation & purification KW - Escherichia coli -- genetics KW - Amino Acid Sequence KW - Adenosine Diphosphate Ribose -- metabolism KW - Plasmids KW - Cloning, Molecular KW - Receptors, Interleukin-2 -- metabolism KW - Base Sequence KW - Promoter Regions, Genetic KW - Chimera KW - Restriction Mapping KW - Molecular Sequence Data KW - Recombinant Fusion Proteins -- pharmacology KW - Cell Line KW - Receptors, Interleukin-2 -- drug effects KW - Interleukin-2 -- pharmacology KW - Cell Survival -- drug effects KW - Diphtheria Toxin -- pharmacology KW - Interleukin-2 -- isolation & purification KW - Interleukin-2 -- genetics KW - Diphtheria Toxin -- genetics KW - Diphtheria Toxin -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72486294?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+proper+amino+terminus+of+diphtheria+toxin+is+important+for+cytotoxicity.&rft.au=Chaudhary%2C+V+K%3BFitzGerald%2C+D+J%3BPastan%2C+I&rft.aulast=Chaudhary&rft.aufirst=V&rft.date=1991-10-31&rft.volume=180&rft.issue=2&rft.spage=545&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 - 1991-12-02 N1 - Date created - 1991-12-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A pharmacogenetic evaluation of the role of local anesthetic actions in the cocaine kindling process. AN - 72610250; 1773340 AB - Repeated administration of subconvulsant doses of lidocaine or cocaine results in the development of an increased susceptibility to seizures induced by the two drugs (pharmacological kindling). It has been hypothesized that the local anesthetic properties of cocaine are responsible for its convulsant and epileptogenic actions. As genetic factors appear to mediate acute sensitivity to the convulsant properties of cocaine and the development of cocaine-kindled seizures, the present studies used a pharmacogenetic approach to address this question further. The convulsant effects of lidocaine were evaluated in BALB, C57, DBA and SJL mice and compared with previous studies evaluating cocaine-induced seizures. We have also evaluated the development of lidocaine- versus cocaine-kindled seizures and the effects of repeated treatment with cocaine or lidocaine on subsequent lidocaine seizure susceptibility in three of these inbred mouse strains. As observed for cocaine, genetic factors influence the convulsant properties of lidocaine; however, the differences between the strains of mice in susceptibility to lidocaine-induced seizures (SJL greater than DBA = BALB = C57) did not parallel those seen for cocaine-induced seizures (C57 greater than DBA = BALB greater than SJL). Similarly, the time course for the expression of kindled seizures and the differences between the various inbred strains were not the same for lidocaine kindling and cocaine kindling. However, depending on the genetic background of the subject, the repeated administration of lidocaine, or cocaine, resulted in the development of sensitization or tolerance to the convulsant effects of lidocaine in an identical manner.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Brain research AU - Marley, R J AU - Witkin, J M AU - Goldberg, S R AD - National Institute on Drug Abuse-Addiction Research Center, Baltimore, MD 21224. Y1 - 1991/10/25/ PY - 1991 DA - 1991 Oct 25 SP - 251 EP - 257 VL - 562 IS - 2 SN - 0006-8993, 0006-8993 KW - Convulsants KW - 0 KW - Lidocaine KW - 98PI200987 KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Mice, Inbred Strains KW - Animals KW - Disease Susceptibility KW - Drug Tolerance -- genetics KW - Mice KW - Male KW - Kindling, Neurologic -- drug effects KW - Cocaine -- toxicity KW - Lidocaine -- toxicity KW - Kindling, Neurologic -- genetics KW - Convulsants -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72610250?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+pharmacogenetic+evaluation+of+the+role+of+local+anesthetic+actions+in+the+cocaine+kindling+process.&rft.au=Marley%2C+R+J%3BWitkin%2C+J+M%3BGoldberg%2C+S+R&rft.aulast=Marley&rft.aufirst=R&rft.date=1991-10-25&rft.volume=562&rft.issue=2&rft.spage=251&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 - 1992-03-03 N1 - Date created - 1992-03-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Functional mapping of anthrax toxin lethal factor by in-frame insertion mutagenesis. AN - 72446999; 1939073 AB - Linker insertion mutagenesis was employed to create structural disruptions of the lethal factor (LF) protein of anthrax toxin to map functional domains. A dodecameric linker was inserted at 17 blunt end restriction enzyme sites throughout the gene. Paired MluI restriction sites within the linker allowed the inserts to be reduced from four to two amino acids. Shuttle vectors containing the mutated genes were transformed into the avirulent Bacillus anthracis UM23C1-1 for expression and secretion of the gene products. Mutations at five sites in the central one-third of the sequence made the protein unstable, and purified protein could not be obtained. Mutated LF proteins with insertions at the other sites were purified and assessed for toxic activity in a macrophage lysis assay and for their ability to bind to the protective antigen (PA) component of anthrax toxin, the receptor binding moiety. Most insertions located in the NH2-terminal one-third of the LF protein eliminated both toxicity and binding to PA, while all four insertions in the COOH-terminal one-third of the protein eliminated toxicity without affecting binding to PA. These data support the hypothesis that the NH2-terminal domain contains the structures required for binding to PA and the COOH-terminal domain contains the putative catalytic domain of LF. JF - The Journal of biological chemistry AU - Quinn, C P AU - Singh, Y AU - Klimpel, K R AU - Leppla, S H AD - Laboratory of Microbial Ecology, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/10/25/ PY - 1991 DA - 1991 Oct 25 SP - 20124 EP - 20130 VL - 266 IS - 30 SN - 0021-9258, 0021-9258 KW - lef KW - Antigens, Bacterial KW - 0 KW - Bacterial Toxins KW - anthrax toxin KW - Index Medicus KW - Phenotype KW - Genes, Bacterial KW - Base Sequence KW - Restriction Mapping KW - Binding, Competitive KW - Molecular Sequence Data KW - Plasmids KW - Bacterial Toxins -- genetics KW - Mutagenesis, Insertional UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72446999?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Functional+mapping+of+anthrax+toxin+lethal+factor+by+in-frame+insertion+mutagenesis.&rft.au=Quinn%2C+C+P%3BSingh%2C+Y%3BKlimpel%2C+K+R%3BLeppla%2C+S+H&rft.aulast=Quinn&rft.aufirst=C&rft.date=1991-10-25&rft.volume=266&rft.issue=30&rft.spage=20124&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 - 1991-12-02 N1 - Date created - 1991-12-02 N1 - Date revised - 2017-01-13 N1 - Gene symbol - lef N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - 1-aminocyclopropanecarboxylates exhibit antidepressant and anxiolytic actions in animal models. AN - 72602119; 1685448 AB - 1-Aminocyclopropanecarboxylic acid (ACPC) is a high affinity ligand at strychnine-insensitive glycine receptors that exhibits partial agonist properties in both biochemical and electrophysiological measures. While ACPC was reported active in animal models commonly used to evaluate potential antidepressants (forced swim) and anxiolytics (plus-maze), the zwitterionic character of this compound could limit both penetration into the central nervous system and oral availability. The present experiments were designed to determine the duration of action of ACPC, its efficacy following oral administration, and to compare these effects with the more lipophilic ACPC methyl ester. Parenterally and orally administered ACPC were equipotent in reducing immobility in the forced swim test, an action manifested for at least 6 h. Both orally and parenterally administered ACPC methyl ester were approximately 3.3-fold more potent than ACPC in the forced swim test. In the elevated plus-maze, both ACPC and ACPC methyl ester were active for 1-2 h after parenteral administration. These findings suggest that 1-aminocyclopropanecarboxylates may constitute a novel class of antidepressant/anxiolytic agents. JF - European journal of pharmacology AU - Trullas, R AU - Folio, T AU - Young, A AU - Miller, R AU - Boje, K AU - Skolnick, P AD - Laboratory of Neuroscience, NIDDK, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/10/22/ PY - 1991 DA - 1991 Oct 22 SP - 379 EP - 385 VL - 203 IS - 3 SN - 0014-2999, 0014-2999 KW - Amino Acids KW - 0 KW - Amino Acids, Cyclic KW - Anti-Anxiety Agents KW - Antidepressive Agents KW - 1-aminocyclopropane-1-carboxylic acid KW - 3K9EJ633GL KW - Strychnine KW - H9Y79VD43J KW - Glycine KW - TE7660XO1C KW - Index Medicus KW - Space life sciences KW - Animals KW - Cerebral Cortex -- drug effects KW - Swimming KW - Synaptosomes -- drug effects KW - Cerebral Cortex -- metabolism KW - Dose-Response Relationship, Drug KW - Glycine -- metabolism KW - Mice KW - Strychnine -- pharmacology KW - Motor Activity -- drug effects KW - Electroshock KW - Synaptosomes -- metabolism KW - Immobilization KW - Male KW - Anti-Anxiety Agents -- pharmacology KW - Antidepressive Agents -- pharmacology KW - Amino Acids -- metabolism KW - Amino Acids -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72602119?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=1-aminocyclopropanecarboxylates+exhibit+antidepressant+and+anxiolytic+actions+in+animal+models.&rft.au=Trullas%2C+R%3BFolio%2C+T%3BYoung%2C+A%3BMiller%2C+R%3BBoje%2C+K%3BSkolnick%2C+P&rft.aulast=Trullas&rft.aufirst=R&rft.date=1991-10-22&rft.volume=203&rft.issue=3&rft.spage=379&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 - 1992-03-05 N1 - Date created - 1992-03-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Potential role of tamoxifen in prevention of breast cancer. AN - 72147957; 1920492 AB - Despite advances in early detection and treatment of breast cancer, primary prevention has not been well explored, especially for women at increased risk of disease due to reproductive factors and family history. There are, however, suggestions that primary prevention of breast cancer may be a realistic objective. Randomized clinical trials of adjuvant therapy for early-stage breast cancer have demonstrated a 35% decrease in contralateral breast cancers among women receiving tamoxifen compared with controls, suggesting a potential role for tamoxifen in chemoprevention of breast cancer in women at increased risk of the disease. Adjuvant therapy studies also demonstrate that tamoxifen is well tolerated by most patients and suggest additional health benefits from alterations in plasma lipid levels and stabilization of bone mineral loss in women receiving tamoxifen. Aspects of tamoxifen pharmacology, laboratory research, and clinical experience which support its investigation as a chemopreventive agent for breast cancer are summarized, and potential toxic effects are discussed. JF - Journal of the National Cancer Institute AU - Nayfield, S G AU - Karp, J E AU - Ford, L G AU - Dorr, F A AU - Kramer, B S AD - Community Oncology and Rehabilitation Branch, National Cancer Institute, Bethesda, Md 20892. Y1 - 1991/10/16/ PY - 1991 DA - 1991 Oct 16 SP - 1450 EP - 1459 VL - 83 IS - 20 SN - 0027-8874, 0027-8874 KW - Lipids KW - 0 KW - Tamoxifen KW - 094ZI81Y45 KW - Index Medicus KW - Lipids -- blood KW - Bone Density -- drug effects KW - Risk Factors KW - Humans KW - Cardiovascular System -- drug effects KW - Female KW - Tamoxifen -- pharmacology KW - Tamoxifen -- therapeutic use KW - Tamoxifen -- adverse effects KW - Breast Neoplasms -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72147957?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Potential+role+of+tamoxifen+in+prevention+of+breast+cancer.&rft.au=Nayfield%2C+S+G%3BKarp%2C+J+E%3BFord%2C+L+G%3BDorr%2C+F+A%3BKramer%2C+B+S&rft.aulast=Nayfield&rft.aufirst=S&rft.date=1991-10-16&rft.volume=83&rft.issue=20&rft.spage=1450&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 - 1991-11-19 N1 - Date created - 1991-11-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Preclinical evaluation of an anti-autocrine growth factor monoclonal antibody for treatment of patients with small-cell lung cancer. AN - 72142860; 1656058 AB - We have evaluated an anti-autocrine growth factor monoclonal antibody for potential use in the treatment of patients with small-cell lung cancer. The monoclonal antibody, designated 2A11, binds to the C-terminal region of the autocrine growth factor gastrin-releasing peptide and neutralizes its growth-promoting effects in vitro and in vivo. Equilibrium-binding analysis demonstrated that the peptide binds to the antibody (dissociation constant = 1.5 x 10(-10) at least as avidly as it binds to the tumor peptide receptor. Pharmacokinetic studies in normal BALB/c mice demonstrated an initial clearance half-life (alpha t1/2) of 24.3 +/- 4 hours and a secondary clearance half-life (beta t1/2) of 1039.6 +/- 309 hours, and biodistribution studies revealed a distribution pattern which generally reflected blood flow. Single intravenous infusions of 2A11 (20 mg/20-25-kg dogs) into normal mongrel dogs with surgically created gastric fistulas antagonized the stimulatory effects of exogenously infused gastrin-releasing peptide or bombesin on plasma gastrin release and gastric acid secretion. Toxicology studies in normal dogs (with gastric fistulas) infused with 50 mg 2A11 intravenously three times a week for 4 weeks failed to reveal any adverse behavioral, clinical, or pathological effects. Four of six dogs developed an immune response to 2A11. Anti-idiotypic antibodies elicited in two cases did not mimic the functional effects of the peptide. We conclude that the concept of immunoblockade of an autocrine growth factor appears feasible in vivo. JF - Journal of the National Cancer Institute AU - Avis, I L AU - Kovacs, T O AU - Kasprzyk, P G AU - Treston, A M AU - Bartholomew, R AU - Walsh, J H AU - Cuttitta, F AU - Mulshine, J L AD - NCI-Navy Medical Oncology Branch, National Naval Medical Center, Bethesda, Md. 20889. Y1 - 1991/10/16/ PY - 1991 DA - 1991 Oct 16 SP - 1470 EP - 1476 VL - 83 IS - 20 SN - 0027-8874, 0027-8874 KW - Antibodies, Monoclonal KW - 0 KW - Gastrins KW - Growth Substances KW - Peptides KW - Gastrin-Releasing Peptide KW - 80043-53-4 KW - Bombesin KW - PX9AZU7QPK KW - Index Medicus KW - Animals KW - Dogs KW - Gastrins -- secretion KW - Mice KW - Tissue Distribution KW - Mice, Inbred BALB C KW - Gastric Acid -- secretion KW - Carcinoma, Small Cell -- therapy KW - Bombesin -- immunology KW - Antibodies, Monoclonal -- metabolism KW - Peptides -- immunology KW - Lung Neoplasms -- therapy KW - Growth Substances -- immunology KW - Antibodies, Monoclonal -- therapeutic use KW - Antibodies, Monoclonal -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72142860?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Preclinical+evaluation+of+an+anti-autocrine+growth+factor+monoclonal+antibody+for+treatment+of+patients+with+small-cell+lung+cancer.&rft.au=Avis%2C+I+L%3BKovacs%2C+T+O%3BKasprzyk%2C+P+G%3BTreston%2C+A+M%3BBartholomew%2C+R%3BWalsh%2C+J+H%3BCuttitta%2C+F%3BMulshine%2C+J+L&rft.aulast=Avis&rft.aufirst=I&rft.date=1991-10-16&rft.volume=83&rft.issue=20&rft.spage=1470&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 - 1991-11-19 N1 - Date created - 1991-11-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Site-directed mutagenesis of a portion of the extracellular domain of the rat thyrotropin receptor important in autoimmune thyroid disease and nonhomologous with gonadotropin receptors. Relationship of functional and immunogenic domains. AN - 72131256; 1655787 AB - Residues 287 to 404 of the rat thyrotropin (TSH) receptor exhibit little homology to gonadotropin receptors. A large segment of this region, residues 303-382, has no determinants important for TSH to bind or elevate cAMP levels nor for the activity of thyroid-stimulating autoantibodies (TSAbs) from the sera of Graves' patients, i.e. deletions, substitutions, or mutations in this segment do not result in a loss of any of these activities in transfected Cos-7 cells. Critical residues for these activities do, however, flank both sides of this segment. Of particular interest, deletion or mutation of residues 299-301 and 387-395 results in a marked decrease in high affinity TSH binding but preserves the ability of a TSAb to increase cAMP levels. Tyrosine 385 is also of particular interest since its mutation to phenylalanine, alanine, threonine, or glutamine results in a receptor with a 20-fold decrease in the ability of TSH to bind or increase cAMP levels, but one whose TSAb activity is, once again, preserved. Because one activity is preserved, we can conclude that (a) the receptor must be fully integrated within the membrane of the cell without malfolding, (b) these sequences represent determinants involved in the high affinity TSH binding site, and (c) separate determinants exist for high affinity TSH binding and TSAb activity, consistent with the existence of autoantibodies in Graves' sera which inhibit TSH binding (TBIAbs) or which increase cAMP levels (TSAbs). Additionally, we show that a 16-mer peptide (residues 352-367), which reacts with the sera of greater than 80% of patients with Graves' disease, can induce the formation of antibodies to a peptide with no sequence homology, residues 377-397. This peptide flanks the region, residues 303-382, with no determinants important for TSH receptor binding or activity. As noted above, it contains residues involved in the high affinity TSH binding site but whose deletion or mutation has no effect on TSAb activity, i.e. residues which would appear to be required at an epitope important for TBIAb but not TSAb antibody activity. JF - The Journal of biological chemistry AU - Kosugi, S AU - Ban, T AU - Akamizu, T AU - Kohn, L D AD - Cell Regulation Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/10/15/ PY - 1991 DA - 1991 Oct 15 SP - 19413 EP - 19418 VL - 266 IS - 29 SN - 0021-9258, 0021-9258 KW - Receptors, Gonadotropin KW - 0 KW - Receptors, Thyrotropin KW - DNA KW - 9007-49-2 KW - Cyclic AMP KW - E0399OZS9N KW - Index Medicus KW - Swine KW - Animals KW - Sequence Homology, Nucleic Acid KW - Humans KW - Amino Acid Sequence KW - Mutagenesis, Site-Directed KW - Rats KW - Transfection KW - DNA -- genetics KW - Cyclic AMP -- metabolism KW - Molecular Sequence Data KW - Enzyme-Linked Immunosorbent Assay KW - Mutation KW - Cell Line KW - Receptors, Thyrotropin -- metabolism KW - Thyroid Diseases -- metabolism KW - Receptors, Gonadotropin -- genetics KW - Autoimmune Diseases -- metabolism KW - Receptors, Thyrotropin -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72131256?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Site-directed+mutagenesis+of+a+portion+of+the+extracellular+domain+of+the+rat+thyrotropin+receptor+important+in+autoimmune+thyroid+disease+and+nonhomologous+with+gonadotropin+receptors.+Relationship+of+functional+and+immunogenic+domains.&rft.au=Kosugi%2C+S%3BBan%2C+T%3BAkamizu%2C+T%3BKohn%2C+L+D&rft.aulast=Kosugi&rft.aufirst=S&rft.date=1991-10-15&rft.volume=266&rft.issue=29&rft.spage=19413&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 - 1991-11-14 N1 - Date created - 1991-11-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pharmacokinetics of pyrazoloacridine in the rhesus monkey. AN - 72118418; 1913666 AB - Pyrazoloacridine is a rationally synthesized acridine derivative with in vitro activity against solid tumor cell lines, noncycling and hypoxic cells, and tumor cell lines that exhibit the multidrug resistance phenotype. The pharmacokinetic behavior of pyrazoloacridine after a 1- or 24-h i.v. infusion was studied in 5 rhesus monkeys that received a total of 10 courses of pyrazoloacridine at 300 or 600 mg/m2. Pyrazoloacridine levels in plasma and cerebrospinal fluid were measured by high-pressure liquid chromatography. For 1-h infusions, the plasma disappearance was biexponential with a t 1/2 alpha of 31 min and t 1/2 beta of 11 h. The mean volume of distribution at steady state was 1380 liters/m2. The clearance was 1660 ml/min/m2. For the 300 mg/m2 dose, the mean area under the concentration-time curve was 759 microM.min, and the mean peak concentration was 1.3 microM. For the 600 mg/m2 dose, the area under the concentration-time curve was 1330 microM.min, and the peak concentration was 2.5 microM. The steady-state plasma concentrations during the 24-h continuous infusions were 0.27 microM for the 300 mg/m2 dose and 0.45 microM for the 600 mg/m2 dose. The mean clearance calculated from these steady-state concentrations was 2420 ml/min/m2. Cerebrospinal fluid levels were less than 0.1 microM for all doses and schedules. There was no evidence of toxicity at any dose or schedule. These results contrast strikingly with those obtained in mice and dogs in which, despite a more rapid clearance of pyrazoloacridine, significant toxicities were observed at doses that were nontoxic in the monkey. These interspecies differences in the pharmacokinetic and pharmacodynamic behavior of pyrazoloacridine have important implications for the design of Phase I trials in humans. JF - Cancer research AU - Berg, S L 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 - 1991/10/15/ PY - 1991 DA - 1991 Oct 15 SP - 5467 EP - 5470 VL - 51 IS - 20 SN - 0008-5472, 0008-5472 KW - Acridines KW - 0 KW - Antineoplastic Agents KW - Pyrazoles KW - NSC 366140 KW - 99009-20-8 KW - Index Medicus KW - Animals KW - Macaca mulatta KW - Male KW - Antineoplastic Agents -- pharmacokinetics KW - Acridines -- pharmacokinetics KW - Antineoplastic Agents -- blood KW - Pyrazoles -- blood KW - Pyrazoles -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72118418?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Pharmacokinetics+of+pyrazoloacridine+in+the+rhesus+monkey.&rft.au=Berg%2C+S+L%3BBalis%2C+F+M%3BMcCully%2C+C+L%3BGodwin%2C+K+S%3BPoplack%2C+D+G&rft.aulast=Berg&rft.aufirst=S&rft.date=1991-10-15&rft.volume=51&rft.issue=20&rft.spage=5467&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 - 1991-11-13 N1 - Date created - 1991-11-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Reversal of drug resistance in a human colon cancer xenograft expressing MDR1 complementary DNA by in vivo administration of MRK-16 monoclonal antibody. AN - 72142180; 1681110 AB - One strategy to overcome multidrug resistance in neoplasia is to inhibit the gp170 glycoprotein (relative molecular mass, 170,000) that functions as a plasma membrane, energy-dependent, drug-efflux pump. The human colon cancer cell line HT-29, which grows as an ascitic tumor in athymic NCr-nu/nu nude mice, was made multidrug resistant by infection with an MDR1 (also known as PGY1) retrovirus. Referred to as HT-29mdr1, it was used to study reversal of drug resistance in vivo by the anti-P-glycoprotein monoclonal antibody MRK-16. Flow cytometry and radioimmunoassay demonstrated a marked increase in MRK-16 reactivity on HT-29mdr1 cells as compared with its reactivity on the parental, uninfected cell line (HT-29par). The 50% inhibitory concentrations (IC50) of vincristine on HT-29par and HT-29mdr1 cells were 2.5 and 15 ng/mL, respectively. The MRK-16 monoclonal antibody did not affect the vincristine sensitivity of the HT-29par cells. Pretreatment of HT-29mdr1 cells with 10 micrograms/mL MRK-16 in tissue culture partially restored the vincristine sensitivity (IC50 = 7 ng/mL). This modulation of vincristine sensitivity by MRK-16 was then tested in vivo. The median survival times of mice given intraperitoneal transplants of 5 x 10(6) HT-29par or HT-29mdr1 were 37 and 39 days, respectively. Treatment of mice with 1 mg/kg vincristine weekly for 3 weeks, beginning 10 days after tumor injection, resulted in a significant increase in the median survival time of the HT-29par tumor-bearing mice (68 days, P less than .0001), but it had no effect on the HT-29mdr1 tumor-bearing mice. However, treatment of mice bearing the HT-29mdr1 tumor with MRK-16 before vincristine therapy reversed the resistance to the drug (median survival time = 64 days, P less than .0001). The MRK-16 monoclonal antibody alone had no effect on the median survival time of mice given an injection of either HT-29par or HT-29mdr1 cells. These results suggest that strategies employing monoclonal antibody against gp170 may be clinically useful to reverse multidrug resistance. JF - Journal of the National Cancer Institute AU - Pearson, J W AU - Fogler, W E AU - Volker, K AU - Usui, N AU - Goldenberg, S K AU - Gruys, E AU - Riggs, C W AU - Komschlies, K AU - Wiltrout, R H AU - Tsuruo, T AD - Laboratory of Experimental Immunology, National Cancer Institute, NCI-Frederick Cancer Research and Development Center (NCI-FCRDC), Md. 21702-1201. Y1 - 1991/10/02/ PY - 1991 DA - 1991 Oct 02 SP - 1386 EP - 1391 VL - 83 IS - 19 SN - 0027-8874, 0027-8874 KW - MDR1 KW - PGY1 KW - Antibodies, Monoclonal KW - 0 KW - DNA, Neoplasm KW - Membrane Glycoproteins KW - P-Glycoprotein KW - Vincristine KW - 5J49Q6B70F KW - Index Medicus KW - Animals KW - Drug Resistance -- genetics KW - Humans KW - Vincristine -- pharmacology KW - Mice KW - Mice, Nude KW - Vincristine -- toxicity KW - Neoplasm Transplantation KW - Tumor Cells, Cultured KW - Cell Survival -- drug effects KW - Membrane Glycoproteins -- immunology KW - Retroviridae Infections -- pathology KW - Female KW - Male KW - Membrane Glycoproteins -- genetics KW - Colonic Neoplasms -- genetics KW - Colonic Neoplasms -- drug therapy KW - DNA, Neoplasm -- genetics KW - Colonic Neoplasms -- pathology KW - Antibodies, Monoclonal -- administration & dosage KW - Antibodies, Monoclonal -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72142180?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Reversal+of+drug+resistance+in+a+human+colon+cancer+xenograft+expressing+MDR1+complementary+DNA+by+in+vivo+administration+of+MRK-16+monoclonal+antibody.&rft.au=Pearson%2C+J+W%3BFogler%2C+W+E%3BVolker%2C+K%3BUsui%2C+N%3BGoldenberg%2C+S+K%3BGruys%2C+E%3BRiggs%2C+C+W%3BKomschlies%2C+K%3BWiltrout%2C+R+H%3BTsuruo%2C+T&rft.aulast=Pearson&rft.aufirst=J&rft.date=1991-10-02&rft.volume=83&rft.issue=19&rft.spage=1386&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 - 1991-10-29 N1 - Date created - 1991-10-29 N1 - Date revised - 2017-01-13 N1 - Gene symbol - MDR1; PGY1 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The Influence of Location upon Profitability and Employment Change in Small Companies AN - 918039854; 13500483 AB - This paper examines the hypothesis that firms located in large urban areas suffer from location diseconomies which significantly reduce their profitability and propensity to create employment. This hypothesis is tested on a sample of companies located within a single region, the north of England, over the period 1974-81. The empirical results suggest that neither trading profits nor employment change are significantly influenced by location. However, the amount taken out of the business in the form of directors' remuneration, which on average swallowed up 61.5 per cent of trading profits, is significantly negatively related to employment change. This suggests that, with respect to employment creation, public policy should focus on influencing the size of directors' remuneration rather than on directly increasing trading profits. Fiscal policies may not be effective in this context, however, with the result that significantly influencing the behaviour of small firm directors may be a policy role best fitted to pro-active local economic development agencies. JF - Urban Studies AU - Coombes, M G AU - Storey, D J AU - Watson, R AU - Wynarczyk, P AD - Centre for Urban and Regional Development Studies. University of Newcastle-upon-Tyne, Newcastle-upon-Tyne NEI 7RU, UK Y1 - 1991/10// PY - 1991 DA - Oct 1991 SP - 723 EP - 734 PB - Sage Publications, Inc., 2455 Teller Road Thousand Oaks CA 91320 USA VL - 28 IS - 5 SN - 0042-0980, 0042-0980 KW - Environment Abstracts KW - employment KW - economic development KW - British Isles, England KW - public policy KW - fiscal policy KW - profits KW - Economics KW - Urban areas KW - ENA 07:General UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/918039854?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aenvabstractsmodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Urban+Studies&rft.atitle=The+Influence+of+Location+upon+Profitability+and+Employment+Change+in+Small+Companies&rft.au=Coombes%2C+M+G%3BStorey%2C+D+J%3BWatson%2C+R%3BWynarczyk%2C+P&rft.aulast=Coombes&rft.aufirst=M&rft.date=1991-10-01&rft.volume=28&rft.issue=5&rft.spage=723&rft.isbn=&rft.btitle=&rft.title=Urban+Studies&rft.issn=00420980&rft_id=info:doi/10.1080%2F00420989120080891 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-01-01 N1 - Last updated - 2012-03-29 N1 - SubjectsTermNotLitGenreText - economic development; employment; public policy; Economics; fiscal policy; Urban areas; profits; British Isles, England DO - http://dx.doi.org/10.1080/00420989120080891 ER - TY - JOUR T1 - Management of the pruritus of cholestasis: potential role of opiate antagonists. AN - 85221124; pmid-1928030 JF - The American Journal of Gastroenterology AU - Bergasa, N V AU - Jones, E A AD - Liver Diseases Section, NIDDK, National Institutes of Health, Bethesda, Maryland. PY - 1991 SP - 1404 EP - 1412 VL - 86 IS - 10 SN - 0002-9270, 0002-9270 KW - Pruritus KW - Cholestasis KW - Human KW - Narcotic Antagonists UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85221124?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+Journal+of+Gastroenterology&rft.atitle=Management+of+the+pruritus+of+cholestasis%3A+potential+role+of+opiate+antagonists.&rft.au=Bergasa%2C+N+V%3BJones%2C+E+A&rft.aulast=Bergasa&rft.aufirst=N&rft.date=1991-10-01&rft.volume=86&rft.issue=10&rft.spage=1404&rft.isbn=&rft.btitle=&rft.title=The+American+Journal+of+Gastroenterology&rft.issn=00029270&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Relevance of metabolic polymorphisms to human carcinogenesis: evaluation of epidemiologic evidence. AN - 72767207; 1844821 AB - Genetic modulation of environmental exposures associated with common malignancies (lung and bladder) is an attractive mechanism to explain differential susceptibility to tobacco or occupation related carcinogens in the population. Epidemiologic studies to test the hypothesis of such associations and to evaluate evidence for a causal role for genetic factors in the etiology of chemically-induced tumors are challenging and require the close collaboration of epidemiologists, clinicians and laboratory investigators. In this work we review the evidence for an association of three polymorphisms of drug or xenobiotic metabolism with human cancers. Methodologic considerations and data relevant to evaluating a causal role for each polymorphism are considered. Fair to good support for both an association of the acetylation phenotype with occupationally-related bladder cancer and for an association of the debrisoquine metabolic phenotype and lung cancer is found, although in neither case is the evidence completely convincing. Epidemiologic evidence for the association of aryl hydrocarbon hydroxylase and lung cancer is presently problematic because of difficulties in the assay and subsequent confounding factors. DNA based assays are at various stages of development for each of the genotypes and promise to simplify future studies while introducing new methodologic pitfalls. Further studies in all three areas are warranted as each has important implications for the understanding of the carcinogenic process, etiology and the public health aspects of common malignancies. JF - Pharmacogenetics AU - Caporaso, N AU - Landi, M T AU - Vineis, P AD - Family Studies Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 4 EP - 19 VL - 1 IS - 1 SN - 0960-314X, 0960-314X KW - Index Medicus KW - Kidney Neoplasms -- genetics KW - Lung Neoplasms -- etiology KW - Age Factors KW - Lung Neoplasms -- epidemiology KW - Sex Factors KW - Humans KW - Lung Neoplasms -- genetics KW - Kidney Neoplasms -- etiology KW - Kidney Neoplasms -- epidemiology KW - Male KW - Female KW - Polymorphism, Genetic KW - Neoplasms -- epidemiology KW - Environmental Exposure KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72767207?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacogenetics&rft.atitle=Relevance+of+metabolic+polymorphisms+to+human+carcinogenesis%3A+evaluation+of+epidemiologic+evidence.&rft.au=Caporaso%2C+N%3BLandi%2C+M+T%3BVineis%2C+P&rft.aulast=Caporaso&rft.aufirst=N&rft.date=1991-10-01&rft.volume=1&rft.issue=1&rft.spage=4&rft.isbn=&rft.btitle=&rft.title=Pharmacogenetics&rft.issn=0960314X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-28 N1 - Date created - 1993-05-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chronic cocaine administration and withdrawal of cocaine modify neurotensin binding in rat brain. AN - 72751026; 1821482 AB - Neurotensin (NT) is a peptide colocalized with dopamine (DA) within some mesocorticolimbic DA neurons that are affected by cocaine. We assessed whether chronic treatment with cocaine and withdrawal from cocaine would alter NT binding within these and other areas in the brain. Rats were given infusions repeatedly of isotonic saline or cocaine (1 mg/kg i.v. every 12 min for 2 hr over 10 days) and then were killed within 15 min of the last treatment session ("cocaine" or "saline") or 10 days later ("withdrawal"). Brains were processed for NT receptor autoradiography. Cocaine affected NT binding in the mesocortical regions differently from other areas. Within the mesocorticolimbic system, NT binding in the parabrachial pigmented nucleus of the ventral tegmental area (VTA) was 67% lower in cocaine-treated rats killed immediately after or 10 days after their final infusion than in rats given saline. In contrast to the perikaryal region, significantly more NT binding occurred postsynaptically in the terminal areas of the VTA (prefrontal cortex [PFC] and substantia nigra, pars compacta) 10 days after withdrawal of cocaine than in the saline controls. NT binding in the nucleus accumbens was unaffected by cocaine or its withdrawal. Cocaine also decreased NT binding in non-mesocorticolimbic areas, including the dorsal hypothalamic area and the zona incerta, but binding returned toward control levels 10 days after withdrawal from cocaine. These data suggest that in central areas poor in DA uptake sites such as the PFC, NT may be a critical element in the inactivation of DA. Chronic cocaine treatment and its withdrawal appear to uncouple the normal NT-DA interaction at both the cell bodies and terminals.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Synapse (New York, N.Y.) AU - Pilotte, N S AU - Mitchell, W M AU - Sharpe, L G AU - De Souza, E B AU - Dax, E M AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, Maryland 21224. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 111 EP - 120 VL - 9 IS - 2 SN - 0887-4476, 0887-4476 KW - Neurotensin KW - 39379-15-2 KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred Lew KW - Tissue Distribution KW - Time Factors KW - Male KW - Binding Sites KW - Substance Withdrawal Syndrome -- metabolism KW - Brain -- metabolism KW - Neurotensin -- metabolism KW - Cocaine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72751026?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Chronic+cocaine+administration+and+withdrawal+of+cocaine+modify+neurotensin+binding+in+rat+brain.&rft.au=Pilotte%2C+N+S%3BMitchell%2C+W+M%3BSharpe%2C+L+G%3BDe+Souza%2C+E+B%3BDax%2C+E+M&rft.aulast=Pilotte&rft.aufirst=N&rft.date=1991-10-01&rft.volume=9&rft.issue=2&rft.spage=111&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 - 1992-08-19 N1 - Date created - 1992-08-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Circular dichroism studies of the coenzyme environment in the active sites of mutant forms of the beta-subunit in the tryptophan synthase alpha 2 beta 2 complex. AN - 72707669; 1812066 AB - The circular dichroism has been used to evaluate the effect of mutation on the environment of the pyridoxal phosphate coenzyme in the active site of the beta-subunit in the tryptophan synthase alpha 2 beta 2 complex from Salmonella typhimurium. Seven mutant forms of the alpha 2 beta 2-complex with single amino acid replacements at residues 87, 109, 188, 306, and 350 of the beta-subunit have been prepared by site-directed mutagenesis, purified to homogeneity, and characterized by absorption and circular dichroism spectroscopy. Since the wild type and mutant alpha 2 beta 2 complexes all exhibit positive circular dichroism in the coenzyme absorption band, pyridoxal phosphate must bind asymmetrically in the active site of these enzymes. However, the coenzyme may have an altered orientation or active site environment in five of the mutant enzymes that display less intense ellipticity bands. The mutant enzyme in which lysine 87 is replaced by threonine has very weak ellipticity at 400 nm. Since lysine 87 forms a Schiff base with pyridoxal phosphate in the wild type enzyme, our results demonstrate the importance of the Schiff base linkage for rigid or asymmetric binding. Although the mutant enzymes display spectra in the presence of L-serine that differ from that of the wild type enzyme, addition of alpha-glycerol 3-phosphate converts the spectra of two of the mutant enzymes to that of the wild type enzyme. We conclude that this alpha-subunit ligand may produce a conformational change in the alpha-subunit that is transmitted to the mutant beta-subunits and partially corrects conformational alterations in the mutant enzymes. JF - Indian journal of biochemistry & biophysics AU - Kayastha, A M AU - Sawa, Y AU - Nagata, S AU - Kanzaki, H AU - Miles, E W AD - Laboratory of Biochemical Pharmacology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. PY - 1991 SP - 352 EP - 357 VL - 28 IS - 5-6 SN - 0301-1208, 0301-1208 KW - Coenzymes KW - 0 KW - DNA, Bacterial KW - Pyridoxal Phosphate KW - 5V5IOJ8338 KW - Tryptophan Synthase KW - EC 4.2.1.20 KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Base Sequence KW - DNA, Bacterial -- genetics KW - Pyridoxal Phosphate -- chemistry KW - Molecular Sequence Data KW - Circular Dichroism KW - Salmonella typhimurium -- genetics KW - Coenzymes -- chemistry KW - Salmonella typhimurium -- enzymology KW - Protein Conformation KW - Binding Sites KW - Tryptophan Synthase -- chemistry KW - Tryptophan Synthase -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72707669?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Indian+journal+of+biochemistry+%26+biophysics&rft.atitle=Circular+dichroism+studies+of+the+coenzyme+environment+in+the+active+sites+of+mutant+forms+of+the+beta-subunit+in+the+tryptophan+synthase+alpha+2+beta+2+complex.&rft.au=Kayastha%2C+A+M%3BSawa%2C+Y%3BNagata%2C+S%3BKanzaki%2C+H%3BMiles%2C+E+W&rft.aulast=Kayastha&rft.aufirst=A&rft.date=1991-10-01&rft.volume=28&rft.issue=5-6&rft.spage=352&rft.isbn=&rft.btitle=&rft.title=Indian+journal+of+biochemistry+%26+biophysics&rft.issn=03011208&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-09 N1 - Date created - 1992-06-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - New genetic approaches to craniofacial growth and malformation in the mouse. AN - 72704439; 1812135 AB - New genetic tools that have been developed in the mouse for the study of genetic variation and molecular biology can be applied to the study of craniofacial growth and malformation. D.W. Bailey (Journal of Heredity, 76:107-114, 1985, 77:17-25, 1986) has used congenic and recombinant inbred strains to identify a large number of genes that result in growth variation in local regions of the mandible. The function of "morphogenes" have not been characterized, but they may act as switches that regulate already recognized structural genes. We have studied the cartilage matrix deficiency (cmd/cmd) mutant mouse and found that their chondrocytes fail to synthesize the cartilage-specific proteoglycan at both protein and mRNA levels. In vitro experiments demonstrate biochemical feedback control in the formation of the cartilage extracellular matrix. Abnormalities of cartilage matrix result in facial clefts and in dental malocclusion in mice. A recombinant plasmid containing the type II collagen promoter and enhancer fused to a reporter gene, chloramphenicol acetyl transferase, has been used to produce transgenic mice. These mice reveal that the type II collagen enhancer controls the high level of tissue-specific expression of the gene. The transgenic mice provide a potential test system for study of development and teratogenesis at the gene level. JF - Journal of craniofacial genetics and developmental biology AU - Brown, K S AU - Yamada, Y AU - Abramczuk, J AU - Kimata, K AD - Laboratory of Developmental Biology and Anomalies, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892. PY - 1991 SP - 357 EP - 365 VL - 11 IS - 4 SN - 0270-4145, 0270-4145 KW - Collagen KW - 9007-34-5 KW - Index Medicus KW - Animals KW - Mice, Mutant Strains KW - Models, Genetic KW - Crosses, Genetic KW - Mice KW - Gene Expression Regulation KW - Plasmids KW - Mice, Transgenic KW - Collagen -- biosynthesis KW - Facial Bones -- abnormalities KW - Skull -- abnormalities KW - Maxillofacial Development -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72704439?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+craniofacial+genetics+and+developmental+biology&rft.atitle=New+genetic+approaches+to+craniofacial+growth+and+malformation+in+the+mouse.&rft.au=Brown%2C+K+S%3BYamada%2C+Y%3BAbramczuk%2C+J%3BKimata%2C+K&rft.aulast=Brown&rft.aufirst=K&rft.date=1991-10-01&rft.volume=11&rft.issue=4&rft.spage=357&rft.isbn=&rft.btitle=&rft.title=Journal+of+craniofacial+genetics+and+developmental+biology&rft.issn=02704145&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-11 N1 - Date created - 1992-06-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Induction of phencyclidine-like behavior in rats by dextrorphan but not dextromethorphan. AN - 72703812; 1805242 AB - The behavioral effects of dextromethorphan (DM), dextrorphan (DO) and phencyclidine (PCP) were compared in rats. DO (15-120 mg/kg) was similar to PCP (1.25-20 mg/kg) in inducing dose-dependent locomotor hyperactivity, stereotypy and ataxia. DM (15-120 mg/kg) induced moderate hyperactivity only at the higher doses about 45 min after treatment. DM and DO modified the locomotor facilitation induced by 10 mg/kg PCP in opposite directions. Pretreatment with DO facilitated, whereas DM dose-dependently inhibited PCP-elicited hyperactivity. Although the metabolism of DM in rats is unknown, the recently reported abuse of DM in humans may occur by its conversion to DO in the organism, i.e., to a metabolite which produces PCP-like effects. JF - Pharmacology, biochemistry, and behavior AU - Székely, J I AU - Sharpe, L G AU - Jaffe, J H AD - National Institute on Drug Abuse, Addiction Research Center, Baltimore, MD 21224. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 381 EP - 386 VL - 40 IS - 2 SN - 0091-3057, 0091-3057 KW - Dextrorphan KW - 04B7QNO9WS KW - Dextromethorphan KW - 7355X3ROTS KW - Phencyclidine KW - J1DOI7UV76 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Ataxia -- chemically induced KW - Dose-Response Relationship, Drug KW - Stereotyped Behavior -- drug effects KW - Motor Activity -- drug effects KW - Male KW - Dextrorphan -- pharmacology KW - Behavior, Animal -- drug effects KW - Phencyclidine -- pharmacology KW - Dextromethorphan -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72703812?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacology%2C+biochemistry%2C+and+behavior&rft.atitle=Induction+of+phencyclidine-like+behavior+in+rats+by+dextrorphan+but+not+dextromethorphan.&rft.au=Sz%C3%A9kely%2C+J+I%3BSharpe%2C+L+G%3BJaffe%2C+J+H&rft.aulast=Sz%C3%A9kely&rft.aufirst=J&rft.date=1991-10-01&rft.volume=40&rft.issue=2&rft.spage=381&rft.isbn=&rft.btitle=&rft.title=Pharmacology%2C+biochemistry%2C+and+behavior&rft.issn=00913057&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-04 N1 - Date created - 1992-05-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Retinoic acid alters epithelial differentiation during palatogenesis. AN - 72699468; 1812132 AB - Retinoids are teratogenic in humans and animals, producing a syndrome of craniofacial malformations that includes cleft palate. This study investigates the mechanism through which retinoic acid induces cleft palate. Murine palatogenesis after exposure to retinoic acid in utero is compared to normal development and to alterations observed after exposure in organ culture to retinoic acid or epidermal growth factor (EGF). Human embryonic palatal shelves were placed in the organ culture system and the responses to retinoic acid and EGF were compared to those of the murine palatal shelves. Growth factors play a role in normal development and are found in the embryonic palate. In other cell culture systems, retinoids alter the expression of EGF receptors. Our results suggest that in the medial epithelial cells of the palate, retinoic acid sustains the expression of the EGF receptor and the binding of EGF at a time when the expression in control medial cells has declined, and these control cells subsequently undergo programmed cell death. The continued DNA synthesis, proliferation, survival, and shift in phenotype of the medial cells is believed to interfere with the adhesion and fusion of opposing palatal shelves, resulting in cleft palate. JF - Journal of craniofacial genetics and developmental biology AU - Abbott, B D AU - Pratt, R M AD - Experimental Teratogenesis Section, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27711. PY - 1991 SP - 315 EP - 325 VL - 11 IS - 4 SN - 0270-4145, 0270-4145 KW - Tretinoin KW - 5688UTC01R KW - Epidermal Growth Factor KW - 62229-50-9 KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Isotretinoin KW - EH28UP18IF KW - Index Medicus KW - Humans KW - DNA Replication -- drug effects KW - Epithelium -- drug effects KW - Receptor, Epidermal Growth Factor -- biosynthesis KW - Pregnancy KW - Maternal-Fetal Exchange KW - Isotretinoin -- adverse effects KW - Cell Death KW - Epithelium -- physiology KW - Cell Differentiation -- drug effects KW - Epidermal Growth Factor -- metabolism KW - Organ Culture Techniques KW - Female KW - Cleft Palate -- chemically induced KW - Tretinoin -- adverse effects KW - Palate -- embryology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72699468?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+craniofacial+genetics+and+developmental+biology&rft.atitle=Retinoic+acid+alters+epithelial+differentiation+during+palatogenesis.&rft.au=Abbott%2C+B+D%3BPratt%2C+R+M&rft.aulast=Abbott&rft.aufirst=B&rft.date=1991-10-01&rft.volume=11&rft.issue=4&rft.spage=315&rft.isbn=&rft.btitle=&rft.title=Journal+of+craniofacial+genetics+and+developmental+biology&rft.issn=02704145&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-11 N1 - Date created - 1992-06-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Saturable transport of Ca into CSF in chronic hypo- and hypercalcemia. AN - 72669209; 1798059 AB - To further characterize possible saturable transport of Ca into CSF during chronic plasma [Ca] changes, weanling rats were fed diets differing in Ca for 10 weeks. Transfer coefficients for unidirectional uptake of 45Ca and 36Cl into CSF (Kcsf) were determined 3 or 10 min after intravenous tracer injection in unanesthetized animals. In rats fed low Ca diet, Kcsfs for 45Ca and 36Cl were elevated above control, but the 45Ca/36Cl ratio for Kcsf, a more specific measure of Ca transport, was also increased. In animals fed high Ca diet, Kcsfs of both radiotracers were not statistically different from control, but the 45Ca/36Cl ratio was decreased. Injection of CaCl2 into hypocalcemic rats elevated plasma [Ca], depressed 45Ca Kcsf, and returned the 45Ca/36Cl ratio to the control value. The inverse relationship between plasma ionized [Ca] and 45Ca Kcsf was fitted to saturation kinetics with Km less than or equal to 0.53 mumol/ml, maximal Ca influx for the saturable component between 27 and 67 x 10(-5) mumol.g-1.s-1, and the passive component of Kcsf less than or equal to 15 x 10(-5) ml.g-1.s-1. We conclude that Ca transport into CSF is saturable and this transport is important in the regulation of CSF [Ca]. JF - Journal of neuroscience research AU - Murphy, V A AU - Smith, Q R AU - Rapoport, S I AD - Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 421 EP - 426 VL - 30 IS - 2 SN - 0360-4012, 0360-4012 KW - Calcium Radioisotopes KW - 0 KW - Calcium, Dietary KW - Radioisotopes KW - Chlorine KW - 4R7X1O2820 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Choroid Plexus -- metabolism KW - Calcium, Dietary -- pharmacokinetics KW - Calcium, Dietary -- pharmacology KW - Body Weight -- drug effects KW - Diet KW - Male KW - Hypercalcemia -- cerebrospinal fluid KW - Calcium -- cerebrospinal fluid KW - Hypocalcemia -- cerebrospinal fluid UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72669209?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Saturable+transport+of+Ca+into+CSF+in+chronic+hypo-+and+hypercalcemia.&rft.au=Murphy%2C+V+A%3BSmith%2C+Q+R%3BRapoport%2C+S+I&rft.aulast=Murphy&rft.aufirst=V&rft.date=1991-10-01&rft.volume=30&rft.issue=2&rft.spage=421&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 - 1992-04-15 N1 - Date created - 1992-04-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Smokeless tobacco and premalignant and malignant lesions of the oral cavity. AN - 72667444; 1797655 AB - The paper compares the prevalence of oral carcinoma and dysplasia in smokeless tobacco users and non users. A total of 3205 subjects were studied. Of the smokeless tobacco users, 1.96 percent had oral carcinoma compared with 0.36 percent of non-users. The prevalence of oral dysplasia in the users' group was 14.4 percent as compared with 6.85 percent in the group of non-users. JF - Indian journal of medical sciences AU - Chakrabarti, R N AU - Dutta, K AU - Sikdar, S AU - Ghosh, K AD - Department of Pathology, Chittaranjan National Cancer Institute, Calcutta. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 273 EP - 275 VL - 45 IS - 10 SN - 0019-5359, 0019-5359 KW - Index Medicus KW - Leukoplakia, Oral -- etiology KW - Risk Factors KW - Humans KW - Male KW - Female KW - Plants, Toxic KW - Precancerous Conditions -- etiology KW - Mouth Neoplasms -- etiology KW - Tobacco, Smokeless -- adverse effects KW - Developing Countries UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72667444?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Indian+journal+of+medical+sciences&rft.atitle=Smokeless+tobacco+and+premalignant+and+malignant+lesions+of+the+oral+cavity.&rft.au=Chakrabarti%2C+R+N%3BDutta%2C+K%3BSikdar%2C+S%3BGhosh%2C+K&rft.aulast=Chakrabarti&rft.aufirst=R&rft.date=1991-10-01&rft.volume=45&rft.issue=10&rft.spage=273&rft.isbn=&rft.btitle=&rft.title=Indian+journal+of+medical+sciences&rft.issn=00195359&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-16 N1 - Date created - 1992-04-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phase I evaluation of recombinant tumor necrosis factor given in combination with recombinant interferon-gamma. AN - 72653650; 1790143 AB - In light of in vitro and preclinical animal model data suggesting potential additive or synergistic antitumor effects from the combined use of interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha), we conducted a phase I study employing escalating doses of each agent in 36 patients with solid tumors to determine the maximum tolerated dose (MTD). Patients were given an intramuscular (i.m.) injection of IFN-gamma, followed 5 min later by an i.m. injection of TNF-alpha, each agent in different sites, every other day for ten doses over 20 days. Patients received 10, 50, or 100 micrograms/m2 of each agent throughout the treatment course. No dose modifications were made. Patients suffering serious toxicity had therapy stopped and were considered to be off-study. All patients experienced fatigue, and 36% spent over half their time in bed on treatment days. Fever and chills were nearly universal. Mild to moderate elevations in serum transaminase levels were noted in 44% of patients, and 44% developed transient microscopic hematuria. Although 81% of patients had anorexia, only 17% of patients lost more than 3 kg of body wt during the 3 weeks of therapy. Because two of three patients receiving 100 micrograms/m2 of both agents developed serious toxicity (one fever greater than 105 degrees F, one thrombocytopenia 43,000/mm3), the MTD was established to be 100 micrograms/m2 of IFN-gamma plus 50 micrograms/m2 of TNF-alpha. The use of aspirin did not significantly alter the toxic effects of the agents. One patient with melanoma had a mixed response and one patient with mesothelioma transiently cleared his ascites of malignant cells. JF - Journal of immunotherapy : official journal of the Society for Biological Therapy AU - Smith, J W AU - Urba, W J AU - Clark, J W AU - Longo, D L AU - Farrell, M AU - Creekmore, S P AU - Conlon, K C AU - Jaffe, H AU - Steis, R G AD - Biological Response Modifiers Program, National Cancer Institute-FCRDC, MD 21701. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 355 EP - 362 VL - 10 IS - 5 SN - 1053-8550, 1053-8550 KW - Recombinant Proteins KW - 0 KW - Tumor Necrosis Factor-alpha KW - Interferon-gamma KW - 82115-62-6 KW - Index Medicus KW - Tumor Necrosis Factor-alpha -- administration & dosage KW - Humans KW - Aged KW - Tumor Necrosis Factor-alpha -- adverse effects KW - Interferon-gamma -- adverse effects KW - Drug Evaluation KW - Hematologic Diseases -- chemically induced KW - Chemical and Drug Induced Liver Injury -- etiology KW - Adult KW - Body Weight -- drug effects KW - Recombinant Proteins -- adverse effects KW - Interferon-gamma -- administration & dosage KW - Middle Aged KW - Drug Synergism KW - Recombinant Proteins -- administration & dosage KW - Male KW - Female KW - Kidney Diseases -- chemically induced KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Neoplasms -- therapy KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72653650?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Phase+I+evaluation+of+recombinant+tumor+necrosis+factor+given+in+combination+with+recombinant+interferon-gamma.&rft.au=Smith%2C+J+W%3BUrba%2C+W+J%3BClark%2C+J+W%3BLongo%2C+D+L%3BFarrell%2C+M%3BCreekmore%2C+S+P%3BConlon%2C+K+C%3BJaffe%2C+H%3BSteis%2C+R+G&rft.aulast=Smith&rft.aufirst=J&rft.date=1991-10-01&rft.volume=10&rft.issue=5&rft.spage=355&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 - 1992-03-31 N1 - Date created - 1992-03-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Toxicology and carcinogenesis studies of two grades of pentachlorophenol in B6C3F1 mice. AN - 72648721; 1794655 AB - Toxicology and carcinogenesis studies of pentachlorophenol (penta), a biocide used primarily as a wood preservative, were conducted by feeding diets containing a technical-grade composite or Dowicide EC-7 (a commercial grade with lower levels of contaminants) to groups of B6C3F1 mice. Based primarily on liver lesions (hepatocellular necrosis, degeneration, and cytomegaly) observed in 6-month studies, diets containing 100 or 200 ppm technical-grade pentachlorophenol or 100, 200, or 600 ppm EC-7 were fed to groups of 50 male and 50 female mice for 2 years. Control groups consisted of 35 animals. For the most part, mean body weights of mice exposed to technical-grade penta were comparable to those of controls. During the second year, the 600-ppm EC-7 female mice averaged 85% of the control body weights. Feed consumption by exposed mice was similar to that by controls. The average daily doses of penta were approximately 0, 17-18, 35, or 114-118 (EC-7) mg/kg. Survival of mice did not appear to be significantly affected by exposure to either technical penta or EC-7 at the doses used in these studies; survival of the control male mice (technical-grade) was comparatively low. Compound-related neoplasms were observed in three organs/systems: liver, adrenal gland medulla, and vascular endothelium. Dose-related increases of hepatocellular adenomas and of carcinomas were observed in male and female mice exposed to both technical penta and EC-7, although the increase was less marked in females exposed to technical penta. Pheochromocytomas of the adrenal gland in exposed male mice were significantly greater than those in controls for both technical penta and EC-7. These neoplasms were also increased in female mice exposed to EC-7 but not to technical penta. Hemangiosarcomas in the spleen and/or liver were increased in female mice that received technical penta and EC-7. The results of these studies show that both technical penta and Dowicide EC-7 are carcinogenic for mice, causing neoplasms in multiple organs/systems. In addition, the results suggest that the carcinogenic responses were due almost exclusively to penta itself, with possibly a minimal potentiating influence by the contaminants in the induction of liver neoplasms in male mice. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - McConnell, E E AU - Huff, J E AU - Hejtmancik, M AU - Peters, A C AU - Persing, R AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 519 EP - 532 VL - 17 IS - 3 SN - 0272-0590, 0272-0590 KW - Pentachlorophenol KW - D9BSU0SE4T KW - Index Medicus KW - Animals KW - Body Weight -- drug effects KW - Carcinogenicity Tests KW - Mice KW - Male KW - Female KW - Neoplasms -- chemically induced KW - Pentachlorophenol -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72648721?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Toxicology+and+carcinogenesis+studies+of+two+grades+of+pentachlorophenol+in+B6C3F1+mice.&rft.au=McConnell%2C+E+E%3BHuff%2C+J+E%3BHejtmancik%2C+M%3BPeters%2C+A+C%3BPersing%2C+R&rft.aulast=McConnell&rft.aufirst=E&rft.date=1991-10-01&rft.volume=17&rft.issue=3&rft.spage=519&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 - 1992-04-06 N1 - Date created - 1992-04-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dissociation of hydroxylase and lyase activities by site-directed mutagenesis of the rat P45017 alpha. AN - 72609668; 1723139 AB - Site-directed mutagenesis of the arginine-rich region within the putative active site of the rat testicular P45017 alpha (17 alpha-hydroxylase cytochrome P-450, the product of P450XVII gene) was performed to identify specific amino acids that contribute to either the hydroxylase or lyase activities catalyzed by this enzyme. The conversion of Arg346 to alanine differentially abolished lyase activity without affecting hydroxylase activity, resulting in an accumulation of the 17 alpha-hydroxylated intermediate, and partial lyase activity was recovered by conversion of this mutant to Lys346. Similar results were obtained with the conversion of Arg357 to alanine, although this mutant also diminished hydroxylase activity, and full lyase and hydroxylase activities were recovered with a lysine in this position. Major reductions in hydroxylase activity were apparent with the conversion of Arg363 to Ala, and this inhibition was reversed by a lysine at position 363. In contrast, differential effects were not observed with the mutants Arg361 Ala, Arg361 Lys, or Tyr334Phe. Both mutations at the Arg361 position resulted in a total loss of hydroxylase and lyase activities, and mutation at the Tyr334 position had no effect on either activity. The identification of specific amino acids that are essential for either the hydroxylase or lyase reaction indicates that the steroid substrate-protein interaction changes during the course of the two consecutive reactions and reveals the potential for separation of the two activities by chemical and biological modulators within the active site region of the P45017 alpha. JF - Molecular endocrinology (Baltimore, Md.) AU - Kitamura, M AU - Buczko, E AU - Dufau, M L AD - Endocrinology and Reproduction Research Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 1373 EP - 1380 VL - 5 IS - 10 SN - 0888-8809, 0888-8809 KW - P450XVII KW - Recombinant Proteins KW - 0 KW - RNA KW - 63231-63-0 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Steroid 17-alpha-Hydroxylase KW - EC 1.14.14.19 KW - Aldehyde-Lyases KW - EC 4.1.2.- KW - Index Medicus KW - Animals KW - Blotting, Northern KW - Amino Acid Sequence KW - Binding Sites KW - Rats KW - Transfection KW - Recombinant Proteins -- metabolism KW - Kinetics KW - Molecular Sequence Data KW - RNA -- isolation & purification KW - Testis -- enzymology KW - Substrate Specificity KW - Cell Line KW - Male KW - RNA -- genetics KW - Mutagenesis, Site-Directed KW - Cytochrome P-450 Enzyme System -- genetics KW - Steroid 17-alpha-Hydroxylase -- metabolism KW - Aldehyde-Lyases -- metabolism KW - Steroid 17-alpha-Hydroxylase -- genetics KW - Cytochrome P-450 Enzyme System -- metabolism KW - Aldehyde-Lyases -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72609668?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Dissociation+of+hydroxylase+and+lyase+activities+by+site-directed+mutagenesis+of+the+rat+P45017+alpha.&rft.au=Kitamura%2C+M%3BBuczko%2C+E%3BDufau%2C+M+L&rft.aulast=Kitamura&rft.aufirst=M&rft.date=1991-10-01&rft.volume=5&rft.issue=10&rft.spage=1373&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 - 1992-03-05 N1 - Date created - 1992-03-05 N1 - Date revised - 2017-01-13 N1 - Gene symbol - P450XVII N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Principles of clinically important drug interactions with carbamazepine. Part II. AN - 72595091; 1765573 JF - Journal of clinical psychopharmacology AU - Ketter, T A AU - Post, R M AU - Worthington, K AD - Biological Psychiatry Branch, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 306 EP - 313 VL - 11 IS - 5 SN - 0271-0749, 0271-0749 KW - Carbamazepine KW - 33CM23913M KW - Index Medicus KW - Drug Therapy, Combination KW - Humans KW - Psychotic Disorders -- blood KW - Carbamazepine -- adverse effects KW - Psychotic Disorders -- psychology KW - Carbamazepine -- pharmacokinetics KW - Carbamazepine -- therapeutic use KW - Drug Interactions -- physiology KW - Psychotic Disorders -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72595091?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Principles+of+clinically+important+drug+interactions+with+carbamazepine.+Part+II.&rft.au=Ketter%2C+T+A%3BPost%2C+R+M%3BWorthington%2C+K&rft.aulast=Ketter&rft.aufirst=T&rft.date=1991-10-01&rft.volume=11&rft.issue=5&rft.spage=306&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 - 1992-02-20 N1 - Date created - 1992-02-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Adverse reactions after injection of adsorbed diphtheria-pertussis-tetanus (DPT) vaccine are not due only to pertussis organisms or pertussis components in the vaccine. AN - 72579280; 1759487 AB - Reactions to adsorbed diphtheria-pertussis-tetanus (DPT) vaccine have mostly been attributed to the pertussis organisms or pertussis components in the vaccine. Nevertheless reactions may also be due to other factors such as sensitization induced by aluminium adjuvants and impurities present in crude toxoids that cannot be removed by purification of toxoids after formalinization. Aluminium compounds such as aluminium phosphate and aluminium hydroxide are the most commonly used adjuvants with vaccines for human use. Due to the increasing concern about the toxicity of aluminium, other adjuvants like calcium phosphate may be evaluated as an alternative to aluminium adjuvants. To minimize reactions after immunization with DPT vaccine due to impurities in the toxoids, the use of toxoided purified toxins is suggested. JF - Vaccine AU - Gupta, R K AU - Relyveld, E H AD - National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 699 EP - 702 VL - 9 IS - 10 SN - 0264-410X, 0264-410X KW - Diphtheria Toxoid KW - 0 KW - Diphtheria-Tetanus-Pertussis Vaccine KW - Tetanus Toxoid KW - Aluminum KW - CPD4NFA903 KW - Index Medicus KW - Tetanus Toxoid -- adverse effects KW - Diphtheria Toxoid -- adverse effects KW - Humans KW - Adsorption KW - Aluminum -- adverse effects KW - Diphtheria-Tetanus-Pertussis Vaccine -- adverse effects KW - Diphtheria-Tetanus-Pertussis Vaccine -- chemistry KW - Bordetella pertussis -- pathogenicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72579280?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Vaccine&rft.atitle=Adverse+reactions+after+injection+of+adsorbed+diphtheria-pertussis-tetanus+%28DPT%29+vaccine+are+not+due+only+to+pertussis+organisms+or+pertussis+components+in+the+vaccine.&rft.au=Gupta%2C+R+K%3BRelyveld%2C+E+H&rft.aulast=Gupta&rft.aufirst=R&rft.date=1991-10-01&rft.volume=9&rft.issue=10&rft.spage=699&rft.isbn=&rft.btitle=&rft.title=Vaccine&rft.issn=0264410X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-06 N1 - Date created - 1992-02-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The role of jun and fos gene family members in 12-O-tetradecanoylphorbol-13-acetate induced hemopoietic differentiation. AN - 72576778; 1751404 AB - Terminal differentiation of the leukemic cell lines U-937 and HL-60 by 12-O-tetradecanoylphorbol-13-acetate is accompanied by marked changes in gene expression. In this study, we demonstrate that the expression of jun and fos gene family members is induced with variable kinetics during 12-O-tetradecanoylphorbol-13-acetate induced differentiation, with c-jun expression best paralleling differentiation. The generation of AP-1 complexes, as measured by DNA binding activity, closely parallels morphological differentiation. Furthermore, the ability of these complexes to regulate gene expression is demonstrated by increased transcription from an AP-1 driven reporter construct and marked increases in the expression of endogenous AP-1 regulated genes. Differentiation assays using water soluble phorbol esters reveal that differentiation becomes irreversible soon after AP-1 appears. This tight correlation between c-jun expression, the generation of AP-1 activity, and differentiation suggests a critical role for this gene and transcriptional complex during this process. JF - Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research AU - Szabo, E AU - Preis, L H AU - Brown, P H AU - Birrer, M J AD - NCI-Navy Medical Oncology Branch, Bethesda, Maryland 20814. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 475 EP - 482 VL - 2 IS - 10 SN - 1044-9523, 1044-9523 KW - fos KW - jun KW - DNA-Binding Proteins KW - 0 KW - Proto-Oncogene Proteins c-jun KW - RNA, Messenger KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Hematopoiesis -- physiology KW - DNA-Binding Proteins -- analysis KW - Gene Expression Regulation -- physiology KW - Humans KW - Cell Line -- drug effects KW - RNA, Messenger -- analysis KW - Macrophages -- physiology KW - Granulocytes -- physiology KW - Proto-Oncogene Proteins c-jun -- analysis KW - Cell Differentiation -- physiology KW - Genes, fos -- physiology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Cell Differentiation -- genetics KW - Genes, jun -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72576778?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cell+growth+%26+differentiation+%3A+the+molecular+biology+journal+of+the+American+Association+for+Cancer+Research&rft.atitle=The+role+of+jun+and+fos+gene+family+members+in+12-O-tetradecanoylphorbol-13-acetate+induced+hemopoietic+differentiation.&rft.au=Szabo%2C+E%3BPreis%2C+L+H%3BBrown%2C+P+H%3BBirrer%2C+M+J&rft.aulast=Szabo&rft.aufirst=E&rft.date=1991-10-01&rft.volume=2&rft.issue=10&rft.spage=475&rft.isbn=&rft.btitle=&rft.title=Cell+growth+%26+differentiation+%3A+the+molecular+biology+journal+of+the+American+Association+for+Cancer+Research&rft.issn=10449523&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-29 N1 - Date created - 1992-01-29 N1 - Date revised - 2017-01-13 N1 - Gene symbol - fos; jun N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Maintenance of LHRH and oxytocin neurons in slice explants cultured in serum-free media: effects of tetrodotoxin on gene expression. AN - 72572914; 1758575 AB - A variety of neuroendocrine cells survive and express specific neuropeptide genes for long periods of time in slice explant cultures in the presence of serum. However, before use of these slice explant cultures as experimental models for physiological and pharmacological studies on the regulation of neuropeptide gene expression, it is first necessary to evaluate their characteristics in defined (e.g. serum free) media and to control for the spontaneous electrical and synaptic activity of neurons in these cultures. In this study, brain slices from postnatal day 4 rats were cultured in serum-containing media (SCM) for 12 days to allow thinning, and then maintained in a serum-free, defined media (SFM) for 6 days. Culture slices transferred to SFM appeared healthy and numerous neuroendocrine neurons containing messenger RNA (mRNA) encoding for LHRH and magnocellular neurons containing mRNA encoding for oxytocin (OT) were detected using in situ hybridization histochemistry (ISHH). Each of these neuronal subtypes robustly produced their appropriate gene products as determined by immunocytochemical analysis. Abundant magnocellular OT neurons were found in cultures grown in either SCM or SFM. In contrast, magnocellular vasopressin (VP) neurons were rarely detected under these conditions. Inhibition of spontaneous electrical and synaptic activity in these slice explant cultures was effectively achieved by incubation for the last 2.5 days of culture in the presence of tetrodotoxin (TTX; 10(-6) M). Densitometric single cell analyses after ISHH was performed on both LHRH and OT cells. Comparisons of the density values (corresponding to mRNA levels), from these slice explants, found that: (1) cellular LHRH mRNA levels decreased in the absence of serum, whereas cellular OT mRNA levels did not significantly change under these conditions; (2) the presence of TTX in the media resulted in an overall decrease in cellular LHRH mRNA values in both SCM and SFM, and (3) the OT neurons in these slice cultures appear to be composed of a heterogeneous population, with one cell subtype responding to TTX with an increase in cellular OT mRNA levels. These data show that factors in serum and spontaneous electrical activity can differentially influence mRNA levels of LHRH cells and magnocellular OT neurons in culture. JF - Neuroendocrinology AU - Wray, S AU - Kusano, K AU - Gainer, H AD - Laboratory of Neurochemistry, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 327 EP - 339 VL - 54 IS - 4 SN - 0028-3835, 0028-3835 KW - Culture Media, Serum-Free KW - 0 KW - RNA, Messenger KW - Vasopressins KW - 11000-17-2 KW - Gonadotropin-Releasing Hormone KW - 33515-09-2 KW - Tetrodotoxin KW - 4368-28-9 KW - Oxytocin KW - 50-56-6 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Culture Techniques KW - RNA, Messenger -- metabolism KW - Vasopressins -- genetics KW - Action Potentials -- drug effects KW - Immunohistochemistry KW - Female KW - Neurons -- physiology KW - Oxytocin -- genetics KW - Gene Expression Regulation -- drug effects KW - Tetrodotoxin -- pharmacology KW - Gonadotropin-Releasing Hormone -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72572914?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroendocrinology&rft.atitle=Maintenance+of+LHRH+and+oxytocin+neurons+in+slice+explants+cultured+in+serum-free+media%3A+effects+of+tetrodotoxin+on+gene+expression.&rft.au=Wray%2C+S%3BKusano%2C+K%3BGainer%2C+H&rft.aulast=Wray&rft.aufirst=S&rft.date=1991-10-01&rft.volume=54&rft.issue=4&rft.spage=327&rft.isbn=&rft.btitle=&rft.title=Neuroendocrinology&rft.issn=00283835&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-06 N1 - Date created - 1992-02-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Altered expression of HLA antigens and CD16 Fc receptors on leukocytes of alcoholic subjects and uremic patients. AN - 72567596; 1836713 AB - The possible influences of ethanol and its metabolic product acetate on the surface expression of HLA class I and class II antigens and CD16 Fc receptors were examined. Fluorescent-labeled monoclonal antibodies and flow cytometry were used to measure these antigens on leukocytes from reference controls, subjects admitted for alcohol detoxification, uremic patients undergoing hemodialysis using Cu-prophan dialyzers and fluids containing 4 to 37 mM acetate, and uremic patients that were not hemodialyzed. In comparison to the controls, the mean intensity of staining for class I antigens was not changed significantly on lymphocytes or monocytes from alcoholics but was depressed on cells from eight of 12 uremic patients. Interferon-gamma above 5 units/ml was detected in less than 15% of plasma samples from controls, uremic patients or alcoholics on admission but was detected in four of eight samples from alcoholics at discharge (2-4 days after admission). The intensity of staining for class II antigens was depressed by more than 50% on lymphocytes from alcoholics and uremic patients. The expression of HLA class I and class II antigens was depressed whether uremic patients were hemodialyzed or not. The percentage of lymphocytes expressing CD16 was depressed in three of seven alcoholics and five of seven hemodialyzed patients. In contrast, the percentage of monocytes expressing CD16 was increased in six of seven hemodialyzed patients and three of five uremic patients not undergoing hemodialysis suggesting activation of monocytes in these patients. Plasma levels of beta 2-microglobulin were elevated by 61% in alcoholics, 50-fold in hemodialyzed patients, and 26-fold in nonhemodialyzed uremic patients.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Alcoholism, clinical and experimental research AU - Jones, J M AU - Veech, R L AU - Abbasi, F AU - Yu, K AU - Yeralan, O AU - Briefel, G R AU - Anderson, J AU - Mezey, E AD - Laboratory of Metabolism and Molecular Biology, NIAAA, Rockville, Maryland 20852. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 790 EP - 795 VL - 15 IS - 5 SN - 0145-6008, 0145-6008 KW - Antigens, Differentiation KW - 0 KW - HLA Antigens KW - Receptors, Fc KW - Receptors, IgG KW - Index Medicus KW - Humans KW - Adult KW - Middle Aged KW - Immune Tolerance -- immunology KW - Male KW - Female KW - Kidney Failure, Chronic -- immunology KW - Antigens, Differentiation -- analysis KW - Uremia -- immunology KW - Leukocytes -- immunology KW - Receptors, Fc -- analysis KW - HLA Antigens -- analysis KW - Renal Dialysis KW - Alcoholism -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72567596?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Altered+expression+of+HLA+antigens+and+CD16+Fc+receptors+on+leukocytes+of+alcoholic+subjects+and+uremic+patients.&rft.au=Jones%2C+J+M%3BVeech%2C+R+L%3BAbbasi%2C+F%3BYu%2C+K%3BYeralan%2C+O%3BBriefel%2C+G+R%3BAnderson%2C+J%3BMezey%2C+E&rft.aulast=Jones&rft.aufirst=J&rft.date=1991-10-01&rft.volume=15&rft.issue=5&rft.spage=790&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 - 1992-01-28 N1 - Date created - 1992-01-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cerebral blood flow and metabolic rate in the conscious, freely moving rat: the effects of hypercapnia, and acute ethanol administration. AN - 72554580; 1755506 AB - We propose a simple method that can be used to measure cerebral blood flow (CBF), cerebral oxygen consumption (CMRO2), and cerebral glucose consumption (CMRglu) in the conscious, freely moving rat. The method is based on the classical Kety-Schmidt approach, and uses a chronic cannula in the confluens sinuum. We tested the method by investigating the response of CBF, CMRO2, and CMRglu to hypercapnia and used the approach to investigate the effects of acute alcohol administration. Severe hypercapnia (PaCO2 approximately 80 mmHg) increased the CBF by a factor of 3.5, decreased the CMRO2 by 30%, and had no significant effect on the CMRglu. Under normocapnic conditions moderate blood alcohol levels (100-200 mg%) caused no significant effects on CBF, CMRO2, or CMRglu, but high blood alcohol levels (250-400 mg%) decreased all three parameters by approximately 25%. Under hypercapnic conditions high blood alcohol levels had no effect on CBF, CMRO2, and CMRglu. JF - Alcoholism, clinical and experimental research AU - Ligeti, L AU - Hines, K AU - Dora, E AU - Sinnwell, T AU - Huang, M T AU - McLaughlin, A C AD - National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20852. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 766 EP - 770 VL - 15 IS - 5 SN - 0145-6008, 0145-6008 KW - Blood Glucose KW - 0 KW - Carbon Dioxide KW - 142M471B3J KW - Ethanol KW - 3K9958V90M KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Oxygen Consumption -- drug effects KW - Blood Glucose -- metabolism KW - Oxygen Consumption -- physiology KW - Regional Blood Flow -- drug effects KW - Regional Blood Flow -- physiology KW - Male KW - Ethanol -- pharmacokinetics KW - Alcoholic Intoxication -- physiopathology KW - Energy Metabolism -- physiology KW - Energy Metabolism -- drug effects KW - Brain -- blood supply KW - Ethanol -- toxicity KW - Carbon Dioxide -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72554580?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cerebral+blood+flow+and+metabolic+rate+in+the+conscious%2C+freely+moving+rat%3A+the+effects+of+hypercapnia%2C+and+acute+ethanol+administration.&rft.au=Ligeti%2C+L%3BHines%2C+K%3BDora%2C+E%3BSinnwell%2C+T%3BHuang%2C+M+T%3BMcLaughlin%2C+A+C&rft.aulast=Ligeti&rft.aufirst=L&rft.date=1991-10-01&rft.volume=15&rft.issue=5&rft.spage=766&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 - 1992-01-28 N1 - Date created - 1992-01-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Treatment-related morbidity in patients with lymphoma. AN - 72538857; 1751579 AB - The evolution of effective therapies for lymphoma has led to cures for many patients. In addition to the acute morbidity associated with cytotoxic therapy, significant delayed treatment-related effects have been identified. Complications include immunologic, cardiovascular, pulmonary, thyroid, and gonadal dysfunction as well as the development of second neoplasms. These complications results from tissue injury caused by the administration of radiation or chemotherapy, persistent immunologic deficits related to the underlying malignancy or its therapy, and complications of surgical staging and splenectomy. Disease or treatment-related immunosuppression and the mutagenic effects of therapy appear to predispose these patients to an increased risk of second cancers. This article reviews data from the recently published literature on these issues. JF - Current opinion in oncology AU - Hubbard, S M AU - Longo, D L AD - National Cancer Institute, Bethesda, Maryland. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 852 EP - 862 VL - 3 IS - 5 SN - 1040-8746, 1040-8746 KW - Index Medicus KW - Cardiovascular Diseases -- etiology KW - Leukemia -- chemically induced KW - Hypothyroidism -- etiology KW - Neoplasms, Multiple Primary -- epidemiology KW - Humans KW - Vomiting -- etiology KW - Quality of Life KW - Child KW - Infertility -- etiology KW - Splenectomy -- adverse effects KW - Leukemia -- epidemiology KW - Adult KW - Neoplasms -- chemically induced KW - Myelodysplastic Syndromes -- epidemiology KW - Myelodysplastic Syndromes -- etiology KW - Male KW - Radiation Injuries -- etiology KW - Growth Disorders -- etiology KW - Nausea -- etiology KW - Neoplasms, Radiation-Induced -- etiology KW - Disease Susceptibility KW - Combined Modality Therapy KW - Neoplasms, Radiation-Induced -- epidemiology KW - Leukemia, Radiation-Induced -- etiology KW - Infertility -- epidemiology KW - Neoplasms -- epidemiology KW - Radiation Injuries -- epidemiology KW - Risk KW - Leukemia, Radiation-Induced -- epidemiology KW - Incidence KW - Female KW - Lymphoma -- therapy KW - Infection -- etiology KW - Bone Marrow Diseases -- chemically induced KW - Bone Marrow Diseases -- therapy KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Radiotherapy -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72538857?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+opinion+in+oncology&rft.atitle=Treatment-related+morbidity+in+patients+with+lymphoma.&rft.au=Hubbard%2C+S+M%3BLongo%2C+D+L&rft.aulast=Hubbard&rft.aufirst=S&rft.date=1991-10-01&rft.volume=3&rft.issue=5&rft.spage=852&rft.isbn=&rft.btitle=&rft.title=Current+opinion+in+oncology&rft.issn=10408746&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-27 N1 - Date created - 1992-01-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Responsiveness of a human parotid epithelial cell line (HSY) to autonomic stimulation: muscarinic control of K+ transport. AN - 72508066; 1960145 AB - Salivary electrolyte secretion is under the control of the autonomic nervous system. In this paper we report that HSY, an epithelial cell line derived from the acinar-intercalated duct region of the human parotid gland, responds to muscarinic-cholinergic (generation of Ca2+ signal) and beta-adrenergic (generation of cAMP signal), but not to alpha-adrenergic (lack of Ca2+ signal), receptor stimulation. The muscarinic response was studied in detail. Carbachol (10(-4) M, muscarinic agonist) or A23187 (5 microM, calcium ionophore) stimulation of HSY cells increases both 86Rb (K+) influx and efflux, resulting in no change in net equilibrium 86Rb content. Atropine (10(-5) M, muscarinic antagonist) blocks both the carbachol-generated Ca2+ signal and carbachol-stimulated 86Rb fluxes, but has no effect on either the A23187-generated Ca2+ signal or A23187-stimulated 86Rb fluxes. Carbachol- and A23187-stimulated 86Rb fluxes are substantially inhibited by two K+ channel blockers, quinine (0.3 mM) and scorpion venom containing charybdotoxin (33 micrograms/ml). The inhibition of these stimulated fluxes by another K+ channel blocker, tetraethylammonium chloride (5 mM), is less pronounced. Protein kinase C (PKC) seems to be involved in the regulation of the 86Rb fluxes as 10(-7) M PMA (phorbol ester, phorbol-12-myristate-13-acetate) substantially inhibits the muscarinic-stimulated 86Rb efflux and influx. Because this concentration of PMA totally inhibits the carbachol-generated Ca2+ signal and only 80% of the muscarinic-stimulated 86Rb influx, it seems that a portion of the carbachol-stimulated 86Rb flux (i.e. that portion not inhibited by PMA) might occur independently of the Ca2+ signal. PMA fails to inhibit the A23187-stimulated 86Rb fluxes, however, suggesting that PKC regulates Ca(2+)-sensitive K+ channel activity by regulating the Ca2+ signal, and not steps distal to this event. 4-alpha-Phorbol-12,13-didecanoate, a phorbol ester which fails to activate PKC, fails to inhibit either the carbachol-stimulated increase in intracellular free Ca2+, or carbachol-stimulated 86Rb fluxes. JF - In vitro cellular & developmental biology : journal of the Tissue Culture Association AU - Patton, L L AU - Pollack, S AU - Wellner, R B AD - Clinical Investigations and Patient Care Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 779 EP - 785 VL - 27A IS - 10 SN - 0883-8364, 0883-8364 KW - Phorbol Esters KW - 0 KW - Tetraethylammonium Compounds KW - Tetraethylammonium KW - 66-40-0 KW - Atropine KW - 7C0697DR9I KW - Carbachol KW - 8Y164V895Y KW - Isoproterenol KW - L628TT009W KW - Rubidium KW - MLT4718TJW KW - Potassium KW - RWP5GA015D KW - Epinephrine KW - YKH834O4BH KW - Index Medicus KW - Phorbol Esters -- pharmacology KW - Parotid Neoplasms KW - Biological Transport, Active -- drug effects KW - Kinetics KW - Humans KW - Tetraethylammonium Compounds -- pharmacology KW - Epithelium -- metabolism KW - Adenocarcinoma KW - Isoproterenol -- pharmacology KW - Epithelium -- drug effects KW - Cell Line KW - Rubidium -- metabolism KW - Epinephrine -- pharmacology KW - Atropine -- pharmacology KW - Parotid Gland -- innervation KW - Carbachol -- pharmacology KW - Potassium -- metabolism KW - Parotid Gland -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72508066?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+vitro+cellular+%26+developmental+biology+%3A+journal+of+the+Tissue+Culture+Association&rft.atitle=Responsiveness+of+a+human+parotid+epithelial+cell+line+%28HSY%29+to+autonomic+stimulation%3A+muscarinic+control+of+K%2B+transport.&rft.au=Patton%2C+L+L%3BPollack%2C+S%3BWellner%2C+R+B&rft.aulast=Patton&rft.aufirst=L&rft.date=1991-10-01&rft.volume=27A&rft.issue=10&rft.spage=779&rft.isbn=&rft.btitle=&rft.title=In+vitro+cellular+%26+developmental+biology+%3A+journal+of+the+Tissue+Culture+Association&rft.issn=08838364&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-06 N1 - Date created - 1992-01-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Perinatal thymocyte antigen expression and postnatal immune development altered by gestational exposure to tetrachlorodibenzo-p-dioxin (TCDD). AN - 72492905; 1683717 AB - In utero exposure to the environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was found to alter expression of murine thymocyte fetal cell-surface markers. Pregnant mice were treated (via gavage) with 0, 1.5, or 3.0 micrograms TCDD/kg/day in corn oil on gestational days (gd) 6-14. Offspring were examined on gd 18 and postnatally on d6, d14, and d21, and at 7, 8, and 10 weeks of age. Severe thymic atrophy and cellular depletion were found both pre- and postnatally in TCDD-exposed mice. Immunocytochemical localization of the Thy 1.2 antigen on gd 18 thymocytes revealed no TCDD-related changes in cellular distribution. Flow cytometric analysis, however, indicated that the TCDD treatment resulted in a significant decrease in the percentage of CD4+8+ fetal thymocytes, as well as significantly increased CD4-8- and CD4-8+ thymocytes. The increased CD4-8+ population after TCDD was not from induction of Ts cells. At 7-8 weeks postnatally, no differences existed between control and treatment groups in mitogen responses and antibody plaque response. However, altered thymocyte antigen expression was found to correlate with altered postnatal immune function, as evidenced by decreased cytotoxic T lymphocyte response at 8 weeks of age. Taken together, these results indicate that immunosuppression following prenatal exposure to TCDD can be readily detected by qualitative and quantitative changes in the cell surface phenotype of fetal thymocytes. Furthermore, the observed altered distribution suggests that TCDD inhibits normal thymocyte maturational processes. JF - Teratology AU - Holladay, S D AU - Lindstrom, P AU - Blaylock, B L AU - Comment, C E AU - Germolec, D R AU - Heindell, J J AU - Luster, M I AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 385 EP - 393 VL - 44 IS - 4 SN - 0040-3709, 0040-3709 KW - Antigens, CD4 KW - 0 KW - Antigens, CD8 KW - Antigens, Surface KW - Antigens, Thy-1 KW - Polychlorinated Dibenzodioxins KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Antigens, CD8 -- analysis KW - T-Lymphocytes, Cytotoxic -- immunology KW - Mice KW - Pregnancy KW - Phenotype KW - Maternal-Fetal Exchange KW - Antigens, CD4 -- analysis KW - Mice, Inbred C57BL KW - Flow Cytometry KW - Cytotoxicity, Immunologic -- drug effects KW - Female KW - Male KW - T-Lymphocytes, Cytotoxic -- drug effects KW - Thymus Gland -- immunology KW - Polychlorinated Dibenzodioxins -- toxicity KW - CD4-CD8 Ratio -- drug effects KW - Thymus Gland -- embryology KW - T-Lymphocytes -- drug effects KW - Thymus Gland -- drug effects KW - T-Lymphocytes -- immunology KW - Antigens, Surface -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72492905?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Teratology&rft.atitle=Perinatal+thymocyte+antigen+expression+and+postnatal+immune+development+altered+by+gestational+exposure+to+tetrachlorodibenzo-p-dioxin+%28TCDD%29.&rft.au=Holladay%2C+S+D%3BLindstrom%2C+P%3BBlaylock%2C+B+L%3BComment%2C+C+E%3BGermolec%2C+D+R%3BHeindell%2C+J+J%3BLuster%2C+M+I&rft.aulast=Holladay&rft.aufirst=S&rft.date=1991-10-01&rft.volume=44&rft.issue=4&rft.spage=385&rft.isbn=&rft.btitle=&rft.title=Teratology&rft.issn=00403709&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-03 N1 - Date created - 1992-01-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Nickel-induced renal lipid peroxidation in different strains of mice: concurrence with nickel effect on antioxidant defense systems. AN - 72475559; 1949071 AB - Lipid peroxidation (LPO) and active oxygen-detoxifying enzymes, catalase (CAT), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD), as well as glutathione (GSH) and some related enzymes, glutathione-S-transferase (GST) and glutathione reductase (GSSG-R) were assayed in kidneys of BALB/cAnNCr (BALB/c), C3H/HeNCr-MTV- (C3H), B6C3F1, and C57BL/6NCr (C57BL) mice 3-48 h after a single intraperitoneal injection of 170 mumol nickel (II) acetate (NiAcet)/kg body wt. In control mice that received 340 mumol sodium acetate/kg, the levels of enzymes and GSH did not significantly vary in time but were different in various strains. The basal activities of CAT and SOD in in the controls were highest in BALB/c and lowest in C57BL mice (1.8:1.0 and 1.4:1.0 respectively) in contrast to that of GSH-Px which was highest in B6CF1 and lowest in BALB/c (1.3:1.0; P less than 0.05). The strain ranking of control concentrations of renal GSH was B6C3F1 greater than C3H greater than or equal to C57BL greater than BALB/c (2.8:2.4:2.3:1.0), and that of GSSG-R was C3H greater than or equal to BALB/c greater than B6C3F1 greater than or equal to C57BL [corrected] (1.5:1.4:1.1:1.0). The basal activity of renal GST in control mice was 25% lower in C3H than in any of the other 3 strains. The renal LPO levels in the control mice did not vary among strains. Nickel treatment transiently increased renal LPO levels in the control mice did not vary among strains. Nickel treatment transiently increased renal LPO in the BALB/c mice by 100%, in B6C3F1 by 30%, and in C57BL by 20% (P less than 0.05), with no significant effect in C3H mice. Thus, the magnitude of nickel-induced renal LPO was greatest in the strain that is lowest in GSH and GSH-Px, but not in CAT and SOD. Nickel effects on GSH and the enzymes were time-dependent and included transient inhibition or enhancement of different proportions with no apparent strain- and/or base level-related patterns, or concurrence with LPO. The results emphasize the importance of GSH and GSH-Px for preventing nickel-induced oxidative cell damage. JF - Toxicology letters AU - Misra, M AU - Rodriguez, R E AU - North, S L AU - Kasprzak, K S AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 121 EP - 133 VL - 58 IS - 2 SN - 0378-4274, 0378-4274 KW - Antioxidants KW - 0 KW - Nickel KW - 7OV03QG267 KW - Catalase KW - EC 1.11.1.6 KW - Glutathione Peroxidase KW - EC 1.11.1.9 KW - Superoxide Dismutase KW - EC 1.15.1.1 KW - Glutathione Reductase KW - EC 1.8.1.7 KW - Glutathione Transferase KW - EC 2.5.1.18 KW - Glutathione KW - GAN16C9B8O KW - Index Medicus KW - Animals KW - Glutathione Reductase -- drug effects KW - Glutathione -- metabolism KW - Glutathione Transferase -- metabolism KW - Superoxide Dismutase -- metabolism KW - Superoxide Dismutase -- drug effects KW - Mice KW - Mice, Inbred BALB C KW - Glutathione Peroxidase -- drug effects KW - Catalase -- metabolism KW - Glutathione Peroxidase -- metabolism KW - Glutathione Reductase -- metabolism KW - Mice, Inbred C57BL KW - Mice, Inbred C3H KW - Catalase -- drug effects KW - Glutathione Transferase -- drug effects KW - Male KW - Kidney -- metabolism KW - Antioxidants -- metabolism KW - Lipid Peroxidation -- drug effects KW - Kidney -- enzymology KW - Kidney -- drug effects KW - Nickel -- adverse effects KW - Mice, Inbred Strains -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72475559?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+letters&rft.atitle=Nickel-induced+renal+lipid+peroxidation+in+different+strains+of+mice%3A+concurrence+with+nickel+effect+on+antioxidant+defense+systems.&rft.au=Misra%2C+M%3BRodriguez%2C+R+E%3BNorth%2C+S+L%3BKasprzak%2C+K+S&rft.aulast=Misra&rft.aufirst=M&rft.date=1991-10-01&rft.volume=58&rft.issue=2&rft.spage=121&rft.isbn=&rft.btitle=&rft.title=Toxicology+letters&rft.issn=03784274&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-27 N1 - Date created - 1991-11-27 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Toxicol Lett 1992 Apr;60(2):239 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Application of molecular encapsulation for toxicology studies: toxicokinetics of p-chloro-alpha,alpha,alpha-trifluorotoluene in alpha-cyclodextrin or corn oil vehicles in male F344 rats. AN - 72475195; 1949027 AB - Toxicokinetics of p-chloro-alpha,alpha,alpha-trifluorotoluene (CTFT) after administration as an aqueous alpha-cyclodextrin (alpha-CD) molecular encapsulation suspension (alpha-CD vehicle) or as a corn oil solution (corn oil vehicle) were compared. Male F344 rats were administered intragastrically CTFT in alpha-CD vehicle or corn oil vehicle at dose levels of 10, 50, or 400 mg/kg. Other male F344 rats were administered CTFT intravenously in a 10% Tween 80 aqueous solution. Serial blood samples were taken from a cannulated jugular vein for up to 52 hr after dosing and the CTFT concentrations in whole blood were determined by gas chromatography. The biological elimination half-life of CTFT from the center compartment was not affected by the vehicle used; however, absorption of CTFT from the alpha-CD vehicle was much faster than from the corn oil vehicle. The average absorption half-lives from the alpha-CD vehicle and corn oil vehicle were 17 and 98 min, respectively. Despite the differences in absorption, no statistical difference was observed in the calculated areas under the blood concentration versus time curves (AUC) obtained from rats dosed with either vehicle. Dose proportionality for CTFT was established up to 400 mg/kg and bioavailability was shown to be complete for both vehicles. JF - Toxicology and applied pharmacology AU - Yuan, J M AU - Jameson, C W AU - Goehl, T J AU - Collins, B J AU - Purdie, W AU - Judd, L AD - National Institutes of Health, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 107 EP - 115 VL - 111 IS - 1 SN - 0041-008X, 0041-008X KW - Cyclodextrins KW - 0 KW - Polysorbates KW - alpha-Cyclodextrins KW - Toluene KW - 3FPU23BG52 KW - 4-chloro-alpha,alpha,alpha-trifluorotoluene KW - 694YO34JHC KW - Corn Oil KW - 8001-30-7 KW - alpha-cyclodextrin KW - Z1LH97KTRM KW - Index Medicus KW - Rats KW - Polysorbates -- administration & dosage KW - Administration, Oral KW - Animals KW - Rats, Inbred F344 KW - Injections, Intravenous KW - Drug Compounding KW - Male KW - Biological Availability KW - Toluene -- analogs & derivatives KW - Toluene -- pharmacokinetics KW - Cyclodextrins -- administration & dosage KW - Corn Oil -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72475195?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Application+of+molecular+encapsulation+for+toxicology+studies%3A+toxicokinetics+of+p-chloro-alpha%2Calpha%2Calpha-trifluorotoluene+in+alpha-cyclodextrin+or+corn+oil+vehicles+in+male+F344+rats.&rft.au=Yuan%2C+J+M%3BJameson%2C+C+W%3BGoehl%2C+T+J%3BCollins%2C+B+J%3BPurdie%2C+W%3BJudd%2C+L&rft.aulast=Yuan&rft.aufirst=J&rft.date=1991-10-01&rft.volume=111&rft.issue=1&rft.spage=107&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 - 1991-12-16 N1 - Date created - 1991-12-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Tissue disposition of boron in male Fischer rats. AN - 72474834; 1949031 AB - Boric acid (H3BO3), an inorganic acid with widespread commercial use and consumer exposure, impairs fertility in male rodents at dose levels lower than those required to cause other adverse effects. Previous studies found a testicular lesion in adult Fischer rats fed 9000 ppm boric acid (1575 ppm boron) and slightly reduced basal serum testosterone levels. A CNS-mediated hormonal component to this lesion was suggested. Detailed data on the tissue disposition of boron in the rat, including accessory sex organs and the brain, are lacking. This study examined the tissue disposition of boron in reproductive, accessory sex organs, and other selected tissues in adult male Fischer rats fed 9000 ppm boric acid to determine if selective accumulation of boron in reproductive tissues, accessory sex organs, and/or the brain might correlate with and explain the apparent selective testicular toxicity. Adult male Fischer rats were fed 9000 ppm boric acid for up to 7 days. Animals were killed at 1, 2, 3, 4, and 7 days after the start of exposure. Plasma and excised tissues were heat-digested in acid and analyzed for boron by inductively coupled argon plasma emission spectrometry (ICAP). With the exception of adrenal glands, control boron levels in all tissues examined were below 4 micrograms/g. There was a rapid increase in plasma and tissue boron 1 day after the start of exposure (range 2- to 20-fold), with the exception of adipose tissue. With the exception of bone and adipose tissue, all soft tissues examined, including the testis, epididymis, accessory sex organs, hypothalamus, and rest of brain, appeared to reach steady-state boron levels (range 12-30 micrograms/g) by 3-4 days. Bone boron levels continued to increase up to the termination at 7 days (40-50 micrograms/g by Day 7). Bone attained the greatest concentration of boron (2- to 3-fold over plasma levels) while levels in adipose tissue were 20% of plasma levels during the 7-day exposure period. All other tissues appeared to show no appreciable accumulation of boron over plasma levels. The data suggest that neither the apparent selective testicular toxicity nor the slight CNS hormonal effect associated with boric acid exposure can be explained on the basis of selective accumulation of boron in the testis or brain/hypothalamus, respectively. Thus, the testicular toxicity is likely the result of certain biological processes that are unique to the testis and which are targets of boron exposure. JF - Toxicology and applied pharmacology AU - Ku, W W AU - Chapin, R E AU - Moseman, R F AU - Brink, R E AU - Pierce, K D AU - Adams, K Y AD - Developmental and Reproductive Toxicology Group, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 145 EP - 151 VL - 111 IS - 1 SN - 0041-008X, 0041-008X KW - Boric Acids KW - 0 KW - Boron KW - N9E3X5056Q KW - boric acid KW - R57ZHV85D4 KW - Index Medicus KW - Genital Diseases, Male -- metabolism KW - Animals KW - Prostate -- drug effects KW - Testis -- metabolism KW - Prostate -- metabolism KW - Brain -- metabolism KW - Tissue Distribution KW - Boric Acids -- pharmacokinetics KW - Seminal Vesicles -- drug effects KW - Rats KW - Boric Acids -- adverse effects KW - Rats, Inbred F344 KW - Boric Acids -- blood KW - Seminal Vesicles -- metabolism KW - Testis -- drug effects KW - Hypothalamus -- metabolism KW - Epididymis -- drug effects KW - Genital Diseases, Male -- chemically induced KW - Epididymis -- metabolism KW - Male KW - Boron -- adverse effects KW - Boron -- blood KW - Boron -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72474834?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Tissue+disposition+of+boron+in+male+Fischer+rats.&rft.au=Ku%2C+W+W%3BChapin%2C+R+E%3BMoseman%2C+R+F%3BBrink%2C+R+E%3BPierce%2C+K+D%3BAdams%2C+K+Y&rft.aulast=Ku&rft.aufirst=W&rft.date=1991-10-01&rft.volume=111&rft.issue=1&rft.spage=145&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 - 1991-12-16 N1 - Date created - 1991-12-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Vaginal cancer: the role of infectious and environmental factors. AN - 72469985; 1659200 AB - Primary cancers of the vagina are rare. They comprise 1% to 2% of all gynecologic malignancies and occur predominantly in older women. The diagnosis of primary carcinoma of the vagina requires that the cervix and vulva be intact and that no clinical evidence of other primary tumors exist. Approximately 90% of all vaginal tumors are squamous cell in type on histologic examination. Adenocarcinoma, which is much less common (2% to 4%), is seen primarily in younger women with in utero exposure to diethylstilbestrol. In addition to exposure to diethylstilbestrol, other environmental factors have been associated with the development of vaginal tumors, including chronic irritation from pessaries, previous hysterectomy for benign disease, immunosuppression therapy, cervical irradiation, and endometriosis. Infectious causes seem to play an even more pernicious role in vaginal cancer. The two agents most often implicated are herpes simplex virus and human papillomavirus. These viruses appear to serve as cofactors in the inducement of various genital cancers, working together or with environmental agents such as diethylstilbestrol and host-related genetic abnormalities. The prognosis of vaginal cancer depends on the stage of the disease, with an overall 5-year survival rate of 80% to 90% for early stages. JF - American journal of obstetrics and gynecology AU - Merino, M J AD - National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 1255 EP - 1262 VL - 165 IS - 4 Pt 2 SN - 0002-9378, 0002-9378 KW - Diethylstilbestrol KW - 731DCA35BT KW - Abridged Index Medicus KW - Index Medicus KW - Pessaries KW - Diethylstilbestrol -- adverse effects KW - Adenocarcinoma -- chemically induced KW - Humans KW - Prognosis KW - Papillomaviridae KW - Adenocarcinoma -- pathology KW - Pregnancy KW - Simplexvirus KW - Survival Rate KW - Hysterectomy -- adverse effects KW - Vaginal Smears KW - Middle Aged KW - Endometriosis -- complications KW - Female KW - Prenatal Exposure Delayed Effects KW - Carcinoma, Squamous Cell -- microbiology KW - Vaginal Neoplasms -- etiology KW - Carcinoma, Squamous Cell -- etiology KW - Carcinoma, Squamous Cell -- pathology KW - Vaginal Neoplasms -- pathology KW - Tumor Virus Infections -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72469985?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+obstetrics+and+gynecology&rft.atitle=Vaginal+cancer%3A+the+role+of+infectious+and+environmental+factors.&rft.au=Merino%2C+M+J&rft.aulast=Merino&rft.aufirst=M&rft.date=1991-10-01&rft.volume=165&rft.issue=4+Pt+2&rft.spage=1255&rft.isbn=&rft.btitle=&rft.title=American+journal+of+obstetrics+and+gynecology&rft.issn=00029378&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-27 N1 - Date created - 1991-11-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Radiation dose and leukaemia risk: general relative risk techniques for dose-response models in a matched case-control study. AN - 72468339; 1947508 AB - Generalized relative risk functions were used to model radiation dose-response information from a large matched case-control study of leukaemia occurring after treatment for cervical cancer. Models suggested by radiobiological theory were investigated and compared to standard analyses of categorical dose-response to the linear model. Local radiation doses to each of fourteen bone marrow compartments for each patient were incorporated into the models, and the corresponding risks were summed. Conditional maximum likelihood methods were used to estimate risk parameters. Unique features of the analysis include modelling both induction and reduction of risk as a function of radiation dose absorbed by different parts of the body within individuals. Detailed statistical aspects of these analyses are presented and discussed. JF - Statistics in medicine AU - Blettner, M AU - Boice, J D AD - Radiation Epidemiology Branch, National Cancer Institute, NIH, Bethesda, MD 20892. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 1511 EP - 1526 VL - 10 IS - 10 SN - 0277-6715, 0277-6715 KW - Index Medicus KW - Age Factors KW - Humans KW - Linear Models KW - Adult KW - Mathematical Computing KW - Case-Control Studies KW - Confidence Intervals KW - Middle Aged KW - Dose-Response Relationship, Radiation KW - Likelihood Functions KW - Female KW - Risk KW - Leukemia, Radiation-Induced -- etiology KW - Models, Statistical KW - Uterine Cervical Neoplasms -- radiotherapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72468339?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Statistics+in+medicine&rft.atitle=Radiation+dose+and+leukaemia+risk%3A+general+relative+risk+techniques+for+dose-response+models+in+a+matched+case-control+study.&rft.au=Blettner%2C+M%3BBoice%2C+J+D&rft.aulast=Blettner&rft.aufirst=M&rft.date=1991-10-01&rft.volume=10&rft.issue=10&rft.spage=1511&rft.isbn=&rft.btitle=&rft.title=Statistics+in+medicine&rft.issn=02776715&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-26 N1 - Date created - 1991-12-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The role of alpha-interferon in patients with human immunodeficiency virus infection. AN - 72467709; 1948129 AB - alpha-Interferon (IFN alpha) blocks replication of human immunodeficiency virus (HIV)-1 in vitro by interfering with the release of mature virions. Clinical trials have addressed the in vivo effects of IFN alpha, both alone and in combination with other agents, in a variety of patients at all stages of HIV-1 infection. Patients with late stages of HIV-1 infection (CD4 counts under 100) show few positive results following treatment with IFN alpha. Patients with earlier stages of HIV infection, however, may benefit from treatment with this agent. Several clinical trials have demonstrated the activity of interferon in the treatment of patients with acquired immunodeficiency syndrome, Kaposi's sarcoma, and CD4 counts over 200. In these trials, response rates of approximately 40% have been reported, with the probability of response directly correlated with the level of CD4 cells. These antitumor effects have been associated with declines in the circulating levels of the HIV-1 core antigen p24. alpha-Interferon activity has also been studied in patients concomitantly receiving zidovudine. In these studies, neutropenia, reversible with the concomitant administration of granulocyte macrophage colony-stimulating factor, has been the most common dose-limiting toxicity. Both the antitumor and antiviral activities of combination therapy appear to be at least as good as those observed when single agents are used. Controlled clinical trials are currently under way to evaluate the role of interferon therapy, both alone and in combination with zidovudine, in patients with early HIV infection. JF - Seminars in oncology AU - Lane, H C AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 46 EP - 52 VL - 18 IS - 5 Suppl 7 SN - 0093-7754, 0093-7754 KW - Interferon-alpha KW - 0 KW - Zidovudine KW - 4B9XT59T7S KW - Index Medicus KW - AIDS/HIV KW - Zidovudine -- therapeutic use KW - Animals KW - Humans KW - Clinical Trials as Topic KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Sarcoma, Kaposi -- therapy KW - Sarcoma, Kaposi -- etiology KW - Interferon-alpha -- therapeutic use KW - HIV Infections -- complications KW - HIV Infections -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72467709?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Seminars+in+oncology&rft.atitle=The+role+of+alpha-interferon+in+patients+with+human+immunodeficiency+virus+infection.&rft.au=Lane%2C+H+C&rft.aulast=Lane&rft.aufirst=H&rft.date=1991-10-01&rft.volume=18&rft.issue=5+Suppl+7&rft.spage=46&rft.isbn=&rft.btitle=&rft.title=Seminars+in+oncology&rft.issn=00937754&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-10 N1 - Date created - 1991-12-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Analysis of clinical trials by treatment actually received: is it really an option? AN - 72463708; 1947515 AB - The primary analysis of a randomized clinical trial should compare patients in their randomly assigned treatment groups (intention to treat analysis). When a substantial number of subjects fail to take a prescribed medication or are switched to a different study medication, it is tempting to consider treatment comparisons using only those subjects with treatment as actually received rather than as prescribed. There are several arguments against this approach: the prognostic balance brought about by randomization is likely to be disturbed; sample size will be reduced; and the validity of the statistical test procedures will be undermined. Further, results of analysis by treatment actually received may suffer from a bias introduced by using compliance, a factor often related to outcome independently of the treatment received, to determine the groups for comparison. The extent and nature of this bias will be related to the definition of compliance in an as treated analysis, a definition which could be unintentionally self-serving. We have investigated the problem of the definition of actual treatment in the context of a recent clinical trial. We used several definitions to classify patients as having received or not received treatment as prescribed. These definitions, when used in as treated analyses, provided results that were at times inconsistent or counter-intuitive, and which neither helped to confirm nor further explain the intention to treat analysis. JF - Statistics in medicine AU - Lee, Y J AU - Ellenberg, J H AU - Hirtz, D G AU - Nelson, K B AD - National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 1595 EP - 1605 VL - 10 IS - 10 SN - 0277-6715, 0277-6715 KW - Phenobarbital KW - YQE403BP4D KW - Index Medicus KW - Infant KW - Probability KW - Life Tables KW - Phenobarbital -- adverse effects KW - Cognition -- drug effects KW - Humans KW - Seizures -- prevention & control KW - Phenobarbital -- therapeutic use KW - Intelligence Tests KW - Child, Preschool KW - Patient Compliance KW - Data Interpretation, Statistical KW - Randomized Controlled Trials as Topic -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72463708?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Statistics+in+medicine&rft.atitle=Analysis+of+clinical+trials+by+treatment+actually+received%3A+is+it+really+an+option%3F&rft.au=Lee%2C+Y+J%3BEllenberg%2C+J+H%3BHirtz%2C+D+G%3BNelson%2C+K+B&rft.aulast=Lee&rft.aufirst=Y&rft.date=1991-10-01&rft.volume=10&rft.issue=10&rft.spage=1595&rft.isbn=&rft.btitle=&rft.title=Statistics+in+medicine&rft.issn=02776715&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-26 N1 - Date created - 1991-12-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - New chemotherapeutic agents for non-Hodgkin's lymphomas. AN - 72447384; 1718938 AB - Combination chemotherapy regimens achieve complete remissions in 60% to 80% of patients with non-Hodgkin's lymphomas; however, the majority of patients will relapse, and resistant disease remains a problem. Attempts to identify new, effective chemotherapy agents have primarily focused on the development of analogues that, unfortunately, have uniformly failed to provide a substantial therapeutic advantage. Drugs with a unique mechanism of action are more likely to be successful; among these are the purine analogues (e.g., fludarabine, 2'-deoxycoformycin, 2-chlorodeoxyadenosine) and agents that can reverse clinical drug resistance. The number of patients who can be cured can be increased only by incorporating new agents into front-line regimens through carefully designed clinical trials. JF - Hematology/oncology clinics of North America AU - Cheson, B D AD - Clinical Investigations Branch, National Cancer Institute, Bethesda, Maryland. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 1027 EP - 1051 VL - 5 IS - 5 SN - 0889-8588, 0889-8588 KW - Antimetabolites, Antineoplastic KW - 0 KW - Antineoplastic Agents KW - Vidarabine Phosphate KW - 106XV160TZ KW - fludarabine phosphate KW - 1X9VK9O1SC KW - Pentostatin KW - 395575MZO7 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Cisplatin -- therapeutic use KW - Vidarabine Phosphate -- therapeutic use KW - Humans KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Antimetabolites, Antineoplastic -- therapeutic use KW - Vidarabine Phosphate -- analogs & derivatives KW - Pentostatin -- therapeutic use KW - Lymphoma, Non-Hodgkin -- drug therapy KW - Antineoplastic Agents -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72447384?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hematology%2Foncology+clinics+of+North+America&rft.atitle=New+chemotherapeutic+agents+for+non-Hodgkin%27s+lymphomas.&rft.au=Cheson%2C+B+D&rft.aulast=Cheson&rft.aufirst=B&rft.date=1991-10-01&rft.volume=5&rft.issue=5&rft.spage=1027&rft.isbn=&rft.btitle=&rft.title=Hematology%2Foncology+clinics+of+North+America&rft.issn=08898588&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-17 N1 - Date created - 1991-12-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - K-ras activation occurs frequently in mucinous adenocarcinomas and rarely in other common epithelial tumors of the human ovary. AN - 72161644; 1656759 AB - To explore the role of mutational activation of members of the ras family of cellular protooncogenes in the development of human ovarian neoplasms, a series of 37 ovarian tumors from Japanese patients was studied. These included 30 common epithelial tumors (1 mucinous tumor of borderline malignancy, 7 mucinous adenocarcinomas, and 22 nonmucinous carcinomas: 10 serous, 3 clear cell, 8 endometrioid, and 1 undifferentiated), 5 tumors of germ cell origin, and 2 sex cord/stromal cell tumors. Polymerase chain reaction was performed from selected areas of deparaffinized sections of formalin-fixed paraffin-embedded tissue, and the presence of activating point mutations in codons 12, 13, and 61 of the H-, N-, and K-ras genes was probed by dot-blot hybridization analysis with mutation specific oligonucleotides. Mutations in K-ras were also looked for by direct genomic sequencing. The overall frequency of ras gene mutations was 10/37 (27%). Mutations were detected only in K-ras, and were found in most of the mucinous tumors, including the one such tumor of borderline malignancy (6/8; 75%). In one mucinous adenocarcinoma, two mutations were detected in paraffin-embedded material that had not previously been found in high molecular weight DNA isolated from frozen tissue from the same case. K-ras mutations occurred significantly more frequently in mucinous tumors (6/8, 75%) than in serous carcinomas (2/10, 20%; P = 0.031) or in all nonmucinous types of epithelial ovarian tumors combined (3/22, 14%; P = 0.0031). JF - The American journal of pathology AU - Enomoto, T AU - Weghorst, C M AU - Inoue, M AU - Tanizawa, O AU - Rice, J M AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick Cancer Research and Development Center, Maryland. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 777 EP - 785 VL - 139 IS - 4 SN - 0002-9440, 0002-9440 KW - K-ras KW - DNA, Neoplasm KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Aged KW - DNA, Neoplasm -- analysis KW - Nucleic Acid Hybridization KW - Gene Amplification KW - Japan -- epidemiology KW - Polymerase Chain Reaction KW - Base Sequence KW - Aged, 80 and over KW - Adult KW - Molecular Sequence Data KW - Mutation -- genetics KW - DNA, Neoplasm -- genetics KW - Middle Aged KW - Adolescent KW - Female KW - Ovarian Neoplasms -- metabolism KW - Adenocarcinoma, Mucinous -- genetics KW - Adenocarcinoma, Mucinous -- epidemiology KW - Genes, ras -- genetics KW - Adenocarcinoma, Mucinous -- metabolism KW - Ovarian Neoplasms -- genetics KW - Ovarian Neoplasms -- epidemiology KW - Gene Expression Regulation, Neoplastic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72161644?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=K-ras+activation+occurs+frequently+in+mucinous+adenocarcinomas+and+rarely+in+other+common+epithelial+tumors+of+the+human+ovary.&rft.au=Enomoto%2C+T%3BWeghorst%2C+C+M%3BInoue%2C+M%3BTanizawa%2C+O%3BRice%2C+J+M&rft.aulast=Enomoto&rft.aufirst=T&rft.date=1991-10-01&rft.volume=139&rft.issue=4&rft.spage=777&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 - 1991-11-19 N1 - Date created - 1991-11-19 N1 - Date revised - 2017-01-13 N1 - Gene symbol - K-ras N1 - SuppNotes - Cited By: Cancer Lett. 1991 Jun 14;58(1-2):107-13 [2049776] Cancer. 1975 Nov;36(5):1709-22 [1192360] Oncogene Res. 1988;3(1):77-86 [3144694] Proc Natl Acad Sci U S A. 1987 Jul;84(14):4974-8 [3110778] Nature. 1987 Jun 4-10;327(6121):430-2 [3295562] Mutat Res. 1988 May;195(3):255-71 [3283542] Nucleic Acids Res. 1989 Jul 11;17(13):5407 [2762140] Proc Natl Acad Sci U S A. 1988 Dec;85(23):9268-72 [3057505] J Exp Med. 1988 Jan 1;167(1):225-30 [2826637] N Engl J Med. 1988 Sep 1;319(9):525-32 [2841597] Nucleic Acids Res. 1988 Aug 25;16(16):7773-82 [3047672] Oncogene. 1988 Feb;2(2):157-65 [3285294] Cancer Res. 1988 Sep 15;48(18):5251-5 [2457438] Cell. 1988 May 20;53(4):549-54 [2453289] Nature. 1987 May 28-Jun 3;327(6120):298-303 [2438556] Cancer Res. 1989 Sep 1;49(17):4682-9 [2547513] Cancer Res. 1989 Mar 1;49(5):1220-2 [2917352] Proc Natl Acad Sci U S A. 1988 Mar;85(5):1629-33 [3278322] Annu Rev Biochem. 1987;56:779-827 [3304147] Nature. 1987 May 28-Jun 3;327(6120):293-7 [3587348] Science. 1990 Aug 10;249(4969):655-9 [2116665] Cancer Res. 1990 Jul 1;50(13):4087-91 [1972347] Cancer Res. 1990 Feb 15;50(4):1121-4 [2153451] Cancer Res. 1990 Oct 1;50(19):6139-45 [2205377] Cell. 1990 Jun 1;61(5):759-67 [2188735] Cancer Res. 1990 May 1;50(9):2724-8 [2328498] Proc Natl Acad Sci U S A. 1983 Jan;80(2):383-7 [6300838] Science. 1989 May 12;244(4905):707-12 [2470152] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Clinical implications of the competitive inhibition of the debrisoquin-metabolizing isozyme by quinidine. AN - 72160867; 1681790 AB - Approximately 10% of western populations are genetically deficient in the enzyme that metabolizes the antihypertensive drug debrisoquin. These "poor metabolizers" process many common medications in an aberrant fashion, resulting in a variety of untoward consequences including exaggerated drug effect, subtherapeutic drug concentrations, or complex drug interactions. A variety of medications, including neuroleptics, antidepressants, beta-blockers, and certain antiarrhythmics, are subject to the influence of this metabolic polymorphism. Quinidine administration changes persons to poor metabolizers of debrisoquin for the duration of therapy. Thus, the use of quinidine with any of the other drugs metabolized by this isozyme may be expected to result in a drug interaction in which a person's response will mimic that of a poor metabolizer. Because no test is commonly available to determine directly the debrisoquin metabolic phenotype, clinicians should be alert to unusual drug reactions in patients receiving quinidine concurrently with the other medications. JF - Archives of internal medicine AU - Caporaso, N E AU - Shaw, G L AD - Environmental Epidemiology Branch, National Cancer Institute NIH, Bethesda, Md 20892. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 1985 EP - 1992 VL - 151 IS - 10 SN - 0003-9926, 0003-9926 KW - Adrenergic beta-Antagonists KW - 0 KW - Anti-Arrhythmia Agents KW - Antidepressive Agents, Tricyclic KW - Antihypertensive Agents KW - Antipsychotic Agents KW - Cytochrome P-450 Enzyme Inhibitors KW - Monoamine Oxidase Inhibitors KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Mixed Function Oxygenases KW - EC 1.- KW - Cytochrome P-450 CYP2D6 KW - EC 1.14.14.1 KW - Quinidine KW - ITX08688JL KW - Abridged Index Medicus KW - Index Medicus KW - Phenotype KW - Drug Interactions KW - Cytochrome P-450 Enzyme System -- deficiency KW - Antidepressive Agents, Tricyclic -- pharmacology KW - Cytochrome P-450 Enzyme System -- genetics KW - Humans KW - Antipsychotic Agents -- pharmacology KW - Antihypertensive Agents -- pharmacology KW - Adrenergic beta-Antagonists -- pharmacology KW - Monoamine Oxidase Inhibitors -- pharmacology KW - Anti-Arrhythmia Agents -- pharmacology KW - Mixed Function Oxygenases -- antagonists & inhibitors KW - Quinidine -- pharmacology KW - Mixed Function Oxygenases -- deficiency KW - Mixed Function Oxygenases -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72160867?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+internal+medicine&rft.atitle=Clinical+implications+of+the+competitive+inhibition+of+the+debrisoquin-metabolizing+isozyme+by+quinidine.&rft.au=Caporaso%2C+N+E%3BShaw%2C+G+L&rft.aulast=Caporaso&rft.aufirst=N&rft.date=1991-10-01&rft.volume=151&rft.issue=10&rft.spage=1985&rft.isbn=&rft.btitle=&rft.title=Archives+of+internal+medicine&rft.issn=00039926&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-07 N1 - Date created - 1991-11-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A double-blind desipramine substitution during long-term clomipramine treatment in children and adolescents with obsessive-compulsive disorder. AN - 72159988; 1929762 AB - Twenty-six children and adolescents with severe primary obsessive-compulsive disorder receiving long-term clomipramine hydrochloride maintenance treatment (mean +/- SD, 17.1 +/- 8.3 months; range, 4 to 32 months) entered an 8-month double-blind desipramine hydrochloride substitution study to assess the necessity of continued drug treatment. All patients received clomipramine for the first 3 months, then half continued with clomipramine therapy (nonsubstituted group) and half had desipramine blindly substituted for the next 2 months; all subjects again received clomipramine for the last 3 study months. Eight (89%) of nine of the substituted and only two (18%) of 11 of the nonsubstituted group subjects relapsed during the 2-month comparison period. Long-term clomipramine treatment seems necessary for this population of children and adolescents with obsessive-compulsive disorder. However, even patients receiving maintenance clomipramine treatment throughout the entire study had continued obsessive-compulsive symptoms, which varied in severity over time. JF - Archives of general psychiatry AU - Leonard, H L AU - Swedo, S E AU - Lenane, M C AU - Rettew, D C AU - Cheslow, D L AU - Hamburger, S D AU - Rapoport, J L AD - National Institute of Mental Health, Child Psychiatry Branch, Bethesda, MD 20892. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 922 EP - 927 VL - 48 IS - 10 SN - 0003-990X, 0003-990X KW - Clomipramine KW - NUV44L116D KW - Desipramine KW - TG537D343B KW - Abridged Index Medicus KW - Index Medicus KW - Drug Administration Schedule KW - Age Factors KW - Psychiatric Status Rating Scales KW - Double-Blind Method KW - Humans KW - Follow-Up Studies KW - Child KW - Adolescent KW - Recurrence KW - Male KW - Female KW - Desipramine -- therapeutic use KW - Desipramine -- adverse effects KW - Obsessive-Compulsive Disorder -- psychology KW - Desipramine -- administration & dosage KW - Obsessive-Compulsive Disorder -- drug therapy KW - Clomipramine -- adverse effects KW - Clomipramine -- administration & dosage KW - Clomipramine -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72159988?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+double-blind+desipramine+substitution+during+long-term+clomipramine+treatment+in+children+and+adolescents+with+obsessive-compulsive+disorder.&rft.au=Leonard%2C+H+L%3BSwedo%2C+S+E%3BLenane%2C+M+C%3BRettew%2C+D+C%3BCheslow%2C+D+L%3BHamburger%2C+S+D%3BRapoport%2C+J+L&rft.aulast=Leonard&rft.aufirst=H&rft.date=1991-10-01&rft.volume=48&rft.issue=10&rft.spage=922&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 - 1991-11-13 N1 - Date created - 1991-11-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - B3(Fv)-PE38KDEL, a single-chain immunotoxin that causes complete regression of a human carcinoma in mice. AN - 72155650; 1924323 AB - The genes encoding the heavy- and light-chain Fv regions of the monoclonal murine antibody B3, which recognizes a carbohydrate antigen on the surface of many human carcinomas, were cloned by PCR techniques and used to generate single-chain immunotoxins containing Pseudomonas exotoxin (PE). The light and heavy chains were connected by a flexible linker to form a single-chain antigen-binding protein, B3(Fv), which was in turn fused to truncated forms of PE lacking the cell-binding domain. The single-chain Fv and two different B3(Fv) immunotoxins, B3(Fv)-PE40 and B3(Fv)-PE38KDEL, were expressed in Escherichia coli and the single-chain immunotoxins were purified to near homogeneity. Both recombinant immunotoxins were shown to be cytotoxic specifically to carcinoma cell lines that express the B3 antigen on their surface; B3(Fv)-PE38KDEL was significantly more active. Furthermore, intravenous administration of B3(Fv)-PE38KDEL caused complete regression of human epidermoid carcinomas growing subcutaneously in immunodeficient mice. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Brinkmann, U AU - Pai, L H AU - FitzGerald, D J AU - Willingham, M AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/10/01/ PY - 1991 DA - 1991 Oct 01 SP - 8616 EP - 8620 VL - 88 IS - 19 SN - 0027-8424, 0027-8424 KW - Antibodies, Neoplasm KW - 0 KW - Antigens, Neoplasm KW - Bacterial Toxins KW - Exotoxins KW - Immunoglobulin Variable Region KW - Immunotoxins KW - Oligonucleotides 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 - Immunoglobulin Variable Region -- genetics KW - Protein Biosynthesis KW - Animals KW - Genes, Immunoglobulin KW - Amino Acid Sequence KW - Mice KW - Mice, Nude KW - Structure-Activity Relationship KW - Cell Survival KW - Cloning, Molecular KW - Neoplasm Transplantation KW - Polymerase Chain Reaction KW - Base Sequence KW - Oligonucleotides -- chemistry KW - Molecular Sequence Data KW - Pseudomonas aeruginosa KW - Exotoxins -- genetics KW - Exotoxins -- administration & dosage KW - Immunotoxins -- toxicity KW - Antibodies, Neoplasm -- genetics KW - Immunotoxins -- metabolism KW - Antigens, Neoplasm -- immunology KW - Carcinoma, Squamous Cell -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72155650?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=B3%28Fv%29-PE38KDEL%2C+a+single-chain+immunotoxin+that+causes+complete+regression+of+a+human+carcinoma+in+mice.&rft.au=Brinkmann%2C+U%3BPai%2C+L+H%3BFitzGerald%2C+D+J%3BWillingham%2C+M%3BPastan%2C+I&rft.aulast=Brinkmann&rft.aufirst=U&rft.date=1991-10-01&rft.volume=88&rft.issue=19&rft.spage=8616&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 - 1991-10-31 N1 - Date created - 1991-10-31 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - S57506; GENBANK; S57504; S57448; S57990; S57444; S57457; S57442; S57981; X59603; S57596 N1 - SuppNotes - Cited By: EMBO J. 1984 Dec 1;3(12):3023-30 [6098462] Proc Natl Acad Sci U S A. 1985 Jan;82(2):488-92 [3881765] Science. 1988 Jan 29;239(4839):487-91 [2448875] J Biol Chem. 1988 Jul 5;263(19):9470-5 [3132465] Proc Natl Acad Sci U S A. 1988 Aug;85(16):5879-83 [3045807] Science. 1988 Oct 21;242(4877):423-6 [3140379] J Biol Chem. 1989 Jan 5;264(1):259-65 [2909518] Nature. 1989 Jun 1;339(6223):394-7 [2498664] J Biol Chem. 1989 Aug 25;264(24):14256-61 [2503515] Proc Natl Acad Sci U S A. 1989 Nov;86(21):8545-9 [2510169] Proc Natl Acad Sci U S A. 1990 Jan;87(1):308-12 [2104981] Proc Natl Acad Sci U S A. 1990 Feb;87(3):1066-70 [2105495] J Biol Chem. 1990 Sep 5;265(25):15198-202 [2118522] Proc Natl Acad Sci U S A. 1990 Dec;87(23):9491-4 [2251289] Proc Natl Acad Sci U S A. 1991 Apr 15;88(8):3358-62 [2014255] J Mol Biol. 1969 May 14;41(3):459-72 [4896022] Nature. 1970 Aug 15;227(5259):680-5 [5432063] Gene. 1977;2(2):95-113 [344137] J Immunol. 1981 Jul;127(1):347-51 [6787129] J Mol Biol. 1986 May 5;189(1):113-30 [3537305] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Archival analysis of p53 genetic and protein alterations in Chinese esophageal cancer. AN - 72153122; 1923503 AB - A strategy and methods for archival analysis of genetic and protein alterations in the p53 tumor-suppressor gene are presented. The tumor series includes 43 paraffin-embedded esophageal carcinomas from two high-incidence regions in the People's Republic of China. More than half contained elevated p53 protein levels which were detected by a high-titer polyclonal antiserum and a sensitive immunohistochemical method. To estimate the frequency of underlying mutations, DNA was isolated from conventional paraffin sections, amplified by the polymerase chain reaction, and examined by dideoxy termination sequencing. Analysis of exons 5-8 in a subset of 10 tumors revealed mis-sense point mutations in 4 out of 5 immunostain-positive tumors and a mutation encoding a stop codon in 1 of 5 immunostain-negative tumors. In this report of archival material, we conclude that detectable levels of p53 protein correlate closely with the occurrence of mis-sense mutations. Furthermore, these methods render large repositories of paraffin-embedded tumor and non-tumor tissues accessible to analysis. Immunohistochemical screening for elevated protein levels followed by sequence analysis represents an efficient strategy for the evaluation of the p53 mutational spectrum. JF - Oncogene AU - Bennett, W P AU - Hollstein, M C AU - He, A AU - Zhu, S M AU - Resau, J H AU - Trump, B F AU - Metcalf, R A AU - Welsh, J A AU - Midgley, C AU - Lane, D P AD - Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 1779 EP - 1784 VL - 6 IS - 10 SN - 0950-9232, 0950-9232 KW - p53 KW - Index Medicus KW - Humans KW - Molecular Sequence Data KW - Amino Acid Sequence KW - China KW - Carcinoma, Squamous Cell -- ethnology KW - Adenocarcinoma -- ethnology KW - Esophageal Neoplasms -- ethnology KW - Genes, p53 -- genetics KW - Esophageal Neoplasms -- genetics KW - Carcinoma, Squamous Cell -- genetics KW - Mutation -- genetics KW - Adenocarcinoma -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72153122?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Archival+analysis+of+p53+genetic+and+protein+alterations+in+Chinese+esophageal+cancer.&rft.au=Bennett%2C+W+P%3BHollstein%2C+M+C%3BHe%2C+A%3BZhu%2C+S+M%3BResau%2C+J+H%3BTrump%2C+B+F%3BMetcalf%2C+R+A%3BWelsh%2C+J+A%3BMidgley%2C+C%3BLane%2C+D+P&rft.aulast=Bennett&rft.aufirst=W&rft.date=1991-10-01&rft.volume=6&rft.issue=10&rft.spage=1779&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=09509232&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-18 N1 - Date created - 1991-11-18 N1 - Date revised - 2017-01-13 N1 - Gene symbol - p53 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Suppression of the chemically transformed phenotype of BHK cells by a human cDNA. AN - 72149293; 1922047 AB - Transformation of the baby hamster kidney cell line BHK SN-10 by chemical carcinogens such as nitrosylmethylurea (NMU) is mediated by the loss of a gene product critical for the suppression of malignant transformation. Somatic cell hybrids between chemically transformed BHK SN-10 cells and either normal hamster kidney or human fibroblast cells are nontransformed; therefore, a recessive mechanism underlies the malignant transformation of BHK SN-10 cells after chemical carcinogenesis (A. Stoler and N. P. Bouck, Proc. Natl. Acad. Sci. USA 82:570-574, 1985). A human fibroblast cDNA library was constructed and introduced into NMU-transformed BHK SN-10 cells (NMU 34m) in order to identify a human cDNA capable of suppressing cellular transformation. NMU-transformed BHK cells were analyzed for reversion to an anchorage-dependent normal cellular phenotype after transfection with human cDNA. The human cDNA capable of inducing stable reversion of NMU 34m cells encodes the intermediate filament protein vimentin, which is apparently required for maintenance of the normal phenotype in BHK SN-10 cells. JF - Molecular and cellular biology AU - Eiden, M V AU - MacArthur, L AU - Okayama, H AD - Laboratory of Cell Biology, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 5321 EP - 5329 VL - 11 IS - 10 SN - 0270-7306, 0270-7306 KW - Vimentin KW - 0 KW - Index Medicus KW - Animals KW - Blotting, Southern KW - Humans KW - Transfection -- genetics KW - Hybrid Cells -- physiology KW - Mice, Nude KW - Mice KW - Cell Line, Transformed KW - Tumor Stem Cell Assay KW - Introns -- genetics KW - Female KW - Genes, Tumor Suppressor -- genetics KW - Suppression, Genetic KW - Cell Transformation, Neoplastic KW - Vimentin -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72149293?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Suppression+of+the+chemically+transformed+phenotype+of+BHK+cells+by+a+human+cDNA.&rft.au=Eiden%2C+M+V%3BMacArthur%2C+L%3BOkayama%2C+H&rft.aulast=Eiden&rft.aufirst=M&rft.date=1991-10-01&rft.volume=11&rft.issue=10&rft.spage=5321&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 - 1991-10-31 N1 - Date created - 1991-10-31 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1973 Jan;70(1):46-9 [4346037] Nature. 1964 Sep 26;203:1355-7 [14207308] Methods Enzymol. 1979;58:296-302 [423770] Mol Cell Biol. 1982 Feb;2(2):97-105 [6810094] Annu Rev Biochem. 1982;51:219-50 [6180679] Cell. 1983 Nov;35(1):215-23 [6194898] Proc Natl Acad Sci U S A. 1985 Jan;82(2):570-4 [3155863] Annu Rev Genet. 1984;18:553-612 [6397126] In Vitro Cell Dev Biol. 1985 Aug;21(8):463-9 [4030628] Mol Cell Biol. 1986 Nov;6(11):3614-20 [3467175] Nature. 1987 Aug 6-12;328(6130):524-6 [3614355] Nature. 1987 Aug 6-12;328(6130):528-30 [2886918] Am J Hum Genet. 1987 Oct;41(4):616-26 [3661560] Mol Cell Biol. 1987 Aug;7(8):2745-52 [3670292] Cell. 1989 Feb 10;56(3):345-55 [2464438] Science. 1989 Feb 17;243(4893):937-40 [2521957] Proc Natl Acad Sci U S A. 1989 Apr;86(8):2747-51 [2539599] Proc Natl Acad Sci U S A. 1989 Dec;86(24):9886-90 [2532364] Biochemistry. 1989 Oct 17;28(21):8263-9 [2690938] Science. 1990 Jun 1;248(4959):1101-4 [2188364] Cell. 1991 Jan 25;64(2):235-48 [1988146] Nature. 1976 Dec 23-30;264(5588):722-7 [827710] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Direct evidence for in vivo hydroxyl-radical generation in experimental iron overload: an ESR spin-trapping investigation. AN - 72148036; 1656444 AB - Although the hydroxyl radical is often implicated as the species responsible for the initiation of oxidative damage in iron-overload conditions, no ESR evidence for the formation of the radical in vivo has been reported. We have employed a secondary radical-trapping technique in which the hydroxyl radical reacts with dimethyl sulfoxide to form the methyl radical, which is then detected as its adduct of the spin trap N-t-butyl-alpha-phenylnitrone in the bile of animals given an intragastric dose of ferrous sulfate. The identity of this adduct was verified by isotope-substitution techniques. We show that unless measures are taken to inactivate the iron excreted in the bile of treated animals, reactions between iron, oxygen, dimethyl sulfoxide, N-t-butyl-alpha-phenylnitrone, and bile components lead to the formation of artifacts during sample collection. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Burkitt, M J AU - Mason, R P AD - Laboratory of Molecular Biophysics, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709. Y1 - 1991/10/01/ PY - 1991 DA - 1991 Oct 01 SP - 8440 EP - 8444 VL - 88 IS - 19 SN - 0027-8424, 0027-8424 KW - Cyclic N-Oxides KW - 0 KW - Free Radicals KW - Hydroxides KW - Nitrogen Oxides KW - Spin Labels KW - phenyl-N-tert-butylnitrone KW - 3I91332OPG KW - 2,2'-Dipyridyl KW - 551W113ZEP KW - Iron KW - E1UOL152H7 KW - Dimethyl Sulfoxide KW - YOW8V9698H KW - Index Medicus KW - Animals KW - Bile -- metabolism KW - Oxidation-Reduction KW - Rats KW - Rats, Inbred Strains KW - Electron Spin Resonance Spectroscopy KW - 2,2'-Dipyridyl -- chemistry KW - Nitrogen Oxides -- chemistry KW - Male KW - Dimethyl Sulfoxide -- chemistry KW - Iron -- chemistry KW - Hydroxides -- chemistry KW - Iron -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72148036?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Direct+evidence+for+in+vivo+hydroxyl-radical+generation+in+experimental+iron+overload%3A+an+ESR+spin-trapping+investigation.&rft.au=Burkitt%2C+M+J%3BMason%2C+R+P&rft.aulast=Burkitt&rft.aufirst=M&rft.date=1991-10-01&rft.volume=88&rft.issue=19&rft.spage=8440&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 - 1991-10-31 N1 - Date created - 1991-10-31 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Clin Invest. 1986 Jan;77(1):90-7 [3944262] Hepatology. 1985 Sep-Oct;5(5):789-97 [4029891] Free Radic Res Commun. 1987;3(1-5):251-5 [2854527] Free Radic Res Commun. 1989;7(3-6):307-13 [2583549] Biochem J. 1989 Aug 1;261(3):787-92 [2803243] Free Radic Res Commun. 1989;5(6):333-44 [2925101] Drug Metab Dispos. 1988 Nov-Dec;16(6):813-7 [2907458] N Engl J Med. 1988 May 26;318(21):1355-62 [3367936] Int J Biochem. 1986;18(9):791-8 [3758461] J Biol Chem. 1990 Feb 15;265(5):2650-6 [2154454] Hepatology. 1990 Jan;11(1):127-37 [2153094] Free Radic Biol Med. 1990;8(2):145-52 [2110108] Free Radic Biol Med. 1990;8(1):95-108 [2182396] Biochem J. 1980 Nov 1;191(2):421-7 [6263247] J Clin Invest. 1983 Mar;71(3):429-39 [6826715] Annu Rev Biochem. 1980;49:357-93 [6996567] Blood. 1977 Sep;50(3):433-9 [328083] N Engl J Med. 1978 Mar 23;298(12):659-68 [24176] Clin Toxicol. 1971 Dec;4(4):615-9 [5317454] Ann N Y Acad Sci. 1967 Mar 15;141(1):110-26 [5232226] Am J Med Sci. 1955 Nov;230(5):491-8 [13268426] Free Radic Res Commun. 1991;14(2):107-23 [1648018] J Biol Chem. 1990 Oct 5;265(28):16733-6 [2170352] J Inorg Biochem. 1989 Jan;35(1):55-69 [2540265] Free Radic Res Commun. 1988;4(5):311-5 [2853109] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Thyroid-specific enhancer-binding protein (T/EBP): cDNA cloning, functional characterization, and structural identity with thyroid transcription factor TTF-1. AN - 72146075; 1922026 AB - A cDNA clone encoding a thyroid-specific enhancer-binding protein (T/EBP) was isolated from a rat thyroid-derived FRTL-5 cell lambda gt 11 expression library, using a double-stranded oligonucleotide probe. This oligonucleotide was previously demonstrated to have the strongest binding affinity among three cis-acting DNA elements within the thyroid-specific enhancer region located 5.5 kbp upstream of the human thyroid peroxidase gene transcription start site. Nucleotide and deduced amino acid sequences of the cDNA revealed that T/EBP is identical to the previously reported thyroid-specific transcription factor 1 (TTF-1), which binds to the promoter of the rat thyroglobulin gene and controls its thyroid-specific expression. Expression of the T/EBP cDNA under control of the human cytomegalovirus major immediate-early gene promoter conferred thyroid-specific enhancer activity of as high as 26-fold to nonpermissive human hepatoma HepG2 cells when cotransfected with a vector containing 6.3 kbp of upstream sequence of the human thyroid peroxidase gene connected to a luciferase reporter gene. T/EBP was further expressed in HepG2 cells by using the vaccinia virus expression system. The expressed protein was partially purified by using sequence-specific affinity column chromatography and was further shown, by gel mobility shift experiments, to specifically bind to the enhancer-derived double-stranded oligonucleotide. These results clearly indicate that the binding of T/EBP (TTF-1) to the specific cis-acting enhancer element is largely responsible for thyroid-specific enhancer activity. JF - Molecular and cellular biology AU - Mizuno, K AU - Gonzalez, F J AU - Kimura, S AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 4927 EP - 4933 VL - 11 IS - 10 SN - 0270-7306, 0270-7306 KW - T/EBP KW - TPO KW - Nuclear Proteins KW - 0 KW - Oligonucleotides KW - Recombinant Fusion Proteins KW - Transcription Factors KW - thyroid nuclear factor 1 KW - Iodide Peroxidase KW - EC 1.11.1.8 KW - Luciferases KW - EC 1.13.12.- KW - Index Medicus KW - Vaccinia virus -- genetics KW - Recombinant Fusion Proteins -- biosynthesis KW - Animals KW - Blotting, Northern KW - Sequence Homology, Nucleic Acid KW - Humans KW - Oligonucleotides -- metabolism KW - Cloning, Molecular KW - Rats KW - Base Sequence KW - Tumor Cells, Cultured KW - Enhancer Elements, Genetic -- physiology KW - Molecular Sequence Data KW - Gene Expression -- physiology KW - Luciferases -- genetics KW - Cell Line KW - Nuclear Proteins -- genetics KW - Transcription Factors -- metabolism KW - Nuclear Proteins -- biosynthesis KW - Iodide Peroxidase -- genetics KW - Nuclear Proteins -- metabolism KW - Transcription Factors -- genetics KW - Transcription Factors -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72146075?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Thyroid-specific+enhancer-binding+protein+%28T%2FEBP%29%3A+cDNA+cloning%2C+functional+characterization%2C+and+structural+identity+with+thyroid+transcription+factor+TTF-1.&rft.au=Mizuno%2C+K%3BGonzalez%2C+F+J%3BKimura%2C+S&rft.aulast=Mizuno&rft.aufirst=K&rft.date=1991-10-01&rft.volume=11&rft.issue=10&rft.spage=4927&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 - 1991-10-31 N1 - Date created - 1991-10-31 N1 - Date revised - 2017-01-13 N1 - Gene symbol - T/EBP; TPO N1 - SuppNotes - Cited By: Mol Cell Biol. 1990 Mar;10(3):1033-40 [2406559] EMBO J. 1991 Jun;10(6):1445-57 [1673926] Biochem Biophys Res Commun. 1990 Apr 16;168(1):281-7 [2158317] Cell. 1990 Jun 29;61(7):1161-4 [2194664] J Clin Endocrinol Metab. 1990 Aug;71(2):384-90 [1974263] Biochem Biophys Res Commun. 1990 Jul 31;170(2):735-41 [2383265] Virology. 1973 Apr;52(2):456-67 [4705382] Metabolism. 1977 Jun;26(6):665-718 [67547] Biochemistry. 1977 Oct 18;16(21):4743-51 [911786] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Biochemistry. 1979 Nov 27;18(24):5294-9 [518835] Methods Enzymol. 1980;65(1):499-560 [6246368] Nucleic Acids Res. 1981 Dec 11;9(23):6505-25 [6275366] Anal Biochem. 1983 Feb 15;129(1):216-23 [6305233] J Virol. 1984 Mar;49(3):857-64 [6321770] Endocrinology. 1984 Apr;114(4):1099-107 [6323129] Proc Natl Acad Sci U S A. 1984 Apr;81(7):1991-5 [6326095] Mol Cell Biol. 1987 Feb;7(2):725-37 [3821727] J Biol Chem. 1987 Mar 25;262(9):4048-52 [3549723] Proc Natl Acad Sci U S A. 1987 Aug;84(16):5555-9 [3475693] Nucleic Acids Res. 1987 Aug 25;15(16):6735 [3453124] Nucleic Acids Res. 1987 Oct 26;15(20):8149-66 [3671079] Methods Enzymol. 1987;153:545-63 [2828850] Cell. 1988 Feb 12;52(3):415-23 [2964277] Proc Natl Acad Sci U S A. 1988 Mar;85(6):1744-8 [3162304] Genes Dev. 1988 Jul;2(7):801-6 [3061875] J Biol Chem. 1989 May 15;264(14):8222-9 [2722778] Biochemistry. 1989 May 16;28(10):4481-9 [2548579] Biochem Biophys Res Commun. 1989 Aug 30;163(1):481-8 [2775280] Cell. 1989 Sep 22;58(6):1135-42 [2476239] Nucleic Acids Res. 1989 Oct 25;17(20):8380 [2813071] Proc Natl Acad Sci U S A. 1989 Nov;86(21):8289-93 [2554307] EMBO J. 1989 Sep;8(9):2537-42 [2583123] Mol Endocrinol. 1989 Nov;3(11):1681-92 [2691880] EMBO J. 1990 Nov;9(11):3631-9 [1976511] Eur J Biochem. 1990 Oct 24;193(2):311-8 [2226454] Mol Endocrinol. 1987 Nov;1(11):856-61 [3153466] Mol Endocrinol. 1990 Jun;4(6):793-9 [2233737] Trends Genet. 1990 Sep;6(9):300-4 [2238088] Mol Cell Biol. 1990 Dec;10(12):6216-24 [2174102] Genes Dev. 1991 Jan;5(1):22-8 [1989905] Cell. 1991 Feb 22;64(4):739-49 [1847666] Biochem Biophys Res Commun. 1990 Feb 14;166(3):1257-64 [2306241] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Monitoring the impact of cocaine. AN - 72145541; 1920729 JF - JAMA AU - Schuster, C R AD - National Institute on Drug Abuse, Rockville, Md. PY - 1991 SP - 2273 VL - 266 IS - 16 SN - 0098-7484, 0098-7484 KW - Cocaine KW - I5Y540LHVR KW - Abridged Index Medicus KW - Index Medicus KW - Drug and Narcotic Control KW - Humans KW - Vital Statistics KW - United States -- epidemiology KW - Population Surveillance KW - Databases, Factual KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72145541?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Monitoring+the+impact+of+cocaine.&rft.au=Schuster%2C+C+R&rft.aulast=Schuster&rft.aufirst=C&rft.date=1991-10-01&rft.volume=266&rft.issue=16&rft.spage=2273&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-12 N1 - Date created - 1991-11-12 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment On: JAMA. 1991 Oct 23-30;266(16):2233-7 [1920721] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dehydroabietic acid, a major anionic contaminant of pulp mill effluent, reduces both active p-aminohippurate transport and passive membrane permeability in isolated renal membranes. AN - 72142556; 1920114 AB - The renal organic anion transport system plays a pivotal role in elimination of potentially toxic anions. This system is driven by indirect coupling to the sodium gradient at the basolateral membrane, i.e., the organic anion enters the cell in exchange for internal alpha-ketoglutarate (alpha KG) and the in greater than out alpha KG gradient is regenerated by Na+/alpha KG cotransport. The resin acid, dehydroabietic acid (DHAA), is one of several anionic xenobiotics which enter the environment secondary to pulp and paper processing. Because it is largely ionized at neutral pH (pKa, 5.7), DHAA should share the organic anion system. Indeed, Na+/glutarate-coupled p-aminohippurate (PAH) uptake by renal basolateral membrane vesicles was inhibited competitively by DHAA (Ki congruent to 150 microM). Despite the reduced rate of PAH uptake, a substantial, but delayed, overshoot was observed, suggesting additional effects. Passive permeabilities to mannitol, PAH and sodium were all decreased by DHAA, consistent with a general tightening of the membrane. Decreased permeability extended the effective lifetime of imposed ion gradients. Thus, sodium driven glutarate uptake was stimulated by 200 microM DHAA, prolonging and more than doubling its overshoot. Because the immediate driving force for PAH uptake into basolateral membrane vesicles is the magnitude of the glutarate gradient, DHAA increased the driving force for PAH uptake and permitted a substantial overshoot despite the reduced rate of PAH uptake. These data indicate that DHAA has several distinctly different effects on the membrane. JF - The Journal of pharmacology and experimental therapeutics AU - Pritchard, J B AU - Walden, R AU - Oikari, A AD - Comparative Membrane Pharmacology Section, National Institutes of Health/National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 156 EP - 163 VL - 259 IS - 1 SN - 0022-3565, 0022-3565 KW - Diterpenes KW - 0 KW - Diterpenes, Abietane KW - Ketoglutaric Acids KW - dehydroabietic acid KW - 0S5XP6S3AU KW - Mannitol KW - 3OWL53L36A KW - alpha-ketoglutaric acid KW - 8ID597Z82X KW - p-Aminohippuric Acid KW - Y79XT83BJ9 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Microvilli -- drug effects KW - Ketoglutaric Acids -- metabolism KW - Mannitol -- metabolism KW - Male KW - Diterpenes -- pharmacology KW - Kidney Cortex -- drug effects KW - Cell Membrane Permeability -- drug effects KW - p-Aminohippuric Acid -- metabolism KW - Kidney Cortex -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72142556?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Dehydroabietic+acid%2C+a+major+anionic+contaminant+of+pulp+mill+effluent%2C+reduces+both+active+p-aminohippurate+transport+and+passive+membrane+permeability+in+isolated+renal+membranes.&rft.au=Pritchard%2C+J+B%3BWalden%2C+R%3BOikari%2C+A&rft.aulast=Pritchard&rft.aufirst=J&rft.date=1991-10-01&rft.volume=259&rft.issue=1&rft.spage=156&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 - 1991-11-21 N1 - Date created - 1991-11-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A pilot study of interferon alfa-2a in combination with fluorouracil plus high-dose leucovorin in metastatic gastrointestinal carcinoma. AN - 72141043; 1919632 AB - Thirty-one assessable patients with metastatic adenocarcinoma of the gastrointestinal tract were entered onto a pilot study designed to assess the impact of recombinant interferon alpha-2a (rIFN alpha-2a) on the toxicity and pharmacokinetics of fluorouracil (5-FU) and leucovorin (LV). Patients received an initial cycle of 5-FU (370 or 425 mg/m2/d) with LV (500 mg/m2/d) for 5 days. If tolerated, the patient received the same dose of 5-FU/LV for the second cycle on days 2 to 6, with rIFN alpha-2a at 5 x 10(6) or 10 x 10(6) U/m2/d on days 1 to 7, or with 3 x 10(6) U/m2/d on days 1 to 14. In 26 matched cycles, rIFN alpha-2a administration was associated with an increased incidence of dose-limiting mucositis and diarrhea and a significantly lower median platelet nadir; rIFN alpha-2a did not significantly affect the median WBC or granulocyte nadir. Dose-limiting toxicity occurred in all six patients entered at 425 mg/m2/d of 5-FU/LV within two cycles. The majority of patients treated with 370 mg/m2/d of 5-FU/LV and 10 x 10(6) U/m2/d rIFN alpha-2a experienced grade 3 to 4 mucositis and diarrhea, whereas patients receiving 3 x 10(6) and 5 x 10(6) U/m2/d rIFN alpha-2a had acceptable toxicity. Administration of rIFN alpha-2a was associated with a dose-dependent decrease in 5-FU clearance. The increase in the area under the 5-FU concentration-time curve (AUC) was 1.3-fold and 1.5-fold in patients receiving 5 x 10(6) and 10 x 10(6) U/m2/d rIFN alpha-2a, respectively. Thus, the increase in 5-FU toxicity with rIFN alpha-2a may be explained by alterations in 5-FU pharmacokinetics. In 22 patients without prior 5-FU therapy, three complete (13.6%) and seven partial (31.8%) responses were seen, for an overall response rate of 45.4% (95% confidence interval, 24.4% to 67.8%). Since the 5 x 10(6) U/m2/d dose of rIFN alpha-2a increased the 5-FU drug exposure and was associated with acceptable toxicity, we recommend its further evaluation as given on days 1 to 7 in combination with 5-FU 370 mg/m2/d, with high-dose LV given on days 2 to 6. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Grem, J L AU - McAtee, N AU - Murphy, R F AU - Balis, F M AU - Steinberg, S M AU - Hamilton, J M AU - Sorensen, J M AU - Sartor, O AU - Kramer, B S AU - Goldstein, L J AD - Clinical Oncology Program, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 1811 EP - 1820 VL - 9 IS - 10 SN - 0732-183X, 0732-183X KW - Interferon-alpha KW - 0 KW - Recombinant Proteins KW - interferon alfa-2a KW - 47RRR83SK7 KW - Leucovorin KW - Q573I9DVLP KW - Fluorouracil KW - U3P01618RT KW - Index Medicus KW - Drug Administration Schedule KW - Interferon-alpha -- administration & dosage KW - Humans KW - Leucovorin -- administration & dosage KW - Aged KW - Leucovorin -- adverse effects KW - Pilot Projects KW - Fluorouracil -- administration & dosage KW - Fluorouracil -- adverse effects KW - Aged, 80 and over KW - Adult KW - Middle Aged KW - Fluorouracil -- pharmacokinetics KW - Male KW - Female KW - Adenocarcinoma -- secondary KW - Gastrointestinal Neoplasms -- drug therapy KW - Gastrointestinal Neoplasms -- pathology KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Adenocarcinoma -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72141043?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+pilot+study+of+interferon+alfa-2a+in+combination+with+fluorouracil+plus+high-dose+leucovorin+in+metastatic+gastrointestinal+carcinoma.&rft.au=Grem%2C+J+L%3BMcAtee%2C+N%3BMurphy%2C+R+F%3BBalis%2C+F+M%3BSteinberg%2C+S+M%3BHamilton%2C+J+M%3BSorensen%2C+J+M%3BSartor%2C+O%3BKramer%2C+B+S%3BGoldstein%2C+L+J&rft.aulast=Grem&rft.aufirst=J&rft.date=1991-10-01&rft.volume=9&rft.issue=10&rft.spage=1811&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 - 1991-11-18 N1 - Date created - 1991-11-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Fluorescent verapamil derivative for monitoring activity of the multidrug transporter. AN - 72140928; 1681415 AB - Multidrug resistance to amphipathic natural product chemotherapeutic drugs is conferred on cancer cells by expression of the MDR1 gene, which encodes the 170-kDa multidrug transporter known as P glycoprotein. The P glycoprotein-mediated efflux of toxic chemotherapeutic drugs can be reversed by agents such as verapamil, which is a substrate for the multidrug transporter and appears to be a competitive inhibitor of the efflux pump. In this study, Bodipy-verapamil, a fluorescent derivative of verapamil, has been shown to be a substrate for the efflux pump activity of P glycoprotein. Single-cell fluorescence analysis reveals that Bodipy-verapamil accumulates in lysosomes of drug-sensitive NIH3T3 and KB cells but is rapidly effluxed from multidrug-resistant derivatives of these cell lines. Although Bodipy-verapamil is a substrate for the multidrug transporter, it is not an efficient inhibitor of the pump and does not reverse resistance to vinblastine and colchicine as effectively as does verapamil. This new derivative may be a useful tool for imaging of lysosomes in drug-sensitive cells and for rapid screening for the multidrug-resistant phenotype in other cell types. JF - Molecular pharmacology AU - Lelong, I H AU - Guzikowski, A P AU - Haugland, R P AU - Pastan, I AU - Gottesman, M M AU - Willingham, M C AD - Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 490 EP - 494 VL - 40 IS - 4 SN - 0026-895X, 0026-895X KW - Fluorescent Dyes KW - 0 KW - Membrane Glycoproteins KW - P-Glycoprotein KW - Bodipy-verapamil KW - 137759-83-2 KW - Verapamil KW - CJ0O37KU29 KW - Index Medicus KW - Animals KW - KB Cells KW - Drug Resistance -- genetics KW - Tumor Cells, Cultured -- metabolism KW - Humans KW - Lysosomes -- metabolism KW - Mice KW - Phenotype KW - Cell Survival -- drug effects KW - 3T3 Cells -- metabolism KW - Microscopy, Fluorescence -- methods KW - Membrane Glycoproteins -- metabolism KW - Verapamil -- analogs & derivatives KW - Verapamil -- pharmacokinetics KW - Fluorescent Dyes -- pharmacokinetics KW - Verapamil -- pharmacology KW - Fluorescent Dyes -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72140928?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Fluorescent+verapamil+derivative+for+monitoring+activity+of+the+multidrug+transporter.&rft.au=Lelong%2C+I+H%3BGuzikowski%2C+A+P%3BHaugland%2C+R+P%3BPastan%2C+I%3BGottesman%2C+M+M%3BWillingham%2C+M+C&rft.aulast=Lelong&rft.aufirst=I&rft.date=1991-10-01&rft.volume=40&rft.issue=4&rft.spage=490&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 - 1991-11-21 N1 - Date created - 1991-11-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - GTP-binding protein G alpha Z: its down-regulation by dexamethasone and its credentials as a mediator of antigen-induced responses in RBL-2H3 cells. AN - 72140111; 1921983 AB - We have investigated the possible role of guanine nucleotide-binding proteins in the process of antigen-induced exocytosis in a cultured rat mast cell line, RBL-2H3 cells. The mRNAs for the alpha subunits of the guanine nucleotide-binding proteins G alpha S (short and long forms), G alpha i-2, G alpha i-3, and G alpha Z were detected by hybridization with G alpha-specific oligonucleotide probes. The corresponding proteins were identified in membranes of RBL-2H3 cells on the basis of size, immunoreactivity with specific antibodies, and their ability to serve as substrates for ADP-ribosylation by cholera toxin or pertussis toxin. Treatment of cells with as little as 10(-9) to 10(-7) M dexamethasone markedly decreased the amount of G alpha Z mRNA and membrane G alpha Z, as well as the responsiveness of the cells to antigen stimulation. In the same cells, the exposure to dexamethasone caused an increase in the amounts of certain other G alpha subunits, particularly G alpha i-3, and in the responsiveness of the cells to an adenosine analog, N(ethylcarboxamido)-adenosine. Because of the apparent decrease in G alpha Z mRNA and protein in dexamethasone-treated cells and the fact that neither cholera toxin nor pertussis toxin inhibits the stimulatory signals to antigen [J. Biol. Chem. 265:745-753 (1990)], we suggest that G alpha Z is a potential candidate for regulating the early signals in antigen-stimulated RBL-2H3 cells. JF - Molecular pharmacology AU - Hide, M AU - Ali, H AU - Price, S R AU - Moss, J AU - Beaven, M A AD - Laboratory of Chemical Pharmacology, National Heart, Lung, and Blood Institute, Bethesda, MD 20892. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 473 EP - 479 VL - 40 IS - 4 SN - 0026-895X, 0026-895X KW - Macromolecular Substances KW - 0 KW - Membrane Proteins KW - Oligonucleotide Probes KW - RNA, Messenger KW - Virulence Factors, Bordetella KW - Adenosine Diphosphate KW - 61D2G4IYVH KW - Dexamethasone KW - 7S5I7G3JQL KW - Cholera Toxin KW - 9012-63-9 KW - Pertussis Toxin KW - EC 2.4.2.31 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Index Medicus KW - Animals KW - Blotting, Northern KW - Membrane Proteins -- metabolism KW - Cholera Toxin -- pharmacology KW - Exocytosis KW - Amino Acid Sequence KW - RNA, Messenger -- genetics KW - Mast Cells -- cytology KW - Rats KW - Virulence Factors, Bordetella -- pharmacology KW - Base Sequence KW - Blotting, Southern KW - Cells, Cultured KW - Mast Cells -- metabolism KW - Molecular Sequence Data KW - Membrane Proteins -- drug effects KW - Adenosine Diphosphate -- metabolism KW - Dexamethasone -- pharmacology KW - GTP-Binding Proteins -- drug effects KW - GTP-Binding Proteins -- physiology KW - Down-Regulation -- drug effects KW - GTP-Binding Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72140111?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=GTP-binding+protein+G+alpha+Z%3A+its+down-regulation+by+dexamethasone+and+its+credentials+as+a+mediator+of+antigen-induced+responses+in+RBL-2H3+cells.&rft.au=Hide%2C+M%3BAli%2C+H%3BPrice%2C+S+R%3BMoss%2C+J%3BBeaven%2C+M+A&rft.aulast=Hide&rft.aufirst=M&rft.date=1991-10-01&rft.volume=40&rft.issue=4&rft.spage=473&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 - 1991-11-21 N1 - Date created - 1991-11-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Measurement of 4-aminobiphenyl-hemoglobin adducts in lung cancer cases and controls. AN - 72122921; 1913645 AB - Hemoglobin adducts of the activated carcinogenic aromatic amine 4-aminobiphenyl have been measured in a case-control study of lung cancer. Data obtained for lung cancer cases are compared to those obtained for controls that consisted of patients with either chronic obstructive pulmonary disease or non-pulmonary cancers. Both simple and multivariate analysis found a positive association of 4-aminobiphenyl-hemoglobin adducts with the quantity of tobacco smoked as determined by either urine cotinine or questionnaire data. No association was found between 4-aminobiphenyl-hemoglobin adducts and cancer diagnosis, and adduct levels were not related to remote tobacco use, i.e., total pack years of smoking. There was no association between the levels of adducts detected and the ability of an individual to metabolize debrisoquine (debrisoquine metabolic phenotype, CYP2D6). Whereas 4-aminobiphenyl-hemoglobin adduct levels reflected recent tobacco smoking, they were not correlated with lung cancer risk. JF - Cancer research AU - Weston, A AU - Caporaso, N E AU - Taghizadeh, K AU - Hoover, R N AU - Tannenbaum, S R AU - Skipper, P L AU - Resau, J H AU - Trump, B F AU - Harris, C C AD - Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/10/01/ PY - 1991 DA - 1991 Oct 01 SP - 5219 EP - 5223 VL - 51 IS - 19 SN - 0008-5472, 0008-5472 KW - Aminobiphenyl Compounds KW - 0 KW - Carcinogens KW - Hemoglobins KW - 4-biphenylamine KW - 16054949HJ KW - Cotinine KW - K5161X06LL KW - Debrisoquin KW - X31CDK040E KW - Index Medicus KW - Cotinine -- urine KW - Debrisoquin -- metabolism KW - Chromatography, Gas KW - Risk Factors KW - Humans KW - Cotinine -- blood KW - Case-Control Studies KW - Smoking -- adverse effects KW - Male KW - Female KW - Multivariate Analysis KW - Carcinogens -- metabolism KW - Hemoglobins -- metabolism KW - Aminobiphenyl Compounds -- metabolism KW - Lung Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72122921?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Measurement+of+4-aminobiphenyl-hemoglobin+adducts+in+lung+cancer+cases+and+controls.&rft.au=Weston%2C+A%3BCaporaso%2C+N+E%3BTaghizadeh%2C+K%3BHoover%2C+R+N%3BTannenbaum%2C+S+R%3BSkipper%2C+P+L%3BResau%2C+J+H%3BTrump%2C+B+F%3BHarris%2C+C+C&rft.aulast=Weston&rft.aufirst=A&rft.date=1991-10-01&rft.volume=51&rft.issue=19&rft.spage=5219&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 - 1991-10-29 N1 - Date created - 1991-10-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - K-ras activation in premalignant and malignant epithelial lesions of the human uterus. AN - 72122478; 1913654 AB - We previously reported (Cancer Res., 50:6139-6145, 1990) a significant frequency of activating point mutations in codon 12 of the K-ras oncogene in endometrial adenocarcinomas of the uterine corpus (series 1). To further define the role of ras activation in the development of endometrial adenocarcinoma, we surveyed cystic, adenomatous, and atypical hyperplasias of uterine endometrium and additional cases of endometrial and cervical carcinoma (series 2) for the presence of activating mutations in cellular protooncogenes of the ras family. Polymerase chain reaction was performed from deparaffinized sections of formalin-fixed paraffin-embedded tissue. We screened for point mutations in codons 12, 13, and 61 of the K-, H-, and N-ras genes by dot blot hybridization analysis with mutation-specific oligomers. Mutations in K-ras were also confirmed by direct genomic DNA sequencing. Of 19 endometrial adenocarcinomas in series 2, point mutations in ras genes were found in 7 tumors. Six contained single-base substitutions, five in codon 12 of K-ras and one in codon 12 of N-ras. The seventh tumor contained two different point mutations in codon 12 of K-ras. In one endometrial adenocarcinoma, tumor cells with point mutations in K-ras were predominantly localized to a portion that had a more aggressive histological pattern. In endometrial hyperplasia, K-ras mutations, one in codon 12 and one in codon 13, were found in 2 of 16 hyperplasias histologically classified as atypical and clinically considered premalignant. None of 6 adenomatous hyperplasias and none of 12 cystic hyperplasias, the latter of which is considered clinically benign, contained any detectable ras mutations. No mutations in H-ras were detected in either carcinomas or hyperplastic tissue. JF - Cancer research AU - Enomoto, T AU - Inoue, M AU - Perantoni, A O AU - Buzard, G S AU - Miki, H AU - Tanizawa, O AU - Rice, J M AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1991/10/01/ PY - 1991 DA - 1991 Oct 01 SP - 5308 EP - 5314 VL - 51 IS - 19 SN - 0008-5472, 0008-5472 KW - K-ras KW - Index Medicus KW - Humans KW - Gene Expression KW - Aged KW - Polymerase Chain Reaction KW - Base Sequence KW - Aged, 80 and over KW - Blotting, Southern KW - Hyperplasia -- genetics KW - Adult KW - Molecular Sequence Data KW - Uterine Cervical Neoplasms -- genetics KW - Middle Aged KW - Epithelium -- pathology KW - Mutation KW - Female KW - Uterine Neoplasms -- genetics KW - Precancerous Conditions -- genetics KW - Genes, ras -- genetics KW - Genes, ras -- physiology KW - Adenocarcinoma -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72122478?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=K-ras+activation+in+premalignant+and+malignant+epithelial+lesions+of+the+human+uterus.&rft.au=Enomoto%2C+T%3BInoue%2C+M%3BPerantoni%2C+A+O%3BBuzard%2C+G+S%3BMiki%2C+H%3BTanizawa%2C+O%3BRice%2C+J+M&rft.aulast=Enomoto&rft.aufirst=T&rft.date=1991-10-01&rft.volume=51&rft.issue=19&rft.spage=5308&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 - 1991-10-29 N1 - Date created - 1991-10-29 N1 - Date revised - 2017-01-13 N1 - Gene symbol - K-ras N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pituitary adenylate cyclase-activating polypeptide (PACAP) potentiates the gonadotropin-releasing activity of luteinizing hormone-releasing hormone. AN - 72122061; 1915106 AB - In order to determine if the newly discovered neuropeptide, pituitary adenylate cyclase activating polypeptide (PACAP), interacts with the known hypothalamic releasing factors to modulate pituitary hormone secretion, the effect of PACAP, either alone or in combination with either LHRH, TRH, CRF or GHRH, was examined in rat anterior pituitary cell cultures. While PACAP alone weakly stimulated LH and FSH release, PACAP and LHRH, in combination, interacted synergistically to stimulate gonadotropin secretion. No significant changes in the secretion of either TSH, ACTH, or GH were observed in response to PACAP, either alone or in combination with the other releasing factors. Addition of an LHRH antagonist demonstrated that the PACAP effect on gonadotropin release was neither mediated by the LHRH receptor nor the result of LHRH contamination of the PACAP preparation. Because of the sequence homology (68%) between the N-terminal 28 amino acids of PACAP and VIP, the addition of a VIP antagonist was used to demonstrate that the PACAP effect is not mediated through the VIP receptor. The observation that PACAP interacts synergistically with LHRH in stimulating gonadotropin release suggests intriguing possibilities for PACAP in regulating gonadotropin secretion and reproductive function. JF - Endocrinology AU - Culler, M D AU - Paschall, C S AD - Reproductive Neuroendocrinology Section, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 2260 EP - 2262 VL - 129 IS - 4 SN - 0013-7227, 0013-7227 KW - Gonadotropins KW - 0 KW - Neuropeptides KW - Pituitary Adenylate Cyclase-Activating Polypeptide KW - Gonadotropin-Releasing Hormone KW - 33515-09-2 KW - Vasoactive Intestinal Peptide KW - 37221-79-7 KW - Abridged Index Medicus KW - Index Medicus KW - Vasoactive Intestinal Peptide -- pharmacology KW - Osmolar Concentration KW - Animals KW - Drug Synergism KW - Neuropeptides -- pharmacology KW - Gonadotropin-Releasing Hormone -- antagonists & inhibitors KW - Gonadotropins -- metabolism KW - Gonadotropin-Releasing Hormone -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72122061?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Pituitary+adenylate+cyclase-activating+polypeptide+%28PACAP%29+potentiates+the+gonadotropin-releasing+activity+of+luteinizing+hormone-releasing+hormone.&rft.au=Culler%2C+M+D%3BPaschall%2C+C+S&rft.aulast=Culler&rft.aufirst=M&rft.date=1991-10-01&rft.volume=129&rft.issue=4&rft.spage=2260&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=00137227&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-10-30 N1 - Date created - 1991-10-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Immortalization of normal human bronchial epithelial cells by human papillomaviruses 16 or 18. AN - 72120682; 1717149 AB - Human papillomaviruses (HPV) are associated with papillomatosis of the larynx, trachea, and bronchi in decreasing order of frequency, and these papillomatosis lesions may become malignant. When the patients are not selected for a history of papillomatosis, the frequency of HPV in bronchogenic carcinoma tissue is 1-5%. In order to develop a model for investigating the role of HPV in human bronchogenic carcinogenesis, normal human bronchial epithelial cells were transfected with cloned full-length HPV16 or HPV18. Two HPV18-transformed cell lines (BEP1 and BEP2) and one HPV16-transformed cell line (BEP3) were established. These nontumorigenic epithelial cell lines have: (a) attained over 100 population doublings in vitro; (b) mutually exclusive human marker chromosomes; (c) HPV DNA in forms that are consistent with chromosomal integration by Southern analysis; (d) HPV E6, E7, and E6* mRNA transcripts by Northern and reverse transcriptase-polymerase chain reaction analysis; and (e) diminished confluence-induced squamous differentiation. These cell lines should be useful for studying mechanisms involved in proliferation, differentiation, and neoplastic transformation of human bronchial epithelial cells. JF - Cancer research AU - Willey, J C AU - Broussoud, A AU - Sleemi, A AU - Bennett, W P AU - Cerutti, P AU - Harris, C C AD - Laboratory of Human Carcinogenesis, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1991/10/01/ PY - 1991 DA - 1991 Oct 01 SP - 5370 EP - 5377 VL - 51 IS - 19 SN - 0008-5472, 0008-5472 KW - Keratins KW - 68238-35-7 KW - Index Medicus KW - Blotting, Northern KW - Humans KW - DNA Fingerprinting KW - Transcription, Genetic KW - Plasmids KW - Chromosome Mapping KW - Keratins -- biosynthesis KW - Polymerase Chain Reaction KW - Base Sequence KW - Transfection KW - Blotting, Southern KW - Molecular Sequence Data KW - Epithelium KW - Bronchi -- microbiology KW - Cell Transformation, Viral -- genetics KW - Papillomaviridae -- genetics KW - Cell Line UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72120682?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Immortalization+of+normal+human+bronchial+epithelial+cells+by+human+papillomaviruses+16+or+18.&rft.au=Willey%2C+J+C%3BBroussoud%2C+A%3BSleemi%2C+A%3BBennett%2C+W+P%3BCerutti%2C+P%3BHarris%2C+C+C&rft.aulast=Willey&rft.aufirst=J&rft.date=1991-10-01&rft.volume=51&rft.issue=19&rft.spage=5370&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 - 1991-10-29 N1 - Date created - 1991-10-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prostratin, a nonpromoting phorbol ester, inhibits induction by phorbol 12-myristate 13-acetate of ornithine decarboxylase, edema, and hyperplasia in CD-1 mouse skin. AN - 72120641; 1913657 AB - Pretreatment of CD-1 mouse skin with prostratin (12-deoxyphorbol 13-acetate) inhibited biological response to phorbol 12-myristate 13-acetate. The three responses examined were hyperplasia, induction of ornithine decarboxylase, and edema; the characteristics of inhibition depended on the specific response. Hyperplasia is the best short-term correlate of tumor promotion. Two or more pretreatments with 2.56 mumol (1 mg) prostratin, administered at intervals of 1-4 days, almost completely blocked the hyperplasia induced by phorbol 12-myristate 13-acetate applied 15 min to 6 h after the last pretreatment. Inducibility of hyperplasia was partially restored at 2 days and recovered by 4 days. Prostratin was more potent for inhibition of ornithine decarboxylase induction (50% inhibitory dose = 25.6 nmol) than it was for hyperplasia: the inhibition was largely attained by the first application, and the recovery from inhibition was slower (8 days). Edema was partially inhibited by prostratin (dose giving 50% of maximal inhibition = 512 nmol). We have previously demonstrated that prostratin is a protein kinase C activator. Our present results show that prostratin is a functional antagonist for a class of protein kinase C mediated responses. The findings emphasize the diversity of biological outcome for protein kinase C activators, presumably driven by the extensive heterogeneity in the protein kinase C pathway. JF - Cancer research AU - Szallasi, Z AU - Blumberg, P M AD - Molecular Mechanisms of Tumor Promotion Section, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/10/01/ PY - 1991 DA - 1991 Oct 01 SP - 5355 EP - 5360 VL - 51 IS - 19 SN - 0008-5472, 0008-5472 KW - Phorbol Esters KW - 0 KW - prostratin KW - 60857-08-1 KW - Ornithine Decarboxylase KW - EC 4.1.1.17 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Hyperplasia -- chemically induced KW - Dose-Response Relationship, Drug KW - Mice KW - Body Water KW - Drug Antagonism KW - Time Factors KW - Female KW - Phorbol Esters -- pharmacology KW - Edema -- chemically induced KW - Skin -- drug effects KW - Skin -- metabolism KW - Skin -- pathology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Ornithine Decarboxylase -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72120641?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Prostratin%2C+a+nonpromoting+phorbol+ester%2C+inhibits+induction+by+phorbol+12-myristate+13-acetate+of+ornithine+decarboxylase%2C+edema%2C+and+hyperplasia+in+CD-1+mouse+skin.&rft.au=Szallasi%2C+Z%3BBlumberg%2C+P+M&rft.aulast=Szallasi&rft.aufirst=Z&rft.date=1991-10-01&rft.volume=51&rft.issue=19&rft.spage=5355&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 - 1991-10-29 N1 - Date created - 1991-10-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Free alpha molecules from pregnancy stimulate secretion of prolactin from human decidual cells: a novel function for free alpha in pregnancy. AN - 72119807; 1717245 AB - Free alpha molecules isolated from pregnancy, as well as highly purified reference preparations of hCG alpha subunit (CR119 or CR123), stimulated the release of prolactin from human decidual cells in culture. The amount of prolactin secreted during a 24 h incubation was concentration-dependent over a range of increasing doses of alpha from 0.2 to 20 ng/ml with an ED50 of about 1.6 ng/ml. These concentrations are well within the physiologic maternal serum free alpha levels which average 350 ng/ml during the third trimester of pregnancy. Incubation of decidual cells with a reference preparation of intact hCG (CR123) at a concentration of 260 ng/ml resulted in stimulated secretion of prolactin, however, the observed stimulation could be attributed to contamination of the preparation with free alpha or dissociated hCG alpha subunit. Purified hCG beta subunit had no stimulatory activity on the decidual cell culture. The effect of alpha subunit on the stimulated release of prolactin was not due to a generalized stimulation of protein synthesis and secretion since no increase was observed in the release of 35S-labeled proteins compared to controls. In addition, the observed increase in prolactin secretion was not due to a toxic effect of the alpha subunit since there was no visible effect on cell viability, and the cellular enzymes, LDH and alkaline phosphatase, were not detected in the culture medium. Addition of exogenous hCG alpha subunit to primary cultures of human trophoblast cultures did not result in stimulated release of human placental lactogen. We conclude that free alpha molecules of pregnancy stimulate release of prolactin from human decidual cells in culture. These results suggest a novel role for free alpha in the paracrine regulation of decidual prolactin secretion. JF - Endocrinology AU - Blithe, D L AU - Richards, R G AU - Skarulis, M C AD - Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 2257 EP - 2259 VL - 129 IS - 4 SN - 0013-7227, 0013-7227 KW - Chorionic Gonadotropin KW - 0 KW - Culture Media KW - Glycoprotein Hormones, alpha Subunit KW - Prolactin KW - 9002-62-4 KW - Abridged Index Medicus KW - Index Medicus KW - Immunoblotting KW - Electrophoresis, Polyacrylamide Gel KW - Dose-Response Relationship, Drug KW - Cells, Cultured KW - Humans KW - Female KW - Densitometry KW - Glycoprotein Hormones, alpha Subunit -- physiology KW - Decidua -- cytology KW - Pregnancy -- urine KW - Decidua -- metabolism KW - Glycoprotein Hormones, alpha Subunit -- urine KW - Glycoprotein Hormones, alpha Subunit -- pharmacology KW - Prolactin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72119807?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Free+alpha+molecules+from+pregnancy+stimulate+secretion+of+prolactin+from+human+decidual+cells%3A+a+novel+function+for+free+alpha+in+pregnancy.&rft.au=Blithe%2C+D+L%3BRichards%2C+R+G%3BSkarulis%2C+M+C&rft.aulast=Blithe&rft.aufirst=D&rft.date=1991-10-01&rft.volume=129&rft.issue=4&rft.spage=2257&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=00137227&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-10-30 N1 - Date created - 1991-10-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chemotherapy and chemosensitization of transgenic mice which express the human multidrug resistance gene in bone marrow: efficacy, potency, and toxicity. AN - 72117489; 1680550 AB - A common form of multidrug resistance in human cancer results from expression of the MDR1 gene which encodes a plasma membrane energy-dependent multidrug efflux pump. We have engineered transgenic mice which express this multidrug transporter in their bone marrow cells and demonstrated that peripheral WBC of these animals provide a rapid and reliable system for assessing the bioactivity of agents that reverse multidrug resistance. Immunocytochemical analysis of bone marrow smears suggests that the activation of the MDR1 transgene has probably occurred at a very early stage of bone marrow differentiation since most bone marrow cells express the transporter. Expression of this transgene in bone marrow produces about 10-fold resistance to leukopenia induced by taxol compared to normal bone marrow. Chemosensitization of MDR1 mice to daunomycin and taxol, measured by a fall in WBC, is detectable at a dose as low as 0.01 mg/kg R-verapamil. A dose of 0.5 mg/kg R-verapamil reduces the WBC by nearly 50%. Chemosensitization of MDR-transgenic mice with 5 mg/kg R-verapamil, which is highly effective in reversing MDR and readily tolerated by mice, necessitates a reduction of the maximum tolerated dose of most chemotherapeutic agents by only 20%. In addition, detailed histopathological examination shows that treatment of mice with chemotherapeutic drugs and R-verapamil does not change the organ-related toxicity pattern but only moderately accentuates inherent toxic side effects of the chemotherapeutic agents. We conclude that MDR1-transgenic mice represent a valid model for evaluating efficacy, potency, and toxicity associated with chemotherapy and chemosensitization of multidrug-resistant cells in animals. JF - Cancer research AU - Mickisch, G H AU - Licht, T AU - Merlino, G T AU - Gottesman, M M AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1991/10/01/ PY - 1991 DA - 1991 Oct 01 SP - 5417 EP - 5424 VL - 51 IS - 19 SN - 0008-5472, 0008-5472 KW - MDR1 KW - Alkaloids KW - 0 KW - Antineoplastic Agents, Phytogenic KW - Membrane Glycoproteins KW - P-Glycoprotein KW - Vincristine KW - 5J49Q6B70F KW - Vinblastine KW - 5V9KLZ54CY KW - Doxorubicin KW - 80168379AG KW - Verapamil KW - CJ0O37KU29 KW - Paclitaxel KW - P88XT4IS4D KW - Daunorubicin KW - ZS7284E0ZP KW - Index Medicus KW - Vinblastine -- pharmacology KW - Animals KW - Intestines -- drug effects KW - Daunorubicin -- toxicity KW - Dose-Response Relationship, Drug KW - Vincristine -- pharmacology KW - Antineoplastic Agents, Phytogenic -- pharmacology KW - Mice KW - Doxorubicin -- toxicity KW - Vinblastine -- toxicity KW - Verapamil -- pharmacology KW - Mice, Transgenic KW - Vincristine -- toxicity KW - Daunorubicin -- pharmacology KW - Leukocyte Count -- drug effects KW - Drug Tolerance KW - Antineoplastic Agents, Phytogenic -- toxicity KW - Doxorubicin -- pharmacology KW - Liver -- drug effects KW - Alkaloids -- toxicity KW - Alkaloids -- pharmacology KW - Spleen -- drug effects KW - Drug Resistance -- genetics KW - Membrane Glycoproteins -- biosynthesis KW - Bone Marrow -- ultrastructure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72117489?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Chemotherapy+and+chemosensitization+of+transgenic+mice+which+express+the+human+multidrug+resistance+gene+in+bone+marrow%3A+efficacy%2C+potency%2C+and+toxicity.&rft.au=Mickisch%2C+G+H%3BLicht%2C+T%3BMerlino%2C+G+T%3BGottesman%2C+M+M%3BPastan%2C+I&rft.aulast=Mickisch&rft.aufirst=G&rft.date=1991-10-01&rft.volume=51&rft.issue=19&rft.spage=5417&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 - 1991-10-29 N1 - Date created - 1991-10-29 N1 - Date revised - 2017-01-13 N1 - Gene symbol - MDR1 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prolonged, continuous treatment of hairy cell leukemia patients with recombinant interferon-alpha 2a. AN - 72114073; 1912555 AB - Interferons are not curative in hairy cell leukemia (HCL), and retreatment is necessary in most patients whose therapy is stopped. In an attempt to maintain or improve responses, we administered recombinant interferon-alpha 2a (rIFN-alpha 2a) continuously to patients with HCL who initially responded to this therapy. Of 53 evaluable patients enrolled in this study, 32 have received rIFN-alpha 2a continuously for a median of 5 years. Patients received 3 million units of rIFN-alpha 2a subcutaneously (SC) daily for 6 months, followed, in responding patients, by the same dose three times weekly. Twenty-one patients (40%) discontinued IFN after a median of 29 months, seven of whom developed resistant disease in association with anti-IFN antibodies. Treatment produced high response rates: complete response plus partial response (CR + PR) = 40 of 53 (76%), CR + PR + minor response (MR) = 43 of 53 (82%), with no differences in response rates between patients with and without splenectomy. Sixteen patients who had MR at 18 months had PR with prolonged treatment, nine of whom had a significant further reduction in the hairy cell infiltrate in the bone marrow (BM). The median granulocyte and platelet counts have continued to increase and the median serum soluble interleukin-2 receptor (sIL-2R) level has continued to decrease with prolonged treatment. Two patients developed erythrocytosis that may be treatment related, but no other new toxicities were noted with prolonged treatment. We conclude that prolonged, continuous rIFN-alpha 2a treatment has acceptable toxicity, is not associated with late development of IFN resistance, and results in continued hematologic improvement with time on treatment. JF - Blood AU - Smith, J W AU - Longo, D L AU - Urba, W J AU - Clark, J W AU - Watson, T AU - Beveridge, J AU - Conlon, K C AU - Sznol, M AU - Creekmore, S P AU - Alvord, W G AD - Biological Response Modifiers Program, NCI-FCRDC, Frederick, MD 21701. Y1 - 1991/10/01/ PY - 1991 DA - 1991 Oct 01 SP - 1664 EP - 1671 VL - 78 IS - 7 SN - 0006-4971, 0006-4971 KW - Antibodies KW - 0 KW - Interferon-alpha KW - Receptors, Interleukin-2 KW - Recombinant Proteins KW - interferon alfa-2a KW - 47RRR83SK7 KW - Abridged Index Medicus KW - Index Medicus KW - Bone Marrow -- pathology KW - Receptors, Interleukin-2 -- metabolism KW - Antibodies -- blood KW - Splenectomy KW - Humans KW - Adult KW - Granulocytes -- pathology KW - Aged KW - Middle Aged KW - Male KW - Leukocyte Count KW - Female KW - Platelet Count KW - Leukemia, Hairy Cell -- blood KW - Interferon-alpha -- therapeutic use KW - Interferon-alpha -- adverse effects KW - Interferon-alpha -- administration & dosage KW - Leukemia, Hairy Cell -- pathology KW - Leukemia, Hairy Cell -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72114073?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Prolonged%2C+continuous+treatment+of+hairy+cell+leukemia+patients+with+recombinant+interferon-alpha+2a.&rft.au=Smith%2C+J+W%3BLongo%2C+D+L%3BUrba%2C+W+J%3BClark%2C+J+W%3BWatson%2C+T%3BBeveridge%2C+J%3BConlon%2C+K+C%3BSznol%2C+M%3BCreekmore%2C+S+P%3BAlvord%2C+W+G&rft.aulast=Smith&rft.aufirst=J&rft.date=1991-10-01&rft.volume=78&rft.issue=7&rft.spage=1664&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=00064971&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-14 N1 - Date created - 1991-11-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of a potent varicella-zoster virus-encoded trans-repressor. AN - 72101108; 1654442 AB - Using a transient expression assay in Vero cells, we have shown that the protein product from gene 61 of varicella-zoster virus (VZV) can repress the function of the VZV encoded trans-activators on putative viral immediate-early, early, and late gene promoters. The repression is exerted at the transcriptional level and requires functional gene 61 protein. This trans-repressor is the herpes simplex type 1 ICP0 (a trans-activator) homolog, as defined by gene location, the sharing of a cysteine-rich putative zinc-binding finger in the amino-terminal region, and limited amino acid homology. Open reading frame 61 (ORF61)-mediated trans-repression appears to be specific for VZV-encoded trans-activators in that it has no effect on simian virus 40 and Rous sarcoma virus promoters. Moreover, it does not inhibit trans-activation of the human T-lymphotropic virus type I and human immunodeficiency virus long terminal repeats by tax and tat genes, respectively. We constructed plasmids with mutations in ORF61 and tested them for their ability to inhibit trans-activator (VZV genes 4 and 62)-mediated activation of the viral thymidine kinase promoter-chloramphenicol acetyltransferase construct. Mutants containing interruptions in ORF61 lost their trans-repressing ability, as demonstrated at both the protein and steady-state RNA levels. These results suggest that the ORF61 protein product can mediate down-regulation of VZV gene expression. JF - Journal of virology AU - Nagpal, S AU - Ostrove, J M AD - Medical Virology Section, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 5289 EP - 5296 VL - 65 IS - 10 SN - 0022-538X, 0022-538X KW - Oligonucleotide Probes KW - 0 KW - RNA, Viral KW - Repressor Proteins KW - Trans-Activators KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Chromosome Deletion KW - Open Reading Frames KW - RNA, Viral -- isolation & purification KW - Chloramphenicol O-Acetyltransferase -- metabolism KW - Plasmids KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Base Sequence KW - Promoter Regions, Genetic KW - Transfection KW - Restriction Mapping KW - Cercopithecus aethiops KW - Molecular Sequence Data KW - Vero Cells KW - RNA, Viral -- genetics KW - Mutagenesis, Insertional KW - Herpesvirus 3, Human -- genetics KW - Trans-Activators -- genetics KW - Genes, Viral KW - Repressor Proteins -- genetics KW - Transcriptional Activation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72101108?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Characterization+of+a+potent+varicella-zoster+virus-encoded+trans-repressor.&rft.au=Nagpal%2C+S%3BOstrove%2C+J+M&rft.aulast=Nagpal&rft.aufirst=S&rft.date=1991-10-01&rft.volume=65&rft.issue=10&rft.spage=5289&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 - 1991-10-22 N1 - Date created - 1991-10-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1985 Aug;82(16):5265-9 [2991915] J Virol. 1988 Dec;62(12):4510-22 [2846867] J Virol. 1988 Nov;62(11):4307-20 [2845144] Nucleic Acids Res. 1987 Apr 10;15(7):3097-111 [3031620] J Virol. 1987 Dec;61(12):3726-32 [2446005] Mol Cell Biol. 1985 Aug;5(8):1997-2008 [3018543] J Virol. 1985 Mar;53(3):751-60 [2983086] J Virol. 1985 Dec;56(3):723-33 [2999428] Cell. 1988 Feb 12;52(3):435-45 [2830987] Cell. 1988 Feb 12;52(3):425-34 [2830986] J Virol. 1988 Jun;62(6):2076-82 [2835512] Proc Natl Acad Sci U S A. 1987 Oct;84(20):7061-5 [2823252] EMBO J. 1987 Jul;6(7):2069-76 [2820720] Proc Natl Acad Sci U S A. 1988 Sep;85(17):6347-51 [2842768] J Gen Virol. 1986 Sep;67 ( Pt 9):1759-816 [3018124] Virology. 1986 Mar;149(2):152-64 [3004024] Mol Cell Biol. 1985 May;5(5):957-63 [2987684] Cell. 1985 Mar;40(3):705-16 [2982503] Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] Science. 1984 Jul 27;225(4660):381-5 [6330891] Cell. 1981 Aug;25(2):373-84 [6269743] Cell. 1981 Oct;26(1 Pt 1):1-2 [6276006] J Virol. 1981 Nov;40(2):516-25 [6275100] Proc Natl Acad Sci U S A. 1984 Jul;81(14):4381-5 [6336330] Proc Natl Acad Sci U S A. 1981 Oct;78(10):6121-5 [6947217] Proc Natl Acad Sci U S A. 1976 Sep;73(9):3083-7 [184459] Biochemistry. 1979 Nov 27;18(24):5294-9 [518835] Cell. 1979 Aug;17(4):935-44 [487437] Virology. 1973 Apr;52(2):456-67 [4705382] J Virol. 1985 Nov;56(2):600-6 [2997479] Science. 1988 Jun 24;240(4860):1759-64 [3289117] Genes Dev. 1988 Mar;2(3):267-81 [3288540] Science. 1988 May 13;240(4854):889-95 [3283939] Proc Natl Acad Sci U S A. 1986 Dec;83(24):9759-63 [2432602] Virology. 1989 Dec;173(2):700-9 [2556848] Nature. 1989 Mar 2;338(6210):39-44 [2521923] Science. 1987 Sep 11;237(4820):1324-9 [2888190] EMBO J. 1984 Dec 20;3(13):3135-41 [6098466] Nature. 1984 Dec 13-19;312(5995):608-12 [6095113] Cell. 1990 Jun 29;61(7):1217-24 [2142019] EMBO J. 1990 Jan;9(1):225-32 [2136830] Science. 1990 Mar 2;247(4946):1082-4 [2309119] Nature. 1970 Aug 15;227(5259):680-5 [5432063] Cell. 1981 Dec;27(3 Pt 2):603-13 [6101224] J Gen Virol. 1990 Dec;71 ( Pt 12):2999-3003 [2177091] Virology. 1989 Dec;173(2):710-4 [2556849] Erratum In: J Virol 1995 Apr;69(4):2723 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Sequence-specific interaction of the Ets1 protein with the long terminal repeat of the human T-lymphotropic virus type I. AN - 72099574; 1895400 AB - We recently demonstrated that members of the c-ets proto-oncogene family, Ets1 and Ets2, are sequence-specific transcriptional activators of the human T-lymphotropic virus type I (HTLV-I) long terminal repeat (LTR). We now report that the HTLV-I LTR contains two distinct Ets1-responsive regions, ERR-1 and ERR-2. Expression of Ets1 with reporter plasmids containing ERR-1 or ERR-2 upstream of a basal promoter resulted in an increase in transcriptional activity. By gel mobility shift assay, the interaction of Ets1 with the downstream ERR-1-binding region was found to be more stable than its interaction with the upstream ERR-2 region. By DNase I footprint, gel mobility shift, and methylation interference analyses, ERR-1 was found to contain two Ets1 binding sites, ERE-A and ERE-B. A recombinant Ets1 protein was found to bind with higher affinity to ERE-A than to ERE-B. Binding of Ets1 to these sites appears to result in a specific and sequential protection of a 37-nucleotide sequence of the HTLV-I LTR from -154 to -118. In view of the high-level expression of Ets1 in lymphoid cells, the c-ets proto-oncogenes encode transcription factors which could play an important role in both basal and Tax1-mediated HTLV-I transcription. JF - Journal of virology AU - Gitlin, S D AU - Bosselut, R AU - Gégonne, A AU - Ghysdael, J AU - Brady, J N AD - Laboratory of Molecular Virology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 5513 EP - 5523 VL - 65 IS - 10 SN - 0022-538X, 0022-538X KW - c-ets-1 KW - d-E74 KW - h.PU.1 KW - m-ets-1 KW - n-ets-1 KW - DNA, Viral KW - 0 KW - DNA-Binding Proteins KW - ETS1 protein, human KW - Proto-Oncogene Protein c-ets-1 KW - Proto-Oncogene Proteins KW - Proto-Oncogene Proteins c-ets KW - Recombinant Proteins KW - Transcription Factors KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Immunoblotting KW - Sequence Homology, Nucleic Acid KW - Multigene Family KW - Humans KW - Insects KW - Binding Sites KW - Mutagenesis, Site-Directed KW - Baculoviridae -- genetics KW - Base Sequence KW - Recombinant Proteins -- metabolism KW - Molecular Sequence Data KW - Cell Nucleus -- physiology KW - Substrate Specificity KW - HeLa Cells -- physiology KW - DNA, Viral -- genetics KW - Cell Line KW - DNA, Viral -- metabolism KW - Human T-lymphotropic virus 1 -- genetics KW - Proto-Oncogene Proteins -- metabolism KW - Repetitive Sequences, Nucleic Acid KW - Proto-Oncogenes KW - Proto-Oncogene Proteins -- genetics KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72099574?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Sequence-specific+interaction+of+the+Ets1+protein+with+the+long+terminal+repeat+of+the+human+T-lymphotropic+virus+type+I.&rft.au=Gitlin%2C+S+D%3BBosselut%2C+R%3BG%C3%A9gonne%2C+A%3BGhysdael%2C+J%3BBrady%2C+J+N&rft.aulast=Gitlin&rft.aufirst=S&rft.date=1991-10-01&rft.volume=65&rft.issue=10&rft.spage=5513&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 - 1991-10-22 N1 - Date created - 1991-10-22 N1 - Date revised - 2017-01-13 N1 - Gene symbol - c-ets-1; d-E74; h.PU.1; m-ets-1; n-ets-1 N1 - SuppNotes - Cited By: Dev Biol. 1988 May;127(1):45-53 [2834248] Genes Dev. 1987 Nov;1(9):962-72 [2828177] Nature. 1988 Feb 11;331(6156):540-3 [2829028] J Virol. 1988 Sep;62(9):3233-41 [2841475] Proc Natl Acad Sci U S A. 1988 Nov;85(21):7862-6 [2847145] Mol Cell Biol. 1985 Nov;5(11):2993-3000 [3018492] Methods Enzymol. 1980;65(1):499-560 [6246368] Nature. 1983 Nov 24-30;306(5941):395-7 [6316156] Nature. 1983 Nov 24-30;306(5941):391-5 [6316155] Leukemia. 1988 Jan;2(1):12-8 [2448555] Mol Cell Biol. 1989 Nov;9(11):5169-81 [2557547] Mol Cell Biol. 1989 Dec;9(12):5718-21 [2555704] Science. 1989 Apr 7;244(4900):66-70 [2539641] J Immunol. 1989 Jan 15;142(2):672-8 [2536061] Oncogene. 1989 Jun;4(6):691-7 [2660071] Mol Cell Biol. 1989 Apr;9(4):1733-45 [2786141] N Engl J Med. 1988 May 5;318(18):1141-7 [2896300] J Virol. 1988 Dec;62(12):4499-509 [3263510] Science. 1984 Jul 27;225(4660):381-5 [6330891] Virology. 1981 Sep;113(2):765-8 [6267807] Cell. 1982 Dec;31(3 Pt 2):643-53 [6297778] Science. 1982 Feb 19;215(4535):975-8 [6760397] Proc Natl Acad Sci U S A. 1982 Mar;79(6):2031-5 [6979048] Anal Biochem. 1980 Mar 1;102(2):459-71 [7425302] Virology. 1979 Dec;99(2):431-6 [229630] Nature. 1979 Oct 11;281(5731):452-5 [226888] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Proc Natl Acad Sci U S A. 1986 Jun;83(11):3982-6 [3012540] Proc Natl Acad Sci U S A. 1986 Sep;83(17):6558-62 [3018737] Mol Cell Biol. 1987 Feb;7(2):806-12 [3029569] J Virol. 1987 Jul;61(7):2175-81 [3035218] Proc Natl Acad Sci U S A. 1985 Nov;82(21):7294-8 [2997781] Science. 1985 Nov 1;230(4725):511-7 [2996137] Cell. 1985 Sep;42(2):559-72 [2992804] EMBO J. 1988 Apr;7(4):977-83 [3136014] Proc Natl Acad Sci U S A. 1987 Oct;84(19):6795-9 [3116543] EMBO J. 1988 Mar;7(3):697-705 [3293999] Virology. 1984 Dec;139(2):340-5 [6097028] Proc Natl Acad Sci U S A. 1987 Sep;84(17):6131-5 [3476934] Proc Natl Acad Sci U S A. 1987 May;84(10):3161-5 [3472202] Genes Dev. 1990 Apr;4(4):667-79 [2163347] Cell. 1990 Apr 6;61(1):85-99 [2107982] Cancer Res. 1990 Aug 15;50(16):5013-6 [2165853] Mol Cell Biol. 1990 Mar;10(3):1249-53 [2137553] Nature. 1990 Jul 12;346(6280):191-3 [2114554] EMBO J. 1990 Aug;9(8):2537-42 [2196176] Proc Natl Acad Sci U S A. 1990 May;87(10):3723-7 [2187191] J Biol Chem. 1990 May 15;265(14):8237-42 [2186038] Genes Dev. 1990 Mar;4(3):401-9 [2186967] Oncogene. 1990 Apr;5(4):603-10 [2183162] Cell. 1990 Apr 6;61(1):113-24 [2180582] Mol Cell Biol. 1990 Aug;10(8):4192-201 [2370863] Cell. 1990 Jun 29;61(7):1165-6 [2364426] J Biol Chem. 1990 May 15;265(14):8230-6 [2335523] EMBO J. 1990 Mar;9(3):957-64 [2311587] Nucleic Acids Res. 1983 Mar 11;11(5):1475-89 [6828386] Proc Natl Acad Sci U S A. 1990 Nov;87(21):8452-6 [2236054] EMBO J. 1990 Oct;9(10):3137-44 [2209540] Genes Dev. 1990 Sep;4(9):1451-3 [2253872] J Virol. 1991 Mar;65(3):1420-6 [1847461] J Virol. 1991 Jan;65(1):464-7 [1985210] Science. 1990 Nov 9;250(4982):814-8 [2237431] Cell. 1990 Oct 5;63(1):47-61 [2208281] Proc Natl Acad Sci U S A. 1988 Feb;85(3):757-61 [3422457] Proc Natl Acad Sci U S A. 1988 Oct;85(19):7124-8 [3174625] Science. 1989 Mar 31;243(4899):1681-8 [2494700] Nature. 1989 Nov 9;342(6246):134 [2572967] Nature. 1988 Oct 27;335(6193):835-7 [3185713] Proc Natl Acad Sci U S A. 1986 Mar;83(6):1714-8 [3006066] Mol Cell Biol. 1989 Oct;9(10):4152-60 [2555684] Nature. 1988 Dec 22-29;336(6201):719 [3060725] EMBO J. 1988 Dec 20;7(13):4179-84 [2468487] Proc Natl Acad Sci U S A. 1986 Nov;83(21):8112-6 [3022280] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Purification and characterization of the heat-labile toxin of Bordetella pertussis. AN - 72098161; 1894374 AB - A procedure is described for purification of pertussis heat-labile toxin (PEHLT) from cells of Bordetella pertussis. The purification procedure, performed in the cold and in the presence of protease inhibitors, gives 1,350-fold purification with yields of about 60%. The toxin was shown to be a single-chain polypeptide of 140 kDa, pI 6.02. It was completely inactivated by heating at 56 degrees C for 60 min. Rabbit antiserum prepared against PEHLT neutralized the toxin and gave a single precipitin line on immunodiffusion. In immunodiffusion assays, this anti-PEHLT serum did not react with pertussis toxin, filamentous hemagglutinin, or preparations of pertussis adenylate cyclase. Purified PEHLT elicited dermonecrosis and atrophy of the spleen. PEHLT is extraordinarily active; 0.4 X 10(-12) g caused necrotic lesions in newborn mice, and with 18- to 20-g mice the 50% lethal dose was about 11 X 10(-9) g. JF - Infection and immunity AU - Zhang, Y L AU - Sekura, R D AD - Laboratory of Molecular and Developmental Immunity, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1991/10// PY - 1991 DA - October 1991 SP - 3754 EP - 3759 VL - 59 IS - 10 SN - 0019-9567, 0019-9567 KW - Bacterial Toxins KW - 0 KW - Virulence Factors, Bordetella KW - dermonecrotic toxin, Bordetella KW - Transglutaminases KW - EC 2.3.2.13 KW - Adenylyl Cyclases KW - EC 4.6.1.1 KW - Index Medicus KW - Hot Temperature KW - Animals KW - Neutralization Tests KW - Adenylyl Cyclases -- isolation & purification KW - Rabbits KW - Mice KW - Molecular Weight KW - Bordetella pertussis -- metabolism KW - Bacterial Toxins -- isolation & purification KW - Bacterial Toxins -- toxicity KW - Bacterial Toxins -- immunology KW - Bordetella pertussis -- pathogenicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72098161?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Purification+and+characterization+of+the+heat-labile+toxin+of+Bordetella+pertussis.&rft.au=Zhang%2C+Y+L%3BSekura%2C+R+D&rft.aulast=Zhang&rft.aufirst=Y&rft.date=1991-10-01&rft.volume=59&rft.issue=10&rft.spage=3754&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 - 1991-10-21 N1 - Date created - 1991-10-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 1983 Feb 25;258(4):2072-5 [6296122] Proc Soc Exp Biol Med. 1950 May;74(1):75-8 [15430395] J Biol Chem. 1983 Dec 10;258(23):14647-51 [6315733] J Med Microbiol. 1984 Feb;17(1):91-103 [6319705] Methods Enzymol. 1984;104:415-6 [6717293] Infect Immun. 1979 Sep;25(3):896-901 [227787] Anal Biochem. 1974 Apr;58(2):541-8 [4827395] J Bacteriol. 1963 Oct;86:648-55 [14066457] J Bacteriol. 1962 Aug;84:269-74 [13864610] J Biol Chem. 1961 May;236:1372-9 [13767412] J Biol Chem. 1951 Nov;193(1):265-75 [14907713] J Immunol. 1951 Jun;66(6):627-33 [14850717] J Med Microbiol. 1985 Jun;19(3):391-400 [2861293] J Biol Chem. 1989 Nov 15;264(32):19379-84 [2553737] Trends Biochem Sci. 1989 Nov;14(11):459-63 [2560273] Dev Biol Stand. 1985;61:93-102 [3011569] Microb Pathog. 1989 May;6(5):361-8 [2770506] Microbiol Immunol. 1986;30(7):659-73 [3773790] Infect Immun. 1986 May;52(2):370-7 [3699886] J Med Microbiol. 1986 May;21(3):265-70 [3701831] Infect Immun. 1990 May;58(5):1456-60 [2323823] Nature. 1983 Apr 21;302(5910):706-9 [6300694] Jpn J Microbiol. 1969 Dec;13(4):359-66 [4311586] Methods Enzymol. 1972;26:3-27 [4680711] Methods Enzymol. 1972;26:28-42 [4680709] J Clin Endocrinol Metab. 1971 Dec;33(6):988-91 [5316354] Science. 1982 Sep 3;217(4563):948-50 [6287574] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alterations of B lymphocyte Fc gamma R II expression and ligand binding capacity induced by various activators. AN - 72069502; 1653115 AB - Murine B lymphocytes cultured with F(ab')2 anti-mouse mu or delta lost (85%) the capacity to bind antigen-IgG antibody complexes as assessed by flow microfluorometry. Anti-mu-induced loss of binding of complexes was concentration, time, and temperature dependent, reversible, and not due to decreased expression of the receptor because binding of monoclonal anti-Fc gamma R II to B lymphocytes cultured with anti-mu was unaffected. Activation of PKC and elevation of [Ca2+]i obtained by culturing B lymphocytes with the combination of PMA and Ca2+ ionophore induced a similar loss of binding of Cx. Since stimulation of B lymphocytes with anti-mu also activates PKC and elevates [Ca2+]i, these changes may be involved in the anti-mu-induced alterations in the binding of complexes to Fc gamma R II. In contrast to the effects of other activators, LPS caused increased expression (threefold) of B lymphocyte Fc gamma R II as measured by the binding of both complexes and monoclonal anti-Fc gamma R II. Thus, different B lymphocyte activators have distinct effects on Fc gamma R II expression or ligand binding capacity and can thereby affect Fc gamma R II-generated regulatory signals. JF - Cellular immunology AU - Laszlo, G AU - Dickler, H B AD - Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/10/01/ PY - 1991 DA - 1991 Oct 01 SP - 24 EP - 35 VL - 137 IS - 1 SN - 0008-8749, 0008-8749 KW - Antigen-Antibody Complex KW - 0 KW - Antigens, Differentiation KW - Histocompatibility Antigens Class II KW - I-E-antigen KW - Immunoglobulin mu-Chains KW - Receptors, Antigen, B-Cell KW - Receptors, Fc KW - Receptors, IgG KW - Interleukin-4 KW - 207137-56-2 KW - Calcimycin KW - 37H9VM9WZL KW - Cycloheximide KW - 98600C0908 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Calcium KW - SY7Q814VUP KW - Emetine KW - X8D5EPO80M KW - Index Medicus KW - Animals KW - Interleukin-4 -- pharmacology KW - Immunoglobulin mu-Chains -- immunology KW - Mice KW - Antigen-Antibody Complex -- metabolism KW - Calcimycin -- pharmacology KW - Mice, Inbred DBA KW - Receptors, Antigen, B-Cell -- immunology KW - Histocompatibility Antigens Class II -- metabolism KW - Cells, Cultured KW - Cycloheximide -- pharmacology KW - Emetine -- pharmacology KW - In Vitro Techniques KW - Calcium -- physiology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Time Factors KW - Female KW - Lymphocyte Activation KW - Antigens, Differentiation -- metabolism KW - B-Lymphocytes -- immunology KW - B-Lymphocytes -- metabolism KW - Receptors, Fc -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72069502?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Alterations+of+B+lymphocyte+Fc+gamma+R+II+expression+and+ligand+binding+capacity+induced+by+various+activators.&rft.au=Laszlo%2C+G%3BDickler%2C+H+B&rft.aulast=Laszlo&rft.aufirst=G&rft.date=1991-10-01&rft.volume=137&rft.issue=1&rft.spage=24&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 - 1991-10-04 N1 - Date created - 1991-10-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Refurbishment of the Electrical Power Equipment at Cruachan AN - 19128908; 9202948 AB - After 25 years of operation, the 400 MW Cruachan pumped-storage plant in Scotland has undergone extensive refurbishment. The power station, owned and operated by Scottish Power, is on the shores of Loch Awe in the Scottish Highlands. Pumped storage was introduced to store energy by pumping at night for generation during the day to meet the system load peaks. The load regime was a single pumping period and two periods of generation, to meet the morning and early evening peaks with an average of 4 to 5 load changes per day. Problems with the units, requiring refurbishment, included: the main stator winding and rotor poles had become saturated with oil; the pony motor stator and rotor windings were coated with carbon dust; insulation resistance levels had deteriorated; the vibration levels of the machine had increased to almost unacceptable levels; the control and excitation system was slow to respond; the level of operational instrumentation had diminished because of the failure of embedded detectors; and high condensation from deterioration of lagging of the cooling water pipework. A new two-layer lap-type winding was provided. The stator-mounted air/water coolers were completely refurbished, and new stainless steel cooling water pipework was fitted inside the enclosure. Mercury-in-steel thermometers in the bearing pads were replaced by resistance temperature detector probes, and duplicate probes were fitted in other pads as insurance against possible future failure. The transformer was filled and circulated with hot oil, during which the tank was lagged to retain heat. In general, to refurbish a hydro power installation, problem areas need to be carefully analyzed, extensive redesign carried out, and solutions incorporated during the refurbishment with the aim of achieving a greatly extended plant life. (Brunone-PTT) JF - International Water Power and Dam Construction IWPCDM, Vol. 43, No. 10, p 43-47, October 1991. 3 tab. AU - Parry, GE AU - Henderson, DMS AD - Peebles Projects, NEI Peebles Ltd, East Pilton, Edinburgh EH5 2XT, Scotland Y1 - 1991/10// PY - 1991 DA - Oct 1991 KW - Water Resources Abstracts KW - *Cruachan Hydroelectric Plant KW - *Electrical equipment KW - *Hydroelectric plants KW - *Maintenance KW - *Project planning KW - *Pumping rates KW - *Rehabilitation KW - *Scotland KW - *Upgrading KW - Peak loads KW - Temporal variation KW - SW 4020:Evaluation process KW - SW 6030:Hydraulic machinery UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/19128908?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Awaterresources&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=&rft.atitle=Refurbishment+of+the+Electrical+Power+Equipment+at+Cruachan&rft.au=Parry%2C+GE%3BHenderson%2C+DMS&rft.aulast=Parry&rft.aufirst=GE&rft.date=1991-10-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-14 ER - TY - JOUR T1 - Arachidonic acid and diacylglycerol act synergistically to activate protein kinase C in vitro and in vivo. AN - 72164021; 1930192 AB - Using a well-defined model membrane bilayer system, incorporation of both lipid second messengers, 1,2-diacylglycerol and arachidonic acid, at submaximal activating concentrations, resulted in a synergistic activation of protein kinase C in a Ca2+/phosphatidylserine-dependent manner as measured by monitoring phosphorylation of phosphoprotein substrates. The arachidonic acid appears to modulate membrane properties both at the hydrocarbon core and the membrane surface increasing the availability of the diacylglycerol which can bind to and subsequently activate the enzyme. Co-application of these two lipid activators to the Hermissenda photoreceptor reduced K+ channel conductance in a synergistic manner via a PKC-dependent pathway. Thus, these in vivo and in vitro studies suggest that the membrane bilayer properties of these PKC lipid activators interact to specifically regulate the cellular lipid microenvironment resulting in PKC activation. JF - Biochemical and biophysical research communications AU - Lester, D S AU - Collin, C AU - Etcheberrigaray, R AU - Alkon, D L AD - National Institutes of Health, Section of Neural Systems, Bethesda, MD 20892. Y1 - 1991/09/30/ PY - 1991 DA - 1991 Sep 30 SP - 1522 EP - 1528 VL - 179 IS - 3 SN - 0006-291X, 0006-291X KW - Diglycerides KW - 0 KW - Lipid Bilayers KW - Arachidonic Acid KW - 27YG812J1I KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Second Messenger Systems KW - Photoreceptor Cells -- drug effects KW - Phorbol 12,13-Dibutyrate -- metabolism KW - Enzyme Activation KW - Kinetics KW - Cytosol -- enzymology KW - Photoreceptor Cells -- physiology KW - Mollusca KW - Drug Synergism KW - Protein Kinase C -- metabolism KW - Brain -- enzymology KW - Diglycerides -- pharmacology KW - Neurons -- drug effects KW - Arachidonic Acid -- pharmacology KW - Neurons -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72164021?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Arachidonic+acid+and+diacylglycerol+act+synergistically+to+activate+protein+kinase+C+in+vitro+and+in+vivo.&rft.au=Lester%2C+D+S%3BCollin%2C+C%3BEtcheberrigaray%2C+R%3BAlkon%2C+D+L&rft.aulast=Lester&rft.aufirst=D&rft.date=1991-09-30&rft.volume=179&rft.issue=3&rft.spage=1522&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 - 1991-11-01 N1 - Date created - 1991-11-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Oxidants and respiratory tract epithelial injury: pathogenesis and strategies for therapeutic intervention. AN - 72159515; 1928210 JF - The American journal of medicine AU - Crystal, R G AD - National Heart, Lung, and Blood Institute, Pulmonary Branch, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/09/30/ PY - 1991 DA - 1991 Sep 30 SP - 39S EP - 44S VL - 91 IS - 3C SN - 0002-9343, 0002-9343 KW - Oxidants KW - 0 KW - Glutathione KW - GAN16C9B8O KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Glutathione -- therapeutic use KW - Pulmonary Fibrosis -- chemically induced KW - Humans KW - Pulmonary Fibrosis -- physiopathology KW - HIV Infections -- drug therapy KW - Smoking -- adverse effects KW - Cystic Fibrosis -- physiopathology KW - Epithelium -- drug effects KW - Oxidants -- toxicity KW - Respiratory System -- pathology KW - Respiratory System -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72159515?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+medicine&rft.atitle=Oxidants+and+respiratory+tract+epithelial+injury%3A+pathogenesis+and+strategies+for+therapeutic+intervention.&rft.au=Crystal%2C+R+G&rft.aulast=Crystal&rft.aufirst=R&rft.date=1991-09-30&rft.volume=91&rft.issue=3C&rft.spage=39S&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+medicine&rft.issn=00029343&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-20 N1 - Date created - 1991-11-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Nested case-control study of lung cancer in the meat industry. AN - 72077665; 1886160 JF - Journal of the National Cancer Institute AU - Johnson, E S AD - Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709. Y1 - 1991/09/18/ PY - 1991 DA - 1991 Sep 18 SP - 1337 EP - 1339 VL - 83 IS - 18 SN - 0027-8874, 0027-8874 KW - Index Medicus KW - Risk Factors KW - Humans KW - Case-Control Studies KW - Baltimore -- epidemiology KW - Male KW - Lung Neoplasms -- etiology KW - Lung Neoplasms -- epidemiology KW - Occupational Diseases -- etiology KW - Meat-Packing Industry KW - Occupational Diseases -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72077665?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Nested+case-control+study+of+lung+cancer+in+the+meat+industry.&rft.au=Johnson%2C+E+S&rft.aulast=Johnson&rft.aufirst=E&rft.date=1991-09-18&rft.volume=83&rft.issue=18&rft.spage=1337&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 - 1991-10-04 N1 - Date created - 1991-10-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Surreptitious self-administration of epinephrine resulting in 'pheochromocytoma'. AN - 72063766; 1880888 JF - JAMA AU - Keiser, H R AD - National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/09/18/ PY - 1991 DA - 1991 Sep 18 SP - 1553 EP - 1555 VL - 266 IS - 11 SN - 0098-7484, 0098-7484 KW - Clonidine KW - MN3L5RMN02 KW - Epinephrine KW - YKH834O4BH KW - Abridged Index Medicus KW - Index Medicus KW - Munchausen Syndrome -- diagnosis KW - Self Administration KW - Humans KW - Adult KW - Tomography, X-Ray Computed KW - Female KW - Epinephrine -- adverse effects KW - Pheochromocytoma -- chemically induced KW - Pheochromocytoma -- diagnosis KW - Adrenal Gland Neoplasms -- psychology KW - Factitious Disorders -- diagnosis KW - Adrenal Gland Neoplasms -- chemically induced KW - Adrenal Gland Neoplasms -- diagnosis KW - Pheochromocytoma -- psychology KW - Epinephrine -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72063766?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&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=Surreptitious+self-administration+of+epinephrine+resulting+in+%27pheochromocytoma%27.&rft.au=Keiser%2C+H+R&rft.aulast=Keiser&rft.aufirst=H&rft.date=1991-09-18&rft.volume=266&rft.issue=11&rft.spage=1553&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-10-01 N1 - Date created - 1991-10-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Postexposure chemoprophylaxis for occupational exposure to human immunodeficiency virus type 1: current status and prospects for the future. AN - 72158410; 1928185 AB - Occupational exposures to the human immunodeficiency virus (HIV) continue to occur in the health care setting. Each such exposure is associated with risk for occupational infection. Although occupational HIV infections have been uncommon in health care workers, the occurrence of even one such infection is traumatic for the health care worker and his or her institution. To attempt to prevent infection following occupational exposures, some institutions and investigators have elected to offer postexposure chemoprophylaxis with zidovudine. Unfortunately, data describing the use of nucleoside analogues in animals and humans as antiviral chemoprophylaxis are quite limited and data simply do not exist that definitely support or refute their use in this setting. One can mount an equally reasonable argument for or against the use of these agents in this setting in 1990. This article reviews the available data regarding postexposure chemoprophylaxis, summarizes the clinical experience with zidovudine use for postexposure chemoprophylaxis to date, and evaluates prospects for additional chemoprophylaxis options in the future. JF - The American journal of medicine AU - Henderson, D K AD - Warren G. Magnuson Clinical Center, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/09/16/ PY - 1991 DA - 1991 Sep 16 SP - 312S EP - 319S VL - 91 IS - 3B SN - 0002-9343, 0002-9343 KW - Antiviral Agents KW - 0 KW - Zidovudine KW - 4B9XT59T7S KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Humans KW - Antiviral Agents -- pharmacology KW - Acquired Immunodeficiency Syndrome -- prevention & control KW - Occupational Diseases -- prevention & control KW - Health Personnel KW - Zidovudine -- administration & dosage KW - HIV-1 -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72158410?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+medicine&rft.atitle=Postexposure+chemoprophylaxis+for+occupational+exposure+to+human+immunodeficiency+virus+type+1%3A+current+status+and+prospects+for+the+future.&rft.au=Henderson%2C+D+K&rft.aulast=Henderson&rft.aufirst=D&rft.date=1991-09-16&rft.volume=91&rft.issue=3B&rft.spage=312S&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+medicine&rft.issn=00029343&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-05 N1 - Date created - 1991-11-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Relationship of hepatocarcinogenicity and hepatocellular proliferation induced by mutagenic noncarcinogens vs carcinogens. II. 1- vs 2-nitropropane. AN - 72476471; 1949017 AB - 2-Nitropropane (2-NP) is mutagenic in a number of short-term mutagenicity assays in vitro and in vivo, and is a potent hepatocarcinogen in rats. A structural isomer, 1-nitropropane (1-NP), is mutagenic in V79 cells and can induce unscheduled DNA synthesis in rat hepatocytes, yet did not induce tumors in rats following chronic exposure. We examined the correlation of cell proliferation and hepatocarcinogenesis induced by this mutagenic noncarcinogen-carcinogen pair in a rat liver proliferation model. Rats were exposed to gavage doses of 0.5, 1, or 2 mmol/kg of 1-NP or 2-NP daily for 10 days; the highest two dose groups were similar to the doses used in the carcinogenesis bioassay. Cell proliferation was quantitated by incorporation of bromodeoxyuridine, detected immunohistochemically, into newly synthesized DNA. Animals exposed to the vehicle exhibited a labeling index (LI) of approximately 1.9% and animals exposed to CCL4 had a LI of approximately 30%. Rats exposed to the hepatocarcinogen 2-NP exhibited a dose-related increase in LI to 6.3 and 11% at the 1 and 2 mmol/kg doses, respectively, and no increase above control at the 0.5 mmol/kg exposure level. Animals exposed to the noncarcinogenic isomer 1-NP showed no statistically significant increase in LI above controls at any dose level tested. Serum chemistries were consistent with mild to moderate decreases in hepatocellular function, cholestasis, and necrosis following 2-NP exposure, but only minimal effects were observed, probably due to slight dehydration resulting from 1-NP exposure. These data indicate a positive association between increased cell proliferation and hepatocarcinogenesis induced by these two nitropropane isomers. JF - Toxicology and applied pharmacology AU - Cunningham, M L AU - Matthews, H B AD - Experimental Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/09/15/ PY - 1991 DA - 1991 Sep 15 SP - 505 EP - 513 VL - 110 IS - 3 SN - 0041-008X, 0041-008X KW - Carcinogens KW - 0 KW - Mutagens KW - Nitroparaffins KW - 1-nitropropane KW - 39W305OW99 KW - Carbon Tetrachloride KW - CL2T97X0V0 KW - L-Iditol 2-Dehydrogenase KW - EC 1.1.1.14 KW - Alanine Transaminase KW - EC 2.6.1.2 KW - Bromodeoxyuridine KW - G34N38R2N1 KW - 2-nitropropane KW - GKV234L2QH KW - Propane KW - T75W9911L6 KW - Index Medicus KW - Animals KW - Propane -- adverse effects KW - Dose-Response Relationship, Drug KW - Propane -- analogs & derivatives KW - Cell Division -- drug effects KW - Rats KW - Carbon Tetrachloride -- adverse effects KW - Rats, Inbred F344 KW - Alanine Transaminase -- blood KW - L-Iditol 2-Dehydrogenase -- blood KW - Body Weight -- drug effects KW - Nitroparaffins -- adverse effects KW - Male KW - Bromodeoxyuridine -- metabolism KW - Liver -- cytology KW - Liver -- drug effects KW - Carcinogens -- toxicity KW - Mutagens -- toxicity KW - Liver Neoplasms, Experimental -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72476471?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Relationship+of+hepatocarcinogenicity+and+hepatocellular+proliferation+induced+by+mutagenic+noncarcinogens+vs+carcinogens.+II.+1-+vs+2-nitropropane.&rft.au=Cunningham%2C+M+L%3BMatthews%2C+H+B&rft.aulast=Cunningham&rft.aufirst=M&rft.date=1991-09-15&rft.volume=110&rft.issue=3&rft.spage=505&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 - 1991-11-27 N1 - Date created - 1991-11-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Tardive dyskinesia: neuropsychological, computerized tomographic, and psychiatric symptom findings. AN - 72175059; 1681948 AB - Prior studies have suggested that schizophrenic patients with tardive dyskinesia (TD) have an unusual incidence of cognitive impairment, structural brain abnormalities, and negative symptoms. Twenty-seven schizophrenic patients with TD and an equal number of age-, gender-, and education-matched schizophrenic controls were studied. Each patient received neuropsychological testing, psychiatric symptom ratings, and most had cerebral computed tomography (CT) scans. Patients with TD significantly differed from controls on only 1 of 23, cognitive measures, and the overall group performance profiles were highly similar. No differences were observed on symptom ratings. Patients with TD had significantly smaller ventricular-brain ratios (VBRs) than controls. These data fail to support an association of TD with global measures of "organicity." Abnormal movements may result from specific dysfunction within the more purely motor circuits of the basal ganglia without compromising other neural systems involved in cognitive processing. JF - Biological psychiatry AU - Gold, J M AU - Egan, M F AU - Kirch, D G AU - Goldberg, T E AU - Daniel, D G AU - Bigelow, L B AU - Wyatt, R J AD - Clinical and Research Services Branch, National Institute of Mental Health, Washington, DC 20032. Y1 - 1991/09/15/ PY - 1991 DA - 1991 Sep 15 SP - 587 EP - 599 VL - 30 IS - 6 SN - 0006-3223, 0006-3223 KW - Antipsychotic Agents KW - 0 KW - Index Medicus KW - Psychiatric Status Rating Scales KW - Dose-Response Relationship, Drug KW - Humans KW - Brain -- pathology KW - Adult KW - Cerebral Ventricles -- pathology KW - Male KW - Female KW - Antipsychotic Agents -- administration & dosage KW - Tomography, X-Ray Computed KW - Neurologic Examination KW - Dyskinesia, Drug-Induced -- psychology KW - Dyskinesia, Drug-Induced -- diagnosis KW - Schizophrenic Psychology KW - Schizophrenia -- drug therapy KW - Neuropsychological Tests KW - Antipsychotic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72175059?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biological+psychiatry&rft.atitle=Tardive+dyskinesia%3A+neuropsychological%2C+computerized+tomographic%2C+and+psychiatric+symptom+findings.&rft.au=Gold%2C+J+M%3BEgan%2C+M+F%3BKirch%2C+D+G%3BGoldberg%2C+T+E%3BDaniel%2C+D+G%3BBigelow%2C+L+B%3BWyatt%2C+R+J&rft.aulast=Gold&rft.aufirst=J&rft.date=1991-09-15&rft.volume=30&rft.issue=6&rft.spage=587&rft.isbn=&rft.btitle=&rft.title=Biological+psychiatry&rft.issn=00063223&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-26 N1 - Date created - 1991-12-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A case-control study of serum folate levels and invasive cervical cancer. AN - 72104557; 1893371 AB - Although small intervention trials have suggested that folate supplementation reduces cervical dysplasia, the association of blood folate concentrations with invasive cervical cancer risk has not been investigated in well-controlled epidemiological studies. A study was conducted with newly diagnosed Stage I and II invasive cervical cancer cases and controls in 4 Latin American countries. Ninety-five% of subjects donated blood samples, resulting in 330 case and 565 control serum samples analyzed for folate concentrations by radioassay. Cases did not differ significantly from controls in mean levels of folate (5.00 and 4.90 ng/ml, respectively). No associations were observed between quartiles of serum folate and risk of cervical cancer after adjustment for other risk factors, and no interactions with established risk factors were observed. Folate levels were also unrelated to risk among women who might have compromised folate status because of recent or extended oral contraceptive usage or multiple pregnancies. Further, mean levels of folate were similar by stage of disease, arguing against an effect of disease progression on serum values. These results do not support a role for serum folate in the etiology of invasive cervical cancer. JF - Cancer research AU - Potischman, N AU - Brinton, L A AU - Laiming, V A AU - Reeves, W C AU - Brenes, M M AU - Herrero, R AU - Tenorio, F AU - de Britton, R C AU - Gaitan, E AD - Environmental Epidemiology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/09/15/ PY - 1991 DA - 1991 Sep 15 SP - 4785 EP - 4789 VL - 51 IS - 18 SN - 0008-5472, 0008-5472 KW - Contraceptives, Oral KW - 0 KW - Folic Acid KW - 935E97BOY8 KW - Index Medicus KW - Parity KW - Contraceptives, Oral -- adverse effects KW - Risk Factors KW - Humans KW - Adult KW - Case-Control Studies KW - Aged KW - Middle Aged KW - South America -- epidemiology KW - Female KW - Pregnancy KW - Uterine Cervical Neoplasms -- etiology KW - Adenocarcinoma -- epidemiology KW - Carcinoma, Squamous Cell -- etiology KW - Adenocarcinoma -- blood KW - Carcinoma, Squamous Cell -- epidemiology KW - Uterine Cervical Neoplasms -- epidemiology KW - Folic Acid -- blood KW - Adenocarcinoma -- etiology KW - Carcinoma, Squamous Cell -- blood KW - Uterine Cervical Neoplasms -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72104557?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=A+case-control+study+of+serum+folate+levels+and+invasive+cervical+cancer.&rft.au=Potischman%2C+N%3BBrinton%2C+L+A%3BLaiming%2C+V+A%3BReeves%2C+W+C%3BBrenes%2C+M+M%3BHerrero%2C+R%3BTenorio%2C+F%3Bde+Britton%2C+R+C%3BGaitan%2C+E&rft.aulast=Potischman&rft.aufirst=N&rft.date=1991-09-15&rft.volume=51&rft.issue=18&rft.spage=4785&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 - 1991-10-21 N1 - Date created - 1991-10-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Integrated microscopic-macroscopic pharmacology of monoclonal antibody radioconjugates: the radiation dose distribution. AN - 72102103; 1893374 AB - Accurate dosimetry is essential for the assessment of radioimmunotherapy. Most often studied to date has been the macroscopic dosimetry related to organ and tumor distribution of the radiolabeled antibody, but the question of microscopic dose heterogeneity is also important. To address the latter issue, we have taken an integrated approach to the pharmacology, taking into account whole-body distribution, transcapillary transport, percolation through the tumor interstitial space, antigen-antibody interaction, and antibody metabolism. The first step is to simulate the spatial antibody concentration profile in a tumor as a function of time after i.v. (e.g., bolus) injection, using reasonable values for the parameters involved. The second step is to calculate, also as a function of time, the absorbed radiation dose distribution resulting from each concentration profile. Parameter values for IgG pharmacology and a radiation point source function for 131I are used to explore the effect of antibody distribution profiles on absorbed dose in the tumor. The geometry simulated corresponds to a spherical nodule of densely packed tumor cells. Absorbed doses are calculated for radiation from a single nodule (e.g., a micrometastasis or prevascular primary tumor) and for a cubic lattice of such nodules (e.g., corresponding to nodular lymphoma). As noted in our previous studies, there is a "binding site barrier." Binding to antigen retards antibody percolation into the nodules; high antibody affinity tends to decrease percolation and give a higher absorbed dose near the surface of each nodule. Heterogeneous antibody distribution results in a heterogeneous absorbed dose. This is more apparent in the case of radiation from a single nodule than it is for radiation from within an array of nodules. Dehalogenation results in a lower absorbed dose over time, and the effect is more apparent at later times after injection. PERC-RAD, the computer program package developed for these analyses, provides a convenient and flexible way to assess the impact of macroscopic and microscopic parameters on the distribution of radioimmunoconjugates and on the consequent profile of absorbed radiation dose in tumors. This mathematical model and the general principles developed here can be applied as well to other radiolabeled biological ligands. JF - Cancer research AU - Fujimori, K AU - Fisher, D R AU - Weinstein, J N AD - Laboratory of Mathematical Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/09/15/ PY - 1991 DA - 1991 Sep 15 SP - 4821 EP - 4827 VL - 51 IS - 18 SN - 0008-5472, 0008-5472 KW - Antibodies, Monoclonal KW - 0 KW - Immunoglobulin G KW - Iodine Radioisotopes KW - Index Medicus KW - Software KW - Radiation Dosage KW - Humans KW - Immunoglobulin G -- pharmacology KW - Immunoglobulin G -- pharmacokinetics KW - Tissue Distribution KW - Models, Biological KW - Radiotherapy Planning, Computer-Assisted KW - Neoplasms -- radiotherapy KW - Antibodies, Monoclonal -- pharmacokinetics KW - Iodine Radioisotopes -- pharmacology KW - Antibodies, Monoclonal -- pharmacology KW - Iodine Radioisotopes -- pharmacokinetics KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72102103?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Integrated+microscopic-macroscopic+pharmacology+of+monoclonal+antibody+radioconjugates%3A+the+radiation+dose+distribution.&rft.au=Fujimori%2C+K%3BFisher%2C+D+R%3BWeinstein%2C+J+N&rft.aulast=Fujimori&rft.aufirst=K&rft.date=1991-09-15&rft.volume=51&rft.issue=18&rft.spage=4821&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 - 1991-10-21 N1 - Date created - 1991-10-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chemical and physical carcinogenesis: advances and perspectives for the 1990s. AN - 72074185; 1884379 AB - Carcinogenesis is a multistage process driven by carcinogen-induced genetic and epigenetic damage in susceptible cells that gain a selective growth advantage and undergo clonal expansion as the result of activation of protooncogenes and/or inactivation of tumor suppressor genes. Therefore, the mutational spectra of chemical and physical carcinogens in these critical genes are of interest to define endogenous and exogenous mutational mechanisms. The p53 tumor suppressor gene is ideally suited for analysis of the mutational spectrum. Such an analysis has revealed evidence for both exogenous and endogenous molecular mechanisms of carcinogenesis. For example, an informative p53 mutational spectrum of frequent G----T transversions in codon 249 is found in hepatocellular carcinomas from either Qidong, People's Republic of China, or southern Africa. This observation links exposure to aflatoxin B1, a known cancer risk factor in these geographic regions, with a specific mutation in a cancer-related gene. Other studies indicate that abnormalities in genes controlling the cell cycle may cause genomic instability and increase the probability of neoplastic transformation. Finally, mechanistic understanding of carcinogenesis is leading to improved cancer risk assessment and to the identification of individuals at high cancer risk. JF - Cancer research AU - Harris, C C AD - Laboratory of Human Carcinogenesis, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1991/09/15/ PY - 1991 DA - 1991 Sep 15 SP - 5023s EP - 5044s VL - 51 IS - 18 Suppl SN - 0008-5472, 0008-5472 KW - Ha-ras KW - Ki-ras KW - Rb KW - aprt KW - dhfr KW - ras KW - Carcinogens KW - 0 KW - Index Medicus KW - Animals KW - DNA Repair KW - Genes, Tumor Suppressor KW - DNA Damage KW - Risk Factors KW - Humans KW - Mutation -- genetics KW - Proto-Oncogenes KW - Neoplasms -- chemically induced KW - Neoplasms -- genetics KW - Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72074185?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Chemical+and+physical+carcinogenesis%3A+advances+and+perspectives+for+the+1990s.&rft.au=Harris%2C+C+C&rft.aulast=Harris&rft.aufirst=C&rft.date=1991-09-15&rft.volume=51&rft.issue=18+Suppl&rft.spage=5023s&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 - 1991-10-04 N1 - Date created - 1991-10-04 N1 - Date revised - 2017-01-13 N1 - Gene symbol - Ha-ras; Ki-ras; Rb; aprt; dhfr; ras N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of the human papillomaviruses in human cancer. AN - 72071328; 1653110 AB - The papillomaviruses associated with human anogenital carcinomas encode two transforming genes, E6 and E7. The oncoprotein products of these two genes complex with the tumor suppressor gene products p53 and pRB, respectively. The loss of the normal function of these tumor suppressor gene products, either as a consequence of their association with E6 and E7 or by mutation, appears to be a common event in human cervical carcinogenesis. JF - Cancer research AU - Howley, P M AD - Laboratory of Tumor Virus Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/09/15/ PY - 1991 DA - 1991 Sep 15 SP - 5019s EP - 5022s VL - 51 IS - 18 Suppl SN - 0008-5472, 0008-5472 KW - E6 KW - E7 KW - Index Medicus KW - Genital Neoplasms, Female -- microbiology KW - Genital Neoplasms, Male -- microbiology KW - Humans KW - Uterine Cervical Neoplasms -- microbiology KW - Male KW - Female KW - Papillomaviridae -- physiology KW - Tumor Virus Infections -- genetics KW - Papillomaviridae -- genetics KW - Neoplasms -- microbiology KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72071328?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Role+of+the+human+papillomaviruses+in+human+cancer.&rft.au=Howley%2C+P+M&rft.aulast=Howley&rft.aufirst=P&rft.date=1991-09-15&rft.volume=51&rft.issue=18+Suppl&rft.spage=5019s&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 - 1991-10-04 N1 - Date created - 1991-10-04 N1 - Date revised - 2017-01-13 N1 - Gene symbol - E6; E7 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vivo brain incorporation of [1-14C]arachidonate in awake rats, with or without cholinergic stimulation, following unilateral lesioning of nucleus basalis magnocellularis. AN - 72637296; 1723641 AB - Regional brain incorporation of a radiolabeled unsaturated fatty acid, [1-14C]arachidonic acid (14C-AA), was measured in awake rats following unilateral lesioning of the nucleus basalis magnocellularis (NBM). Right-sided lesions were produced in 3-month-old, male rats by stereotaxic injection of 10 micrograms ibotenic acid. Two weeks after lesioning, rats were subjected to one of two protocols: (1) 5 min intravenous infusion of 14C-AA (170 microCi/kg); or (2) i.p. injection of arecoline (5 mg/kg), a cholinergic agonist, followed by 5 min intravenous infusion of 14C-AA. All animals were killed 15 min postinfusion. Brains were frozen and sectioned for quantitative autoradiography or were stained for acetylcholinesterase (AChE). Animals with unilateral NBM lesions displayed reduced AChE staining in prefrontal, frontal and parietal cortices of the lesioned side, but there was no right-left difference in incorporation of 14C-AA without cholinergic stimulation. Arecoline administration increased 14C-AA incorporation into the prefrontal and frontal cortices ipsilateral to the NBM lesion as compared to the contralateral side and the increase was most prominent in deeper cortical layers such as layers IV and V. Right-left differences in incorporation were not apparent in parietal, temporal, or occipital cortices, where reduction of AChE activity was minimal or absent, nor in subcortical structures. The results suggest that the intravenous 14C-AA technique combined with cholinergic stimulation can be used to detect compensatory regulation of phospholipid-coupled signal transduction caused by a deficit in cholinergic input into the cerebral cortex. JF - Brain research AU - Nariai, T AU - DeGeorge, J J AU - Lamour, Y AU - Rapoport, S I AD - Laboratory of Neurosciences, National Institute on Aging, National Institute of Health, Bethesda, MD 20892. Y1 - 1991/09/13/ PY - 1991 DA - 1991 Sep 13 SP - 1 EP - 9 VL - 559 IS - 1 SN - 0006-8993, 0006-8993 KW - Ibotenic Acid KW - 2552-55-8 KW - Arachidonic Acid KW - 27YG812J1I KW - Arecoline KW - 4ALN5933BH KW - Acetylcholinesterase KW - EC 3.1.1.7 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Arecoline -- pharmacology KW - Acetylcholinesterase -- metabolism KW - Ibotenic Acid -- toxicity KW - Electric Stimulation KW - Staining and Labeling KW - Male KW - Parasympathetic Nervous System -- physiology KW - Parasympathetic Nervous System -- enzymology KW - Basal Ganglia -- physiology KW - Basal Ganglia -- anatomy & histology KW - Arachidonic Acid -- metabolism KW - Brain Chemistry -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72637296?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=In+vivo+brain+incorporation+of+%5B1-14C%5Darachidonate+in+awake+rats%2C+with+or+without+cholinergic+stimulation%2C+following+unilateral+lesioning+of+nucleus+basalis+magnocellularis.&rft.au=Nariai%2C+T%3BDeGeorge%2C+J+J%3BLamour%2C+Y%3BRapoport%2C+S+I&rft.aulast=Nariai&rft.aufirst=T&rft.date=1991-09-13&rft.volume=559&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Brain+research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-19 N1 - Date created - 1992-03-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Structural function of residue-209 in coumarin 7-hydroxylase (P450coh). Enzyme-kinetic studies and site-directed mutagenesis. AN - 72076853; 1885576 AB - Residue-209 plays a critical role in determining the substrate and product specificity of cytochrome P450coh. In order to investigate further the structural function of residue-209 in coumarin 7-hydroxylase reaction, we measured the enzyme-kinetic properties of wild-type P450coh and its mutants in which residue-209 was substituted with various amino acids. In general, the Km and Vmax values for coumarin increased as the size of residue-209 became smaller and Vmax values decreased. The size of residue-209, therefore, was a principle factor determining Km, Kd, and Vmax values of P450coh. Although the polarity and charge also increased the Km value consistently, they altered Vmax and Kd values in an irregular manner. The substitution of serine for residue-209 increased the Vmax, while the substitution of lysine decreased it. Coumarin 7-hydroxylase activity was inhibited weakly by indan, but competitively and strongly by 2-coumaranone. Moreover, Ki values for the inhibitor were similar to Km values of the corresponding, mutated P450s. The results indicate, therefore, that residue-209 is localized in a proposed substrate-binding sequence 1 which binds to the 2-keto group of coumarin and directs its 7-position toward the sixth ligand of heme. Consequently, the identity of residue-209 determines not only the binding of coumarin in P450coh, but also the other reaction step(s) of coumarin 7-hydroxylation. JF - The Journal of biological chemistry AU - Juvonen, R O AU - Iwasaki, M AU - Negishi, M AD - Pharmacogenetics Section, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. Y1 - 1991/09/05/ PY - 1991 DA - 1991 Sep 05 SP - 16431 EP - 16435 VL - 266 IS - 25 SN - 0021-9258, 0021-9258 KW - Amino Acids KW - 0 KW - Coumarins KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Mixed Function Oxygenases KW - EC 1.- KW - Aryl Hydrocarbon Hydroxylases KW - EC 1.14.14.1 KW - Cytochrome P-450 CYP2A6 KW - Index Medicus KW - Molecular Structure KW - Binding Sites KW - Cloning, Molecular KW - Hydroxylation KW - Mutagenesis, Site-Directed KW - Base Sequence KW - Amino Acids -- chemistry KW - Coumarins -- metabolism KW - Kinetics KW - Molecular Sequence Data KW - Substrate Specificity KW - Coumarins -- chemistry KW - Mixed Function Oxygenases -- chemistry KW - Mixed Function Oxygenases -- metabolism KW - Cytochrome P-450 Enzyme System -- genetics KW - Cytochrome P-450 Enzyme System -- chemistry KW - Cytochrome P-450 Enzyme System -- metabolism KW - Mixed Function Oxygenases -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72076853?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Structural+function+of+residue-209+in+coumarin+7-hydroxylase+%28P450coh%29.+Enzyme-kinetic+studies+and+site-directed+mutagenesis.&rft.au=Juvonen%2C+R+O%3BIwasaki%2C+M%3BNegishi%2C+M&rft.aulast=Juvonen&rft.aufirst=R&rft.date=1991-09-05&rft.volume=266&rft.issue=25&rft.spage=16431&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 - 1991-10-04 N1 - Date created - 1991-10-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - CD4+ and CD8+ T cells acquire specific lymphokine secretion potentials during thymic maturation. AN - 72064779; 1831881 AB - Peripheral CD4+ and CD8+ T lymphocytes carry out different functions during immune reactions, partly as a result of the distinct patterns of lymphokines that they secrete upon stimulation. Using thymic cells from adult and newborn mice as well as from fetal organ cultures, we show here that this functional differentiation occurs inside the thymus and is completed during the single positive stage by the time the T-cell receptor becomes fully coupled to the intracellular activation pathways leading to lymphokine secretion. Surprisingly, CD4+8- thymocytes differ from their immediate progeny, naive peripheral CD4+ cells, in that they secrete a broader range of lymphokines, including interleukins 4, 5 and 10 and gamma-interferon, and more closely resemble immunologically experienced (activated or memory) CD4+ lymphocytes. JF - Nature AU - Bendelac, A AU - Schwartz, R H AD - Laboratory of Cellular and Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/09/05/ PY - 1991 DA - 1991 Sep 05 SP - 68 EP - 71 VL - 353 IS - 6339 SN - 0028-0836, 0028-0836 KW - Interleukin-2 KW - 0 KW - Interleukin-5 KW - Interleukins KW - Lymphokines KW - Receptors, Antigen, T-Cell KW - Interleukin-10 KW - 130068-27-8 KW - Interleukin-4 KW - 207137-56-2 KW - Ionomycin KW - 56092-81-0 KW - Interferon-gamma KW - 82115-62-6 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Interleukin-4 -- secretion KW - Interleukin-5 -- secretion KW - Interleukins -- secretion KW - Ionomycin -- pharmacology KW - Mice KW - Receptors, Antigen, T-Cell -- physiology KW - Lymphocyte Activation KW - Animals, Newborn KW - Interferon-gamma -- secretion KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Interleukin-2 -- secretion KW - Thymus Gland -- growth & development KW - T-Lymphocytes, Regulatory -- physiology KW - Thymus Gland -- embryology KW - T-Lymphocytes, Helper-Inducer -- physiology KW - Lymphokines -- secretion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72064779?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=CD4%2B+and+CD8%2B+T+cells+acquire+specific+lymphokine+secretion+potentials+during+thymic+maturation.&rft.au=Bendelac%2C+A%3BSchwartz%2C+R+H&rft.aulast=Bendelac&rft.aufirst=A&rft.date=1991-09-05&rft.volume=353&rft.issue=6339&rft.spage=68&rft.isbn=&rft.btitle=&rft.title=Nature&rft.issn=00280836&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-10-03 N1 - Date created - 1991-10-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Case-control study of canine malignant lymphoma: positive association with dog owner's use of 2,4-dichlorophenoxyacetic acid herbicides. AN - 72031223; 1870148 AB - A hospital-based case-control study of companion dogs examined the risk of developing canine malignant lymphoma associated with the use of chemicals in and about the home. Information from a self-administered owner questionnaire and/or a telephone interview of about 491 cases, 466 nontumor controls, and 479 tumor controls indicated that owners in households with dogs that developed malignant lymphoma applied 2,4-dichlorophenoxyacetic acid (2,4-D) herbicides to their lawn and/or employed commercial lawn care companies to treat their yard significantly more frequently than control owners (odds ratio = 1.3). In addition, the risk of canine malignant lymphoma rose to a twofold excess with four or more yearly owner applications of 2,4-D. The findings in this study are consistent with occupational studies in humans, which have reported modest associations between agricultural exposure to 2,4-D and increased risk of non-Hodgkin's lymphoma, the histology and epidemiology of which are similar to those of canine malignant lymphoma. The present study suggests that human health implications of 2,4-D exposure in the home environment should receive further investigation. JF - Journal of the National Cancer Institute AU - Hayes, H M AU - Tarone, R E AU - Cantor, K P AU - Jessen, C R AU - McCurnin, D M AU - Richardson, R C AD - Epidemiology and Biostatistics Program, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/09/04/ PY - 1991 DA - 1991 Sep 04 SP - 1226 EP - 1231 VL - 83 IS - 17 SN - 0027-8874, 0027-8874 KW - 2,4-Dichlorophenoxyacetic Acid KW - 2577AQ9262 KW - Index Medicus KW - Animals KW - Surveys and Questionnaires KW - Dogs KW - Case-Control Studies KW - Interviews as Topic KW - Male KW - Female KW - Multivariate Analysis KW - Lymphoma -- etiology KW - 2,4-Dichlorophenoxyacetic Acid -- adverse effects KW - Dog Diseases -- etiology KW - Lymphoma -- veterinary UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72031223?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Case-control+study+of+canine+malignant+lymphoma%3A+positive+association+with+dog+owner%27s+use+of+2%2C4-dichlorophenoxyacetic+acid+herbicides.&rft.au=Hayes%2C+H+M%3BTarone%2C+R+E%3BCantor%2C+K+P%3BJessen%2C+C+R%3BMcCurnin%2C+D+M%3BRichardson%2C+R+C&rft.aulast=Hayes&rft.aufirst=H&rft.date=1991-09-04&rft.volume=83&rft.issue=17&rft.spage=1226&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 - 1991-09-18 N1 - Date created - 1991-09-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: J Natl Cancer Inst. 1991 Sep 4;83(17):1198-9 [1870140] J Natl Cancer Inst. 1992 Feb 19;84(4):271 [1734089] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Photochemical effects of laser irradiation on neuritic outgrowth of olfactory neuroepithelial explants. AN - 85212504; pmid-1945434 AB - The photochemical effect of low-intensity laser irradiation (LILI) on the maturation and regeneration of olfactory-immature estrus day 15 (E15) and olfactory-mature estrus day 22 (E22) rat fetuses was studied. Neuritic outgrowths of olfactory bipolar receptor cells were quantified in olfactory neuroepithelial explants. Explants in the experimental groups were irradiated with a helium-neon laser using different incident energy densities (IEDs). Explants in another group were exposed to fluorescent light. Control explants did not receive laser or fluorescent light irradiation. Neuritic outgrowths were analyzed on a regular basis for 12 days. Analysis of variance was used to evaluate the data. The parameters of neuritic outgrowth in E15 fetuses showed a significant increase of 30% to 50% vs. the control with a single laser irradiation of 0.5 J/cm2 IED. The rate of neuritic outgrowth observed in the E22 fetuses was less than in the E15 fetuses. The parameters of neuritic outgrowth in E22 fetuses showed a significant and substantially greater percentage increase than in the E15 fetuses with daily laser irradiations of 0.05 and 0.5 J/cm2 IED when compared to the control. The magnitude of these increases appears to be of biological significance as well as statistical significance. JF - Otolaryngology--Head and Neck Surgery AU - Mester, A F AU - Snow, J B AU - Shaman, P AD - Department of Otorhinolaryngology and Human Communication, University of Pennsylvania Medical Center, Philadelphia.; National Institute on Deafness and other Communication Disorders, Bethesda, Maryland 20892, USA. PY - 1991 SP - 449 EP - 456 VL - 105 IS - 3 SN - 0194-5998, 0194-5998 KW - Rats KW - Rats, Inbred Strains KW - Fetus KW - Analysis of Variance KW - Growth KW - Support, U.S. Gov't, P.H.S. KW - Animal KW - Female KW - Neurites KW - Olfactory Mucosa KW - Receptors, Sensory KW - Lasers UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85212504?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Otolaryngology--Head+and+Neck+Surgery&rft.atitle=Photochemical+effects+of+laser+irradiation+on+neuritic+outgrowth+of+olfactory+neuroepithelial+explants.&rft.au=Mester%2C+A+F%3BSnow%2C+J+B%3BShaman%2C+P&rft.aulast=Mester&rft.aufirst=A&rft.date=1991-09-01&rft.volume=105&rft.issue=3&rft.spage=449&rft.isbn=&rft.btitle=&rft.title=Otolaryngology--Head+and+Neck+Surgery&rft.issn=01945998&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Managing heritable hearing loss: the audiologist's role. AN - 85153162; pmid-1750843 JF - ASHA AU - Pikus, A T AD - National Institute on Deafness and Other Communication Disorders, National Institutes of Health. PY - 1991 SP - 38 EP - 9, 48 VL - 33 IS - 9 SN - 0001-2475, 0001-2475 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85153162?accountid=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=ASHA&rft.atitle=Managing+heritable+hearing+loss%3A+the+audiologist%27s+role.&rft.au=Pikus%2C+A+T&rft.aulast=Pikus&rft.aufirst=A&rft.date=1991-09-01&rft.volume=33&rft.issue=9&rft.spage=38&rft.isbn=&rft.btitle=&rft.title=ASHA&rft.issn=00012475&rft_id=info:doi/ LA - English DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - A new institute. A promising future of research. AN - 85153083; pmid-1750841 JF - ASHA AU - Snow, J B AD - National Institute on Deafness and other Communication Disorders, Bethesda, Maryland 20892, USA. PY - 1991 SP - 33 EP - 34 VL - 33 IS - 9 SN - 0001-2475, 0001-2475 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85153083?accountid=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=ASHA&rft.atitle=A+new+institute.+A+promising+future+of+research.&rft.au=Snow%2C+J+B&rft.aulast=Snow&rft.aufirst=J&rft.date=1991-09-01&rft.volume=33&rft.issue=9&rft.spage=33&rft.isbn=&rft.btitle=&rft.title=ASHA&rft.issn=00012475&rft_id=info:doi/ LA - English DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Prolonged alterations in canine striatal dopamine metabolism following subtoxic doses of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 4'-amino-MPTP are linked to the persistence of pyridinium metabolites. AN - 80714953; 1677682 AB - Single toxic doses of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).HCl (2.5 mg/kg i.v.) and 4'-amino-MPTP.2HCl (22.5 mg/kg) induce loss of striatal dopamine (DA) and tyrosine hydroxylase (TH) activity and of nigral DA neurons in the dog. To examine the subacute neurochemical changes induced by low doses of MPTP and 4'-amino-MPTP, dose-response studies of these compounds were carried out in the dog, using 6- and 3-week survival times for these two compounds, respectively. Low single doses of MPTP (1.0, 0.5, and 0.1 mg/kg i.v.) and 4'-amino-MPTP (15, 7.5, and 3.75 mg/kg i.v.) did not cause depletion of canine striatal DA or TH or a loss of nigral neurons. However, levels of the DA metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were decreased in a dose-related fashion, with significant loss of DOPAC being evident 6 weeks after the lowest administered dose of MPTP and 3 weeks after 4'-amino-MPTP. This selective loss of DA metabolites following nontoxic doses of MPTP and 4'-amino-MPTP led to a shift in the ratio of DA to DOPAC or HVA, which was characteristic for each compound. The measurement of striatal 1-methyl-4-phenylpyridinium (MPP+) and 4'-amino-MPP+ levels revealed that high concentrations (up to 150 microM) persist in the striatum for weeks following administration of a single nontoxic dose of MPTP or 4'-amino-MPTP. A causal relationship between the striatal concentration of MPP+ or 4'-amino-MPP+ and the change in DA metabolism as reflected in the DA/DOPAC ratio is suggested by a significant correlation between these measures. It is suggested that presynaptic sequestration and retention of MPP+ and 4'-amino-MPP+ by striatal DA terminals result in the inhibition of the monoamine oxidase contained within these terminals. JF - Journal of neurochemistry AU - Johannessen, J N AU - Sobotka, T J AU - Weise, V K AU - Markey, S P AD - Laboratory of Clinical Science, National Institute of Mental Health, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 981 EP - 990 VL - 57 IS - 3 SN - 0022-3042, 0022-3042 KW - Pyridinium Compounds KW - 0 KW - 3,4-Dihydroxyphenylacetic Acid KW - 102-32-9 KW - 4'-amino-1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 106362-30-5 KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Tyrosine 3-Monooxygenase KW - EC 1.14.16.2 KW - Dopamine KW - VTD58H1Z2X KW - Homovanillic Acid KW - X77S6GMS36 KW - Index Medicus KW - Animals KW - Tyrosine 3-Monooxygenase -- metabolism KW - Dose-Response Relationship, Drug KW - 3,4-Dihydroxyphenylacetic Acid -- metabolism KW - Dogs KW - Homovanillic Acid -- metabolism KW - Male KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- analogs & derivatives KW - Pyridinium Compounds -- metabolism KW - Corpus Striatum -- metabolism KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- pharmacology KW - Dopamine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80714953?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Prolonged+alterations+in+canine+striatal+dopamine+metabolism+following+subtoxic+doses+of+1-methyl-4-phenyl-1%2C2%2C3%2C6-tetrahydropyridine+%28MPTP%29+and+4%27-amino-MPTP+are+linked+to+the+persistence+of+pyridinium+metabolites.&rft.au=Johannessen%2C+J+N%3BSobotka%2C+T+J%3BWeise%2C+V+K%3BMarkey%2C+S+P&rft.aulast=Johannessen&rft.aufirst=J&rft.date=1991-09-01&rft.volume=57&rft.issue=3&rft.spage=981&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 - 1991-09-04 N1 - Date created - 1991-09-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A Balanced Approach To Risk Assessment AN - 760215891; 13641552 AB - Abstract not available. JF - Toxicology and Industrial Health AU - Hoel, David G AD - National Institute of Environmental Health Sciences, U.S.A Y1 - 1991/09// PY - 1991 DA - Sep 1991 SP - 305 EP - 311 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU UK VL - 7 IS - 5-6 SN - 0748-2337, 0748-2337 KW - Toxicology Abstracts KW - Risk assessment KW - X 24350:Industrial Chemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/760215891?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+Industrial+Health&rft.atitle=A+Balanced+Approach+To+Risk+Assessment&rft.au=Hoel%2C+David+G&rft.aulast=Hoel&rft.aufirst=David&rft.date=1991-09-01&rft.volume=7&rft.issue=5-6&rft.spage=305&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+Industrial+Health&rft.issn=07482337&rft_id=info:doi/10.1177%2F074823379100700533 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2010-10-01 N1 - Number of references - 11 N1 - Last updated - 2015-04-09 N1 - SubjectsTermNotLitGenreText - Risk assessment DO - http://dx.doi.org/10.1177/074823379100700533 ER - TY - JOUR T1 - Identifying glycoconjugate-binding domains. Building on the past. AN - 72758640; 1820195 AB - The molecular details of how glycoconjugate-binding proteins interact with their ligands have been revealed by a variety of techniques. For example, proteases, chemical-modifying reagents and antibodies have served as effective probes of lectin functional domains. Protein crystallography has providing insight into how lectins are structured, and aided in determining which amino acids in these proteins are positioned appropriately for bond formation with glycoconjugates. In addition, the characterization and sequencing of naturally occurring, non-functional lectin variants have led to the identification of amino acids which play critical roles in a lectin's glycoconjugate-binding domain. Similarly, studies of lectin mutants produced by site-directed mutagenesis, and of synthetic peptides that mimic lectin binding properties, have demonstrated the importance of particular amino acids for glycoconjugate binding. An alternate approach to understanding lectin functional domains has been to compare the primary sequences of these proteins to reveal common sequence elements which allow them to be organized into families. For example, the discovery of amino acid homologies dispersed over long segments of the primary sequences of several lectins has suggested that many of these proteins have a related three-dimensional organization. In addition, the identification of more highly focused regions of sequence homology has indicated that many structures within the lectin glycoconjugate-binding domains themselves may be conserved. Scanning protein data banks for sequences homologous to known lectins has led to the identification of several previously unrecognized lectins, and aided in determining what portions of these proteins function in their glycoconjugate-binding domains.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Glycobiology AU - Holt, G D AD - Laboratory of Structural Biology, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 329 EP - 336 VL - 1 IS - 4 SN - 0959-6658, 0959-6658 KW - Glycoproteins KW - 0 KW - Lectins KW - Serpins KW - Fibroblast Growth Factors KW - 62031-54-3 KW - Heparin KW - 9005-49-6 KW - Index Medicus KW - Sequence Homology, Nucleic Acid KW - Molecular Sequence Data KW - Serpins -- chemistry KW - Heparin -- metabolism KW - Heparin -- chemistry KW - Fibroblast Growth Factors -- chemistry KW - Amino Acid Sequence KW - Fibroblast Growth Factors -- metabolism KW - Serpins -- metabolism KW - Binding Sites KW - Glycoproteins -- metabolism KW - Glycoproteins -- chemistry KW - Lectins -- chemistry KW - Lectins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72758640?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Glycobiology&rft.atitle=Identifying+glycoconjugate-binding+domains.+Building+on+the+past.&rft.au=Holt%2C+G+D&rft.aulast=Holt&rft.aufirst=G&rft.date=1991-09-01&rft.volume=1&rft.issue=4&rft.spage=329&rft.isbn=&rft.btitle=&rft.title=Glycobiology&rft.issn=09596658&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 - [The health surveillance of those exposed to low concentrations of anesthetic gases]. TT - Sorveglianza sanitaria in esposti a basse concentrazioni di gas anestetici. AN - 72744874; 1726297 JF - Annali di igiene : medicina preventiva e di comunita AU - Viganò, G AU - Villa, L AU - Ronconi, C AU - Sarcinella, G G AU - Vitiello, L AD - Servizio Igiene Pubblica-Ambientale, Tutela della Salute nei Luoghi di Lavoro, USSL 22, Sondrio. PY - 1991 SP - 277 EP - 286 VL - 3 IS - 5 SN - 1120-9135, 1120-9135 KW - Anesthetics KW - 0 KW - Nitrous Oxide KW - K50XQU1029 KW - Index Medicus KW - Nitrous Oxide -- adverse effects KW - Operating Rooms KW - Dose-Response Relationship, Drug KW - Humans KW - Italy KW - Anesthetics -- adverse effects KW - Occupational Exposure -- adverse effects KW - Population Surveillance UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72744874?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annali+di+igiene+%3A+medicina+preventiva+e+di+comunita&rft.atitle=%5BThe+health+surveillance+of+those+exposed+to+low+concentrations+of+anesthetic+gases%5D.&rft.au=Vigan%C3%B2%2C+G%3BVilla%2C+L%3BRonconi%2C+C%3BSarcinella%2C+G+G%3BVitiello%2C+L&rft.aulast=Vigan%C3%B2&rft.aufirst=G&rft.date=1991-09-01&rft.volume=3&rft.issue=5&rft.spage=277&rft.isbn=&rft.btitle=&rft.title=Annali+di+igiene+%3A+medicina+preventiva+e+di+comunita&rft.issn=11209135&rft_id=info:doi/ LA - Italian DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-15 N1 - Date created - 1992-07-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - [Anesthetics in operating rooms: environmental and biological monitoring in relation to functional restructuring]. TT - Anestetici nelle sale operatorie: monitoraggio ambientale e biologico, in relazione ad una razionale ristrutturazione. AN - 72730672; 1726296 JF - Annali di igiene : medicina preventiva e di comunita AU - Villa, L AU - Viganò, G AU - Pini, A AU - Pradella, G AU - Ruggeri, R AU - Sarcinella, G G AU - Vitiello, L AD - Servizio Igiene Pubblica-Ambientale, Tutela della Salute nei Luoghi di Lavoro, USSL 22, Sondrio. PY - 1991 SP - 269 EP - 276 VL - 3 IS - 5 SN - 1120-9135, 1120-9135 KW - Air Pollutants, Occupational KW - 0 KW - Anesthetics KW - Index Medicus KW - Occupational Exposure KW - Ventilation KW - Humans KW - Adult KW - Italy KW - Environmental Monitoring KW - Anesthetics -- analysis KW - Operating Rooms KW - Air Pollutants, Occupational -- analysis KW - Facility Design and Construction UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72730672?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annali+di+igiene+%3A+medicina+preventiva+e+di+comunita&rft.atitle=%5BAnesthetics+in+operating+rooms%3A+environmental+and+biological+monitoring+in+relation+to+functional+restructuring%5D.&rft.au=Villa%2C+L%3BVigan%C3%B2%2C+G%3BPini%2C+A%3BPradella%2C+G%3BRuggeri%2C+R%3BSarcinella%2C+G+G%3BVitiello%2C+L&rft.aulast=Villa&rft.aufirst=L&rft.date=1991-09-01&rft.volume=3&rft.issue=5&rft.spage=269&rft.isbn=&rft.btitle=&rft.title=Annali+di+igiene+%3A+medicina+preventiva+e+di+comunita&rft.issn=11209135&rft_id=info:doi/ LA - Italian DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-15 N1 - Date created - 1992-07-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The large-scale isolation of bryostatin 1 from Bugula neritina following current good manufacturing practices. AN - 72697939; 1800630 AB - A novel process was designed for the large-scale isolation of bryostatin 1 from the bryozoan Bugula neritina L. in order to obtain multigram quantities of highly pure material for formulation studies, preclinical toxicology, and clinical trials in cancer patients. Multigram quantities of bryostatin 1 were obtained from a collection of approximately 10,000 gallons of wet animal. A phorbol dibutyrate (PDBu) receptor binding assay and hplc with photodiode array detection were used for the design, validation, and control of the isolation process. JF - Journal of natural products AU - Schaufelberger, D E AU - Koleck, M P AU - Beutler, J A AU - Vatakis, A M AU - Alvarado, A B AU - Andrews, P AU - Marzo, L V AU - Muschik, G M AU - Roach, J AU - Ross, J T AD - Chemical Synthesis and Analysis Laboratory, PRI/DynCorp, National Cancer Institute--Frederick Cancer Research and Development Center, Maryland 21702. PY - 1991 SP - 1265 EP - 1270 VL - 54 IS - 5 SN - 0163-3864, 0163-3864 KW - Bryostatins KW - 0 KW - Lactones KW - Macrolides KW - bryostatin 1 KW - 37O2X55Y9E KW - Index Medicus KW - Molecular Structure KW - Animals KW - Lactones -- isolation & purification KW - Bryozoa -- chemistry KW - Lactones -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72697939?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+natural+products&rft.atitle=The+large-scale+isolation+of+bryostatin+1+from+Bugula+neritina+following+current+good+manufacturing+practices.&rft.au=Schaufelberger%2C+D+E%3BKoleck%2C+M+P%3BBeutler%2C+J+A%3BVatakis%2C+A+M%3BAlvarado%2C+A+B%3BAndrews%2C+P%3BMarzo%2C+L+V%3BMuschik%2C+G+M%3BRoach%2C+J%3BRoss%2C+J+T&rft.aulast=Schaufelberger&rft.aufirst=D&rft.date=1991-09-01&rft.volume=54&rft.issue=5&rft.spage=1265&rft.isbn=&rft.btitle=&rft.title=Journal+of+natural+products&rft.issn=01633864&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-21 N1 - Date created - 1992-04-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Long-term (imprinting) effects of transplacental treatment of mice with 3-methylcholanthrene or beta-naphthoflavone on hepatic metabolism of 3-methylcholanthrene. AN - 72659700; 1796059 AB - Foetal mice of genotype AhbAhd (responsive to induction of metabolism of polycyclic aromatic hydrocarbons [PAH]) or AhdAhd (non-responsive) were exposed transplacentally on gestation day 17 to a single dose of 3-methylcholanthrene (MC, 5-175 mg/kg) with or without prior treatment on day 15 with beta-naphthoflavone (beta NF, 150 mg/kg). The mothers were themselves either induction-responsive [(C57BL/6 x DBA/2)F1] or non-responsive (DBA/2). Metabolism of [14C]MC by homogenates of livers from the transplacentally-exposed offspring was quantified at 9 months of age (first experiment) or 13 months (second experiment) with or without prior inducing treatment with MC. The foetal exposure to MC had a permanent effect on MC metabolism by the adult hepatic homogenates in both experiments. In most instances the effect was positive in direction and small in magnitude (15-30%). It was dose-dependent with regard to transplacental MC, occurred in both induced (AhbAhd) and non-induced (AhdAhd) individuals, and was significant only when the mother and/or the foetus was inducible. beta NF itself did not have a positive imprinting effect. In some cases it either reduced or potentiated the long-term imprinting effect of MC, depending on the MC dose and the phenotype of the mother. These results confirm that transplacental exposure to a carcinogenic PAH may permanently alter metabolism of the chemical in later life, and indicate that this imprinting action is dependent on induced metabolism of the chemical in the mother and/or foetus. JF - Pharmacology & toxicology AU - Anderson, L M AU - Jones, A B AU - Riggs, C W AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21701. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 178 EP - 188 VL - 69 IS - 3 SN - 0901-9928, 0901-9928 KW - Benzoflavones KW - 0 KW - Methylcholanthrene KW - 56-49-5 KW - beta-Naphthoflavone KW - 6051-87-2 KW - Aryl Hydrocarbon Hydroxylases KW - EC 1.14.14.1 KW - Index Medicus KW - Phenotype KW - Maternal-Fetal Exchange KW - Animals KW - Aryl Hydrocarbon Hydroxylases -- metabolism KW - Mice, Inbred C57BL KW - Mice KW - Gene Expression Regulation KW - Longitudinal Studies KW - Male KW - Female KW - Pregnancy KW - Mice, Inbred DBA KW - Methylcholanthrene -- pharmacology KW - Liver -- metabolism KW - Methylcholanthrene -- metabolism KW - Benzoflavones -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72659700?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacology+%26+toxicology&rft.atitle=Long-term+%28imprinting%29+effects+of+transplacental+treatment+of+mice+with+3-methylcholanthrene+or+beta-naphthoflavone+on+hepatic+metabolism+of+3-methylcholanthrene.&rft.au=Anderson%2C+L+M%3BJones%2C+A+B%3BRiggs%2C+C+W&rft.aulast=Anderson&rft.aufirst=L&rft.date=1991-09-01&rft.volume=69&rft.issue=3&rft.spage=178&rft.isbn=&rft.btitle=&rft.title=Pharmacology+%26+toxicology&rft.issn=09019928&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-06 N1 - Date created - 1992-04-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Current state-of-the-art in human cell transformation in culture. AN - 72627969; 1781179 AB - The immortalization and transformation of cultured human cells has far-reaching implications for both cell and cancer biology. Human cell transformation studies will increase our understanding of the mechanisms underlying carcinogenesis and differentiation. The neoplastic process can now be studied in a model human cell culture system. The accompanying biochemical and genetic changes, once identified, will help define the relationship between malignancy and differentiation. The present studies indeed demonstrate that the neoplastic process can now be studied in a human cell model system. Primary human cells treated with various carcinogens became immortalized in culture but were not tumorigenic. Additional exposure to either retroviruses, chemical carcinogenes or X-ŗay irradiation to these cells induced morphological alterations associated with the acquisition of neoplastic properties. These findings demonstrate the malignant transformation of human primary cells in culture by the combined action of either a DNA transforming virus and a retrovirus or a DNA virus and a chemical or X-ray irradiation, and support an multistep process for neoplastic conversion. It has been known that normal human cells in culture are remarkably resistant to experimentally induced tumorigenicity. However, as shown above, normal human cells could now be transformed into tumorigenic cells. JF - Yonsei medical journal AU - Rhim, J S AD - Laboratory of Cellular and Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 195 EP - 206 VL - 32 IS - 3 SN - 0513-5796, 0513-5796 KW - DNA, Viral KW - 0 KW - Index Medicus KW - Fibroblasts -- pathology KW - Cells, Cultured KW - Humans KW - Osteosarcoma -- pathology KW - Osteosarcoma -- genetics KW - Keratinocytes -- cytology KW - Keratinocytes -- pathology KW - Cell Transformation, Neoplastic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72627969?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Yonsei+medical+journal&rft.atitle=Current+state-of-the-art+in+human+cell+transformation+in+culture.&rft.au=Rhim%2C+J+S&rft.aulast=Rhim&rft.aufirst=J&rft.date=1991-09-01&rft.volume=32&rft.issue=3&rft.spage=195&rft.isbn=&rft.btitle=&rft.title=Yonsei+medical+journal&rft.issn=05135796&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-12 N1 - Date created - 1992-03-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - 3H-paroxetine binding in brains of alcoholics. AN - 72557539; 1836640 AB - High affinity 3H-paroxetine binding was studied in human frontal cortex and hippocampus obtained from normal controls and alcoholics. On the basis of Scatchard analyses, a significant decrease in the maximal number of binding sites (Bmax) was found in the hippocampus of alcoholics (n = 8) as compared with that of controls (n = 10) (mean +/- SD = 63 +/- 35 vs. 114 +/- 70 fmoles/mg protein). There was no significant difference in the dissociation constants (Kd) between the two groups. The presumed effect of chronic alcohol abuse on 3H-paroxetine binding may be region-specific since no significant difference in either Bmax or Kd for 3H-paroxetine binding was found in the frontal cortex between normal controls and alcoholics. No significant correlation of 3H-paroxetine binding with age or postmortem interval was observed. The decrease in 3H-paroxetine binding in the hippocampus of alcoholics is probably indicative of reduced density of serotonergic nerve terminals either as a preexisting condition or as a result of neuronal damage caused by ethanol or the sequelae of alcoholism, such as nutritional deficiencies. JF - Psychiatry research AU - Chen, H T AU - Casanova, M F AU - Kleinman, J E AU - Zito, M AU - Goldman, D AU - Linnoila, M AD - Laboratory of Clinical Studies, DICBR, National Institute of Alcohol Abuse and Alcoholism (NIAAA), Bethesda, MD. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 293 EP - 299 VL - 38 IS - 3 SN - 0165-1781, 0165-1781 KW - Piperidines KW - 0 KW - Serotonin Antagonists KW - Paroxetine KW - 41VRH5220H KW - Index Medicus KW - Humans KW - Adult KW - Data Interpretation, Statistical KW - Aged KW - Middle Aged KW - Male KW - Female KW - Binding Sites -- physiology KW - Alcoholism -- pathology KW - Cerebral Cortex -- pathology KW - Serotonin Antagonists -- metabolism KW - Hippocampus -- pathology KW - Piperidines -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72557539?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=3H-paroxetine+binding+in+brains+of+alcoholics.&rft.au=Chen%2C+H+T%3BCasanova%2C+M+F%3BKleinman%2C+J+E%3BZito%2C+M%3BGoldman%2C+D%3BLinnoila%2C+M&rft.aulast=Chen&rft.aufirst=H&rft.date=1991-09-01&rft.volume=38&rft.issue=3&rft.spage=293&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 - 1992-01-28 N1 - Date created - 1992-01-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Recovery of function after lesions in the superior temporal sulcus in the monkey. AN - 72556562; 1753278 AB - 1. Ibotenic acid lesions in the monkey's middle temporal area (MT) and the medial superior temporal area (MST) in the superior temporal sulcus (STS) have previously been shown to produce a deficit in initiation of smooth-pursuit eye movements to moving visual targets. The deficits, however, recovery within a few days. In the present experiments we investigated the factors that influence that recovery. 2. We tested two aspects of the monkey's ability to use motion information to acquire moving targets. We used eye-position error as a measure of the monkey's ability to make accurate initial saccades to the moving target. We measured eye speed within the first 100 ms after the saccade to evaluate the monkey's initial smooth pursuit. 3. We determined that pursuit recovery was not dependent specifically on the use of neurotoxic lesions. Although the rate of recovery was slightly altered by replacing the usual neurotoxin (ibotenic acid) with another neurotoxin [alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)] or with an electrolytic lesion, pursuit recovery still occurred within a period of days to weeks. 4. There was a relationship between the size and location of the lesion and the recovery time. The time to recovery for eye-position error and initial eye speed increased with the fraction of MT removed. Whether the rate of recovery and size of lesions within regions on the anterior bank were related was unresolved. 5. We found that a large AMPA lesion within the STS that removed all of MT and nearly all of MST drastically altered the rate of recovery. Recovery was incomplete more than 7 mo after the lesion. Even with this lesion, however, the monkey's ability to use motion information for pursuit was not completely eliminated. 6. The large lesion also included parts of areas V1, V2, V3, and V4, but analysis of the visual fields associated with this lesion indicated that these areas probably did not have a substantial effect on recovery. 7. We tested whether visual motion experience of the monkey after a lesion was necessary for recovery by limiting the monkey's experience either by using a mask or by using 4-Hz stroboscopic illumination. In one monkey the eye-position error component of pursuit was prolonged to greater than 2 wk, but recovery of eye speed was not. Reduced motion experience had little effect on recovery in the other two monkeys. These results suggest that such visual motion experience is not necessary for the recovery of pursuit.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Journal of neurophysiology AU - Yamasaki, D S AU - Wurtz, R H AD - Laboratory of Sensorimotor Research, National Eye Institute, Bethesda, Maryland 20892. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 651 EP - 673 VL - 66 IS - 3 SN - 0022-3077, 0022-3077 KW - Index Medicus KW - Space life sciences KW - Animals KW - Cerebral Cortex -- physiology KW - Brain Mapping KW - Visual Fields -- physiology KW - Macaca mulatta KW - Neuronal Plasticity KW - Vision, Ocular -- physiology KW - Eye Movements -- physiology KW - Temporal Lobe -- physiology KW - Pursuit, Smooth -- physiology KW - Pursuit, Smooth -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72556562?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+neurophysiology&rft.atitle=Recovery+of+function+after+lesions+in+the+superior+temporal+sulcus+in+the+monkey.&rft.au=Yamasaki%2C+D+S%3BWurtz%2C+R+H&rft.aulast=Yamasaki&rft.aufirst=D&rft.date=1991-09-01&rft.volume=66&rft.issue=3&rft.spage=651&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurophysiology&rft.issn=00223077&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-30 N1 - Date created - 1992-01-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Induction of tubules in rat metanephrogenic mesenchyme in the absence of an inductive tissue. AN - 72510556; 1743431 AB - Differentiation of metanephrogenic mesenchyme to renal tubular epithelium requires induction by the ureteric bud in vivo or any of several embryonic tissues in vitro. In an effort to eliminate the tissue requirement in embryonic induction, extracellular matrices and soluble factors were analyzed individually or in combination for their ability to stimulate tubulogenesis in uninduced metanephrogenic mesenchyme from 13-gestation-day rat embryos. These evaluations have established that pituitary extract and epidermal growth factor (EGF) in concert with a matrix can promote morphogenesis of mesenchymal rudiments in culture. While type I collagen, laminin, or fibronectin matrices all promoted tubulogenesis in the presence of pituitary extract and EGF, type IV collagen proved the most effective. Under these conditions, tubules were induced in 23/24 mesenchymal rudiments by 9 days in culture. Mesenchyme was not induced prior to explanation since it formed no tubules when cultured in a medium that allowed tubulogenesis in intact embryonic kidneys. Preliminary characterization of the undefined factor in pituitary extract was consistent with a protein of molecular weight greater than 100,000 but less than 300,000. When uninduced metanephrogenic mesenchyme from mouse was used instead of rat tissue, a similar pattern of morphogenesis was not observed, suggesting that the described medium is inappropriate for promoting differentiation in mouse or, less likely, that different mechanisms mediate differentiation in rat and mouse. These studies show that embryonic induction can occur in explanted rat renal mesenchyme in an appropriate environment and does not require the presence of an inductive tissue. JF - Differentiation; research in biological diversity AU - Perantoni, A O AU - Dove, L F AU - Williams, C L AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick, MD 21702. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 25 EP - 31 VL - 48 IS - 1 SN - 0301-4681, 0301-4681 KW - Culture Media KW - 0 KW - Epidermal Growth Factor KW - 62229-50-9 KW - Collagen KW - 9007-34-5 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Cell Differentiation KW - Mice KW - Epidermal Growth Factor -- pharmacology KW - Collagen -- pharmacology KW - Embryonic Induction KW - Mesoderm -- physiology KW - Kidney Tubules -- embryology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72510556?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Differentiation%3B+research+in+biological+diversity&rft.atitle=Induction+of+tubules+in+rat+metanephrogenic+mesenchyme+in+the+absence+of+an+inductive+tissue.&rft.au=Perantoni%2C+A+O%3BDove%2C+L+F%3BWilliams%2C+C+L&rft.aulast=Perantoni&rft.aufirst=A&rft.date=1991-09-01&rft.volume=48&rft.issue=1&rft.spage=25&rft.isbn=&rft.btitle=&rft.title=Differentiation%3B+research+in+biological+diversity&rft.issn=03014681&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-10 N1 - Date created - 1992-01-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Testing human hair for drugs of abuse. II. Identification of unique cocaine metabolites in hair of drug abusers and evaluation of decontamination procedures. AN - 72509521; 1960975 AB - Two unique metabolites of cocaine, cocaethylene and norcocaine, were identified by GC/MS in the hair of cocaine users. Their presence cannot be explained by environmental contamination; thus, their presence together with cocaine provides convincing evidence that cocaine is excreted in hair after active cocaine administration. The amount of cocaine in hair predominated over all metabolites generally by a factor of 5-10. Two washing procedures were evaluated for their efficiency in removal of cocaine from environmentally contaminated hair. Neither procedure completely removed cocaine, suggesting that false positives can result from environmental contamination. Analysis of the methanolic wash of the hair of cocaine users also revealed the presence of cocaine metabolites, indicating that washing removes cocaine from the interior as well as from the exterior surface of hair during decontamination procedures. JF - Journal of analytical toxicology AU - Cone, E J AU - Yousefnejad, D AU - Darwin, W D AU - Maguire, T AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, Maryland 21224. PY - 1991 SP - 250 EP - 255 VL - 15 IS - 5 SN - 0146-4760, 0146-4760 KW - norcocaine KW - 3SL7BR2M1E KW - cocaethylene KW - FJO3071W5Y KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Gas Chromatography-Mass Spectrometry -- methods KW - Humans KW - Adult KW - Male KW - Female KW - Substance-Related Disorders -- diagnosis KW - Cocaine -- analysis KW - Cocaine -- analogs & derivatives KW - Hair -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72509521?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+analytical+toxicology&rft.atitle=Testing+human+hair+for+drugs+of+abuse.+II.+Identification+of+unique+cocaine+metabolites+in+hair+of+drug+abusers+and+evaluation+of+decontamination+procedures.&rft.au=Cone%2C+E+J%3BYousefnejad%2C+D%3BDarwin%2C+W+D%3BMaguire%2C+T&rft.aulast=Cone&rft.aufirst=E&rft.date=1991-09-01&rft.volume=15&rft.issue=5&rft.spage=250&rft.isbn=&rft.btitle=&rft.title=Journal+of+analytical+toxicology&rft.issn=01464760&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-07 N1 - Date created - 1992-01-07 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: J Anal Toxicol. 1992 Nov-Dec;16(6):402 [1293409] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - [Inhibitors of HIV-1 reverse transcriptase and protease as chemotherapeutics for AIDS]. AN - 72506503; 1720470 JF - Nihon rinsho. Japanese journal of clinical medicine AU - Mitsuya, H AD - National Cancer Institute, National Institutes of Health. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 2062 EP - 2069 VL - 49 IS - 9 SN - 0047-1852, 0047-1852 KW - Antiviral Agents KW - 0 KW - HIV Protease Inhibitors KW - Reverse Transcriptase Inhibitors KW - 1-((2-hydroxyethoxy)methyl)-6-(phenylthio)thymine KW - 123027-56-5 KW - Zidovudine KW - 4B9XT59T7S KW - Zalcitabine KW - 6L3XT8CB3I KW - HIV Reverse Transcriptase KW - EC 2.7.7.49 KW - Didanosine KW - K3GDH6OH08 KW - Thymine KW - QR26YLT7LT KW - Index Medicus KW - AIDS/HIV KW - Thymine -- pharmacology KW - Animals KW - Thymine -- analogs & derivatives KW - Zidovudine -- adverse effects KW - Humans KW - Zidovudine -- pharmacology KW - Zalcitabine -- pharmacology KW - HIV-1 -- enzymology KW - Didanosine -- pharmacology KW - Didanosine -- adverse effects KW - Antiviral Agents -- pharmacology KW - Acquired Immunodeficiency Syndrome -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72506503?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nihon+rinsho.+Japanese+journal+of+clinical+medicine&rft.atitle=%5BInhibitors+of+HIV-1+reverse+transcriptase+and+protease+as+chemotherapeutics+for+AIDS%5D.&rft.au=Mitsuya%2C+H&rft.aulast=Mitsuya&rft.aufirst=H&rft.date=1991-09-01&rft.volume=49&rft.issue=9&rft.spage=2062&rft.isbn=&rft.btitle=&rft.title=Nihon+rinsho.+Japanese+journal+of+clinical+medicine&rft.issn=00471852&rft_id=info:doi/ LA - Japanese DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-07 N1 - Date created - 1992-01-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Drug discrimination using a conditioned taste-aversion paradigm in rhesus monkeys. AN - 72492059; 1659608 AB - The development of drug discrimination was assessed in rhesus monkeys using the conditioned taste-aversion paradigm. Monkeys were initially trained to respond under a fixed-ratio 30-response schedule of food-pellet delivery to assess the rate-decreasing effects of alprazolam (0.03 to 3 mg/kg, i.m., 60 min presession). Alprazolam decreased responding at doses greater than 0.1 mg/kg. Discriminative stimulus effects of alprazolam were then assessed by giving 0.03 mg/kg before sessions in which 1.8 mEq/kg lithium chloride was given immediately after the session (alprazolam/lithium session). On intervening days, saline was given before and after the session (saline/saline session). Rates of responding decreased over successive alprazolam/lithium sessions and also during the saline/saline session that immediately followed an alprazolam/lithium session. During subsequent saline/saline sessions, rates of responding returned to levels near baseline rates within two to four sessions. The discriminative stimulus effects of alprazolam were then assessed by giving 0.1 mg/kg before sessions in which 1 mg/kg d-amphetamine was given immediately after the session (alprazolam/d-amphetamine session). Rates of responding decreased during subsequent alprazolam/d-amphetamine sessions in drug-experienced monkeys, but did not decrease during intervening saline/saline sessions. These findings demonstrate that drug stimuli associated with postsession drug injections can rapidly develop control over behavior and suggest that similar methods be explored in the assessment of drug discrimination. JF - Journal of the experimental analysis of behavior AU - Glowa, J R AU - Jeffreys, R D AU - Riley, A L AD - Biopsychology Unit, NIMH, Bethesda, Maryland 20892. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 303 EP - 312 VL - 56 IS - 2 SN - 0022-5002, 0022-5002 KW - Chlorides KW - 0 KW - Lithium KW - 9FN79X2M3F KW - Lithium Chloride KW - G4962QA067 KW - Alprazolam KW - YU55MQ3IZY KW - Index Medicus KW - Chlorides -- toxicity KW - Animals KW - Dose-Response Relationship, Drug KW - Macaca mulatta KW - Lithium -- toxicity KW - Male KW - Discrimination Learning -- drug effects KW - Reinforcement Schedule KW - Conditioning, Classical -- drug effects KW - Alprazolam -- pharmacology KW - Avoidance Learning -- drug effects KW - Taste -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72492059?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+experimental+analysis+of+behavior&rft.atitle=Drug+discrimination+using+a+conditioned+taste-aversion+paradigm+in+rhesus+monkeys.&rft.au=Glowa%2C+J+R%3BJeffreys%2C+R+D%3BRiley%2C+A+L&rft.aulast=Glowa&rft.aufirst=J&rft.date=1991-09-01&rft.volume=56&rft.issue=2&rft.spage=303&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+experimental+analysis+of+behavior&rft.issn=00225002&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-30 N1 - Date created - 1991-12-30 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Psychopharmacologia. 1962 Oct 31;3:374-85 [13947088] Pharmacol Biochem Behav. 1986 Nov;25(5):973-8 [3024186] Eur J Pharmacol. 1986 Sep 23;129(1-2):39-47 [3021479] J Pharmacol Exp Ther. 1988 Dec;247(3):1120-7 [2974486] Psychopharmacology (Berl). 1989;98(1):20-30 [2567033] Psychopharmacologia. 1975 Jun 19;42(3):283-7 [1161987] J Pharmacol Exp Ther. 1990 Jun;253(3):1070-6 [2113579] Drugs. 1984 Feb;27(2):132-47 [6141930] J Exp Anal Behav. 1983 Jan;39(1):165-73 [6833938] Pharmacol Biochem Behav. 1978 Feb;8(2):107-11 [652820] Fed Proc. 1975 Aug;34(9):1870-9 [238868] Pharmacol Biochem Behav. 1989 Jan;32(1):1-8 [2734321] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mouse dominant lethal and bone marrow micronucleus studies on methyl vinyl sulfone and divinyl sulfone. AN - 72467752; 1944356 AB - Methyl vinyl sulfone and divinyl sulfone were tested for the induction of dominant lethal mutations and micronucleated bone-marrow erythrocytes in male mice. These chemicals were chosen for study because of their similarities in structure and chemical reactivity to acrylamide which is known to induce both effects. Following administration of the test compounds by intraperitoneal injection at the maximum tolerated doses, no evidence of induced dominant lethal mutations or micronucleated bone-marrow cells was observed for either chemical. It is concluded that structures and Michael reactivities similar to acrylamide are not sufficient to impart similar in vivo genetic toxicity to MVS and DVS. JF - Mutation research AU - Shelby, M D AU - Gutierrez-Espeleta, G A AU - Generoso, W M AU - McFee, A F AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. PY - 1991 SP - 431 EP - 437 VL - 250 IS - 1-2 SN - 0027-5107, 0027-5107 KW - Mutagens KW - 0 KW - Sulfones KW - methyl vinyl sulfone KW - 3680-02-2 KW - divinyl sulfone KW - 5PFN71LP8M KW - Index Medicus KW - Animals KW - Micronucleus Tests KW - Mice, Inbred C3H KW - Crosses, Genetic KW - Mice KW - Bone Marrow -- ultrastructure KW - Male KW - Female KW - Pregnancy KW - Genes, Dominant KW - Sulfones -- toxicity KW - Mutagens -- toxicity KW - Genes, Lethal UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72467752?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mouse+dominant+lethal+and+bone+marrow+micronucleus+studies+on+methyl+vinyl+sulfone+and+divinyl+sulfone.&rft.au=Shelby%2C+M+D%3BGutierrez-Espeleta%2C+G+A%3BGeneroso%2C+W+M%3BMcFee%2C+A+F&rft.aulast=Shelby&rft.aufirst=M&rft.date=1991-09-01&rft.volume=250&rft.issue=1-2&rft.spage=431&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 - 1991-11-27 N1 - Date created - 1991-11-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A multistage model of carcinogenesis incorporating DNA damage and repair. AN - 72464523; 1947359 AB - Mathematical models of carcinogenesis are one tool used for research into the mechanisms of carcinogenesis and for assessing risks from exposure to carcinogenic agents. Recent research into carcinogenic mechanisms has focused on the role of cell replication in fixing damage to cellular DNA and increasing the incidence of malignancies. The most commonly used multistage model of carcinogenesis does not explicitly account for DNA damage and the contribution of cell replication rates on the transformation of cells through the various stages. In this manuscript, a generalized multistage model of carcinogenesis is developed in which DNA damage, cell replication, and DNA repair are explicitly included. JF - Risk analysis : an official publication of the Society for Risk Analysis AU - Portier, C J AU - Kopp-Schneider, A AD - Division of Biometry and Risk Assessment, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 535 EP - 543 VL - 11 IS - 3 SN - 0272-4332, 0272-4332 KW - Carcinogens KW - 0 KW - DNA, Neoplasm KW - Mutagens KW - Index Medicus KW - Animals KW - Humans KW - Models, Statistical KW - DNA, Neoplasm -- analysis KW - DNA Repair KW - DNA Damage KW - Environmental Exposure KW - Models, Biological UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72464523?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Risk+analysis+%3A+an+official+publication+of+the+Society+for+Risk+Analysis&rft.atitle=A+multistage+model+of+carcinogenesis+incorporating+DNA+damage+and+repair.&rft.au=Portier%2C+C+J%3BKopp-Schneider%2C+A&rft.aulast=Portier&rft.aufirst=C&rft.date=1991-09-01&rft.volume=11&rft.issue=3&rft.spage=535&rft.isbn=&rft.btitle=&rft.title=Risk+analysis+%3A+an+official+publication+of+the+Society+for+Risk+Analysis&rft.issn=02724332&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-16 N1 - Date created - 1991-12-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Analytical DNA fingerprinting in lions: parentage, genetic diversity, and kinship. AN - 72452942; 1940281 AB - The application of hypervariable minisatellite genomic families to the reconstruction of population genetic structure holds great promise in describing the demographic history and future prospects of free-ranging populations. This potential has not yet been realized due to unforeseen empirical constraints associated with the use of heterologous species probes, to theoretical limitations on the power of the procedure to track genic heterozygosity and kinship, and to the absence of extensive field studies to test genetic predictions. We combine here the technical development of feline-specific VNTR (variable number tandem repeat) families of genetic loci with the long-term demographic and behavioral observations of lion populations of the Serengeti ecosystem in East Africa. Minisatellite variation was used to quantify the extent of genetic variation in several populations that differed in their natural history and levels of inbreeding. Definitive parentage, both maternal and paternal, was assessed for 78 cubs born in 11 lion prides, permitting the assessment of precise genealogical relationships among some 200 lions. The extent of DNA restriction fragment sharing between lions was empirically calibrated with the coefficient of relatedness, r, in two different populations that had distinct demographic histories. The results suggest that reliable estimates of relative genetic diversity, of parentage, and of individual relatedness can be achieved in free-ranging populations, provided the minisatellite family is calibrated in established pedigrees for the species. JF - The Journal of heredity AU - Gilbert, D A AU - Packer, C AU - Pusey, A E AU - Stephens, J C AU - O'Brien, S J AD - Biological Carcinogenesis and Development Program, Program Resources, Inc./DynCorp, NCI-Frederick Cancer Research and Development Center, Maryland 21702-1201. PY - 1991 SP - 378 EP - 386 VL - 82 IS - 5 SN - 0022-1503, 0022-1503 KW - DNA Probes KW - 0 KW - DNA, Satellite KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Pedigree KW - Genetic Variation KW - Animals KW - Base Sequence KW - Blotting, Southern KW - Humans KW - Cats KW - Molecular Sequence Data KW - Male KW - Female KW - Lions -- genetics KW - DNA Fingerprinting UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72452942?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+heredity&rft.atitle=Analytical+DNA+fingerprinting+in+lions%3A+parentage%2C+genetic+diversity%2C+and+kinship.&rft.au=Gilbert%2C+D+A%3BPacker%2C+C%3BPusey%2C+A+E%3BStephens%2C+J+C%3BO%27Brien%2C+S+J&rft.aulast=Gilbert&rft.aufirst=D&rft.date=1991-09-01&rft.volume=82&rft.issue=5&rft.spage=378&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+heredity&rft.issn=00221503&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-17 N1 - Date created - 1991-12-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prior exposures to the laboratory enhance the effect of alcohol. AN - 72451951; 1943103 AB - We compared responses to 0.6 g/kg alcohol of normal male drinkers in a laboratory environment that was new to the subjects with the responses of a second group in the same environment who had two prior exposures to the laboratory environment and procedures. Alcohol-induced increases in heart rate, cheek temperature and self-reported intoxication were greater in the subjects who had previous exposure to the laboratory environment than in the subjects who had no such previous exposure. Differences in blood alcohol concentration (BAC) also were found between the two environments. However, differences in the physiological and self-report measures were found after matching subjects in terms of BAC. These results suggest that novelty effects may contaminate alcohol responses in novel laboratory environments, and they add to our understanding of nonpharmacological factors in the responses to drugs. JF - Journal of studies on alcohol AU - Newlin, D B AU - Pretorius, M B AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, Maryland 21224. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 470 EP - 473 VL - 52 IS - 5 SN - 0096-882X, 0096-882X KW - Ethanol KW - 3K9958V90M KW - Index Medicus KW - Heart Rate -- drug effects KW - Ethanol -- pharmacokinetics KW - Alcoholic Intoxication -- psychology KW - Humans KW - Adult KW - Skin Temperature -- drug effects KW - Motor Activity -- drug effects KW - Male KW - Arousal -- drug effects KW - Alcohol Drinking -- psychology KW - Alcohol Drinking -- blood KW - Social Environment UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72451951?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Prior+exposures+to+the+laboratory+enhance+the+effect+of+alcohol.&rft.au=Newlin%2C+D+B%3BPretorius%2C+M+B&rft.aulast=Newlin&rft.aufirst=D&rft.date=1991-09-01&rft.volume=52&rft.issue=5&rft.spage=470&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 - 1991-11-26 N1 - Date created - 1991-11-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Local and systemic carcinogenic effects of alkylating carcinogens in rats treated by intravesicular administration. AN - 72447174; 1938603 AB - Several nitrosamines and an azoxyalkane have been administered intravesically to groups of 12 female F344 rats, twice a week for 20 or 30 weeks. Many of the nitrosamines were as efficacious in giving rise to the same tumors of internal organs as when similar doses were administered orally, showing that absorption from the bladder was as rapid as from other sites. The tumors produced included lung and kidney tumors by nitrosodimethylamine, colon and Zymbal gland tumors by azoxymethane, liver tumors by methylnitrosoethylamine (but not by nitrosodimethylamine), liver and esophagus tumors by nitrosodiethylamine, liver and lung tumors by methylnitrosamino-3-pyridylbutanone, liver tumors by nitrosomorpholine, and tumors of the esophagus by methylnitroso-n-butylamine, 2,6-dimethyl-nitrosomorpholine and methylnitrosamino-N,N-dimethylethylamine. Bladder tumors were induced by intravesicular administration of only low doses of nitrosobis-(2-oxopropyl)amine and to a lesser extent by methylnitroso-n-hexylamine and nitroso-(2-hydroxypropyl)(2-oxopropyl)amine, which all induced tumors systemically in addition. The bladder mucosa seemed to lack enzymes necessary to activate most nitrosamines to locally acting proximate carcinogens, but was quite transparent to the passage of carcinogenic nitrosamines present in the urine into the body to induce tumors in distant organs. JF - Japanese journal of cancer research : Gann AU - Lijinsky, W AU - Thomas, B J AU - Kovatch, R M AD - ABL-Basic Research Program, NCI-Frederick Cancer Research and Development Center, MD 21702. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 980 EP - 986 VL - 82 IS - 9 SN - 0910-5050, 0910-5050 KW - Alkylating Agents KW - 0 KW - Carcinogens KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Neoplasms, Experimental -- chemically induced KW - Kidney Neoplasms -- chemically induced KW - Carcinoma, Transitional Cell -- chemically induced KW - Papilloma -- chemically induced KW - Female KW - Administration, Intravesical KW - Urinary Bladder -- drug effects KW - Carcinogens -- administration & dosage KW - Carcinogens -- toxicity KW - Alkylating Agents -- toxicity KW - Alkylating Agents -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72447174?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Local+and+systemic+carcinogenic+effects+of+alkylating+carcinogens+in+rats+treated+by+intravesicular+administration.&rft.au=Lijinsky%2C+W%3BThomas%2C+B+J%3BKovatch%2C+R+M&rft.aulast=Lijinsky&rft.aufirst=W&rft.date=1991-09-01&rft.volume=82&rft.issue=9&rft.spage=980&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 - 1991-12-06 N1 - Date created - 1991-12-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparing age at onset of major depression and other psychiatric disorders by birth cohorts in five US community populations. AN - 72163757; 1929768 AB - Using data collected in the National Institute of Mental Health (Rockville, Md) Epidemiologic Catchment Area Program, we examined the proposed hypothesis that there has been a shift in major depression to younger ages at onset, or increased prevalence in younger age periods, for recent birth cohorts. Life-table survival methods were used to examine the hazard rates for major depression as well as for other specific mental disorders. The findings are consistent with a gradual shift to increased rates for major depression between the ages of 15 and 19 years for Epidemiologic Catchment Area respondents born more recently. The findings also suggest a similar shift for drug abuse/dependence; similar but less pronounced changes were found for alcohol abuse/dependence and obsessive-compulsive disorder. However, in this study, bipolar disorder, panic disorder, and phobias did not exhibit a consistent increase in onset at younger ages. Further research is required to determine if the shifts in major depression, drug abuse/dependence, and possibly alcohol abuse/dependence are linked. It is important to note that these shifts to adolescent onset are occurring when nearly half the 31 million Americans without health insurance are aged 24 years or younger. JF - Archives of general psychiatry AU - Burke, K C AU - Burke, J D AU - Rae, D S AU - Regier, D A AD - Office of the Institute Director, National Institute of Mental Health, Rockville, Md. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 789 EP - 795 VL - 48 IS - 9 SN - 0003-990X, 0003-990X KW - Abridged Index Medicus KW - Index Medicus KW - Age Factors KW - Humans KW - Child KW - Catchment Area (Health) KW - Life Tables KW - Psychiatric Status Rating Scales KW - Alcoholism -- epidemiology KW - Adult KW - Cohort Studies KW - Adolescent KW - Anxiety Disorders -- epidemiology KW - United States -- epidemiology KW - Substance-Related Disorders -- epidemiology KW - Prevalence KW - Proportional Hazards Models KW - Depressive Disorder -- epidemiology KW - Mental Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72163757?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Comparing+age+at+onset+of+major+depression+and+other+psychiatric+disorders+by+birth+cohorts+in+five+US+community+populations.&rft.au=Burke%2C+K+C%3BBurke%2C+J+D%3BRae%2C+D+S%3BRegier%2C+D+A&rft.aulast=Burke&rft.aufirst=K&rft.date=1991-09-01&rft.volume=48&rft.issue=9&rft.spage=789&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 - 1991-11-13 N1 - Date created - 1991-11-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Psychological reactions and retention by cocaine addicts during treatment according to HIV-serostatus: a matched-control study. AN - 72158006; 1928028 AB - We compared retention in treatment and psychological reactions during drug abuse treatment by 22 HIV-antibody positive, physically asymptomatic cocaine addicts to 22 matched HIV-seronegative cocaine addicts. All subjects participated in an outpatient clinical research project. There were no significant differences between groups in sociodemographics and psychiatric symptom scores on entrance or cocaine use except for route of administration (chi 2 = 11.59, df = 2, p less than .005). There were no significant differences among groups regarding being informed of serostatus and beginning treatment. There was a trend (p = .079) for more seropositives to complete treatment. Using end-point analysis to compare 11 seropositive subjects who completed a minimum of 2 weeks of treatment to a matched seronegative comparison groups, there were no significant differences in mood states except for "anger/hostility" (interaction of group x time; F = 2.24, df = 13/260, p less than .05). Informing drug abusers in treatment regarding positive HIV-serostatus was not associated with a lower treatment-retention rate or adverse psychological reactions when counseling regarding HIV issues was integrated with drug abuse treatment. JF - The American journal of drug and alcohol abuse AU - Weddington, W W AU - Haertzen, C A AU - Hess, J M AU - Brown, B S AD - National Institute on Drug Abuse, Rockville, Maryland 20857. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 355 EP - 368 VL - 17 IS - 3 SN - 0095-2990, 0095-2990 KW - Fluoxetine KW - 01K63SUP8D KW - Amantadine KW - BF4C9Z1J53 KW - Cocaine KW - I5Y540LHVR KW - Desipramine KW - TG537D343B KW - Index Medicus KW - AIDS/HIV KW - Baltimore KW - Amantadine -- administration & dosage KW - Affect -- drug effects KW - Psychotherapy KW - Combined Modality Therapy KW - Humans KW - Fluoxetine -- administration & dosage KW - Desipramine -- administration & dosage KW - Adult KW - AIDS Serodiagnosis -- psychology KW - Male KW - Female KW - HIV Seropositivity -- psychology KW - Adaptation, Psychological KW - Sick Role KW - Patient Dropouts -- psychology KW - Substance-Related Disorders -- rehabilitation KW - Substance-Related Disorders -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72158006?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+journal+of+drug+and+alcohol+abuse&rft.atitle=Psychological+reactions+and+retention+by+cocaine+addicts+during+treatment+according+to+HIV-serostatus%3A+a+matched-control+study.&rft.au=Weddington%2C+W+W%3BHaertzen%2C+C+A%3BHess%2C+J+M%3BBrown%2C+B+S&rft.aulast=Weddington&rft.aufirst=W&rft.date=1991-09-01&rft.volume=17&rft.issue=3&rft.spage=355&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+drug+and+alcohol+abuse&rft.issn=00952990&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-21 N1 - Date created - 1991-11-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - An enhancement method for immunohistochemical staining of proliferating cell nuclear antigen in archival rodent tissues. AN - 72123166; 1680544 AB - An enhanced immunohistochemical procedure to detect proliferating cell nuclear antigen (PCNA), an endogenous cell replication marker, has been successfully applied to formalin-fixed, paraffin-embedded archival rat and mouse tissues. The procedure involves microwave oven heating of tissue sections in a commercially available antigen retrieval solution of heavy metal salts. Successful immunohistochemical staining of PCNA can be consistently obtained in tissues fixed for over 24 months in formalin and in sections made from paraffin blocks stored in our tissue archives for up to 19 months. Use of this technique will allow retrospective staining of rodent tissues for identification of S phase cells as an indication of DNA replicative activity in previously conducted toxicity and carcinogenicity studies. JF - Cancer letters AU - Greenwell, A AU - Foley, J F AU - Maronpot, R R AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 251 EP - 256 VL - 59 IS - 3 SN - 0304-3835, 0304-3835 KW - Antigens KW - 0 KW - Nuclear Proteins KW - Proliferating Cell Nuclear Antigen KW - Formaldehyde KW - 1HG84L3525 KW - Index Medicus KW - Rats KW - Animals KW - Paraffin Embedding KW - Formaldehyde -- chemistry KW - Cell Nucleus -- chemistry KW - Mice KW - Immunohistochemistry -- methods KW - Antigens -- immunology KW - Cell Division KW - Nuclear Proteins -- analysis KW - Nuclear Proteins -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72123166?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=An+enhancement+method+for+immunohistochemical+staining+of+proliferating+cell+nuclear+antigen+in+archival+rodent+tissues.&rft.au=Greenwell%2C+A%3BFoley%2C+J+F%3BMaronpot%2C+R+R&rft.aulast=Greenwell&rft.aufirst=A&rft.date=1991-09-01&rft.volume=59&rft.issue=3&rft.spage=251&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 - 1991-11-07 N1 - Date created - 1991-11-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Molecular genetics of the debrisoquin-sparteine polymorphism. AN - 72122598; 1680592 JF - Clinical pharmacology and therapeutics AU - Gonzalez, F J AU - Meyer, U A AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 233 EP - 238 VL - 50 IS - 3 SN - 0009-9236, 0009-9236 KW - CYP2D KW - Sparteine KW - 298897D62S KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Debrisoquin KW - X31CDK040E KW - Abridged Index Medicus KW - Index Medicus KW - Genotype KW - Polymorphism, Restriction Fragment Length KW - Humans KW - Mutation KW - Chromosome Mapping KW - Pharmacogenetics KW - Sparteine -- metabolism KW - Alleles KW - Debrisoquin -- metabolism KW - Cytochrome P-450 Enzyme System -- deficiency KW - Cytochrome P-450 Enzyme System -- genetics KW - Polymorphism, Genetic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72122598?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Molecular+genetics+of+the+debrisoquin-sparteine+polymorphism.&rft.au=Gonzalez%2C+F+J%3BMeyer%2C+U+A&rft.aulast=Gonzalez&rft.aufirst=F&rft.date=1991-09-01&rft.volume=50&rft.issue=3&rft.spage=233&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 - 1991-10-25 N1 - Date created - 1991-10-25 N1 - Date revised - 2017-01-13 N1 - Gene symbol - CYP2D N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Activation of the rasHa gene in urethane-initiated papillomas induced by protocols with high and low frequencies of malignant conversion. AN - 72110419; 1911043 AB - The number of papillomas that develop in mice initiated with a single exposure to urethane and promoted by repeated applications of 12-O-tetradecanoylphorbol-13-acetate (TPA) is increased greater than 4-fold by pretreating the skin once with TPA 24 hr before administration of urethane. In contrast, the carcinoma incidence was increased only 2-fold by the TPA pretreatment. Individual papillomas developed from the two protocols, differing in the potential for conversion to malignancy, were compared for activation of the rasHa gene. An activated oncogene that transformed 3T3 cells was found in the DNA of four of five papillomas from urethane-initiated, TPA-promoted mice and in eight of eleven papillomas from similarly promoted mice exposed to TPA before urethane initiation. Southern analysis of DNA from tumors or 3T3 foci demonstrated that the rasHa gene was activated by an A----T transversion at the second base of codon 61 in all mutated alleles. Thus, tumors induced by the two protocols did not differ in rasHa activation. JF - Cancer communications AU - Hennings, H AU - Robinson, V A AU - Yuspa, S H AU - Welty, D J AU - Greenhalgh, D G AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 277 EP - 281 VL - 3 IS - 9 SN - 0955-3541, 0955-3541 KW - rasHa KW - Carcinogens KW - 0 KW - DNA, Neoplasm KW - Urethane KW - 3IN71E75Z5 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - 3T3 Cells KW - Animals KW - Carcinogens -- pharmacology KW - Drug Interactions KW - Carcinoma, Squamous Cell -- chemically induced KW - Mice, Nude KW - Mice KW - Gene Expression Regulation, Neoplastic -- drug effects KW - Neoplasm Transplantation KW - Tumor Cells, Cultured KW - Transfection KW - Blotting, Southern KW - Carcinoma, Squamous Cell -- genetics KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Urethane -- pharmacology KW - Cell Transformation, Neoplastic -- genetics KW - Female KW - Male KW - Genes, ras -- drug effects KW - DNA, Neoplasm -- genetics KW - Papilloma -- genetics KW - Papilloma -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72110419?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+communications&rft.atitle=Activation+of+the+rasHa+gene+in+urethane-initiated+papillomas+induced+by+protocols+with+high+and+low+frequencies+of+malignant+conversion.&rft.au=Hennings%2C+H%3BRobinson%2C+V+A%3BYuspa%2C+S+H%3BWelty%2C+D+J%3BGreenhalgh%2C+D+G&rft.aulast=Hennings&rft.aufirst=H&rft.date=1991-09-01&rft.volume=3&rft.issue=9&rft.spage=277&rft.isbn=&rft.btitle=&rft.title=Cancer+communications&rft.issn=09553541&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-14 N1 - Date created - 1991-11-14 N1 - Date revised - 2017-01-13 N1 - Gene symbol - rasHa N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transient reversal of bone marrow aplasia associated with lymphocyte depleted Hodgkin's disease after combination chemotherapy. AN - 72109588; 1897515 AB - This report describes a patient with lymphocyte depleted Hodgkin's disease who presented with bone marrow aplasia. The aplastic marrow reverted to normal after initiation of MOPP chemotherapy; however, 4 months after completion of therapy, bone marrow aplasia recurred in the absence of recurrent Hodgkin's disease. The patient remains free of Hodgkin's disease 34 months after completion of chemotherapy. Bone marrow abnormalities in Hodgkin's disease are reviewed and the current understanding of the pathological mechanisms leading to aplastic anemia is discussed. JF - American journal of hematology AU - Johnston, P G AU - Ruscetti, F W AU - Connaghan, D G AU - Sullivan, F J AU - Longo, D L AD - Medicine Branch, N.C.I., N.I.H., Bethesda, MD 20892. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 54 EP - 60 VL - 38 IS - 1 SN - 0361-8609, 0361-8609 KW - Procarbazine KW - 35S93Y190K KW - Mechlorethamine KW - 50D9XSG0VR KW - Vincristine KW - 5J49Q6B70F KW - Prednisone KW - VB0R961HZT KW - Index Medicus KW - Procarbazine -- therapeutic use KW - Mechlorethamine -- therapeutic use KW - Neoplasm Staging KW - Vincristine -- therapeutic use KW - Prednisone -- therapeutic use KW - Humans KW - Adult KW - Biopsy KW - Radiography KW - Time Factors KW - Female KW - Lymphocytes -- pathology KW - Bone Marrow -- pathology KW - Hodgkin Disease -- pathology KW - Bone Marrow -- diagnostic imaging KW - Hodgkin Disease -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72109588?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+hematology&rft.atitle=Transient+reversal+of+bone+marrow+aplasia+associated+with+lymphocyte+depleted+Hodgkin%27s+disease+after+combination+chemotherapy.&rft.au=Johnston%2C+P+G%3BRuscetti%2C+F+W%3BConnaghan%2C+D+G%3BSullivan%2C+F+J%3BLongo%2C+D+L&rft.aulast=Johnston&rft.aufirst=P&rft.date=1991-09-01&rft.volume=38&rft.issue=1&rft.spage=54&rft.isbn=&rft.btitle=&rft.title=American+journal+of+hematology&rft.issn=03618609&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-10-23 N1 - Date created - 1991-10-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Treatment of corneal allograft rejection with the cytotoxin IL-2-PE40. AN - 72105769; 1897019 AB - IL-2-PE40 is a recombinant chimeric protein composed of IL-2, fused to a modified pseudomonas exotoxin. This molecule is extremely toxic to activated T cells expressing high-affinity IL-2R. We used this new molecule for selective immunosuppression to treat corneal allograft rejection in the rat, using Fisher and Lewis rats, a strain combination differing only in medial and minor histocompatibility antigens. The effect of IL-2-PE40 on the immunologic response was studied using both a heterotopic corneal graft model and orthotopic grafts. At the dose of 0.31 micrograms/g given intraperitoneally every 12 hr, IL-2-PE40 produced a significant reduction of both total lymph node cells and cytotoxic-T-cell (CTL) activity in draining lymph nodes (DLN) of heterotopically grafted animals. IL-2-PE40 treatment also significantly reduced the clinical rejection score and cumulative rejection rate (CRR) in orthotopic grafts and appears to be a very effective immunosuppressive agent. JF - Transplantation AU - Herbort, C P AU - de Smet, M D AU - Roberge, F G AU - Nussenblatt, R B AU - FitzGerald, D AU - Lorberboum-Galski, H AU - Pastan, I AD - Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 470 EP - 474 VL - 52 IS - 3 SN - 0041-1337, 0041-1337 KW - Bacterial Proteins KW - 0 KW - Cyclosporins KW - Exotoxins KW - IL-2-PE40 chimeric protein, recombinant KW - Immunotoxins KW - Interleukin-2 KW - Receptors, Interleukin-2 KW - Recombinant Proteins KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred Lew KW - Rats, Inbred F344 KW - Transplantation, Heterotopic KW - Receptors, Interleukin-2 -- analysis KW - Cyclosporins -- therapeutic use KW - T-Lymphocytes, Cytotoxic -- immunology KW - Interleukin-2 -- pharmacology KW - Exotoxins -- pharmacology KW - Bacterial Proteins -- pharmacology KW - Graft Rejection -- drug effects KW - Immunotoxins -- pharmacology KW - Corneal Transplantation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72105769?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Transplantation&rft.atitle=Treatment+of+corneal+allograft+rejection+with+the+cytotoxin+IL-2-PE40.&rft.au=Herbort%2C+C+P%3Bde+Smet%2C+M+D%3BRoberge%2C+F+G%3BNussenblatt%2C+R+B%3BFitzGerald%2C+D%3BLorberboum-Galski%2C+H%3BPastan%2C+I&rft.aulast=Herbort&rft.aufirst=C&rft.date=1991-09-01&rft.volume=52&rft.issue=3&rft.spage=470&rft.isbn=&rft.btitle=&rft.title=Transplantation&rft.issn=00411337&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-10-18 N1 - Date created - 1991-10-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Levels of chromosomally encoded Umu proteins and requirements for in vivo UmuD cleavage. AN - 72104575; 1654503 AB - Most of the inducible mutagenesis observed in Escherichia coli after treatment with many DNA damaging agents is dependent upon the products of the umuD,C operon. RecA-mediated proteolytic processing of UmuD yields a carboxyl-terminal fragment (UmuD') that is active for mutagenesis. Processing of UmuD is therefore a critical step in the fixation of mutations. In this paper we have analyzed the requirements for UmuD processing in vivo. Standard immuno-detection assays, coupled with a sensitive chemiluminescence detection assay, have been utilized to probe levels of chromosomally encoded Umu proteins from whole-cell E. coli extracts. We found that the derepression of additional SOS gene products, other than RecA, was not required for UmuD processing. Moreover, efficient cleavage of UmuD was observed only in the presence of elevated levels of activated RecA, suggesting that efficient processing would occur only under conditions of severe DNA damage. Detection of chromosomally encoded Umu proteins has allowed us, for the first time, to measure directly the cellular steady-state levels of these proteins under various SOS inducing conditions. UmuD was present at approximately 180 copies per uninduced cell and was measured at approximately 2400 copies per cell in strains that lacked a functional repressor. Induced levels of UmuC were approximately 12-fold lower than UmuD with approximately 200 molecules per cell. These levels of cellular UmuC protein suggest that it functions through specific protein-DNA or protein-protein interactions, possibly as a lesion recognition protein or by interacting with DNA polymerase III. JF - Molecular & general genetics : MGG AU - Woodgate, R AU - Ennis, D G AD - Section on Viruses and Cellular Biology, National Institute of Child Health and Human Development, Bethesda, MD 20892. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 10 EP - 16 VL - 229 IS - 1 SN - 0026-8925, 0026-8925 KW - Bacterial Proteins KW - 0 KW - Escherichia coli Proteins KW - LexA protein, Bacteria KW - Rec A Recombinases KW - EC 2.7.7.- KW - DNA-Directed DNA Polymerase KW - EC 2.7.7.7 KW - UmuD protein, E coli KW - Serine Endopeptidases KW - EC 3.4.21.- KW - Index Medicus KW - DNA Repair -- physiology KW - Operon -- physiology KW - Luminescent Measurements KW - Protein Processing, Post-Translational KW - Mutagenesis -- physiology KW - Enzyme-Linked Immunosorbent Assay KW - Rec A Recombinases -- metabolism KW - Gene Expression Regulation KW - Rec A Recombinases -- analysis KW - SOS Response (Genetics) -- physiology KW - Escherichia coli -- metabolism KW - Bacterial Proteins -- metabolism KW - Bacterial Proteins -- analysis KW - Escherichia coli -- genetics KW - Escherichia coli -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72104575?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+%26+general+genetics+%3A+MGG&rft.atitle=Levels+of+chromosomally+encoded+Umu+proteins+and+requirements+for+in+vivo+UmuD+cleavage.&rft.au=Woodgate%2C+R%3BEnnis%2C+D+G&rft.aulast=Woodgate&rft.aufirst=R&rft.date=1991-09-01&rft.volume=229&rft.issue=1&rft.spage=10&rft.isbn=&rft.btitle=&rft.title=Molecular+%26+general+genetics+%3A+MGG&rft.issn=00268925&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-10-23 N1 - Date created - 1991-10-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Polymerase chain reaction-directed identification, cloning, and quantification of human CYP2C18 mRNA. AN - 72102117; 1896026 AB - Sequencing of genomic polymerase chain reaction (PCR) products synthesized using primers generated from the CYP2C8 and CYP2C9 cDNAs revealed the presence of a new CYP2C gene in the human genome. Primers specific to exons of this new gene were used to perform PCR on human liver cDNA libraries and cDNA synthesized from human liver mRNA to generate a cDNA containing a complete cytochrome P450 amino acid reading frame. This cytochrome P450 cDNA, designated CYP2C18, displayed 85% and 87% nucleotide and 77% and 81% amino acid sequence similarities, respectively, with cDNAs and proteins corresponding to CYP2C8 and CYP2C9. cDNA-directed synthesis of CYP2C18 revealed a protein with relative Mr 49,000 on sodium dodecyl sulfate-polyacrylamide gels, which is considerably less than that calculated from the deduced amino acid composition, Mr 55,747. A preferred substrate for this enzyme has not been uncovered. Levels of CYP2C8, CYP2C9, and CYP2C18 mRNAs were examined in 17 human liver specimens using a PCR-based assay. CYP2C18 mRNA was found in all livers examined, albeit at mean levels 7-8-fold lower than those of mRNAs encoding CYP2C8 and CYP2C9. Marked interindividual differences in levels of expression of all three CYP2C mRNAs were also found. JF - Molecular pharmacology AU - Furuya, H AU - Meyer, U A AU - Gelboin, H V AU - Gonzalez, F J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 375 EP - 382 VL - 40 IS - 3 SN - 0026-895X, 0026-895X KW - CYP2C18 KW - RNA, Messenger KW - 0 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Base Sequence KW - Humans KW - Molecular Sequence Data KW - Gene Expression KW - Amino Acid Sequence KW - Liver -- chemistry KW - Polymerase Chain Reaction KW - Cytochrome P-450 Enzyme System -- genetics KW - RNA, Messenger -- analysis KW - Cloning, Molecular UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72102117?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Polymerase+chain+reaction-directed+identification%2C+cloning%2C+and+quantification+of+human+CYP2C18+mRNA.&rft.au=Furuya%2C+H%3BMeyer%2C+U+A%3BGelboin%2C+H+V%3BGonzalez%2C+F+J&rft.aulast=Furuya&rft.aufirst=H&rft.date=1991-09-01&rft.volume=40&rft.issue=3&rft.spage=375&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 - 1991-10-18 N1 - Date created - 1991-10-18 N1 - Date revised - 2017-01-13 N1 - Gene symbol - CYP2C18 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Changes in inositol phosphate metabolism are associated with terminal differentiation and neoplasia in mouse keratinocytes. AN - 72097792; 1893524 AB - Cultured murine keratinocytes respond to specific Ca2+ levels in medium (Ca0) by expressing markers of terminal differentiation. A Ca0 of 0.05 mM selects for a basal cell phenotype, whereas spinous cell characteristics occur in 0.12 mM Ca2+ and cornified envelopes develop in 1.0 mM Ca2+. An increase in inositol phosphate (InsP) metabolism is associated with higher Ca2+ in the medium. The magnitude of Ca(2+)-stimulated InsP turnover is Ca0-dependent, whereas Ca0 of 0.05, 0.12 or 1.4 mM resulted in a graded, sustained (greater than 24 h) increase in InsPs. Diacylglycerol (DAG) levels similarly increased in a graded manner. The major inositol trisphosphate (InsP3) to accumulate was Ins-1,3,4-P3 while Ins-1,4,5-P3 increased transiently. Neoplastic keratinocyte cell lines, 308 and SP-1, which produce benign tumors and have a mutated c-rasHa gene, do not express markers of differentiation in response to Ca2+. Basal InsP and DAG are 2- and 5-fold higher respectively in the neoplastic cells relative to normal keratinocytes. However, the metabolic profiles of InsPs were similar in normal and neoplastic cells. In neoplastic cells, InsP metabolism was stimulated even further following a Ca2+ increase, and this was graded to the Ca0. The unusual, sustained Ca(2+)-graded InsP response in normal cells is consistent with the turnover of InsP contributing to the signals controlling expression of markers of differentiation. Very high InsP turnover and DAG levels, as in neoplastic cells, may be inhibitory to marker expression. JF - Carcinogenesis AU - Lee, E AU - Yuspa, S H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, NIH, Bethesda, MD 20892. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 1651 EP - 1658 VL - 12 IS - 9 SN - 0143-3334, 0143-3334 KW - Diglycerides KW - 0 KW - Inositol Phosphates KW - Phosphatidylinositols KW - Phospholipids KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Calcium -- metabolism KW - Phosphatidylinositols -- metabolism KW - Animals KW - Blotting, Western KW - Phosphorylation KW - Electrophoresis, Polyacrylamide Gel KW - Cells, Cultured KW - Phospholipids -- metabolism KW - Mice KW - Mice, Inbred BALB C KW - Diglycerides -- metabolism KW - Cell Transformation, Neoplastic -- pathology KW - Inositol Phosphates -- metabolism KW - Cell Transformation, Neoplastic -- metabolism KW - Cell Differentiation KW - Keratinocytes -- pathology KW - Keratinocytes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72097792?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Changes+in+inositol+phosphate+metabolism+are+associated+with+terminal+differentiation+and+neoplasia+in+mouse+keratinocytes.&rft.au=Lee%2C+E%3BYuspa%2C+S+H&rft.aulast=Lee&rft.aufirst=E&rft.date=1991-09-01&rft.volume=12&rft.issue=9&rft.spage=1651&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-10-23 N1 - Date created - 1991-10-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Anticarcinogenic effects of cadmium in B6C3F1 mouse liver and lung. AN - 72095691; 1891777 AB - The B6C3F1 mouse liver has been widely used for the evaluation of carcinogenic or tumor promoting efficacy of various organic compounds, although little is known about the actions of metallic carcinogens in this system. Thus, the ability of cadmium to initiate or promote tumors in B6C3F1 mouse liver was studied. In promotion studies, diethylnitrosamine (DEN; 90 mg/kg, ip) was given as an initiator to 5-week-old mice followed 2 weeks later by 500 or 1000 ppm of cadmium in drinking water for 50 weeks. DEN caused an elevation of liver tumor incidence (13 tumor bearing mice/45 total) over control (1/48) which was prevented by cadmium (DEN + 500 ppm cadmium, 3/42; DEN + 1000 cadmium, 0/47). Cadmium alone did not further reduce the very low spontaneous liver and lung tumor incidence at approximately 1 year of age. DEN-induced lung tumor incidence (15/45) was also reduced by cadmium (DEN + 500 ppm cadmium, 11/42; DEN + 1000 ppm cadmium, 1/47) to control levels (0/48). In initiation studies, cadmium (20 or 22.5 mumol/kg, sc) was given to 5-week-old mice (n = 30-60) 2 weeks before an established promoting regimen of sodium barbital (BB) in drinking water at 500 ppm level was begun. Barbital in drinking water was given continuously for up to 92 weeks. Such cadmium doses caused acute, focal hepatic necrosis. Mice treated with BB and killed at 97 weeks of age showed an elevation of liver tumor multiplicity (7.44 tumors/liver) over control (2.24) that was prevented by cadmium in a dose-related manner (20 mumol/kg cadmium + BB, 3.93; 22.5 mumol/kg cadmium + BB, 1.87). Cadmium alone given by injection also reduced spontaneous liver tumor multiplicity. These results indicate that cadmium inhibits tumor formation in the B6C3F1 mouse liver initiation/promotion system regardless of route of exposure or sequence of administration. The possibility exists that cadmium has a specific toxicity toward previously initiated cells within liver and lung. JF - Toxicology and applied pharmacology AU - Waalkes, M P AU - Diwan, B A AU - Weghorst, C M AU - Bare, R M AU - Ward, J M AU - Rice, J M AD - Inorganic Carcinogenesis Section, National Cancer Institute, Frederick Cancer Research and Development Center, Frederick, Maryland 21702-1201. Y1 - 1991/09/01/ PY - 1991 DA - 1991 Sep 01 SP - 327 EP - 335 VL - 110 IS - 2 SN - 0041-008X, 0041-008X KW - Antineoplastic Agents KW - 0 KW - Cadmium KW - 00BH33GNGH KW - Diethylnitrosamine KW - 3IQ78TTX1A KW - Barbital KW - 5WZ53ENE2P KW - Cadmium Chloride KW - J6K4F9V3BA KW - Index Medicus KW - Administration, Oral KW - Mice, Inbred Strains KW - Animals KW - Dose-Response Relationship, Drug KW - Mice KW - Male KW - Barbital -- pharmacology KW - Lung Neoplasms -- prevention & control KW - Liver Neoplasms -- prevention & control KW - Cadmium -- administration & dosage KW - Liver Neoplasms -- chemically induced KW - Lung Neoplasms -- chemically induced KW - Cadmium -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72095691?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Anticarcinogenic+effects+of+cadmium+in+B6C3F1+mouse+liver+and+lung.&rft.au=Waalkes%2C+M+P%3BDiwan%2C+B+A%3BWeghorst%2C+C+M%3BBare%2C+R+M%3BWard%2C+J+M%3BRice%2C+J+M&rft.aulast=Waalkes&rft.aufirst=M&rft.date=1991-09-01&rft.volume=110&rft.issue=2&rft.spage=327&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 - 1991-10-17 N1 - Date created - 1991-10-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparative toxicity and tissue distribution of antimony potassium tartrate in rats and mice dosed by drinking water or intraperitoneal injection. AN - 72093137; 1890693 AB - Antimony potassium tartrate (APT) is a complex salt that until recently was used worldwide as an antischistosomal drug. Treatment was efficacious only if APT was administered intravenously to humans at a near lethal total dose of 36 mg/kg. Because unconfirmed epidemiologic studies suggested there might be an association between APT treatment and bladder cancer, we initiated prechronic toxicity studies with the drug to select a route of administration and doses in the event that chronic studies of APT were needed. The toxicity and concentration of tissue antimony levels were compared in 14-d studies with F344 rats and B6C3F1 mice administered APT in the drinking water or by ip injection to determine the most appropriate route for longer term studies. Drinking water doses estimated by water consumption were 0, 16, 28, 59, 94 and 168 mg/kg in rats and 0, 59, 98, 174, 273, and 407 mg/kg in mice. APT was poorly absorbed and relatively nontoxic orally, whereas ip administration of the drug caused mortality, body weight decrements, and lesions in the liver and kidney at doses about one order of magnitude below those in drinking water. Because of these data and the dose-related accumulation of antimony in the target organs, an ip dose regimen was selected for subsequent studies. Both sexes of F344 rats and B6C3F1 mice were given 0, 1.5, 3, 6, 12, and 24 mg/kg doses of APT every other day for 90 d by ip injection. There were no clinical signs of toxicity nor gross or microscopic lesions in mice that could be attributed to toxicity of APT, although elevated concentrations of antimony were detected in the liver and spleen of mice. Rats were more sensitive than mice to the toxic effects of APT, exhibiting dose-related mortality, body weight decrements, and hepatotoxicity. The concentrations of antimony measured in liver, blood, kidney, spleen, and heart of rats were proportional to dose, but there were no biochemical changes indicative of toxicity except in the liver. Hepatocellular degeneration and necrosis occurred in association with dose-related elevations in activities of the liver-specific serum enzymes sorbitol dehydrogenase and alanine aminotransferase. By alternating the site of abdominal injection and the days of treatment, mesenteric inflammation at the site of administration was minimized in the rats and mice, indicating that the ip route would be suitable for chronic studies.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Journal of toxicology and environmental health AU - Dieter, M P AU - Jameson, C W AU - Elwell, M R AU - Lodge, J W AU - Hejtmancik, M AU - Grumbein, S L AU - Ryan, M AU - Peters, A C AD - National Institutes of Health, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 51 EP - 82 VL - 34 IS - 1 SN - 0098-4108, 0098-4108 KW - Antimony Potassium Tartrate KW - DL6OZ476V3 KW - L-Iditol 2-Dehydrogenase KW - EC 1.1.1.14 KW - Alanine Transaminase KW - EC 2.6.1.2 KW - Index Medicus KW - Administration, Oral KW - Drinking KW - Injections, Intraperitoneal KW - Regression Analysis KW - Animals KW - Kidney -- metabolism KW - Spleen -- metabolism KW - Dose-Response Relationship, Drug KW - Kidney -- drug effects KW - Liver -- metabolism KW - Mice KW - Intestinal Absorption KW - Tissue Distribution KW - Myocardium -- metabolism KW - Rats KW - Rats, Inbred F344 KW - Alanine Transaminase -- blood KW - Liver -- drug effects KW - L-Iditol 2-Dehydrogenase -- blood KW - Body Weight -- drug effects KW - Male KW - Female KW - Antimony Potassium Tartrate -- pharmacokinetics KW - Antimony Potassium Tartrate -- blood KW - Antimony Potassium Tartrate -- toxicity KW - Antimony Potassium Tartrate -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72093137?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Comparative+toxicity+and+tissue+distribution+of+antimony+potassium+tartrate+in+rats+and+mice+dosed+by+drinking+water+or+intraperitoneal+injection.&rft.au=Dieter%2C+M+P%3BJameson%2C+C+W%3BElwell%2C+M+R%3BLodge%2C+J+W%3BHejtmancik%2C+M%3BGrumbein%2C+S+L%3BRyan%2C+M%3BPeters%2C+A+C&rft.aulast=Dieter&rft.aufirst=M&rft.date=1991-09-01&rft.volume=34&rft.issue=1&rft.spage=51&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 - 1991-10-11 N1 - Date created - 1991-10-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Survivors of Hodgkin's disease: prevention of sequelae. AN - 72092469; 1909813 AB - Increasing numbers of patients are surviving Hodgkin's disease in their youth, creating an ever larger cohort who need careful attention to long-term preventive medicine in their older years. Vigilance is especially needed for those who received laparotomy, splenectomy, and irradiation for early stage I through stage III disease, the majority of whom are destined to be long-term survivors. With the frequent migration of the young, these patients often fall under the care of a physician other than their original oncologist. The diligent internist, oncologist, emergency room physician, and general practitioner can avoid several simple pitfalls in the long-term care of these young patients now entering middle age. JF - Southern medical journal AU - Goffman, T E AU - Raubitschek, A AU - Glatstein, E AD - Radiation Oncology Branch, National Institutes of Health, National Cancer Institute, Bethesda, Md 20892. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 1108 EP - 1110 VL - 84 IS - 9 SN - 0038-4348, 0038-4348 KW - Antineoplastic Agents KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Combined Modality Therapy KW - Humans KW - Adult KW - Middle Aged KW - Long-Term Care KW - Male KW - Female KW - Radiotherapy -- adverse effects KW - Antineoplastic Agents -- adverse effects KW - Hodgkin Disease -- therapy KW - Hodgkin Disease -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72092469?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Southern+medical+journal&rft.atitle=Survivors+of+Hodgkin%27s+disease%3A+prevention+of+sequelae.&rft.au=Goffman%2C+T+E%3BRaubitschek%2C+A%3BGlatstein%2C+E&rft.aulast=Goffman&rft.aufirst=T&rft.date=1991-09-01&rft.volume=84&rft.issue=9&rft.spage=1108&rft.isbn=&rft.btitle=&rft.title=Southern+medical+journal&rft.issn=00384348&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-10-16 N1 - Date created - 1991-10-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Thromboxane stimulates synthesis of extracellular matrix proteins in vitro. AN - 72079639; 1887910 AB - The vasoconstrictor eicosanoid thromboxane plays an important role in the pathogenesis of several renal diseases. As an autacoid, its local release alters blood flow and induces platelet aggregation. We report a direct stimulatory effect of thromboxane on extracellular matrix protein production and gene expression in vitro. Treatment of two cell types, differentiated mouse teratocarcinoma cells (F9+) and human glomerular mesangial cells, with two different thromboxane analogues resulted in increased production of components of the extracellular matrix including fibronectin and the basement membrane proteins laminin and type IV collagen. These responses to thromboxane were not the result of a mitogenic effect of thromboxane nor the result of an increase in total cellular protein. The increased production of extracellular matrix proteins was, at least in part, due to an increase in the steady-state level of mRNA for these genes. Furthermore, the effect of thromboxane was markedly inhibited by cotreatment with a thromboxane-receptor antagonist. These results suggest a new potential role for thromboxane as a mediator of the sclerotic and fibrotic responses to injury. JF - The American journal of physiology AU - Bruggeman, L A AU - Horigan, E A AU - Horikoshi, S AU - Ray, P E AU - Klotman, P E AD - Molecular Medicine Section, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - F488 EP - F494 VL - 261 IS - 3 Pt 2 SN - 0002-9513, 0002-9513 KW - Biphenyl Compounds KW - 0 KW - Bridged Bicyclo Compounds KW - Bridged Bicyclo Compounds, Heterocyclic KW - Extracellular Matrix Proteins KW - Fatty Acids, Unsaturated KW - Fibronectins KW - Heptanoic Acids KW - Laminin KW - Prostaglandin Endoperoxides, Synthetic KW - RNA, Messenger KW - Thromboxanes KW - 7-(3-(3-hydroxy-4-(4'-iodophenoxy)-1-butenyl)-7-oxabicyclo(2.2.1)heptan-2-yl)-5-heptenoic acid KW - 124924-85-2 KW - 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid KW - 76898-47-0 KW - Collagen KW - 9007-34-5 KW - vapiprost KW - H84XT1COAU KW - Thymidine KW - VC2W18DGKR KW - Index Medicus KW - Animals KW - Laminin -- genetics KW - Humans KW - Cell Division -- drug effects KW - Biphenyl Compounds -- pharmacology KW - Mice KW - Fibronectins -- genetics KW - RNA, Messenger -- genetics KW - Thymidine -- metabolism KW - Collagen -- genetics KW - Bridged Bicyclo Compounds -- pharmacology KW - RNA, Messenger -- metabolism KW - Cells, Cultured KW - Kinetics KW - Adult KW - Fatty Acids, Unsaturated -- pharmacology KW - Teratoma KW - RNA, Messenger -- isolation & purification KW - Cell Line KW - Heptanoic Acids -- pharmacology KW - Prostaglandin Endoperoxides, Synthetic -- pharmacology KW - Glomerular Mesangium -- drug effects KW - Extracellular Matrix Proteins -- genetics KW - Extracellular Matrix Proteins -- biosynthesis KW - Glomerular Mesangium -- metabolism KW - Thromboxanes -- pharmacology KW - DNA Replication -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72079639?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+physiology&rft.atitle=Thromboxane+stimulates+synthesis+of+extracellular+matrix+proteins+in+vitro.&rft.au=Bruggeman%2C+L+A%3BHorigan%2C+E+A%3BHorikoshi%2C+S%3BRay%2C+P+E%3BKlotman%2C+P+E&rft.aulast=Bruggeman&rft.aufirst=L&rft.date=1991-09-01&rft.volume=261&rft.issue=3+Pt+2&rft.spage=F488&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+physiology&rft.issn=00029513&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-10-04 N1 - Date created - 1991-10-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effect of site-directed mutagenic alterations on ADP-ribosyltransferase activity of the A subunit of Escherichia coli heat-labile enterotoxin. AN - 72063551; 1908825 AB - Previous studies of the S1 subunit of pertussis toxin, an NAD(+)-dependent ADP-ribosyltransferase, suggested that a small amino-terminal region of amino acid sequence similarity to the active fragments of both cholera toxin and Escherichia coli heat-labile enterotoxin represents a region containing critical active-site residues that might be involved in the binding of the substrate NAD+. Other studies of two other bacterial toxins possessing ADP-ribosyltransferase activity, diphtheria toxin and Pseudomonas exotoxin A, have revealed the presence of essential glutamic acid residues vicinal to the active site. To help determine the relevance of these observations to activities of the enterotoxins, the A-subunit gene of the E. coli heat-labile enterotoxin was subjected to site-specific mutagenesis in the region encoding the amino-terminal region of similarity to the S1 subunit of pertussis toxin delineated by residues 6 through 17 and at two glutamic acid residues, 110 and 112, that are conserved in the active domains of all of the heat-labile enterotoxin variants and in cholera toxin. Mutant proteins in which arginine 7 was either deleted or replaced with lysine exhibited undetectable levels of ADP-ribosyltransferase activity. However, limited trypsinolysis of the arginine 7 mutants yielded fragmentation kinetics that were different from that yielded by the wild-type recombinant subunit or the authentic A subunit. In contrast, mutant proteins in which glutamic acid residues at either position 110 or 112 were replaced with aspartic acid responded like the wild-type subunit upon limited trypsinolysis, while exhibiting severely depressed, but detectable, ADP-ribosyltransferase activity. The latter results may indicate that either glutamic acid 110 or glutamic acid 112 of the A subunit of heat-labile enterotoxin is analogous to those active-site glutamic acids identified in several other ADP-ribosylating toxins. JF - Infection and immunity AU - Lobet, Y AU - Cluff, C W AU - Cieplak, W AD - Laboratory of Vectors and Pathogens, National Institute of Allergy and Infectious Diseases, Hamilton, Montana 59840. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 2870 EP - 2879 VL - 59 IS - 9 SN - 0019-9567, 0019-9567 KW - Bacterial Toxins KW - 0 KW - DNA, Bacterial KW - Enterotoxins KW - Escherichia coli Proteins KW - Recombinant Proteins KW - heat-labile enterotoxin, E coli KW - Adenosine Diphosphate Ribose KW - 20762-30-5 KW - Guanylyl Imidodiphosphate KW - 34273-04-6 KW - Poly(ADP-ribose) Polymerases KW - EC 2.4.2.30 KW - Dithiothreitol KW - T8ID5YZU6Y KW - Index Medicus KW - Animals KW - Immunoblotting KW - Plasmids -- genetics KW - Gene Expression KW - Escherichia coli -- genetics KW - Amino Acid Sequence KW - Escherichia coli -- enzymology KW - Adenosine Diphosphate Ribose -- metabolism KW - Structure-Activity Relationship KW - Mutagenesis, Site-Directed KW - Base Sequence KW - Cattle KW - Guanylyl Imidodiphosphate -- pharmacology KW - Recombinant Proteins -- metabolism KW - DNA, Bacterial -- genetics KW - Dithiothreitol -- pharmacology KW - Molecular Sequence Data KW - Rod Cell Outer Segment -- drug effects KW - Bacterial Toxins -- genetics KW - Bacterial Toxins -- metabolism KW - Enterotoxins -- metabolism KW - Enterotoxins -- genetics KW - Poly(ADP-ribose) Polymerases -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72063551?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Effect+of+site-directed+mutagenic+alterations+on+ADP-ribosyltransferase+activity+of+the+A+subunit+of+Escherichia+coli+heat-labile+enterotoxin.&rft.au=Lobet%2C+Y%3BCluff%2C+C+W%3BCieplak%2C+W&rft.aulast=Lobet&rft.aufirst=Y&rft.date=1991-09-01&rft.volume=59&rft.issue=9&rft.spage=2870&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 - 1991-10-02 N1 - Date created - 1991-10-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Infect Immun. 1982 Aug;37(2):687-94 [6889574] J Biol Chem. 1990 Dec 25;265(36):22520-5 [2266142] Proc Natl Acad Sci U S A. 1989 May;86(9):3075-9 [2470088] Infect Immun. 1989 Nov;57(11):3660-2 [2807541] Proc Natl Acad Sci U S A. 1988 Dec;85(23):8880-4 [3143111] Infect Immun. 1987 Nov;55(11):2546-53 [3117686] J Biol Chem. 1988 Feb 5;263(4):1768-72 [3123477] Infect Immun. 1988 Aug;56(8):1934-41 [3135265] Proc Natl Acad Sci U S A. 1988 Aug;85(15):5488-91 [3135549] J Bacteriol. 1987 Nov;169(11):4967-71 [2889718] Proc Natl Acad Sci U S A. 1985 Feb;82(4):1074-8 [3156376] J Biol Chem. 1985 Sep 5;260(19):10392-4 [2863266] J Biol Chem. 1987 Jun 25;262(18):8707-11 [2885323] J Bacteriol. 1988 May;170(5):2208-11 [3129402] Science. 1988 Oct 7;242(4875):72-4 [2459776] Proc Natl Acad Sci U S A. 1988 Jul;85(13):4667-71 [2455296] Rev Infect Dis. 1987 May-Jun;9(3):544-61 [2440089] FEBS Lett. 1986 Nov 24;208(2):194-8 [2430831] Science. 1989 Oct 27;246(4929):497-500 [2683073] J Bacteriol. 1989 Sep;171(9):4945-52 [2670900] N Engl J Med. 1989 Sep 28;321(13):879-83 [2671741] Eur J Biochem. 1989 Aug 1;183(2):311-6 [2667996] Infect Immun. 1989 Nov;57(11):3549-54 [2807535] Vaccine. 1988 Apr;6(2):197-9 [2898844] Proc Natl Acad Sci U S A. 1988 Oct;85(20):7521-5 [2902632] Microbiol Rev. 1984 Sep;48(3):199-221 [6436655] J Bacteriol. 1987 Mar;169(3):1352-7 [3546273] Infect Immun. 1987 Jan;55(1):24-8 [3539804] Science. 1986 Jun 6;232(4755):1258-64 [3704651] Proc Natl Acad Sci U S A. 1985 Jan;82(2):488-92 [3881765] Anal Biochem. 1985 Oct;150(1):76-85 [3843705] DNA. 1985 Apr;4(2):165-70 [3996185] Biochemistry. 1990 Jul 24;29(29):6866-73 [2397218] J Biol Chem. 1990 Mar 15;265(8):4552-9 [2155232] J Biol Chem. 1984 May 25;259(10):6228-34 [6327671] J Biol Chem. 1982 Sep 25;257(18):10540-3 [6125514] Proc Natl Acad Sci U S A. 1982 May;79(10):3129-33 [6954463] J Infect Dis. 1980 Jan;141(1):64-70 [6988518] J Biol Chem. 1982 Jun 10;257(11):6452-60 [7076677] Proc Natl Acad Sci U S A. 1984 Jun;81(11):3307-11 [6145155] J Biol Chem. 1981 Dec 25;256(24):12861-5 [6273411] J Biol Chem. 1982 May 25;257(10):5716-21 [6279611] J Bacteriol. 1984 May;158(2):713-20 [6427184] J Mol Biol. 1983 Jun 5;166(4):557-80 [6345791] Infect Immun. 1981 Sep;33(3):677-82 [7026442] J Biol Chem. 1980 Apr 10;255(7):2835-42 [7358713] J Bacteriol. 1979 Sep;139(3):850-8 [383697] J Clin Invest. 1978 Aug;62(2):281-5 [209060] Proc Natl Acad Sci U S A. 1978 Jul;75(7):3050-4 [210449] Infect Immun. 1979 Jun;24(3):760-9 [89088] Proc Natl Acad Sci U S A. 1979 Sep;76(9):4350-4 [388439] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Nature. 1970 Aug 15;227(5259):680-5 [5432063] FEBS Lett. 1990 Dec 17;277(1-2):59-64 [2269370] Proc Natl Acad Sci U S A. 1986 Jul;83(13):4631-5 [2873570] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transforming growth factor-beta improves healing of radiation-impaired wounds. AN - 72052678; 1875042 AB - Exogenously applied TGF-beta 1 has been shown to increase wound strength in incisional wounds early in the healing process. An impaired wound healing model was first established in guinea pigs by isolating flaps of skin and irradiating the flaps to 15 Gray in one fraction using a 4-MeV linear accelerator. Incisions made 2 d after irradiation were excised 7 d later, and showed decreased linear wound bursting strength (WBS) as compared to non-irradiated control wounds on the contralateral side of each animal (p = 0.001). The effect of TGF-beta on healing of radiation-impaired wounds was studied using this model. Skin on both left and right sides of guinea pigs was irradiated as above. A linear incision was made in each side. Collagen with either 1, 5, or 20 micrograms of TGF-beta was applied to one side prior to closure with staples, whereas the contralateral side received saline in collagen. Wounds given either 1 or 5 micrograms of TGF-beta were found to be stronger than controls at 7 d (p less than 0.05), whereas those receiving the higher 20-micrograms dose were weaker than controls (p less than 0.05). Thus, TGF-beta in lower doses improved healing at 7 d but very large amounts of the growth factor actually impaired healing. In situ hybridization done on wound samples showed increased type I collagen gene expression by fibroblasts in wounds treated with 1 micrograms TGF-beta over control wounds. These results indicate that TGF-beta improved wound healing as demonstrated by increased WBS. This improvement is accompanied by an up-regulation of collagen gene expression by resident fibroblasts. JF - The Journal of investigative dermatology AU - Bernstein, E F AU - Harisiadis, L AU - Salomon, G AU - Norton, J AU - Sollberg, S AU - Uitto, J AU - Glatstein, E AU - Glass, J AU - Talbot, T AU - Russo, A AD - Radiation Oncology Branch, National Institutes of Health, Bethesda, Maryland. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 430 EP - 434 VL - 97 IS - 3 SN - 0022-202X, 0022-202X KW - Transforming Growth Factor beta KW - 0 KW - Collagen KW - 9007-34-5 KW - Index Medicus KW - Collagen -- genetics KW - Animals KW - Guinea Pigs KW - Gene Expression KW - Disease Models, Animal KW - Nucleic Acid Hybridization KW - Female KW - Transforming Growth Factor beta -- pharmacology KW - Radiation Injuries -- drug therapy KW - Wound Healing -- physiology KW - Radiation Injuries -- complications KW - Wound Healing -- radiation effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72052678?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Transforming+growth+factor-beta+improves+healing+of+radiation-impaired+wounds.&rft.au=Bernstein%2C+E+F%3BHarisiadis%2C+L%3BSalomon%2C+G%3BNorton%2C+J%3BSollberg%2C+S%3BUitto%2C+J%3BGlatstein%2C+E%3BGlass%2C+J%3BTalbot%2C+T%3BRusso%2C+A&rft.aulast=Bernstein&rft.aufirst=E&rft.date=1991-09-01&rft.volume=97&rft.issue=3&rft.spage=430&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 - 1991-09-20 N1 - Date created - 1991-09-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Staurosporine induces protein kinase C agonist effects and maturation of normal and neoplastic mouse keratinocytes in vitro. AN - 72042550; 1678684 AB - Staurosporine is a potent but nonselective inhibitor of protein kinase C (PKC) and blocks responses to 12-O-tetradecanoylphorbol-13-acetate (TPA) in several cell types in vitro. In cultured primary mouse keratinocytes, however, staurosporine fails to inhibit TPA-mediated keratinocyte maturation and itself elicits responses that are similar to TPA (T. Sako et al., Cancer Res., 48: 4646-4650, 1988). After exposure to 10 nM staurosporine for 24 h, essentially all keratinocytes undergo morphological differentiation, whereas 160 nM TPA induces this response in about 50% of epidermal cells. These concentrations of staurosporine and TPA cause a 4-5-fold induction of epidermal transglutaminase activity and cornified envelopes, both markers of the terminal stage of keratinocyte differentiation. Staurosporine, but not TPA, also induces morphological and biochemical maturation in 2 neoplastic mouse keratinocyte cell lines, 308 and SP-1. The ability of staurosporine to elicit the same responses as TPA suggested that it may be functioning paradoxically as a PKC agonist in intact keratinocytes. In support of this hypothesis, staurosporine induces ornithine decarboxylase activity, inhibits 125I-labeled epidermal growth factor binding, and induces expression of c-fos mRNA. Down-regulation of PKC by pretreatment of primary keratinocytes with 60 nM bryostatin partially blocks staurosporine-mediated induction of cornified envelopes and inhibition of 125I-labeled epidermal growth factor binding, implicating PKC in these responses. The ability of staurosporine to mimic and/or enhance certain responses to TPA suggests that this agent is acting as a functional PKC agonist in cultured keratinocytes. JF - Cancer research AU - Dlugosz, A A AU - Yuspa, S H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/09/01/ PY - 1991 DA - 1991 Sep 01 SP - 4677 EP - 4684 VL - 51 IS - 17 SN - 0008-5472, 0008-5472 KW - Alkaloids KW - 0 KW - Proto-Oncogene Proteins KW - Proto-Oncogene Proteins c-fos KW - RNA, Messenger KW - Epidermal Growth Factor KW - 62229-50-9 KW - Transglutaminases KW - EC 2.3.2.13 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Staurosporine KW - H88EPA0A3N KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Dimethyl Sulfoxide KW - YOW8V9698H KW - Index Medicus KW - Tetradecanoylphorbol Acetate -- toxicity KW - Animals KW - Epidermal Growth Factor -- biosynthesis KW - Tumor Cells, Cultured -- drug effects KW - Skin Neoplasms -- pathology KW - Mice KW - Mice, Inbred BALB C KW - RNA, Messenger -- biosynthesis KW - Proto-Oncogene Proteins -- biosynthesis KW - Enzyme Induction -- drug effects KW - Skin Neoplasms -- chemically induced KW - Carcinogenicity Tests KW - Dimethyl Sulfoxide -- toxicity KW - Tumor Cells, Cultured -- pathology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Cell Differentiation -- drug effects KW - Proto-Oncogene Proteins -- genetics KW - Protein Kinase C -- antagonists & inhibitors KW - Keratinocytes -- enzymology KW - Keratinocytes -- drug effects KW - Alkaloids -- toxicity KW - Transglutaminases -- biosynthesis KW - Alkaloids -- pharmacology KW - Keratinocytes -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72042550?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Economic+Review&rft.atitle=Rational+Decision+Making+in+Business+Organizations&rft.au=Simon%2C+H+A&rft.aulast=Simon&rft.aufirst=H&rft.date=1979-09-01&rft.volume=69&rft.issue=4&rft.spage=493&rft.isbn=&rft.btitle=&rft.title=The+American+Economic+Review&rft.issn=00028282&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-23 N1 - Date created - 1991-09-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Metabolic activation of 4-ipomeanol by complementary DNA-expressed human cytochromes P-450: evidence for species-specific metabolism. AN - 72042394; 1651809 AB - 4-Ipomeanol is a pulmonary toxin in cattle and rodents that is metabolically activated by cytochromes P-450 (P-450s). P-450-mediated activation of 4-ipomeanol to DNA binding metabolites was evaluated using a vaccinia virus complementary DNA expression system and an in situ DNA-binding assay. Twelve human P-450s and two rodent P-450s were expressed in human hepatoma Hep G2 cells and examined for their abilities to metabolically activate this toxin. Three forms, designated CYP1A2, CYP3A3, and CYP3A4, were able to catalyze significant production of DNA-bound metabolites of 20-, 8-, and 5-fold, respectively, above binding catalyzed by Hep G2 cells infected with wild-type vaccinia virus. These enzymes, with highest activities, are not known to be expressed in human or rodent lung. CYP2F1 and CYP4B1, two enzymes that are expressed in lung, display only modest 3- and 2-fold respective increased abilities to metabolically activate 4-ipomeanol. Two human forms were inactive and seven other human forms showed activities ranging from 0.5- to 2-fold above control level. Surprisingly, rabbit complementary DNA-expressed CYP4B1 was the most active enzyme (180-fold above control) among all P-450s tested in producing DNA-binding metabolites from this mycotoxin. These studies demonstrate a species difference in 4-ipomeanol metabolism and suggest caution when attempting to extrapolate rodent data to humans. JF - Cancer research AU - Czerwinski, M AU - McLemore, T L AU - Philpot, R M AU - Nhamburo, P T AU - Korzekwa, K AU - Gelboin, H V AU - Gonzalez, F J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1991/09/01/ PY - 1991 DA - 1991 Sep 01 SP - 4636 EP - 4638 VL - 51 IS - 17 SN - 0008-5472, 0008-5472 KW - Terpenes KW - 0 KW - Toxins, Biological KW - 4-ipomeanol KW - 32954-58-8 KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - CYP3A4 protein, human KW - EC 1.14.13.67 KW - CYP3A protein, human KW - EC 1.14.14.1 KW - Cytochrome P-450 CYP3A KW - Index Medicus KW - Vaccinia virus -- enzymology KW - Liver Neoplasms -- metabolism KW - Carcinoma, Hepatocellular -- metabolism KW - Cells, Cultured KW - Biotransformation KW - Humans KW - Species Specificity KW - Toxins, Biological -- metabolism KW - Terpenes -- metabolism KW - DNA -- metabolism KW - Cytochrome P-450 Enzyme System -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72042394?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Metabolic+activation+of+4-ipomeanol+by+complementary+DNA-expressed+human+cytochromes+P-450%3A+evidence+for+species-specific+metabolism.&rft.au=Czerwinski%2C+M%3BMcLemore%2C+T+L%3BPhilpot%2C+R+M%3BNhamburo%2C+P+T%3BKorzekwa%2C+K%3BGelboin%2C+H+V%3BGonzalez%2C+F+J&rft.aulast=Czerwinski&rft.aufirst=M&rft.date=1991-09-01&rft.volume=51&rft.issue=17&rft.spage=4636&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 - 1991-09-23 N1 - Date created - 1991-09-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Adeno-associated viruses having nonsense mutations in the capsid genes: growth in mammalian cells containing an inducible amber suppressor. AN - 72036982; 1651593 AB - When an adeno-associated virus (AAV) genome contained in a recombinant plasmid is transfected into adenovirus-infected cells, infectious AAV particles are efficiently generated. We previously described the construction of a conditional lethal mutant of AAV having an amber termination codon inserted in the rep gene. This mutant was propagated on a monkey kidney cell line (SupD12) having an inducible amber suppressor tRNAser. We now describe the construction and propagation of two additional conditional lethal mutants of AAV having amber codons affecting all three capsid proteins (AAV Capam) or only the VP1 capsid protein (AAV VP1am). Suppression of the amber mutations in the capsid proteins was demonstrated directly by immunoblot analysis. The efficiency of amber suppression on the SupD12 cell was about 6 to 10% for AAV VP1am and 4 to 5% for AAV Capam. The reversion frequency of either mutant was apparently less than 10(-5). On nonsuppressing cells AAV VP1am exhibited an Lip (Inf) phenotype, whereas AAV Capam exhibited a Cap phenotype. JF - Virology AU - Smuda, J W AU - Carter, B J AD - Laboratory of Molecular and Cellular Biology, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 310 EP - 318 VL - 184 IS - 1 SN - 0042-6822, 0042-6822 KW - Oligonucleotide Probes KW - 0 KW - RNA, Messenger KW - Index Medicus KW - Animals KW - Base Sequence KW - Transfection KW - HeLa Cells KW - Humans KW - Molecular Sequence Data KW - Escherichia coli -- genetics KW - RNA, Messenger -- genetics KW - Plasmids KW - Cell Line KW - Cloning, Molecular KW - Mutagenesis, Site-Directed KW - Dependovirus -- growth & development KW - Dependovirus -- physiology KW - Capsid -- genetics KW - Dependovirus -- genetics KW - Genes, Viral KW - Genes, Suppressor UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72036982?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Adeno-associated+viruses+having+nonsense+mutations+in+the+capsid+genes%3A+growth+in+mammalian+cells+containing+an+inducible+amber+suppressor.&rft.au=Smuda%2C+J+W%3BCarter%2C+B+J&rft.aulast=Smuda&rft.aufirst=J&rft.date=1991-09-01&rft.volume=184&rft.issue=1&rft.spage=310&rft.isbn=&rft.btitle=&rft.title=Virology&rft.issn=00426822&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-18 N1 - Date created - 1991-09-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutations within the human immunodeficiency virus type 1 gp160 envelope glycoprotein alter its intracellular transport and processing. AN - 72036125; 1871974 AB - Intracellular transport and processing of the human immunodeficiency virus type 1 (HIV-1) envelope precursor polyprotein, gp160, proceeds via the endoplasmic reticulum (ER) and Golgi complex. We examined gp160 processing during the production of HIV-1 virions in transfected HeLa cells using wild-type and env mutant proviral molecular clones. Results from pulse-chase analyses indicated that a single amino acid substitution within a highly conserved domain of the env gene impaired gp160 export from the ER, leading to an increase in oligomeric forms of gp160 and a decrease in gp120 production. In contrast, gp160 which contained a mutated cleavage site was able to traverse the ER/Golgi complex, even in the absence of proteolytic processing, and become incorporated into budding virions. These findings indicate that export from the ER is a point in the intracellular trafficking of gp160 that is crucial to the production of the mature envelope components. JF - Virology AU - Willey, R L AU - Klimkait, T AU - Frucht, D M AU - Bonifacino, J S AU - Martin, M A AD - Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 319 EP - 329 VL - 184 IS - 1 SN - 0042-6822, 0042-6822 KW - Gene Products, env KW - 0 KW - HIV Envelope Protein gp160 KW - Macromolecular Substances KW - Oligonucleotide Probes KW - Protein Precursors KW - Viral Envelope Proteins KW - Glycoside Hydrolases KW - EC 3.2.1.- KW - Index Medicus KW - AIDS/HIV KW - Endoplasmic Reticulum -- metabolism KW - Virion -- genetics KW - Electrophoresis, Polyacrylamide Gel KW - Humans KW - Viral Envelope Proteins -- biosynthesis KW - Viral Envelope Proteins -- isolation & purification KW - Amino Acid Sequence KW - Molecular Weight KW - Base Sequence KW - Transfection KW - Molecular Sequence Data KW - HeLa Cells -- physiology KW - Golgi Apparatus -- metabolism KW - Viral Envelope Proteins -- genetics KW - Mutagenesis, Site-Directed KW - Gene Products, env -- isolation & purification KW - HIV-1 -- genetics KW - Protein Precursors -- biosynthesis KW - Protein Processing, Post-Translational KW - Protein Precursors -- genetics KW - Gene Products, env -- biosynthesis KW - Protein Precursors -- isolation & purification KW - Gene Products, env -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72036125?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mutations+within+the+human+immunodeficiency+virus+type+1+gp160+envelope+glycoprotein+alter+its+intracellular+transport+and+processing.&rft.au=Willey%2C+R+L%3BKlimkait%2C+T%3BFrucht%2C+D+M%3BBonifacino%2C+J+S%3BMartin%2C+M+A&rft.aulast=Willey&rft.aufirst=R&rft.date=1991-09-01&rft.volume=184&rft.issue=1&rft.spage=319&rft.isbn=&rft.btitle=&rft.title=Virology&rft.issn=00426822&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-18 N1 - Date created - 1991-09-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Immunologic responses to repeated ivermectin treatment in patients with onchocerciasis. AN - 72029879; 1822959 AB - To assess the effect of ivermectin treatment on the immunologic status of individuals with onchocerciasis, 27 patients from Guatemala were studied before and at 6-month intervals during 2 years of repeated semiannual treatment with ivermectin. T cell proliferative responses to onchocercal antigen increased transiently by 6 months (mean stimulation index [SI] rising from 4.17 to 12.81) but returned to preivermectin levels thereafter. Changes in SI to nonparasite antigen paralleled those induced by parasite antigen. There were also significant decreases in levels of blood eosinophils, polyclonal IgG and IgE, parasite-specific IgG antibody, and IgG subclass antibodies by the end of the study. This study emphasizes the apparent long-term safety of ivermectin by demonstrating the absence of immunopathogenic responses induced by repeated ivermectin treatments. JF - The Journal of infectious diseases AU - Steel, C AU - Lujan-Trangay, A AU - Gonzalez-Peralta, C AU - Zea-Flores, G AU - Nutman, T B AD - Laboratory of Parasitic Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/09// PY - 1991 DA - September 1991 SP - 581 EP - 587 VL - 164 IS - 3 SN - 0022-1899, 0022-1899 KW - Antibodies, Helminth KW - 0 KW - Antigens, Helminth KW - Ivermectin KW - 70288-86-7 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Antibodies, Helminth -- immunology KW - Humans KW - Microfilariae -- immunology KW - Guatemala KW - Cell Division -- drug effects KW - Leukocytes -- drug effects KW - Leukocyte Count -- drug effects KW - Adult KW - Eosinophils -- drug effects KW - Middle Aged KW - T-Lymphocytes -- drug effects KW - Adolescent KW - Immunity -- drug effects KW - Antibodies, Helminth -- blood KW - Male KW - Antigens, Helminth -- immunology KW - Onchocerciasis -- drug therapy KW - Ivermectin -- therapeutic use KW - Ivermectin -- adverse effects KW - Onchocerciasis -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72029879?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+infectious+diseases&rft.atitle=Immunologic+responses+to+repeated+ivermectin+treatment+in+patients+with+onchocerciasis.&rft.au=Steel%2C+C%3BLujan-Trangay%2C+A%3BGonzalez-Peralta%2C+C%3BZea-Flores%2C+G%3BNutman%2C+T+B&rft.aulast=Steel&rft.aufirst=C&rft.date=1991-09-01&rft.volume=164&rft.issue=3&rft.spage=581&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+infectious+diseases&rft.issn=00221899&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-16 N1 - Date created - 1991-09-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: J Infect Dis. 1992 Jun;165(6):1161-2 [1583341] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of regions of fibronectin besides the arginine-glycine-aspartic acid sequence required for adhesive function of the cell-binding domain using site-directed mutagenesis. AN - 72044577; 1874740 AB - Previous studies of adhesion mediated by the central cell-binding domain of fibronectin suggest that additional polypeptide information besides the Arg-Gly-Asp sequence is required for full activity. We analyzed this putative second, synergistic region of fibronectin more extensively by deletion analysis and oligonucleotide-based site-directed mutagenesis. Resulting mutated fusion proteins expressed using lambda gt11 were assayed for baby hamster kidney fibroblast cell spreading activity. Deletion mutants truncating from the amino terminus showed a decrease of activity in two apparently discrete steps. Complementary studies using a series of overlapped internal deletions designed to retain the repetitive fibronectin structure also indicated that two distinct peptide regions besides the RGD sequence were necessary for full activity. Removal of the carboxyl-terminal region resulted in the greatest loss of activity (greater than or equal to 20- versus 3-5-fold). Very similar results were obtained with HT-1080 cells dependent on the alpha 5 beta 1 integrin receptor for adhesion to fibronectin. An anti-fibronectin monoclonal antibody that inhibits cell adhesion was found to bind to the carboxyl-terminal functional region, and a point mutation caused specific loss of its epitope. These studies reveal unexpected complexity in the organization of these functional regions, which contrasts with adhesion models based only on simple, short peptide recognition sequences. JF - The Journal of biological chemistry AU - Aota, S AU - Nagai, T AU - Yamada, K M AD - Laboratory of Developmental Biology, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/08/25/ PY - 1991 DA - 1991 Aug 25 SP - 15938 EP - 15943 VL - 266 IS - 24 SN - 0021-9258, 0021-9258 KW - Antibodies, Monoclonal KW - 0 KW - Fibronectins KW - Aspartic Acid KW - 30KYC7MIAI KW - Arginine KW - 94ZLA3W45F KW - Glycine KW - TE7660XO1C KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Animals KW - Kidney -- metabolism KW - Molecular Sequence Data KW - Kidney -- cytology KW - Amino Acid Sequence KW - Mutation KW - Cricetinae KW - Binding Sites KW - Glycine -- genetics KW - Aspartic Acid -- genetics KW - Arginine -- genetics KW - Fibronectins -- immunology KW - Fibronectins -- metabolism KW - Fibronectins -- genetics KW - Cell Adhesion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72044577?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+regions+of+fibronectin+besides+the+arginine-glycine-aspartic+acid+sequence+required+for+adhesive+function+of+the+cell-binding+domain+using+site-directed+mutagenesis.&rft.au=Aota%2C+S%3BNagai%2C+T%3BYamada%2C+K+M&rft.aulast=Aota&rft.aufirst=S&rft.date=1991-08-25&rft.volume=266&rft.issue=24&rft.spage=15938&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 - 1991-09-26 N1 - Date created - 1991-09-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Halichondrin B and homohalichondrin B, marine natural products binding in the vinca domain of tubulin. Discovery of tubulin-based mechanism of action by analysis of differential cytotoxicity data. AN - 72043387; 1874739 AB - Data generated in the new National Cancer Institute drug evaluation program, which is based on inhibition of cell growth in 60 human tumor cell lines, were used to compare new compounds with agents of known mechanism of action in terms of their differential cytotoxicity. Two marine natural products, halichondrin B and homohalichondrin B, appeared repeatedly when the data base was probed with known antimitotic agents. We confirmed that both compounds were highly cytotoxic (IC50 values for L1210 murine leukemia cells of 0.3 and 1 nM, respectively), with accumulation of cells arrested in mitosis at toxic concentrations, that both inhibited the polymerization of purified tubulin, and that both inhibited microtubule assembly dependent on microtubule-associated proteins. Limited amounts of homohalichondrin B, the less active agent, were available, so only halichondrin B was studied in detail. Halichondrin B did not interfere with colchicine binding to tubulin, but it was a noncompetitive inhibitor of the binding of vinblastine to tubulin (apparent Ki, 5.0 microM). Halichondrin B was therefore compared with other agents which interfere with the binding of vinca alkaloids to tubulin (vinblastine, maytansine, dolastatin 10, phomopsin A, rhizoxin) in terms of its effects on tubulin polymerization, inhibition of GTP hydrolysis, inhibition of nucleotide exchange, and stabilization of tubulin, as well as the quantitative assessment of its effects on vinca alkaloid binding and inhibition of cell growth. Since halichondrin B was originally isolated from the same organism as the phosphatase inhibitor okadaic acid, and since it is about 50-fold more effective than okadaic acid as an inhibitor of L1210 cell growth, perturbations of cellular microtubules observed following treatment with okadaic acid should be interpreted cautiously. JF - The Journal of biological chemistry AU - Bai, R L AU - Paull, K D AU - Herald, C L AU - Malspeis, L AU - Pettit, G R AU - Hamel, E AD - Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/08/25/ PY - 1991 DA - 1991 Aug 25 SP - 15882 EP - 15889 VL - 266 IS - 24 SN - 0021-9258, 0021-9258 KW - Antineoplastic Agents KW - 0 KW - Depsipeptides KW - Ethers, Cyclic KW - Macrolides KW - Oligopeptides KW - Polymers KW - Tubulin KW - homohalichondrin B KW - 101383-39-5 KW - halichondrin B KW - 103614-76-2 KW - dolastatin 10 KW - 110417-88-4 KW - Maytansine KW - 14083FR882 KW - Vinblastine KW - 5V9KLZ54CY KW - Guanosine Triphosphate KW - 86-01-1 KW - Colchicine KW - SML2Y3J35T KW - Index Medicus KW - Animals KW - Drug Screening Assays, Antitumor KW - Vinblastine -- metabolism KW - Porifera KW - Maytansine -- pharmacology KW - Microtubules -- metabolism KW - Microtubules -- drug effects KW - Hydrolysis KW - Guanosine Triphosphate -- metabolism KW - Leukemia L1210 KW - Colchicine -- pharmacology KW - Oligopeptides -- pharmacology KW - Mitosis -- drug effects KW - Tubulin -- drug effects KW - Ethers, Cyclic -- metabolism KW - Antineoplastic Agents -- metabolism KW - Tubulin -- metabolism KW - Ethers, Cyclic -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72043387?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Halichondrin+B+and+homohalichondrin+B%2C+marine+natural+products+binding+in+the+vinca+domain+of+tubulin.+Discovery+of+tubulin-based+mechanism+of+action+by+analysis+of+differential+cytotoxicity+data.&rft.au=Bai%2C+R+L%3BPaull%2C+K+D%3BHerald%2C+C+L%3BMalspeis%2C+L%3BPettit%2C+G+R%3BHamel%2C+E&rft.aulast=Bai&rft.aufirst=R&rft.date=1991-08-25&rft.volume=266&rft.issue=24&rft.spage=15882&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 - 1991-09-26 N1 - Date created - 1991-09-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cloning and characterization of Rrp1, the gene encoding Drosophila strand transferase: carboxy-terminal homology to DNA repair endo/exonucleases. AN - 19795867; 8737207 AB - We previously reported the purification of a protein from Drosophila embryo extracts that carries out the strand transfer step in homologous recombination (Lowenhaupt, K., Sander, M., Hauser, C. and A. Rich, 1989, J. Biol. Chem. 264, 20568). We report here the isolation of the gene encoding this protein. Partial amino acid sequence from a tryptic digest of gel purified strand transfer protein was used to design a pair of degenerate oligonucleotide primers which amplified a 635 bp region of Drosophila genomic DNA. Recombinant bacteriophage were isolated from genomic and embryo cDNA libraries by screening with the amplified DNA fragment. These bacteriophage clones identify a single copy gene that expresses a single mRNA transcript in early embryos and in embryo-derived tissue culture cells. The cDNA nucleotide sequence contains an open reading frame of 679 amino acids within which are found 5 tryptic peptides from the strand transfer protein. Expression of this cDNA in E. coli produces a polypeptide with the same electrophoretic mobility as the purified protein. The deduced protein sequence has two distinct regions. The first 427 residues are basic, rich in glutamic acid and lysine residues and unrelated to known proteins. The carboxy-terminal 252 residues are average in amino acid composition and are homologous to the DNA repair proteins, Escherichia coli exonuclease III and Streptococcus pneumoniae exonuclease A. This protein, which we name Rrp1 (Recombination Repair Protein 1), may facilitate recombinational repair of DNA damage. Images JF - Nucleic Acids Research AU - Sander, M AU - Lowenhaupt, K AU - Lane, W S AU - Rich, A AD - Laboratory of Genetics D3-04, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/08/25/ PY - 1991 DA - 1991 Aug 25 SP - 4523 EP - 4529 PB - Oxford University Press, Oxford Journals, Great Clarendon Street VL - 19 IS - 16 SN - 0305-1048, 0305-1048 KW - Virology & AIDS Abstracts; Microbiology Abstracts B: Bacteriology; Genetics Abstracts; Entomology Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - Phages KW - Nucleotide sequence KW - Amino acid composition KW - Lysine KW - protein purification KW - Electrophoretic mobility KW - Oligonucleotides KW - Escherichia coli KW - Embryos KW - Tryptic peptides KW - genomics KW - homologous recombination KW - Transcription KW - Tissue culture KW - DNA repair KW - DNA damage KW - Streptococcus pneumoniae KW - Homology KW - exonuclease KW - Primers KW - Glutamic acid KW - Drosophila KW - Open reading frames KW - Amino acid sequence KW - J 02310:Genetics & Taxonomy KW - N 14820:DNA Metabolism & Structure KW - Z 05360:Genetics and Evolution KW - V 22310:Genetics, Taxonomy & Structure KW - G 07760:Viruses & Phages UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/19795867?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+Acids+Research&rft.atitle=Cloning+and+characterization+of+Rrp1%2C+the+gene+encoding+Drosophila+strand+transferase%3A+carboxy-terminal+homology+to+DNA+repair+endo%2Fexonucleases.&rft.au=Sander%2C+M%3BLowenhaupt%2C+K%3BLane%2C+W+S%3BRich%2C+A&rft.aulast=Sander&rft.aufirst=M&rft.date=1991-08-25&rft.volume=19&rft.issue=16&rft.spage=4523&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 - Phages; Nucleotide sequence; Transcription; Lysine; Amino acid composition; Tissue culture; protein purification; DNA repair; Electrophoretic mobility; Oligonucleotides; DNA damage; Homology; exonuclease; Tryptic peptides; Primers; Embryos; Glutamic acid; genomics; homologous recombination; Open reading frames; Amino acid sequence; Streptococcus pneumoniae; Escherichia coli; Drosophila ER - TY - JOUR T1 - Cytokine-induced activation of the neuroendocrine stress axis persists in endotoxin-tolerant mice. AN - 72547430; 1747764 AB - Chronic administration of lipopolysaccharide (LPS) to mice markedly reduced activation of the neuroendocrine stress axis elicited by an acute challenge dose of LPS. LPS-induced elevation in norepinephrine turnover in the hypothalamus showed complete tolerance whereas elevation of plasma corticosterone showed only partial tolerance. Challenge-induced increased turnover of dopamine in hypothalamus persisted in LPS-tolerant animals. Neuroendocrine activation persisted following acute challenge with interleukin-1 and tumor necrosis factor following chronic LPS exposure. JF - Brain research AU - Mefford, I N AU - Masters, C F AU - Heyes, M P AU - Eskay, R L AD - Section of Clinical Pharmacology, National Institute of Mental Health, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892. Y1 - 1991/08/23/ PY - 1991 DA - 1991 Aug 23 SP - 327 EP - 330 VL - 557 IS - 1-2 SN - 0006-8993, 0006-8993 KW - Biogenic Monoamines KW - 0 KW - Cytokines KW - Endotoxins KW - Interleukin-1 KW - Lipopolysaccharides KW - Tumor Necrosis Factor-alpha KW - Dopamine KW - VTD58H1Z2X KW - Corticosterone KW - W980KJ009P KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Animals KW - Interleukin-1 -- pharmacology KW - Hypothalamus -- drug effects KW - Tumor Necrosis Factor-alpha -- pharmacology KW - Dopamine -- metabolism KW - Mice KW - Macrophages -- drug effects KW - Biogenic Monoamines -- metabolism KW - Corticosterone -- metabolism KW - Drug Tolerance KW - Norepinephrine -- metabolism KW - Hypothalamus -- metabolism KW - Mice, Inbred C57BL KW - Lipopolysaccharides -- toxicity KW - Male KW - Cytokines -- pharmacology KW - Neurosecretory Systems -- drug effects KW - Neurosecretory Systems -- physiology KW - Endotoxins -- toxicity KW - Stress, Physiological -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72547430?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cytokine-induced+activation+of+the+neuroendocrine+stress+axis+persists+in+endotoxin-tolerant+mice.&rft.au=Mefford%2C+I+N%3BMasters%2C+C+F%3BHeyes%2C+M+P%3BEskay%2C+R+L&rft.aulast=Mefford&rft.aufirst=I&rft.date=1991-08-23&rft.volume=557&rft.issue=1-2&rft.spage=327&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 - 1992-01-22 N1 - Date created - 1992-01-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Requirement for positive selection of gamma delta receptor-bearing T cells. AN - 72050729; 1831565 AB - The alpha beta and gamma delta T cell receptors for antigen (TCR) delineate distinct T cell populations. TCR alpha beta-bearing thymocytes must be positively selected by binding of the TCR to major histocompatibility complex (MHC) molecules on thymic epithelium. To examine the requirement for positive selection of TCR gamma delta T cells, mice bearing a class I MHC-specific gamma delta transgene (Tg) were crossed to mice with disrupted beta 2 microglobulin (beta 2M) genes. The Tg+beta 2M- (class I MHC-) offspring had Tg+ thymocytes that did not proliferate to antigen or Tg-specific monoclonal antibody and few peripheral Tg+ cells. This is evidence for positive selection within the gamma delta T cell subset. JF - Science (New York, N.Y.) AU - Wells, F B AU - Gahm, S J AU - Hedrick, S M AU - Bluestone, J A AU - Dent, A AU - Matis, L A AD - Biological Carcinogenesis and Development Program, Program Resources, Inc./DynCorp, NCI-Frederick Cancer Research and Development Center, MD 21701-0201. Y1 - 1991/08/23/ PY - 1991 DA - 1991 Aug 23 SP - 903 EP - 905 VL - 253 IS - 5022 SN - 0036-8075, 0036-8075 KW - H-2 Antigens KW - 0 KW - Histocompatibility Antigens Class I KW - Receptors, Antigen, T-Cell KW - beta 2-Microglobulin KW - Index Medicus KW - Animals KW - Spleen -- cytology KW - T-Lymphocytes, Helper-Inducer -- cytology KW - Histocompatibility Antigens Class I -- immunology KW - H-2 Antigens -- immunology KW - Mice KW - Mice, Nude KW - Mice, Inbred BALB C KW - Mice, Transgenic KW - beta 2-Microglobulin -- genetics KW - T-Lymphocytes, Helper-Inducer -- immunology KW - Lymph Nodes -- cytology KW - Thymus Gland -- immunology KW - T-Lymphocytes, Regulatory -- cytology KW - Epithelium -- immunology KW - Flow Cytometry KW - T-Lymphocytes, Regulatory -- immunology KW - Cell Division KW - T-Lymphocytes -- cytology KW - Receptors, Antigen, T-Cell -- metabolism KW - Receptors, Antigen, T-Cell -- immunology KW - T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72050729?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Requirement+for+positive+selection+of+gamma+delta+receptor-bearing+T+cells.&rft.au=Wells%2C+F+B%3BGahm%2C+S+J%3BHedrick%2C+S+M%3BBluestone%2C+J+A%3BDent%2C+A%3BMatis%2C+L+A&rft.aulast=Wells&rft.aufirst=F&rft.date=1991-08-23&rft.volume=253&rft.issue=5022&rft.spage=903&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 - 1991-09-25 N1 - Date created - 1991-09-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of hematopoietic growth factors on the survival of primitive stem cells in liquid suspension culture. AN - 80734271; 1714328 AB - We have examined the effects of 10 different growth factors either alone or in combination on colony-forming unit-spleen (CFU-S) and repopulating stem cell survival in vitro. Either interleukin-3 (IL-3), granulocyte-colony-stimulating factor (G-CSF), or IL-4 alone support CFU-S in vitro. The effects of IL-3 or G-CSF could be neutralized by adding antibodies against IL-3 or G-CSF, respectively. However, the effects of IL-4 could be neutralized with antibodies to IL-4 as well as with antibodies to IL-3 and G-CSF. The combinations of IL-3 and IL-6, IL-3 and G-CSF, IL-3 and IL-1 alpha, IL-3 and granulocyte-macrophage CSF (GM-CSF), and IL-4 and IL-6 acted synergistically to increase CFU-S number. Addition of macrophage inflammatory protein-1 alpha (MIP-1 alpha) to IL-3 and IL-6 inhibited the increase in CFU-S number. Repopulating stem cell function was measured in a competitive repopulation assay. Either IL-3 or IL-4 alone could preserve stem cell function in vitro. The combinations of IL-3 and IL-6, and IL-3 and G-CSF increased stem cell function approximately twofold. The combinations of IL-3 + G-CSF + IL-6, and IL-4 and IL-6 (both of which increased CFU-S number fivefold to 10-fold) decreased stem cell function approximately fourfold. These results demonstrate that certain combinations of growth factors can increase CFU-S number at the expense of stem cell function. JF - Blood AU - Bodine, D M AU - Crosier, P S AU - Clark, S C AD - Clinical Hematology Branch, NHLBI, National Institutes of Health Bethesda, MD 20892. Y1 - 1991/08/15/ PY - 1991 DA - 1991 Aug 15 SP - 914 EP - 920 VL - 78 IS - 4 SN - 0006-4971, 0006-4971 KW - Growth Substances KW - 0 KW - Interleukin-1 KW - Interleukin-3 KW - Interleukin-6 KW - Granulocyte Colony-Stimulating Factor KW - 143011-72-7 KW - Interleukin-4 KW - 207137-56-2 KW - Granulocyte-Macrophage Colony-Stimulating Factor KW - 83869-56-1 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Interleukin-1 -- pharmacology KW - Spleen -- cytology KW - Interleukin-3 -- pharmacology KW - Interleukin-4 -- pharmacology KW - Interleukin-6 -- pharmacology KW - Mice KW - Granulocyte Colony-Stimulating Factor -- pharmacology KW - Granulocyte-Macrophage Colony-Stimulating Factor -- pharmacology KW - Mice, Inbred DBA KW - Cells, Cultured KW - Mice, Inbred C57BL KW - Colony-Forming Units Assay KW - Drug Synergism KW - Growth Substances -- pharmacology KW - Hematopoietic Stem Cells -- cytology KW - Cell Survival UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80734271?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Effects+of+hematopoietic+growth+factors+on+the+survival+of+primitive+stem+cells+in+liquid+suspension+culture.&rft.au=Bodine%2C+D+M%3BCrosier%2C+P+S%3BClark%2C+S+C&rft.aulast=Bodine&rft.aufirst=D&rft.date=1991-08-15&rft.volume=78&rft.issue=4&rft.spage=914&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=00064971&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-13 N1 - Date created - 1991-09-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Anti-retroviral therapy of human immunodeficiency virus infection: current strategies and challenges for the future. AN - 80733029; 1714326 JF - Blood AU - Yarchoan, R AU - Pluda, J M AU - Perno, C F AU - Mitsuya, H AU - Broder, S AD - Clinical Oncology Program, National Cancer Institute, Bethesda, MD. Y1 - 1991/08/15/ PY - 1991 DA - 1991 Aug 15 SP - 859 EP - 884 VL - 78 IS - 4 SN - 0006-4971, 0006-4971 KW - Antiviral Agents KW - 0 KW - Reverse Transcriptase Inhibitors KW - Zidovudine KW - 4B9XT59T7S KW - Zalcitabine KW - 6L3XT8CB3I KW - Didanosine KW - K3GDH6OH08 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Zidovudine -- therapeutic use KW - Acquired Immunodeficiency Syndrome -- complications KW - HIV -- drug effects KW - Humans KW - Acquired Immunodeficiency Syndrome -- drug therapy KW - Drug Resistance KW - Acquired Immunodeficiency Syndrome -- pathology KW - Didanosine -- therapeutic use KW - HIV -- physiology KW - Zidovudine -- adverse effects KW - Virus Replication -- drug effects KW - Lymphoma, Non-Hodgkin -- etiology KW - Zalcitabine -- therapeutic use KW - T-Lymphocytes, Helper-Inducer -- pathology KW - Antiviral Agents -- therapeutic use KW - HIV Infections -- complications KW - Retroviridae -- drug effects KW - Antiviral Agents -- pharmacology KW - HIV Infections -- drug therapy KW - HIV Infections -- pathology KW - Antiviral Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80733029?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Anti-retroviral+therapy+of+human+immunodeficiency+virus+infection%3A+current+strategies+and+challenges+for+the+future.&rft.au=Yarchoan%2C+R%3BPluda%2C+J+M%3BPerno%2C+C+F%3BMitsuya%2C+H%3BBroder%2C+S&rft.aulast=Yarchoan&rft.aufirst=R&rft.date=1991-08-15&rft.volume=78&rft.issue=4&rft.spage=859&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=00064971&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-13 N1 - Date created - 1991-09-13 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Blood 1991 Dec 15;78(12):3330 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differences in the regulation of intracellular calcium in normal and neoplastic keratinocytes are not caused by ras gene mutations. AN - 80731322; 1907882 AB - The development of resistance to terminal differentiation is an early event in epidermal neoplasia. Altered differentiation can be detected in vitro since normal epidermal cells are induced to differentiate in medium with Ca2+ greater than 0.1 mM while neoplastic epidermal cells and keratinocytes transduced with a v-rasHa gene are resistant to Ca2+. In normal epidermal cells, the elevation of extracellular Ca2+ (Cao) from 0.05 to 1.2 mM causes a biphasic intracellular Ca2+ (Cai) response in which a transient (10 min) peak of 4-5-fold over basal values is followed by a sustained (greater than 24 h) 2-fold increase in steady-state Cai. The transient peak in Cai is dependent on a serum component and independent of Cao, while the sustained plateau is directly dependent on Cao. The transient peak responding to a serum factor is lost in normal cells after 24 h in 1.2 mM Ca2+, a time when these cells are differentiating. Two neoplastic keratinocyte cell lines, SP-1 and 308, which produce benign tumors in vivo, also have a biphasic Cai response to an increase in Cao. In these cells, the transient peak is also serum dependent and amplified to 10-fold over basal values. However, the plateau value is not sustained and returns to basal values by 8 h, independent of Cao. Furthermore, 308 cells remain sensitive to the serum-induced Cai transient after 24 h in 1.2 mM Ca2+. To determine whether the activating c-rasHa mutation in 308 and SP-1 cells was responsible for the altered Cai regulation, a v-rasHa gene was introduced into normal keratinocytes by a defective retrovirus. This also produces the papilloma phenotype in vivo. Recipient cells were resistant to Ca(2+)-induced terminal differentiation although they did not proliferate in 1.2 mM Ca2+. The Cai profile in response to 1.2 mM Ca2+ was identical in normal and v-rasHa keratinocytes, and these cells lost the serum-induced transient Cai peak after 24 h. Thus, the activation of the c-rasHa gene in 308 or SP-1 cells is probably not solely responsible for the altered Cai response in neoplastic cell lines. Sustained physiological elevation of Cai may be relevant to the loss of proliferative potential in both normal and v-rasHa keratinocytes in 1.2 mM Ca2+. In addition, v-rasHa-mediated or activated c-rasHa-mediated changes in a complementary pathway may contribute to the block in terminal differentiation in neoplastic cells. JF - Cancer research AU - Kruszewski, F H AU - Hennings, H AU - Tucker, R W AU - Yuspa, S H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/08/15/ PY - 1991 DA - 1991 Aug 15 SP - 4206 EP - 4212 VL - 51 IS - 16 SN - 0008-5472, 0008-5472 KW - ras KW - 9,10-Dimethyl-1,2-benzanthracene KW - 57-97-6 KW - Calcium KW - SY7Q814VUP KW - Fura-2 KW - TSN3DL106G KW - Index Medicus KW - Mice, Inbred Strains KW - Animals KW - Reference Values KW - Spectrometry, Fluorescence KW - Kinetics KW - Gene Expression KW - Mice KW - Mice, Inbred BALB C KW - Cell Line KW - Skin Neoplasms -- genetics KW - Genes, ras KW - Calcium -- metabolism KW - Skin Neoplasms -- chemically induced KW - Keratinocytes -- metabolism KW - Skin Neoplasms -- metabolism KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80731322?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Differences+in+the+regulation+of+intracellular+calcium+in+normal+and+neoplastic+keratinocytes+are+not+caused+by+ras+gene+mutations.&rft.au=Kruszewski%2C+F+H%3BHennings%2C+H%3BTucker%2C+R+W%3BYuspa%2C+S+H&rft.aulast=Kruszewski&rft.aufirst=F&rft.date=1991-08-15&rft.volume=51&rft.issue=16&rft.spage=4206&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 - 1991-09-13 N1 - Date created - 1991-09-13 N1 - Date revised - 2017-01-13 N1 - Gene symbol - ras N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Randomized, double-masked study of cyclosporine compared to prednisolone in the treatment of endogenous uveitis. AN - 80729126; 1867297 AB - Fifty-six patients with bilateral sight-threatening noninfectious intermediate or posterior uveitis participated in a randomized double-masked study of the use of cyclosporine vs prednisolone in their treatment. Applying the end-point definitions, visual acuity or vitreal haze improved in only 13 of 28 (46%) patients in each group. The macular edema resolved in seven of 15 patients of the cyclosporine-treated group, and in ten of 16 patients of the prednisolone-treated group (P = .376). Patients whose therapies failed both cyclosporine and prednisolone trials were treated with both drugs, which resulted in additional patient improvements. Secondary effects were observed in both therapeutic alternatives, the most notable being alterations in serum creatinine concentration and hypertension with the dosage of cyclosporine used. JF - American journal of ophthalmology AU - Nussenblatt, R B AU - Palestine, A G AU - Chan, C C AU - Stevens, G AU - Mellow, S D AU - Green, S B AD - Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/08/15/ PY - 1991 DA - 1991 Aug 15 SP - 138 EP - 146 VL - 112 IS - 2 SN - 0002-9394, 0002-9394 KW - Cyclosporins KW - 0 KW - Prednisolone KW - 9PHQ9Y1OLM KW - Creatinine KW - AYI8EX34EU KW - Abridged Index Medicus KW - Index Medicus KW - Anterior Chamber -- drug effects KW - Double-Blind Method KW - Humans KW - Child KW - Creatinine -- blood KW - Hypertension -- chemically induced KW - Vitreous Body -- drug effects KW - Anterior Chamber -- pathology KW - Vitreous Body -- pathology KW - Visual Acuity -- drug effects KW - Adult KW - Middle Aged KW - Adolescent KW - Female KW - Male KW - Uveitis -- blood KW - Cyclosporins -- therapeutic use KW - Uveitis -- physiopathology KW - Uveitis -- drug therapy KW - Prednisolone -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80729126?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+ophthalmology&rft.atitle=Randomized%2C+double-masked+study+of+cyclosporine+compared+to+prednisolone+in+the+treatment+of+endogenous+uveitis.&rft.au=Nussenblatt%2C+R+B%3BPalestine%2C+A+G%3BChan%2C+C+C%3BStevens%2C+G%3BMellow%2C+S+D%3BGreen%2C+S+B&rft.aulast=Nussenblatt&rft.aufirst=R&rft.date=1991-08-15&rft.volume=112&rft.issue=2&rft.spage=138&rft.isbn=&rft.btitle=&rft.title=American+journal+of+ophthalmology&rft.issn=00029394&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-06 N1 - Date created - 1991-09-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparability of data obtained from farmers and surrogate respondents on use of agricultural pesticides. AN - 72053121; 1877595 AB - Information from surrogates is increasingly being used in case-control studies to evaluate cancer risks from pesticides; however, little is known about the quality of this type of information. To address this concern, the authors compared interview data collected in 1987 from 95 male Iowa farmers and their wives or other surrogates on the use of specific agricultural pesticides. Agreement between direct and surrogate interviews was excellent (83-100%) for responses to dichotomous (yes/no) questions regarding past agricultural use of specific pesticides. Although there were more discrepancies for detailed questions (e.g., the number of days per year on which each pesticide was handled), responses from spouses appear to be adequate for epidemiologic studies of pesticides and cancer. JF - American journal of epidemiology AU - Brown, L M AU - Dosemeci, M AU - Blair, A AU - Burmeister, L AD - Epidemiology and Biostatistics Program, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/08/15/ PY - 1991 DA - 1991 Aug 15 SP - 348 EP - 355 VL - 134 IS - 4 SN - 0002-9262, 0002-9262 KW - Pesticides KW - 0 KW - Index Medicus KW - Evaluation Studies as Topic KW - Reproducibility of Results KW - Aged, 80 and over KW - Humans KW - Adult KW - Case-Control Studies KW - Aged KW - Middle Aged KW - Male KW - Female KW - Occupational Exposure KW - Data Collection -- standards KW - Agriculture KW - Interviews as Topic -- standards KW - Data Collection -- methods KW - Interviews as Topic -- methods KW - Marriage KW - Pesticides -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72053121?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=unknown&rft.jtitle=Cognition&rft.atitle=Implicit+learning%3A+An+analysis+of+the+form+and+structure+of+a+body+of+tacit+knowledge&rft.au=Reber%2C+Arthur+S.%3BLewis%2C+Selma&rft.aulast=Reber&rft.aufirst=Arthur&rft.date=1977-01-01&rft.volume=5&rft.issue=4&rft.spage=333&rft.isbn=&rft.btitle=&rft.title=Cognition&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-20 N1 - Date created - 1991-09-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Blind assignment of exposure does not always prevent differential misclassification. AN - 72051530; 1877603 AB - The authors argue that one can never be certain whether an exposure variable which is measured with error is subject to differential misclassification in either a case-control study or a cohort study. They present hypothetic examples that demonstrate that even when misclassification is nondifferential in a 2 x 3 table, the observed odds ratios in the 2 x 2 table created by collapsing over two exposure levels can be either in the opposite direction from or more extreme than the odds ratio that would be obtained if exposures were classified correctly. The anomalies are explained by the observation that the 2 x 2 tables exhibit differential misclassification. In general, collapsing over categories which have different risks of disease and different probabilities of exposure misclassification can induce differential misclassification and even nonconservative estimates of relative risk. Collapsing of exposure levels can occur in the analysis or at the exposure assessment stage. Since indistinguishable categories can be collapsed implicitly, blind assessment of exposure, i.e., assignment without knowledge of disease status, does not guarantee that misclassification is nondifferential. JF - American journal of epidemiology AU - Wacholder, S AU - Dosemeci, M AU - Lubin, J H AD - Epidemiology and Biostatistics Program, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/08/15/ PY - 1991 DA - 1991 Aug 15 SP - 433 EP - 437 VL - 134 IS - 4 SN - 0002-9262, 0002-9262 KW - Index Medicus KW - Odds Ratio KW - Double-Blind Method KW - Epidemiologic Methods KW - Risk Factors KW - Humans KW - Classification KW - Cohort Studies KW - Environmental Exposure KW - Case-Control Studies KW - Observer Variation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72051530?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+epidemiology&rft.atitle=Blind+assignment+of+exposure+does+not+always+prevent+differential+misclassification.&rft.au=Wacholder%2C+S%3BDosemeci%2C+M%3BLubin%2C+J+H&rft.aulast=Wacholder&rft.aufirst=S&rft.date=1991-08-15&rft.volume=134&rft.issue=4&rft.spage=433&rft.isbn=&rft.btitle=&rft.title=American+journal+of+epidemiology&rft.issn=00029262&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-20 N1 - Date created - 1991-09-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Randomized recruitment in case-control studies. AN - 72048638; 1877602 AB - A new sampling approach for case-control studies offers a flexible alternative to frequency matching. In the "randomized recruitment" method, subjects are individually randomized to be recruited or not on the basis of investigator-imposed recruitment probabilities that can depend on both disease status and values of covariates already available or ascertained in a screening interview. When there is prior information about the odds ratios associated with the screening variables, such a design can achieve "probability matching," without the well-known disadvantages that encumber traditional matching. The method can also be used to enlarge the relative size of subsamples of interest. Following randomized recruitment, a modified logistic regression analysis allows unbiased estimation of effects associated with all variables studied, including the "matching" variables. One can also readily fit an additive model. The method is illustrated by developing the recruitment probabilities required for probability matching on age, sex, and cigarette smoking status in an ongoing study of lung cancer and exposure to radon progeny in which smoking cases are undersampled. JF - American journal of epidemiology AU - Weinberg, C R AU - Sandler, D P AD - Statistics and Biomathematics Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/08/15/ PY - 1991 DA - 1991 Aug 15 SP - 421 EP - 432 VL - 134 IS - 4 SN - 0002-9262, 0002-9262 KW - Radon KW - Q74S4N8N1G KW - Index Medicus KW - Software KW - Probability KW - Odds Ratio KW - Epidemiologic Methods KW - Humans KW - Linear Models KW - Radon -- adverse effects KW - Selection Bias KW - Registries KW - Lung Neoplasms -- epidemiology KW - Classification KW - Logistic Models KW - Connecticut -- epidemiology KW - Research Design -- standards KW - Mass Screening -- standards KW - Lung Neoplasms -- chemically induced KW - Random Allocation KW - Case-Control Studies UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72048638?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+epidemiology&rft.atitle=Randomized+recruitment+in+case-control+studies.&rft.au=Weinberg%2C+C+R%3BSandler%2C+D+P&rft.aulast=Weinberg&rft.aufirst=C&rft.date=1991-08-15&rft.volume=134&rft.issue=4&rft.spage=421&rft.isbn=&rft.btitle=&rft.title=American+journal+of+epidemiology&rft.issn=00029262&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-20 N1 - Date created - 1991-09-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Glucagon induces disaggregation of polymer-like structures of the alpha subunit of the stimulatory G protein in liver membranes. AN - 72039953; 1908089 AB - The hydrodynamic behavior of G alpha s, the alpha subunit of the stimulatory guanine nucleotide-binding regulatory protein (G protein), in octyl glucoside extracts of rat liver membranes was investigated. As was previously shown for G proteins similarly extracted from brain synaptoneurosomes, G alpha s behaved as polydisperse structures with S values higher than that of heterotrimeric G proteins. At concentrations of guanosine 5'-[gamma-thio]triphosphate (GTP[gamma S]) greater than 100 microM, incubation with membranes led to smaller structures having S values in the range of 4-5 S. Incubation of liver membranes with glucagon also caused a marked increase in structures having these S values; glucagon action required the presence of low concentrations of GTP[gamma S] (maximal, 10 microM), was rapid (within 10 sec), and was not observed with vasopressin, angiotensin II, or glucagon-(19-29). When G alpha s in its membrane-bound form was [32P]ADP-ribosylated by cholera toxin and the treated membranes were extracted with octyl glucoside, greater than 35% of the labeled G alpha s was found in material that sedimented through sucrose gradients and contained relatively low levels of immunoreactive G alpha s. Glucagon selectively converted the apparently large molecular weight structures to the 4-5 S structures in the presence of GTP[gamma S], even at 1 mM (the maximal effect of the nucleotide alone), when incubated with the toxin-treated membranes. These findings suggest that the glucagon receptor selectively interacts with polymer-like structures of G alpha s and that activation by GTP[gamma S] results in disaggregation. The role of the beta and gamma subunits of G proteins in the hormone-induced process is not clear since the polymer-like structures extracted with octyl glucoside are devoid of beta and gamma subunits. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Nakamura, S AU - Rodbell, M AD - Signal Transduction Section, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/08/15/ PY - 1991 DA - 1991 Aug 15 SP - 7150 EP - 7154 VL - 88 IS - 16 SN - 0027-8424, 0027-8424 KW - Macromolecular Substances KW - 0 KW - NAD KW - 0U46U6E8UK KW - Vasopressins KW - 11000-17-2 KW - Angiotensin II KW - 11128-99-7 KW - Guanosine 5'-O-(3-Thiotriphosphate) KW - 37589-80-3 KW - Glucagon KW - 9007-92-5 KW - Cholera Toxin KW - 9012-63-9 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Index Medicus KW - Rats KW - Centrifugation, Density Gradient KW - NAD -- metabolism KW - Animals KW - Cell Membrane -- drug effects KW - Kinetics KW - Cholera Toxin -- pharmacology KW - Vasopressins -- pharmacology KW - Cell Membrane -- metabolism KW - Angiotensin II -- pharmacology KW - Cholera Toxin -- metabolism KW - GTP-Binding Proteins -- metabolism KW - GTP-Binding Proteins -- isolation & purification KW - Glucagon -- pharmacology KW - GTP-Binding Proteins -- chemistry KW - Liver -- metabolism KW - Guanosine 5'-O-(3-Thiotriphosphate) -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72039953?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Glucagon+induces+disaggregation+of+polymer-like+structures+of+the+alpha+subunit+of+the+stimulatory+G+protein+in+liver+membranes.&rft.au=Nakamura%2C+S%3BRodbell%2C+M&rft.aulast=Nakamura&rft.aufirst=S&rft.date=1991-08-15&rft.volume=88&rft.issue=16&rft.spage=7150&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 - 1991-09-18 N1 - Date created - 1991-09-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1990 Aug;87(16):6413-7 [2117281] Biochem J. 1985 Jun 15;228(3):593-603 [3896232] Proc Natl Acad Sci U S A. 1990 May;87(10):3645-9 [2111013] Cell. 1990 Mar 23;60(6):883-5 [2138513] Nature. 1980 Mar 6;284(5751):17-22 [6101906] J Biol Chem. 1979 Jun 25;254(12):5168-76 [221464] Adv Cyclic Nucleotide Res. 1977;8:85-118 [335847] J Biol Chem. 1971 Mar 25;246(6):1877-82 [4926550] FASEB J. 1990 Nov;4(14):3178-88 [2172060] Biochim Biophys Acta. 1990 Dec 10;1055(3):265-72 [2265214] Annu Rev Biochem. 1987;56:615-49 [3113327] J Biol Chem. 1987 Mar 15;262(8):3697-705 [3102494] Biochim Biophys Acta. 1989 Feb 9;1010(2):227-32 [2536285] J Biochem. 1989 Feb;105(2):190-5 [2722765] J Biol Chem. 1990 Jun 15;265(17):9876-80 [2141022] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Oxidative modification by low levels of HOOH can transform myoglobin to an oxidase. AN - 72039715; 1871123 AB - It is generally thought that the oxidative modification of hemoproteins leads to their inactivation. In the current study, however, a transiently activated form of myoglobin was shown to be formed when the prosthetic heme group became covalently bound to the polypeptide during the reaction of myoglobin with low levels of HOOH. In the presence of an enzymatic metmyoglobin reducing system containing diaphorase and methylene blue with excess NADH, this HOOH-altered myoglobin catalyzed NADH oxidation and oxygen consumption; the overall stoichiometry indicated a two-electron reduction of oxygen to HOOH. This reaction was not catalyzed by iron released from heme, as desferrioxamine had no effect on the activity. Stoichiometric amounts of HOOH were sufficient to produce the activated oxidase state of myoglobin, whereas larger amounts of HOOH lead to heme destruction, iron release, and inactivation of the oxidase activity. The alteration of myoglobin to an enzyme that can form toxic oxygen metabolites may have pathological importance, especially in myocardial injury caused by ischemia and reperfusion, where myoglobin is present in large amounts and HOOH is formed. Furthermore, the oxidase form may be involved in the mechanism of destruction of the heme seen with oxidative treatment of myoglobin. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Osawa, Y AU - Korzekwa, K AD - Laboratory of Chemical Pharmacology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/08/15/ PY - 1991 DA - 1991 Aug 15 SP - 7081 EP - 7085 VL - 88 IS - 16 SN - 0027-8424, 0027-8424 KW - Myoglobin KW - 0 KW - NAD KW - 0U46U6E8UK KW - Hydrogen Peroxide KW - BBX060AN9V KW - Oxidoreductases KW - EC 1.- KW - Catalase KW - EC 1.11.1.6 KW - Superoxide Dismutase KW - EC 1.15.1.1 KW - Index Medicus KW - Oxidation-Reduction KW - NAD -- metabolism KW - Animals KW - Superoxide Dismutase -- pharmacology KW - Oxygen Consumption KW - Kinetics KW - Horses KW - Catalase -- pharmacology KW - Whales KW - Myocardium -- metabolism KW - Chromatography, High Pressure Liquid KW - Binding Sites KW - Oxidoreductases -- metabolism KW - Hydrogen Peroxide -- pharmacology KW - Myoglobin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72039715?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Oxidative+modification+by+low+levels+of+HOOH+can+transform+myoglobin+to+an+oxidase.&rft.au=Osawa%2C+Y%3BKorzekwa%2C+K&rft.aulast=Osawa&rft.aufirst=Y&rft.date=1991-08-15&rft.volume=88&rft.issue=16&rft.spage=7081&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 - 1991-09-18 N1 - Date created - 1991-09-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Chem Res Toxicol. 1989 May-Jun;2(3):131-41 [2519716] Biochem J. 1952 Nov;52(3):511-7 [13018268] Free Radic Res Commun. 1990;10(6):361-70 [2175284] Biochim Biophys Acta. 1990 Oct 18;1041(1):43-7 [2223846] Biochemistry. 1985 Jun 18;24(13):3254-63 [3927975] Am J Physiol. 1988 Sep;255(3 Pt 2):F539-44 [3414810] Biochem Pharmacol. 1989 Jun 1;38(11):1819-25 [2735939] J Biol Chem. 1987 Sep 15;262(26):12603-6 [3040760] Biochem Biophys Res Commun. 1986 Jul 16;138(1):193-8 [2874799] Free Radic Res Commun. 1988;4(6):415-22 [2854107] Arch Biochem Biophys. 1987 Nov 1;258(2):381-90 [2823714] Biochem J. 1987 Aug 1;245(3):925-8 [2822034] Biochem Biophys Res Commun. 1986 Aug 29;139(1):327-32 [3021127] J Biol Chem. 1987 Dec 15;262(35):16892-9 [3119593] Arch Biochem Biophys. 1986 Sep;249(2):273-85 [3092738] FEBS Lett. 1986 Jun 9;201(2):291-5 [2423372] Biochem J. 1989 Nov 1;263(3):731-6 [2557008] Semin Hematol. 1989 Apr;26(2):105-13 [2658086] Am Heart J. 1989 May;117(5):1177-88 [2653014] Free Radic Biol Med. 1989;7(1):45-52 [2753395] J Biol Chem. 1989 Jun 25;264(18):10534-41 [2732236] Lab Invest. 1988 Dec;59(6):824-30 [3199797] Biochem Pharmacol. 1987 May 1;36(9):1447-55 [3579983] Mol Pharmacol. 1990 Mar;37(3):435-42 [2314391] J Biol Chem. 1990 Jun 25;265(18):10340-6 [2355004] Cardiovasc Res. 1980 Dec;14(11):646-53 [7226174] Biochem J. 1983 Jun 15;212(3):759-72 [6882393] Int J Biochem. 1981;13(7):823-30 [6268466] Arch Biochem Biophys. 1983 Mar;221(2):417-27 [6301376] J Biol Chem. 1982 May 10;257(9):4966-77 [6279655] Biochemistry. 1978 Aug 22;17(17):3633-9 [28754] Methods Enzymol. 1978;52:342-50 [672638] Biochem J. 1977 Dec 15;168(3):417-22 [606245] J Biol Chem. 1969 Dec 25;244(24):6702-6 [4391279] Arch Biochem Biophys. 1973 Oct;158(2):842-52 [4150126] Biochim Biophys Acta. 1967 Sep 12;146(1):91-101 [4293968] J Biol Chem. 1967 Apr 25;242(8):1974-9 [4290448] Biochim Biophys Acta. 1967;146(2):397-408 [4294448] Biochemistry. 1974 Dec 3;13(25):5178-86 [4433514] Aust J Biol Sci. 1966 Feb;19(1):211-7 [5917210] Biochim Biophys Acta. 1959 Oct;35:543 [13837237] J Biol Chem. 1963 Apr;238:1520-8 [14032861] J Biol Chem. 1991 Feb 15;266(5):3208-14 [1993694] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Nonhuman primate model of alcohol abuse: effects of early experience, personality, and stress on alcohol consumption. AN - 72034488; 1871131 AB - Twenty-two 50-month-old rhesus monkeys were provided concurrent free access to an aspartame-sweetened 7% ethanol solution and an aspartame-sweetened vehicle before, during, and after social separation. Subjects had been reared for their first 6 months of life either without access to adults but with constant access to age mates (peer reared), a condition producing reduced exploration and increased fear-related behaviors, or as controls with their mothers; thereafter, all subjects received identical treatment. During home-cage periods, for 1 hr each day, 4 days a week, when the ethanol solution and vehicle were freely available, peer-reared subjects consumed significantly more alcohol than mother-reared subjects. When stress was increased via social separation, mother-reared animals increased their alcohol consumption to a level nearly as high as that of peer-reared monkeys. Average individual differences in alcohol consumption were markedly stable over time. In addition, there were strong positive correlations between alcohol consumption and distress behaviors. Biological indices of increased stress, such as plasma cortisol and corticotropin, were higher in peer-reared subjects. Within the peer- and mother-reared groups, these indices were positively correlated with alcohol consumption. The results suggest that early rearing experiences that predispose monkeys to increased fear-related behaviors produce excessive alcohol consumption under normal living conditions. Furthermore, a major challenge such as social separation increases alcohol consumption to levels producing intoxication even in monkeys not particularly vulnerable to stress. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Higley, J D AU - Hasert, M F AU - Suomi, S J AU - Linnoila, M AD - Laboratories of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism, National Institute of Child Health and Human Development, Bethesda, MD 20892. Y1 - 1991/08/15/ PY - 1991 DA - 1991 Aug 15 SP - 7261 EP - 7265 VL - 88 IS - 16 SN - 0027-8424, 0027-8424 KW - Ethanol KW - 3K9958V90M KW - Aspartame KW - Z0H242BBR1 KW - Index Medicus KW - Animals KW - Anxiety KW - Motor Activity KW - Disease Models, Animal KW - Macaca mulatta KW - Stress, Psychological KW - Personality KW - Alcoholism -- physiopathology KW - Alcohol Drinking KW - Alcoholism -- psychology KW - Behavior, Animal UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72034488?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Nonhuman+primate+model+of+alcohol+abuse%3A+effects+of+early+experience%2C+personality%2C+and+stress+on+alcohol+consumption.&rft.au=Higley%2C+J+D%3BHasert%2C+M+F%3BSuomi%2C+S+J%3BLinnoila%2C+M&rft.aulast=Higley&rft.aufirst=J&rft.date=1991-08-15&rft.volume=88&rft.issue=16&rft.spage=7261&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 - 1991-09-18 N1 - Date created - 1991-09-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Psychopharmacology (Berl). 1985;85(4):444-8 [3927341] Arch Gen Psychiatry. 1981 Aug;38(8):861-8 [7259422] Science. 1987 Apr 24;236(4800):410-6 [2882604] Alcohol Clin Exp Res. 1988 Dec;12(6):742-7 [3064633] J Clin Psychiatry. 1988 Oct;49 Suppl:17-9 [3049562] J Stud Alcohol. 1979 Jul;40(7):723-8 [491672] J Stud Alcohol. 1976 Nov;37(11):1548-55 [1003971] Psychosom Med. 1972 Mar-Apr;34(2):139-64 [5017102] J Comp Physiol Psychol. 1972 Sep;80(3):422-34 [5071897] J Pharmacol Exp Ther. 1970 May;173(1):101-16 [5442292] Ann N Y Acad Sci. 1972 May 25;197:49-53 [4504603] Am Psychol. 1989 Oct;44(10):1285-92 [2679255] Science. 1988 Apr 8;240(4849):167-71 [3353713] Am J Psychiatry. 1986 Feb;143(2):140-7 [3511739] Child Dev. 1987 Dec;58(6):1459-73 [3691195] J Abnorm Psychol. 1987 Aug;96(3):230-6 [3680762] Physiol Behav. 1987;40(5):673-6 [3671534] Physiol Behav. 1987;40(3):401-6 [3659157] J Stud Alcohol. 1987 Jan;48(1):1-8 [3821113] Pharmacol Biochem Behav. 1986 Apr;24(4):879-81 [3714781] Arch Gen Psychiatry. 1990 Jan;47(1):21-6 [2294852] Psychopharmacology (Berl). 1981;73(4):307-10 [6789348] J Stud Alcohol. 1981 Nov;42(11):918-24 [7334807] Anal Biochem. 1983 May;131(1):246-53 [6193730] J Exp Psychol Gen. 1981 Mar;110(1):56-85 [6453185] Br J Psychiatry. 1984 Jan;144:53-7 [6692076] Alcohol Clin Exp Res. 1988 Dec;12(6):780-4 [3064639] Psychopharmacology (Berl). 1987;92(2):196-205 [3110841] J Stud Alcohol. 1987 May;48(3):272-6 [3657171] Arch Gen Psychiatry. 1986 Dec;43(12):1131-6 [3778110] Psychopharmacology (Berl). 1985;86(1-2):182-9 [3927354] Drug Alcohol Depend. 1981 Apr;7(2):113-24 [7195797] J Abnorm Psychol. 1982 Oct;91(5):350-67 [7142573] J Med Primatol. 1986;15(3):183-97 [2874229] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W7) stimulation of K+ transport in a human salivary epithelial cell line. AN - 72040443; 1714731 AB - Treatment of a human salivary epithelial cell line, HSG-PA, with the calmodulin antagonist N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W7; 20-70 microM) increased 86Rb (K+) influx and efflux in a manner similar to that resulting from muscarinic (carbachol; Cch) or calcium ionophore (A23187) stimulation. Unlike the Cch or A23187 responses, the W7 responses were not blocked by 0.1 mM atropine (muscarinic antagonist) or phorbol-12-myristate-13-acetate (0.1 microM). Like Cch- or A23187-stimulated 86Rb fluxes, W7-stimulated 86Rb fluxes were substantially blocked by the K+ channel inhibitors quinine (0.25 mM) and scorpion venom-containing charybdotoxin (33 micrograms/mL), while 5 mM tetraethylammonium chloride (K+ channel blocker), furosemide (0.1 mM; Na+,K+,2Cl- co-transport inhibitor) and ouabain (10 microM; Na+,K(+)-ATPase inhibitor) were ineffective. Purified charybdotoxin (10 nM) also blocked W7-stimulated 86Rb influx, as well as 86Rb influx stimulated by Cch or A23187. Although Quin 2 fluorescence measurements indicated that W7 increased free intracellular Ca2+ concentration ([Ca2+]i), the magnitude of the increase appeared to be insufficient to solely account for the W7-stimulated increases in 86Rb fluxes (i.e. K+ channel activity). Ca2+ was involved in the W7 response, however, as lack of Ca2+ in the incubation medium reduced the W7-stimulated increases in 86Rb influx and efflux. Taken together, our results suggest that W7 increased K+ fluxes in HSG-PA cells by interacting, directly or indirectly, with the K+ transport machinery (K+ channels) in a manner different from that observed during muscarinic stimulation, and also in a manner not accounted for solely by the formation of a typical muscarinic- or calcium ionophore-generated calcium signal. JF - Biochemical pharmacology AU - Patton, L AU - Ship, J AU - Wellner, R AD - Clinical Investigations and Patient Care Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/08/08/ PY - 1991 DA - 1991 Aug 08 SP - 1039 EP - 1044 VL - 42 IS - 5 SN - 0006-2952, 0006-2952 KW - Aminoquinolines KW - 0 KW - Calmodulin KW - Potassium Channels KW - Rubidium Radioisotopes KW - Scorpion Venoms KW - Sulfonamides KW - Charybdotoxin KW - 115422-61-2 KW - W 7 KW - 65595-90-6 KW - Quin2 KW - O448IDK23O KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Calcium -- metabolism KW - Scorpion Venoms -- pharmacology KW - Dose-Response Relationship, Drug KW - Humans KW - Cell Line -- drug effects KW - Epithelium -- drug effects KW - Biological Transport -- drug effects KW - Aminoquinolines -- pharmacology KW - Potassium Channels -- metabolism KW - Salivary Glands -- drug effects KW - Sulfonamides -- antagonists & inhibitors KW - Sulfonamides -- pharmacology KW - Calmodulin -- antagonists & inhibitors KW - Salivary Glands -- metabolism KW - Potassium Channels -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72040443?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=N-%286-aminohexyl%29-5-chloro-1-naphthalenesulfonamide+%28W7%29+stimulation+of+K%2B+transport+in+a+human+salivary+epithelial+cell+line.&rft.au=Patton%2C+L%3BShip%2C+J%3BWellner%2C+R&rft.aulast=Patton&rft.aufirst=L&rft.date=1991-08-08&rft.volume=42&rft.issue=5&rft.spage=1039&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 - 1991-09-16 N1 - Date created - 1991-09-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Molecular epidemiology and the genetics of environmental cancer. AN - 80688154; 2072479 AB - Environmental, occupational, and recreational exposures to carcinogens contribute to cancer risk in humans. Cancer formation is a multistage process involving tumor initiation, promotion, conversion, and progression. Carcinogens can affect any of these stages through genetic and epigenetic mechanisms. The association of a suspected carcinogenic exposure and cancer risk can be studied in populations with classic epidemiologic techniques. However, these techniques are not applicable to the assessment of risk in individuals. Molecular epidemiology, in contrast, is a field that integrates molecular biology, in vitro and in vivo laboratory models, biochemistry, and epidemiology to infer individual cancer risk. Carcinogen-macromolecular adduct levels, and somatic cell mutations can be measured to determine the biologically effective dose of a carcinogen. Molecular epidemiology also explores host cancer susceptibilities, such as carcinogen metabolic activation, DNA repair, endogenous mutation rates, and inheritance of mutated tumor suppressor genes. Substantial interindividual variation for each of these biologic end points has been shown and, therefore, highlights the need for assessing cancer risk on an individual basis. Given the pace of the last decade, it is feasible that the next 10 years will allow molecular epidemiologists to develop a cancer-risk profile for an individual that includes assessment of a number of factors. This will help focus preventive strategies and strengthen quantitative risk assessments. JF - JAMA AU - Shields, P G AU - Harris, C C AD - Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/08/07/ PY - 1991 DA - 1991 Aug 07 SP - 681 EP - 687 VL - 266 IS - 5 SN - 0098-7484, 0098-7484 KW - Carcinogens, Environmental KW - 0 KW - DNA KW - 9007-49-2 KW - Abridged Index Medicus KW - Index Medicus KW - Environmental Monitoring KW - Risk KW - Disease Susceptibility KW - Humans KW - DNA -- metabolism KW - Epidemiological Monitoring KW - Cell Transformation, Neoplastic -- genetics KW - DNA -- drug effects KW - Carcinogens, Environmental -- adverse effects KW - Neoplasms -- chemically induced KW - Neoplasms -- epidemiology KW - Carcinogens, Environmental -- metabolism KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80688154?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Molecular+epidemiology+and+the+genetics+of+environmental+cancer.&rft.au=Shields%2C+P+G%3BHarris%2C+C+C&rft.aulast=Shields&rft.aufirst=P&rft.date=1991-08-07&rft.volume=266&rft.issue=5&rft.spage=681&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-22 N1 - Date created - 1991-08-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparison of protein synthesis inhibition kinetics and cell killing induced by immunotoxins. AN - 80712845; 1860832 AB - Immunotoxins comprised of a monoclonal antibody covalently coupled to recombinant ricin A chain or to a binding-defective form of diphtheria toxin were compared with respect to their rates of protein synthesis inhibition and efficiencies of killing target cells. Protein synthesis inhibition rates were established by measuring the incorporation of L-[14C]leucine in toxin-treated cells relative to untreated cells at several times after exposure of cells to an immunotoxin. Cell killing was assessed by a limiting dilution assay which measures the number of cells surviving toxin treatment relative to untreated cells. At equivalent protein concentrations, the diphtheria toxin immunotoxin inhibited protein synthesis significantly more rapidly than the ricin A immunotoxin but, contrary to previous predictions, achieved a significantly lower cell kill. Thus, the kinetics of protein synthesis inactivation do not necessarily correlate with killing efficiencies. Possible explanations for these results are that the effect of the diphtheria toxin immunotoxin on protein synthesis is partially reversible or that the diphtheria toxin immunotoxin enters the cytosol at a faster rate than the ricin A immunotoxin but also is degraded at a faster rate. JF - The Journal of biological chemistry AU - Sung, C AU - Wilson, D AU - Youle, R J AD - Chemical Engineering Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/08/05/ PY - 1991 DA - 1991 Aug 05 SP - 14159 EP - 14162 VL - 266 IS - 22 SN - 0021-9258, 0021-9258 KW - Antibodies, Monoclonal KW - 0 KW - Diphtheria Toxin KW - Immunotoxins KW - Protein Synthesis Inhibitors KW - Ricin KW - 9009-86-3 KW - Index Medicus KW - Kinetics KW - Antibodies, Monoclonal -- immunology KW - Ricin -- toxicity KW - Immunotoxins -- toxicity KW - Cell Survival -- drug effects KW - Diphtheria Toxin -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80712845?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+protein+synthesis+inhibition+kinetics+and+cell+killing+induced+by+immunotoxins.&rft.au=Sung%2C+C%3BWilson%2C+D%3BYoule%2C+R+J&rft.aulast=Sung&rft.aufirst=C&rft.date=1991-08-05&rft.volume=266&rft.issue=22&rft.spage=14159&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 - 1991-09-04 N1 - Date created - 1991-09-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Trans-1-aminocyclopentane-1,3-dicarboxylic acid (t-ACPD) decreases synaptic excitation in rat striatal slices through a presynaptic action. AN - 72145672; 1656337 AB - Excitatory synaptic transmission was decreased in the presence of trans-1-aminocyclopentane-1,3-dicarboxylic acid (t-ACPD) during whole-cell recordings from striatal slices. This effect of t-ACPD increased in a concentration-dependent manner at drug concentrations from 5-100 microM. Decreased transmission appeared to result from a presynaptic effect as indicated by the observations that: (1) t-ACPD decreased the amplitude of excitatory postsynaptic potentials (EPSPs) mediated by either quisqualate alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA) or N-methyl-D-aspartate (NMDA) receptors, but did not block responses to agonist application; indicating that t-ACPD is not a glutamate receptor antagonist; (2) t-ACPD decreased transmission in the absence of changes in postsynaptic cell properties. The t-ACPD-activated receptor appears to differ from previously identified presynaptic receptors. These findings indicate that t-ACPD activates a presynaptic receptor; most likely a glutamate receptor. JF - Neuroscience letters AU - Lovinger, D M AD - Section of Electrophysiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20852. Y1 - 1991/08/05/ PY - 1991 DA - 1991 Aug 05 SP - 17 EP - 21 VL - 129 IS - 1 SN - 0304-3940, 0304-3940 KW - Neurotoxins KW - 0 KW - Receptors, AMPA KW - Receptors, N-Methyl-D-Aspartate KW - Receptors, Neurotransmitter KW - Cycloleucine KW - 0TQU7668EI KW - 1-amino-1,3-dicarboxycyclopentane KW - 111900-32-4 KW - Index Medicus KW - Rats KW - Animals KW - Receptors, N-Methyl-D-Aspartate -- drug effects KW - In Vitro Techniques KW - Receptors, Neurotransmitter -- drug effects KW - Membrane Potentials -- drug effects KW - Male KW - Hippocampus -- drug effects KW - Synapses -- physiology KW - Corpus Striatum -- physiology KW - Synapses -- drug effects KW - Cycloleucine -- pharmacology KW - Cycloleucine -- analogs & derivatives KW - Neurotoxins -- pharmacology KW - Corpus Striatum -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72145672?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Trans-1-aminocyclopentane-1%2C3-dicarboxylic+acid+%28t-ACPD%29+decreases+synaptic+excitation+in+rat+striatal+slices+through+a+presynaptic+action.&rft.au=Lovinger%2C+D+M&rft.aulast=Lovinger&rft.aufirst=D&rft.date=1991-08-05&rft.volume=129&rft.issue=1&rft.spage=17&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 - 1991-11-05 N1 - Date created - 1991-11-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Crystal structure of a Y35G mutant of bovine pancreatic trypsin inhibitor. AN - 72037491; 1714504 AB - The structure of a Y35G mutant of bovine pancreatic trypsin inhibitor (BPTI) was solved by molecular replacement and was refined by both simulated annealing and restrained least-squares at 1.8 A resolution. The crystals belong to the space group P42212, with unit cell dimensions a = b = 46.75 A, c = 50.61 A. The final R-factor is 0.159 and the deviation from ideality for bond distances is 0.02 A. The structure of the mutant differs from that of the native protein, showing an overall root-mean-square (r.m.s.) difference of 1.86 A for main-chain atoms. However, the change is mostly localized in the two loops (respective r.m.s. values of 2.04 A and 3.93 A) and the C terminus (r.m.s. 6.79 A), while the core of the protein is well conserved (r.m.s. 0.45 A). The change in the loop regions can be clearly attributed to the mutation while the difference in the C terminus might be only due to a different crystal packing. Seventy water molecules were included in the model but only seven of them are shared with the native structure. Thermal parameters are showing a good correlation with those for the wild-type of BPTI. JF - Journal of molecular biology AU - Housset, D AU - Kim, K S AU - Fuchs, J AU - Woodward, C AU - Wlodawer, A AD - Macromolecular Structure Laboratory, NCI-Frederick Cancer Research and Development Center, MD 21702. Y1 - 1991/08/05/ PY - 1991 DA - 1991 Aug 05 SP - 757 EP - 770 VL - 220 IS - 3 SN - 0022-2836, 0022-2836 KW - Disulfides KW - 0 KW - Recombinant Proteins KW - Solutions KW - Aprotinin KW - 9087-70-1 KW - Index Medicus KW - Animals KW - Disulfides -- analysis KW - Cattle KW - X-Ray Diffraction -- methods KW - Computer Simulation KW - Models, Molecular KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Recombinant Proteins -- chemistry KW - Protein Conformation KW - Mutagenesis, Site-Directed KW - Aprotinin -- genetics KW - Aprotinin -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72037491?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+molecular+biology&rft.atitle=Crystal+structure+of+a+Y35G+mutant+of+bovine+pancreatic+trypsin+inhibitor.&rft.au=Housset%2C+D%3BKim%2C+K+S%3BFuchs%2C+J%3BWoodward%2C+C%3BWlodawer%2C+A&rft.aulast=Housset&rft.aufirst=D&rft.date=1991-08-05&rft.volume=220&rft.issue=3&rft.spage=757&rft.isbn=&rft.btitle=&rft.title=Journal+of+molecular+biology&rft.issn=00222836&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-13 N1 - Date created - 1991-09-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Protection and potentiation of MPTP-induced toxicity by cytochrome P-450 inhibitors and inducer: in vitro studies with brain slices. AN - 72170432; 1933335 AB - Exposure to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) causes loss of dopaminergic neurons in humans, primates and mice. Exposure of sagittal slices of mouse brain to MPTP (100 pM) caused inhibition of mitochondrial NADH-dehydrogenase activity. Leakage of lactate dehydrogenase from the slice into the medium was observed following incubation of slices with 1 nM MPTP. Neurotoxicity induced by MPTP was prevented by prior exposure of the slices to the dopamine uptake inhibitor GBR 12935. Deprenyl and pargyline (inhibitors of monoamine oxidase), also protected the slices from MPTP-induced toxicity. However, both pargyline and deprenyl also inhibited cytochrome P-450 mediated aminopyrine N-demethylase activity in brain slices. Pargyline, when administered in vivo to mice, decreased brain cytochrome P-450 levels significantly. Other cytochrome P-450 inhibitors, namely, piperonyl butoxide and SKF 525A were found to offer protection against MPTP induced neurotoxicity in slices without affecting monoamine oxidase activity. MPTP toxicity was potentiated significantly in brain slices prepared from mice pretreated with phenobarbital, an inducer of cytochrome P-450. The present study suggests the possible involvement of cytochrome P-450 in MPTP-induced neurotoxicity, in vitro, in brain slices. JF - Brain research AU - Pai, K S AU - Ravindranath, V AD - Department of Neurochemistry, National Institute of Mental Health and Neuro Sciences, Bangalore, India. Y1 - 1991/08/02/ PY - 1991 DA - 1991 Aug 02 SP - 239 EP - 244 VL - 555 IS - 2 SN - 0006-8993, 0006-8993 KW - Cytochrome P-450 Enzyme Inhibitors KW - 0 KW - Monoamine Oxidase Inhibitors KW - Piperazines KW - Selegiline KW - 2K1V7GP655 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - 1-(2 (diphenylmethoxy)ethyl)-4-(3-phenylpropyl)piperazine KW - 9J9974WIBA KW - Pargyline KW - 9MV14S8G3E KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Proadifen KW - A510CA4CBT KW - Mixed Function Oxygenases KW - EC 1.- KW - L-Lactate Dehydrogenase KW - EC 1.1.1.27 KW - NADPH-Ferrihemoprotein Reductase KW - EC 1.6.2.4 KW - Piperonyl Butoxide KW - LWK91TU9AH KW - Phenobarbital KW - YQE403BP4D KW - Index Medicus KW - Animals KW - NADPH-Ferrihemoprotein Reductase -- antagonists & inhibitors KW - NADPH-Ferrihemoprotein Reductase -- metabolism KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Mice KW - Piperazines -- pharmacology KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- antagonists & inhibitors KW - Monoamine Oxidase Inhibitors -- pharmacology KW - Piperonyl Butoxide -- pharmacology KW - Selegiline -- pharmacology KW - Proadifen -- pharmacology KW - Phenobarbital -- pharmacology KW - Mixed Function Oxygenases -- metabolism KW - Enzyme Induction -- drug effects KW - Mixed Function Oxygenases -- antagonists & inhibitors KW - Pargyline -- pharmacology KW - In Vitro Techniques KW - L-Lactate Dehydrogenase -- antagonists & inhibitors KW - L-Lactate Dehydrogenase -- metabolism KW - Male KW - Brain -- enzymology KW - MPTP Poisoning KW - Brain -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72170432?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Protection+and+potentiation+of+MPTP-induced+toxicity+by+cytochrome+P-450+inhibitors+and+inducer%3A+in+vitro+studies+with+brain+slices.&rft.au=Pai%2C+K+S%3BRavindranath%2C+V&rft.aulast=Pai&rft.aufirst=K&rft.date=1991-08-02&rft.volume=555&rft.issue=2&rft.spage=239&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 - 1991-12-23 N1 - Date created - 1991-12-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Nodular regenerative hyperplasia of the liver in idiopathic hypereosinophilic syndrome. AN - 85201216; pmid-1918853 AB - We report a 52-year-old man with idiopathic hypereosinophilic syndrome and nodular regenerative hyperplasia of the liver. We postulate that nodular regenerative hyperplasia may be the result of an eosinophil-induced vascular lesion. JF - Journal of Clinical Gastroenterology AU - Baker, B L AU - Axiotis, C AU - Hurwitz, E S AU - Leavitt, R AU - Di Bisceglie A M AD - Liver Diseases Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institute of Health, Bethesda, MD 20892. PY - 1991 SP - 452 EP - 456 VL - 13 IS - 4 SN - 0192-0790, 0192-0790 KW - Hyperplasia KW - Human KW - Esophageal and Gastric Varices KW - Liver KW - Middle Age KW - Case Report KW - Liver Regeneration KW - Eosinophilia KW - Male UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85201216?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Clinical+Gastroenterology&rft.atitle=Nodular+regenerative+hyperplasia+of+the+liver+in+idiopathic+hypereosinophilic+syndrome.&rft.au=Baker%2C+B+L%3BAxiotis%2C+C%3BHurwitz%2C+E+S%3BLeavitt%2C+R%3BDi+Bisceglie+A+M&rft.aulast=Baker&rft.aufirst=B&rft.date=1991-08-01&rft.volume=13&rft.issue=4&rft.spage=452&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Gastroenterology&rft.issn=01920790&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Mouse bronchiolar cell carcinogenesis. Histologic characterization and expression of Clara cell antigen in lesions induced by N-nitrosobis-(2-chloroethyl) ureas. AN - 80728971; 1651059 AB - Female Swiss mice (Cr:NIH(S)) developed bronchiolar cell hyperplasia, dysplasia, metaplasia, and various morphologic types of bronchiolar cell tumors after topical (skin) application of N-nitroso-methyl-bis-chloroethylurea (NMBCU) or N-nitroso-tris-chloroethylurea (NTCU). These compounds are the first found to induce systemically bronchiolar cell tumors in mice in high incidence. Twice a week, with a 3-day interval, a 25-microliter drop of 0.04 mol/l (molar) NMBCU or NTCU in acetone was applied to the shaved interscapular integument for a maximum of 35 to 40 weeks. The earliest lung neoplasms were seen in mice that died after 23 weeks of treatment and affected 11 of 19 with NMBCU and 14 of 19 with NTCU treatment. Tumor growth pattern was nodular or the neoplastic tissue was frequently disseminated throughout the parenchyma, starting from multicentric peribronchiolar foci. The most common tumor types were squamous cell carcinomas and adenosquamous carcinomas, followed by adenocarcinomas with or without secretory cells, and a single ciliated-cell tumor. Histochemical and immunohistochemical studies were carried out on paraffin-embedded lungs using the avidin-biotin immunoperoxidase complex procedure and antisera against keratin, Clara cell antigen, surfactant apoprotein, neuron-specific enolase, bombesin, and chromogranin A. In several mice from both groups, hyperplasias and tumors were composed of cells expressing Clara cell antigen. No tumor cells were found expressing alveolar type II or neuroendocrine cell markers. It appeared that bronchiolar cells, in particular Clara cells, had migrated from terminal bronchioles or invaded bronchiolar walls to extend into the alveolar parenchyma. Squamous cell metaplasia with keratin expression was seen within airways or associated with glandular tumors, especially at the periphery. A unique cell type, with large eosinophilic globules and associated eosinophilic crystals, was seen lining airways or forming hyperplastic and neoplastic lesions. N-nitroso-methyl-bis-chloroethylurea- and NTCU-induced mouse bronchiolar cell alterations could be an interesting new model to study mechanisms of bronchiolar cell differentiation and tumor formation. JF - The American journal of pathology AU - Rehm, S AU - Lijinsky, W AU - Singh, G AU - Katyal, S L AD - Division of Cancer Etiology, National Cancer Institute, Frederick, Maryland 21702-1201. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 413 EP - 422 VL - 139 IS - 2 SN - 0002-9440, 0002-9440 KW - N-nitroso-tris-chloroethylurea KW - 0 KW - Nitrosourea Compounds KW - Proteins KW - Scgb1a1 protein, mouse KW - Uteroglobin KW - 9060-09-7 KW - Carmustine KW - U68WG3173Y KW - Abridged Index Medicus KW - Index Medicus KW - Mice, Inbred Strains KW - Animals KW - Carcinoma, Squamous Cell -- immunology KW - Carcinoma, Squamous Cell -- pathology KW - Metaplasia KW - Mice KW - Immunohistochemistry KW - Female KW - Adenocarcinoma, Bronchiolo-Alveolar -- chemically induced KW - Adenocarcinoma, Bronchiolo-Alveolar -- pathology KW - Lung Neoplasms -- immunology KW - Carmustine -- analogs & derivatives KW - Proteins -- analysis KW - Lung Neoplasms -- chemically induced KW - Adenocarcinoma, Bronchiolo-Alveolar -- immunology KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80728971?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mouse+bronchiolar+cell+carcinogenesis.+Histologic+characterization+and+expression+of+Clara+cell+antigen+in+lesions+induced+by+N-nitrosobis-%282-chloroethyl%29+ureas.&rft.au=Rehm%2C+S%3BLijinsky%2C+W%3BSingh%2C+G%3BKatyal%2C+S+L&rft.aulast=Rehm&rft.aufirst=S&rft.date=1991-08-01&rft.volume=139&rft.issue=2&rft.spage=413&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 - 1991-09-06 N1 - Date created - 1991-09-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Arch Pathol. 1961 Jun;71:693-713 [13703918] Cancer Res. 1968 Nov;28(11):2197-210 [5723964] Toxicol Pathol. 1991;19(1):35-46 [2047706] Am J Pathol. 1990 Oct;137(4):833-43 [2221015] J Histochem Cytochem. 1987 Jul;35(7):789-94 [2438324] J Histochem Cytochem. 1988 Jan;36(1):73-80 [3275712] Ultrastruct Pathol. 1985;9(3-4):283-318 [3003994] J Pathol. 1988 Jul;155(3):231-40 [2457672] Am J Clin Pathol. 1987 Oct;88(4):472-7 [2821793] Am J Pathol. 1989 Jan;134(1):79-87 [2464284] J Cancer Res Clin Oncol. 1988;114(3):245-9 [3384841] Carcinogenesis. 1988 Feb;9(2):293-6 [3338113] Cancer Res. 1988 Jan 1;48(1):148-60 [3334989] Exp Lung Res. 1984;6(3-4):175-89 [6548441] Vet Pathol. 1987 May;24(3):216-25 [3300004] J Thorac Cardiovasc Surg. 1986 Nov;92(5):880-9 [3773544] Am J Pathol. 1986 Apr;123(1):126-33 [3963147] Am J Pathol. 1985 Mar;118(3):493-9 [3883798] Lab Anim. 1985 Jul;19(3):224-35 [4033063] Prog Exp Tumor Res. 1963;3:186-215 [14148380] Am J Pathol. 1985 Apr;119(1):168-70 [3985122] Vet Pathol. 1990 Jul;27(4):274-81 [2169666] Am J Surg Pathol. 1990 May;14(5):464-73 [2158243] Arch Pathol Lab Med. 1984 Jan;108(1):44-8 [6318684] Cancer Res. 1980 Nov;40(11):4301-7 [6258778] J Histochem Cytochem. 1984 Jan;32(1):49-54 [6418790] Cancer Res. 1981 Dec;41(12 Pt 1):5027-32 [7307005] Am J Pathol. 1981 May;103(2):174-80 [7234960] Lab Invest. 1976 Dec;35(6):558-68 [62893] Lab Invest. 1979 May;40(5):562-7 [374864] J Cancer Res Clin Oncol. 1979 Jun 8;94(2):131-7 [468904] Lab Invest. 1979 Jun;40(6):708-16 [449277] Vet Pathol. 1978 Mar;15(2):170-8 [664185] Eur J Cancer. 1977 Nov;13(11):1325-40 [590290] Adv Cancer Res. 1975;21:1-58 [1108612] Lab Invest. 1972 Feb;26(2):210-9 [5059985] Arch Pathol Lab Med. 1976 Mar;100(3):147-53 [946402] J Natl Cancer Inst. 1971 Sep;47(3):697-701 [5157586] Exp Lung Res. 1991 Mar-Apr;17(2):229-44 [1646707] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A transduction pathway associated with receptors coupled to the inhibitory guanine nucleotide binding protein Gi that amplifies ATP-mediated arachidonic acid release. AN - 80717639; 1650470 AB - ATP is copackaged and coreleased with adrenergic, serotonergic, and cholinergic neurotransmitters, suggesting a possible interaction between the signaling pathways for ATP and these coreleased neurotransmitters. Muscarinic m2 and m4, alpha 2-adrenergic, and D2-dopaminergic neurotransmitter receptors, which have in common their ability to inhibit adenylate cyclase through the inhibitory guanine nucleotide binding protein Gi, were transfected and expressed in Chinese hamster ovary (CHO) cells that contain endogenous ATP receptors coupled to the release of arachidonic acid. Normal functional coupling of m2, m4, alpha 2, and D2 receptors was demonstrated by their ability to inhibit forskolin-stimulated cAMP accumulation with dose-response activities consistent with previous reports for these Gi-coupled receptors. Stimulation of m2, m4, alpha 2, and D2 receptors resulted in an augmentation of ATP-stimulated arachidonic acid release. With the exception of the m4 receptor, none of the receptors tested was able to stimulate arachidonic acid release in the absence of ATP. Potentiation of ATP-stimulated arachidonic acid release was independent of changes in cAMP. The augmentation of ATP-stimulated arachidonic acid release and the inhibition of cAMP accumulation were both blocked by pertussis toxin, an inhibitor of Gi, but with different dose-response characteristics. Inhibition of protein kinase C with staurosporine or long-term pretreatment of the cells with the phorbol ester phorbol 12-myristate 13-acetate blocked the augmentation response. This demonstrates that Gi-coupled inhibitory receptors can amplify ATP-receptor-stimulated arachidonic acid release through a pertussis-toxin-sensitive G protein, independent of their ability to inhibit adenylate cyclase activity. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Felder, C C AU - Williams, H L AU - Axelrod, J AD - Laboratory of Cell Biology, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1991/08/01/ PY - 1991 DA - 1991 Aug 01 SP - 6477 EP - 6480 VL - 88 IS - 15 SN - 0027-8424, 0027-8424 KW - Adenylate Cyclase Toxin KW - 0 KW - Alkaloids KW - Arachidonic Acids KW - Receptors, Adrenergic, alpha KW - Receptors, Dopamine KW - Receptors, Dopamine D2 KW - Receptors, Muscarinic KW - Receptors, Purinergic KW - Recombinant Proteins KW - Virulence Factors, Bordetella KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Carbachol KW - 8Y164V895Y KW - Cyclic AMP KW - E0399OZS9N KW - Pertussis Toxin KW - EC 2.4.2.31 KW - Protein Kinase C KW - EC 2.7.11.13 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Staurosporine KW - H88EPA0A3N KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Receptors, Dopamine -- drug effects KW - Receptors, Muscarinic -- genetics KW - Animals KW - Receptors, Dopamine -- genetics KW - Receptors, Adrenergic, alpha -- drug effects KW - Receptors, Adrenergic, alpha -- genetics KW - Virulence Factors, Bordetella -- pharmacology KW - Receptors, Dopamine -- physiology KW - Protein Kinase C -- antagonists & inhibitors KW - Transfection KW - Recombinant Proteins -- metabolism KW - Cyclic AMP -- metabolism KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Receptors, Muscarinic -- drug effects KW - Alkaloids -- pharmacology KW - Receptors, Muscarinic -- physiology KW - Carbachol -- pharmacology KW - Receptors, Adrenergic, alpha -- physiology KW - Cell Line KW - Receptors, Purinergic -- genetics KW - Receptors, Purinergic -- physiology KW - Adenosine Triphosphate -- metabolism KW - GTP-Binding Proteins -- physiology KW - Arachidonic Acids -- metabolism KW - Receptors, Purinergic -- drug effects KW - Signal Transduction KW - Adenosine Triphosphate -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80717639?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=A+transduction+pathway+associated+with+receptors+coupled+to+the+inhibitory+guanine+nucleotide+binding+protein+Gi+that+amplifies+ATP-mediated+arachidonic+acid+release.&rft.au=Felder%2C+C+C%3BWilliams%2C+H+L%3BAxelrod%2C+J&rft.aulast=Felder&rft.aufirst=C&rft.date=1991-08-01&rft.volume=88&rft.issue=15&rft.spage=6477&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 - 1991-09-04 N1 - Date created - 1991-09-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Trends Pharmacol Sci. 1990 Sep;11(9):367-73 [2122564] J Biol Chem. 1990 May 25;265(15):8369-72 [2341388] Trends Neurosci. 1988 Mar;11(3):117-23 [2465609] Science. 1987 Oct 30;238(4827):672-5 [2823384] Mol Pharmacol. 1991 Mar;39(3):364-9 [1848657] Nature. 1990 Sep 27;347(6291):386-8 [1977083] FEBS Lett. 1991 Jan 14;278(1):45-50 [1704314] J Pharmacol Exp Ther. 1990 Dec;255(3):1140-7 [2124620] J Biol Chem. 1988 Feb 25;263(6):2577-80 [2830256] Proc Natl Acad Sci U S A. 1986 Oct;83(19):7201-5 [3020540] J Biol Chem. 1989 Dec 5;264(34):20356-62 [2555356] Methods Enzymol. 1988;159:159-72 [2842582] Annu Rev Neurosci. 1987;10:195-236 [2436543] J Biol Chem. 1986 Sep 5;261(25):11608-12 [3017936] Biochem J. 1986 Jan 15;233(2):309-19 [3006665] Science. 1987 Jul 31;237(4814):527-32 [3037705] Nature. 1989 Dec 21-28;342(6252):926-9 [2480527] Nature. 1989 Oct 26;341(6244):739-42 [2571939] J Biol Chem. 1989 Sep 5;264(25):14848-52 [2549039] J Biol Chem. 1986 Sep 25;261(27):12604-9 [3462188] Science. 1990 Aug 10;249(4969):662-6 [2166341] Nature. 1990 Sep 13;347(6289):182-4 [1975645] J Biol Chem. 1990 Jun 25;265(18):10320-6 [2162345] Biochem J. 1989 Nov 1;263(3):715-23 [2512911] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Oxathiin carboxanilide, a potent inhibitor of human immunodeficiency virus reproduction. AN - 80716812; 1713689 AB - Oxathiin carboxanilide (OC), NSC 615985, a compound originally synthesized as a potential fungicide, was demonstrated to be highly active in preventing human immunodeficiency virus (HIV)-induced cell killing and in inhibiting HIV reproduction. Virus-infected CD4+ lymphocytes were completely protected by 0.5 microM OC, whereas no toxicity was observed at concentrations below 50 microM OC. Production of infectious virus, viral p24 antigen, and virion reverse transcriptase were reduced by OC at concentrations that prevented viral cell killing. A variety of CD4+ T-cell lines were protected by OC from HIV cytopathicity, and OC inhibited two distinct strains of HIV-1. However, HIV-2 infections were unaffected by OC. OC had no direct effect on virions of HIV or on the enzymatic activities of HIV reverse transcriptase or HIV protease. Time-limited treatments of cells with OC before, during, or after exposure of cells to virus failed to protect cells from the eventual cytopathic effects of HIV, and OC failed to inhibit the production of virus from cells in which infection was established or from chronically infected cells. We conclude that the highly active OC has a reversible effect on some early stage of HIV-1 reproduction and cytopathicity. Pilot in vivo experiments showed that circulating concentrations of OC exceeding 1 microM could be achieved and sustained in hamsters for at least a week with no remarkable toxicological sequelae. OC represents a new class of anti-HIV agents that are promising candidates for drug development. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Bader, J P AU - McMahon, J B AU - Schultz, R J AU - Narayanan, V L AU - Pierce, J B AU - Harrison, W A AU - Weislow, O S AU - Midelfort, C F AU - Stinson, S F AU - Boyd, M R AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/08/01/ PY - 1991 DA - 1991 Aug 01 SP - 6740 EP - 6744 VL - 88 IS - 15 SN - 0027-8424, 0027-8424 KW - Antigens, CD4 KW - 0 KW - Antiviral Agents KW - HIV Protease Inhibitors KW - NSC 615985 KW - Reverse Transcriptase Inhibitors KW - Carboxin KW - 5A8K850HDE KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Antigens, CD4 -- analysis KW - Humans KW - Drug Evaluation, Preclinical KW - Cell Line KW - Cricetinae KW - Carboxin -- toxicity KW - Virus Replication -- drug effects KW - Carboxin -- pharmacology KW - Antiviral Agents -- pharmacology KW - HIV-1 -- enzymology KW - HIV-1 -- physiology KW - Carboxin -- analogs & derivatives KW - HIV-1 -- drug effects KW - Carboxin -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80716812?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Oxathiin+carboxanilide%2C+a+potent+inhibitor+of+human+immunodeficiency+virus+reproduction.&rft.au=Bader%2C+J+P%3BMcMahon%2C+J+B%3BSchultz%2C+R+J%3BNarayanan%2C+V+L%3BPierce%2C+J+B%3BHarrison%2C+W+A%3BWeislow%2C+O+S%3BMidelfort%2C+C+F%3BStinson%2C+S+F%3BBoyd%2C+M+R&rft.aulast=Bader&rft.aufirst=J&rft.date=1991-08-01&rft.volume=88&rft.issue=15&rft.spage=6740&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 - 1991-09-04 N1 - Date created - 1991-09-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Virology. 1965 Jun;26:253-61 [14323993] Lancet. 1968 Mar 16;1(7542):575-6 [4170280] Biochem Biophys Res Commun. 1989 Feb 28;159(1):87-94 [2647085] N Engl J Med. 1987 Jul 23;317(4):185-91 [3299089] Biochem Pharmacol. 1987 Nov 15;36(22):3797-800 [3120727] Proc Natl Acad Sci U S A. 1989 Jun;86(11):4244-8 [2471199] Science. 1989 Mar 31;243(4899):1731-4 [2467383] Antimicrob Agents Chemother. 1988 Dec;32(12):1784-7 [2469387] Nature. 1987 Aug 20-26;328(6132):728-30 [2441266] J Acquir Immune Defic Syndr. 1989;2(4):311-34 [2666638] Lancet. 1988 Jan 16;1(8577):76-81 [2891981] N Engl J Med. 1987 Jul 23;317(4):192-7 [3299090] Science. 1990 Jan 26;247(4941):454-6 [2405486] AIDS Res Hum Retroviruses. 1990 Jun;6(6):753-64 [1694680] Nature. 1990 Feb 1;343(6257):470-4 [1689015] Science. 1984 May 4;224(4648):500-3 [6200936] Science. 1983 May 20;220(4599):868-71 [6189183] J Natl Cancer Inst. 1989 Apr 19;81(8):577-86 [2495366] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Protein kinase C redistribution within CA3 stratum oriens during acquisition of nictitating membrane conditioning in the rabbit. AN - 80716399; 1862086 AB - This manuscript describes experiments designed to investigate protein kinase C redistribution occurring during acquisition of the rabbit nictitating membrane (NM) conditioned response (CR). The first experiment defined the acquisition phase of the NM response for our laboratory. A group of rabbits (n = 6) was given 2 days of paired NM training; a second group (n = 6) was given 2 days of unpaired NM training. The data document a variable level of responding on day 1 for rabbits given paired training (mean +/- SEM, 21 +/- 11% CRs) but show that on day 2 most rabbits reached the behavioral asymptote (five of six rabbits responding with greater than 85% CRs). Rabbits responding at the behavioral asymptote were defined as having acquired the NM conditioned response. These data were interpreted to indicate that 1 day of training initiated processes necessary for behavioral acquisition (i.e., responding at the behavioral asymptote). A quantitative film autoradiographic study of [3H]phorbol 12,13-dibutyrate binding was then used to determine the distribution of hippocampal protein kinase C in rabbits sacrificed after receiving either 1 day of paired stimuli (n = 10), 1 day of unpaired stimuli (n = 6), or no stimuli (n = 6). Autoradiograms were analyzed by measuring binding in strictly defined regions of interest and from transept profiles. A significant increase in binding of the phorbol ester was found in the CA3 stratum oriens in the paired group relative to unpaired and naive controls. No other significant differences were found. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Scharenberg, A M AU - Olds, J L AU - Schreurs, B G AU - Craig, A M AU - Alkon, D L AD - Section on Neural Systems, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/08/01/ PY - 1991 DA - 1991 Aug 01 SP - 6637 EP - 6641 VL - 88 IS - 15 SN - 0027-8424, 0027-8424 KW - Tritium KW - 10028-17-8 KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Index Medicus KW - Animals KW - Analysis of Variance KW - Phorbol 12,13-Dibutyrate -- metabolism KW - Rabbits KW - Autoradiography KW - Protein Binding KW - Male KW - Protein Kinase C -- metabolism KW - Conditioning (Psychology) KW - Pyramidal Tracts -- enzymology KW - Nictitating Membrane -- physiology KW - Hippocampus -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80716399?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Protein+kinase+C+redistribution+within+CA3+stratum+oriens+during+acquisition+of+nictitating+membrane+conditioning+in+the+rabbit.&rft.au=Scharenberg%2C+A+M%3BOlds%2C+J+L%3BSchreurs%2C+B+G%3BCraig%2C+A+M%3BAlkon%2C+D+L&rft.aulast=Scharenberg&rft.aufirst=A&rft.date=1991-08-01&rft.volume=88&rft.issue=15&rft.spage=6637&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 - 1991-09-04 N1 - Date created - 1991-09-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Prog Neurobiol. 1986;26(1):1-54 [2870537] J Neurophysiol. 1989 May;61(5):971-81 [2542473] Proc Natl Acad Sci U S A. 1988 Mar;85(5):1672-6 [2830626] Science. 1986 Jul 18;233(4761):305-12 [3014651] Neurosci Lett. 1986 Sep 25;70(1):132-7 [3022192] Science. 1986 Feb 7;231(4738):587-9 [3003904] Nature. 1985 May 16-22;315(6016):233-5 [3158820] J Biol Chem. 1987 Nov 15;262(32):15714-20 [3119580] J Biol Chem. 1986 Apr 25;261(12):5307-13 [3082882] J Neurosci. 1989 Nov;9(11):3915-28 [2585060] Behav Neurosci. 1989 Oct;103(5):935-43 [2803560] Science. 1989 Aug 25;245(4920):866-9 [2772638] Brain Res. 1988 Oct 11;462(1):118-25 [3179727] Brain Res. 1984 Dec 17;324(1):160-4 [6097340] Proc Natl Acad Sci U S A. 1986 Apr;83(8):2733-7 [3458232] J Neurosci. 1986 Jan;6(1):199-207 [3456012] Brain Res Bull. 1987 Apr;18(4):533-45 [3607523] Brain Res. 1987 Mar 3;405(1):196-8 [3567594] Brain Res. 1986 Jun 4;375(1):102-16 [3719349] Brain Res. 1986 Jan 1;362(1):98-113 [3942871] Proc Natl Acad Sci U S A. 1984 Apr;81(8):2548-52 [6144101] Proc Natl Acad Sci U S A. 1983 Jul;80(14):4208-12 [6308606] Nature. 1983 Nov 10-16;306(5939):176-9 [6316143] Science. 1983 Dec 2;222(4627):1036-8 [6316499] Brain Res. 1984 May 7;299(1):121-31 [6326959] J Neurosci. 1983 Jun;3(6):1189-98 [6304260] Brain Res. 1986 Aug 13;380(1):59-68 [3756473] Neuroscience. 1981;6(10):1961-73 [6272155] Behav Neurosci. 1984 Apr;98(2):333-44 [6721930] J Neurophysiol. 1983 Nov;50(5):1197-219 [6644367] Cancer Res. 1981 Jul;41(7):2640-7 [6941848] Nature. 1980 Dec 4;288(5790):451-5 [7442792] Ciba Found Symp. 1977;(58):5-24 [83225] J Biochem. 1979 Aug;86(2):575-8 [225310] Ciba Found Symp. 1977;(58):145-77 [215389] J Biol Chem. 1979 May 25;254(10):3692-5 [438153] Brain Res. 1978 Apr 28;145(2):323-46 [638791] Brain Res. 1977 Nov 25;137(1):127-43 [922505] Cond Reflex. 1973 Jan-Mar;8(1):41-56 [4714915] Exp Neurol. 1975 Oct;49(1 Pt 1):58-85 [1183532] J Comp Neurol. 1979 Aug 15;186(4):621-55 [15116692] J Neurosci. 1990 Nov;10(11):3707-13 [2230955] Proc Natl Acad Sci U S A. 1988 Mar;85(6):1988-92 [3162320] J Neurosci. 1989 Feb;9(2):507-12 [2493078] J Biol Chem. 1986 Dec 25;261(36):17099-106 [3782155] Neuron. 1988 Apr;1(2):97-103 [2856092] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cytotoxic effects of a recombinant chimeric toxin on rapidly proliferating vascular smooth muscle cells. AN - 80711130; 1860221 AB - Restenosis after percutaneous transluminal coronary angioplasty is associated with activation of medial smooth muscle cells (SMCs); they proliferate, migrate to the subintima, and narrow the vessel lumen. Cancer cells often express more cell surface receptors than do normal cells. This has allowed tumor cells to be specifically targeted using cytotoxic agents. We have examined whether a similar concept can be applied to rapidly proliferating but nontransformed SMCs. Pseudomonas exotoxin (PE; MW, 66 kDa) is a potent toxin that kills cells by inhibiting protein synthesis; its toxicity is diminished when its cell recognition domain is deleted to produce a 40-kDa protein (PE40). A complementary DNA encoding transforming growth factor alpha (TGF alpha) was ligated to that encoding PE40 and the chimeric toxin TGF alpha-PE40, which is cytotoxic to cancer cells displaying epidermal growth factor (EGF) receptors, was expressed in Escherichia coli. The ability of this toxin to kill proliferating SMCs was tested. When cells were seeded at low density (2,500 cells/cm2) and grown in medium supplemented with 10% fetal bovine serum, they were found to be rapidly proliferating; these cells were very sensitive to the cytotoxic effects of TGF alpha-PE40 (ID50, 4.0 +/- 0.17 ng/ml). In contrast, cytotoxicity was 30-fold less (ID50, 125 +/- 23 ng/ml; p less than 0.0004) when cells were in a quiescent state (grown in medium supplemented with 0.5% fetal bovine serum). Competition studies using excess EGF indicated that the cytotoxic effects of TGF alpha-PE40 are specifically mediated by the EGF receptor. EGF receptor binding analysis demonstrated that rapidly proliferating SMCs display 10-fold more EGF receptors than do quiescent SMCs in vitro. Thus, a chimeric toxin targeted toward the EGF receptor can selectively kill rapidly proliferating SMCs. Whether this toxin or other chimeric toxins directed against other cell surface receptors will effectively inhibit SMCs proliferating in vivo or be useful in preventing restenosis remains to be determined. JF - Circulation AU - Epstein, S E AU - Siegall, C B AU - Biro, S AU - Fu, Y M AU - FitzGerald, D AU - Pastan, I AD - Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 778 EP - 787 VL - 84 IS - 2 SN - 0009-7322, 0009-7322 KW - Bacterial Toxins KW - 0 KW - Cytotoxins KW - Exotoxins KW - Recombinant Proteins KW - Transforming Growth Factor alpha KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Abridged Index Medicus KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Bacterial Toxins -- genetics KW - Animals KW - Receptor, Epidermal Growth Factor -- physiology KW - Rabbits KW - Bacterial Toxins -- pharmacology KW - Cell Division KW - Exotoxins -- genetics KW - Exotoxins -- pharmacology KW - Recombinant Proteins -- pharmacology KW - Transforming Growth Factor alpha -- genetics KW - Muscle, Smooth, Vascular -- drug effects KW - Transforming Growth Factor alpha -- pharmacology KW - Muscle, Smooth, Vascular -- cytology KW - Cytotoxins -- pharmacology KW - Recombinant Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80711130?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cytotoxic+effects+of+a+recombinant+chimeric+toxin+on+rapidly+proliferating+vascular+smooth+muscle+cells.&rft.au=Epstein%2C+S+E%3BSiegall%2C+C+B%3BBiro%2C+S%3BFu%2C+Y+M%3BFitzGerald%2C+D%3BPastan%2C+I&rft.aulast=Epstein&rft.aufirst=S&rft.date=1991-08-01&rft.volume=84&rft.issue=2&rft.spage=778&rft.isbn=&rft.btitle=&rft.title=Circulation&rft.issn=00097322&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-30 N1 - Date created - 1991-08-30 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Circulation. 1991 Aug;84(2):945-7 [1860242] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - O(6)-methylguanine-DNA methyltransferase and uracil DNA glycosylase in human broncho-alveolar lavage cells and peripheral blood mononuclear cells from tobacco smokers and non-smokers. AN - 80709896; 1860159 AB - Because interindividual variations in the activities of DNA repair enzymes may be a risk factor in the pathogenesis of lung diseases, O(6)-methylguanine-DNA methyltransferase (O(6)-MT) and uracil DNA glycosylase (UDG) were measured in broncho-alveolar lavage cell (BALC) and peripheral blood mononuclear cell (PBM) samples from 57 healthy volunteers (25 smokers and 32 non-smokers). According to cotinine determination in 39 cases where serum for this was available, 38% of the self-acclaimed non-smokers had greater than 10 ng/ml of cotinine in their serum. Whether grouped into smokers and non-smokers according to clinical history or by serum cotinine, there were no statistically significant differences between these groups in O(6)-MT or UDG in either of the cell types. However, a tendency towards lower values in smokers was seen. The highest intraindividual variation in O(6)-MT activity was 7-fold, while the highest interindividual variation reached 18-fold. For UDG, the respective values were 24- and 307-fold. Although the distribution of O(6)-MT in BALC was different from that in PBM, the data are consistent with unimodality in both of the cell types. These findings suggest that exposure to cigarette smoke is not entirely responsible for the wide interindividual variation in O(6)-MT and UDG DNA repair activities. JF - Carcinogenesis AU - Vähäkangas, K AU - Trivers, G E AU - Plummer, S AU - Hayes, R B AU - Krokan, H AU - Rowe, M AU - Swartz, R P AU - Yeager, H AU - Harris, C C AD - Laboratory of Human Carcinogenesis, National Cancer Institute, NIH, Bethesda, MD 20892. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 1389 EP - 1394 VL - 12 IS - 8 SN - 0143-3334, 0143-3334 KW - Methyltransferases KW - EC 2.1.1.- KW - O(6)-Methylguanine-DNA Methyltransferase KW - EC 2.1.1.63 KW - DNA Glycosylases KW - EC 3.2.2.- KW - N-Glycosyl Hydrolases KW - Uracil-DNA Glycosidase KW - Index Medicus KW - Humans KW - Adult KW - Male KW - Female KW - Leukocytes, Mononuclear -- enzymology KW - Smoking -- blood KW - Smoking -- metabolism KW - Methyltransferases -- analysis KW - N-Glycosyl Hydrolases -- analysis KW - Bronchoalveolar Lavage Fluid -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80709896?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=O%286%29-methylguanine-DNA+methyltransferase+and+uracil+DNA+glycosylase+in+human+broncho-alveolar+lavage+cells+and+peripheral+blood+mononuclear+cells+from+tobacco+smokers+and+non-smokers.&rft.au=V%C3%A4h%C3%A4kangas%2C+K%3BTrivers%2C+G+E%3BPlummer%2C+S%3BHayes%2C+R+B%3BKrokan%2C+H%3BRowe%2C+M%3BSwartz%2C+R+P%3BYeager%2C+H%3BHarris%2C+C+C&rft.aulast=V%C3%A4h%C3%A4kangas&rft.aufirst=K&rft.date=1991-08-01&rft.volume=12&rft.issue=8&rft.spage=1389&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-04 N1 - Date created - 1991-09-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Long-term preservation of renal function in patients with lupus nephritis receiving treatment that includes cyclophosphamide versus those treated with prednisone only. AN - 80708605; 1859488 AB - The purpose of this study was to assess long-term preservation of renal function in 111 patients with systemic lupus erythematosus and active glomerulonephritis who participated in a randomized treatment trial. Four different drug treatment programs, each of which allowed the use of low-dose oral prednisone in addition to the study drug(s), were compared with a regimen consisting solely of high-dose oral prednisone. Patients randomized to receive intravenous cyclophosphamide, oral cyclophosphamide, or oral azathioprine plus cyclophosphamide had significantly better preservation of renal function than did patients who were randomized to receive prednisone only. Results in the azathioprine group did not differ from those in the prednisone-only group. Cyclophosphamide appears to have long-term benefit in the delay or prevention of end-stage renal disease in patients with lupus nephritis. JF - Arthritis and rheumatism AU - Steinberg, A D AU - Steinberg, S C AD - Arthritis and Rheumatism Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 945 EP - 950 VL - 34 IS - 8 SN - 0004-3591, 0004-3591 KW - Cyclophosphamide KW - 8N3DW7272P KW - Azathioprine KW - MRK240IY2L KW - Prednisone KW - VB0R961HZT KW - Abridged Index Medicus KW - Index Medicus KW - Administration, Oral KW - Injections, Intravenous KW - Dose-Response Relationship, Drug KW - Azathioprine -- therapeutic use KW - Humans KW - Azathioprine -- pharmacology KW - Drug Therapy, Combination KW - Prospective Studies KW - Risk Factors KW - Azathioprine -- administration & dosage KW - Kidney Failure, Chronic -- physiopathology KW - Adult KW - Kidney Failure, Chronic -- mortality KW - Middle Aged KW - Follow-Up Studies KW - Adolescent KW - Time Factors KW - Prednisone -- pharmacology KW - Cyclophosphamide -- administration & dosage KW - Lupus Nephritis -- physiopathology KW - Lupus Nephritis -- drug therapy KW - Cyclophosphamide -- therapeutic use KW - Lupus Nephritis -- epidemiology KW - Prednisone -- therapeutic use KW - Kidney -- physiology KW - Kidney -- drug effects KW - Prednisone -- administration & dosage KW - Cyclophosphamide -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80708605?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Long-term+preservation+of+renal+function+in+patients+with+lupus+nephritis+receiving+treatment+that+includes+cyclophosphamide+versus+those+treated+with+prednisone+only.&rft.au=Steinberg%2C+A+D%3BSteinberg%2C+S+C&rft.aulast=Steinberg&rft.aufirst=A&rft.date=1991-08-01&rft.volume=34&rft.issue=8&rft.spage=945&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 - 1991-08-29 N1 - Date created - 1991-08-29 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Arthritis Rheum. 1992 May;35(5):605-7 [1575797] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Fluorescence detection of benzo[a]pyrene--DNA adducts in human lung. AN - 80708433; 1860165 AB - Improved techniques are described for the specific identification of benzo[a]pyrene-diolepoxide (BPDE)--DNA adducts in human tissues. Immunoaffinity chromatography, synchronous fluorescence spectroscopy and second-derivative synchronous fluorescence spectroscopy have previously been used to detect BPDE-DNA adducts in human placenta. Here we report how these methods, together with HPLC and the generation of complete fluorescence excitation--emission matrices, have been used to identify unequivocally BPDE-DNA adducts in samples of human lung. BPDE nucleotide adducts were isolated with immunoaffinity chromatography columns bearing antibodies raised against the (+/-)anti-7,8-diol-9,10-epoxide-deoxyguanosine adduct of benzo[a]pyrene. These adducts were hydrolyzed to tetrahydrotetrols and the hydrolysis products subjected to HPLC. The major product isolated by HPLC, benzo[a]-pyrene-7,10/8,9-tetrahydrotetrol, was determined by fluorescence spectroscopy. Using this method, levels of BPDE-DNA adducts in the range of 1-40 in 10(8) nucleotides were measured in 6 out of 25 samples, with a lower detection limit of one adduct in 10(8) nucleotides. The data may also indicate that adduct levels show regional variation in different parts of the same lung. JF - Carcinogenesis AU - Weston, A AU - Bowman, E D AD - Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 1445 EP - 1449 VL - 12 IS - 8 SN - 0143-3334, 0143-3334 KW - DNA Adducts KW - 0 KW - benzo(a)pyrene-DNA adduct KW - Benzo(a)pyrene KW - 3417WMA06D KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Infant KW - Chromatography, Affinity KW - Aged, 80 and over KW - Humans KW - Adult KW - Infant, Newborn KW - Aged KW - Middle Aged KW - Adolescent KW - Male KW - Female KW - Chromatography, High Pressure Liquid KW - Benzo(a)pyrene -- analysis KW - Lung -- chemistry KW - DNA -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80708433?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Fluorescence+detection+of+benzo%5Ba%5Dpyrene--DNA+adducts+in+human+lung.&rft.au=Weston%2C+A%3BBowman%2C+E+D&rft.aulast=Weston&rft.aufirst=A&rft.date=1991-08-01&rft.volume=12&rft.issue=8&rft.spage=1445&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-04 N1 - Date created - 1991-09-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - New potent verapamil derivatives that reverse multidrug resistance in human renal carcinoma cells and in transgenic mice expressing the human MDR1 gene. AN - 80705243; 1677434 AB - Multidrug resistance in human renal cell carcinoma is mainly caused by expression of the MDR1 gene and is characterized by a broad spectrum cross resistance to many natural product chemotherapeutic agents. This resistance can be overcome by applying chemosensitizers which inhibit the function of the MDR1 gene product P-glycoprotein. The development of new reversing agents with fewer side effects and a higher potency in modifying resistance is a high priority of research on drug resistance. We have evaluated four new verapamil derivatives on 21 primary human renal cell carcinomas in vitro, and also tested them in an MDR-transgenic mice model. These mice express the human MDR1 gene in their bone marrow cells and measurement of their white blood counts provides a simple, rapid and reliable system to screen for the potency of MDR-reversing agents in vivo. We demonstrate here that all four drugs are effective in reversing multidrug resistance in primary cultures of human renal cell carcinomas when used in combination with vinblastine chemotherapy, and to a lesser extent with doxorubicin or daunomycin chemotherapy. Our in vivo data indicate that two of these reversing agents display low toxicity at high concentrations and are more effective at low, clinically achievable concentrations, than the other two drugs and R-verapamil. These results make the two new drugs attractive candidates to be taken into clinical trials. JF - The Journal of urology AU - Mickisch, G H AU - Merlino, G T AU - Aiken, P M AU - Gottesman, M M AU - Pastan, I AD - Laboratories of Molecular Biology and Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 447 EP - 453 VL - 146 IS - 2 SN - 0022-5347, 0022-5347 KW - MDR1 KW - Membrane Glycoproteins KW - 0 KW - Neoplasm Proteins KW - P-Glycoprotein KW - Vinblastine KW - 5V9KLZ54CY KW - Doxorubicin KW - 80168379AG KW - Verapamil KW - CJ0O37KU29 KW - Daunorubicin KW - ZS7284E0ZP KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Drug Screening Assays, Antitumor KW - Drug Resistance -- genetics KW - Dose-Response Relationship, Drug KW - Tumor Cells, Cultured -- drug effects KW - Doxorubicin -- antagonists & inhibitors KW - Humans KW - Vinblastine -- antagonists & inhibitors KW - Mice KW - Daunorubicin -- antagonists & inhibitors KW - Female KW - Male KW - Kidney Neoplasms -- genetics KW - Neoplasm Proteins -- drug effects KW - Kidney Neoplasms -- drug therapy KW - Membrane Glycoproteins -- drug effects KW - Verapamil -- analogs & derivatives KW - Carcinoma, Renal Cell -- drug therapy KW - Gene Expression Regulation, Neoplastic -- drug effects KW - Genes -- genetics KW - Neoplasm Proteins -- genetics KW - Genes -- drug effects KW - Verapamil -- therapeutic use KW - Carcinoma, Renal Cell -- genetics KW - Gene Expression Regulation, Neoplastic -- genetics KW - Membrane Glycoproteins -- genetics KW - Mice, Transgenic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80705243?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+urology&rft.atitle=New+potent+verapamil+derivatives+that+reverse+multidrug+resistance+in+human+renal+carcinoma+cells+and+in+transgenic+mice+expressing+the+human+MDR1+gene.&rft.au=Mickisch%2C+G+H%3BMerlino%2C+G+T%3BAiken%2C+P+M%3BGottesman%2C+M+M%3BPastan%2C+I&rft.aulast=Mickisch&rft.aufirst=G&rft.date=1991-08-01&rft.volume=146&rft.issue=2&rft.spage=447&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+urology&rft.issn=00225347&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-29 N1 - Date created - 1991-08-29 N1 - Date revised - 2017-01-13 N1 - Gene symbol - MDR1 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pentoxifylline suppression of tumor necrosis factor gene transcription. AN - 80702863; 1858029 AB - Pentoxifylline decreases lung injury after intravenous endotoxin; the mechanism is unknown. Tumor necrosis factor-alpha (TNF) is secreted by macrophages in response to endotoxin and mediates some of the toxicity of endotoxin. This study investigates the effects of pentoxifylline on endotoxin-stimulated TNF production in vitro and in vivo. Pentoxifylline concentrations of 100 and 1000 micrograms/ml inhibited TNF production by murine adherent peritoneal exudate cells incubated with endotoxin 1 microgram/ml. Similarly, pentoxifylline at 100 and 1000 micrograms/ml decreased the number of available TNF messenger RNA transcripts in peritoneal exudate cells assessed by Northern blot. Pentoxifylline had no effect on TNF mRNA stability, but appeared to act by inhibiting the rate of TNF mRNA production (transcription). In murine in vivo experiments at each dose of endotoxin administered from 0.01 to 30 mg/kg, pentoxifylline treatment significantly reduced serum TNF levels, suggesting a favorable shift of the endotoxin dose-response curve. Expression of murine TNF gene in the livers of these animals showed fewer TNF transcripts in the pentoxifylline-treated animals compared to controls. Pentoxifylline inhibited endotoxin-induced TNF production both in vivo and in vitro and exerted this control by inhibiting endotoxin-induced transcription of the TNF gene. This study suggests that pentoxifylline may ameliorate endotoxic shock by decreasing macrophage TNF production. JF - Surgery AU - Doherty, G M AU - Jensen, J C 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 - 1991/08// PY - 1991 DA - August 1991 SP - 192 EP - 198 VL - 110 IS - 2 SN - 0039-6060, 0039-6060 KW - Endotoxins KW - 0 KW - RNA, Messenger KW - Tumor Necrosis Factor-alpha KW - Pentoxifylline KW - SD6QCT3TSU KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Blotting, Northern KW - Dose-Response Relationship, Drug KW - In Vitro Techniques KW - RNA, Messenger -- physiology KW - Mice, Inbred C57BL KW - Biological Assay KW - Enzyme-Linked Immunosorbent Assay KW - Mice KW - Female KW - Pentoxifylline -- pharmacology KW - Transcription, Genetic -- drug effects KW - Tumor Necrosis Factor-alpha -- biosynthesis KW - Tumor Necrosis Factor-alpha -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80702863?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Surgery&rft.atitle=Pentoxifylline+suppression+of+tumor+necrosis+factor+gene+transcription.&rft.au=Doherty%2C+G+M%3BJensen%2C+J+C%3BAlexander%2C+H+R%3BBuresh%2C+C+M%3BNorton%2C+J+A&rft.aulast=Doherty&rft.aufirst=G&rft.date=1991-08-01&rft.volume=110&rft.issue=2&rft.spage=192&rft.isbn=&rft.btitle=&rft.title=Surgery&rft.issn=00396060&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-28 N1 - Date created - 1991-08-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chemotherapy amplifies production of tumor necrosis factor. AN - 80702265; 1858032 AB - Several chemotherapeutic agents exert cytotoxicity through the generation of reactive oxygen species (ROS), and our laboratory has shown that ROS increase tumor necrosis factor (TNF) production. Therefore, we hypothesized that cis-dichlorodiammine platinum (CDDP), mitomycin-C, and doxorubicin hydrochloride (Adriamycin), by the release of ROS, would increase macrophage TNF production. Murine macrophages were incubated for 20 hours with varying doses of the chemotherapeutic drugs and 2.5 micrograms/ml endotoxin. Both CDDP and mitomycin-C increased TNF production compared to nondrug-exposed cells. Peak TNF values occurred at 10 micrograms/ml CDDP and 62.5 micrograms/ml mitomycin-C with 377 +/- 38 and 427 +/- 54 units/ml TNF produced, respectively. These increases were significant (p2 less than 0.05) compared to the nonchemotherapy; but endotoxin-exposed macrophages (CDDP 11 +/- 3 units/ml; mitomycin-C 10 +/- 3 units/ml). Only CDDP-increased production of TNF from non-endotoxin-primed macrophages (0 microgram/ml CDDP - 0 +/- 0 unit/ml TNF; 50 micrograms/ml CDDP - 13 +/- 5 units/ml TNF; p2 less than 0.038). 5-Fluorouracil, a non-ROS-generating chemotherapeutic, and Adriamycin failed to amplify TNF production. By Northern blot analysis, CDDP induced transcription of the TNF gene in non-endotoxin-primed macrophages as early as 3 hours after exposure to 50 micrograms/ml CDDP, and this preceded the increase in TNF protein in kinetic studies. Because CDDP, mitomycin-C, and Adriamycin all produce ROS, the mechanism for this selective chemotherapy-induced cytokine amplification remains unclear. This finding may explain both indirect toxic and tumoricidal properties of CDDP and mitomycin-C. JF - Surgery AU - Pogrebniak, H W AU - Matthews, W AU - Pass, H I AD - Thoracic Oncology Section, National Cancer Institute, National Institutes of Health, Bethesda, Md 20892. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 231 EP - 237 VL - 110 IS - 2 SN - 0039-6060, 0039-6060 KW - Antineoplastic Agents KW - 0 KW - Mitomycins KW - Tumor Necrosis Factor-alpha KW - transplatin KW - 14913-33-8 KW - Doxorubicin KW - 80168379AG KW - Cisplatin KW - Q20Q21Q62J KW - Oxygen KW - S88TT14065 KW - Fluorouracil KW - U3P01618RT KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Transcription, Genetic -- drug effects KW - Blotting, Northern KW - Doxorubicin -- pharmacology KW - Cell Survival -- drug effects KW - Oxygen -- metabolism KW - Mice, Inbred C57BL KW - Cisplatin -- pharmacology KW - Fluorouracil -- pharmacology KW - Mice KW - Mitomycins -- pharmacology KW - Female KW - Tumor Necrosis Factor-alpha -- biosynthesis KW - Macrophages -- drug effects KW - Antineoplastic Agents -- pharmacology KW - Macrophages -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80702265?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Surgery&rft.atitle=Chemotherapy+amplifies+production+of+tumor+necrosis+factor.&rft.au=Pogrebniak%2C+H+W%3BMatthews%2C+W%3BPass%2C+H+I&rft.aulast=Pogrebniak&rft.aufirst=H&rft.date=1991-08-01&rft.volume=110&rft.issue=2&rft.spage=231&rft.isbn=&rft.btitle=&rft.title=Surgery&rft.issn=00396060&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-28 N1 - Date created - 1991-08-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Genetic analysis of human esophageal tumors from two high incidence geographic areas: frequent p53 base substitutions and absence of ras mutations. AN - 80700912; 1855226 AB - Esophageal squamous cell carcinoma (ESC) samples from patients residing in Uruguay and in Normandy, France, where alcoholic beverages and tobacco smoke are major risk factors, were analyzed for point mutations in the p53 tumor suppressor gene. Among 34 tumors (15 from Normandy and 19 from Uruguay) 15 point mutations in the p53 gene that result in amino acid substitutions or chain termination were identified by polymerase chain reaction amplification of exons 5-8 and direct DNA sequencing. Base substitutions in ESC from these high-incidence areas are dispersed over the midregion of the p53 gene. There are differences between ESC and other types of gastrointestinal cancer in the nature of frequent base substitutions. CpG to TpG transitions were far less prevalent in these ESC than in colorectal tumors, whereas G to T transversions, rarely found in colon cancers, were found in one-fourth of the ESC samples. Base substitutions at A:T pairs constitute an important fraction of ESC p53 mutations, in contrast to mutation patterns in most other types of solid tumors. In contrast to the frequent mutation of the p53 gene in these samples, no mutations in the H-, K-, or N-ras genes were found in 16 tumors from Uruguay by direct sequencing of exons in which transforming mutations are known to occur. A previous study on ras mutations in ESC from France was also negative (M. C. Hollstein et al., Cancer Res., 48: 5119-5123, 1988). The role of distinct etiological factors in generating these differences and the potential for linking patient exposure histories with patterns of p53 mutations in high risk populations are considered. JF - Cancer research AU - Hollstein, M C AU - Peri, L AU - Mandard, A M AU - Welsh, J A AU - Montesano, R AU - Metcalf, R A AU - Bak, M AU - Harris, C C AD - Laboratory of Human Carcinogenesis, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1991/08/01/ PY - 1991 DA - 1991 Aug 01 SP - 4102 EP - 4106 VL - 51 IS - 15 SN - 0008-5472, 0008-5472 KW - H-ras KW - K-ras KW - N-ras KW - Codon KW - 0 KW - Index Medicus KW - Codon -- genetics KW - Humans KW - Aged KW - Uruguay -- epidemiology KW - DNA Damage -- genetics KW - Base Sequence KW - Aged, 80 and over KW - Adult KW - France -- epidemiology KW - Molecular Sequence Data KW - Middle Aged KW - Female KW - Male KW - Genes, ras -- genetics KW - Carcinoma, Squamous Cell -- epidemiology KW - Genes, p53 -- genetics KW - Esophageal Neoplasms -- genetics KW - Carcinoma, Squamous Cell -- genetics KW - Mutation -- genetics KW - Esophageal Neoplasms -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80700912?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Genetic+analysis+of+human+esophageal+tumors+from+two+high+incidence+geographic+areas%3A+frequent+p53+base+substitutions+and+absence+of+ras+mutations.&rft.au=Hollstein%2C+M+C%3BPeri%2C+L%3BMandard%2C+A+M%3BWelsh%2C+J+A%3BMontesano%2C+R%3BMetcalf%2C+R+A%3BBak%2C+M%3BHarris%2C+C+C&rft.aulast=Hollstein&rft.aufirst=M&rft.date=1991-08-01&rft.volume=51&rft.issue=15&rft.spage=4102&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 - 1991-08-28 N1 - Date created - 1991-08-28 N1 - Date revised - 2017-01-13 N1 - Gene symbol - H-ras; K-ras; N-ras N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - p53 mutations, ras mutations, and p53-heat shock 70 protein complexes in human lung carcinoma cell lines. AN - 80699640; 1855224 AB - The p53 tumor suppressor gene is frequently mutated and the K-ras oncogene is occasionally mutated in primary specimens of human lung carcinomas. These mutated genes also cooperate in the immortalization and neoplastic transformation of rodent cells. To determine whether these mutations are necessary for maintenance of the immortalized and/or neoplastically transformed states of human bronchial epithelial cells, the p53 gene and regions of the ras (K-, H-, and N-) genes were sequenced in nine human lung carcinoma cell lines. Detection of p53 mutations by polymerase chain amplification and direct DNA sequencing was corroborated by p53 immunocytochemistry and coimmunoprecipitation of p53 with heat shock protein 70. p53 and ras genes were frequently, but not always, mutated in the carcinoma cell lines. These data are consistent with the hypothesis that multiple genetic changes involving both protooncogenes and tumor suppressor genes occur during lung carcinogenesis. JF - Cancer research AU - Lehman, T A AU - Bennett, W P AU - Metcalf, R A AU - Welsh, J A AU - Ecker, J AU - Modali, R V AU - Ullrich, S AU - Romano, J W AU - Appella, E AU - Testa, J R AD - Laboratory of Human Carcinogenesis, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1991/08/01/ PY - 1991 DA - 1991 Aug 01 SP - 4090 EP - 4096 VL - 51 IS - 15 SN - 0008-5472, 0008-5472 KW - p53 KW - ras KW - Heat-Shock Proteins KW - 0 KW - Tumor Suppressor Protein p53 KW - Index Medicus KW - Exons -- physiology KW - Base Sequence KW - Tumor Cells, Cultured KW - Epithelial Cells KW - Bronchi -- cytology KW - Humans KW - Molecular Sequence Data KW - Precipitin Tests KW - Bronchi -- physiology KW - Protein Binding KW - Immunohistochemistry KW - Cell Transformation, Neoplastic -- genetics KW - Heat-Shock Proteins -- metabolism KW - Genes, ras -- genetics KW - Genes, p53 -- genetics KW - Mutation -- genetics KW - Lung Neoplasms -- genetics KW - Tumor Suppressor Protein p53 -- genetics KW - Tumor Suppressor Protein p53 -- metabolism KW - Lung Neoplasms -- pathology KW - Lung Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80699640?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=p53+mutations%2C+ras+mutations%2C+and+p53-heat+shock+70+protein+complexes+in+human+lung+carcinoma+cell+lines.&rft.au=Lehman%2C+T+A%3BBennett%2C+W+P%3BMetcalf%2C+R+A%3BWelsh%2C+J+A%3BEcker%2C+J%3BModali%2C+R+V%3BUllrich%2C+S%3BRomano%2C+J+W%3BAppella%2C+E%3BTesta%2C+J+R&rft.aulast=Lehman&rft.aufirst=T&rft.date=1991-08-01&rft.volume=51&rft.issue=15&rft.spage=4090&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 - 1991-08-28 N1 - Date created - 1991-08-28 N1 - Date revised - 2017-01-13 N1 - Gene symbol - p53; ras N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Disturbances of hypothalamic-pituitary-adrenal axis functioning during ethanol withdrawal in six men. AN - 80693430; 1853950 AB - Excessive exposure to glucocorticoids can have neurotoxic effects. The behavioral, cognitive, and neurochemical changes observed following the cessation of heavy drinking, therefore, may be associated with disturbances of the hypothalamic-pituitary-adrenal (HPA) axis. To investigate HPA axis disturbances during the ethanol withdrawal syndrome, the authors examined diurnal changes in plasma cortisol in six alcohol-dependent men following the abrupt discontinuation of alcohol intake. Plasma cortisol concentrations were quantified every 30 minutes for 24 hours in the early stage (1 day after cessation) and the middle to late stage (3 days after cessation) of the ethanol withdrawal syndrome as well as after the resolution of acute symptoms (8 days or more after cessation). Plasma cortisol concentrations were almost twice as high during acute withdrawal as they were following recovery. The duration of the cortisol diurnal cycle on the first day of withdrawal was negatively correlated with the severity of withdrawal. There is a marked activation of the HPA axis associated with the ethanol withdrawal syndrome. The authors hypothesize that this activation may account for some of the signs and symptoms of acute and subacute withdrawal. They discuss the potential long-term physiological effects of the episodic increases in cortisol associated with repeated episodes of ethanol withdrawal. The alterations in cortisol rhythmicity during early withdrawal may also have clinical implications. JF - The American journal of psychiatry AU - Adinoff, B AU - Risher-Flowers, D AU - De Jong, J AU - Ravitz, B AU - Bone, G H AU - Nutt, D J AU - Roehrich, L AU - Martin, P R AU - Linnoila, M AD - Laboratory of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Md. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 1023 EP - 1025 VL - 148 IS - 8 SN - 0002-953X, 0002-953X KW - Ethanol KW - 3K9958V90M KW - Hydrocortisone KW - WI4X0X7BPJ KW - Abridged Index Medicus KW - Index Medicus KW - Circadian Rhythm KW - Hypothalamo-Hypophyseal System -- physiopathology KW - Humans KW - Pituitary-Adrenal System -- physiopathology KW - Adult KW - Temperance KW - Male KW - Ethanol -- adverse effects KW - Substance Withdrawal Syndrome -- physiopathology KW - Substance Withdrawal Syndrome -- etiology KW - Hydrocortisone -- physiology KW - Substance Withdrawal Syndrome -- blood KW - Hydrocortisone -- blood KW - Alcoholism -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80693430?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+journal+of+psychiatry&rft.atitle=Disturbances+of+hypothalamic-pituitary-adrenal+axis+functioning+during+ethanol+withdrawal+in+six+men.&rft.au=Adinoff%2C+B%3BRisher-Flowers%2C+D%3BDe+Jong%2C+J%3BRavitz%2C+B%3BBone%2C+G+H%3BNutt%2C+D+J%3BRoehrich%2C+L%3BMartin%2C+P+R%3BLinnoila%2C+M&rft.aulast=Adinoff&rft.aufirst=B&rft.date=1991-08-01&rft.volume=148&rft.issue=8&rft.spage=1023&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+psychiatry&rft.issn=0002953X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-20 N1 - Date created - 1991-08-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Contribution of NF-kappa B and Sp1 binding motifs to the replicative capacity of human immunodeficiency virus type 1: distinct patterns of viral growth are determined by T-cell types. AN - 80686228; 2072454 AB - Starting with a replication-incompetent molecular clone of human immunodeficiency virus type 1, lacking all the NF-kappa B and Sp1 binding sites present in the native long terminal repeat (LTR), proviruses containing reconstructed LTRs with individual or combinations of NF-kappa B and Sp1 elements were generated and evaluated for their capacity to produce virus progeny following transfection-cocultivation. Virus stocks obtained from these experiments exhibited a continuum of replicative capacities in different human T-cell types depending on which element(s) was present in the LTR. For example, in experiments involving proviral clones with LTRs containing one or two NF-kappa B elements (and no Sp1 binding sites), a hierarchy of cellular permissivity to virus replication (peripheral blood lymphocytes = MT4 greater than H9 greater than CEM greater than Jurkat) was observed. Of note was the associated emergence of second-site LTR revertants which involved an alteration of the TATA box. These results suggest that the human immunodeficiency virus type 1 LTR possesses functional redundancy which ensures virus replication in different T-cell types and is capable of changing depending on the particular combination of transcriptional factors present. JF - Journal of virology AU - Ross, E K AU - Buckler-White, A J AU - Rabson, A B AU - Englund, G AU - Martin, M A AD - Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 4350 EP - 4358 VL - 65 IS - 8 SN - 0022-538X, 0022-538X KW - DNA, Viral KW - 0 KW - NF-kappa B KW - RNA, Viral KW - Sp1 Transcription Factor KW - Index Medicus KW - AIDS/HIV KW - Mutagenesis, Site-Directed KW - Polymerase Chain Reaction KW - Base Sequence KW - Transfection KW - Humans KW - Enhancer Elements, Genetic KW - RNA, Viral -- chemistry KW - Proviruses -- genetics KW - Molecular Sequence Data KW - DNA Replication KW - Cell Line KW - Virus Replication KW - Sp1 Transcription Factor -- genetics KW - HIV-1 -- genetics KW - DNA, Viral -- biosynthesis KW - DNA, Viral -- chemistry KW - T-Lymphocytes -- microbiology KW - Sp1 Transcription Factor -- metabolism KW - HIV-1 -- growth & development KW - HIV-1 -- physiology KW - Repetitive Sequences, Nucleic Acid KW - NF-kappa B -- genetics KW - NF-kappa B -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80686228?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Contribution+of+NF-kappa+B+and+Sp1+binding+motifs+to+the+replicative+capacity+of+human+immunodeficiency+virus+type+1%3A+distinct+patterns+of+viral+growth+are+determined+by+T-cell+types.&rft.au=Ross%2C+E+K%3BBuckler-White%2C+A+J%3BRabson%2C+A+B%3BEnglund%2C+G%3BMartin%2C+M+A&rft.aulast=Ross&rft.aufirst=E&rft.date=1991-08-01&rft.volume=65&rft.issue=8&rft.spage=4350&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 - 1991-08-19 N1 - Date created - 1991-08-19 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1988 Jul;85(13):4700-4 [3133660] Hum Gene Ther. 1990 Summer;1(2):135-49 [1964093] Mol Cell Biol. 1988 Jun;8(6):2555-61 [2841583] Cell. 1988 Sep 23;54(7):943-53 [2843294] Science. 1988 Sep 16;241(4872):1481-5 [3262235] Genes Dev. 1988 Dec;2(12B):1764-78 [2853685] EMBO J. 1989 Mar;8(3):765-78 [2721501] Genes Dev. 1989 Apr;3(4):547-58 [2470647] J Virol. 1989 Jun;63(6):2585-91 [2657100] J Virol. 1989 Sep;63(9):4115-9 [2760991] J Virol. 1989 Nov;63(11):4919-24 [2795721] Cell. 1989 Oct 20;59(2):273-82 [2478293] Nucleic Acids Res. 1989 Oct 25;17(20):8197-206 [2510129] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Cell. 1983 Nov;35(1):79-87 [6313230] Science. 1984 May 4;224(4648):497-500 [6200935] J Immunol. 1984 Jul;133(1):123-8 [6327821] DNA. 1984 Dec;3(6):479-88 [6096101] Science. 1985 Jan 11;227(4683):171-3 [2981427] Proc Natl Acad Sci U S A. 1985 Jan;82(2):488-92 [3881765] Cell. 1985 Jul;41(3):813-23 [2988790] Proc Natl Acad Sci U S A. 1985 Jul;82(13):4539-43 [2989831] Science. 1985 Jul 5;229(4708):69-73 [2990040] Science. 1985 Jul 5;229(4708):74-7 [2990041] Science. 1986 May 9;232(4751):755-9 [3008338] EMBO J. 1986 Jun;5(6):1367-71 [3015602] J Virol. 1986 Aug;59(2):284-91 [3016298] Mol Cell Biol. 1986 Nov;6(11):3847-53 [3540601] Nature. 1987 Apr 16-22;326(6114):662-9 [3031510] Nature. 1987 Apr 16-22;326(6114):711-3 [3031512] Proc Natl Acad Sci U S A. 1987 Jun;84(11):3658-62 [3035545] J Virol. 1988 Jan;62(1):139-47 [3257102] Science. 1987 Dec 11;238(4833):1575-8 [2825351] Cell. 1988 Mar 11;52(5):723-9 [2830991] Nature. 1988 May 5;333(6168):40-5 [2834649] Mol Cell Biol. 1988 Apr;8(4):1715-24 [3260003] Nature. 1988 Jul 14;334(6178):165-7 [3386755] J Virol. 1989 Dec;63(12):5501-4 [2479775] Nature. 1990 Mar 15;344(6263):260-2 [2156167] Proc Natl Acad Sci U S A. 1990 Jun;87(12):4732-6 [2191301] EMBO J. 1990 Dec;9(13):4417-23 [2124973] J Virol. 1991 Mar;65(3):1414-9 [1995951] Science. 1988 Jul 8;241(4862):202-5 [3260404] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Treatment of advanced-stage Hodgkin's disease: alternating noncrossresistant MOPP/CABS is not superior to MOPP. AN - 80684860; 1712836 AB - One hundred twenty-five assessable patients with advanced-stage Hodgkin's disease were randomized to receive mechlorethamine, vincristine, procarbazine, and prednisone (MOPP) or MOPP alternating with lomustine (CCNU), doxorubicin, bleomycin, and streptozocin (CABS). The median follow-up is 7.7 years. The complete response rate was 60 of 66 MOPP-treated patients (91%) and 54 of 59 MOPP/CABS-treated patients (92%) (difference not significant). The level of the disease-free survival curve at longest follow-up is 65% for MOPP-treated patients and 72% for MOPP/CABS-treated patients (difference not significant). The overall survival at 12 years is projected at 68% for MOPP-treated patients and 54% for MOPP/CABS-treated patients (difference not significant). Thus, there were no significant differences in efficacy between MOPP and MOPP/CABS. However, MOPP/CABS was more emetogenic than MOPP, and four MOPP/CABS-treated patients went on to develop secondary acute leukemia. No MOPP-treated patients developed leukemia. High initial erythrocyte sedimentation rate (ESR) and high platelet counts adversely affected treatment outcome. MOPP-treated patients who received greater than 81% of the projected dose intensity of vincristine over the first three cycles had significantly improved disease-free survival rates over those receiving less than 81%. MOPP/CABS-treated patients who received greater than 82% of the projected dose intensity of vincristine had significantly better overall survival than those who received less than 82%. Disease-free survival on both arms was significantly better in patients who received greater than 84% of the projected dose intensity of all agents. The effect of dose intensity was particularly apparent in patients with poor prognostic factors where those who received greater than 84% of the projected dose intensity of all agents had significantly improved disease-free and overall survival. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Longo, D L AU - Duffey, P L AU - DeVita, V T AU - Wiernik, P H AU - Hubbard, S M AU - Phares, J C AU - Bastian, A W AU - Jaffe, E S AU - Young, R C AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, MD. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 1409 EP - 1420 VL - 9 IS - 8 SN - 0732-183X, 0732-183X KW - Bleomycin KW - 11056-06-7 KW - Procarbazine KW - 35S93Y190K KW - Mechlorethamine KW - 50D9XSG0VR KW - Vincristine KW - 5J49Q6B70F KW - Streptozocin KW - 5W494URQ81 KW - Lomustine KW - 7BRF0Z81KG KW - Doxorubicin KW - 80168379AG KW - Prednisone KW - VB0R961HZT KW - Index Medicus KW - Acute Disease KW - Mechlorethamine -- administration & dosage KW - Neoplasm Staging KW - Bleomycin -- administration & dosage KW - Dose-Response Relationship, Drug KW - Humans KW - Vincristine -- administration & dosage KW - Doxorubicin -- administration & dosage KW - Lomustine -- administration & dosage KW - Streptozocin -- administration & dosage KW - Procarbazine -- administration & dosage KW - Survival Rate KW - Adult KW - Middle Aged KW - Follow-Up Studies KW - Leukemia -- etiology KW - Adolescent KW - Prednisone -- administration & dosage KW - Female KW - Male KW - Remission Induction KW - Hodgkin Disease -- pathology KW - Hodgkin Disease -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Hodgkin Disease -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80684860?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Treatment+of+advanced-stage+Hodgkin%27s+disease%3A+alternating+noncrossresistant+MOPP%2FCABS+is+not+superior+to+MOPP.&rft.au=Longo%2C+D+L%3BDuffey%2C+P+L%3BDeVita%2C+V+T%3BWiernik%2C+P+H%3BHubbard%2C+S+M%3BPhares%2C+J+C%3BBastian%2C+A+W%3BJaffe%2C+E+S%3BYoung%2C+R+C&rft.aulast=Longo&rft.aufirst=D&rft.date=1991-08-01&rft.volume=9&rft.issue=8&rft.spage=1409&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 - 1991-08-22 N1 - Date created - 1991-08-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Host genetic background effect on the frequency of mouse mammary tumor virus-induced rearrangements of the int-1 and int-2 loci in mouse mammary tumors. AN - 80684443; 1712864 AB - The frequency with which int-1 and int-2 are rearranged in mouse mammary tumors by mouse mammary tumor virus (MMTV)-induced insertional mutagenesis is a consequence of the host genetic background. In 75% of C3H mammary tumors, int-1 is rearranged by MMTV insertion, whereas only 30% of BALB/cfC3H tumors contain a virus-induced rearrangement of int-1. This difference is significant (P less than 0.005) and could not be accounted for by the potentially additive effect of the genetically transmitted Mtv-1-encoded virus in C3H mice. Similarly, MMTV-induced rearrangement of the int-2 gene in mammary tumors of the R111 mouse strain (59%) occurred at a significantly (P less than 0.025) higher frequency than in BALB/cfR111 (25%) mammary tumors. Moreover, in BALB/cfR111 mammary tumors, there is evidence that rearrangement of int-1 and int-2 does not occur independently (P less than 0.025). These results suggest that the long history of inbreeding for high tumor incidence of C3H and R111 mouse strains has selected for the fixation of host mutations which either complement the action of the particular int gene or affect the sensitivity of specific subpopulations of mammary epithelium to infection by particular strains of MMTV. JF - Journal of virology AU - Marchetti, A AU - Robbins, J AU - Campbell, G AU - Buttitta, F AU - Squartini, F AU - Bistocchi, M AU - Callahan, R AD - Laboratory of Tumor Immunology and Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 4550 EP - 4554 VL - 65 IS - 8 SN - 0022-538X, 0022-538X KW - hst/K-fgf KW - int-1 KW - int-2 KW - DNA Probes KW - 0 KW - DNA, Viral KW - RNA, Messenger KW - Poly A KW - 24937-83-5 KW - RNA KW - 63231-63-0 KW - Index Medicus KW - Animals KW - Blotting, Northern KW - Transcription, Genetic KW - RNA -- analysis KW - Mice KW - Mice, Inbred BALB C KW - Base Sequence KW - Poly A -- analysis KW - DNA, Viral -- chemistry KW - Blotting, Southern KW - Mice, Inbred C3H KW - Molecular Sequence Data KW - Inbreeding KW - Repetitive Sequences, Nucleic Acid KW - Mutagenesis, Insertional KW - Female KW - Mammary Neoplasms, Experimental -- microbiology KW - Mammary Neoplasms, Experimental -- genetics KW - Gene Rearrangement KW - Mammary Tumor Virus, Mouse -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80684443?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Host+genetic+background+effect+on+the+frequency+of+mouse+mammary+tumor+virus-induced+rearrangements+of+the+int-1+and+int-2+loci+in+mouse+mammary+tumors.&rft.au=Marchetti%2C+A%3BRobbins%2C+J%3BCampbell%2C+G%3BButtitta%2C+F%3BSquartini%2C+F%3BBistocchi%2C+M%3BCallahan%2C+R&rft.aulast=Marchetti&rft.aufirst=A&rft.date=1991-08-01&rft.volume=65&rft.issue=8&rft.spage=4550&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 - 1991-08-19 N1 - Date created - 1991-08-19 N1 - Date revised - 2017-01-13 N1 - Gene symbol - hst/K-fgf; int-1; int-2 N1 - SuppNotes - Cited By: Nature. 1963 Feb 2;197:505-6 [13978585] Biochem Biophys Res Commun. 1966 Jun 13;23(5):641-6 [5963888] Proc Natl Acad Sci U S A. 1989 Aug;86(15):5678-82 [2548184] Cell. 1987 Aug 28;50(5):729-37 [2957062] Nature. 1986 Apr 17-23;320(6063):628-31 [3010125] Virology. 1985 Apr 30;142(2):278-90 [2997987] Proc Natl Acad Sci U S A. 1987 Oct;84(20):7305-9 [2959959] EMBO J. 1988 Mar;7(3):691-5 [3293998] Proc Natl Acad Sci U S A. 1986 Oct;83(20):7806-10 [2429320] J Virol. 1989 Nov;63(11):4972-5 [2552179] Virus Res. 1989 Feb;12(2):123-37 [2539705] Cell. 1988 Nov 18;55(4):619-25 [3180222] Cell. 1987 Jul 3;50(1):89-95 [3594566] Nature. 1987 Apr 30-May 6;326(6116):833 [3574458] EMBO J. 1990 Mar;9(3):907-13 [1690126] Cell. 1990 Sep 21;62(6):1073-85 [2205396] Nature. 1990 Aug 30;346(6287):847-50 [2202907] Nature. 1984 May 17-23;309(5965):273-5 [6325949] Cell. 1984 Jun;37(2):529-36 [6327073] Cell. 1981 Jan;23(1):165-73 [6260372] J Virol. 1981 Jan;37(1):226-38 [6260976] Cell. 1982 Nov;31(1):99-109 [6297757] Int J Cancer. 1977 Mar 15;19(3):383-90 [191409] Int J Cancer. 1975 Dec 15;16(6):922-31 [172460] Cell Growth Differ. 1990 Oct;1(10):503-10 [2278881] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Leukoregulin, a novel cytokine enhances the anti-herpesvirus actions of acyclovir. AN - 80677876; 1649027 AB - Leukoregulin is a naturally occurring immunologic cytokine which increases membrane permeability and drug uptake in tumor cells but not in normal cells. In this paper we show that leukoregulin also increases membrane permeability of Herpes simplex virus type 1 (HSV-1)-infected cells. More importantly, we demonstrate that leukoregulin significantly enhances the ability of acyclovir (acycloguanosine, ACV) to inhibit the cellular release of infectious HSV-1. The ability of 1-100 microM ACV to inhibit infectious HSV-1 production is increased up to 100-fold when HSV-1-infected human amnion (WISH) cells are treated with 5 units leukoregulin/ml and ACV 3 hr after virus infection. Under these conditions, leukoregulin alone is unable to inhibit HSV-1 infectivity. In addition, three unrelated cytokines, interleukin-1 alpha (IL-1), interferon (IFN)-alpha and IFN-gamma lack the ability to enhance the anti-HSV actions of ACV when their treatment is initiated after HSV-1 infection. These findings demonstrate that a combination of immunotherapy and chemotherapy can produce a substantial inhibition of herpesvirus replication and provide a rationale for the application of this approach to the interventive treatment of virus infection. JF - Clinical immunology and immunopathology AU - Hooks, J J AU - Detrick, B AU - Evans, C H AD - Immunology & Virology Section, National Eye Institute, Bethesda, Maryland 20892. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 244 EP - 253 VL - 60 IS - 2 SN - 0090-1229, 0090-1229 KW - Antineoplastic Agents KW - 0 KW - Interferon Type I KW - Interleukin-1 KW - Lymphokines KW - leukoregulin KW - Interferon-gamma KW - 82115-62-6 KW - Acyclovir KW - X4HES1O11F KW - Index Medicus KW - Interleukin-1 -- pharmacology KW - Virus Replication -- drug effects KW - Interferon Type I -- pharmacology KW - Dose-Response Relationship, Drug KW - Cell Membrane Permeability -- drug effects KW - Interferon-gamma -- pharmacology KW - Flow Cytometry KW - Drug Synergism KW - Simplexvirus -- drug effects KW - Acyclovir -- pharmacology KW - Simplexvirus -- pathogenicity KW - Lymphokines -- pharmacology KW - Simplexvirus -- physiology KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80677876?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+immunology+and+immunopathology&rft.atitle=Leukoregulin%2C+a+novel+cytokine+enhances+the+anti-herpesvirus+actions+of+acyclovir.&rft.au=Hooks%2C+J+J%3BDetrick%2C+B%3BEvans%2C+C+H&rft.aulast=Hooks&rft.aufirst=J&rft.date=1991-08-01&rft.volume=60&rft.issue=2&rft.spage=244&rft.isbn=&rft.btitle=&rft.title=Clinical+immunology+and+immunopathology&rft.issn=00901229&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-20 N1 - Date created - 1991-08-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Nonsteroidal anti-inflammatory drugs and the risk for chronic renal disease. AN - 80644039; 2058870 AB - To evaluate the risk for chronic renal disease associated with regular use of nonaspirin nonsteroidal anti-inflammatory drugs (NSAIDs). Multicenter case-control study. Patients were 554 North Carolina residents (age range, 30 to 79 years) hospitalized between 1980 and 1982 with a discharge diagnosis indicating newly diagnosed chronic renal dysfunction and a serum creatinine level consistently at or above 130 mumol/L (1.5 mg/dL). Controls were 516 persons chosen randomly by telephone screening (if younger than 65 years of age) and from listings of Medicare recipients (if 65 years of age or older), frequency-matched to patients by age, race, sex, and proximity to study hospitals. Data on use of prescription NSAIDs and other analgesics before 1980, other risk factors, and potential confounders were obtained by telephone interviews. Patients were classified by frequency and duration of use; daily users were those who took an NSAID for at least 360 consecutive days. A twofold risk for chronic renal disease was associated with previous daily use of NSAIDs (adjusted odds ratio, 2.1; 95% Cl, 1.1 to 4.1). Increased risk was predominantly limited to men older than 65 years, for whom the odds ratio for daily use was 10.0 (Cl, 1.2 to 82.7) after adjusting for use of other analgesics. In other age-sex groups, the risk associated with NSAID use tended to be increased among those with heart disease or other factors that might indicate compromised renal circulation. These findings did not result from confounding by known renal disease risk factors and were not readily explained by potential biases. Regular use of NSAIDs may increase the risk for chronic kidney disease in some high-risk groups. With the recent over-the-counter availability and increasing popularity of NSAIDs, the possibility of an increased risk for chronic renal disease associated with their use may warrant further scrutiny. JF - Annals of internal medicine AU - Sandler, D P AU - Burr, F R AU - Weinberg, C R AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina. Y1 - 1991/08/01/ PY - 1991 DA - 1991 Aug 01 SP - 165 EP - 172 VL - 115 IS - 3 SN - 0003-4819, 0003-4819 KW - Anti-Inflammatory Agents, Non-Steroidal KW - 0 KW - Caffeine KW - 3G6A5W338E KW - Creatinine KW - AYI8EX34EU KW - Abridged Index Medicus KW - Index Medicus KW - Odds Ratio KW - Age Factors KW - Sex Factors KW - Humans KW - Aged KW - Creatinine -- blood KW - Risk Factors KW - Adult KW - Confounding Factors (Epidemiology) KW - Caffeine -- adverse effects KW - Case-Control Studies KW - Confidence Intervals KW - Middle Aged KW - Chronic Disease KW - Bias (Epidemiology) KW - Male KW - Female KW - Kidney Diseases -- blood KW - Anti-Inflammatory Agents, Non-Steroidal -- adverse effects KW - Kidney Diseases -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80644039?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+internal+medicine&rft.atitle=Nonsteroidal+anti-inflammatory+drugs+and+the+risk+for+chronic+renal+disease.&rft.au=Sandler%2C+D+P%3BBurr%2C+F+R%3BWeinberg%2C+C+R&rft.aulast=Sandler&rft.aufirst=D&rft.date=1991-08-01&rft.volume=115&rft.issue=3&rft.spage=165&rft.isbn=&rft.btitle=&rft.title=Annals+of+internal+medicine&rft.issn=00034819&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-30 N1 - Date created - 1991-07-30 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Ann Intern Med. 1991 Aug 1;115(3):227-8 [2058878] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ghetto legacy. AN - 80362698; 15336121 JF - Current biology : CB AU - O'Brien, S J AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick Cancer Research and Development Center, Frederick, Maryland 21702-1201, USA. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 209 EP - 211 VL - 1 IS - 4 SN - 0960-9822, 0960-9822 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80362698?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+biology+%3A+CB&rft.atitle=Ghetto+legacy.&rft.au=O%27Brien%2C+S+J&rft.aulast=O%27Brien&rft.aufirst=S&rft.date=1991-08-01&rft.volume=1&rft.issue=4&rft.spage=209&rft.isbn=&rft.btitle=&rft.title=Current+biology+%3A+CB&rft.issn=09609822&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2005-03-01 N1 - Date created - 2004-08-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - To T or not to T: is it selection? AN - 80359526; 15336139 JF - Current biology : CB AU - Matis, L AU - Hedrick, S AU - Bluestone, J AD - Biological Carcinogenesis and Development Program, NCI-FCRDC, Frederick, Maryland 21701, USA. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 262 EP - 264 VL - 1 IS - 4 SN - 0960-9822, 0960-9822 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80359526?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+biology+%3A+CB&rft.atitle=To+T+or+not+to+T%3A+is+it+selection%3F&rft.au=Matis%2C+L%3BHedrick%2C+S%3BBluestone%2C+J&rft.aulast=Matis&rft.aufirst=L&rft.date=1991-08-01&rft.volume=1&rft.issue=4&rft.spage=262&rft.isbn=&rft.btitle=&rft.title=Current+biology+%3A+CB&rft.issn=09609822&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2005-03-01 N1 - Date created - 2004-08-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Diet and the risk of vulvar cancer. AN - 72778592; 1669523 AB - In this case-control study, 201 case patients with vulvar cancer and 342 community control subjects responded to a 61-item food frequency questionnaire. Risk was unrelated to intake of dark green vegetables, citrus fruits, legumes, and vitamins A and C and folate. Risk increased modestly with decreased intake of dark yellow-orange vegetables; the relative risk for the lowest versus the highest quartile was 1.6. Analyses using preliminary determinations of the major carotenoids in common fruits and vegetables suggested that alpha carotene might be the protective constituent in dark yellow-orange vegetables. Intake of beta carotene and provitamin A carotenoids was unrelated to risk. Multivitamin users were at lower risk, compared to nonusers, but no trend was observed with increasing years of use, suggesting that this association was due to unmeasured differences in life-style factors. Risk increased irregularly with the number of cups of coffee consumed per week whereas consumption of alcohol was unrelated to risk. JF - Annals of epidemiology AU - Sturgeon, S R AU - Ziegler, R G AU - Brinton, L A AU - Nasca, P C AU - Mallin, K AU - Gridley, G AD - Environmental Epidemiology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 427 EP - 437 VL - 1 IS - 5 SN - 1047-2797, 1047-2797 KW - Carotenoids KW - 36-88-4 KW - Caffeine KW - 3G6A5W338E KW - Index Medicus KW - United States KW - Risk Factors KW - Humans KW - Diet Surveys KW - Case-Control Studies KW - Caffeine -- adverse effects KW - Aged KW - Middle Aged KW - Carotenoids -- administration & dosage KW - Female KW - Vulvar Neoplasms -- epidemiology KW - Diet KW - Vulvar Neoplasms -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72778592?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+epidemiology&rft.atitle=Diet+and+the+risk+of+vulvar+cancer.&rft.au=Sturgeon%2C+S+R%3BZiegler%2C+R+G%3BBrinton%2C+L+A%3BNasca%2C+P+C%3BMallin%2C+K%3BGridley%2C+G&rft.aulast=Sturgeon&rft.aufirst=S&rft.date=1991-08-01&rft.volume=1&rft.issue=5&rft.spage=427&rft.isbn=&rft.btitle=&rft.title=Annals+of+epidemiology&rft.issn=10472797&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1994-02-03 N1 - Date created - 1994-02-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A phase II study of epirubicin in breast cancer. AN - 72669300; 1797193 AB - We evaluated the efficacy of epirubicin in a phase II trial in breast cancer, as well as its cardiac toxicity. The study was carried out on 40 female patients with advanced, metastatic, or recurrent breast cancer. The patients were grouped into two groups: group I received 30 mg/m2 epirubicin weekly, and group II 90 mg/m2 epirubicin every 3 weeks. Cardiac monitoring was by ECG, roentgenography, echocardiography and endomyocardial biopsies. Clinical results were 35.3% overall response in group I, and 50% overall response in group II. No untoward cardiac toxicities were encountered. We conclude that epirubicin is an effective agent in breast cancer with relatively little cardiac toxicity. JF - Anti-cancer drugs AU - el Mawla, N G AU - Hamza, M R AU - el Khodari, A AU - Khaled, H AU - Gaafar, R AU - el Zawahry, H AU - abdel Wareth, A AU - Dardir, M D AU - Habboubi, N AD - National Cancer Institute, Department of Medical Oncology, Cairo, Egypt. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 371 EP - 374 VL - 2 IS - 4 SN - 0959-4973, 0959-4973 KW - Epirubicin KW - 3Z8479ZZ5X KW - Index Medicus KW - Drug Evaluation KW - Myocardium -- pathology KW - Humans KW - Heart Diseases -- chemically induced KW - Electrocardiography KW - Echocardiography KW - Adult KW - Neoplasm Metastasis KW - Middle Aged KW - Heart Diseases -- diagnostic imaging KW - Radiography KW - Heart Diseases -- pathology KW - Female KW - Breast Neoplasms -- drug therapy KW - Epirubicin -- therapeutic use KW - Epirubicin -- adverse effects KW - Epirubicin -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72669300?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+phase+II+study+of+epirubicin+in+breast+cancer.&rft.au=el+Mawla%2C+N+G%3BHamza%2C+M+R%3Bel+Khodari%2C+A%3BKhaled%2C+H%3BGaafar%2C+R%3Bel+Zawahry%2C+H%3Babdel+Wareth%2C+A%3BDardir%2C+M+D%3BHabboubi%2C+N&rft.aulast=el+Mawla&rft.aufirst=N&rft.date=1991-08-01&rft.volume=2&rft.issue=4&rft.spage=371&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 - 1992-04-13 N1 - Date created - 1992-04-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Clinical use of thymidine as a rescue agent from methotrexate toxicity. AN - 72651928; 1838364 AB - Thymidine has been available for clinical research as a rescue agent since 1978 under sponsorship of the Division of Cancer Treatment, National Cancer Institute. Renal insufficiency following administration of high dose methotrexate results in prolonged exposure to toxic concentrations of drug. Thymidine has been used in conjunction with leucovorin and alkaline hydration to protect patients with acute renal dysfunction from life-threatening methotrexate toxicity. The outcome of eight cases in which thymidine was released under the special exception mechanism to treat patients who developed acute renal failure following methotrexate are reported. The clinical trials using thymidine in combination with methotrexate in patients with normal renal function are also reviewed. JF - Investigational new drugs AU - Grem, J L AU - King, S A AU - Sorensen, J M AU - Christian, M C AD - Medicine Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 281 EP - 290 VL - 9 IS - 3 SN - 0167-6997, 0167-6997 KW - Thymidine KW - VC2W18DGKR KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - Humans KW - Kidney -- drug effects KW - Kidney -- physiology KW - Aged KW - Child KW - Adult KW - Middle Aged KW - Adolescent KW - Meta-Analysis as Topic KW - Female KW - Kidney Diseases -- drug therapy KW - Male KW - Kidney Diseases -- chemically induced KW - Methotrexate -- adverse effects KW - Thymidine -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72651928?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Investigational+new+drugs&rft.atitle=Clinical+use+of+thymidine+as+a+rescue+agent+from+methotrexate+toxicity.&rft.au=Grem%2C+J+L%3BKing%2C+S+A%3BSorensen%2C+J+M%3BChristian%2C+M+C&rft.aulast=Grem&rft.aufirst=J&rft.date=1991-08-01&rft.volume=9&rft.issue=3&rft.spage=281&rft.isbn=&rft.btitle=&rft.title=Investigational+new+drugs&rft.issn=01676997&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-16 N1 - Date created - 1992-03-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of substance abuse on ventricular and sulcal measures assessed by computerised tomography. AN - 72619229; 1773237 AB - Computerised tomography (CT) was used to assess the possible effects of substance abuse on brain morphology. Polydrug abusers had significantly wider third ventricles than normal controls, with a positive correlation between age and ventricle:brain ratio (VBR). Assuming no effect of age, estimated quantity of substance abuse was not significantly related to ventricular and sulcal measures, except that alcohol consumption correlated positively with VBR and severity of cocaine use correlated negatively with sulcal width. When age of the subjects was partialled out, alcohol use showed a tendency for association with VBR; however, severity of cocaine use did not remain a significant predictor of cortical sulcal width. The findings suggest that chronic use of alcohol, but not necessarily of other commonly abused substances, produces brain atrophy. JF - The British journal of psychiatry : the journal of mental science AU - Cascella, N G AU - Pearlson, G AU - Wong, D F AU - Broussolle, E AU - Nagoshi, C AU - Margolin, R A AU - London, E D AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 217 EP - 221 VL - 159 SN - 0007-1250, 0007-1250 KW - Psychotropic Drugs KW - 0 KW - Ethanol KW - 3K9958V90M KW - Index Medicus KW - Ethanol -- adverse effects KW - Psychiatric Status Rating Scales KW - Alcoholism -- pathology KW - Humans KW - Adult KW - Follow-Up Studies KW - Atrophy KW - Alcoholism -- psychology KW - Male KW - Substance-Related Disorders -- pathology KW - Brain -- pathology KW - Tomography, X-Ray Computed KW - Cerebral Ventricles -- pathology KW - Psychotropic Drugs -- adverse effects KW - Substance-Related Disorders -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72619229?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+British+journal+of+psychiatry+%3A+the+journal+of+mental+science&rft.atitle=Effects+of+substance+abuse+on+ventricular+and+sulcal+measures+assessed+by+computerised+tomography.&rft.au=Cascella%2C+N+G%3BPearlson%2C+G%3BWong%2C+D+F%3BBroussolle%2C+E%3BNagoshi%2C+C%3BMargolin%2C+R+A%3BLondon%2C+E+D&rft.aulast=Cascella&rft.aufirst=N&rft.date=1991-08-01&rft.volume=159&rft.issue=&rft.spage=217&rft.isbn=&rft.btitle=&rft.title=The+British+journal+of+psychiatry+%3A+the+journal+of+mental+science&rft.issn=00071250&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-03 N1 - Date created - 1992-03-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Toxicity studies of acetone administered in the drinking water of rodents. AN - 72597202; 1765222 AB - Two- and thirteen-week toxicity studies were conducted using male and female F344/N rats and B6C3F1 mice. Animals were exposed to the following concentrations of acetone in their drinking water: two-week studies 0; 5000; 10,000; 20,000; 50,000; or 100,000 ppm acetone. Thirteen-week rat and female mouse studies 0; 2500; 5000; 10,000; 20,000; or 50,000 ppm acetone. Thirteen week male mice were exposed to 0; 1250; 2500; 5000; 10,000; or 20,000 ppm acetone. Depressed body weight gain was restricted to the 50,000 and 100,000 ppm exposure groups. Male and female mice exposed respectively to 20,000 or 50,000 ppm acetone for 2 weeks developed hepatocellular hypertrophy. This change was not apparent after 13 weeks of exposure although relative and absolute liver weight was increased in high dose female mice. Bone marrow hypoplasia was observed in 5/5 high dose (100,000 ppm) male rats during the 2-week studies. Treatment of male rats for 13 weeks resulted in a variety of mild and subtle hematological changes that often occurred at relatively low levels of exposure (5000 ppm) and resembled those seen during the clinical condition of megaloblastic anemia. Changes characteristic of hypogonadism (depressed sperm motility and cauda epididymal and epididymal weight and elevated incidence of abnormal sperm) were observed in male rats receiving 50,000 ppm acetone for 13 weeks. The incidence and severity of a kidney lesion that is morphologically similar to the spontaneously occurring nephropathy among aging F-344 rats were increased at 20,000 and 50,000 ppm acetone, respectively, in 13-week male rats. In summary, the effects of acetone were either subtle in nature or occurred during very high levels of exposure confirming acetone's low level of toxicity. The daily levels of acetone exposure were often several-fold greater than possibly encountered by humans during the accidental consumption of contaminated groundwater (250 ppm; 5 mg/day) and frequently exceeded maximum levels reported following acute toxic exposures (2,500 mg/kg). JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Dietz, D D AU - Leininger, J R AU - Rauckman, E J AU - Thompson, M B AU - Chapin, R E AU - Morrissey, R L AU - Levine, B S AD - Division of Toxicology Research and Testing, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 347 EP - 360 VL - 17 IS - 2 SN - 0272-0590, 0272-0590 KW - Hemoglobins KW - 0 KW - Water KW - 059QF0KO0R KW - Acetone KW - 1364PS73AF KW - Index Medicus KW - Administration, Oral KW - Animals KW - Reproduction -- drug effects KW - Mice KW - Blood Cell Count KW - Rats KW - Mice, Inbred Strains KW - Rats, Inbred F344 KW - Hemoglobins -- metabolism KW - Drinking -- drug effects KW - Body Weight -- drug effects KW - Female KW - Male KW - Organ Size -- drug effects KW - Acetone -- administration & dosage KW - Acetone -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72597202?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+studies+of+acetone+administered+in+the+drinking+water+of+rodents.&rft.au=Dietz%2C+D+D%3BLeininger%2C+J+R%3BRauckman%2C+E+J%3BThompson%2C+M+B%3BChapin%2C+R+E%3BMorrissey%2C+R+L%3BLevine%2C+B+S&rft.aulast=Dietz&rft.aufirst=D&rft.date=1991-08-01&rft.volume=17&rft.issue=2&rft.spage=347&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 - 1992-02-19 N1 - Date created - 1992-02-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparative toxicity and carcinogenicity studies of tetracycline and oxytetracycline in rats and mice. AN - 72588521; 1765221 AB - Two-year toxicity and carcinogenicity studies of oxytetracycline hydrochloride and tetracycline hydrochloride, two structurally similar and widely used antibiotics, were performed in F344/N rats and B6C3F1 mice. Rats and mice were continuously exposed via their diet to the following levels of antibiotic: oxytetracycline HCl--rats 0, 25,000, or 50,000 ppm; mice 0,6,300, or 12,500 ppm; tetracycline HCl--rats and mice 0, 12,500, or 25,000 ppm. On a milligram per kilogram of body weight basis these exposures represent doses that are 20 to 140 times daily human therapeutic doses. Dose-related increased survival was noted among oxytetracycline-treated male rats and tetracycline-treated female rats and male mice, while treatment-related reduced body weight gain occurred in oxytetracycline- and tetracycline-treated mice. Microscopic changes included fatty metamorphosis and focal cellular change in livers of oxytetracycline-treated male rats and basophilic cytoplasmic and clear cell change in livers of tetracycline-treated male rats. The only neoplastic changes were a marginally increased trend in pheochromocytoma of the adrenal medulla (equivocal evidence only) among oxytetracycline-exposed male rats (12/50 controls, 19/50 low dose, 24/50 high dose) and an increased incidence of pituitary adenoma or adenocarcinoma among high-dose oxytetracycline-treated female rats (20/50 controls, 32/50 high dose). Although oxytetracycline and tetracycline appeared to increase the incidence of pituitary hyperplasia in high-dose male and female rats, respectively, the total incidence of proliferative changes (hyperplasia, adenoma, and adenocarcinoma) was not affected by antibiotic exposure. The results from these studies therefore support the notion that neither antibiotic is carcinogenic in rodents. There were several negative trends suggesting possible protective effects by both these tetracycline analogs against certain spontaneous neoplastic and non-neoplastic changes. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Dietz, D D AU - Abdo, K M AU - Haseman, J K AU - Eustis, S L AU - Huff, J E AD - Division of Toxicology Research and Testing, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 335 EP - 346 VL - 17 IS - 2 SN - 0272-0590, 0272-0590 KW - Anticarcinogenic Agents KW - 0 KW - Carcinogens KW - Tetracycline KW - F8VB5M810T KW - Oxytetracycline KW - X20I9EN955 KW - Index Medicus KW - Rats KW - Eating -- drug effects KW - Mice, Inbred Strains KW - Animals KW - Rats, Inbred F344 KW - Neoplasms, Experimental -- chemically induced KW - Body Weight -- drug effects KW - Anticarcinogenic Agents -- pharmacology KW - Mice KW - Neoplasms, Experimental -- prevention & control KW - Male KW - Female KW - Tetracycline -- toxicity KW - Carcinogens -- toxicity KW - Oxytetracycline -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72588521?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.atitle=Comparative+toxicity+and+carcinogenicity+studies+of+tetracycline+and+oxytetracycline+in+rats+and+mice.&rft.au=Dietz%2C+D+D%3BAbdo%2C+K+M%3BHaseman%2C+J+K%3BEustis%2C+S+L%3BHuff%2C+J+E&rft.aulast=Dietz&rft.aufirst=D&rft.date=1991-08-01&rft.volume=17&rft.issue=2&rft.spage=335&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 - 1992-02-19 N1 - Date created - 1992-02-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparison of the effects of repeated oral versus subcutaneous fenfluramine administration on rat brain monoamine neurons: pharmacokinetic and dose-response data. AN - 72582800; 1763116 AB - The importance of the route of drug administration (oral vs. subcutaneous) on the neurochemical effects and pharmacokinetics of repeated d,1-fenfluramine administration in rats (1-24 mg/kg b.i.d., i.e., 2-48 mg/kg/day for 4 days) was examined. Overall, comparable dose-dependent alterations in brain monoamine markers were observed following repeated oral (PO) and subcutaneous (SC) administration of fenfluramine. Doses of 1 and 2 mg/kg fenfluramine were without significant effects on the density of 3H-paroxetine-labeled serotonin (5-HT) uptake sites. Higher doses of fenfluramine (4, 12 and 24 mg/kg) produced dose-dependent decreases in 5-HT, 5-hydroxyindoleacetic acid and 5-HT uptake sites with maximal decreases (80-90%) occurring at the 12 mg/kg dose. Fenfluramine administration produced dose-dependent and biphasic effects on brain dopamine markers with increases in homovanillic acid (HVA) observed at 2 hours, whereas decreases in the levels of dopamine, HVA and dihydroxyphenylacetic acid were evident at 18 hours posttreatment. Norepinephrine levels were only decreased at the highest dose of fenfluramine. Significantly higher levels of brain fenfluramine were observed following SC than following PO administration of the drug. On the other hand, comparable levels of its active metabolite norfenfluramine were present in the brain following the two routes of fenfluramine administration. These data suggest the importance of norfenfluramine levels in the brain in determining the high-dose neurotoxic effects of fenfluramine on brain 5-HT neurons in rats. JF - Pharmacology, biochemistry, and behavior AU - De Souza, E B AU - Zaczek, R AU - Culp, S AU - Appel, N M AU - Contrera, J F AD - Neurobiology Laboratory, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 963 EP - 969 VL - 39 IS - 4 SN - 0091-3057, 0091-3057 KW - Biogenic Monoamines KW - 0 KW - Norfenfluramine KW - 1886-26-6 KW - Fenfluramine KW - 2DS058H2CF KW - Serotonin KW - 333DO1RDJY KW - Dopamine KW - VTD58H1Z2X KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Administration, Oral KW - Animals KW - Dose-Response Relationship, Drug KW - Dopamine -- metabolism KW - Chromatography, High Pressure Liquid KW - Rats, Inbred Strains KW - Rats KW - Norfenfluramine -- pharmacokinetics KW - Norfenfluramine -- pharmacology KW - Norepinephrine -- metabolism KW - Body Weight -- drug effects KW - Injections, Subcutaneous KW - Serotonin -- metabolism KW - Male KW - Fenfluramine -- administration & dosage KW - Neurons -- drug effects KW - Brain Chemistry -- drug effects KW - Biogenic Monoamines -- physiology KW - Neurons -- physiology KW - Fenfluramine -- pharmacokinetics KW - Fenfluramine -- pharmacology KW - Biogenic Monoamines -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72582800?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacology%2C+biochemistry%2C+and+behavior&rft.atitle=Comparison+of+the+effects+of+repeated+oral+versus+subcutaneous+fenfluramine+administration+on+rat+brain+monoamine+neurons%3A+pharmacokinetic+and+dose-response+data.&rft.au=De+Souza%2C+E+B%3BZaczek%2C+R%3BCulp%2C+S%3BAppel%2C+N+M%3BContrera%2C+J+F&rft.aulast=De+Souza&rft.aufirst=E&rft.date=1991-08-01&rft.volume=39&rft.issue=4&rft.spage=963&rft.isbn=&rft.btitle=&rft.title=Pharmacology%2C+biochemistry%2C+and+behavior&rft.issn=00913057&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-10 N1 - Date created - 1992-02-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - CONF T1 - Toxicology testing requirements and the U.S.-Japan collaborative study on in vitro tests for chromosomal aberrations. AN - 72500191; 1683283 AB - As part of the U.S.-Japan Agreement on Cooperation in Research and Development in Science and Technology, Japanese and American scientists met in North Carolina to exchange information on toxicology testing requirements and guidelines in the two countries and to review progress in a collaborative study on detection of chemically induced chromosomal aberrations in cultured mammalian cells. JF - Environmental health perspectives AU - Shelby, M D AU - Sofuni, T Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 255 EP - 259 VL - 94 KW - Index Medicus KW - Animals KW - International Cooperation KW - Cells, Cultured KW - Biotransformation KW - Humans KW - Mutagenicity Tests -- methods KW - Chromosome Aberrations UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72500191?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&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=Toxicology+testing+requirements+and+the+U.S.-Japan+collaborative+study+on+in+vitro+tests+for+chromosomal+aberrations.&rft.au=Shelby%2C+M+D%3BSofuni%2C+T&rft.aulast=Shelby&rft.aufirst=M&rft.date=1991-08-01&rft.volume=94&rft.issue=&rft.spage=255&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 - 1992-01-02 N1 - Date created - 1992-01-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - CONF T1 - In vitro teratology. AN - 72499152; 1683285 AB - The purpose of this conference was to reevaluate the need for and use of in vitro teratology assays; to examine the validation process for in vitro tests; and to discuss progress in the validation of in vitro teratology screens. Participants enthusiastically supported further development of short-term in vivo and in vitro systems both as prescreens for developmental toxicity and as experimental systems to explore mechanisms of action of toxicants. The group strongly endorsed the development of an updated reference list ("gold standard") of known developmental toxicants and nontoxicants as essential to further progress in developing and validating prescreening efforts. Independently, an expert group should further evaluate the performance characteristics for a validated prescreen. The limits of usefulness of prescreens for product development, regulatory use, and mechanistic investigations need to be clearly defined. Finally, too few in vitro teratology prescreens have been evaluated under multiple-laboratory conditions with common, agreed-upon test agents to draw firm conclusions regarding the merit and reproducibility of in vitro teratology prescreens. There was general agreement regarding the need to move several of the assays further along the validation pathway, at least using a short list of reference compounds. JF - Environmental health perspectives AU - Schwetz, B A AU - Morrissey, R E AU - Welsch, F AU - Kavlock, R A Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 265 EP - 268 VL - 94 KW - Teratogens KW - 0 KW - Index Medicus KW - Evaluation Studies as Topic KW - Animals KW - Humans KW - In Vitro Techniques KW - Drug Evaluation, Preclinical -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72499152?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&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=In+vitro+teratology.&rft.au=Schwetz%2C+B+A%3BMorrissey%2C+R+E%3BWelsch%2C+F%3BKavlock%2C+R+A&rft.aulast=Schwetz&rft.aufirst=B&rft.date=1991-08-01&rft.volume=94&rft.issue=&rft.spage=265&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-02 N1 - Date created - 1992-01-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Teratology. 1991 Feb;43(2):159-85 [2014481] Teratog Carcinog Mutagen. 1982;2(3-4):221-9 [6130622] Teratog Carcinog Mutagen. 1983;3(6):461-80 [6140767] Environ Health Perspect. 1985 Sep;61:55-67 [3905381] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Multidrug resistant transgenic mice as a novel pharmacologic tool. AN - 72487569; 1683231 AB - Multidrug resistance resulting from expression of an energy-dependent drug efflux pump encoded by the human MDR1 gene is a major impediment to effective cancer therapy. Pharmacologic intervention aimed at inhibiting this multidrug transporter should improve existing chemotherapy of human cancer, but drug development has been delayed by the difficulty and expense of developing valid animal models. Using recombinant DNA technology, a transgenic mouse has been engineered whose bone marrow is protected from the toxic effects of chemotherapy by expression of the MDR1 gene. This animal system allows the rapid screening of drugs which inhibit the multidrug transporter and heralds a new era of using transgenic animals for pharmacologic screening. JF - BioEssays : news and reviews in molecular, cellular and developmental biology AU - Mickisch, G H AU - Pastan, I AU - Gottesman, M M AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 381 EP - 387 VL - 13 IS - 8 SN - 0265-9247, 0265-9247 KW - Actins KW - 0 KW - Antineoplastic Agents KW - Membrane Glycoproteins KW - P-Glycoprotein KW - Index Medicus KW - Animals KW - Homozygote KW - Actins -- genetics KW - Humans KW - Mice KW - Drug Resistance -- genetics KW - Mice, Transgenic KW - Antineoplastic Agents -- pharmacology KW - Membrane Glycoproteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72487569?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BioEssays+%3A+news+and+reviews+in+molecular%2C+cellular+and+developmental+biology&rft.atitle=Multidrug+resistant+transgenic+mice+as+a+novel+pharmacologic+tool.&rft.au=Mickisch%2C+G+H%3BPastan%2C+I%3BGottesman%2C+M+M&rft.aulast=Mickisch&rft.aufirst=G&rft.date=1991-08-01&rft.volume=13&rft.issue=8&rft.spage=381&rft.isbn=&rft.btitle=&rft.title=BioEssays+%3A+news+and+reviews+in+molecular%2C+cellular+and+developmental+biology&rft.issn=02659247&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-13 N1 - Date created - 1991-12-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Epidemiology and health consequences of drug abuse among pregnant women. AN - 72470449; 1948137 JF - Seminars in perinatology AU - Khalsa, J H AU - Gfroerer, J AD - Division of Epidemiology and Prevention Research, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 265 EP - 270 VL - 15 IS - 4 SN - 0146-0005, 0146-0005 KW - Index Medicus KW - Humans KW - Adult KW - Adolescent KW - United States -- epidemiology KW - Female KW - Pregnancy KW - Pregnancy Complications -- etiology KW - Substance-Related Disorders -- complications KW - Substance-Related Disorders -- epidemiology KW - Pregnancy Complications -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72470449?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+perinatology&rft.atitle=Epidemiology+and+health+consequences+of+drug+abuse+among+pregnant+women.&rft.au=Khalsa%2C+J+H%3BGfroerer%2C+J&rft.aulast=Khalsa&rft.aufirst=J&rft.date=1991-08-01&rft.volume=15&rft.issue=4&rft.spage=265&rft.isbn=&rft.btitle=&rft.title=Seminars+in+perinatology&rft.issn=01460005&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-26 N1 - Date created - 1991-12-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Proenkephalin gene expression in C6 rat glioma cells: potentiation of cyclic adenosine 3',5'-monophosphate-dependent transcription by glucocorticoids. AN - 72455650; 1658636 AB - Glucocorticoids enhance proenkephalin gene expression in several cell types. To elucidate the mechanism(s) involved, we analyzed the potentiation by dexamethasone of the cAMP-dependent increase in proenkephalin mRNA levels elicited by forskolin in C6 rat glioma cells. This potentiation did not require ongoing protein synthesis. In nuclear run-on transcription assays, dexamethasone alone did not alter proenkephalin transcription, but strongly increased the magnitude and duration of transcriptional elevation by forskolin through a direct action not requiring ongoing protein synthesis. Dexamethasone did not alter basal or stimulated cAMP levels. To search for functionally cooperative glucocorticoid and cAMP regulatory elements, we transfected C6 cells with plasmids containing the chloramphenicol acetyltransferase (CAT) gene under the control of rat proenkephalin sequences from bases -5800 to +703. Maximum stimulation of transiently expressed CAT activity by forskolin required more than 145 and 190 or fewer base pairs of 5'-flanking sequence, implicating sequences up-stream from the previously described cAMP-inducible enhancer. Dexamethasone reduced forskolin-stimulated CAT expression from plasmids with 190 or more base-pairs of 5'-flanking sequence, an effect apparently involving multiple up-stream regions. Dexamethasone also reduced forskolin-stimulated CAT mRNA levels in C6 cells stably transfected with proenkephalin/CAT chimeric genes in the presence or absence of proteins synthesis. In summary, we demonstrate that glucocorticoids and cAMP synergize positively in regulating transcription of the endogenous gene, but interact negatively in regulating the chimeric constructs, which may lack the context or distal element(s) required for positive synergism. JF - Molecular endocrinology (Baltimore, Md.) AU - Joshi, J AU - Sabol, S L AD - Laboratory of Biochemical Genetics, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 1069 EP - 1080 VL - 5 IS - 8 SN - 0888-8809, 0888-8809 KW - Enkephalins KW - 0 KW - Protein Precursors KW - RNA, Messenger KW - proenkephalin KW - Colforsin KW - 1F7A44V6OU KW - Dexamethasone KW - 7S5I7G3JQL KW - DNA KW - 9007-49-2 KW - Cyclic AMP KW - E0399OZS9N KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Index Medicus KW - Rats KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Animals KW - Colforsin -- pharmacology KW - Tumor Cells, Cultured KW - RNA, Messenger -- metabolism KW - Transfection KW - DNA -- genetics KW - Plasmids KW - Drug Synergism KW - Cloning, Molecular KW - Enkephalins -- genetics KW - Transcription, Genetic -- drug effects KW - Dexamethasone -- pharmacology KW - Cyclic AMP -- pharmacology KW - Protein Precursors -- genetics KW - Gene Expression KW - Glioma -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72455650?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Proenkephalin+gene+expression+in+C6+rat+glioma+cells%3A+potentiation+of+cyclic+adenosine+3%27%2C5%27-monophosphate-dependent+transcription+by+glucocorticoids.&rft.au=Joshi%2C+J%3BSabol%2C+S+L&rft.aulast=Joshi&rft.aufirst=J&rft.date=1991-08-01&rft.volume=5&rft.issue=8&rft.spage=1069&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 - 1991-12-10 N1 - Date created - 1991-12-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alternatives to continuous social housing. AN - 72455507; 1658483 AB - Although social housing is desirable for social species of nonhuman primates, circumstances arise whereby social housing is precluded (for example, certain kinds of infectious disease or toxicologic research, when the health of the animal(s) would be compromised by social housing, and animals which respond behaviorally in an inappropriate manner to social housing). Nonsocial alternatives that provide increased environmental complexity to the home cage should then be considered. Nonsocial "environmental enrichment" schemes can be designed to enhance the expression of an individually housed nonhuman primate's locomotive/postural, manipulative, and foraging behaviors. In this way, nonsocial, but species-typical, behaviors can be promoted in the single cage housing condition. JF - Laboratory animal science AU - Bayne, K AD - National Center for Research Resources, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 355 EP - 359 VL - 41 IS - 4 SN - 0023-6764, 0023-6764 KW - Index Medicus KW - Animals KW - Primates -- physiology KW - Primates -- psychology KW - Housing, Animal KW - Social Behavior KW - Behavior, Animal UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72455507?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Alternatives+to+continuous+social+housing.&rft.au=Bayne%2C+K&rft.aulast=Bayne&rft.aufirst=K&rft.date=1991-08-01&rft.volume=41&rft.issue=4&rft.spage=355&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 - 1991-12-23 N1 - Date created - 1991-12-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Trends in diagnosed drug problems among newborns: United States, 1979-1987. AN - 72448287; 1935566 AB - Between 1979 and 1987, there was an estimated 361% increase in the number of drug-affected newborns discharged from the 6000 non-federal, short-stay hospitals in the United States. Per 10,000 newborns, the rate increased 339%, mostly occurring after 1983. The estimated number of drug affected newborns in 1987 was about 13,000 (95% confidence interval: 10,000-15,000). Recognizing that underreporting could have occurred, multiplicative correction factors derived from the literature were employed to produce 'adjusted' estimates. While somewhat arbitrary, the number of drug-affected newborns, adjusted for underreporting, was about 38,000 (95% confidence interval: 30,000-45,000). Both adjusted and unadjusted estimates of the numbers of newborns identified as drug-affected by the present study is much smaller than most of the estimates reported in the literature. Possible reasons for this finding are discussed. JF - Drug and alcohol dependence AU - Dicker, M AU - Leighton, E A AD - National Institute on Drug Abuse, Division of Applied Research, Rockville, MD 20857. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 151 EP - 165 VL - 28 IS - 2 SN - 0376-8716, 0376-8716 KW - Street Drugs KW - 0 KW - Index Medicus KW - Cross-Sectional Studies KW - Humans KW - Birth Rate KW - Infant, Newborn KW - Incidence KW - United States -- epidemiology KW - Male KW - Female KW - Neonatal Abstinence Syndrome -- epidemiology KW - Street Drugs -- adverse effects KW - Neonatal Abstinence Syndrome -- diagnosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72448287?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Drug+and+alcohol+dependence&rft.atitle=Trends+in+diagnosed+drug+problems+among+newborns%3A+United+States%2C+1979-1987.&rft.au=Dicker%2C+M%3BLeighton%2C+E+A&rft.aulast=Dicker&rft.aufirst=M&rft.date=1991-08-01&rft.volume=28&rft.issue=2&rft.spage=151&rft.isbn=&rft.btitle=&rft.title=Drug+and+alcohol+dependence&rft.issn=03768716&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-11 N1 - Date created - 1991-12-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chronic aluminum-induced motor neuron degeneration: clinical, neuropathological and molecular biological aspects. AN - 72444727; 1933693 AB - The monthly intracisternal inoculation of young adult New Zealand white rabbits with low-dose (100 micrograms) aluminum chloride induces aggregates of phosphorylated neurofilament that mimics the intraneuronal inclusions of amyotrophic lateral sclerosis. The chronic progressive myelopathy and topographically-specific motor neuron degeneration that occurs in the absence of suppressions of neurofilament messenger RNA levels in this model contrasts with the acute fulminant encephalomyelopathy and nonspecific gene suppressions that occur subsequent to high-dose (1000 micrograms) aluminum chloride inoculations. Further analysis of this unique model of chronic motor system degeneration can be expected to provide additional insights into the pathogenesis of amyotrophic lateral sclerosis. JF - The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques AU - Strong, M J AU - Garruto, R M AD - Laboratory of Central Nervous System Studies, National Institutes of Health, Bethesda. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 428 EP - 431 VL - 18 IS - 3 Suppl SN - 0317-1671, 0317-1671 KW - Aluminum KW - CPD4NFA903 KW - Index Medicus KW - Animals KW - In Vitro Techniques KW - Disease Models, Animal KW - Rabbits KW - Time Factors KW - Immunohistochemistry KW - Intermediate Filaments -- drug effects KW - Amyotrophic Lateral Sclerosis -- pathology KW - Amyotrophic Lateral Sclerosis -- metabolism KW - Aluminum -- metabolism KW - Aluminum -- toxicity KW - Motor Neurons -- ultrastructure KW - Motor Neurons -- drug effects KW - Amyotrophic Lateral Sclerosis -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72444727?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Canadian+journal+of+neurological+sciences.+Le+journal+canadien+des+sciences+neurologiques&rft.atitle=Chronic+aluminum-induced+motor+neuron+degeneration%3A+clinical%2C+neuropathological+and+molecular+biological+aspects.&rft.au=Strong%2C+M+J%3BGarruto%2C+R+M&rft.aulast=Strong&rft.aufirst=M&rft.date=1991-08-01&rft.volume=18&rft.issue=3+Suppl&rft.spage=428&rft.isbn=&rft.btitle=&rft.title=The+Canadian+journal+of+neurological+sciences.+Le+journal+canadien+des+sciences+neurologiques&rft.issn=03171671&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-19 N1 - Date created - 1991-12-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Regulation of c-myc and ornithine decarboxylase expression by distinct protein kinase systems in IL-3-dependent myeloid cells. AN - 72442000; 1718453 AB - We have investigated whether PK-C-regulated events are independent of those biochemical events related to IL-3-induced tyrosine kinase activation by 32Dcl cells. The depletion of functional PK-C isoform activity by prolonged PMA treatment reduced the proliferative response to IL-3 by half that of untreated control cells. PK-C-deficient 32Dcl cells were unable to respond to PMA for the induction of c-myc and ODC mRNA accumulation. PK-C down-regulation did not affect IL-3-induced tyrosine phosphorylation and inhibited IL-3-regulated c-myc and ODC mRNA expression by only 30%. However, PK-C down-regulation had a pronounced inhibitory effect on IL-3 regulation of ODC enzymatic activity. While a PK-C-dependent and -independent pathway for the regulation of c-myc and ODC mRNA expression could be demonstrated, the regulation of ODC enzymatic activity appeared to require an intact PK-C system. The data suggest that the optimum biological and biochemical responses to IL-3 requires both pathways intact, however, tyrosine kinase activation and significant increases in gene products associated with proliferation can be achieved in the absence of a functional PK-C system. JF - Lymphokine and cytokine research AU - Farrar, W L AU - Willette-Brown, J AU - Linnekin, D AD - Cytokine Molecular Mechanisms Section, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702-1201. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 291 EP - 299 VL - 10 IS - 4 SN - 1056-5477, 1056-5477 KW - Interleukin-3 KW - 0 KW - Proto-Oncogene Proteins c-myc KW - RNA, Messenger KW - Phosphotyrosine KW - 21820-51-9 KW - Tyrosine KW - 42HK56048U KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Ornithine Decarboxylase KW - EC 4.1.1.17 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Blotting, Northern KW - Cell Division -- drug effects KW - Gene Expression KW - Mice KW - RNA, Messenger -- genetics KW - In Vitro Techniques KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Tyrosine -- metabolism KW - Tyrosine -- analogs & derivatives KW - Down-Regulation -- drug effects KW - Cell Line KW - Ornithine Decarboxylase -- genetics KW - Genes, myc KW - Interleukin-3 -- pharmacology KW - Proto-Oncogene Proteins c-myc -- genetics KW - Hematopoietic Stem Cells -- physiology KW - Protein-Tyrosine Kinases -- metabolism KW - Protein Kinase C -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72442000?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Lymphokine+and+cytokine+research&rft.atitle=Regulation+of+c-myc+and+ornithine+decarboxylase+expression+by+distinct+protein+kinase+systems+in+IL-3-dependent+myeloid+cells.&rft.au=Farrar%2C+W+L%3BWillette-Brown%2C+J%3BLinnekin%2C+D&rft.aulast=Farrar&rft.aufirst=W&rft.date=1991-08-01&rft.volume=10&rft.issue=4&rft.spage=291&rft.isbn=&rft.btitle=&rft.title=Lymphokine+and+cytokine+research&rft.issn=10565477&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-02 N1 - Date created - 1991-12-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pharmacotherapies for alcoholism: promising agents and clinical issues. AN - 72161703; 1928636 AB - The past 10 years have witnessed important advances in research on pharmacotherapy for alcoholism. Promising drugs are discussed under six headings: agents to treat alcohol withdrawal; anticraving agents; agents that make drinking an aversive experience; agents to alleviate concomitant psychiatric problems; agents to treat concurrent drug abuse; and amethystic ("sobering-up") agents. Research on the drug classes is summarized and clinical issues surrounding specific agents and alcoholism pharmacotherapy in general are discussed. Finally, long-range therapeutic implications of recent findings on the actions of alcohol on basic mechanisms of the brain are offered. JF - Alcoholism, clinical and experimental research AU - Litten, R Z AU - Allen, J P AD - Treatment Research Branch, National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20857. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 620 EP - 633 VL - 15 IS - 4 SN - 0145-6008, 0145-6008 KW - Alcohol Deterrents KW - 0 KW - Index Medicus KW - Humans KW - Substance Withdrawal Syndrome -- drug therapy KW - Alcohol Deterrents -- therapeutic use KW - Alcoholism -- complications KW - Alcoholism -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72161703?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Pharmacotherapies+for+alcoholism%3A+promising+agents+and+clinical+issues.&rft.au=Litten%2C+R+Z%3BAllen%2C+J+P&rft.aulast=Litten&rft.aufirst=R&rft.date=1991-08-01&rft.volume=15&rft.issue=4&rft.spage=620&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 - 1991-11-20 N1 - Date created - 1991-11-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Neuroanatomic specificity and time course of alterations in rat brain serotonergic pathways induced by MDMA (3,4-methylenedioxymethamphetamine): assessment using quantitative autoradiography. AN - 72155383; 1681594 AB - The widely abused "designer" drug MDMA (3,4-methylenedioxymethamphetamine) has been shown to cause marked and long-lasting changes in brain serotonergic systems. The present study uses quantitative in vitro autoradiography of 3H-paroxetine labeled 5-HT uptake sites to assess the time-dependent effects of MDMA on 5-HT neurons in specific neuroanatomic loci. Following treatment with MDMA (20 mg/kg, b.i.d. for 4 days), marked decreases in 5-HT uptake sites were observed in a number of brain regions known to receive projections of 5-HT neurons. These regions included cerebral cortex, caudate nucleus, hippocampus, nucleus accumbens, olfactory tubercle, superior and inferior colliculi, geniculate nuclei, and most thalamic nuclei. In contrast, other areas such as the septal nuclei and some thalamic nuclei which also receive 5-HT projections were not substantially affected by this drug. In most regions, decreases in 5-HT uptake sites occurred within 24 hours of the last dose of MDMA and persisted at the 2 week time point. Some regions such as dorsal striatum exhibited a time-dependent reduction with greater reductions occurring at 2 weeks rather than immediately following the MDMA treatment regimen. The density of 5-HT uptake sites in other regions such as endopiriform nucleus and substantia nigra at the 2 week versus 18 hour time point indicated some degree of region-specific recovery. Regions which demonstrated no significant reduction in 5-HT uptake sites included the dorsal and median raphe nuclei, ventral tegmental area, central grey, interpeduncular nucleus, locus coerulus, pontine reticular formation and cerebellum. Likewise, regions containing 5-HT axons of passage (e.g., indusium griseum and lateral hypothalamus) appeared to be insensitive to the neurotoxic effects of MDMA on 5-HT neurons. Furthermore, the neurotoxic effects of MDMA showed specificity in that the catecholamine neurons labeled by 3H-mazindol were unaffected by the treatment regimen. These data indicate that the preferential degeneration of serotonergic neurons by MDMA is mediated primarily at 5-HT terminal regions, whereas regions containing 5-HT perikarya and axons of passage remain relatively unaffected. In addition, the observed time-dependent reductions and recovery of 5-HT uptake sites which were detected within 2 weeks of the treatment regimen in certain brain regions suggest region-specific differences in recovery of 5-HT systems from MDMA-induced lesion. JF - Synapse (New York, N.Y.) AU - Battaglia, G AU - Sharkey, J AU - Kuhar, M J AU - de Souza, E B AD - Neuroscience Branch, National Institute on Drug Abuse, Baltimore, Maryland 21224. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 249 EP - 260 VL - 8 IS - 4 SN - 0887-4476, 0887-4476 KW - Piperidines KW - 0 KW - Serotonin KW - 333DO1RDJY KW - Paroxetine KW - 41VRH5220H KW - 3,4-Methylenedioxyamphetamine KW - 4764-17-4 KW - Mazindol KW - C56709M5NH KW - N-Methyl-3,4-methylenedioxyamphetamine KW - KE1SEN21RM KW - 3,4-methylenedioxyethamphetamine KW - ML1I4KK67B KW - Dopamine KW - VTD58H1Z2X KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Animals KW - Reference Values KW - Norepinephrine -- pharmacokinetics KW - Neural Pathways -- metabolism KW - Autoradiography KW - Neural Pathways -- drug effects KW - Rats, Inbred Strains KW - Rats KW - Dopamine -- pharmacokinetics KW - Neural Pathways -- anatomy & histology KW - Time Factors KW - Male KW - Brain -- drug effects KW - 3,4-Methylenedioxyamphetamine -- analogs & derivatives KW - Brain -- anatomy & histology KW - 3,4-Methylenedioxyamphetamine -- pharmacology KW - Brain -- metabolism KW - Serotonin -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72155383?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Neuroanatomic+specificity+and+time+course+of+alterations+in+rat+brain+serotonergic+pathways+induced+by+MDMA+%283%2C4-methylenedioxymethamphetamine%29%3A+assessment+using+quantitative+autoradiography.&rft.au=Battaglia%2C+G%3BSharkey%2C+J%3BKuhar%2C+M+J%3Bde+Souza%2C+E+B&rft.aulast=Battaglia&rft.aufirst=G&rft.date=1991-08-01&rft.volume=8&rft.issue=4&rft.spage=249&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 - 1991-11-14 N1 - Date created - 1991-11-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - CONF T1 - Highlights of the 1990 Leesburg, Virginia, International Workshop on Retrospective Exposure Assessment for Occupational Epidemiology Studies. AN - 72150808; 1925441 JF - Scandinavian journal of work, environment & health AU - Stewart, P A AU - Herrick, R F AU - Blair, A AU - Checkoway, H AU - Droz, P AU - Fine, L AU - Fischer, L AU - Harris, R AU - Kauppinen, T AU - Saracci, R Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 281 EP - 285 VL - 17 IS - 4 KW - Index Medicus KW - Evaluation Studies as Topic KW - Humans KW - Retrospective Studies KW - Monitoring, Physiologic KW - Occupational Exposure KW - Environmental Monitoring -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72150808?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&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=Scandinavian+journal+of+work%2C+environment+%26+health&rft.atitle=Highlights+of+the+1990+Leesburg%2C+Virginia%2C+International+Workshop+on+Retrospective+Exposure+Assessment+for+Occupational+Epidemiology+Studies.&rft.au=Stewart%2C+P+A%3BHerrick%2C+R+F%3BBlair%2C+A%3BCheckoway%2C+H%3BDroz%2C+P%3BFine%2C+L%3BFischer%2C+L%3BHarris%2C+R%3BKauppinen%2C+T%3BSaracci%2C+R&rft.aulast=Stewart&rft.aufirst=P&rft.date=1991-08-01&rft.volume=17&rft.issue=4&rft.spage=281&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 - 1991-11-14 N1 - Date created - 1991-11-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of chorioretinal biopsy in inflammatory eye disease. AN - 72146061; 1923367 AB - Two patients who had similar clinical presentations of bilateral multiple chorioretinal lesions and needed a correct diagnosis underwent chorioretinal biopsy. The biopsy from one patient demonstrated mainly a B cell infiltrate in choroidal and subretinal nodules, while the biopsy from the second patient showed mainly macrophages in the retina. These findings directed the therapeutic approach taken in each patient. Although chorioretinal biopsy is an invasive procedure with the potential for serious complications, the resultant finding may aid in the diagnosis and guide the subsequent management of certain patients presenting with serious ocular findings of undefined etiology. JF - Ophthalmology AU - Chan, C C AU - Palestine, A G AU - Davis, J L AU - de Smet, M D AU - McLean, I W AU - Burnier, M AU - Drouilhet, J H AU - Nussenblatt, R B AD - Laboratory of Immunology, National Eye Institute, Bethesda, MD 20892. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 1281 EP - 1286 VL - 98 IS - 8 SN - 0161-6420, 0161-6420 KW - Cyclosporins KW - 0 KW - Cyclophosphamide KW - 8N3DW7272P KW - Index Medicus KW - Sarcoidosis -- pathology KW - Fundus Oculi KW - Cyclophosphamide -- therapeutic use KW - Humans KW - Cyclosporins -- therapeutic use KW - Middle Aged KW - Biopsy KW - Female KW - Retinitis -- pathology KW - Choroid -- pathology KW - Choroiditis -- pathology KW - Retina -- pathology KW - Choroiditis -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72146061?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Ophthalmology&rft.atitle=Role+of+chorioretinal+biopsy+in+inflammatory+eye+disease.&rft.au=Chan%2C+C+C%3BPalestine%2C+A+G%3BDavis%2C+J+L%3Bde+Smet%2C+M+D%3BMcLean%2C+I+W%3BBurnier%2C+M%3BDrouilhet%2C+J+H%3BNussenblatt%2C+R+B&rft.aulast=Chan&rft.aufirst=C&rft.date=1991-08-01&rft.volume=98&rft.issue=8&rft.spage=1281&rft.isbn=&rft.btitle=&rft.title=Ophthalmology&rft.issn=01616420&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-04 N1 - Date created - 1991-11-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dental amalgam. Designs for research in human populations. AN - 72141957; 1918688 AB - Questions have been raised about the safety of dental amalgam. The main point of contention is whether the mercury contained in dental restorations is released in sufficient quantities to pose a public health hazard. Most scientists agree that current evidence is not sufficient to show that amalgam restorations pose a general health threat. But researchers on both sides of this debate agree that much remains to be learned about any potential toxicity of dental amalgam--an issue serious enough to merit additional research. JF - Journal of the American Dental Association (1939) AU - Brown, L J AD - Epidemiology and Disease Prevention Program, National Institute of Dental Research, National Institutes of Health, Bethesda, Md 20892. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 73 EP - 77 VL - 122 IS - 8 SN - 0002-8177, 0002-8177 KW - Dental Amalgam KW - 8049-85-2 KW - Mercury KW - FXS1BY2PGL KW - Dentistry KW - Index Medicus KW - Mercury -- blood KW - Mercury -- urine KW - Humans KW - Mercury -- analysis KW - Cohort Studies KW - Dental Records KW - United States -- epidemiology KW - Research Design KW - Mercury Poisoning -- etiology KW - Dental Amalgam -- adverse effects KW - Mercury Poisoning -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72141957?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+American+Dental+Association+%281939%29&rft.atitle=Dental+amalgam.+Designs+for+research+in+human+populations.&rft.au=Brown%2C+L+J&rft.aulast=Brown&rft.aufirst=L&rft.date=1991-08-01&rft.volume=122&rft.issue=8&rft.spage=73&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+American+Dental+Association+%281939%29&rft.issn=00028177&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-13 N1 - Date created - 1991-11-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A controlled comparison of adjuvant lithium carbonate or thyroid hormone in clomipramine-treated patients with obsessive-compulsive disorder. AN - 72134507; 1918422 AB - In this study, 16 patients with obsessive-compulsive disorder (OCD) who had partially improved during at least 6 months of treatment with clomipramine were sequentially treated with triiodothyronine and lithium carbonate in an 8-week double-blind cross-over study. Both triiodothyronine and lithium carbonate have been reported to be efficacious in open trials as adjunctive agents when combined with tricyclics in the treatment of OCD and depressed patients. However, in our controlled study, OCD and depressive symptoms, as assessed by standardized rating scales in the patient group as a whole, did not significantly change after either adjuvant treatment. Further analysis on an individual patient basis revealed that neither adjuvant medication was associated with a clinically meaningful change (greater than 25%) in OCD symptoms. However, lithium, but not triiodothyronine, adjuvant therapy was associated with a 25% or greater reduction in depression scores in 44% of the patients. This controlled study lends further support to the contention that OCD may represent a disorder with characteristics distinct from affective disorders. JF - Journal of clinical psychopharmacology AU - Pigott, T A AU - Pato, M T AU - L'Heureux, F AU - Hill, J L AU - Grover, G N AU - Bernstein, S E AU - Murphy, D L AD - Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 242 EP - 248 VL - 11 IS - 4 SN - 0271-0749, 0271-0749 KW - Triiodothyronine KW - 06LU7C9H1V KW - Lithium Carbonate KW - 2BMD2GNA4V KW - Clomipramine KW - NUV44L116D KW - Index Medicus KW - Drug Therapy, Combination KW - Psychiatric Status Rating Scales KW - Double-Blind Method KW - Humans KW - Electrocardiography KW - Adult KW - Drug Resistance KW - Middle Aged KW - Male KW - Female KW - Lithium Carbonate -- therapeutic use KW - Triiodothyronine -- adverse effects KW - Triiodothyronine -- blood KW - Obsessive-Compulsive Disorder -- psychology KW - Lithium Carbonate -- adverse effects KW - Obsessive-Compulsive Disorder -- drug therapy KW - Clomipramine -- blood KW - Triiodothyronine -- therapeutic use KW - Lithium Carbonate -- blood KW - Clomipramine -- adverse effects KW - Clomipramine -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72134507?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+controlled+comparison+of+adjuvant+lithium+carbonate+or+thyroid+hormone+in+clomipramine-treated+patients+with+obsessive-compulsive+disorder.&rft.au=Pigott%2C+T+A%3BPato%2C+M+T%3BL%27Heureux%2C+F%3BHill%2C+J+L%3BGrover%2C+G+N%3BBernstein%2C+S+E%3BMurphy%2C+D+L&rft.aulast=Pigott&rft.aufirst=T&rft.date=1991-08-01&rft.volume=11&rft.issue=4&rft.spage=242&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 - 1991-11-18 N1 - Date created - 1991-11-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mast cell adhesion to fibronectin. AN - 72127819; 1916899 AB - The MCP-5 murine mast cell line, as well as primary bone marrow-derived cultured mast cells (BMCMC), are demonstrated to bind to fibronectin, a ubiquitous adhesion protein of the extracellular matrix. BMCMC required activation by phorbol myristate acetate (PMA) to adhere to fibronectin, whereas MCP-5 displayed spontaneous adherence. The binding of both MCP-5 and BMCMC was dose dependent, with maximal adhesion at a fibronectin concentration of 20 micrograms/ml. The 120,000 molecular weight (MW) proteolytic fragment of fibronectin containing the RGDS cell attachment site was able to substitute for the native fibronectin molecule in promoting mast cell attachment. Mast cell adhesion to fibronectin, in addition, could be inhibited by the RGDS peptide alone. These data suggest that, in addition to the previously described mast cell-laminin interactions, mast cells also adhere to fibronectin, thus providing further insight into their tissue localization and possible roles in processes such as wound healing and fibrosis. JF - Immunology AU - Dastych, J AU - Costa, J J AU - Thompson, H L AU - Metcalfe, D D AD - Mast Cell Physiology Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 478 EP - 484 VL - 73 IS - 4 SN - 0019-2805, 0019-2805 KW - Fibronectins KW - 0 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Bone Marrow Cells KW - Animals KW - Cattle KW - Dose-Response Relationship, Drug KW - Cells, Cultured KW - Kinetics KW - Humans KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Rabbits KW - Cell Adhesion -- drug effects KW - Cell Line KW - Structure-Activity Relationship KW - Fibronectins -- chemistry KW - Mast Cells -- metabolism KW - Fibronectins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72127819?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Immunology&rft.atitle=Mast+cell+adhesion+to+fibronectin.&rft.au=Dastych%2C+J%3BCosta%2C+J+J%3BThompson%2C+H+L%3BMetcalfe%2C+D+D&rft.aulast=Dastych&rft.aufirst=J&rft.date=1991-08-01&rft.volume=73&rft.issue=4&rft.spage=478&rft.isbn=&rft.btitle=&rft.title=Immunology&rft.issn=00192805&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-10-30 N1 - Date created - 1991-10-30 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Immunol. 1990 Nov 15;145(10):3425-31 [2146320] Nature. 1970 Aug 15;227(5259):680-5 [5432063] J Cell Biol. 1989 Sep;109(3):1341-9 [2475511] Nature. 1989 Oct 19;341(6243):619-24 [2477710] J Cell Biol. 1988 Nov;107(5):1881-91 [2846588] Cell. 1987 Feb 27;48(4):549-54 [3028640] Exp Cell Res. 1986 Mar;163(1):47-62 [3002832] J Cell Biol. 1988 Nov;107(5):1873-80 [2972733] Biochem Biophys Res Commun. 1988 Sep 15;155(2):603-7 [2971352] Cancer Res. 1986 Jan;46(1):1-7 [2998604] Nature. 1989 Jul 27;340(6231):307-9 [2473404] Cell. 1989 Apr 7;57(1):59-69 [2467745] J Immunol. 1989 Oct 1;143(7):2323-7 [2528592] J Exp Med. 1989 May 1;169(5):1589-605 [2523953] J Cell Biol. 1989 Sep;109(3):1321-30 [2527858] J Cell Biol. 1989 Aug;109(2):863-75 [2527241] Dev Biol. 1989 Jun;133(2):489-501 [2525104] Cell. 1989 Dec 22;59(6):1203-11 [2688898] J Cell Physiol. 1989 Nov;141(2):334-45 [2808541] J Immunol. 1988 Apr 1;140(7):2340-9 [3351302] Annu Rev Cell Biol. 1985;1:91-113 [3916324] J Biol Chem. 1990 Apr 15;265(11):5934-7 [2138612] Cell. 1981 Oct;26(2 Pt 2):259-67 [6174240] Nature. 1984 May 3-9;309(5963):30-3 [6325925] J Exp Med. 1981 Jan 1;153(1):42-60 [6256467] J Cell Biol. 1983 Nov;97(5 Pt 1):1500-6 [6355120] J Immunol. 1982 Oct;129(4):1612-8 [7108218] J Cell Biol. 1989 Aug;109(2):877-89 [2547805] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effect of manganese on biogenic amine metabolism in regions of the rat brain. AN - 72098571; 1894225 AB - The effect of prolonged exposure to low-level manganese (Mn) on regional levels of biogenic amines in the rat brain was studied. Rats were given Mn in drinking-water for 90 days, which resulted in a two- to three-fold accumulation of Mn in all regions of the brain. After exposure, dopamine beta-hydroxylase (DBH), monoamine oxidase (MAO), dopamine (DA) and serotonin (5-HT) were measured in regions of the brain. There was a significant inhibition of DBH in the striatum (P less than 0.01), hypothalamus (P less than 0.01), mid-brain (P less than 0.001) and cortex (P less than 0.01). MAO was also decreased significantly in the cerebellum and cortex (both P less than 0.01). The striatum showed a decrease in DA content, but this was not significant. However, the hippocampus showed a significant decrease (P less than 0.01) and the mid-brain showed a significant increase (P less than 0.01) in DA levels. No significant changes were observed in 5-HT levels in any region, except for an increase in the cortex (P less than 0.01). It was observed that prolonged exposure of rats to low-level Mn affects both DBH and MAO, and that this effect is region-specific. However, the effect of Mn on biogenic amines seems to be variable, and this might explain the variable signs and symptoms observed in the various phases of Mn toxicity in humans. JF - Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association AU - Subhash, M N AU - Padmashree, T S AD - Department of Neurochemistry, National Institute of Mental Health and Neuro Sciences, Bangalore, India. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 579 EP - 582 VL - 29 IS - 8 SN - 0278-6915, 0278-6915 KW - Serotonin KW - 333DO1RDJY KW - Dopamine beta-Hydroxylase KW - EC 1.14.17.1 KW - Monoamine Oxidase KW - EC 1.4.3.4 KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Rats KW - Administration, Oral KW - Animals KW - Dopamine beta-Hydroxylase -- metabolism KW - Brain Chemistry -- drug effects KW - Monoamine Oxidase -- metabolism KW - Male KW - Brain -- enzymology KW - Manganese Poisoning KW - Brain -- drug effects KW - Dopamine -- metabolism KW - Serotonin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72098571?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Effect+of+manganese+on+biogenic+amine+metabolism+in+regions+of+the+rat+brain.&rft.au=Subhash%2C+M+N%3BPadmashree%2C+T+S&rft.aulast=Subhash&rft.aufirst=M&rft.date=1991-08-01&rft.volume=29&rft.issue=8&rft.spage=579&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 - 1991-10-23 N1 - Date created - 1991-10-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Selenium-dependent glutathione peroxidase expression is inversely related to estrogen receptor content of human breast cancer cells. AN - 72088928; 1653587 AB - The absence of estrogen receptors (ER) in human breast tumors has been associated with a poorer prognosis compared to patients with ER positive breast cancer. Previous studies from our laboratory have shown that a multidrug resistant human breast cancer cell line selected for resistance to Adriamycin (ADR) exhibited markedly increased expression of both the pi class glutathione S-transferase (GST-pi) and the selenium-dependent glutathione peroxidase. These studies also revealed that the ER status was inversely related to the expression of GST-pi in six human breast cancer cell lines and primary tumor specimens. In the present study, we have examined the relationship between ER status and several biological properties of these cells, including their levels of glutathione peroxidase (GSH-Px) and catalase expression, their capacity to generate toxic hydroxyl radicals (degrees OH) by redox cycling of ADR, and their sensitivities to the cytotoxic effects of ADR and the oxidant, H2O2. Our results show that expression of GSH-Px, but not catalase, is inversely related to the ER status in these cell lines. Formation of the degree OH induced by treatment of cells with ADR was inversely proportional to the GSH-Px activity in these cell lines, and thus directly related to the ER status. Sensitivity of these cells to ADR or to H2O2, however, was not consistently related to ER status, GSH-Px, or catalase activity, or to ADR induced degree OH radical formation. These results indicate that these parameters are not predictive of cellular susceptibility to oxidative damage in these cell lines under the conditions studied. JF - Cancer communications AU - Townsend, A J AU - Morrow, C S AU - Sinha, B K AU - Cowan, K H AD - Medicine Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 265 EP - 270 VL - 3 IS - 8 SN - 0955-3541, 0955-3541 KW - RNA, Neoplasm KW - 0 KW - Receptors, Estrogen KW - Doxorubicin KW - 80168379AG KW - Hydrogen Peroxide KW - BBX060AN9V KW - Catalase KW - EC 1.11.1.6 KW - Glutathione Peroxidase KW - EC 1.11.1.9 KW - Selenium KW - H6241UJ22B KW - Index Medicus KW - Blotting, Northern KW - Doxorubicin -- pharmacology KW - Cell Survival -- drug effects KW - Tumor Cells, Cultured -- drug effects KW - Humans KW - Electron Spin Resonance Spectroscopy KW - Hydrogen Peroxide -- pharmacology KW - RNA, Neoplasm -- analysis KW - Tumor Cells, Cultured -- enzymology KW - Catalase -- analysis KW - Breast Neoplasms -- genetics KW - Breast Neoplasms -- metabolism KW - Receptors, Estrogen -- analysis KW - Glutathione Peroxidase -- genetics KW - Breast Neoplasms -- enzymology KW - Glutathione Peroxidase -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72088928?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+communications&rft.atitle=Selenium-dependent+glutathione+peroxidase+expression+is+inversely+related+to+estrogen+receptor+content+of+human+breast+cancer+cells.&rft.au=Townsend%2C+A+J%3BMorrow%2C+C+S%3BSinha%2C+B+K%3BCowan%2C+K+H&rft.aulast=Townsend&rft.aufirst=A&rft.date=1991-08-01&rft.volume=3&rft.issue=8&rft.spage=265&rft.isbn=&rft.btitle=&rft.title=Cancer+communications&rft.issn=09553541&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-10-16 N1 - Date created - 1991-10-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Nickel-induced lipid peroxidation in the liver of different strains of mice and its relation to nickel effects on antioxidant systems. AN - 72064722; 1882388 AB - After a single intraperitoneal injection of 170 mumol nickel(II)acetate/kg body wt., the activity of hepatic catalase (CAT) decreased by 25-56% in a strain- and time-dependent manner, the most susceptible being C57BL/6NCr greater than C3H/HeNCr-MTV- greater than B6C3F1 greater than or equal to BALB/cAnNCr mice. The glutathione (GSH) levels in all 4 strains were inhibited by nickel with the C57BL/6NCr mice showing the biggest decrease (68%) followed by BALB/cAnNCr (46%) greater than or equal to B6C3F1 (42%) greater than C3H/HeNCr-MTV- (22%). The response of hepatic glutathione peroxidase (GSH-Px) to nickel was variable and included 30% enhancement in C3H/HeNCr-MTV- or lack of biologically significant effect (max. +/- 10% variations in time) in the remaining strains. The activity of glutathione reductase (GSSG-R) increased gradually by up to 30% (48 h post-injection) in B6C3F1 and C3H/HeNCr-MTV- mice or, transiently, by 15-18% (3 h), in C57BL/6NCr and BALB/cAnNCr mice. Also, in some strains, nickel significantly affected superoxide dismutase (SOD) (14-19% loss in C57BL/6NCr and B6C3F1 mice, respectively), and GSH-S-transferase (GST) (26% loss in C3H/HeNCr-MTV- mice). Lipid peroxidation (LPO) in the liver reached its highest value 24 h after nickel treatment in C57BL/6NCr (549% over the control) greater than or equal to BALB/cAnNCr (519%) greater than B6C3F1 (426%) much greater than C3H/HeNCr-MTV- (39%). In conclusion, the magnitude of nickel-induced LPO shows a reverse correlation with the extent and direction of nickel effect on GSH, GSH-Px and GSSG-R, but not on CAT, SOD or GST. JF - Toxicology letters AU - Rodriguez, R E AU - Misra, M AU - North, S L AU - Kasprzak, K S AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702-1201. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 269 EP - 281 VL - 57 IS - 3 SN - 0378-4274, 0378-4274 KW - Nickel KW - 7OV03QG267 KW - Catalase KW - EC 1.11.1.6 KW - Glutathione Peroxidase KW - EC 1.11.1.9 KW - Superoxide Dismutase KW - EC 1.15.1.1 KW - Glutathione KW - GAN16C9B8O KW - Index Medicus KW - Superoxide Dismutase -- analysis KW - Mice, Inbred Strains KW - Animals KW - Glutathione -- analysis KW - Mice KW - Species Specificity KW - Glutathione Peroxidase -- analysis KW - Catalase -- analysis KW - Liver -- drug effects KW - Lipid Peroxidation -- drug effects KW - Liver -- metabolism KW - Nickel -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72064722?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+letters&rft.atitle=Nickel-induced+lipid+peroxidation+in+the+liver+of+different+strains+of+mice+and+its+relation+to+nickel+effects+on+antioxidant+systems.&rft.au=Rodriguez%2C+R+E%3BMisra%2C+M%3BNorth%2C+S+L%3BKasprzak%2C+K+S&rft.aulast=Rodriguez&rft.aufirst=R&rft.date=1991-08-01&rft.volume=57&rft.issue=3&rft.spage=269&rft.isbn=&rft.btitle=&rft.title=Toxicology+letters&rft.issn=03784274&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-27 N1 - Date created - 1991-09-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Retrospective cohort mortality study of workers at an aircraft maintenance facility. I. Epidemiological results. AN - 72055926; 1878308 AB - A retrospective cohort study of 14,457 workers at an aircraft maintenance facility was undertaken to evaluate mortality associated with exposures in their workplace. The purpose was to determine whether working with solvents, particularly trichloroethylene, posed any excess risk of mortality. The study group consisted of all civilian employees who worked for at least one year at Hill Air Force Base, Utah, between 1 January 1952 and 31 December 1956. Work histories were obtained from records at the National Personnel Records Centre, St. Louis, Missouri, and the cohort was followed up for ascertainment of vital state until 31 December 1982. Observed deaths among white people were compared with the expected number of deaths, based on the Utah white population, and adjusted for age, sex, and calendar period. Significant deficits occurred for mortality from all causes (SMR 92, 95% confidence interval (95% CI) 90-95), all malignant neoplasms (SMR 90, 95% CI 83-97), ischaemic heart disease (SMR 93, 95% CI 88-98), non-malignant respiratory disease (SMR 87, 95% CI 76-98), and accidents (SMR 61, 95% CI 52-70). Mortality was raised for multiple myeloma (MM) in white women (SMR 236, 95% CI 87-514), non-Hodgkin's lymphoma (NHL) in white women (SMR 212, 95% CI 102-390), and cancer of the biliary passages and liver in white men dying after 1980 (SMR 358, 95% CI 116-836). Detailed analysis of the 6929 employees occupationally exposed to trichloroethylene, the most widely used solvent at the base during the 1950s and 1960s, did not show any significant or persuasive association between several measures of exposure to trichloroethylene and any excess of cancer. Women employed in departments in which fabric cleaning and parachute repair operations were performed had more deaths than expected from MM and NHL. The inconsistent mortality patterns by sex, multiple and overlapping exposures, and small numbers made it difficult to ascribe these excesses to any particular substance. Hypothesis generating results are presented by a variety of exposures for causes of death not showing excesses in the overall cohort. JF - British journal of industrial medicine AU - Spirtas, R AU - Stewart, P A AU - Lee, J S AU - Marano, D E AU - Forbes, C D AU - Grauman, D J AU - Pettigrew, H M AU - Blair, A AU - Hoover, R N AU - Cohen, J L AD - US National Cancer Institute, NIH. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 515 EP - 530 VL - 48 IS - 8 SN - 0007-1072, 0007-1072 KW - Solvents KW - 0 KW - Trichloroethylene KW - 290YE8AR51 KW - Index Medicus KW - Occupational Exposure KW - Evaluation Studies as Topic KW - Lymphoma, Non-Hodgkin -- mortality KW - Trichloroethylene -- adverse effects KW - Risk Factors KW - Humans KW - Cohort Studies KW - Retrospective Studies KW - Solvents -- adverse effects KW - Multiple Myeloma -- mortality KW - Male KW - Female KW - Aircraft KW - Occupational Diseases -- etiology KW - Occupational Diseases -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72055926?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+industrial+medicine&rft.atitle=Retrospective+cohort+mortality+study+of+workers+at+an+aircraft+maintenance+facility.+I.+Epidemiological+results.&rft.au=Spirtas%2C+R%3BStewart%2C+P+A%3BLee%2C+J+S%3BMarano%2C+D+E%3BForbes%2C+C+D%3BGrauman%2C+D+J%3BPettigrew%2C+H+M%3BBlair%2C+A%3BHoover%2C+R+N%3BCohen%2C+J+L&rft.aulast=Spirtas&rft.aufirst=R&rft.date=1991-08-01&rft.volume=48&rft.issue=8&rft.spage=515&rft.isbn=&rft.btitle=&rft.title=British+journal+of+industrial+medicine&rft.issn=00071072&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-10-03 N1 - Date created - 1991-10-03 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Br J Ind Med. 1991 Aug;48(8):531-7 [1878309] N Engl J Med. 1976 Jan 15;294(3):129-33 [1244508] Int J Cancer. 1987 Feb 15;39(2):155-61 [3804490] J Occup Med. 1985 Aug;27(8):580-4 [3897488] JAMA. 1986 Sep 5;256(9):1141-7 [3801091] J Urol. 1986 Oct;136(4):834-6 [3020259] Arch Environ Health. 1989 May-Jun;44(3):150-6 [2751350] Scand J Work Environ Health. 1988 Dec;14(6):356-65 [3212412] JAMA. 1988 May 20;259(19):2867-71 [3367453] Am J Ind Med. 1988;13(1):59-69 [3344756] Am J Public Health. 1984 Nov;74(11):1278-80 [6496825] Int Arch Occup Environ Health. 1984;54(2):147-53 [6480122] N Engl J Med. 1987 Jan 1;316(1):1-5 [3491316] J Occup Med. 1987 Jun;29(6):535-41 [3612328] J Occup Med. 1987 Apr;29(4):340-4 [3585565] N Engl J Med. 1987 May 7;316(19):1174-80 [3574368] J Occup Med. 1987 Mar;29(3):217-28 [3559766] Appl Environ Microbiol. 1985 May;49(5):1080-3 [3923927] Scand J Work Environ Health. 1985;11 Suppl 1:45-52 [3906868] J Occup Med. 1985 Dec;27(12):881-4 [4087053] Br J Ind Med. 1990 Mar;47(3):162-8 [2328223] Br J Cancer. 1981 Feb;43(2):169-76 [7470379] Int J Cancer. 1982 Mar 15;29(3):239-47 [7040259] Lancet. 1982 Jan 30;1(8266):267-70 [6120284] Lancet. 1983 Feb 5;1(8319):293-4 [6130308] Br Med J (Clin Res Ed). 1983 Mar 12;286(6368):846 [6403111] J Natl Cancer Inst. 1984 May;72(5):1051-7 [6585583] Comput Biomed Res. 1983 Apr;16(2):116-26 [6851488] Scand J Work Environ Health. 1983;9 Suppl 1:1-38 [6857191] Am J Epidemiol. 1983 Jan;117(1):35-45 [6823951] Am J Public Health. 1981 Mar;71(3):305-7 [7468868] Am J Public Health. 1981 Mar;71(3):242-50 [7468855] J Occup Med. 1980 Nov;22(11):737-40 [7441393] Arch Environ Health. 1980 Jan-Feb;35(1):51-3 [7362270] J Natl Cancer Inst. 1977 Mar;58(3):525-47 [557114] J Occup Med. 1978 Oct;20(10):657-66 [722350] J Occup Med. 1978 Mar;20(3):194-6 [627938] Am J Epidemiol. 1977 May;105(5):488-95 [871121] Cancer. 1977 Jun;39(6):2608-18 [872060] Arch Environ Health. 1972 Nov;25(5):342-8 [4651547] J Natl Cancer Inst. 1969 Jul;43(1):1-14 [5804605] Endeavour. 1975 Jan;34(121):13-8 [54249] J Occup Med. 1976 Mar;18(3):165-8 [1255276] Br J Ind Med. 1989 Aug;46(8):516-20 [2775671] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Retrospective cohort mortality study of workers at an aircraft maintenance facility. II. Exposures and their assessment. AN - 72054019; 1878309 AB - Methods are presented that were used for assessing exposures in a cohort mortality study of 15,000 employees who held 150,000 jobs at an Air Force base from 1939 to 1982. Standardisation of the word order and spelling of the job titles identified 43,000 unique job title organisation combinations. Walkthrough surveys were conducted, long term employees were interviewed, and available industrial hygiene data were collected to evaluate historic exposures. Because of difficulties linking air monitoring data and use of specific chemicals to the departments identified in the work histories, position descriptions were used to identify the tasks in each job. From knowledge of the tasks and the chemicals used in those tasks the presence or absence of 23 chemicals or groups of chemicals were designated for each job organisation combination. Also, estimates of levels of exposure were made for trichloroethylene and for mixed solvents, a category comprising several solvents including trichloroethylene, Stoddard solvent, carbon tetrachloride, JP4 gasoline, freon, alcohols, 1,1,1-trichloroethane, acetone, toluene, methyl ethyl ketone, methylene chloride, o-dichlorobenzene, perchloroethylene, chloroform, styrene, and xylene. JF - British journal of industrial medicine AU - Stewart, P A AU - Lee, J S AU - Marano, D E AU - Spirtas, R AU - Forbes, C D AU - Blair, A AD - US National Cancer Institute, NIH. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 531 EP - 537 VL - 48 IS - 8 SN - 0007-1072, 0007-1072 KW - Solvents KW - 0 KW - Trichloroethylene KW - 290YE8AR51 KW - Index Medicus KW - Environmental Monitoring KW - Humans KW - Cohort Studies KW - Retrospective Studies KW - Male KW - Female KW - Aircraft KW - Occupational Diseases -- chemically induced KW - Occupational Exposure -- analysis KW - Occupational Diseases -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72054019?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+industrial+medicine&rft.atitle=Retrospective+cohort+mortality+study+of+workers+at+an+aircraft+maintenance+facility.+II.+Exposures+and+their+assessment.&rft.au=Stewart%2C+P+A%3BLee%2C+J+S%3BMarano%2C+D+E%3BSpirtas%2C+R%3BForbes%2C+C+D%3BBlair%2C+A&rft.aulast=Stewart&rft.aufirst=P&rft.date=1991-08-01&rft.volume=48&rft.issue=8&rft.spage=531&rft.isbn=&rft.btitle=&rft.title=British+journal+of+industrial+medicine&rft.issn=00071072&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-10-03 N1 - Date created - 1991-10-03 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Am Ind Hyg Assoc J. 1984 Oct;45(10):689-96 [6093492] Int J Cancer. 1986 Nov 15;38(5):677-83 [3770995] J Occup Med. 1985 Jun;27(6):420-6 [4020500] Am J Ind Med. 1983;4(3):399-419 [6846338] J Occup Med. 1981 May;23(5):353-8 [7195425] Am Ind Hyg Assoc J. 1979 Jan;40(1):58-65 [484451] Am Ind Hyg Assoc J. 1979 Jan;40(1):47-57 [484450] Arch Environ Health. 1972 Mar;24(3):189-97 [5059627] J Occup Med. 1970 May;12(5):151-7 [5423391] J Natl Cancer Inst. 1969 Jun;42(6):1045-52 [5797547] J Occup Med. 1968 May;10(5):213-32 [5651782] Br J Ind Med. 1991 Aug;48(8):515-30 [1878308] Am J Ind Med. 1987;11(1):1-14 [3028135] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Glyburide-sensitive K+ channels in cultured rat hippocampal neurons: activation by cromakalim and energy-depleting conditions. AN - 72049724; 1715018 AB - Previous studies in our laboratory have shown that cromakalim activates a tetraethylammonium-sensitive K+ current in cultured embryonic rat hippocampal neurons. This phenomenon was further characterized using whole-cell voltage-clamp and single-channel recording techniques. Glyburide (1-25 microM), an antagonist of ATP-sensitive K+ channels, produced a concentration-dependent depression of the cromakalim-activated current. In contrast, charybdotoxin (100 nM), an antagonist of some Ca(2+)-dependent and other K+ channels, not only failed to block the effect of cromakalim but actually produced a moderate enhancement of the cromakalim-activated K+ current. Neither glyburide nor charybdotoxin affected resting or voltage-activated K+ currents in the absence of cromakalim. Exposure of the cells to energy-depleting conditions (0.24 micrograms/ml oligomycin and 10 mM 2-deoxy-D-glucose) also activated an outward current. Single-channel recordings in the cell-attached configuration showed that cromakalim (100 microM) stimulated the opening of flickery single channels having a unitary conductance of approximately 26 pS and a prolonged burst duration (mean open time, approximately 131 msec); similar channel openings were observed in patches from cells exposed to energy-depleting conditions. In patches containing a single K+ channel, the open probability in the presence of cromakalim was approximately 0.6 and in the presence of energy-depleting conditions was approximately 0.8; in the absence of either of these treatments, channel openings were not observed. Glyburide produced a reversible inhibition of the channels activated by cromakalim and energy-depleting conditions. These data provide additional support for the existence of ATP-sensitive K+ channels in central neurons and indicate that the K+ channels whose opening is stimulated by cromakalim are likely to be of the ATP-sensitive type. JF - Molecular pharmacology AU - Politi, D M AU - Rogawski, M A AD - Neuronal Excitability Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 308 EP - 315 VL - 40 IS - 2 SN - 0026-895X, 0026-895X KW - Benzopyrans KW - 0 KW - Oligomycins KW - Potassium Channels KW - Pyrroles KW - Scorpion Venoms KW - Cromakalim KW - 0G4X367WA3 KW - Charybdotoxin KW - 115422-61-2 KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Deoxyglucose KW - 9G2MP84A8W KW - Glyburide KW - SX6K58TVWC KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Scorpion Venoms -- pharmacology KW - Cells, Cultured KW - Neurons -- drug effects KW - Oligomycins -- pharmacology KW - Deoxyglucose -- pharmacology KW - Adenosine Triphosphate -- pharmacology KW - Benzopyrans -- pharmacology KW - Potassium Channels -- physiology KW - Pyrroles -- pharmacology KW - Potassium Channels -- drug effects KW - Glyburide -- pharmacology KW - Hippocampus -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72049724?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Glyburide-sensitive+K%2B+channels+in+cultured+rat+hippocampal+neurons%3A+activation+by+cromakalim+and+energy-depleting+conditions.&rft.au=Politi%2C+D+M%3BRogawski%2C+M+A&rft.aulast=Politi&rft.aufirst=D&rft.date=1991-08-01&rft.volume=40&rft.issue=2&rft.spage=308&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 - 1991-09-24 N1 - Date created - 1991-09-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Site-directed mutagenesis of alpha 2A-adrenergic receptors: identification of amino acids involved in ligand binding and receptor activation by agonists. AN - 72049488; 1678850 AB - Molecular cloning of the alpha 2A-adrenergic receptor has shown that this receptor is a member of the gene superfamily of guanine nucleotide-binding protein (G protein)-coupled receptors. The alpha 2A-adrenergic receptor expressed in Chinese hamster ovary (CHO) cells attenuates and potentiates forskolin-stimulated cAMP production through independent signaling pathways. To examine the role of three conserved aspartic acid and two conserved serine residues in alpha 2A-adrenergic receptor function, we substituted asparagine for aspartic acid or alanine for serine and characterized the mutant receptors in stably transfected CHO cells. Asn113 mutant alpha 2-adrenergic receptors display no [3H] yohimbine specific binding, at concentrations up to 1000 nM. In transfected cells expressing the Asn113 mutant receptor, agonists, at concentrations up to 0.1 mM, produce small decreases (approximately 10% of wild-type values) in forskolin-stimulated cAMP and potentiate forskolin-stimulated cAMP concentrations in a dose-dependent manner, with EC50 values approximately 500-fold higher than those for the wild-type receptor. These findings suggest that Asp113 may be involved in high affinity binding of agonists and antagonists, as has been previously reported for beta 2-adrenergic and m1 muscarinic acetylcholine receptors. Asn79 mutant alpha 2-adrenergic receptors display high affinity agonist binding that is insensitive to guanine nucleotides, suggesting an altered receptor-G protein coupling. Furthermore, agonist binding to Asn79 mutant receptors elicits no change in forskolin-stimulated cAMP concentrations, similar to earlier findings that the corresponding residue in beta 2-adrenergic and muscarinic receptors is required for effector stimulation. Asp130 appears to influence receptor-G protein coupling. Mutation of this residue eliminates high affinity, guanine nucleotide-sensitive, agonist binding and produces a rightward shift in the dose-response curves for agonist-mediated inhibition of forskolin-stimulated cAMP production, compared with the wild-type receptor. Moreover, agonist potentiation of forskolin-stimulated cAMP levels is abolished if Asp130 is replaced by Asn, supporting the hypothesis that inhibition and potentiation of forskolin-stimulated cAMP production in CHO cells proceed through distinct signaling pathways. Characterization of Ala204 mutant alpha 2A-adrenergic receptors suggests a possible role for Ser204 in hydrogen bond interactions with the para-hydroxyl group of the phenyl ring of the catecholamines, as has been previously described for the corresponding serine in beta 2-adrenergic receptors.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Molecular pharmacology AU - Wang, C D AU - Buck, M A AU - Fraser, C M AD - Section on Molecular Neurobiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20852. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 168 EP - 179 VL - 40 IS - 2 SN - 0026-895X, 0026-895X KW - Adrenergic alpha-Agonists KW - 0 KW - Adrenergic alpha-Antagonists KW - Receptors, Adrenergic, alpha KW - Cyclic AMP KW - E0399OZS9N KW - Index Medicus KW - Animals KW - Guinea Pigs KW - Cells, Cultured KW - Molecular Sequence Data KW - Cyclic AMP -- metabolism KW - Amino Acid Sequence KW - Hydrogen Bonding KW - Adrenergic alpha-Antagonists -- metabolism KW - Structure-Activity Relationship KW - Protein Conformation KW - Mutagenesis KW - Binding Sites KW - Adrenergic alpha-Agonists -- pharmacology KW - Receptors, Adrenergic, alpha -- drug effects KW - Receptors, Adrenergic, alpha -- physiology KW - Receptors, Adrenergic, alpha -- chemistry KW - Adrenergic alpha-Agonists -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72049488?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Site-directed+mutagenesis+of+alpha+2A-adrenergic+receptors%3A+identification+of+amino+acids+involved+in+ligand+binding+and+receptor+activation+by+agonists.&rft.au=Wang%2C+C+D%3BBuck%2C+M+A%3BFraser%2C+C+M&rft.aulast=Wang&rft.aufirst=C&rft.date=1991-08-01&rft.volume=40&rft.issue=2&rft.spage=168&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 - 1991-09-24 N1 - Date created - 1991-09-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - An alternative view minimizing the significance of cyclosporine nephrotoxicity and in favor of enhanced immunosuppression for long-term kidney transplant recipients. AN - 72039799; 1871827 JF - Transplantation proceedings AU - Salomon, D R AD - Laboratory of Immunology, National Institutes of Health, Bethesda, Maryland, NIAID 20892. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 2115 EP - 2118 VL - 23 IS - 4 SN - 0041-1345, 0041-1345 KW - Cyclosporins KW - 0 KW - Index Medicus KW - Humans KW - Retrospective Studies KW - Follow-Up Studies KW - Florida KW - Kidney Transplantation -- pathology KW - Cyclosporins -- adverse effects KW - Kidney Transplantation -- immunology KW - Cyclosporins -- therapeutic use KW - Immunosuppression -- methods KW - Kidney Transplantation -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72039799?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Transplantation+proceedings&rft.atitle=An+alternative+view+minimizing+the+significance+of+cyclosporine+nephrotoxicity+and+in+favor+of+enhanced+immunosuppression+for+long-term+kidney+transplant+recipients.&rft.au=Salomon%2C+D+R&rft.aulast=Salomon&rft.aufirst=D&rft.date=1991-08-01&rft.volume=23&rft.issue=4&rft.spage=2115&rft.isbn=&rft.btitle=&rft.title=Transplantation+proceedings&rft.issn=00411345&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-19 N1 - Date created - 1991-09-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Isolation of the mutagenic and DNA adduct-inducing components from a commercial preparation of HC blue 1 using Salmonella (TA98) bioassay-directed HPLC fractionation. AN - 72035518; 1870626 AB - In the present study we report the separation of the mutagenic impurities from the nitrophenylenediamine hair dye HC Blue 1. This was accomplished by bioassay-directed HPLC fractionation, using Salmonella strain TA98 and reverse phase HPLC analysis. The mutagenic fraction eluted between 80 and 90% methanol, whereas the HPLC fraction containing the parent compound HC Blue 1 eluted with 30% methanol and was non-mutagenic. 100% of the mutagenic activity applied to the column was recovered in fractions that did not possess the blue color of HC Blue 1. Also, HPLC-purified HC Blue 1 did not form DNA adducts (32P-postlabeling) in Salmonella strain TA98. On the other hand, commercial HC Blue 1 and the mutagenic fraction derived from commercial HC Blue 1 (HPLC-isolated) gave similar DNA-adduct profiles that consisted of 7 adducts. DNA adduction was examined concomitantly with mutagenicity and toxicity studies on the HC Blue 1 samples in TA98. The data indicated that, in Salmonella, both the mutagenicity and DNA adduction of commercial HC Blue 1 are due to impurities and not the parent compound. JF - Mutation research AU - Abu-Shakra, A AU - Johnson, L AU - Earley, K AU - Jameson, C W AU - Kari, F W AU - Gupta, R AU - Langenbach, R AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 377 EP - 385 VL - 260 IS - 4 SN - 0027-5107, 0027-5107 KW - Hair Dyes KW - 0 KW - Mutagens KW - Phenylenediamines KW - N-methylamino-2-nitro-4-N',N'-bis(2-hydroxyethyl)aminobenzene KW - 2784-94-3 KW - Index Medicus KW - Mutagenicity Tests KW - Spectrophotometry, Ultraviolet KW - Salmonella typhimurium -- drug effects KW - Autoradiography KW - Chromatography, High Pressure Liquid KW - Phenylenediamines -- toxicity KW - DNA Damage KW - Hair Dyes -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72035518?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Isolation+of+the+mutagenic+and+DNA+adduct-inducing+components+from+a+commercial+preparation+of+HC+blue+1+using+Salmonella+%28TA98%29+bioassay-directed+HPLC+fractionation.&rft.au=Abu-Shakra%2C+A%3BJohnson%2C+L%3BEarley%2C+K%3BJameson%2C+C+W%3BKari%2C+F+W%3BGupta%2C+R%3BLangenbach%2C+R&rft.aulast=Abu-Shakra&rft.aufirst=A&rft.date=1991-08-01&rft.volume=260&rft.issue=4&rft.spage=377&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 - 1991-09-17 N1 - Date created - 1991-09-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Methyl carbamate: negative results in mouse bone-marrow micronucleus test. AN - 72033235; 1870620 JF - Mutation research AU - Shelby, M D AU - Tice, R R AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 311 VL - 260 IS - 4 SN - 0027-5107, 0027-5107 KW - Carbamates KW - 0 KW - Mutagens KW - methyl carbamate KW - 9WFX634X2T KW - Index Medicus KW - Bone Marrow Cells KW - Animals KW - Micronucleus Tests KW - Mice KW - Male KW - Carbamates -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72033235?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Methyl+carbamate%3A+negative+results+in+mouse+bone-marrow+micronucleus+test.&rft.au=Shelby%2C+M+D%3BTice%2C+R+R&rft.aulast=Shelby&rft.aufirst=M&rft.date=1991-08-01&rft.volume=260&rft.issue=4&rft.spage=311&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 - 1991-09-17 N1 - Date created - 1991-09-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inactivation of a sperm motility gene by insertion of an epidermal growth factor receptor transgene whose product is overexpressed and compartmentalized during spermatogenesis. AN - 72031801; 1714416 AB - Transgenic mice were generated with a human epidermal growth factor (EGF) receptor cDNA driven by the chicken beta-actin gene promoter. One line (AE24) that exhibited a unique expression pattern in which dramatically elevated levels of EGF receptor RNA were found only in the testis was established, suggesting that the beta-actin promoter was being influenced by an adjacent testis-specific enhancer. EGF receptor RNA was detected in primary spermatocytes, whereas the synthesis of receptor protein was restricted to elongate spermatids, indicating that transgene expression was under translational control. At spermiation, the EGF receptor was sequestered in residual bodies and excluded from mature sperm by a compartmentalization mechanism. About half of AE24 homozygous males were sterile because of sperm paralysis, whereas heterozygous males and females of either genotype were completely fertile. Electron microscopic analysis of sperm flagella from sterile AE24 homozygotes revealed an aberrant axonemal structure in which outer doublet microtubules were missing from the middle piece, resembling changes observed in the sperm of some infertile humans. Flagellar axonemal disassembly was observed in the vas deferens and epididymis but not in the testis, suggesting that outer doublets were assembled in a grossly normal manner but possessed a latent instability. These results demonstrate that in the AE24 mouse line the EGF receptor transgene was integrated into and inactivated an endogenous autosomal gene, causing sperm flagellar axonemal disruption and male sterility. JF - Genes & development AU - Merlino, G T AU - Stahle, C AU - Jhappan, C AU - Linton, R AU - Mahon, K A AU - Willingham, M C AD - Laboratory of Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/08// PY - 1991 DA - August 1991 SP - 1395 EP - 1406 VL - 5 IS - 8 SN - 0890-9369, 0890-9369 KW - Actins KW - 0 KW - RNA KW - 63231-63-0 KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Index Medicus KW - Animals KW - Protein Biosynthesis KW - Humans KW - Sperm Tail -- ultrastructure KW - Gene Expression KW - Mice KW - Nucleic Acid Hybridization KW - Mice, Transgenic KW - Chickens KW - Promoter Regions, Genetic KW - Actins -- genetics KW - RNA -- isolation & purification KW - Immunohistochemistry KW - Male KW - RNA -- genetics KW - Genes KW - Receptor, Epidermal Growth Factor -- genetics KW - Infertility, Male -- pathology KW - Infertility, Male -- genetics KW - Gene Expression Regulation KW - Receptor, Epidermal Growth Factor -- analysis KW - Sperm Motility KW - Spermatogenesis KW - Mutagenesis, Insertional UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72031801?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Genes+%26+development&rft.atitle=Inactivation+of+a+sperm+motility+gene+by+insertion+of+an+epidermal+growth+factor+receptor+transgene+whose+product+is+overexpressed+and+compartmentalized+during+spermatogenesis.&rft.au=Merlino%2C+G+T%3BStahle%2C+C%3BJhappan%2C+C%3BLinton%2C+R%3BMahon%2C+K+A%3BWillingham%2C+M+C&rft.aulast=Merlino&rft.aufirst=G&rft.date=1991-08-01&rft.volume=5&rft.issue=8&rft.spage=1395&rft.isbn=&rft.btitle=&rft.title=Genes+%26+development&rft.issn=08909369&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-13 N1 - Date created - 1991-09-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Opisthorchis viverrini infestation and endogenous nitrosamines as risk factors for cholangiocarcinoma in Thailand. AN - 80708415; 1650329 AB - Cholangiocarcinoma (CCA) is one of the most common cancers in north-east Thailand and has been associated with infestation by the liver fluke Opisthorchis viverrini (OV). Two samples of 12-hr overnight urine (after dosing with proline and ascorbic acid or proline alone) were collected from 20 inhabitants from each of 5 contrasting incidence areas for CCA. The incidence of CCA was not correlated with either the amount of NPRO or other nitrosamino acids, endogenous nitrosation potential (difference in NPRO levels between proline dose and proline and ascorbic dose), or nitrate level. However, when urinary levels of nitrosamino acids were compared in subjects living in high-risk areas, subjects who were positive for OV antibody excreted significantly more (p less than 0.01) NPRO (12.3 +/- 18.7 micrograms/12 hr) after proline ingestion than those who were negative (3.5 +/- 3.2 micrograms/12 hr). After ingestion of ascorbic acid, the NPRO levels in the positive subjects were significantly reduced (p less than 0.01) to 2.4 +/- 2.0 micrograms/12 hr, suggesting that endogenous nitrosation of proline was inhibited. Thus, endogenous nitrosation potential estimated from the difference between NPRO and the sum of nitrosamino acids excreted in the 2 urine samples was significantly higher in subjects positive for the OV antibody. Small amounts of pre-formed nitrosamines were found in fermented fish and pork food items, which are consumed frequently in the high-risk area for CCA. These results suggest that the interaction between chemical carcinogens, especially nitrosamines, and OV infestation may play a role in the development of cholangiocarcinoma in Thailand. JF - International journal of cancer AU - Srivatanakul, P AU - Ohshima, H AU - Khlat, M AU - Parkin, M AU - Sukaryodhin, S AU - Brouet, I AU - Bartsch, H AD - National Cancer Institute of Thailand, Bangkok. Y1 - 1991/07/30/ PY - 1991 DA - 1991 Jul 30 SP - 821 EP - 825 VL - 48 IS - 6 SN - 0020-7136, 0020-7136 KW - Amino Acids KW - 0 KW - Nitrates KW - Nitrosamines KW - Proline KW - 9DLQ4CIU6V KW - Creatinine KW - AYI8EX34EU KW - Index Medicus KW - Demography KW - Proline -- metabolism KW - Creatinine -- urine KW - Fermentation KW - Thailand KW - Humans KW - Food Analysis KW - Adult KW - Incidence KW - Male KW - Female KW - Amino Acids -- urine KW - Nitrates -- urine KW - Bile Duct Neoplasms -- epidemiology KW - Adenoma, Bile Duct -- epidemiology KW - Opisthorchiasis -- complications KW - Opisthorchiasis -- physiopathology KW - Nitrosamines -- urine KW - Bile Duct Neoplasms -- etiology KW - Adenoma, Bile Duct -- etiology KW - Diet UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80708415?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Opisthorchis+viverrini+infestation+and+endogenous+nitrosamines+as+risk+factors+for+cholangiocarcinoma+in+Thailand.&rft.au=Srivatanakul%2C+P%3BOhshima%2C+H%3BKhlat%2C+M%3BParkin%2C+M%3BSukaryodhin%2C+S%3BBrouet%2C+I%3BBartsch%2C+H&rft.aulast=Srivatanakul&rft.aufirst=P&rft.date=1991-07-30&rft.volume=48&rft.issue=6&rft.spage=821&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 - 1991-09-04 N1 - Date created - 1991-09-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Analysis of sequences in domain II of Pseudomonas exotoxin A which mediate translocation. AN - 80699766; 1906738 AB - Pseudomonas exotoxin (PE) contains 613 amino acids that are arranged into 3 structural domains. PE exerts its cell-killing effects in a series of steps initiated by binding to the cell surface and internalization into endocytic vesicles. The toxin is then cleaved within domain II near arginine-279, generating a C-terminal 37-kDa fragment that is translocated into the cytosol where it ADP-ribosylates elongation factor 2 and arrests protein synthesis. In this study, we have focused on the functions of PE which are encoded by domain II. We have used the chimeric toxin TGF alpha-PE40 to deliver the toxin's ADP-ribosylating activity to the cell cytosol. Deletion analysis revealed that sequences from 253 to 345 were essential for toxicity but sequences from 346 to 364 were dispensable. Additional point mutants were constructed which identified amino acids 339 and 343 as important residues while amino acids 344 and 345 could be altered without loss of cytotoxic activity. Our data support the idea that domain II functions by first allowing PE to be processed to a 37-kDa fragment and then key sequences such as those identified in this study mediate the translocation of ADP-ribosylation activity to the cytosol. JF - Biochemistry AU - Siegall, C B AU - Ogata, M AU - Pastan, I AU - FitzGerald, D J AD - Division of Cancer Biology Diagnosis Centers, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/07/23/ PY - 1991 DA - 1991 Jul 23 SP - 7154 EP - 7159 VL - 30 IS - 29 SN - 0006-2960, 0006-2960 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - Transforming Growth Factor alpha KW - Virulence Factors KW - Adenosine Diphosphate Ribose KW - 20762-30-5 KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - Chromosome Deletion KW - Chimera KW - Transforming Growth Factor alpha -- genetics KW - Models, Molecular KW - Electrophoresis, Polyacrylamide Gel KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Plasmids KW - Biological Transport, Active KW - Adenosine Diphosphate Ribose -- metabolism KW - Mutation KW - Bacterial Toxins -- genetics KW - Exotoxins -- genetics KW - Pseudomonas aeruginosa -- genetics KW - Bacterial Toxins -- metabolism KW - Exotoxins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80699766?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+sequences+in+domain+II+of+Pseudomonas+exotoxin+A+which+mediate+translocation.&rft.au=Siegall%2C+C+B%3BOgata%2C+M%3BPastan%2C+I%3BFitzGerald%2C+D+J&rft.aulast=Siegall&rft.aufirst=C&rft.date=1991-07-23&rft.volume=30&rft.issue=29&rft.spage=7154&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-27 N1 - Date created - 1991-08-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modulation of cytolytic T lymphocyte functions by an inhibitor of serine/threonine phosphatase, okadaic acid. Enhancement of cytolytic T lymphocyte-mediated cytotoxicity. AN - 80681817; 1649222 AB - A specific and potent inhibitor of protein phosphatases 1 and 2A, okadaic acid (OA), and its inactive analog, tetramethyl ether (OA-TME), were tested in the cytotoxicity and granule exocytosis assays of CTL activation. At low concentrations OA enhanced, whereas at higher concentrations OA inhibited, CTL responses. The Ag-specific and retargeted cytotoxicity, granule exocytosis induced by target cell (TC), anti-TCR mAb, or PMA and A23187, and conjugate formation with TC were inhibited by pretreatment of CTL with OA as expected if protein phosphatases and protein dephosphorylation were indeed involved in the TCR-mediated signal transduction and effector responses of CTL. Cytotoxicity and granule exocytosis were unaffected by pretreatment of CTL with OA-TME. The inhibitory effect of OA on the exocytic response of CTL induced by TC and anti-TCR mAb can be dissociated from the inhibition of the response to PMA and A23187, suggesting the involvement of a serine and/or threonine protein phosphatase in the early events of transmembrane signaling. At lower concentrations, OA, but not OA-TME, was able to enhance the Ag-specific cytotoxicity and TC-induced exocytosis from CTL clones. The enhancement of these TCR-mediated responses of CTL was observed only if the activation was induced by the Ag on the TC surface, because OA did not enhance either the anti-TCR mAb-induced exocytosis of granules from the CTL clone or lysis of the Ag-nonbearing TC by CTL in a retargeting assay. The biphasic character of the effects of OA on CTL-TC interactions suggests the existence of at least two functionally distinct phosphatases in CTL. The ability of OA to enhance the Ag-specific response is unique and indicates the presence of an inhibitory phosphoprotein phosphatase that should be considered as a participant in the down-regulation of the cell-cell interactions between CTL and TC. The inhibitory effects of OA on both TC-induced and anti-TCR mAb-triggered CTL responses at higher concentrations point to the importance of yet another phosphatase in the CTL-TC interactions and in the TCR-mediated transmembrane signaling. The use of OA may help to decipher the details of biochemical changes involved in T lymphocyte effector functions. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Taffs, R E AU - Redegeld, F A AU - Sitkovsky, M V AD - Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/07/15/ PY - 1991 DA - 1991 Jul 15 SP - 722 EP - 728 VL - 147 IS - 2 SN - 0022-1767, 0022-1767 KW - Antigens KW - 0 KW - Antigens, CD8 KW - Antigens, Differentiation, T-Lymphocyte KW - Ethers, Cyclic KW - Lymphocyte Function-Associated Antigen-1 KW - Okadaic Acid KW - 1W21G5Q4N2 KW - Phosphoprotein Phosphatases KW - EC 3.1.3.16 KW - Abridged Index Medicus KW - Index Medicus KW - Clone Cells KW - Animals KW - Antigens, Differentiation, T-Lymphocyte -- physiology KW - In Vitro Techniques KW - Mice KW - Antigens -- immunology KW - Lymphocyte Function-Associated Antigen-1 -- physiology KW - Cell Line KW - Cell Degranulation -- drug effects KW - Phosphoprotein Phosphatases -- antagonists & inhibitors KW - T-Lymphocytes, Cytotoxic -- immunology KW - Ethers, Cyclic -- pharmacology KW - Cytotoxicity, Immunologic -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80681817?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Modulation+of+cytolytic+T+lymphocyte+functions+by+an+inhibitor+of+serine%2Fthreonine+phosphatase%2C+okadaic+acid.+Enhancement+of+cytolytic+T+lymphocyte-mediated+cytotoxicity.&rft.au=Taffs%2C+R+E%3BRedegeld%2C+F+A%3BSitkovsky%2C+M+V&rft.aulast=Taffs&rft.aufirst=R&rft.date=1991-07-15&rft.volume=147&rft.issue=2&rft.spage=722&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 - 1991-08-20 N1 - Date created - 1991-08-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Nitric oxide mediates glutamate neurotoxicity in primary cortical cultures. AN - 80673490; 1648740 AB - Nitric oxide (NO) mediates several biological actions, including relaxation of blood vessels, cytotoxicity of activated macrophages, and formation of cGMP by activation of glutamate receptors in cerebellar slices. Nitric oxide synthase (EC 1.14.23.-) immunoreactivity is colocalized with nicotinamide adenine di-nucleotide phosphate diaphorase in neurons that are uniquely resistant to toxic insults. We show that the nitric oxide synthase inhibitors, N omega-nitro-L-arginine (EC50 = 20 microM) and N omega-monomethyl-L-arginine (EC50 = 170 microM), prevent neurotoxicity elicited by N-methyl-D-aspartate and related excitatory amino acids. This effect is competitively reversed by L-arginine. Depletion of the culture medium of arginine by arginase or arginine-free growth medium completely attenuates N-methyl-D-aspartate toxicity. Sodium nitroprusside, which spontaneously releases NO, produces dose-dependent cell death that parallels cGMP formation. Hemoglobin, which complexes NO, prevents neurotoxic effects of both N-methyl-D-aspartate and sodium nitroprusside. These data establish that NO mediates the neurotoxicity of glutamate. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Dawson, V L AU - Dawson, T M AU - London, E D AU - Bredt, D S AU - Snyder, S H AD - Neuropharmacology Laboratory, National Institute on Drug Abuse Addiction Research Center, Baltimore, MD 21224. Y1 - 1991/07/15/ PY - 1991 DA - 1991 Jul 15 SP - 6368 EP - 6371 VL - 88 IS - 14 SN - 0027-8424, 0027-8424 KW - Glutamates KW - 0 KW - Hemoglobins KW - Neurotoxins KW - Receptors, N-Methyl-D-Aspartate KW - Citrulline KW - 29VT07BGDA KW - Nitric Oxide KW - 31C4KY9ESH KW - N-Methylaspartate KW - 6384-92-5 KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - Arginine KW - 94ZLA3W45F KW - Superoxide Dismutase KW - EC 1.15.1.1 KW - Cyclic GMP KW - H2D2X058MU KW - Index Medicus KW - Animals KW - Fetus KW - Dizocilpine Maleate -- metabolism KW - Arginine -- metabolism KW - Receptors, N-Methyl-D-Aspartate -- metabolism KW - Hemoglobins -- pharmacology KW - Arginine -- pharmacology KW - Rats KW - Cyclic GMP -- metabolism KW - Superoxide Dismutase -- pharmacology KW - Cell Survival -- drug effects KW - Cells, Cultured KW - N-Methylaspartate -- pharmacology KW - Kinetics KW - Citrulline -- metabolism KW - Hippocampus -- physiology KW - Glutamates -- pharmacology KW - Neurons -- drug effects KW - Neurons -- cytology KW - Hippocampus -- cytology KW - Neurons -- physiology KW - Nitric Oxide -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80673490?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Nitric+oxide+mediates+glutamate+neurotoxicity+in+primary+cortical+cultures.&rft.au=Dawson%2C+V+L%3BDawson%2C+T+M%3BLondon%2C+E+D%3BBredt%2C+D+S%3BSnyder%2C+S+H&rft.aulast=Dawson&rft.aufirst=V&rft.date=1991-07-15&rft.volume=88&rft.issue=14&rft.spage=6368&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 - 1991-08-14 N1 - Date created - 1991-08-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1990 Nov;87(21):8607-11 [1978327] Pflugers Arch. 1981 Aug;391(2):85-100 [6270629] Biochem Biophys Res Commun. 1991 May 15;176(3):1136-41 [1710109] Trends Neurosci. 1991 Feb;14(2):60-7 [1708538] Trends Pharmacol Sci. 1991 Apr;12(4):125-8 [1712138] Nature. 1990 Oct 25;347(6295):768-70 [1700301] Trends Pharmacol Sci. 1990 Sep;11(9):379-87 [2238094] Biochem Pharmacol. 1989 Jun 1;38(11):1709-15 [2567594] Trends Biochem Sci. 1989 Dec;14(12):488-92 [2696179] Science. 1986 Oct 3;234(4772):73-6 [2875522] Science. 1985 Nov 1;230(4725):561-3 [2931802] Ann Neurol. 1988 Feb;23(2):105-14 [2897822] J Immunol. 1987 Jan 15;138(2):550-65 [2432129] Proc Natl Acad Sci U S A. 1989 Nov;86(22):9030-3 [2573074] Eur J Pharmacol. 1989 Dec 19;174(2-3):297-9 [2630304] Br J Pharmacol. 1989 Dec;98(4):1080-2 [2611482] Proc Natl Acad Sci U S A. 1989 Jul;86(13):5159-62 [2567995] Eur J Pharmacol. 1989 Oct 17;172(4-5):413-6 [2555211] Proc Natl Acad Sci U S A. 1989 Jan;86(2):740-4 [2536176] J Exp Med. 1989 May 1;169(5):1543-55 [2497225] Biochem Biophys Res Commun. 1988 Nov 30;157(1):87-94 [3196352] J Neurosci. 1988 Jun;8(6):2153-63 [3385492] Acta Physiol Scand. 1990 Jun;139(2):257-70 [2164317] Annu Rev Pharmacol Toxicol. 1990;30:535-60 [2188578] Nature. 1990 May 24;345(6273):346-7 [1971425] Biochem Biophys Res Commun. 1990 Mar 30;167(3):1037-43 [2322257] Ann Neurol. 1990 Jun;27(6):620-5 [1972876] J Neurosci. 1990 Feb;10(2):693-705 [2406381] Proc Natl Acad Sci U S A. 1990 Jan;87(2):682-5 [1689048] J Neurosci. 1990 Aug;10(8):2493-501 [1974918] Proc Natl Acad Sci U S A. 1990 Feb;87(4):1620-4 [2154753] J Neurochem. 1991 Mar;56(3):990-5 [1704427] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cellular pharmacology of cyclopentenyl cytosine in Molt-4 lymphoblasts. AN - 80665693; 1712247 AB - The toxicity, uptake, and metabolism of the oncolytic nucleoside cyclopentenyl cytosine (CPEC) have been examined in the Molt-4 line of human lymphoblasts. This compound is known to be converted to its 5'-triphosphate, which inhibits CTP synthetase and depletes the pools of cytidine nucleotides. In the Molt-4 system, the concentration of drug reducing proliferation by 50% in a 24-h incubation was between 50 and 100 nM. Cytidine, uridine, and nitrobenzylthioinosine almost fully prevented the cytotoxicity of CPEC when introduced shortly before or together with the drug, but only cytidine was effective as an antidote when added 12 h after 200 nM CPEC. Studies of the cellular entry of CPEC revealed that nitrobenzylthioinosine fully blocked this process over a 60-s interval and for as long as 2 h, suggesting that the initial interiorization was mediated by facilitated diffusion. In Molt-4 cells incubated with tritiated CPEC, 9 metabolites could be distinguished: prominent among these was cyclopentenyl uridine (CPEU), the deamination product of CPEC; other major metabolites included the 5'-mono-, di-, and triphosphates of CPEC, and of CPEU, along with two phosphodiesters provisionally identified as CPEC-diphosphate choline and CPEC-diphosphate ethanolamine. When the accumulation of CPEC-5'-triphosphate was measured as a function of concentration of the drug in the medium, the process was found not to be saturable by levels of CPEC up to 1000 nM. In cells incubated with 200 nM drug, CPEC-5'-triphosphate accumulated rapidly and linearly for approximately 4 h, the time for doubling of the concentration being 2 h. After a 16-h incubation with 100 nM CPEC, the concentration of CPEC-5'-triphosphate was 50-fold that of the parent drug in the medium and could be readily monitored spectrophotometrically in high-pressure liquid chromatography effluents without recourse to radiolabeled nucleoside. In 2-h incubations, the concentration of free CPEC required to reduce CTP by 50% was 150 nM; this corresponded to a CPEC-5'-triphosphate level of 750 nM. After washout of extracellular CPEC, CPEC-5'-triphosphate decayed with a half-life that ranged from 9 to 14 h. Twenty-four h after washout of 200 nM CPEC (the concentration of drug reducing proliferation by 80%), cells had not resumed proliferation, and CTP pools were still depressed by 90%. Cytidine, uridine, and nitrobenzylthioinosine all strongly repressed the anabolic phosphorylation of CPEC when added to Molt-4 cells along with the drug.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Cancer research AU - Ford, H AU - Cooney, D A AU - Ahluwalia, G S AU - Hao, Z AU - Rommel, M E AU - Hicks, L AU - Dobyns, K A AU - Tomaszewski, J E AU - Johns, D G AD - Laboratory of Medicinal Chemistry, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/07/15/ PY - 1991 DA - 1991 Jul 15 SP - 3733 EP - 3740 VL - 51 IS - 14 SN - 0008-5472, 0008-5472 KW - Antineoplastic Agents KW - 0 KW - Cytidine KW - 5CSZ8459RP KW - RNA KW - 63231-63-0 KW - Cytidine Triphosphate KW - 65-47-4 KW - cyclopentenyl cytosine KW - 69MO0NDN8K KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Protein Biosynthesis KW - RNA -- metabolism KW - Cytidine Triphosphate -- metabolism KW - Humans KW - DNA -- metabolism KW - Cell Line KW - Antineoplastic Agents -- metabolism KW - Cytidine -- pharmacology KW - Lymphocytes -- metabolism KW - Cytidine -- metabolism KW - Cytidine -- antagonists & inhibitors KW - Cytidine -- analogs & derivatives KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80665693?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cellular+pharmacology+of+cyclopentenyl+cytosine+in+Molt-4+lymphoblasts.&rft.au=Ford%2C+H%3BCooney%2C+D+A%3BAhluwalia%2C+G+S%3BHao%2C+Z%3BRommel%2C+M+E%3BHicks%2C+L%3BDobyns%2C+K+A%3BTomaszewski%2C+J+E%3BJohns%2C+D+G&rft.aulast=Ford&rft.aufirst=H&rft.date=1991-07-15&rft.volume=51&rft.issue=14&rft.spage=3733&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 - 1991-08-12 N1 - Date created - 1991-08-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human bronchial epithelial cells transformed by the c-raf-1 and c-myc protooncogenes induce multidifferentiated carcinomas in nude mice: a model for lung carcinogenesis. AN - 80663551; 1712250 AB - We have previously described the neoplastic transformation of immortalized human bronchial epithelial cells (BEAS-2B) by the combination of the c-raf-1 and c-myc protooncogenes and the concomitant induction of neuron-specific enolase mRNA expression (A. Pfeifer et al., Proc. Natl. Acad. Sci. USA, 86: 10075-10079, 1989). In this paper we describe the morphological, biochemical, and immunohistochemical characteristics of the primary c-raf-1/c-myc tumors, xenografts of these tumors, and tumors that originated from cell lines of the primary neoplasm. The tumors were morphologically characterized by the appearance of desmosomes and tonofilaments, microvilli, and dense core granules representing markers of squamous, glandular, and neuroendocrine differentiation, respectively. A total of 11 of 13 tumors were positive by immunohistochemical techniques for neuron-specific enolase, serotonin (nine of 13), and calcitonin (six of 13). Keratins were expressed in 11 of 13 tumors, and while specific keratins (K5, K7, K16/K17) decreased, there was an increase of vimentin in the tumor cells. Gastrin-releasing peptide immunoreactivity was detectable in a small number of tumors (five of 13). BEAS-2B cells transfected with the c-raf-1 and c-myc protooncogenes and cell lines established from the primary tumors expressed major histocompatibility Class II antigen which has been found on small cell lung carcinoma cells. The tumors induced by the c-raf-1 and c-myc protooncogenes resemble the multidifferentiated phenotype of small cell lung cancer frequently detected in vivo and present a defined model to study the relation between molecular markers, phenotypical appearance, and response to chemotherapeutic agents and radiation. JF - Cancer research AU - Pfeifer, A M AU - Jones, R T AU - Bowden, P E AU - Mann, D AU - Spillare, E AU - Klein-Szanto, A J AU - Trump, B F AU - Harris, C C AD - Laboratory of Human Carcinogenesis, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1991/07/15/ PY - 1991 DA - 1991 Jul 15 SP - 3793 EP - 3801 VL - 51 IS - 14 SN - 0008-5472, 0008-5472 KW - Antigens, Neoplasm KW - 0 KW - Histocompatibility Antigens Class II KW - Proto-Oncogene Proteins KW - Keratins KW - 68238-35-7 KW - Proto-Oncogene Proteins c-raf KW - EC 2.7.11.1 KW - Phosphopyruvate Hydratase KW - EC 4.2.1.11 KW - Index Medicus KW - Neoplasm Transplantation KW - Animals KW - Phosphopyruvate Hydratase -- analysis KW - Humans KW - Antigens, Neoplasm -- analysis KW - Transplantation, Heterologous KW - Mice KW - Keratins -- analysis KW - Histocompatibility Antigens Class II -- analysis KW - Epithelium -- pathology KW - Immunohistochemistry KW - Cell Line KW - Genes, myc KW - Adenocarcinoma -- genetics KW - Carcinoma, Squamous Cell -- ultrastructure KW - Proto-Oncogenes KW - Bronchi -- pathology KW - Adenocarcinoma -- pathology KW - Lung Neoplasms -- ultrastructure KW - Carcinoma, Squamous Cell -- pathology KW - Adenocarcinoma -- ultrastructure KW - Carcinoma, Squamous Cell -- genetics KW - Lung Neoplasms -- genetics KW - Proto-Oncogene Proteins -- genetics KW - Cell Transformation, Neoplastic KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80663551?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Human+bronchial+epithelial+cells+transformed+by+the+c-raf-1+and+c-myc+protooncogenes+induce+multidifferentiated+carcinomas+in+nude+mice%3A+a+model+for+lung+carcinogenesis.&rft.au=Pfeifer%2C+A+M%3BJones%2C+R+T%3BBowden%2C+P+E%3BMann%2C+D%3BSpillare%2C+E%3BKlein-Szanto%2C+A+J%3BTrump%2C+B+F%3BHarris%2C+C+C&rft.aulast=Pfeifer&rft.aufirst=A&rft.date=1991-07-15&rft.volume=51&rft.issue=14&rft.spage=3793&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 - 1991-08-12 N1 - Date created - 1991-08-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Oct-3 and the beginning of mammalian development. AN - 80690440; 1853199 JF - Science (New York, N.Y.) AU - Rosner, M H AU - Vigano, M A AU - Rigby, P W AU - Arnheiter, H AU - Staudt, L M AD - Metabolism Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/07/12/ PY - 1991 DA - 1991 Jul 12 SP - 144 EP - 145 VL - 253 IS - 5016 SN - 0036-8075, 0036-8075 KW - DNA-Binding Proteins KW - 0 KW - Octamer Transcription Factor-3 KW - Pou5f1 protein, mouse KW - Transcription Factors KW - Index Medicus KW - Teratoma -- genetics KW - Animals KW - Teratoma -- pathology KW - Mice KW - Gene Expression Regulation KW - Stem Cells -- physiology KW - DNA Replication KW - Transcription Factors -- physiology KW - Embryo, Mammalian -- physiology KW - DNA-Binding Proteins -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80690440?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Oct-3+and+the+beginning+of+mammalian+development.&rft.au=Rosner%2C+M+H%3BVigano%2C+M+A%3BRigby%2C+P+W%3BArnheiter%2C+H%3BStaudt%2C+L+M&rft.aulast=Rosner&rft.aufirst=M&rft.date=1991-07-12&rft.volume=253&rft.issue=5016&rft.spage=144&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 - 1991-08-19 N1 - Date created - 1991-08-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Developmental regulation of transcription factor AP-2 during Xenopus laevis embryogenesis. AN - 80686965; 1852613 AB - We have isolated a cDNA clone encoding the Xenopus homologue of the transcription factor AP-2 (XAP-2). The predicted amino acid sequence derived from the Xenopus cDNA shows very strong conservation with the amino acid sequence of human AP-2, suggesting that this protein is evolutionarily conserved, at least among vertebrates. This is further substantiated by the demonstration that an in vitro translation product of XAP-2 cDNA bound specifically to an AP-2 binding site from the human MT-IIA gene. Northern blot analysis of Xenopus embryo RNA revealed the existence of three major XAP-2 mRNA species that were only detectable after the midblastula transition (when embryonic transcription is activated), with peak accumulation of the transcripts occurring during gastrulation. Therefore, in contrast to other Xenopus transcription factors, XAP-2 is not maternally derived but arises exclusively from zygotic transcription. Unlike the situation in cultured human teratocarcinoma (NT2) cells, retinoic acid treatment did not induce XAP-2 mRNA in Xenopus embryos, even though the treatment had a pronounced morphogenetic effect on the embryos. Our results suggest that XAP-2 may play a distinctive role during Xenopus embryogenesis. JF - Nucleic acids research AU - Winning, R S AU - Shea, L J AU - Marcus, S J AU - Sargent, T D AD - Laboratory of Molecular Genetics, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/07/11/ PY - 1991 DA - 1991 Jul 11 SP - 3709 EP - 3714 VL - 19 IS - 13 SN - 0305-1048, 0305-1048 KW - XAP-2 KW - DNA-Binding Proteins KW - 0 KW - Transcription Factor AP-2 KW - Transcription Factors KW - Xenopus Proteins KW - tfap2a protein, Xenopus KW - Tretinoin KW - 5688UTC01R KW - Index Medicus KW - Animals KW - Tretinoin -- pharmacology KW - Blotting, Northern KW - Sequence Homology, Nucleic Acid KW - Humans KW - Amino Acid Sequence KW - Cloning, Molecular KW - Base Sequence KW - Blotting, Southern KW - Molecular Sequence Data KW - Open Reading Frames -- genetics KW - Xenopus laevis -- genetics KW - DNA-Binding Proteins -- genetics KW - Gene Expression Regulation KW - Xenopus laevis -- embryology KW - Transcription Factors -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80686965?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+acids+research&rft.atitle=Developmental+regulation+of+transcription+factor+AP-2+during+Xenopus+laevis+embryogenesis.&rft.au=Winning%2C+R+S%3BShea%2C+L+J%3BMarcus%2C+S+J%3BSargent%2C+T+D&rft.aulast=Winning&rft.aufirst=R&rft.date=1991-07-11&rft.volume=19&rft.issue=13&rft.spage=3709&rft.isbn=&rft.btitle=&rft.title=Nucleic+acids+research&rft.issn=03051048&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-20 N1 - Date created - 1991-08-20 N1 - Date revised - 2017-01-13 N1 - Gene symbol - XAP-2 N1 - Genetic sequence - X56865; GENBANK; X57510; X59607; M59455; X58106; X57509; X58496; X58524; X58105; X58104 N1 - SuppNotes - Cited By: Dev Biol. 1986 Mar;114(1):170-9 [3956861] In Vitro. 1976 Mar;12(3):173-9 [944165] Methods Enzymol. 1990;185:60-89 [2199796] Genes Dev. 1990 Jun;4(6):932-42 [2384214] Dev Genet. 1990;11(1):97-109 [2361336] Proc Natl Acad Sci U S A. 1984 Apr;81(7):1991-5 [6326095] Methods Enzymol. 1983;100:255-66 [6194404] J Mol Biol. 1964 May;8:669-87 [14187393] Development. 1990 May;109(1):157-65 [1698604] Genes Dev. 1991 Jan;5(1):105-19 [1989904] Development. 1990 Oct;110(2):427-33 [2133546] Cell. 1987 Jun 19;49(6):729-39 [3034432] Cell. 1987 Oct 23;51(2):251-60 [2822255] Nature. 1986 Sep 25-Oct 1;323(6086):353-6 [3020428] Proc Natl Acad Sci U S A. 1985 Dec;82(24):8572-6 [3866241] Dev Biol. 1986 Mar;114(1):238-46 [3956863] Nature. 1989 Jul 13;340(6229):140-4 [2739735] Cell. 1987 Sep 11;50(6):847-61 [3040262] Nature. 1988 Aug 11;334(6182):535-7 [3136397] Genes Dev. 1988 Dec;2(12A):1557-69 [3063603] Genes Dev. 1989 Oct;3(10):1507-17 [2482225] J Cell Physiol. 1989 Aug;140(2):239-45 [2501316] EMBO J. 1989 Apr;8(4):1153-61 [2743976] EMBO J. 1988 Jul;7(7):2075-87 [3262058] Proc Natl Acad Sci U S A. 1988 Nov;85(21):8086-90 [3186710] Science. 1987 Jun 5;236(4806):1237-45 [3296191] Cell. 1987 Dec 4;51(5):773-81 [3677172] Biochem Cell Biol. 1987 Apr;65(4):310-6 [3606855] Nature. 1987 Jun 18-24;327(6123):625-8 [3600758] Cell. 1982 Oct;30(3):675-86 [6183003] Cell. 1982 Oct;30(3):687-96 [7139712] Nature. 1982 Apr 8;296(5857):564-6 [7070499] Science. 1977 Feb 25;195(4280):785-7 [65013] Dev Biol. 1985 Feb;107(2):483-9 [3972166] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Results and conclusions of the National Toxicology Program's rodent carcinogenicity studies with sodium fluoride. AN - 80681381; 2071234 AB - The US National Toxicology Program (NTP) has conducted toxicity and carcinogenicity studies with sodium fluoride administered in the drinking water to F344/N rats and B6C3F1 mice. The drinking water concentrations used in the 2-year studies were 0, 25, 100, or 175 ppm sodium fluoride (equivalent to 0, 11, 45 or 79 ppm fluoride). Survival and weight gains of rats and mice were not affected by fluoride treatment. Animals receiving sodium fluoride developed effects typical of dental fluorosis, and female rats given 175 ppm had increased osteosclerosis. There were no increases in neoplasms in female rats or in male or female mice that were attributed to sodium fluoride administration. There was equivocal evidence of carcinogenic activity of sodium fluoride in male rats based on the occurrence of a small number of osteosarcomas in treated animals. JF - International journal of cancer AU - Bucher, J R AU - Hejtmancik, M R AU - Toft, J D AU - Persing, R L AU - Eustis, S L AU - Haseman, J K AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/07/09/ PY - 1991 DA - 1991 Jul 09 SP - 733 EP - 737 VL - 48 IS - 5 SN - 0020-7136, 0020-7136 KW - Carcinogens KW - 0 KW - Sodium Fluoride KW - 8ZYQ1474W7 KW - Fluorides KW - Q80VPU408O KW - Index Medicus KW - United States KW - Rats KW - Animals KW - Bone and Bones -- chemistry KW - Water Supply KW - Toxicology -- methods KW - Fluorides -- analysis KW - Male KW - Female KW - Neoplasms, Experimental -- chemically induced KW - Sodium Fluoride -- pharmacokinetics KW - Sodium Fluoride -- administration & dosage KW - Sodium Fluoride -- toxicity KW - Neoplasms, Experimental -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80681381?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Results+and+conclusions+of+the+National+Toxicology+Program%27s+rodent+carcinogenicity+studies+with+sodium+fluoride.&rft.au=Bucher%2C+J+R%3BHejtmancik%2C+M+R%3BToft%2C+J+D%3BPersing%2C+R+L%3BEustis%2C+S+L%3BHaseman%2C+J+K&rft.aulast=Bucher&rft.aufirst=J&rft.date=1991-07-09&rft.volume=48&rft.issue=5&rft.spage=733&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 - 1991-08-20 N1 - Date created - 1991-08-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A human bronchial epithelial cell strain with unusual in vitro growth potential which undergoes neoplastic transformation after SV40 T antigen gene transfection. AN - 80679117; 1712759 AB - Bronchial epithelial cells were cultured from an individual with no evidence of malignant disease. These cells, designated HB56B, had a greatly extended in vitro life-span, being able to undergo 50 passages and 200 population doublings in contrast to the usual 3 to 4 passages and 20 to 30 population doublings characteristic of normal human bronchial epithelial cells. HB56B cells had karyotypic evidence of an amplified region on the short arm of chromosome II. Unlike normal bronchial epithelial cells, which undergo terminal squamous differentiation in vitro in response to fetal bovine serum, HB56B cells were only minimally affected by serum. These cells were readily established as an immortalized cell line, HB56B/5T, following transfection with a plasmid containing SV40 early region DNA. HB56B cells were non-tumorigenic in athymic nude mice, but HB56B/5T cells within a few passages of transfection with the SV40 plasmid formed tumors of which 28/37 regressed. HB56B cells may offer an experimental system for the study of proliferation, differentiation, and senescence control in human bronchial epithelial cells. JF - International journal of cancer AU - Reddel, R R AU - Hsu, I C AU - Mass, M J AU - Hukku, B AU - Gerwin, B I AU - Salghetti, S E AU - Somers, A N AU - Galati, A J AU - Gunning, W T AU - Harris, C C AD - Laboratory of Human Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/07/09/ PY - 1991 DA - 1991 Jul 09 SP - 764 EP - 773 VL - 48 IS - 5 SN - 0020-7136, 0020-7136 KW - Antigens, Polyomavirus Transforming KW - 0 KW - DNA, Neoplasm KW - Isoenzymes KW - Keratins KW - 68238-35-7 KW - Index Medicus KW - Karyotyping KW - Animals KW - Culture Techniques -- methods KW - Humans KW - Chromosome Disorders KW - Mice, Nude KW - Mice KW - Keratins -- analysis KW - DNA, Neoplasm -- isolation & purification KW - Isoenzymes -- genetics KW - Chromosomes, Human, Pair 11 KW - Neoplasm Transplantation KW - Isoenzymes -- analysis KW - Oncogenes KW - Epithelial Cells KW - Adult KW - Chromosome Aberrations KW - Transplantation, Heterologous KW - Cell Line KW - Female KW - Bronchi -- cytology KW - Transfection KW - Simian virus 40 -- genetics KW - Antigens, Polyomavirus Transforming -- genetics KW - Cell Transformation, Neoplastic KW - Cell Division UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80679117?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+human+bronchial+epithelial+cell+strain+with+unusual+in+vitro+growth+potential+which+undergoes+neoplastic+transformation+after+SV40+T+antigen+gene+transfection.&rft.au=Reddel%2C+R+R%3BHsu%2C+I+C%3BMass%2C+M+J%3BHukku%2C+B%3BGerwin%2C+B+I%3BSalghetti%2C+S+E%3BSomers%2C+A+N%3BGalati%2C+A+J%3BGunning%2C+W+T%3BHarris%2C+C+C&rft.aulast=Reddel&rft.aufirst=R&rft.date=1991-07-09&rft.volume=48&rft.issue=5&rft.spage=764&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 - 1991-08-20 N1 - Date created - 1991-08-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Sequence-dependent interaction of 5-fluorouracil and arabinosyl-5-azacytosine or 1-beta-D-arabinofuranosylcytosine. AN - 80707210; 1713459 AB - We studied the cytotoxicity of arabinosyl-5-azacytosine (Ara-AC), a dCyd antagonist which inhibits DNA synthesis, in combination with 5-fluorouracil (FUra) in two human colon cancer cell lines, HCT 116 and SNU-C4. Clonogenic assays done following sequential or concurrent 24-hr exposures to Ara-AC and FUra showed that the sequence Ara-AC followed by FUra resulted in more than additive lethality in the HCT 116 cell lines and additive lethality in the SNU-C4 cells. In contrast, the reverse sequence, FUra followed by Ara-AC, was antagonistic in both cell lines. A similar interaction between FUra and 1-beta-D-arabinofuranosylcytosine (Ara-C) was evident in HCT 116 cells; at concentrations which individually diminished viability by 34 and 62%, respectively, the sequence Ara-C followed by FUra decreased viability by 97%. Pulse-labeling with [3H]dUrd showed profound inhibition of DNA synthesis by the sequence Ara-AC followed by FUra, with over 90% inhibition lasting for up to 48 hr following Ara-AC exposure. When FUra preceded Ara-AC, however, earlier recovery from inhibition of DNA synthesis occurred. FUra pretreatment did not appreciably alter the quantity or distribution of [3H]Ara-AC or [3H]Ara-C nucleotides after a 4- to 6-hr exposure. Pre-exposure to FUra decreased Ara-AC incorporation into DNA by 37 and 73% at 6 hr in HCT 116 and SNU-C4, respectively. FUra pretreatment also inhibited Ara-C incorporation into DNA by over 50% at 6 and 24 hr. The antagonism of Ara-AC and Ara-C cytotoxicity by FUra pretreatment can thus be explained by diminished incorporation of the dCyd analogs into DNA resulting from inhibition of DNA synthesis by FUra-induced dTTP and dCTP depletion. In contrast, when Ara-AC or Ara-C preceded FUra, their incorporation into DNA was not disturbed, and prolonged inhibition of DNA synthesis was observed. JF - Biochemical pharmacology AU - Grem, J L AU - Allegra, C J AD - Gastrointestinal Tumor Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/07/05/ PY - 1991 DA - 1991 Jul 05 SP - 409 EP - 418 VL - 42 IS - 2 SN - 0006-2952, 0006-2952 KW - DNA, Neoplasm KW - 0 KW - Deoxycytosine Nucleotides KW - Nucleic Acids KW - Thymine Nucleotides KW - Cytarabine KW - 04079A1RDZ KW - 2'-deoxycytidine 5'-triphosphate KW - 2056-98-6 KW - Cytidine KW - 5CSZ8459RP KW - fazarabine KW - 5V71D8JOKK KW - Azacitidine KW - M801H13NRU KW - thymidine 5'-triphosphate KW - QOP4K539MU KW - Fluorouracil KW - U3P01618RT KW - Index Medicus KW - Drug Administration Schedule KW - Drug Interactions KW - Thymine Nucleotides -- metabolism KW - Cell Line -- drug effects KW - Humans KW - Cell Division -- drug effects KW - Cell Nucleus -- drug effects KW - Nucleic Acids -- metabolism KW - Deoxycytosine Nucleotides -- metabolism KW - Cell Survival -- drug effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Tumor Stem Cell Assay KW - Cytidine -- antagonists & inhibitors KW - DNA, Neoplasm -- biosynthesis KW - Fluorouracil -- administration & dosage KW - Cytarabine -- pharmacology KW - Azacitidine -- pharmacology KW - Colonic Neoplasms -- drug therapy KW - Fluorouracil -- pharmacology KW - Cytarabine -- administration & dosage KW - Colonic Neoplasms -- pathology KW - Azacitidine -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80707210?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Sequence-dependent+interaction+of+5-fluorouracil+and+arabinosyl-5-azacytosine+or+1-beta-D-arabinofuranosylcytosine.&rft.au=Grem%2C+J+L%3BAllegra%2C+C+J&rft.aulast=Grem&rft.aufirst=J&rft.date=1991-07-05&rft.volume=42&rft.issue=2&rft.spage=409&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 - 1991-08-23 N1 - Date created - 1991-08-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - p53 mutations in human cancers. AN - 80655676; 1905840 AB - Mutations in the evolutionarily conserved codons of the p53 tumor suppressor gene are common in diverse types of human cancer. The p53 mutational spectrum differs among cancers of the colon, lung, esophagus, breast, liver, brain, reticuloendothelial tissues, and hemopoietic tissues. Analysis of these mutations can provide clues to the etiology of these diverse tumors and to the function of specific regions of p53. Transitions predominate in colon, brain, and lymphoid malignancies, whereas G:C to T:A transversions are the most frequent substitutions observed in cancers of the lung and liver. Mutations at A:T base pairs are seen more frequently in esophageal carcinomas than in other solid tumors. Most transitions in colorectal carcinomas, brain tumors, leukemias, and lymphomas are at CpG dinucleotide mutational hot spots. G to T transversions in lung, breast, and esophageal carcinomas are dispersed among numerous codons. In liver tumors in persons from geographic areas in which both aflatoxin B1 and hepatitis B virus are cancer risk factors, most mutations are at one nucleotide pair of codon 249. These differences may reflect the etiological contributions of both exogenous and endogenous factors to human carcinogenesis. JF - Science (New York, N.Y.) AU - Hollstein, M AU - Sidransky, D AU - Vogelstein, B AU - Harris, C C AD - Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/07/05/ PY - 1991 DA - 1991 Jul 05 SP - 49 EP - 53 VL - 253 IS - 5015 SN - 0036-8075, 0036-8075 KW - Index Medicus KW - Rats KW - Animals KW - Chickens KW - Base Sequence KW - Trout KW - Sequence Homology, Nucleic Acid KW - Humans KW - DNA Mutational Analysis KW - Molecular Sequence Data KW - Xenopus KW - Mice KW - Amino Acid Sequence KW - Haplorhini KW - Genes, p53 KW - Mutation KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80655676?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=p53+mutations+in+human+cancers.&rft.au=Hollstein%2C+M%3BSidransky%2C+D%3BVogelstein%2C+B%3BHarris%2C+C+C&rft.aulast=Hollstein&rft.aufirst=M&rft.date=1991-07-05&rft.volume=253&rft.issue=5015&rft.spage=49&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 - 1991-08-02 N1 - Date created - 1991-08-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Tumorigenicity of the tobacco-specific carcinogen 4-(methyl-nitrosamino)-1-(3-pyridyl)-1-butanone in infant mice. AN - 80700053; 1855194 AB - The tobacco-specific nitrosamine, 4-(methyl-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK), is a potent carcinogen in adult rodents and variably effective transplacentally, depending on species. In pursuit of the thesis that human infants may be especially vulnerable targets for tumor initiation by tobacco smoke constituents, we tested the efficacy of NNK as a tumor initiator in infant mice. Cr:NIH(S) (NIH Swiss outbred) mice were given 50 mg/kg NNK i.p. on postnatal days 1, 4, 7, 10 and 14, with saline to controls. At an average age of 13-15 months, 57% of the NNK-exposed male offspring had hepatocellular tumors, with a multiplicity of 1.15 +/- 1.4, including 4 with carcinoma. Liver tumors including 2 carcinomas were found in 8 (14%) of the NNK-exposed female offspring. There were no hepatocellular neoplasms in any control. A significant increase in primary lung tumors also occurred in the NNK-treated males, with an incidence of 30/55 (57%) and a multiplicity of 0.7 +/- 0.2, vs. 7/33 (21%), multiplicity 0.3 +/- 0.6, in controls (P less than 0.025). An apparent increase in the incidence of lung tumors in NNK-treated females, 21/57 (37%) vs. 7/32 (22%) in controls, approached significance (P less than 0.1). Thus NNK was a moderately potent neonatal carcinogen for liver and lung in infant Swiss mice and more efficacious in this regard than when received transplacentally by mice of the same strain. JF - Cancer letters AU - Anderson, L M AU - Hecht, S S AU - Kovatch, R M AU - Amin, S AU - Hoffmann, D AU - Rice, J M AD - Division of Cancer Etiology, National Cancer Institute, Frederick, MD 21702. Y1 - 1991/07/04/ PY - 1991 DA - 1991 Jul 04 SP - 177 EP - 181 VL - 58 IS - 3 SN - 0304-3835, 0304-3835 KW - Carcinogens KW - 0 KW - Nitrosamines KW - 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone KW - 7S395EDO61 KW - Index Medicus KW - Animals, Newborn KW - Animals KW - Liver Neoplasms -- chemically induced KW - Mice KW - Lung Neoplasms -- chemically induced KW - Male KW - Female KW - Nitrosamines -- toxicity KW - Neoplasms, Experimental -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80700053?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Tumorigenicity+of+the+tobacco-specific+carcinogen+4-%28methyl-nitrosamino%29-1-%283-pyridyl%29-1-butanone+in+infant+mice.&rft.au=Anderson%2C+L+M%3BHecht%2C+S+S%3BKovatch%2C+R+M%3BAmin%2C+S%3BHoffmann%2C+D%3BRice%2C+J+M&rft.aulast=Anderson&rft.aufirst=L&rft.date=1991-07-04&rft.volume=58&rft.issue=3&rft.spage=177&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 - 1991-08-26 N1 - Date created - 1991-08-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Failure of senescent cells to phosphorylate the RB protein. AN - 80719763; 1861860 AB - The product of the RB susceptibility gene has been shown to be differentially phosphorylated during the cell cycle, suggesting a role in the regulation of cell cycle progression. We examined the expression and phosphorylation status of the RB protein in senescent Syrian hamster embryo cells. Both phosphorylated and unphosphorylated forms of the RB protein were observed in cells at early passages; however, only unphosphorylated RB protein was found in senescent cells. When nonsenescent cells at low population doubling levels were made quiescent by reducing the serum concentration of the media, the RB protein in these cells was mostly in the unphosphorylated form. When stimulated with serum, phosphorylation of the RB protein occurred between 10-20 h after stimulation, which corresponded with the induction of DNA synthesis. Senescent cells, in contrast, did not show any phosphorylation of the RB protein in response to serum. In addition, cell lines that had escaped cellular senescence at various stages of neoplastic progression were examined; all 25 cell lines examined expressed RB protein, which was phosphorylated normally. These results suggest that the RB protein plays a role in cellular senescence with phosphorylation status determining this role. Factors controlling this phosphorylation are potential key factors in controlling cellular life span in culture. JF - Oncogene AU - Futreal, P A AU - Barrett, J C AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 1109 EP - 1113 VL - 6 IS - 7 SN - 0950-9232, 0950-9232 KW - v-HA-ras KW - v-myc KW - Phosphoproteins KW - 0 KW - Retinoblastoma Protein KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - DNA -- biosynthesis KW - Genes, ras KW - Blood KW - Blotting, Western KW - Oncogenes KW - Phosphorylation KW - Mesocricetus KW - Time Factors KW - Embryo, Mammalian KW - Cell Line KW - Cell Transformation, Neoplastic -- genetics KW - Cell Division KW - Cricetinae KW - Retinoblastoma Protein -- metabolism KW - Phosphoproteins -- metabolism KW - Cell Survival UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80719763?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Failure+of+senescent+cells+to+phosphorylate+the+RB+protein.&rft.au=Futreal%2C+P+A%3BBarrett%2C+J+C&rft.aulast=Futreal&rft.aufirst=P&rft.date=1991-07-01&rft.volume=6&rft.issue=7&rft.spage=1109&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=09509232&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-05 N1 - Date created - 1991-09-05 N1 - Date revised - 2017-01-13 N1 - Gene symbol - v-HA-ras; v-myc N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Aluminum fluoride stimulates inositol phosphate metabolism and inhibits expression of differentiation markers in mouse keratinocytes. AN - 80711663; 1860890 AB - Mouse keratinocytes are induced to differentiate in vitro by elevating the level of extracellular calcium from 0.05 mM, where keratinocytes express a basal cell phenotype, to greater than 0.10 mM, where they express the differentiated phenotype. This process has been associated with a rapid, sustained increase in inositol phosphate (InsP) turnover, which precedes the expression of differentiation-specific proteins. In 0.05 mM Ca2+ medium, aluminum and fluoride salts (AIF4-), which combine to activate nonspecifically heterotrimeric guanine nucleotide-binding (G) proteins, cause a concentration-dependent increase in InsP metabolism in keratinocytes, and generate elevated intracellular diacylglycerol levels. This is associated with an inhibition of cell growth. Treatment with both AIF4- and Ca2+ greater than 0.10 mM resulted in an additive increase in InsP turnover, implying the presence of at least two responsive InsP pools. AIF4- inhibited the expression of differentiation markers induced by Ca2+ greater than 0.10 mM and altered the morphology of keratinocytes from squamous to dendritic, which was reversible upon withdrawal of AIF4-. Neoplastic keratinocytes, in which basal levels of InsP metabolism are higher than in normal cells, do not differentiate in response to Ca2+. Neoplastic keratinocytes responded to AIF-4 treatment with an even greater rise in InsP metabolism. AIF-4 also inhibited cell growth and reversibly altered morphology in neoplastic keratinocytes. These data suggest that InsP metabolism in keratinocytes is at least partially regulated by a G protein mechanism. Furthermore, an increase in InsP metabolism is not sufficient to stimulate differentiation and may be inhibitory to differentiation if exceeding limited increases. However, these observations cannot exclude the possibility that other AIF-4 stimulated pathways involving G or non-G proteins can also influence keratinocyte biology. JF - Journal of cellular physiology AU - Lee, E AU - Yuspa, S H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 106 EP - 115 VL - 148 IS - 1 SN - 0021-9541, 0021-9541 KW - Aluminum Compounds KW - 0 KW - Biomarkers KW - Diglycerides KW - Inositol Phosphates KW - Aluminum KW - CPD4NFA903 KW - Fluorides KW - Q80VPU408O KW - aluminum fluoride KW - Z77H3IKW94 KW - Index Medicus KW - Animals KW - Dose-Response Relationship, Drug KW - Cells, Cultured KW - Mice KW - Mice, Inbred BALB C KW - Time Factors KW - Diglycerides -- metabolism KW - Inositol Phosphates -- metabolism KW - Aluminum -- pharmacology KW - Keratinocytes -- cytology KW - Fluorides -- pharmacology KW - Keratinocytes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80711663?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Aluminum+fluoride+stimulates+inositol+phosphate+metabolism+and+inhibits+expression+of+differentiation+markers+in+mouse+keratinocytes.&rft.au=Lee%2C+E%3BYuspa%2C+S+H&rft.aulast=Lee&rft.aufirst=E&rft.date=1991-07-01&rft.volume=148&rft.issue=1&rft.spage=106&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 - 1991-09-05 N1 - Date created - 1991-09-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inhibitors of IMP dehydrogenase stimulate the phosphorylation of the anti-human immunodeficiency virus nucleosides 2',3'-dideoxyadenosine and 2',3'-dideoxyinosine. AN - 80704116; 1677450 AB - 2',3'-Dideoxyadenosine (ddAdo) and its deamination product 2',3'-dideoxyinosine (ddIno) (didanosine) inhibit the replication and infectivity of the human immunodeficiency virus (HIV) in a number of in vitro assay systems. Early clinical studies (phase I) have indicated a role for ddIno in the treatment of patients with severe HIV infection. In the present in vitro study, the formation in human T cells (MOLT-4, ATH8, and CCRF-CEM) of the pharmacologically active metabolite of ddIno and ddAdo, 2',3'-dideoxyadenosine-5'-triphosphate (ddATP), was found to be stimulated 2-4-fold by appropriate concentrations of inosinate dehydrogenase (IMPD) inhibitors such as ribavirin, tiazofurin, and mycophenolic acid. Concomitant with this increase in ddATP formation from ddIno was an increase in anti-HIV activity of this agent when it was combined with ribavirin in the ATH8 cell assay system and with tiazofurin in the MOLT-4 assay system. No change was noted in the intracellular concentration of the corresponding physiological deoxynucleoside-5'-triphosphate, dATP; positive correlation was observed, however, between the increase in ddATP formation from ddIno and the increase in intracellular IMP occurring as a consequence of IMPD inhibition. The results support the hypothesis that the stimulation of ddATP formation seen when ddIno is combined with ribavirin or other IMPD inhibitors is a consequence of an increased concentration of IMP, the major phosphate donor for the initial phosphorylation step in the anabolism of ddIno to ddATP, i.e., ddIno----ddIMP. JF - Molecular pharmacology AU - Hartman, N R AU - Ahluwalia, G S AU - Cooney, D A AU - Mitsuya, H AU - Kageyama, S AU - Fridland, A AU - Broder, S AU - Johns, D G AD - Laboratory of Medicinal Chemistry, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 118 EP - 124 VL - 40 IS - 1 SN - 0026-895X, 0026-895X KW - Antiviral Agents KW - 0 KW - Nucleotides KW - Inosine Monophosphate KW - 131-99-7 KW - Ribavirin KW - 49717AWG6K KW - Dideoxyadenosine KW - 4Q86AH641A KW - Inosine KW - 5A614L51CT KW - IMP Dehydrogenase KW - EC 1.1.1.205 KW - Didanosine KW - K3GDH6OH08 KW - Index Medicus KW - AIDS/HIV KW - Nucleotides -- metabolism KW - HIV -- drug effects KW - Chromatography KW - Ribavirin -- pharmacology KW - Humans KW - Inosine Monophosphate -- metabolism KW - Phosphorylation -- drug effects KW - Stimulation, Chemical KW - Nucleotides -- isolation & purification KW - Inosine -- pharmacology KW - Cells, Cultured KW - Antiviral Agents -- pharmacology KW - Drug Synergism KW - Dideoxyadenosine -- metabolism KW - Didanosine -- metabolism KW - IMP Dehydrogenase -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80704116?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Inhibitors+of+IMP+dehydrogenase+stimulate+the+phosphorylation+of+the+anti-human+immunodeficiency+virus+nucleosides+2%27%2C3%27-dideoxyadenosine+and+2%27%2C3%27-dideoxyinosine.&rft.au=Hartman%2C+N+R%3BAhluwalia%2C+G+S%3BCooney%2C+D+A%3BMitsuya%2C+H%3BKageyama%2C+S%3BFridland%2C+A%3BBroder%2C+S%3BJohns%2C+D+G&rft.aulast=Hartman&rft.aufirst=N&rft.date=1991-07-01&rft.volume=40&rft.issue=1&rft.spage=118&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 - 1991-08-29 N1 - Date created - 1991-08-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - 2-amino-3-(methylamino)-propanoic acid (BMAA) pharmacokinetics and blood-brain barrier permeability in the rat. AN - 80682909; 2072299 AB - 2-Amino-3-(methylamino)-propanoic acid (BMAA) is a neurotoxic, excitatory amino acid which has been linked through cycad use and consumption with the onset of a variant of amyotrophic lateral sclerosis occurring with high incidence in the western Pacific region. We have studied BMAA pharmacokinetics, oral bioavailability and blood-brain barrier permeability in the rat in an attempt to better define the possible role for BMAA in this disease. To evaluate its kinetics and uptake, BMAA (25-400 mg/kg) was administered to rats, either acutely or chronically, and then plasma and brain concentrations were determined at various times thereafter by combined gas chromatography mass spectrometry. After single dose i.v. injection, BMAA was cleared from plasma in a rapid distribution phase (Vd approximately 16 liters/kg) followed by a slower elimination phase (t1/2 approximately 1 day). Brain uptake was limited by a low blood-brain barrier permeability-surface area product of 2 to 5 x 10(-5) ml/sed/g. Brain BMAA levels peaked within 8 hr after injection, and then declined with a t1/2 similar to that of plasma. After two weeks of continuous infusion (100 mg/kg/day), steady-state brain concentrations equalled 10 to 30 micrograms/g, and only moderately exceeded those in plasma. The results suggest that BMAA may reach potentially toxic levels in brain (i.e., greater than 250 microM) after large doses (greater than 100 mg/kg). However, such doses are orders of magnitude greater than those available from dietary or medicinal use of cycads. JF - The Journal of pharmacology and experimental therapeutics AU - Duncan, M W AU - Villacreses, N E AU - Pearson, P G AU - Wyatt, L AU - Rapoport, S I AU - Kopin, I J AU - Markey, S P AU - Smith, Q R AD - Intramural Research Program, National Institute of Neurological Disorders and Stroke, National Institute of Mental Health, Bethesda, Maryland. Y1 - 1991/07/01/ PY - 1991 DA - 1991 Jul 01 SP - 27 EP - 35 VL - 258 IS - 1 SN - 0022-3565, 0022-3565 KW - Amino Acids, Diamino KW - 0 KW - beta-N-methylamino-L-alanine KW - 108SA6URTV KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Administration, Oral KW - Animals KW - Injections, Intravenous KW - Half-Life KW - Gas Chromatography-Mass Spectrometry KW - Tissue Distribution KW - Male KW - Biological Availability KW - Blood-Brain Barrier -- drug effects KW - Amino Acids, Diamino -- pharmacology KW - Amino Acids, Diamino -- pharmacokinetics KW - Blood-Brain Barrier -- physiology KW - Amino Acids, Diamino -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80682909?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=2-amino-3-%28methylamino%29-propanoic+acid+%28BMAA%29+pharmacokinetics+and+blood-brain+barrier+permeability+in+the+rat.&rft.au=Duncan%2C+M+W%3BVillacreses%2C+N+E%3BPearson%2C+P+G%3BWyatt%2C+L%3BRapoport%2C+S+I%3BKopin%2C+I+J%3BMarkey%2C+S+P%3BSmith%2C+Q+R&rft.aulast=Duncan&rft.aufirst=M&rft.date=1991-07-01&rft.volume=258&rft.issue=1&rft.spage=27&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 - 1991-08-20 N1 - Date created - 1991-08-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Regulating the retention of T-cell receptor alpha chain variants within the endoplasmic reticulum: Ca(2+)-dependent association with BiP. AN - 80680781; 1649196 AB - Immunoglobulin heavy chain binding protein (BiP, GRP 78) coprecipitates with soluble and membrane-associated variants of the T-cell antigen receptor alpha chain (TCR-alpha) which are stably retained within the ER. Chelation of Ca2+ during solubilization of cells leads to the dissociation of BiP from the TCR-alpha variants, which is dependent upon the availability of Mg2+ and hydrolyzable ATP; this suggests that Ca2+ levels can serve to modulate the association/dissociation of these proteins with BiP. In vivo treatment of cells expressing either the soluble or membrane-anchored TCR-alpha variants with the Ca2+ ionophore, A23187, or an inhibitor of an ER Ca(2+)-ATPase, thapsigargin, or the membrane-permeant Ca2+ chelator BAPTA-AM, results in the redistribution of these proteins out of the ER and their subsequent secretion or cell surface expression. Under the same assay conditions, no movement of BiP out of the ER is observed. Taken together, these observations indicate that decreased Ca2+ levels result in the dissociation of a protein bound to BiP, leading to its release from ER retention. These data suggest that the intracellular fate of newly synthesized proteins stably associated with BiP can be regulated by Ca2+ levels in the ER. JF - The Journal of cell biology AU - Suzuki, C K AU - Bonifacino, J S AU - Lin, A Y AU - Davis, M M AU - Klausner, R D AD - Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 189 EP - 205 VL - 114 IS - 2 SN - 0021-9525, 0021-9525 KW - Carcinogens KW - 0 KW - Carrier Proteins KW - Heat-Shock Proteins KW - Immunoglobulin alpha-Chains KW - Molecular Chaperones KW - Receptors, Antigen, T-Cell KW - Terpenes KW - molecular chaperone GRP78 KW - Calcimycin KW - 37H9VM9WZL KW - Thapsigargin KW - 67526-95-8 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Carcinogens -- pharmacology KW - Immunoblotting KW - Ovary -- chemistry KW - Ovary -- ultrastructure KW - Cricetulus KW - Dose-Response Relationship, Drug KW - Gene Rearrangement, alpha-Chain T-Cell Antigen Receptor KW - Calcimycin -- pharmacology KW - Precipitin Tests KW - Ovary -- metabolism KW - Ovary -- cytology KW - Genetic Variation -- genetics KW - Terpenes -- pharmacology KW - Fluorescent Antibody Technique KW - Immunoglobulin alpha-Chains -- genetics KW - Cell Line KW - Female KW - Cricetinae KW - Endoplasmic Reticulum -- metabolism KW - Endoplasmic Reticulum -- chemistry KW - Carrier Proteins -- metabolism KW - Receptors, Antigen, T-Cell -- metabolism KW - Carrier Proteins -- analysis KW - Calcium -- pharmacology KW - Endoplasmic Reticulum -- ultrastructure KW - Receptors, Antigen, T-Cell -- genetics KW - Receptors, Antigen, T-Cell -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80680781?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+cell+biology&rft.atitle=Regulating+the+retention+of+T-cell+receptor+alpha+chain+variants+within+the+endoplasmic+reticulum%3A+Ca%282%2B%29-dependent+association+with+BiP.&rft.au=Suzuki%2C+C+K%3BBonifacino%2C+J+S%3BLin%2C+A+Y%3BDavis%2C+M+M%3BKlausner%2C+R+D&rft.aulast=Suzuki&rft.aufirst=C&rft.date=1991-07-01&rft.volume=114&rft.issue=2&rft.spage=189&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+cell+biology&rft.issn=00219525&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-19 N1 - Date created - 1991-08-19 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cell Calcium. 1990 Feb-Mar;11(2-3):157-79 [2191780] Cell Calcium. 1990 Feb-Mar;11(2-3):57-62 [2191781] Cell Calcium. 1990 Feb-Mar;11(2-3):93-109 [2354507] Science. 1990 Jan 5;247(4938):79-82 [2294595] Proc Natl Acad Sci U S A. 1983 Nov;80(22):6972-6 [6316339] Nature. 1982 Jul 29;298(5873):478-81 [6283392] Nature. 1983 Nov 24-30;306(5941):387-9 [6417546] J Cell Biol. 1982 Jan;92(1):92-107 [7199056] Cell. 1977 Dec;12(4):1133-41 [23215] J Biol Chem. 1974 Feb 10;249(3):811-7 [4204552] Annu Rev Cell Biol. 1990;6:403-31 [2275818] Cell. 1990 Nov 2;63(3):503-13 [2225064] Annu Rev Cell Biol. 1988;4:257-88 [3058161] Cell. 1986 Jul 18;46(2):291-300 [3087629] Nature. 1989 Jul 20;340(6230):236-9 [2787892] Cell. 1989 Mar 10;56(5):801-13 [2647301] Nature. 1989 Nov 9;342(6246):192-5 [2554146] Nature. 1989 Nov 2;342(6245):32-8 [2554142] J Cell Biol. 1987 Dec;105(6 Pt 1):2665-74 [3121636] J Cell Biol. 1989 Dec;109(6 Pt 2):3273-89 [2557352] Cell. 1989 Nov 17;59(4):729-37 [2510935] Cell. 1986 Sep 12;46(6):939-50 [3757030] J Cell Biol. 1986 Oct;103(4):1179-91 [2429970] Agents Actions. 1989 Apr;27(1-2):17-23 [2787587] J Biol Chem. 1988 Oct 15;263(29):15024-31 [2844796] J Cell Biol. 1988 Dec;107(6 Pt 1):2149-61 [2974039] J Biol Chem. 1988 Jan 5;263(1):340-3 [2961745] Nature. 1985 Oct 3-9;317(6036):430-4 [2995827] Cell. 1986 Apr 11;45(1):3-13 [2937542] Cell. 1986 Sep 26;46(7):959-61 [2944601] Nature. 1988 May 5;333(6168):90-3 [3129663] Proc Natl Acad Sci U S A. 1987 Dec;84(24):9199-203 [3122216] J Cell Biol. 1987 Mar;104(3):761-7 [3102505] J Cell Biol. 1986 May;102(5):1558-66 [3084497] Cell. 1988 Jul 15;54(2):209-20 [3292055] Hybridoma. 1985 Summer;4(2):91-102 [2408992] Cell. 1989 Nov 17;59(4):591-601 [2573430] Cell. 1989 Jul 14;58(1):133-45 [2526682] Annu Rev Cell Biol. 1989;5:277-307 [2688707] EMBO J. 1989 May;8(5):1461-7 [2670554] J Cell Biol. 1989 Jul;109(1):73-83 [2663883] Science. 1989 Jul 28;245(4916):385-90 [2756425] J Cell Biol. 1989 Jun;108(6):2117-26 [2738090] J Cell Sci. 1988 Sep;91 ( Pt 1):61-70 [3253304] Proc Natl Acad Sci U S A. 1988 Apr;85(8):2499-503 [3357878] Nature. 1988 Mar 31;332(6163):462-4 [3352747] Methods Enzymol. 1987;154:367-82 [3323813] Nature. 1987 Oct 29-Nov 4;329(6142):840-2 [3313052] Annu Rev Biochem. 1987;56:395-433 [3304139] Cell. 1985 Nov;43(1):223-31 [3878228] J Biol Chem. 1985 Mar 25;260(6):3440-50 [3838314] EMBO J. 1985 Dec 1;4(12):3137-43 [4092680] Science. 1990 Aug 10;249(4969):677-9 [1696397] Cell. 1990 Mar 9;60(5):781-90 [2107027] Proc Natl Acad Sci U S A. 1990 Apr;87(7):2466-70 [2138778] J Biol Chem. 1990 Jul 5;265(19):10893-9 [2162823] J Biol Chem. 1990 Apr 25;265(12):6879-83 [2157712] J Cell Biol. 1990 Sep;111(3):829-37 [2118144] Cell. 1990 Apr 20;61(2):197-9 [2184940] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Discrimination of mutagenic intermediates derived from alkylating agents by mutational patterns generated in Escherichia coli. AN - 80679506; 2070480 AB - Reactive intermediates (ultimate mutagens/carcinogens) generated by alkylating agents are unstable and difficult to characterize by chemical means. We have used a genetic system to distinguish the in vivo interactions of eight carcinogenic methylating agents and five ethylating agents by the patterns of induced mutations at different target sites in Escherichia coli WU3610. For this multiple locus assay, target sites were an amber (TAG) and an ochre (TAA) triplet, DNA encoding five suppressor tRNA anticodons, and one unidentified locus. Most of the mutations could be classified as specific sequence changes at the target loci by suppressor analysis using T4 bacteriophage. Ratios of the slopes of dose-response curves for induced mutations were used to generate a profile of preferred sites for mutagenesis independent of mutagen potency. 'Mutational fingerprints' derived from different methylating and ethylating agents were compared, as evidence for the existence of common intermediates responsible for their biological effects. Six methylating agents thought to act via SN1 mechanisms were found to generate similar mutational patterns, indicative of a common mechanism, while two methylating agents reacting via SN2 mechanisms gave different patterns. The mutational fingerprints of SN1- and SN-type ethylating agents were also distinct. Mutational fingerprints may be useful in distinguishing the interactions of different ultimate mutagens. JF - Carcinogenesis AU - Elespuru, R K AU - Stupar, L L AU - Gordon, J A AD - Laboratory of Chemical and Physical Carcinogenesis, NCI-Frederick Cancer Research and Development Facility, MD 21702-1201. Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 1161 EP - 1167 VL - 12 IS - 7 SN - 0143-3334, 0143-3334 KW - Alkylating Agents KW - 0 KW - DNA, Bacterial KW - Mutagens KW - Index Medicus KW - Phenotype KW - Dose-Response Relationship, Drug KW - DNA, Bacterial -- metabolism KW - Chromosome Mapping KW - Alkylating Agents -- metabolism KW - Mutagens -- metabolism KW - Escherichia coli -- genetics KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80679506?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Discrimination+of+mutagenic+intermediates+derived+from+alkylating+agents+by+mutational+patterns+generated+in+Escherichia+coli.&rft.au=Elespuru%2C+R+K%3BStupar%2C+L+L%3BGordon%2C+J+A&rft.aulast=Elespuru&rft.aufirst=R&rft.date=1991-07-01&rft.volume=12&rft.issue=7&rft.spage=1161&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-20 N1 - Date created - 1991-08-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Platinum-DNA damage in leukocyte DNA of patients receiving carboplatin and cisplatin chemotherapy, measured by atomic absorption spectrometry. AN - 80677823; 2070490 AB - Previous studies have shown that platinum-DNA adduct level in leukocyte DNA (measured by antibody methodology) is directly related to disease response in ovarian cancer and testicular cancer. To determine if this principle could be more broadly applied, platinum-DNA damage was studied in a blinded fashion in leukocyte DNA of 21 cancer patients who received carboplatin (day 1) and cisplatin (day 3) in a phase 1 clinical trial. Fifteen different tumor types were included in this cohort. Using atomic absorption spectrometry with Zeeman background correction, DNA-bound platinum was measured during cycles 1 (C1) and 2 (C2) of therapy for most patients. For each of two cycles of therapy, most patients developed measurable levels of adduct after carboplatin, and in most patients adduct levels increased further after cisplatin, often in a supra-additive fashion. Total mg dose levels varied by less than 2-fold, whereas individual patients differed by as much as 10(3) in their adduct measurements after C1 and after C2, and by 29-fold after the very first carboplatin dose. All patients had refractory disease at the initiation of therapy, and 19 patients were evaluable for disease response. Adduct determinations were made 24 h after the first dose of platinum therapy in 17 of these individuals. Mean adduct levels after the first dose of carboplatin were higher in six responders (50 fmol/micrograms DNA +/- 26) than in 11 non-responders (14 fmol/micrograms DNA +/- 10); Wilcoxon two sample test two-sided P = 0.0071. The six responders were patients with pleural mesothelioma (2), breast cancer, buccal mucosa cancer, esophageal cancer and ovarian cancer. Adduct levels were consistently higher in the group of responders on each day that adduct was measured, with a summary two-sided P value of 0.00011. We conclude that analysis of platinum-DNA adduct formation may help determine whether pharmacogenetics are important in cancer drug resistance; and may help to determine the relationship between DNA damage in the peripheral blood compartment and internal organ response to in vivo exposures to DNA-damaging agents. JF - Carcinogenesis AU - Parker, R J AU - Gill, I AU - Tarone, R AU - Vionnet, J A AU - Grunberg, S AU - Muggia, F M AU - Reed, E AD - Medicine Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 1253 EP - 1258 VL - 12 IS - 7 SN - 0143-3334, 0143-3334 KW - Platinum KW - 49DFR088MY KW - DNA KW - 9007-49-2 KW - Carboplatin KW - BG3F62OND5 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Drug Administration Schedule KW - Prospective Studies KW - Double-Blind Method KW - Humans KW - Spectrophotometry, Atomic KW - Male KW - Female KW - Leukocytes -- metabolism KW - Platinum -- metabolism KW - Neoplasms -- drug therapy KW - Cisplatin -- therapeutic use KW - DNA Damage KW - DNA -- metabolism KW - Carboplatin -- metabolism KW - Carboplatin -- therapeutic use KW - Cisplatin -- metabolism KW - Carboplatin -- administration & dosage KW - Neoplasms -- metabolism KW - Cisplatin -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80677823?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Platinum-DNA+damage+in+leukocyte+DNA+of+patients+receiving+carboplatin+and+cisplatin+chemotherapy%2C+measured+by+atomic+absorption+spectrometry.&rft.au=Parker%2C+R+J%3BGill%2C+I%3BTarone%2C+R%3BVionnet%2C+J+A%3BGrunberg%2C+S%3BMuggia%2C+F+M%3BReed%2C+E&rft.aulast=Parker&rft.aufirst=R&rft.date=1991-07-01&rft.volume=12&rft.issue=7&rft.spage=1253&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-20 N1 - Date created - 1991-08-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Theoretical and experimental measures of DNA helix stability and their relation to sequence specific repair of O6-ethylguanine lesions. AN - 80673383; 2067552 AB - Recent work (Breslauer et al. (1986) Proc. Natl. Acad. Sci. (U.S.A.), 83, 3746) has provided a method for calculating empirical thermodynamic quantities for helix to coil transitions from the base sequence of any oligomer. It is shown in this work that the DNA helix binding energy, calculated with the AMBER force field, for 9-mers of the type 5'-GGGXGeYGGG-3', where X and Y are any base and the central Ge is O6-ethylguanine, correlates well with the empirical delta G for helix to strand transitions. The mutation spectrum of ethane methylsulfonate (EMS) in the lacI gene of Escherichia coli can be modeled using the calculated local binding energy but the empirical free energies, enthalpies and melting temperatures predict these levels of repair less well. The relation of the binding energy to the mutation spectrum can be somewhat improved by including entropic effects in a theoretical free energy of binding as given by delta G theoretical identical to delta E binding - T delta S. JF - Mutation research AU - Foley, C K AU - Pedersen, L G AU - Darden, T A AU - Glickman, B W AU - Anderson, M W AD - Laboratory of Molecular Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 89 EP - 93 VL - 255 IS - 1 SN - 0027-5107, 0027-5107 KW - DNA, Bacterial KW - 0 KW - 6-ethylguanine KW - 51866-19-4 KW - Guanine KW - 5Z93L87A1R KW - Ethyl Methanesulfonate KW - 9H154DI0UP KW - Index Medicus KW - Escherichia coli -- metabolism KW - Base Sequence KW - Thermodynamics KW - Kinetics KW - Molecular Sequence Data KW - Escherichia coli -- drug effects KW - Escherichia coli -- genetics KW - Ethyl Methanesulfonate -- toxicity KW - DNA Repair -- physiology KW - DNA, Bacterial -- chemistry KW - DNA Damage KW - Guanine -- analogs & derivatives KW - DNA, Bacterial -- metabolism KW - Nucleic Acid Conformation KW - Guanine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80673383?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Theoretical+and+experimental+measures+of+DNA+helix+stability+and+their+relation+to+sequence+specific+repair+of+O6-ethylguanine+lesions.&rft.au=Foley%2C+C+K%3BPedersen%2C+L+G%3BDarden%2C+T+A%3BGlickman%2C+B+W%3BAnderson%2C+M+W&rft.aulast=Foley&rft.aufirst=C&rft.date=1991-07-01&rft.volume=255&rft.issue=1&rft.spage=89&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 - 1991-08-12 N1 - Date created - 1991-08-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Targeted therapy of human immunodeficiency virus-related disease. AN - 80666676; 1712326 AB - Since the discovery of human immunodeficiency virus (HIV) as a pathogenic retrovirus linked to acquired immunodeficiency syndrome (AIDS), a number of potentially useful strategies for antiretroviral therapy of AIDS and its related diseases have emerged. One such strategy involves use of the broad family of 2',3'-dideoxynucleosides, to which 3'-azido-2',3'-dideoxythymidine (AZT) belongs. AZT has been shown to reduce the replication of HIV in vivo and to confer significant clinical benefits in patients in both early and advanced stages of infection. Other members of the family, 2',3'-dideoxycytidine (ddC), 2',3'-dideoxyinosine (ddI), and 2',3'-didehydro-2',3'-dideoxythymidine (d4T), have also been reported to be active against HIV in short-term clinical trials. The armamentarium of antiretroviral agents is rapidly growing. Various nonnucleoside agents have recently been identified to be active against HIV in vitro. HIV-1 protease inhibitors are notable as possible new therapies for HIV-1-related diseases. However, we have faced several new challenges in the antiretroviral therapy in AIDS. These include long-term drug-related toxicities; emergence of drug-resistant HIV variants; and development of various cancers, particularly as effective therapies prolong survival. Progress in understanding structure-activity relations and clinical effectiveness will continue with dideoxynucleoside analogs. However, it seems certain that a variety of nonnucleoside analogs affecting multiple steps in viral replication will become available before long, and combination therapies using multiple antiretroviral drugs will be available. Such therapies will exert major effects against the moribidity and mortality caused by HIV. JF - FASEB journal : official publication of the Federation of American Societies for Experimental Biology AU - Mitsuya, H AU - Yarchoan, R AU - Kageyama, S AU - Broder, S AD - Division of Cancer Treatment, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 2369 EP - 2381 VL - 5 IS - 10 SN - 0892-6638, 0892-6638 KW - Antigens, CD4 KW - 0 KW - Antiviral Agents KW - Dideoxynucleosides KW - Interferon Type I KW - Organophosphonates KW - Zidovudine KW - 4B9XT59T7S KW - Dipyridamole KW - 64ALC7F90C KW - adefovir KW - 6GQP90I798 KW - Zalcitabine KW - 6L3XT8CB3I KW - Stavudine KW - BO9LE4QFZF KW - RNA-Directed DNA Polymerase KW - EC 2.7.7.49 KW - HIV Protease KW - EC 3.4.23.- KW - Adenine KW - JAC85A2161 KW - Didanosine KW - K3GDH6OH08 KW - 3'-azido-2',3'-dideoxyuridine KW - PS28W65479 KW - Index Medicus KW - AIDS/HIV KW - HIV -- drug effects KW - Transcription, Genetic -- drug effects KW - HIV Protease -- drug effects KW - Didanosine -- adverse effects KW - Zidovudine -- adverse effects KW - Genes, rev -- physiology KW - Dipyridamole -- therapeutic use KW - Antigens, CD4 -- therapeutic use KW - Zalcitabine -- pharmacology KW - Drug Synergism KW - Didanosine -- pharmacology KW - Zidovudine -- therapeutic use KW - Zidovudine -- analogs & derivatives KW - Zidovudine -- pharmacology KW - Interferon Type I -- therapeutic use KW - Adenine -- therapeutic use KW - RNA-Directed DNA Polymerase -- physiology KW - Dideoxynucleosides -- pharmacology KW - Genes, tat -- physiology KW - Antiviral Agents -- pharmacology KW - Dideoxynucleosides -- adverse effects KW - RNA-Directed DNA Polymerase -- drug effects KW - Adenine -- analogs & derivatives KW - HIV -- pathogenicity KW - RNA-Directed DNA Polymerase -- genetics KW - Genes, nef -- physiology KW - Gene Expression Regulation, Viral -- drug effects KW - Acquired Immunodeficiency Syndrome -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80666676?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Targeted+therapy+of+human+immunodeficiency+virus-related+disease.&rft.au=Mitsuya%2C+H%3BYarchoan%2C+R%3BKageyama%2C+S%3BBroder%2C+S&rft.aulast=Mitsuya&rft.aufirst=H&rft.date=1991-07-01&rft.volume=5&rft.issue=10&rft.spage=2369&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 - 1991-08-15 N1 - Date created - 1991-08-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The state of the p53 and retinoblastoma genes in human cervical carcinoma cell lines. AN - 80652758; 1648218 AB - Human cervical carcinoma cell lines that were either positive or negative for human papillomavirus (HPV) DNA sequences were analyzed for evidence of mutation of the p53 and retinoblastoma genes. Each of five HPV-positive cervical cancer cell lines expressed normal pRB and low levels of wild-type p53 proteins, which are presumed to be altered in function as a consequence of association with HPV E7 and E6 oncoproteins, respectively. In contrast, mutations were identified in the p53 and RB genes expressed in the C-33A and HT-3 cervical cancer cell lines, which lack HPV DNA sequences. Mutations in the p53 genes mapped to codon 273 and codon 245 in the C33-A and HT-3 cell lines, respectively, located in the highly conserved regions of p53, where mutations appear in a variety of human cancers. Mutations in RB occurred at splice junctions, resulting in in-frame deletions, affecting exons 13 and 20 in the HT-3 and C-33A cell lines, respectively. These mutations resulted in aberrant proteins that were not phosphorylated and were unable to complex with the adenovirus E1A oncoprotein. These results support the hypothesis that the inactivation of the normal functions of the tumor-suppressor proteins pRB and p53 are important steps in human cervical carcinogenesis, either by mutation or from complex formation with the HPV E6 and E7 oncoproteins. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Scheffner, M AU - Münger, K AU - Byrne, J C AU - Howley, P M AD - Laboratory of Tumor Virus Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/07/01/ PY - 1991 DA - 1991 Jul 01 SP - 5523 EP - 5527 VL - 88 IS - 13 SN - 0027-8424, 0027-8424 KW - DNA, Neoplasm KW - 0 KW - Oligonucleotides KW - Tumor Suppressor Protein p53 KW - Index Medicus KW - Humans KW - Keratinocytes -- physiology KW - Polymerase Chain Reaction KW - Base Sequence KW - Blotting, Western KW - Genes KW - Tumor Cells, Cultured KW - Papillomaviridae -- analysis KW - Oligonucleotides -- chemistry KW - Molecular Sequence Data KW - DNA, Neoplasm -- genetics KW - Mutation KW - Female KW - Uterine Cervical Neoplasms -- genetics KW - Tumor Suppressor Protein p53 -- immunology KW - Tumor Suppressor Protein p53 -- genetics KW - Genes, Retinoblastoma -- genetics KW - Genes, Retinoblastoma -- immunology KW - Carcinoma -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80652758?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=The+state+of+the+p53+and+retinoblastoma+genes+in+human+cervical+carcinoma+cell+lines.&rft.au=Scheffner%2C+M%3BM%C3%BCnger%2C+K%3BByrne%2C+J+C%3BHowley%2C+P+M&rft.aulast=Scheffner&rft.aufirst=M&rft.date=1991-07-01&rft.volume=88&rft.issue=13&rft.spage=5523&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 - 1991-08-02 N1 - Date created - 1991-08-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Eur J Biochem. 1986 Sep 15;159(3):529-34 [2428616] Proc Natl Acad Sci U S A. 1979 Sep;76(9):4350-4 [388439] EMBO J. 1989 Dec 20;8(13):4099-105 [2556261] EMBO J. 1989 Dec 1;8(12):3905-10 [2555178] J Virol. 1989 Nov;63(11):4898-903 [2552162] Science. 1989 Feb 17;243(4893):934-7 [2537532] Proc Natl Acad Sci U S A. 1989 Nov;86(22):8763-7 [2530586] J Virol. 1989 Mar;63(3):1465-9 [2536847] J Virol. 1989 Mar;63(3):1247-55 [2536832] J Virol. 1989 Feb;63(2):965-9 [2536119] Cell. 1989 Jun 30;57(7):1083-93 [2525423] Cell. 1990 Dec 21;63(6):1129-36 [2175676] J Clin Microbiol. 1991 Mar;29(3):573-7 [1645370] Mol Cell Biol. 1990 Dec;10(12):6299-305 [2247057] Nature. 1989 Dec 7;342(6250):705-8 [2531845] Oncogene Res. 1988 Sep;3(2):167-75 [2852339] Mol Cell Biol. 1988 Feb;8(2):531-9 [2832726] Oncogene. 1987 May;1(2):201-11 [2830579] Cell. 1988 May 20;53(4):539-47 [2836062] Virology. 1988 Jul;165(1):321-5 [2838969] Cell. 1988 Jul 15;54(2):275-83 [2839300] Int J Cancer. 1988 Jun 15;41(6):896-900 [2836322] Proc Natl Acad Sci U S A. 1987 Nov;84(21):7716-9 [2823272] Proc Natl Acad Sci U S A. 1986 Jul;83(13):4680-4 [3014503] EMBO J. 1986 Sep;5(9):2285-92 [3023067] J Virol. 1987 Apr;61(4):962-71 [3029430] Nature. 1985 Mar 7-13;314(6006):111-4 [2983228] Nature. 1988 Jul 14;334(6178):124-9 [2968522] J Virol. 1989 Oct;63(10):4417-21 [2476573] EMBO J. 1988 Jun;7(6):1815-20 [2458921] EMBO J. 1988 Oct;7(10):3181-7 [2460337] Gene. 1989 Aug 1;80(1):119-28 [2701949] Cell. 1989 Sep 22;58(6):1193-8 [2673546] Cell. 1989 Sep 22;58(6):1097-105 [2673543] Cell. 1989 Jan 13;56(1):57-65 [2910497] Mol Cell Biol. 1981 Feb;1(2):101-10 [6100960] Mol Cell Biol. 1987 Aug;7(8):2863-9 [3313006] Proc Natl Acad Sci U S A. 1987 Dec;84(24):9059-63 [3480530] EMBO J. 1990 Jun;9(6):1815-22 [2189724] Lancet. 1990 May 19;335(8699):1171-4 [1971033] Proc Natl Acad Sci U S A. 1990 Sep;87(17):6922-6 [2168563] Mol Cell Biol. 1990 Jul;10(7):3761-9 [2162480] Science. 1990 Apr 6;248(4951):76-9 [2157286] J Virol. 1990 Mar;64(3):1353-6 [2154613] Cell. 1990 Feb 9;60(3):387-96 [2154332] Cell. 1990 Jun 1;61(5):777-85 [2140528] EMBO J. 1990 Apr;9(4):1147-55 [2138977] Proc Natl Acad Sci U S A. 1990 Apr;87(7):2775-9 [2181449] Cell. 1984 Aug;38(1):119-26 [6088057] Cell. 1982 Feb;28(2):387-94 [6277513] J Virol. 1980 Nov;36(2):395-407 [6253665] Cell. 1979 May;17(1):43-52 [222475] Nature. 1979 Mar 15;278(5701):261-3 [218111] Eur J Biochem. 1986 Feb 3;154(3):665-72 [2419131] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Photodynamic therapy for chest wall recurrence in breast cancer. AN - 80652353; 2061120 AB - Photodynamic therapy is the use of a sensitizer (dihematoporphyrin ethers) which is preferentially retained in tumor cells and activated by subsequent light delivery resulting in a selective tumoricidal effect. Between 1986 and 1989, we treated 20 patients with photodynamic therapy for chest wall recurrence of breast cancer. Responses were seen (20% complete response, 45% partial response, 35% no response), but the duration of response was short (average 2.5 months). Complications, in decreasing frequency, included pain, ecchymoses, blistering, ulceration and necrosis in the area of tumor involvement on the chest wall. One patient required skin flap reconstruction for full thickness necrosis. A limitation to this mode of therapy is that the sensitizer currently used is activated by light at a wavelength of 630 nm. This light can penetrate to a tissue depth of only 0.5 to 1.0 cm; thus, deeper disease cannot be treated. Future research must focus on the development of a clinically useful photosensitizer that can be activated by light at longer wavelengths and thereby achieve deeper tissue penetration. This would greatly expand the patient population for which this therapy is useful. JF - International journal of radiation oncology, biology, physics AU - Sperduto, P W AU - DeLaney, T F AU - Thomas, G AU - Smith, P AU - Dachowski, L J AU - Russo, A AU - Bonner, R AU - Glatstein, E AD - Radiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 441 EP - 446 VL - 21 IS - 2 SN - 0360-3016, 0360-3016 KW - Index Medicus KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Female KW - Breast Neoplasms -- drug therapy KW - Neoplasm Recurrence, Local -- drug therapy KW - Photochemotherapy -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80652353?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+radiation+oncology%2C+biology%2C+physics&rft.atitle=Photodynamic+therapy+for+chest+wall+recurrence+in+breast+cancer.&rft.au=Sperduto%2C+P+W%3BDeLaney%2C+T+F%3BThomas%2C+G%3BSmith%2C+P%3BDachowski%2C+L+J%3BRusso%2C+A%3BBonner%2C+R%3BGlatstein%2C+E&rft.aulast=Sperduto&rft.aufirst=P&rft.date=1991-07-01&rft.volume=21&rft.issue=2&rft.spage=441&rft.isbn=&rft.btitle=&rft.title=International+journal+of+radiation+oncology%2C+biology%2C+physics&rft.issn=03603016&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-08 N1 - Date created - 1991-08-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - CONF T1 - Report on the Fourth Conference for Federally Supported Human Nutrition Research Units and Centers. AN - 80646808; 2058579 AB - The Fourth Conference for Federally Supported Human Nutrition Research Units and Centers, sponsored by the Interagency Committee on Human Nutrition Research, addressed two topics: nutrition and function, and nutrient interactions and toxicities. This article summarizes the conference's introductory remarks and the contents of the 34 papers presented. Future meetings of federally supported nutrition research units and centers will focus on other human nutrition research topics and will be held biennially. JF - The American journal of clinical nutrition AU - Danford, D E AU - Hubbard, V S AU - Combs, G F AU - Hall, C A AU - Larsen, L A AU - Schnakenberg, D D Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 164 EP - 168 VL - 54 IS - 1 KW - Abridged Index Medicus KW - Index Medicus KW - United States KW - Humans KW - National Institutes of Health (U.S.) KW - Research KW - Nutritional Physiological Phenomena UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80646808?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=The+American+journal+of+clinical+nutrition&rft.atitle=Report+on+the+Fourth+Conference+for+Federally+Supported+Human+Nutrition+Research+Units+and+Centers.&rft.au=Danford%2C+D+E%3BHubbard%2C+V+S%3BCombs%2C+G+F%3BHall%2C+C+A%3BLarsen%2C+L+A%3BSchnakenberg%2C+D+D&rft.aulast=Danford&rft.aufirst=D&rft.date=1991-07-01&rft.volume=54&rft.issue=1&rft.spage=164&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+clinical+nutrition&rft.issn=00029165&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-26 N1 - Date created - 1991-07-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A phase I/II trial of zidovudine, interferon-alpha, and granulocyte-macrophage colony-stimulating factor in the treatment of human immunodeficiency virus type 1 infection. AN - 80639941; 1676045 AB - Twenty-four patients infected with human immunodeficiency virus type 1 (HIV-1) who had CD4+ counts of 0.2-0.5 x 10(9) cells/l received granulocyte-macrophage colony-stimulating factor (GM-CSF) in combination with zidovudine plus escalating doses of daily subcutaneous interferon-alpha. Mean neutropenia-inducing doses of interferon-alpha were 9.4 x 10(6) and 10.6 x 10(6) IU/day for groups receiving 100 or 200 mg zidovudine every 4 h, respectively. Mean GM-CSF doses used to reverse neutropenia were 0.64 and 0.63 microgram/kg/day for these two groups, respectively, although the mean minimum effective GM-CSF dose for both was only 0.30 microgram/kg/day. Serum p24 antigen declined greater than 70% in all 5 antigenemic patients. Toxicities included a dose-dependent increase in lymphokine-like side effects (100%), anorexia and weight loss (42%), fatigue (42%), and anemia (50%). While toxicities of the combination can be significant, low-dose GM-CSF readily ameliorated neutropenia associated with zidovudine and interferon-alpha therapy without adversely affecting the antiviral properties of the combination. JF - The Journal of infectious diseases AU - Davey, R T AU - Davey, V J AU - Metcalf, J A AU - Zurlo, J J AU - Kovacs, J A AU - Falloon, J AU - Polis, M A AU - Zunich, K M AU - Masur, H AU - Lane, H C AD - Critical Care Medicine Department, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 43 EP - 52 VL - 164 IS - 1 SN - 0022-1899, 0022-1899 KW - Gene Products, gag KW - 0 KW - HIV Antigens KW - HIV Core Protein p24 KW - Interferon-alpha KW - Recombinant Proteins KW - Viral Core Proteins KW - interferon alfa-2b KW - 43K1W2T1M6 KW - Zidovudine KW - 4B9XT59T7S KW - Granulocyte-Macrophage Colony-Stimulating Factor KW - 83869-56-1 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Administration, Oral KW - Gene Products, gag -- blood KW - Humans KW - Neutropenia -- chemically induced KW - Sarcoma, Kaposi -- complications KW - Leukocyte Count KW - CD4-Positive T-Lymphocytes KW - Erythema -- chemically induced KW - Drug Therapy, Combination KW - Drug Evaluation KW - Viral Core Proteins -- blood KW - Adult KW - Recombinant Proteins -- adverse effects KW - Injections, Subcutaneous KW - Follow-Up Studies KW - HIV Antigens -- blood KW - Recombinant Proteins -- therapeutic use KW - Male KW - Zidovudine -- therapeutic use KW - Granulocyte-Macrophage Colony-Stimulating Factor -- administration & dosage KW - Interferon-alpha -- therapeutic use KW - Interferon-alpha -- adverse effects KW - Zidovudine -- adverse effects KW - Interferon-alpha -- administration & dosage KW - HIV Infections -- drug therapy KW - Zidovudine -- administration & dosage KW - Granulocyte-Macrophage Colony-Stimulating Factor -- therapeutic use KW - Granulocyte-Macrophage Colony-Stimulating Factor -- adverse effects KW - HIV-1 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80639941?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+infectious+diseases&rft.atitle=A+phase+I%2FII+trial+of+zidovudine%2C+interferon-alpha%2C+and+granulocyte-macrophage+colony-stimulating+factor+in+the+treatment+of+human+immunodeficiency+virus+type+1+infection.&rft.au=Davey%2C+R+T%3BDavey%2C+V+J%3BMetcalf%2C+J+A%3BZurlo%2C+J+J%3BKovacs%2C+J+A%3BFalloon%2C+J%3BPolis%2C+M+A%3BZunich%2C+K+M%3BMasur%2C+H%3BLane%2C+H+C&rft.aulast=Davey&rft.aufirst=R&rft.date=1991-07-01&rft.volume=164&rft.issue=1&rft.spage=43&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+infectious+diseases&rft.issn=00221899&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-01 N1 - Date created - 1991-08-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A physicians's guide to preventing tobacco use during childhood and adolescence. AN - 80637715; 2057249 AB - Physicians who care for children can and should help patients avoid the use of tobacco. Physicians are well aware of the health hazards associated with tobacco use, inasmuch as smoking is the chief, single cause of premature mortality in this country. Each day, more than 3000 children in the United States begin to use tobacco. Physicians who care for children have patients at vastly different stages of intellectual and social maturity. Both the theory and practical details of tobacco-related interventions differ among infants, children, and adolescents. The physician is in a unique position to intervene in the early stages. Anticipatory guidance--the practice of providing counsel regarding potential problems--is a key part of health care for the young. If physicians provide messages about tobacco use that are appropriate to the patient's age and developmental stage, the potential for broad public health impact is great. Based on a series of clinical trials, the National Cancer Institute developed a manual to assist physicians in helping their patients stop smoking. The recommendations in this manual include four physician activities that begin with the letter A (four A's): Ask, Advise, Assist, and Arrange follow-up. For physicians who treat children, a fifth A, Anticipatory guidance, is added. JF - Pediatrics AU - Epps, R P AU - Manley, M W AD - Division of Cancer Prevention and Control, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 140 EP - 144 VL - 88 IS - 1 SN - 0031-4005, 0031-4005 KW - Abridged Index Medicus KW - Index Medicus KW - United States KW - Age Factors KW - Attitude to Health KW - Humans KW - Professional-Family Relations KW - Child KW - Adolescent KW - Parents -- psychology KW - Child, Preschool KW - Tobacco Use Disorder -- psychology KW - Tobacco Use Disorder -- prevention & control KW - Physician's Role KW - Smoking -- psychology KW - Smoking -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80637715?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pediatrics&rft.atitle=A+physicians%27s+guide+to+preventing+tobacco+use+during+childhood+and+adolescence.&rft.au=Epps%2C+R+P%3BManley%2C+M+W&rft.aulast=Epps&rft.aufirst=R&rft.date=1991-07-01&rft.volume=88&rft.issue=1&rft.spage=140&rft.isbn=&rft.btitle=&rft.title=Pediatrics&rft.issn=00314005&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-31 N1 - Date created - 1991-07-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Treatment with recombinant human tumor necrosis factor-alpha protects rats against the lethality, hypotension, and hypothermia of gram-negative sepsis. AN - 80635332; 2056127 AB - Tumor necrosis factor (TNF) is a peptide secreted by macrophages in response to endotoxin that can produce many of the changes seen in septic shock. After cecal ligation and puncture (CLP) rats gradually develop tachycardia, hypotension, tachypnea, and hypothermia. At 5 h post-CLP, rats have a peak in serum levels of endotoxin and 60% of rats have blood cultures that grow Gram-negative rods (Escherichia coli and Klebsiella pneumonia). At 20 h post-CLP all rats develop positive blood cultures. Serum levels of TNF are not reproducibly measurable in rats following CLP. Rats undergoing CLP have a 50-80% mortality with deaths usually occurring 24-72 h postinjury. Repetitive (twice daily x 6 d) i.p. injection of sublethal doses of recombinant human TNF-alpha (100 micrograms/kg) to rats undergoing CLP 1 d after the treatment period resulted in a significant reduction in mortality compared to control rats previously unexposed to rTNF (P less than 0.03). Animals treated with rTNF had no hypotension or hypothermia after CLP and regained normal food intake faster than control rats. 12 h after CLP the gene expression for manganous superoxide dismutase (MnSOD), an inducible mitochondrial metalloenzyme responsible for cellular resistance to injury from toxic reactive oxygen species, was higher in livers of rats treated with rTNF suggesting that the TNF treatment augmented expression of this protective enzyme. Unlike MnSOD, expression of the gene for copper-zinc SOD was not affected by CLP or rTNF treatment. The results suggest that prior treatment with recombinant TNF can ameliorate the lethality, hypotension, hypothermia, and anorexia of Gram-negative sepsis in rats and that the mechanism may be related to enhanced hepatic expression of the gene for MnSOD. Repeated administration of recombinant TNF may be a strategy to minimize mortality and morbidity of Gram-negative sepsis. JF - The Journal of clinical investigation AU - Alexander, H R AU - Sheppard, B C AU - Jensen, J C AU - Langstein, H N AU - Buresh, C M AU - Venzon, D AU - Walker, E C AU - Fraker, D L AU - Stovroff, M C AU - Norton, J A AD - Surgical Metabolism Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 34 EP - 39 VL - 88 IS - 1 SN - 0021-9738, 0021-9738 KW - Recombinant Proteins KW - 0 KW - Tumor Necrosis Factor-alpha KW - Superoxide Dismutase KW - EC 1.15.1.1 KW - Abridged Index Medicus KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Gene Expression KW - Superoxide Dismutase -- genetics KW - Recombinant Proteins -- therapeutic use KW - Male KW - Hypothermia -- prevention & control KW - Tumor Necrosis Factor-alpha -- analysis KW - Hypotension -- prevention & control KW - Sepsis -- drug therapy KW - Sepsis -- complications KW - Tumor Necrosis Factor-alpha -- therapeutic use KW - Gram-Negative Bacteria -- pathogenicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80635332?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Treatment+with+recombinant+human+tumor+necrosis+factor-alpha+protects+rats+against+the+lethality%2C+hypotension%2C+and+hypothermia+of+gram-negative+sepsis.&rft.au=Alexander%2C+H+R%3BSheppard%2C+B+C%3BJensen%2C+J+C%3BLangstein%2C+H+N%3BBuresh%2C+C+M%3BVenzon%2C+D%3BWalker%2C+E+C%3BFraker%2C+D+L%3BStovroff%2C+M+C%3BNorton%2C+J+A&rft.aulast=Alexander&rft.aufirst=H&rft.date=1991-07-01&rft.volume=88&rft.issue=1&rft.spage=34&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 - 1991-08-01 N1 - Date created - 1991-08-01 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Surg Res. 1980 Aug;29(2):189-201 [6997619] Proc Natl Acad Sci U S A. 1990 Nov;87(21):8331-5 [2172983] Science. 1985 Aug 30;229(4716):869-71 [3895437] Science. 1986 Oct 24;234(4775):470-4 [3764421] J Immunol. 1987 Feb 1;138(3):963-74 [3805720] Lancet. 1987 Feb 14;1(8529):355-7 [2880163] Surg Gynecol Obstet. 1987 May;164(5):415-22 [3576418] Cancer Res. 1987 Aug 15;47(16):4318-22 [3300963] CRC Crit Rev Biochem. 1987;22(2):111-80 [3315461] J Clin Invest. 1987 Dec;80(6):1587-96 [3500186] J Immunol. 1987 Dec 1;139(11):3783-91 [2824615] Nature. 1987 Dec 17-23;330(6149):662-4 [3317066] J Immunol. 1987 Dec 15;139(12):4225-31 [3693903] Surg Gynecol Obstet. 1988 Feb;166(2):147-53 [3122336] Immunology. 1988 Mar;63(3):507-12 [2832316] J Immunol. 1988 May 1;140(9):2994-9 [3258889] J Exp Med. 1988 May 1;167(5):1743-8 [3367098] N Engl J Med. 1988 Jun 9;318(23):1481-6 [2835680] J Exp Med. 1988 Jun 1;167(6):1957-62 [3385359] Lancet. 1988 Jul 9;2(8602):72-4 [2898700] Cancer Res. 1988 Aug 15;48(16):4567-72 [3165053] J Exp Med. 1988 Jul 1;168(1):95-105 [3294337] N Engl J Med. 1988 Aug 18;319(7):397-400 [3135497] Am J Med. 1988 Sep;85(3):289-91 [3414726] Arch Surg. 1988 Nov;123(11):1383-8 [3178487] J Biol Chem. 1980 Feb 10;255(3):1054-7 [7356650] Science. 1988 Nov 11;242(4880):941-4 [3263703] J Immunol. 1989 Jul 15;143(2):736-9 [2661690] Biochem Biophys Res Commun. 1989 Jul 31;162(2):794-801 [2547375] Surgery. 1989 Aug;106(2):156-61; discussion 161-2 [2669193] Immunol Today. 1988 Jan;9(1):28-31 [3076757] Cell. 1989 Sep 8;58(5):923-31 [2476237] Circ Shock. 1989 Dec;29(4):279-90 [2598414] Infect Immun. 1990 Feb;58(2):439-42 [2298485] J Clin Pathol. 1983 Oct;36(10):1145-9 [6352744] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Tobacco smoking as a risk factor for colon polyps. AN - 80626000; 2053658 AB - Data from a cancer screening project among pattern makers were used to evaluate the association between tobacco smoking and prevalence of colon polyps. From 1981-1983, 549 White men were examined by flexible sigmoidoscopy and completed self-administered questionnaires including smoking histories. One or more colon polyps were detected in 76 men. Standardized prevalence rates (SPR) for polyps increased by smoking category (never smoked = 0.094; ex-smokers = 0.118, current smokers = 0.214) and by cigarettes per day, years of smoking, and pack-years among both current and ex-smokers. Both adenomatous and hyperplastic polyps showed an association with smoking while other types of polyps and polyps with unspecified histology did not. The risk associated with smoking was greater for polyps greater than one centimeter in diameter. An interaction with occupational exposures was suggested by a greater increase in the SPR for polyps among current smokers employed as pattern makers for more than 10 years than among current smokers similarly employed for 10 years or less. Since at least some colon polyps are considered precursor lesions to colon cancer, one of the most common cancers in the United States, this report suggests that the possible link between colon polyps and smoking deserves further evaluation. JF - American journal of public health AU - Zahm, S H AU - Cocco, P AU - Blair, A AD - Occupational Studies Section, National Cancer Institute, Rockville, MD 20892. Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 846 EP - 849 VL - 81 IS - 7 SN - 0090-0036, 0090-0036 KW - Abridged Index Medicus KW - Index Medicus KW - Sigmoidoscopy KW - Mass Screening KW - Risk Factors KW - Humans KW - Adult KW - Surveys and Questionnaires KW - Middle Aged KW - United States -- epidemiology KW - Male KW - Prevalence KW - Colonic Polyps -- epidemiology KW - Occupational Diseases -- prevention & control KW - Smoking -- adverse effects KW - Occupational Diseases -- pathology KW - Occupational Diseases -- epidemiology KW - Smoking -- epidemiology KW - Colonic Polyps -- prevention & control KW - Colonic Polyps -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80626000?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Tobacco+smoking+as+a+risk+factor+for+colon+polyps.&rft.au=Zahm%2C+S+H%3BCocco%2C+P%3BBlair%2C+A&rft.aulast=Zahm&rft.aufirst=S&rft.date=1991-07-01&rft.volume=81&rft.issue=7&rft.spage=846&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 - 1991-07-25 N1 - Date created - 1991-07-25 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Occup Med. 1985 Nov;27(11):809-12 [4067686] Cancer Detect Prev. 1985;8(3):393-8 [4064061] J Occup Med. 1986 Aug;28(8):709-13 [3746495] J Occup Med. 1986 Aug;28(8):719-27 [3746497] Scand J Gastroenterol. 1987 Jan;22(1):13-6 [3563406] Prev Med. 1988 May;17(3):295-309 [3405986] J Natl Cancer Inst. 1988 Oct 19;80(16):1329-33 [3172257] Gastroenterology. 1989 Sep;97(3):660-4 [2753326] Int J Epidemiol. 1989 Sep;18(3):556-62 [2807657] Surg Forum. 1963;14:137-8 [14064485] Natl Cancer Inst Monogr. 1966 Jan;19:127-204 [5905667] Natl Cancer Inst Monogr. 1966 Jan;19:1-125 [5905668] Surg Gynecol Obstet. 1972 Mar;134(3):499-508 [4551198] Br Med J. 1976 Dec 25;2(6051):1525-36 [1009386] J Natl Cancer Inst. 1977 Mar;58(3):525-47 [557114] Cancer. 1979 May;43(5):1847-57 [445371] Int J Epidemiol. 1979 Dec;8(4):295-303 [541153] Br Med J. 1980 Apr 5;280(6219):967-71 [7417764] J Occup Med. 1982 Apr;24(4):315-9 [7069524] Am J Ind Med. 1980;1(2):159-65 [7342763] Cancer. 1982 Dec 1;50(11 Suppl):2601-8 [7139554] J Natl Cancer Inst. 1983 Mar;70(3):389-400 [6300495] Int J Cancer. 1985 Aug 15;36(2):179-86 [4018911] J Occup Med. 1986 Aug;28(8):704-8 [3746494] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Tyrosine mutations within the alpha platelet-derived growth factor receptor kinase insert domain abrogate receptor-associated phosphatidylinositol-3 kinase activity without affecting mitogenic or chemotactic signal transduction. AN - 80611683; 1646396 AB - A phosphatidylinositol-3 (PI-3) kinase activity of unknown biological function associates with tyrosine kinase-containing proteins, including a number of growth factor receptors after ligand stimulation. In the beta platelet-derived growth factor (beta PDGF) receptor, phosphorylation of a specific tyrosine residue within the kinase insert domain was required for its interaction with this enzyme. We show that substitutions of phenylalanine for tyrosine residue 731 or 742 within the kinase insert domain of the alpha PDGF receptor do not impair PDGF-induced tyrosine phosphorylation of the receptor or of an in vivo substrate, phospholipase C-gamma. Moreover, phosphatidylinositol turnover in response to ligand stimulation is unaffected. However, both lesions markedly impair receptor association with PI-3 kinase. Antiphosphotyrosine antibody-recoverable PI-3 kinase was also dramatically reduced in PDGF-stimulated cells expressing either mutant receptor. Since neither mutation abolished PDGF-induced mitogenesis or chemotaxis, we conclude that alpha PDGF receptor-associated PI-3 kinase activity is not required for either of these major PDGF signalling functions. JF - Molecular and cellular biology AU - Yu, J C AU - Heidaran, M A AU - Pierce, J H AU - Gutkind, J S AU - Lombardi, D AU - Ruggiero, M AU - Aaronson, S A AD - Laboratory of Cellular and Molecular Biology, National Cancer Institute (37-1E24), Bethesda, Maryland 20892. Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 3780 EP - 3785 VL - 11 IS - 7 SN - 0270-7306, 0270-7306 KW - Interleukin-3 KW - 0 KW - Oligonucleotide Probes KW - Platelet-Derived Growth Factor KW - Recombinant Proteins KW - Tyrosine KW - 42HK56048U KW - Phosphotransferases KW - EC 2.7.- KW - Protein Kinases KW - Phosphatidylinositol 3-Kinases KW - EC 2.7.1.- KW - Receptors, Platelet-Derived Growth Factor KW - EC 2.7.10.1 KW - Index Medicus KW - Animals KW - Recombinant Proteins -- pharmacology KW - Sequence Homology, Nucleic Acid KW - Interleukin-3 -- pharmacology KW - Platelet-Derived Growth Factor -- pharmacology KW - Amino Acid Sequence KW - Mutagenesis, Site-Directed KW - Base Sequence KW - Phosphorylation KW - Transfection KW - Kinetics KW - Molecular Sequence Data KW - Cell Line KW - Protein Kinases -- metabolism KW - Signal Transduction -- drug effects KW - Protein Kinases -- genetics KW - Cell Division -- drug effects KW - Chemotaxis -- drug effects KW - Phosphotransferases -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80611683?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Tyrosine+mutations+within+the+alpha+platelet-derived+growth+factor+receptor+kinase+insert+domain+abrogate+receptor-associated+phosphatidylinositol-3+kinase+activity+without+affecting+mitogenic+or+chemotactic+signal+transduction.&rft.au=Yu%2C+J+C%3BHeidaran%2C+M+A%3BPierce%2C+J+H%3BGutkind%2C+J+S%3BLombardi%2C+D%3BRuggiero%2C+M%3BAaronson%2C+S+A&rft.aulast=Yu&rft.aufirst=J&rft.date=1991-07-01&rft.volume=11&rft.issue=7&rft.spage=3780&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 - 1991-07-17 N1 - Date created - 1991-07-17 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nature. 1989 Dec 7;342(6250):699-702 [2556641] EMBO J. 1990 Oct;9(10):3279-86 [2170111] Science. 1987 Oct 23;238(4826):542-5 [2821624] Cell. 1987 Sep 25;50(7):1021-9 [2441878] Science. 1988 Feb 5;239(4840):628-31 [3257584] Cell. 1987 Dec 24;51(6):1063-70 [3500791] Cell. 1988 Aug 26;54(5):641-9 [2842060] Nature. 1988 Sep 1;335(6185):85-7 [2842689] Nature. 1988 Apr 14;332(6165):644-6 [2833705] Cell. 1987 Sep 25;50(7):1031-7 [2441879] Biochem J. 1987 Oct 1;247(1):165-74 [2825654] J Biol Chem. 1988 Oct 5;263(28):14497-504 [2459119] Annu Rev Biochem. 1987;56:159-93 [3304132] Proc Natl Acad Sci U S A. 1990 Sep;87(17):6738-42 [2168557] Cell. 1990 Apr 6;61(1):125-33 [2156626] Nature. 1990 Jan 25;343(6256):377-81 [1689011] Mol Cell Biol. 1991 Feb;11(2):1107-13 [1846663] Mol Cell Biol. 1989 Apr;9(4):1651-8 [2542773] Cell. 1989 Apr 7;57(1):167-75 [2467744] Cell. 1989 Jun 30;57(7):1109-22 [2472219] Science. 1989 Mar 24;243(4898):1564-70 [2538922] Cell. 1989 Sep 22;58(6):1121-33 [2550144] Mol Cell Biol. 1989 Jul;9(7):2934-43 [2550789] Mol Cell Biol. 1989 Oct;9(10):4473-8 [2479827] Proc Natl Acad Sci U S A. 1989 Nov;86(21):8314-8 [2554309] Proc Natl Acad Sci U S A. 1989 Nov;86(21):8232-6 [2554305] Nature. 1989 Dec 7;342(6250):711-4 [2480526] Mol Cell Biol. 1990 Jul;10(7):3806-9 [2162481] Proc Natl Acad Sci U S A. 1990 Feb;87(4):1411-5 [2154747] Mol Cell Biol. 1990 May;10(5):2359-66 [1691440] EMBO J. 1990 Aug;9(8):2415-21 [2164469] J Virol. 1990 Aug;64(8):3895-904 [2164601] Proc Natl Acad Sci U S A. 1984 Apr;81(7):2117-21 [6326105] Proc Natl Acad Sci U S A. 1982 Feb;79(4):973-7 [6280176] Mol Cell Biol. 1991 Jan;11(1):134-42 [1702511] J Biol Chem. 1990 Nov 15;265(32):19704-11 [2174051] Science. 1989 Mar 3;243(4895):1191-4 [2466336] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Lamina propria lymphocytes are derived from circulating cells that lack the Leu-8 lymph node homing receptor. AN - 80599161; 2044931 AB - The Leu-8 membrane glycoprotein is the primate homologue of the murine MEL-14 peripheral lymph node homing receptor and is expressed on a majority of circulating lymphocytes but on few lymphocytes in the intestinal lamina propria. To examine the mechanisms regulating expression of the Leu-8-molecule on lymphocytes in different tissue sites, studies of Leu-8 membrane antigen expression, Leu-8 messenger RNA, and the Leu-8 gene were performed using normal human and nonhuman primate lymphocytes. Activation of resting peripheral blood lymphocytes caused a rapid decrease in membrane Leu-8 expression, a more gradual decrease in Leu-8 messenger RNA, and an increase in expression of interleukin 2 and interleukin 2 receptor messenger RNA. However, the down regulation of Leu-8 expression during activation was reversible because both membrane Leu-8 antigen and Leu-8 messenger RNA were reexpressed after 5 days of culture. Leu-8 messenger RNA was present in lymphocytes isolated from peripheral blood, spleen, and, particularly, mesenteric lymph node, but intestinal lamina propria lymphocytes contained very low levels of Leu-8 messenger RNA. The absence of Leu-8 messenger RNA in intestinal lymphocytes and circulating Leu-8 negative lymphocytes was not caused by recent activation in vivo because these cells did not have detectable interleukin 2 messenger RNA, and intestinal lymphocytes did not express Leu-8 after culture in vitro. Phorbol myristate acetate was found to be a strong inducer of Leu-8 messenger RNA in Leu-8-positive lymphocytes; however, phorbol myristate acetate did not induce membrane Leu-8 expression or Leu-8 messenger RNA in lamina propria lymphocytes. Leu-8-negative lymphocytes in peripheral blood or lamina propria did not have evidence of deletion or rearrangement of the Leu-8 gene. Leu-8-positive Jurkat cells and peripheral blood lymphocytes and Leu-8-negative peripheral blood and intestinal lymphocytes had partial methylation of an Msp I site in proximity to the Leu-8 gene, suggesting that in Leu-8-negative lymphocytes, the Leu-8 gene previously was transcriptionally active. In summary, these studies demonstrate that intestinal lamina propria lymphocytes have the same characteristics as circulating Leu-8-negative lymphocytes with respect to their state of activation and inability to express the Leu-8 antigen. The results suggest that the majority of lymphocytes that migrate to the intestinal lamina propria are derived from the subpopulation of circulating Leu-8-negative lymphocytes. JF - Gastroenterology AU - Berg, M AU - Murakawa, Y AU - Camerini, D AU - James, S P AD - Mucosal Immunity Section, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland. Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 90 EP - 99 VL - 101 IS - 1 SN - 0016-5085, 0016-5085 KW - Antigens, Differentiation, T-Lymphocyte KW - 0 KW - RNA, Messenger KW - Receptors, Lymphocyte Homing KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Lymphocyte Activation KW - Animals KW - RNA, Messenger -- metabolism KW - Down-Regulation KW - Humans KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Gene Expression Regulation KW - Time Factors KW - Cell Line KW - Intestinal Mucosa -- cytology KW - Lymphocytes -- chemistry KW - Lymphocytes -- immunology KW - Antigens, Differentiation, T-Lymphocyte -- analysis KW - Receptors, Lymphocyte Homing -- analysis KW - Lymphocytes -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80599161?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gastroenterology&rft.atitle=Lamina+propria+lymphocytes+are+derived+from+circulating+cells+that+lack+the+Leu-8+lymph+node+homing+receptor.&rft.au=Berg%2C+M%3BMurakawa%2C+Y%3BCamerini%2C+D%3BJames%2C+S+P&rft.aulast=Berg&rft.aufirst=M&rft.date=1991-07-01&rft.volume=101&rft.issue=1&rft.spage=90&rft.isbn=&rft.btitle=&rft.title=Gastroenterology&rft.issn=00165085&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-12 N1 - Date created - 1991-07-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutational analysis of the equine infectious anemia virus Tat-responsive element. AN - 80592804; 1645778 AB - A hairpinlike structure is predicted to exist at the 5' end of equine infectious anemia virus (EIAV) RNA which is similar in many ways to the human immunodeficiency type 1 (HIV-1) Tat-responsive element (TAR). In EIAV, this structure has a shorter stem than in HIV-1 and lacks the uridine bulge. Primer extension analysis of EIAV RNA was used to identify the transcriptional start site in the viral long terminal repeat. Premature termination of primer elongation at the predicted double-stranded RNA region was frequently observed and suggests that the inferred hairpin structure exists under these conditions. We have functionally characterized EIAV TAR by site-directed mutagenesis and transient gene expression analysis. It is demonstrated here that the secondary structure of this element is essential for Tat action. Mutations that disrupted base pairing abolished TAR function, and compensatory mutations that restored the stem structure resulted in Tat activation. The TAR loop appears to be closed by two U.G base pairs that are likely to provide a unique structural motif recognized by the Tat protein. With one exception, substitutions of nucleotides within the EIAV loop sequence decreased TAR function. All nucleotide substitutions of the cytidine at position +14 increased EIAV Tat responsiveness; however, its deletion abolished trans activation. Our results lead us to propose that the EIAV and HIV-1 Tat systems employ closely related cis- and trans-acting components that probably act by the same mechanism. JF - Journal of virology AU - Carvalho, M AU - Derse, D AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick, Maryland 21702-1201. Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 3468 EP - 3474 VL - 65 IS - 7 SN - 0022-538X, 0022-538X KW - Gene Products, tat KW - 0 KW - Oligonucleotides KW - RNA, Viral KW - Index Medicus KW - AIDS/HIV KW - Base Sequence KW - Oligonucleotides -- chemistry KW - DNA Mutational Analysis KW - Molecular Sequence Data KW - RNA, Viral -- ultrastructure KW - RNA, Viral -- genetics KW - Repetitive Sequences, Nucleic Acid KW - Nucleic Acid Conformation KW - Hydrogen Bonding KW - Regulatory Sequences, Nucleic Acid KW - Gene Expression Regulation, Viral KW - Infectious Anemia Virus, Equine -- genetics KW - Gene Products, tat -- genetics KW - Transcriptional Activation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80592804?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+equine+infectious+anemia+virus+Tat-responsive+element.&rft.au=Carvalho%2C+M%3BDerse%2C+D&rft.aulast=Carvalho&rft.aufirst=M&rft.date=1991-07-01&rft.volume=65&rft.issue=7&rft.spage=3468&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 - 1991-07-11 N1 - Date created - 1991-07-11 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nature. 1988 Jul 14;334(6178):165-7 [3386755] EMBO J. 1989 Mar;8(3):765-78 [2721501] Cell. 1986 Sep 26;46(7):973-82 [3530501] Biochemistry. 1990 May 1;29(17):4215-26 [1694459] J Virol. 1990 Aug;64(8):3716-25 [2164593] J Virol. 1990 Apr;64(4):1616-24 [2157047] Cell. 1990 Aug 24;62(4):769-76 [2117500] J Virol. 1990 Apr;64(4):1803-7 [2108259] Science. 1990 Sep 14;249(4974):1281-5 [2205002] Virology. 1990 Sep;178(1):1-5 [2202146] Virology. 1990 May;176(1):178-83 [2184574] J Virol. 1990 Mar;64(3):1402-6 [2406460] Proc Natl Acad Sci U S A. 1990 May;87(9):3624-8 [2333305] Nature. 1983 Dec 8-14;306(5943):557-61 [6358900] Natl Inst Anim Health Q (Tokyo). 1967 Spring;7(1):1-7 [4293211] New Biol. 1989 Oct;1(1):101-10 [2562188] EMBO J. 1990 Dec;9(12):4145-53 [2249668] J Virol. 1991 Jul;65(7):3460-7 [1645777] Trends Genet. 1991 Jan;7(1):9-14 [2003337] Genes Dev. 1990 Aug;4(8):1365-73 [2227414] Cell. 1987 Feb 27;48(4):691-701 [3643816] Genes Dev. 1989 Apr;3(4):547-58 [2470647] Cell. 1985 Jul;41(3):813-23 [2988790] Mol Cell Biol. 1988 Jun;8(6):2555-61 [2841583] J Virol. 1988 Mar;62(3):673-9 [2828663] J Virol. 1988 Sep;62(9):3522-6 [2841502] Proc Natl Acad Sci U S A. 1988 Dec;85(24):9753-7 [2849115] Science. 1985 Jul 5;229(4708):74-7 [2990041] Cell. 1989 Oct 20;59(2):273-82 [2478293] J Virol. 1989 Dec;63(12):5501-4 [2479775] Proc Natl Acad Sci U S A. 1989 Sep;86(18):6925-9 [2476805] Science. 1988 Dec 23;242(4886):1681-4 [2462282] Virology. 1986 Dec;155(2):309-21 [2431539] Virus Genes. 1989 Nov;3(2):99-110 [2559542] Proc Natl Acad Sci U S A. 1989 Jul;86(13):4858-62 [2544877] Proc Natl Acad Sci U S A. 1989 Oct;86(20):7828-32 [2510154] Methods Enzymol. 1987;154:367-82 [3323813] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Identification of lentivirus tat functional domains through generation of equine infectious anemia virus/human immunodeficiency virus type 1 tat gene chimeras. AN - 80592613; 1645777 AB - The structural regions that comprise the functional domains of lentivirus Tat proteins were examined. Chimeric tat genes and chimeric viral promoters were constructed between the distantly related human immunodeficiency virus type 1 (HIV-1) and equine infectious anemia virus (EIAV). These exchange experiments revealed that the EIAV Tat-responsive element recognition domain is formed by two distinct structural regions. Activation domains of both HIV-1 and EIAV Tat contain a conserved core element, but at least HIV-1 Tat requires the presence of additional structural regions. The interchangeable nature of Tat activation domains suggests that these domains act through a common or ubiquitous cellular transcription factor. JF - Journal of virology AU - Carroll, R AU - Martarano, L AU - Derse, D AD - Laboratory of Viral Carcinogenesis, NCI-Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 3460 EP - 3467 VL - 65 IS - 7 SN - 0022-538X, 0022-538X KW - tat KW - Gene Products, tat KW - 0 KW - Recombinant Fusion Proteins KW - tat Gene Products, Human Immunodeficiency Virus KW - Index Medicus KW - AIDS/HIV KW - Gene Expression Regulation, Viral KW - DNA Mutational Analysis KW - HIV Long Terminal Repeat -- genetics KW - Amino Acid Sequence KW - Transcriptional Activation KW - Cloning, Molecular KW - Structure-Activity Relationship KW - Regulatory Sequences, Nucleic Acid KW - Promoter Regions, Genetic KW - Restriction Mapping KW - Molecular Sequence Data KW - HIV-1 -- genetics KW - Infectious Anemia Virus, Equine -- genetics KW - Lentivirus -- genetics KW - Gene Products, tat -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80592613?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Identification+of+lentivirus+tat+functional+domains+through+generation+of+equine+infectious+anemia+virus%2Fhuman+immunodeficiency+virus+type+1+tat+gene+chimeras.&rft.au=Carroll%2C+R%3BMartarano%2C+L%3BDerse%2C+D&rft.aulast=Carroll&rft.aufirst=R&rft.date=1991-07-01&rft.volume=65&rft.issue=7&rft.spage=3460&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 - 1991-07-11 N1 - Date created - 1991-07-11 N1 - Date revised - 2017-01-13 N1 - Gene symbol - tat N1 - SuppNotes - Cited By: Cell. 1989 Oct 20;59(2):273-82 [2478293] J Virol. 1989 Dec;63(12):5501-4 [2479775] Proc Natl Acad Sci U S A. 1989 Sep;86(18):6925-9 [2476805] Virus Genes. 1989 Nov;3(2):99-110 [2559542] Proc Natl Acad Sci U S A. 1989 Oct;86(19):7397-401 [2552444] J Virol. 1989 Nov;63(11):4925-31 [2552171] Nucleic Acids Res. 1989 May 11;17(9):3551-61 [2542902] Proc Natl Acad Sci U S A. 1989 Jul;86(13):4858-62 [2544877] J Virol. 1989 Mar;63(3):1181-7 [2536828] Biotechniques. 1989 Mar;7(3):282-9 [2698649] Cell. 1989 Oct 20;59(2):229-30 [2680105] Science. 1989 Jul 28;245(4916):371-8 [2667136] J Virol. 1991 Jul;65(7):3468-74 [1645778] Genes Dev. 1990 Aug;4(8):1365-73 [2227414] Cell. 1987 Feb 27;48(4):691-701 [3643816] J Virol. 1989 Jan;63(1):1-8 [2535718] Cell. 1989 Oct 20;59(2):283-92 [2553266] Genes Dev. 1989 Apr;3(4):547-58 [2470647] J Virol. 1986 Nov;60(2):385-93 [3021973] Nature. 1987 Dec 3-9;330(6147):489-93 [2825027] Cell. 1985 Jul;41(3):813-23 [2988790] Virology. 1986 Jan 15;148(1):226-31 [3002031] Mol Cell Biol. 1988 Jun;8(6):2555-61 [2841583] Nature. 1988 Apr 7;332(6164):551-3 [2833703] J Virol. 1988 Mar;62(3):673-9 [2828663] J Virol. 1988 Sep;62(9):3522-6 [2841502] J Virol. 1988 Jan;62(1):120-6 [2824840] Genes Dev. 1988 Sep;2(9):1101-14 [2847959] Cell. 1988 Dec 23;55(6):1179-88 [2849509] Cell. 1986 Oct 10;47(1):29-35 [3019564] Proc Natl Acad Sci U S A. 1986 Dec;83(24):9734-8 [3025848] Nature. 1987 Apr 16-22;326(6114):662-9 [3031510] Science. 1985 Jul 5;229(4708):74-7 [2990041] Science. 1985 Jul 5;229(4708):69-73 [2990040] EMBO J. 1988 Jul;7(7):2117-30 [3138113] Nature. 1988 Oct 20;335(6192):683-9 [3050531] Nature. 1989 Oct 12;341(6242):539-41 [2797181] Nature. 1989 Jun 1;339(6223):389-92 [2786147] EMBO J. 1989 Mar;8(3):765-78 [2721501] Proc Natl Acad Sci U S A. 1988 Dec;85(23):9224-8 [3194421] EMBO J. 1988 Oct;7(10):3143-7 [3181132] Nature. 1988 Jul 14;334(6178):165-7 [3386755] Nature. 1988 Jun 2;333(6172):457-61 [3374586] Science. 1984 Dec 7;226(4679):1165-71 [6095449] Methods Enzymol. 1987;154:367-82 [3323813] Cell. 1986 Sep 26;46(7):973-82 [3530501] Science. 1986 Nov 21;234(4779):988-92 [3490693] Proc Natl Acad Sci U S A. 1987 Sep;84(18):6364-8 [3476953] Nature. 1987 Aug 6-12;328(6130):543-7 [3649576] J Virol. 1990 Apr;64(4):1864-8 [2181156] Nature. 1990 May 24;345(6273):356-9 [2188136] Virology. 1990 May;176(1):280-8 [2158694] J Virol. 1990 Apr;64(4):1616-24 [2157047] Cell. 1990 Aug 24;62(4):769-76 [2117500] J Virol. 1990 Apr;64(4):1803-7 [2108259] Science. 1990 Sep 14;249(4974):1281-5 [2205002] Virology. 1990 Sep;178(1):1-5 [2202146] Nature. 1990 Jun 14;345(6276):640-2 [2190099] Virology. 1990 May;176(1):178-83 [2184574] Virology. 1990 Apr;175(2):391-409 [2183467] J Virol. 1990 Mar;64(3):1402-6 [2406460] Proc Natl Acad Sci U S A. 1990 May;87(9):3624-8 [2333305] Virology. 1973 Apr;52(2):456-67 [4705382] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Acute myeloid leukemia induction by amphotropic murine retrovirus (4070A): clonal integrations involve c-myb in some but not all leukemias. AN - 80591629; 1645785 AB - Amphotropic murine retrovirus 4070A was demonstrated to be highly leukemogenic when inoculated intravenously into adult DBA/2 mice that were undergoing an intense chronic inflammatory response, but was nonleukemogenic in the absence of inflammation. The virus-induced promoonocytic leukemias, designated AMPH-ML, are similar morphologically and in cell surface marker expression to monocytic leukemias, called MML and MF-ML, previously shown to be induced by Moloney murine leukemia virus and MF-3 virus (a recombinant between Friend murine leukemia virus and Moloney murine leukemia virus) and resemble certain mature acute monocytic leukemias in humans (AML subtype M5). Approximately two-thirds of the AMPH-MLs (subgroup I) were demonstrated to have alterations in the 5' end of the c-myb locus, an event which occurs in 100% of MML and MF-ML. Data indicate that proviral insertions in AMPH-ML subgroup I resulted in aberrant c-myb mRNA expression and truncation of its translation product at the amino terminus. Approximately one-third of the AMPH-MLs (subgroup II) had not undergone any DNA rearrangements at the c-myb locus. In addition, their transcripts and protein products were of normal size. These latter leukemias also had not undergone DNA rearrangements in c-myc, although retroviruses expressing myc have previously been shown to induce monocyte-macrophage tumors in mice undergoing a chronic inflammation. That subgroup II leukemias had at least one clonal viral insertion suggests that there may be other sites in the cellular genome that can be activated by insertional mutagenesis in these murine acute monocytic leukemias. JF - Journal of virology AU - Wolff, L AU - Koller, R AU - Davidson, W AD - Laboratory of Genetics, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 3607 EP - 3616 VL - 65 IS - 7 SN - 0022-538X, 0022-538X KW - DNA, Neoplasm KW - 0 KW - Proto-Oncogene Proteins KW - Proto-Oncogene Proteins c-myb KW - Proto-Oncogene Proteins c-myc KW - RNA, Messenger KW - Index Medicus KW - Clone Cells KW - Animals KW - Blotting, Northern KW - Gene Expression KW - Gene Rearrangement KW - Proto-Oncogene Proteins c-myc -- genetics KW - Mice KW - RNA, Messenger -- genetics KW - Proto-Oncogenes KW - Precipitin Tests KW - Mice, Inbred DBA KW - Blotting, Southern KW - Restriction Mapping KW - DNA, Neoplasm -- genetics KW - Leukemia, Myeloid, Acute -- genetics KW - Leukemia, Myeloid, Acute -- microbiology KW - Leukemia Virus, Murine -- pathogenicity KW - Proto-Oncogene Proteins -- genetics KW - Cell Transformation, Viral UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80591629?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Acute+myeloid+leukemia+induction+by+amphotropic+murine+retrovirus+%284070A%29%3A+clonal+integrations+involve+c-myb+in+some+but+not+all+leukemias.&rft.au=Wolff%2C+L%3BKoller%2C+R%3BDavidson%2C+W&rft.aulast=Wolff&rft.aufirst=L&rft.date=1991-07-01&rft.volume=65&rft.issue=7&rft.spage=3607&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 - 1991-07-11 N1 - Date created - 1991-07-11 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Oncogene Res. 1989;4(4):259-69 [2549488] J Virol. 1983 Feb;45(2):539-46 [6300418] J Virol. 1989 Apr;63(4):1630-40 [2538646] J Virol. 1987 Oct;61(10):3284-7 [3041047] J Virol. 1988 Apr;62(4):1423-32 [2831403] Mol Cell Biol. 1986 Feb;6(2):380-92 [3023843] Mol Cell Biol. 1986 Nov;6(11):3677-84 [3025608] Mol Cell Biol. 1988 Jun;8(6):2504-12 [3043180] Proc Natl Acad Sci U S A. 1986 Jul;83(14):5010-4 [3014527] J Virol. 1981 Sep;39(3):777-91 [6270351] J Immunol. 1978 Aug;121(2):641-7 [308074] Biochemistry. 1979 Nov 27;18(24):5294-9 [518835] J Virol. 1987 Sep;61(9):2754-63 [2441077] Nucleic Acids Res. 1986 Jul 11;14(13):5309-20 [3016644] J Immunol. 1988 Jul 15;141(2):681-9 [2838552] J Virol. 1987 Dec;61(12):3721-5 [2824810] J Virol. 1986 Aug;59(2):276-83 [3016297] Proc Natl Acad Sci U S A. 1986 May;83(10):3204-8 [3010282] Curr Top Microbiol Immunol. 1986;132:33-9 [3024920] J Virol. 1987 Jun;61(6):1861-6 [3033317] J Exp Med. 1986 Aug 1;164(2):443-57 [3088206] Proc Natl Acad Sci U S A. 1986 Jul;83(13):4685-9 [3088565] J Virol. 1989 Jan;63(1):205-15 [2535727] Curr Top Microbiol Immunol. 1989;149:79-87 [2659284] J Virol. 1989 Jan;63(1):328-37 [2783259] Science. 1984 Nov 30;226(4678):1077-80 [6093260] J Virol. 1984 Dec;52(3):945-52 [6092722] Mol Cell Biol. 1984 Nov;4(11):2486-97 [6513926] Science. 1987 Feb 13;235(4790):787-9 [3810165] Nature. 1986 Feb 13-19;319(6054):604-6 [3753748] J Virol. 1985 Jul;55(1):184-92 [4009793] J Virol. 1985 Jun;54(3):864-8 [3999195] Nature. 1990 Apr 5;344(6266):517-22 [2157164] J Virol. 1990 Jan;64(1):155-60 [2403439] J Virol. 1990 Feb;64(2):757-66 [2153240] Blood. 1990 Aug 15;76(4):655-63 [2200535] Nature. 1984 Mar 29-Apr 4;308(5958):467-70 [6323995] Mol Cell Biol. 1989 Dec;9(12):5456-63 [2685565] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human cytotoxic effector cells: definition and analysis of activity. AN - 72750966; 1726345 AB - Studies have indicated that the complexity of NK and LAK activities goes beyond the question of which effector cell mediates most of this activity. Examination of Nk activity reveals that numerous effector phenotypes can mediate spontaneous, non-MHC-restricted cytotoxicity. These effector cells are predominantly the CD3-, Leu19 (NKH1)+ and the CD3+, Leu19 (NKH1)+ lymphocytes. However, the existence of other effector cells capable of mediating NK activity and the relative contribution of each type of effector cell in vivo situations requires further study. In addition, LAK activity has been attributed to numerous cell types, and an indepth examination of the regulation and recognition events involved in LAK activity indicates a greater degree of heterogeneity than was initially anticipated. The preliminary data presented above support the contention that although NK and LAK activities are quite similar with regard to their lytic properties (e.g. effector phenotype, target selection), their mechanisms of targets cell recognition and lytic attack appear to be quite different. Our investigation of recognition events indicated that IL-2-activated effector cells do not recognize the same structure that is recognized by freshly isolated NK cells. These data suggest that a recognition event occurs on activated cells that can be dissociated from the events involved in NK binding by fresh CD3- LGL. With regard to CD3+ effectors, the role of the TcR and the nature of the receptor mediating LAK activity require further study to determine whether multiple receptors or a single, unique receptor class are expressed after IL-2 stimulation. In addition, the role of IFN gamma and other regulatory cytokines must be further examined to determine their importance in human LAK activity. JF - Allergologia et immunopathologia AU - Ortaldo, J R AD - Laboratory of Experimental Immunology, National Cancer Institute, Frederick Cancer Research Facility, MD 21701-1013. PY - 1991 SP - 145 EP - 156 VL - 19 IS - 4 SN - 0301-0546, 0301-0546 KW - Antibodies, Monoclonal KW - 0 KW - Antigens KW - Antigens, CD KW - Antigens, CD3 KW - Antigens, CD56 KW - Antigens, Differentiation, T-Lymphocyte KW - Cytokines KW - Cytotoxins KW - Receptors, Antigen, T-Cell KW - Receptors, Immunologic KW - Index Medicus KW - Animals KW - Antigens, CD -- analysis KW - Humans KW - Cytokines -- secretion KW - Killer Cells, Lymphokine-Activated -- immunology KW - T-Lymphocytes, Cytotoxic -- immunology KW - Mice KW - Terminology as Topic KW - Receptors, Antigen, T-Cell -- analysis KW - Models, Biological KW - Receptors, Immunologic -- isolation & purification KW - Antibodies, Monoclonal -- immunology KW - Receptors, Immunologic -- immunology KW - Antigens, Differentiation, T-Lymphocyte -- analysis KW - Antigens -- immunology KW - Cytotoxins -- secretion KW - Killer Cells, Natural -- immunology KW - Cytotoxicity, Immunologic KW - T-Lymphocyte Subsets -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72750966?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Allergologia+et+immunopathologia&rft.atitle=Human+cytotoxic+effector+cells%3A+definition+and+analysis+of+activity.&rft.au=Ortaldo%2C+J+R&rft.aulast=Ortaldo&rft.aufirst=J&rft.date=1991-07-01&rft.volume=19&rft.issue=4&rft.spage=145&rft.isbn=&rft.btitle=&rft.title=Allergologia+et+immunopathologia&rft.issn=03010546&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 - A clinical trial of nifedipine in schizophrenia and tardive dyskinesia. AN - 72643920; 1686106 AB - Effects of the dihydropyridine calcium channel inhibitor nifedipine on chronic schizophrenia and tardive dyskinesia were studied in an 8-week double-blind crossover trial. Four of the ten patients had tardive dyskinesia, and three of these were not receiving neuroleptics. No effects on symptoms of chronic schizophrenia were found using Psychiatric Symptom Assessment Scale ratings. In the four patients with tardive dyskinesia, an average improvement in total Abnormal Involuntary Movement Scale scores of 57% was observed. These data suggest that dihydropyridine calcium channel inhibitors may be effective in the treatment of tardive dyskinesia in schizophrenic patients. JF - Pharmacology, biochemistry, and behavior AU - Suddath, R L AU - Straw, G M AU - Freed, W J AU - Bigelow, L B AU - Kirch, D G AU - Wyatt, R J AD - Neuropsychiatry Branch, NIMH Neuroscience Center at St. Elizabeths, Washington, DC 20032. Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 743 EP - 745 VL - 39 IS - 3 SN - 0091-3057, 0091-3057 KW - Antipsychotic Agents KW - 0 KW - Benztropine KW - 1NHL2J4X8K KW - Nifedipine KW - I9ZF7L6G2L KW - Index Medicus KW - Psychiatric Status Rating Scales KW - Double-Blind Method KW - Humans KW - Antipsychotic Agents -- therapeutic use KW - Adult KW - Benztropine -- therapeutic use KW - Male KW - Female KW - Dyskinesia, Drug-Induced -- drug therapy KW - Nifedipine -- therapeutic use KW - Schizophrenia -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72643920?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacology%2C+biochemistry%2C+and+behavior&rft.atitle=A+clinical+trial+of+nifedipine+in+schizophrenia+and+tardive+dyskinesia.&rft.au=Suddath%2C+R+L%3BStraw%2C+G+M%3BFreed%2C+W+J%3BBigelow%2C+L+B%3BKirch%2C+D+G%3BWyatt%2C+R+J&rft.aulast=Suddath&rft.aufirst=R&rft.date=1991-07-01&rft.volume=39&rft.issue=3&rft.spage=743&rft.isbn=&rft.btitle=&rft.title=Pharmacology%2C+biochemistry%2C+and+behavior&rft.issn=00913057&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-19 N1 - Date created - 1992-03-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Influence of endogenous Thy1.1 cells upon the efficacy of an anti-Thy1.1 antibody-diphtheria toxin conjugate. AN - 72623048; 1685330 AB - The chemical conjugation of antibodies to protein toxins results in cell-specific cytotoxic agents that can be defined in terms of in vitro potency and efficacy; however, it is the in vivo utilities that are largely being pursued in clinical trials. The nature of in vivo target cell depletion by toxin conjugates is largely unknown. The anti-murine Thy1.1 antibody-diphtheria toxin conjugate possesses high in vitro efficacy, and because mice are remarkably resistant to the native toxin, the conjugate possesses in vivo efficacy. When administered intravenously, the conjugate is shown to deplete peripheral blood Thy1.1+ target cells in a concentration-dependent fashion. When the log kill of Thy1.1+ tumor cells was analyzed by the life span extension method, it was determined, however, that the log kill is inversely proportional to the number of target cells. That is, the presence of an endogenous cell population, which is expressing the same surface antigen targeted by the antibody conjugate as on the pathological cell, may drastically lower the clinical efficacy of the immunotoxin. Thus, the greatest potential for antibody-toxin conjugates will be for low target cell burdens and for pathogenic cell populations expressing unique surface antigens. These are important considerations in the design of bioconjugates to insure high in vivo efficacy in elimination of intended target cells. JF - Bioconjugate chemistry AU - Yan, B AU - Baker, P D AU - Evans, C H AU - Marsh, J W AD - Laboratory of Molecular Biology, National Institute of Mental Health, Bethesda, Maryland 20892. PY - 1991 SP - 207 EP - 210 VL - 2 IS - 4 SN - 1043-1802, 1043-1802 KW - Antigens, Neoplasm KW - 0 KW - Antigens, Surface KW - Antigens, Thy-1 KW - Diphtheria Toxin KW - Immunotoxins KW - Isoantibodies KW - anti-Thy antibody KW - Index Medicus KW - Animals KW - Dose-Response Relationship, Immunologic KW - Mice KW - T-Lymphocytes -- drug effects KW - Cell Death -- drug effects KW - Antigens, Neoplasm -- immunology KW - T-Lymphocytes -- immunology KW - Mice, Inbred AKR KW - Cell Cycle -- drug effects KW - Tumor Cells, Cultured -- immunology KW - Leukemia, Experimental -- immunology KW - Leukemia, Experimental -- drug therapy KW - Diphtheria Toxin -- pharmacology KW - Immunotoxins -- therapeutic use KW - Leukemia, Experimental -- pathology KW - Antigens, Surface -- immunology KW - Antigens, Surface -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72623048?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bioconjugate+chemistry&rft.atitle=Influence+of+endogenous+Thy1.1+cells+upon+the+efficacy+of+an+anti-Thy1.1+antibody-diphtheria+toxin+conjugate.&rft.au=Yan%2C+B%3BBaker%2C+P+D%3BEvans%2C+C+H%3BMarsh%2C+J+W&rft.aulast=Yan&rft.aufirst=B&rft.date=1991-07-01&rft.volume=2&rft.issue=4&rft.spage=207&rft.isbn=&rft.btitle=&rft.title=Bioconjugate+chemistry&rft.issn=10431802&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-28 N1 - Date created - 1992-02-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Psychological support for the patient on chemotherapy. AN - 72599444; 1837479 AB - The benefits of chemotherapy are frequently accompanied by side effects that can cause significant toxicity. Specific aspects of treatment contribute to the patient's psychological distress and should be identified by care-givers. Practical support interventions are possible and include both prevention and management techniques. Such strategies should be used in an ongoing manner as part of the professional relationship with the patient and may be enhanced by the inclusion of outside resources. JF - Oncology (Williston Park, N.Y.) AU - McCabe, M S AD - Investigational Drug Branch, NCI, Bethesda, Maryland 20892. Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 91 EP - 8, 103; discussion 103-4, 107 VL - 5 IS - 7 SN - 0890-9091, 0890-9091 KW - Antineoplastic Agents KW - 0 KW - Index Medicus KW - Emotions KW - Self Concept KW - Humans KW - Physician-Patient Relations KW - Neoplasms -- drug therapy KW - Neoplasms -- psychology KW - Stress, Psychological -- prevention & control KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72599444?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncology+%28Williston+Park%2C+N.Y.%29&rft.atitle=Psychological+support+for+the+patient+on+chemotherapy.&rft.au=McCabe%2C+M+S&rft.aulast=McCabe&rft.aufirst=M&rft.date=1991-07-01&rft.volume=5&rft.issue=7&rft.spage=91&rft.isbn=&rft.btitle=&rft.title=Oncology+%28Williston+Park%2C+N.Y.%29&rft.issn=08909091&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-24 N1 - Date created - 1992-02-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Soluble HTLV-I Tax1 protein stimulates proliferation of human peripheral blood lymphocytes. AN - 72582939; 1751450 AB - Human T-cell leukemia virus type I (HTLV-I) is associated with two human diseases, adult T-cell leukemia (ATL) and tropical spastic paraparesis/HTLV-I associated myelopathy (TSP/HAM). Lymphocytes from patients with ATL or TSP/HAM display abnormal proliferation properties in culture. Here we report that purified, soluble Tax1 protein can be taken up by, and stimulate proliferation of, uninfected human peripheral blood lymphocytes (PBLs) that have been stimulated with phytohemagglutinin (PHA). Tax1 was 40 to 70% as active as interleukin-2 (IL-2) in stimulating proliferation of PBLs. Heat inactivation, chloroform extraction, and immunoprecipitation with antisera specific for Tax1 each abolished the ability of the protein to stimulate lymphocyte proliferation. Tax1 failed to stimulate PBL proliferation in the absence of PHA. After an initial round of cell division, Tax1-treated PBLs exhibited prolonged sensitivity to IL-2-induced proliferation. These results indicate that Tax1 can stimulate lymphocyte proliferation in culture and imply that extracellular Tax1 may be involved in the spontaneous proliferation of TSP/HAM lymphocytes and the IL-2-dependent proliferation of ATL lymphocytes. JF - The New biologist AU - Marriott, S J AU - Lindholm, P F AU - Reid, R L AU - Brady, J N AD - Laboratory of Molecular Virology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 678 EP - 686 VL - 3 IS - 7 SN - 1043-4674, 1043-4674 KW - Gene Products, tax KW - 0 KW - Interleukin-2 KW - Phytohemagglutinins KW - Chloroform KW - 7V31YC746X KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Index Medicus KW - AIDS/HIV KW - Interleukin-2 -- pharmacology KW - Drug Interactions KW - Chloroform -- pharmacology KW - Blotting, Western KW - Gene Expression Regulation, Viral KW - Chloramphenicol O-Acetyltransferase -- biosynthesis KW - Humans KW - In Vitro Techniques KW - Leukemia, T-Cell KW - Hot Temperature -- adverse effects KW - Cell Division -- drug effects KW - Lymphocytes -- metabolism KW - Time Factors KW - Transcriptional Activation KW - Lymphocyte Activation -- drug effects KW - Gene Products, tax -- pharmacokinetics KW - Gene Products, tax -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72582939?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+biologist&rft.atitle=Soluble+HTLV-I+Tax1+protein+stimulates+proliferation+of+human+peripheral+blood+lymphocytes.&rft.au=Marriott%2C+S+J%3BLindholm%2C+P+F%3BReid%2C+R+L%3BBrady%2C+J+N&rft.aulast=Marriott&rft.aufirst=S&rft.date=1991-07-01&rft.volume=3&rft.issue=7&rft.spage=678&rft.isbn=&rft.btitle=&rft.title=The+New+biologist&rft.issn=10434674&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-28 N1 - Date created - 1992-01-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prolonged disease-free survival in pediatric non-Hodgkin's lymphoma using ifosfamide-containing combination chemotherapy. AN - 72507768; 1743631 AB - Pediatric non-Hodgkin's lymphoma (NHL) constitutes 16 per cent of pediatric malignancies reported to the National Cancer Institute (NCI) in Cairo. The adopted treatment for these cases was, from 1982 to July 1985, a modified St Jude's regimen consisting of: vincristine, cyclophosphamide, adriamycin, prednisone and intrathecal methotrexate for the first 6 weeks for induction, followed by cranial irradiation for cranial prophylaxis. Patients in remission received maintenance therapy for 18 months. Of 32 patients complete remission (CR) was achieved in 24 patients (75 per cent); partial remission (PR) in one patient (3 per cent); five patients showed no response (15 per cent) while two patients died during the induction phase. At 60+ months follow-up, 60 per cent of cases are still alive, disease-free, and overall survival is 66 per cent. A new protocol was adopted in 1985, consisting of alternating cycles: A and B, for 4-8 cycles. Cycle A: cyclophosphamide, high dose ara-C, adriamycin, and vincristine. Cycle B: ifosfamide, methotrexate, VP 16, with intrathecal methotrexate. The response in 39 cases is: CR in 31 cases (82 per cent); PR in four cases (10 per cent); no response in three cases (8 per cent). At 60+ months, the disease-free survival is 60 per cent, and overall survival 80 per cent. This new protocol has the advantage of: short duration of therapy and so better patient compliance, no maintenance therapy or cranial irradiation with its sequelae in the future. Moreover, it has a better overall survival. JF - Hematological oncology AU - Gad-el-Mawla, N AU - Hamza, M R AU - Abdel-Hadi, S AU - el-Tannir, O AU - Hussein, M H AU - el-Haddad, A AU - Adde, M AU - Magrath, I AD - National Cancer Institute, Cairo, Egypt. PY - 1991 SP - 281 EP - 286 VL - 9 IS - 4-5 SN - 0278-0232, 0278-0232 KW - Vincristine KW - 5J49Q6B70F KW - Doxorubicin KW - 80168379AG KW - Cyclophosphamide KW - 8N3DW7272P KW - Prednisolone KW - 9PHQ9Y1OLM KW - 6-Mercaptopurine KW - E7WED276I5 KW - Ifosfamide KW - UM20QQM95Y KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - Dose-Response Relationship, Drug KW - Humans KW - Prognosis KW - Child KW - Child, Preschool KW - Drug Therapy, Combination KW - Survival Rate KW - Adolescent KW - Female KW - Male KW - Lymphoma, Non-Hodgkin -- drug therapy KW - Lymphoma, Non-Hodgkin -- mortality KW - Ifosfamide -- therapeutic use KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72507768?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hematological+oncology&rft.atitle=Prolonged+disease-free+survival+in+pediatric+non-Hodgkin%27s+lymphoma+using+ifosfamide-containing+combination+chemotherapy.&rft.au=Gad-el-Mawla%2C+N%3BHamza%2C+M+R%3BAbdel-Hadi%2C+S%3Bel-Tannir%2C+O%3BHussein%2C+M+H%3Bel-Haddad%2C+A%3BAdde%2C+M%3BMagrath%2C+I&rft.aulast=Gad-el-Mawla&rft.aufirst=N&rft.date=1991-07-01&rft.volume=9&rft.issue=4-5&rft.spage=281&rft.isbn=&rft.btitle=&rft.title=Hematological+oncology&rft.issn=02780232&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-14 N1 - Date created - 1992-01-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pediatric non-Hodgkin's lymphoma abdominal presentations: a comparative study between two treatment regimens at the National Cancer Institute Cairo. AN - 72506975; 1743630 AB - Abdominal presentations of pediatric NHL are rarely amenable to complete surgical resection. Chemotherapy is the hallmark of treatment for pediatric NHL. Treatment of various types of this disease including intra-abdominal NHL in children with various protocols have not exceeded 54 per cent two-year disease-free survival. We have attempted to study and compare the effects of two treatment regimen upon two groups of previously untreated children up to the age of 16 years who presented to the Pediatric Oncology Unit at the NCI. The first group included 18 children who presented between 1983 and 1985 and were treated by a modified St Jude regimen: while the second group of patients was comprised of 19 children who presented between 1985 and 1987 and were treated by a multi-national protocol: the MCP 842. The two groups will be compared with respect to various patient characteristics, response to therapy and their two-year disease-free survival as well as overall survival. JF - Hematological oncology AU - Abdel Hadi, S S AU - el Taneer, O M AU - Hussein, M H AU - el Haddad, A AU - el Badawi, S AU - Mokhtar, N AU - Hamza, M R AU - el Mawla, N G AD - Department of Pediatric Oncology, National Cancer Institute, Cairo University, Egypt. PY - 1991 SP - 275 EP - 279 VL - 9 IS - 4-5 SN - 0278-0232, 0278-0232 KW - Cytarabine KW - 04079A1RDZ KW - Vincristine KW - 5J49Q6B70F KW - Etoposide KW - 6PLQ3CP4P3 KW - Doxorubicin KW - 80168379AG KW - Cyclophosphamide KW - 8N3DW7272P KW - Prednisolone KW - 9PHQ9Y1OLM KW - 6-Mercaptopurine KW - E7WED276I5 KW - Ifosfamide KW - UM20QQM95Y KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - Cyclophosphamide -- administration & dosage KW - Humans KW - Lymphoma, B-Cell -- epidemiology KW - Child KW - Prednisolone -- therapeutic use KW - Lymphoma, B-Cell -- drug therapy KW - Cyclophosphamide -- therapeutic use KW - Vincristine -- therapeutic use KW - 6-Mercaptopurine -- administration & dosage KW - Adolescent KW - Time Factors KW - Male KW - Ifosfamide -- administration & dosage KW - Dose-Response Relationship, Drug KW - 6-Mercaptopurine -- therapeutic use KW - Vincristine -- administration & dosage KW - Prognosis KW - Doxorubicin -- administration & dosage KW - Cytarabine -- administration & dosage KW - Child, Preschool KW - Lymphoma, B-Cell -- mortality KW - Survival Rate KW - Etoposide -- administration & dosage KW - Egypt -- epidemiology KW - Methotrexate -- therapeutic use KW - Doxorubicin -- therapeutic use KW - Prednisolone -- administration & dosage KW - Methotrexate -- administration & dosage KW - Female KW - Lymphoma, Non-Hodgkin -- epidemiology KW - Lymphoma, Non-Hodgkin -- drug therapy KW - Lymphoma, Non-Hodgkin -- mortality KW - Abdominal Neoplasms -- mortality KW - Abdominal Neoplasms -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Antineoplastic Combined Chemotherapy Protocols -- standards KW - Abdominal Neoplasms -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72506975?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hematological+oncology&rft.atitle=Pediatric+non-Hodgkin%27s+lymphoma+abdominal+presentations%3A+a+comparative+study+between+two+treatment+regimens+at+the+National+Cancer+Institute+Cairo.&rft.au=Abdel+Hadi%2C+S+S%3Bel+Taneer%2C+O+M%3BHussein%2C+M+H%3Bel+Haddad%2C+A%3Bel+Badawi%2C+S%3BMokhtar%2C+N%3BHamza%2C+M+R%3Bel+Mawla%2C+N+G&rft.aulast=Abdel+Hadi&rft.aufirst=S&rft.date=1991-07-01&rft.volume=9&rft.issue=4-5&rft.spage=275&rft.isbn=&rft.btitle=&rft.title=Hematological+oncology&rft.issn=02780232&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-14 N1 - Date created - 1992-01-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The dopamine hypothesis of the reinforcing properties of cocaine. AN - 72481471; 1719677 AB - A variety of evidence suggests a 'dopamine hypothesis' for the reinforcing properties of cocaine. This hypothesis proposes that cocaine binds at the dopamine transporter and mainly inhibits neurotransmitter re-uptake; the resulting potentiation of dopaminergic neurotransmission in mesolimbocortical pathways ultimately causes reinforcement. This model suggests potential medications for treatment of cocaine abuse and dependence. Some, but not all, pharmacological data in humans support the hypothesis and additional experimentation is needed. JF - Trends in neurosciences AU - Kuhar, M J AU - Ritz, M C AU - Boja, J W AD - Neuroscience Branch, Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 299 EP - 302 VL - 14 IS - 7 SN - 0166-2236, 0166-2236 KW - Carrier Proteins KW - 0 KW - Dopamine Plasma Membrane Transport Proteins KW - Membrane Glycoproteins KW - Membrane Transport Proteins KW - Nerve Tissue Proteins KW - Neurotransmitter Uptake Inhibitors KW - Amphetamine KW - CK833KGX7E KW - Cocaine KW - I5Y540LHVR KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Substance-Related Disorders -- physiopathology KW - Euphoria -- drug effects KW - Animals KW - Self Administration KW - Carrier Proteins -- metabolism KW - Reward KW - Humans KW - Euphoria -- physiology KW - Protein Binding KW - Models, Biological KW - Amphetamine -- pharmacology KW - Limbic System -- drug effects KW - Limbic System -- physiology KW - Neurotransmitter Uptake Inhibitors -- pharmacology KW - Reinforcement (Psychology) KW - Dopamine -- physiology KW - Cocaine -- pharmacology KW - Cocaine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72481471?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Trends+in+neurosciences&rft.atitle=The+dopamine+hypothesis+of+the+reinforcing+properties+of+cocaine.&rft.au=Kuhar%2C+M+J%3BRitz%2C+M+C%3BBoja%2C+J+W&rft.aulast=Kuhar&rft.aufirst=M&rft.date=1991-07-01&rft.volume=14&rft.issue=7&rft.spage=299&rft.isbn=&rft.btitle=&rft.title=Trends+in+neurosciences&rft.issn=01662236&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-02 N1 - Date created - 1991-12-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cancer among farmers. AN - 72473894; 1835166 JF - Occupational medicine (Philadelphia, Pa.) AU - Blair, A AU - Zahm, S H AD - Occupational Studies Section, National Cancer Institute, Rockville, MD 20892. PY - 1991 SP - 335 EP - 354 VL - 6 IS - 3 SN - 0885-114X, 0885-114X KW - Index Medicus KW - Causality KW - Risk Factors KW - Humans KW - Cohort Studies KW - Adult KW - Aged KW - Middle Aged KW - Data Collection KW - Meta-Analysis as Topic KW - Male KW - Female KW - Cause of Death KW - Agricultural Workers' Diseases -- mortality KW - Neoplasms -- mortality KW - Agricultural Workers' Diseases -- etiology KW - Agricultural Workers' Diseases -- epidemiology KW - Neoplasms -- epidemiology KW - Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72473894?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Occupational+medicine+%28Philadelphia%2C+Pa.%29&rft.atitle=Cancer+among+farmers.&rft.au=Blair%2C+A%3BZahm%2C+S+H&rft.aulast=Blair&rft.aufirst=A&rft.date=1991-07-01&rft.volume=6&rft.issue=3&rft.spage=335&rft.isbn=&rft.btitle=&rft.title=Occupational+medicine+%28Philadelphia%2C+Pa.%29&rft.issn=0885114X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-04 N1 - Date created - 1991-12-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Spontaneous and agonist-induced calcium oscillations in pituitary gonadotrophs. AN - 72459304; 1944300 AB - Basal and receptor-regulated changes in cytoplasmic calcium concentration ([Ca2+]i) were monitored by fluorescence analysis in individual rat pituitary gonadotrophs loaded with the calcium-sensitive dye indo-1. Most gonadotrophs exhibited low amplitude spontaneous oscillations in basal [Ca2+]i that were interspersed by quiescent periods and abolished by removal of extracellular Ca2+ or addition of calcium channel blockers. Such random fluctuations in [Ca2+]i, which reflect the operation of a plasma membrane oscillator, were not coupled to basal gonadotropin secretion. The physiological agonist GnRH induced high amplitude [Ca2+]i oscillations; when a threshold [Ca2+]i level was reached, a cytoplasmic oscillator began to generate extremely regular Ca2+ transients. The time required to reach the threshold [Ca2+]i level was inversely correlated with agonist dose; the frequency, but not the amplitude, of agonist-induced Ca2+ spiking increased with agonist concentration. The duration of the latent period decreased and the frequency of Ca2+ spiking increased with the increase in ambient temperature. At high GnRH concentrations, the calcium transients merged into biphasic responses similar to those observed in cell suspensions at all GnRH concentrations. The presence of spontaneous fluctuations in basal [Ca2+]i did not significantly change the patterns of agonist-induced [Ca2+]i responses. Also, removal of extracellular Ca2+ did not interfere with the frequency or amplitude of Ca2+ spikes, but caused the loss of the plateau phase. Blockade of intracellular Ca(2+)-ATPase pumps by thapsigargin was usually accompanied by a subthreshold increase in [Ca2+]i. In such cells the agonist-induced oscillatory pattern was transformed into the biphasic response. In about 10% of the cells, however, high thapsigargin concentrations induced coarse [Ca2+]i oscillations; subsequent stimulation of such cells with GnRH was ineffective. The cytoplasmic oscillatory and biphasic responses may represent a mechanism for differential activation of Ca(2+)-dependent enzymes and their dependent cellular processes, including hormone secretion. The membrane oscillator is probably responsible for refilling of agonist-sensitive pools during and after agonist stimulation. JF - Molecular endocrinology (Baltimore, Md.) AU - Iida, T AU - Stojilković, S S AU - Izumi, S 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 - 1991/07// PY - 1991 DA - July 1991 SP - 949 EP - 958 VL - 5 IS - 7 SN - 0888-8809, 0888-8809 KW - Carcinogens KW - 0 KW - Gonadotropins, Pituitary KW - Terpenes KW - Gonadotropin-Releasing Hormone KW - 33515-09-2 KW - Potassium Chloride KW - 660YQ98I10 KW - Thapsigargin KW - 67526-95-8 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Endoplasmic Reticulum -- metabolism KW - Animals KW - Carcinogens -- pharmacology KW - Dose-Response Relationship, Drug KW - Potassium Chloride -- pharmacology KW - Temperature KW - Gonadotropin-Releasing Hormone -- administration & dosage KW - Rats KW - Rats, Inbred Strains KW - Terpenes -- pharmacology KW - Cell Membrane -- metabolism KW - Gonadotropin-Releasing Hormone -- pharmacology KW - Female KW - Endoplasmic Reticulum -- drug effects KW - Calcium -- metabolism KW - Pituitary Gland, Anterior -- drug effects KW - Pituitary Gland, Anterior -- metabolism KW - Periodicity KW - Gonadotropins, Pituitary -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72459304?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Spontaneous+and+agonist-induced+calcium+oscillations+in+pituitary+gonadotrophs.&rft.au=Iida%2C+T%3BStojilkovi%C4%87%2C+S+S%3BIzumi%2C+S%3BCatt%2C+K+J&rft.aulast=Iida&rft.aufirst=T&rft.date=1991-07-01&rft.volume=5&rft.issue=7&rft.spage=949&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 - 1991-12-13 N1 - Date created - 1991-12-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Adverse virus-drug interactions. AN - 72154785; 1925290 AB - Over the last 3 decades, epidemiologists and clinicians have identified a few clinical entities that appear to result when a viral infection and a chemical exposure overlap and interact. Ampicillin rash during infectious mononucleosis, Reye's syndrome following salicylate ingestion and certain viral infections, and the association of AIDS-related Kaposi's sarcoma with abuse of nitrite inhalants and infection due to human immunodeficiency virus are examples of such phenomena. Preclinical research provides additional evidence that viruses and chemicals may interact and produce illnesses in animals. We hypothesize that other virus-drug interactions may exist. Identifying such interactions may lead to a better understanding of the pathogenesis of currently baffling illnesses and may provide insights into ways of preventing and/or treating diseases that appear uncontrollable now. JF - Reviews of infectious diseases AU - Haverkos, H W AU - Amsel, Z AU - Drotman, D P AD - Division of Clinical Research, National Institute on Drug Abuse, Alcohol, Drug Abuse, and Mental Health Administration, Rockville, Maryland 20857. PY - 1991 SP - 697 EP - 704 VL - 13 IS - 4 SN - 0162-0886, 0162-0886 KW - Nitrites KW - 0 KW - Ampicillin KW - 7C782967RD KW - Aspirin KW - R16CO5Y76E KW - Index Medicus KW - AIDS/HIV KW - Acquired Immunodeficiency Syndrome -- complications KW - Animals KW - Infectious Mononucleosis -- complications KW - Humans KW - Disease Models, Animal KW - Reye Syndrome -- chemically induced KW - Ampicillin -- adverse effects KW - Exanthema -- chemically induced KW - Nitrites -- administration & dosage KW - Sarcoma, Kaposi -- chemically induced KW - Aspirin -- adverse effects KW - Nitrites -- adverse effects KW - Administration, Inhalation KW - Sarcoma, Kaposi -- etiology KW - Virus Diseases -- complications KW - Drug-Related Side Effects and Adverse Reactions UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72154785?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Reviews+of+infectious+diseases&rft.atitle=Adverse+virus-drug+interactions.&rft.au=Haverkos%2C+H+W%3BAmsel%2C+Z%3BDrotman%2C+D+P&rft.aulast=Haverkos&rft.aufirst=H&rft.date=1991-07-01&rft.volume=13&rft.issue=4&rft.spage=697&rft.isbn=&rft.btitle=&rft.title=Reviews+of+infectious+diseases&rft.issn=01620886&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-18 N1 - Date created - 1991-11-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Rev Infect Dis. 1991 Nov-Dec;13(6):1256-7 [1775871] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - PHS commissioned officers and EPA: a natural coalition for environmental quality and public health. AN - 72149137; 1922845 AB - Commissioned officers of the U.S. Public Health Service play a vital role in enabling EPA to achieve its objectives and responsibilities to protect the environment and the health of the country. Of the 220 officers currently (as of April 1990) detailed to EPA, most are in the engineer category. Table III lists, by category, the PHS officers on detail to EPA. Table IV lists the approximate distribution of officers among various geographical assignments at EPA. JF - Military medicine AU - Holcomb, W F AU - Clark, R L AD - National Institutes of Health, Radiation Safety Branch, Bethesda, MD 20892. Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 346 EP - 350 VL - 156 IS - 7 SN - 0026-4075, 0026-4075 KW - Index Medicus KW - United States KW - Humans KW - Environmental Pollution -- prevention & control KW - United States Public Health Service KW - United States Environmental Protection Agency KW - Environmental Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72149137?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Military+medicine&rft.atitle=PHS+commissioned+officers+and+EPA%3A+a+natural+coalition+for+environmental+quality+and+public+health.&rft.au=Holcomb%2C+W+F%3BClark%2C+R+L&rft.aulast=Holcomb&rft.aufirst=W&rft.date=1991-07-01&rft.volume=156&rft.issue=7&rft.spage=346&rft.isbn=&rft.btitle=&rft.title=Military+medicine&rft.issn=00264075&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-20 N1 - Date created - 1991-11-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - FK506 treatment of S-antigen induced uveitis in primates. AN - 72126014; 1717199 AB - FK506 is a new immunosuppressive agent which has been found more potent than cyclosporine based on the dosage. FK506 was examined here for its effect on the development of uveitis in primates immunized with S-antigen. FK506 successfully inhibited uveitis in monkeys, even when administered three weeks after the first immunization, at the time when the immunopathogenic mechanism of uveitis is assumed to be developed. All four monkeys injected with 0.5 mg/kg/day of FK506 did not develop uveitis, 2 out of 4 treated with the 0.25 mg and 3 out of 4 of those receiving the 0.125 mg also did not develop disease. FK506 suppressed to some extent the cellular and humoral immune responses to S-antigen. The main side effect of FK506 was weight loss. We consider that this drug may be considered as a new potential therapeutic agent for immune-mediated ocular disease in humans. JF - Current eye research AU - Fujino, Y AU - Mochizuki, M AU - Chan, C C AU - Raber, J AU - Kotake, S AU - Gery, I AU - Nussenblatt, R B AD - Laboratory of Immunology, National Eye Institute, Bethesda, MD. Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 679 EP - 690 VL - 10 IS - 7 SN - 0271-3683, 0271-3683 KW - Antigens KW - 0 KW - Arrestin KW - Eye Proteins KW - Phosphodiesterase Inhibitors KW - Tacrolimus KW - WM0HAQ4WNM KW - Index Medicus KW - Animals KW - Macaca fascicularis KW - Injections, Intramuscular KW - Fluorescein Angiography KW - Disease Models, Animal KW - Lymphocyte Activation KW - Fundus Oculi KW - Immunity, Cellular KW - Eye Proteins -- immunology KW - Phosphodiesterase Inhibitors -- immunology KW - Macaca mulatta KW - Antigens -- immunology KW - Male KW - Female KW - Uveitis -- prevention & control KW - Tacrolimus -- blood KW - Tacrolimus -- adverse effects KW - Uveitis -- pathology KW - Tacrolimus -- therapeutic use KW - Uveitis -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72126014?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:book&rft.genre=book&rft.jtitle=&rft.atitle=&rft.au=Barnard%2C+C.I.&rft.aulast=Barnard&rft.aufirst=C.I.&rft.date=1938-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=The+functions+of+the+executive&rft.title=The+functions+of+the+executive&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-07 N1 - Date created - 1991-11-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Hematologic toxicity of AZT and ddC administered as single agents and in combination to rats and mice. AN - 72124504; 1655546 AB - Toxicity studies of 3'-azido-2',3'-dideoxythymidine (AZT) and 2',3'-dideoxycytidine (ddC) were conducted in F344/N rats and B6C3F1 mice. The drugs were administered as single agents and in combination. In all studies, animals were treated by oral gavage twice a day, 7 days a week. In studies of the individual compounds, each was administered for 13 weeks at the following concentrations: AZT in rats, 0, 125, 250, 500, 1000 mg/kg and in mice, 0, 25, 50, 100, 400, 1000 mg/kg; ddC in rats and mice, 0, 250, 1000, 2000 mg/kg. Additional male rats and female mice that were treated with 0, 250, 1000, or 2000 mg/kg ddC and male and female mice treated with 0, 50, 400, 1000 mg/kg AZT were maintained for 30 days after treatment was stopped (at 94 days) to evaluate the reversibility of toxic effects. Hematologic variables were measured on Days 5, 23, and 94 (last day of dosing), and on Day 123 (after a 30-day period without treatment). AZT and ddC produced dose-related, poorly regenerative, macrocytic anemias as evidenced by decreases in erythrocyte counts, hematocrits, and hemoglobin concentrations and increases in mean corpuscular hemoglobin and mean corpuscular volume. Bone marrow samples in rats treated with AZT were hyperplastic whereas those in mice treated with AZT and rats and mice treated with ddC were hypoplastic. The hematologic toxicity of AZT was more severe than that of ddC. Generally, toxic effects of either chemical were greater in mice than in rats and more pronounced in female than in male animals. After 30 days without dosing, hematologic effects either resolved or dramatically improved. In studies in which ddC and AZT were administered in combination for 4 weeks at concentrations of 0/0, 0/500, 500/0, 10/500, 100/500, 500/500, and 500/1000 mg/kg ddC/AZT, there was macrocytic anemia in animals in the lower doses and marked microcytic anemia in surviving male mice in higher dose groups. Most female mice died in the 500/500 and 500/1000 mg/kg ddC/AZT dose groups. At lower concentrations (100/500, 500/1000 mg/kg ddC/AZT), effects of the two drugs were similar to those in the single drug studies. At higher concentrations (500/500 and 500/1000 mg/kg ddC/AZT), the combination treatment produced enhanced hematopoietic toxicity. These studies demonstrated the early and progressive time course of toxicity of AZT and ddC, species differences in sensitivities and responses, and reversibility of effects after termination of treatment. Based on these findings, a chronic toxicity study is being conducted with AZT in mice. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Thompson, M B AU - Dunnick, J K AU - Sutphin, M E AU - Giles, H D AU - Irwin, R D AU - Prejean, J D AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 159 EP - 176 VL - 17 IS - 1 SN - 0272-0590, 0272-0590 KW - Hemoglobins KW - 0 KW - Zidovudine KW - 4B9XT59T7S KW - Zalcitabine KW - 6L3XT8CB3I KW - Index Medicus KW - AIDS/HIV KW - Rats KW - Eating -- drug effects KW - Bone Marrow Cells KW - Mice, Inbred Strains KW - Animals KW - Rats, Inbred F344 KW - Hemoglobins -- metabolism KW - Body Weight -- drug effects KW - Thrombocytopenia -- chemically induced KW - Mice KW - Thrombocytopenia -- blood KW - Bone Marrow -- drug effects KW - Male KW - Female KW - Blood Cell Count KW - Hematologic Diseases -- chemically induced KW - Zidovudine -- toxicity KW - Hematologic Diseases -- physiopathology KW - Zalcitabine -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72124504?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Hematologic+toxicity+of+AZT+and+ddC+administered+as+single+agents+and+in+combination+to+rats+and+mice.&rft.au=Thompson%2C+M+B%3BDunnick%2C+J+K%3BSutphin%2C+M+E%3BGiles%2C+H+D%3BIrwin%2C+R+D%3BPrejean%2C+J+D&rft.aulast=Thompson&rft.aufirst=M&rft.date=1991-07-01&rft.volume=17&rft.issue=1&rft.spage=159&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 - 1991-11-13 N1 - Date created - 1991-11-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The mouse biliary glycoprotein gene (Bgp): partial nucleotide sequence, expression, and chromosomal assignment. AN - 72089625; 1653760 AB - Transcripts related to the human carcinoembryonic antigen were found in mRNA isolated from both dimethylbenzanthracene-induced and mouse mammary tumor virus-induced mammary tumors. A cDNA library was prepared from a dimethylbenzanthracene-induced tumor, and a clone was isolated by hybridization with a human carcinoembryonic antigen cDNA probe. Its sequence, when compared to those of members of the human carcinoembryonic antigen gene family, was most homologous to the sequence of the human biliary glycoprotein (BGP) gene. Thus, this clone appears to encode a portion of the mouse biliary glycoprotein gene. Southern blot analysis of EcoRI-digested mouse cellular DNA with this probe detected four restriction fragments, all of which appear to be located on mouse chromosome 7, Northern blot analysis using the mouse probe demonstrated that related mRNA species were expressed in some normal adult mouse tissues. JF - Genomics AU - Robbins, J AU - Robbins, P F AU - Kozak, C A AU - Callahan, R AD - Laboratory of Tumor Immunology and Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 583 EP - 587 VL - 10 IS - 3 SN - 0888-7543, 0888-7543 KW - BGP KW - Bgp KW - Antigens, CD KW - 0 KW - CD66 antigens KW - Carcinoembryonic Antigen KW - Cell Adhesion Molecules KW - Genetic Markers KW - Glycoproteins KW - Neoplasm Proteins KW - RNA, Messenger KW - RNA, Neoplasm KW - 9,10-Dimethyl-1,2-benzanthracene KW - 57-97-6 KW - Index Medicus KW - Animals KW - Cricetulus KW - Sequence Homology, Nucleic Acid KW - Humans KW - Mammary Tumor Virus, Mouse KW - Organ Specificity KW - Amino Acid Sequence KW - Chromosome Mapping KW - Gene Expression Regulation, Neoplastic KW - Base Sequence KW - Genes KW - Genes, Neoplasm KW - Molecular Sequence Data KW - Hybrid Cells KW - Carcinoembryonic Antigen -- genetics KW - Cricetinae KW - Mammary Neoplasms, Experimental -- chemically induced KW - Mammary Neoplasms, Experimental -- microbiology KW - Multigene Family KW - Neoplasm Proteins -- genetics KW - Mice -- genetics KW - Mammary Neoplasms, Experimental -- genetics KW - RNA, Neoplasm -- genetics KW - RNA, Messenger -- genetics KW - Glycoproteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72089625?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Genomics&rft.atitle=The+mouse+biliary+glycoprotein+gene+%28Bgp%29%3A+partial+nucleotide+sequence%2C+expression%2C+and+chromosomal+assignment.&rft.au=Robbins%2C+J%3BRobbins%2C+P+F%3BKozak%2C+C+A%3BCallahan%2C+R&rft.aulast=Robbins&rft.aufirst=J&rft.date=1991-07-01&rft.volume=10&rft.issue=3&rft.spage=583&rft.isbn=&rft.btitle=&rft.title=Genomics&rft.issn=08887543&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-10-17 N1 - Date created - 1991-10-17 N1 - Date revised - 2017-01-13 N1 - Gene symbol - BGP; Bgp N1 - Genetic sequence - M61177; GENBANK; M61178; S54795; M61179; S54791; S54809; S54803; M61907; M61181; M61180 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The feasibility of collecting drug abuse data by telephone. AN - 72054666; 1908589 AB - An evaluation was made of the use of telephone survey methods to collect illicit drug use data. Using data from a national survey that collects data by personal interviews, marijuana and cocaine use prevalence rates among households with telephones and those without were compared in order to assess coverage errors in telephone surveys. Drug use rates were substantially higher among households without telephones, with 24.9 percent of those living in households without telephones reporting use of marijuana in the past year, compared with only 9.4 percent of persons living in households with telephones. Trends in drug use were divergent, with substantial decreases in use occurring between 1985 and 1988 in households with telephones, but not in those without. National prevalence patterns and trends among households with telephone appear to be consistent with national patterns and trends in the total household population, because about 93 percent of the population lives in households with telephones. However, surveys conducted by telephone were found to produce underestimates of illicit drug use prevalence. In a 1988 national telephone survey, estimated rates of past year use were 5.2 percent for marijuana and 1.4 percent for cocaine. Comparable data from a personal visit survey (including only households with telephones and reedited and reweighted to control for differences in data collection protocols) were 8.0 percent for marijuana and 3.1 percent for cocaine use. Comparisons with several other telephone surveys collecting illicit drug use data showed similar results. Based on these results, researchers are advised to use caution in using telephone surveys to produce drug use prevalence estimates. JF - Public health reports (Washington, D.C. : 1974) AU - Gfroerer, J C AU - Hughes, A L AD - National Institute on Drug Abuse, Division of Epidemiology and Prevention Research, Survey and Analysis Branch, Rockville, MD 20857. PY - 1991 SP - 384 EP - 393 VL - 106 IS - 4 SN - 0033-3549, 0033-3549 KW - Cocaine KW - I5Y540LHVR KW - Abridged Index Medicus KW - Index Medicus KW - Mass Screening KW - Feasibility Studies KW - Reproducibility of Results KW - Risk Factors KW - Humans KW - Adult KW - Adolescent KW - Male KW - Female KW - Prevalence KW - Data Collection -- standards KW - Data Collection -- methods KW - Telephone -- statistics & numerical data KW - Marijuana Abuse -- epidemiology KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72054666?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Public+health+reports+%28Washington%2C+D.C.+%3A+1974%29&rft.atitle=The+feasibility+of+collecting+drug+abuse+data+by+telephone.&rft.au=Gfroerer%2C+J+C%3BHughes%2C+A+L&rft.aulast=Gfroerer&rft.aufirst=J&rft.date=1991-07-01&rft.volume=106&rft.issue=4&rft.spage=384&rft.isbn=&rft.btitle=&rft.title=Public+health+reports+%28Washington%2C+D.C.+%3A+1974%29&rft.issn=00333549&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-20 N1 - Date created - 1991-09-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Followup study of possible HIV seropositivity among abusers of parenteral drugs in 1971-72. AN - 72051691; 1908596 AB - Serum specimens obtained from a nationwide sample of parenteral drug abusers (PDAs) during the period 1971-72 had previously been screened for human immunodeficiency virus (HIV) antibodies. Some specimens were considered to be positive to both ELISA and Western blot (WB) analysis. These findings have been a topic of controversy, since HIV was not thought to have penetrated at-risk populations at such an early date. This study was a followup of those PDAs with apparent seropositivity to WB analysis. Of 10 persons followed, only one death (in 1985) was documented, and postmortem findings were inconsistent with HIV infection. Eight of the remaining PDAs were traced and found to be alive and well in 1989. Fresh specimens were obtained from the two persons with the strongest 1971-72 WB staining and were found to be both ELISA and WB negative on retesting. Their T-cell parameters were within normal limits. We concluded that the earlier WB results were most likely false positives and that definitive evidence of HIV infection in the U.S. addict population as early as 1971-72 is still lacking. JF - Public health reports (Washington, D.C. : 1974) AU - Lange, W R AU - Ball, J C AU - Adler, W H AU - Brown, E AU - Pyle, R AU - Hoffman, W AU - Dax, E M AD - Public Health Service, National Institute on Drug Abuse's Addiction Research Center, Baltimore, MD 21224. PY - 1991 SP - 451 EP - 455 VL - 106 IS - 4 SN - 0033-3549, 0033-3549 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Mortality KW - Blotting, Western KW - Humans KW - Enzyme-Linked Immunosorbent Assay KW - Follow-Up Studies KW - T-Lymphocyte Subsets -- chemistry KW - Male KW - Female KW - Cross Reactions KW - Population Surveillance KW - Kentucky -- epidemiology KW - False Positive Reactions KW - Substance Abuse, Intravenous -- complications KW - HIV Seropositivity -- immunology KW - HIV Seropositivity -- epidemiology KW - HIV Seropositivity -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72051691?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Public+health+reports+%28Washington%2C+D.C.+%3A+1974%29&rft.atitle=Followup+study+of+possible+HIV+seropositivity+among+abusers+of+parenteral+drugs+in+1971-72.&rft.au=Lange%2C+W+R%3BBall%2C+J+C%3BAdler%2C+W+H%3BBrown%2C+E%3BPyle%2C+R%3BHoffman%2C+W%3BDax%2C+E+M&rft.aulast=Lange&rft.aufirst=W&rft.date=1991-07-01&rft.volume=106&rft.issue=4&rft.spage=451&rft.isbn=&rft.btitle=&rft.title=Public+health+reports+%28Washington%2C+D.C.+%3A+1974%29&rft.issn=00333549&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-20 N1 - Date created - 1991-09-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Transfusion. 1988 Sep-Oct;28(5):412-8 [3420668] JAMA. 1984 Sep 7;252(9):1152-9 [6471338] Int J Addict. 1989 Jul;24(7):609-26 [2599682] Rev Infect Dis. 1987 Nov-Dec;9(6):1102-8 [3321360] Ann Intern Med. 1985 Nov;103(5):755-9 [4051350] N Engl J Med. 1986 May 22;314(21):1387-8 [3010112] J Infect Dis. 1986 Apr;153(4):736-42 [3005434] Anal Biochem. 1988 May 15;171(1):1-32 [3044183] Ann Intern Med. 1988 Jun;108(6):785-90 [3285743] Mayo Clin Proc. 1989 Oct;64(10):1226-34 [2593713] South Med J. 1989 Sep;82(9):1075-8 [2772675] Ann Intern Med. 1987 May;106(5):671-6 [3551711] Am J Med. 1984 Mar;76(3):493-500 [6322585] J Infect Dis. 1983 Aug;148(2):339-45 [6604115] Clin Exp Immunol. 1983 Aug;53(2):465-72 [6224612] Immunol Commun. 1983;12(2):223-237 [6603416] JAMA. 1988 Oct 14;260(14):2085-7 [3418874] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Marriage and Family among China's Minority Nationalities as Viewed from Beijing AN - 61276698; 92Z1206 AB - The social development of minority nationalities in the People's Republic of China & their diverse forms of marriage & family are examined, paying particular attention to the government's desire to reshape the traditional outlook on marriage, ie, as an institution intended to facilitate procreation, especially the production of male heirs. National census data, 1953-1982, reveal the highest birth & lowest death rates in the world among these minorities, resulting in a growth rate that has generally surpassed the level that their economic development can support. Despite the recognition that economic development must be accelerated, minorities (particularly in the outlying regions) have maintained the traditional attitude toward reproduction. Women account for 70% of the illiterates & semi-illiterates of the minority nationalities. Ancient matrimonial customs (eg, arranged & mercenary marriages, sexual freedom before & after marriage, & polygamy) continue to be perpetuated, despite their adverse impact on people's mental health & aspirations. A number of reforms of these traditions occurring in various regions are discussed, & it is suggested that developing countries accelerate their process of modernization, & that ethnology be employed in the process. 3 Tables, 6 References. S. Millett JF - The Mankind Quarterly AU - Ruxian, Yan AD - Instit Nationality Studies Chinese Academy Social Sciences, 5 Jianguomen Nei Da Jie 5 Hao Beijing People's Republic China Y1 - 1991/07// PY - 1991 DA - July 1991 SP - 345 EP - 355 VL - 31 IS - 4 SN - 0025-2344, 0025-2344 KW - marriage/family patterns, minority nationalities, People's Republic of China KW - 1953-1982 census data KW - Peoples Republic of China KW - Family Structure KW - National Identity KW - Nationalism KW - Marriage Patterns KW - article KW - 1941: the family and socialization; sociology of the family UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/61276698?accountid=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=The+Mankind+Quarterly&rft.atitle=Marriage+and+Family+among+China%27s+Minority+Nationalities+as+Viewed+from+Beijing&rft.au=Ruxian%2C+Yan&rft.aulast=Ruxian&rft.aufirst=Yan&rft.date=1991-07-01&rft.volume=31&rft.issue=4&rft.spage=345&rft.isbn=&rft.btitle=&rft.title=The+Mankind+Quarterly&rft.issn=00252344&rft_id=info:doi/ LA - English DB - Sociological Abstracts N1 - Date revised - 2007-04-01 N1 - Last updated - 2016-09-28 N1 - CODEN - MKQUA4 N1 - SubjectsTermNotLitGenreText - Peoples Republic of China; Marriage Patterns; Family Structure; Nationalism; National Identity ER - TY - JOUR T1 - Cooperative effect of 8-Cl-cAMP and rhGM-CSF on the differentiation of HL-60 human leukemia cells. AN - 80645553; 2059204 AB - In HL-60 leukemia cells the site-selective cAMP analog, 8-Cl-cAMP, at a dose of 5 microM produced growth inhibition with no signs of toxicity, whereas granulocyte-macrophage colony stimulating factor (GM-CSF) exerted an early transient increase of cell proliferation which was followed by differentiation toward monocytes. 8-Cl-cAMP in combination with GM-CSF blocked the growth stimulation due to GM-CSF and demonstrated a synergistic effect on the differentiation of HL-60 cells. The early proliferative effect of GM-CSF was correlated with an increased expression of type I regulatory subunit of cAMP-dependent protein kinase (RI alpha). Treatment with an RI alpha antisense oligodeoxynucleotide suppressed the GM-CSF-inducible cell proliferation and differentiation. Conversely, an RII beta antisense oligodeoxynucleotide, which suppresses the RII beta and causes a compensatory increase in RI alpha level, greatly enhanced the early proliferative input and the differentiation induced by GM-CSF. These results provide an insight into the mechanism of action of GM-CSF and the rationale for a combination differentiation therapy with 8-Cl-cAMP and GM-CSF. JF - Biochemical and biophysical research communications AU - Tortora, G AU - Pepe, S AU - Yokozaki, H AU - Meissner, S AU - Cho-Chung, Y S AD - Laboratory of Tumor Immunology and Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/06/28/ PY - 1991 DA - 1991 Jun 28 SP - 1133 EP - 1140 VL - 177 IS - 3 SN - 0006-291X, 0006-291X KW - Antineoplastic Agents KW - 0 KW - Oligonucleotides, Antisense KW - Recombinant Proteins KW - 8-Bromo Cyclic Adenosine Monophosphate KW - 23583-48-4 KW - 8-chloro-cyclic adenosine monophosphate KW - 41941-56-4 KW - Granulocyte-Macrophage Colony-Stimulating Factor KW - 83869-56-1 KW - Protein Kinases KW - EC 2.7.- KW - Index Medicus KW - Base Sequence KW - Recombinant Proteins -- pharmacology KW - Monocytes -- cytology KW - Kinetics KW - Humans KW - Protein Kinases -- genetics KW - Molecular Sequence Data KW - Leukemia, Promyelocytic, Acute KW - Cell Division -- drug effects KW - Oligonucleotides, Antisense -- pharmacology KW - Drug Synergism KW - Cell Line KW - 8-Bromo Cyclic Adenosine Monophosphate -- analogs & derivatives KW - Granulocyte-Macrophage Colony-Stimulating Factor -- pharmacology KW - Cell Differentiation -- drug effects KW - Antineoplastic Agents -- pharmacology KW - 8-Bromo Cyclic Adenosine Monophosphate -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80645553?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cooperative+effect+of+8-Cl-cAMP+and+rhGM-CSF+on+the+differentiation+of+HL-60+human+leukemia+cells.&rft.au=Tortora%2C+G%3BPepe%2C+S%3BYokozaki%2C+H%3BMeissner%2C+S%3BCho-Chung%2C+Y+S&rft.aulast=Tortora&rft.aufirst=G&rft.date=1991-06-28&rft.volume=177&rft.issue=3&rft.spage=1133&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 - 1991-07-31 N1 - Date created - 1991-07-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Neuronal localization of cannabinoid receptors and second messengers in mutant mouse cerebellum. AN - 72121632; 1913192 AB - Four lines of mutant mice were used to investigate (1) the neuronal localization of cannabinoid receptors in the cerebellar molecular layer and (2) the anatomical association of these receptors with elements of the two second messenger systems in the brain. Two of the mutant lines--Purkinje cell degeneration and nervous--are selectively deficient in Purkinje cells; the other two--weaver and reeler--are deficient in granule cells. In the heterozygous mice, [3H]CP 55,940 binding to cannabinoid receptors was discretely and densely localized to the molecular layer, as was [3H]forskolin binding to adenylate cyclase and [3H]phorbol 12,13-dibutyrate binding to protein kinase C, a component of the phosphoinositide cycle. [3H]CP 55,940 and [3H]forskolin binding was selectively reduced in weaver and reeler homozygous mice but unchanged in Purkinje cell deficient and nervous homozygotes. No decreases in [3H]phorbol 12,13-dibutyrate binding were found in any of the homozygous mutants relative to the heterozygous littermates. The results suggest that cannabinoid receptors and adenylate cyclase are localized to granule cell axons in the molecular layer, whereas protein kinase C is equally distributed in parallel fibers and Purkinje cell dendrites. JF - Brain research AU - Herkenham, M AU - Groen, B G AU - Lynn, A B AU - De Costa, B R AU - Richfield, E K AD - Section on Functional Neuroanatomy, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1991/06/28/ PY - 1991 DA - 1991 Jun 28 SP - 301 EP - 310 VL - 552 IS - 2 SN - 0006-8993, 0006-8993 KW - Cannabinoids KW - 0 KW - Cyclohexanols KW - Receptors, Cannabinoid KW - Receptors, Drug KW - Tritium KW - 10028-17-8 KW - Colforsin KW - 1F7A44V6OU KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - 3-(2-hydroxy-4-(1,1-dimethylheptyl)phenyl)-4-(3-hydroxypropyl)cyclohexanol KW - 83003-12-7 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Adenylyl Cyclases KW - EC 4.6.1.1 KW - Index Medicus KW - Animals KW - Homozygote KW - Phorbol 12,13-Dibutyrate -- metabolism KW - Adenylyl Cyclases -- metabolism KW - Mice KW - Autoradiography KW - Protein Kinase C -- metabolism KW - Protein Kinase C -- analysis KW - Adenylyl Cyclases -- analysis KW - Heterozygote KW - Mice, Neurologic Mutants KW - Colforsin -- metabolism KW - Second Messenger Systems KW - Receptors, Drug -- metabolism KW - Cerebellum -- cytology KW - Cyclohexanols -- metabolism KW - Cannabinoids -- metabolism KW - Neurons -- cytology KW - Neurons -- physiology KW - Cyclohexanols -- analysis KW - Receptors, Drug -- analysis KW - Cerebellum -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72121632?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Neuronal+localization+of+cannabinoid+receptors+and+second+messengers+in+mutant+mouse+cerebellum.&rft.au=Herkenham%2C+M%3BGroen%2C+B+G%3BLynn%2C+A+B%3BDe+Costa%2C+B+R%3BRichfield%2C+E+K&rft.aulast=Herkenham&rft.aufirst=M&rft.date=1991-06-28&rft.volume=552&rft.issue=2&rft.spage=301&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 - 1991-10-31 N1 - Date created - 1991-10-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alterations in opiate receptor binding in MPTP-induced hemiparkinsonian monkeys. AN - 72061420; 1652716 AB - Quantitative autoradiography was used to study [3H]naloxone binding in the striatum of normal monkeys and monkeys made hemiparkinsonian by the unilateral infusion of the neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The density of [3H]naloxone binding sites was significantly higher in the caudate and putamen on the MPTP-treated side of hemiparkinsonian monkeys, as compared with binding on the untreated side and in the striatum of normal monkeys. A more extensive patchy distribution of binding sites was evident throughout the striatum on the MPTP-treated side than seen in the striatum of the untreated side or in normal striatum. JF - Neuroscience letters AU - Porrino, L J AU - Viola, J J AU - Crane, A M AU - Pontieri, F E AD - Laboratory of Cerebral Metabolism, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1991/06/24/ PY - 1991 DA - 1991 Jun 24 SP - 155 EP - 159 VL - 127 IS - 2 SN - 0304-3940, 0304-3940 KW - Receptors, Opioid KW - 0 KW - Naloxone KW - 36B82AMQ7N KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Index Medicus KW - Animals KW - Receptors, Opioid -- metabolism KW - Macaca mulatta KW - Male KW - Functional Laterality KW - Female KW - Parkinson Disease, Secondary -- metabolism KW - Naloxone -- metabolism KW - Corpus Striatum -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72061420?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Alterations+in+opiate+receptor+binding+in+MPTP-induced+hemiparkinsonian+monkeys.&rft.au=Porrino%2C+L+J%3BViola%2C+J+J%3BCrane%2C+A+M%3BPontieri%2C+F+E&rft.aulast=Porrino&rft.aufirst=L&rft.date=1991-06-24&rft.volume=127&rft.issue=2&rft.spage=155&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 - 1991-10-02 N1 - Date created - 1991-10-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A fluorescence study of the interactions of benzo[a]pyrene, cytochrome P450c and NADPH-cytochrome P450 reductase. AN - 80672133; 1906275 AB - Fluorescence quenching of benzo[a]pyrene (BP) by cytochrome P450c was used to probe this substrate-enzyme binding interaction. Addition of NADPH-cytochrome P450 reductase, an essential electron carrier during P450 catalysis, resulted in increased quenching and thus strengthened binding of BP to P450c. This shows that the role of reductase extends beyond that of an electron transfer agent to influence substrate binding. Fluorescence titration measurements revealed that reductase and P450c formed a complex with an apparent KD of 13.7 +/- 0.9 nM. Reductase had no effect in the presence of an anti-P450c monoclonal antibody which inhibits BP hydroxylation, which suggests that this monoclonal antibody binds P450c near its reductase binding region. JF - Biochemical pharmacology AU - Omata, Y AU - Friedman, F K AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/06/21/ PY - 1991 DA - 1991 Jun 21 SP - 97 EP - 101 VL - 42 IS - 1 SN - 0006-2952, 0006-2952 KW - Antibodies, Monoclonal KW - 0 KW - Benzo(a)pyrene KW - 3417WMA06D KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - NADPH-Ferrihemoprotein Reductase KW - EC 1.6.2.4 KW - Index Medicus KW - Rats KW - Animals KW - Drug Interactions KW - Spectrometry, Fluorescence KW - Antibodies, Monoclonal -- pharmacology KW - Male KW - Binding Sites KW - Mitochondria, Liver -- enzymology KW - NADPH-Ferrihemoprotein Reductase -- pharmacology KW - Cytochrome P-450 Enzyme System -- immunology KW - NADPH-Ferrihemoprotein Reductase -- metabolism KW - Cytochrome P-450 Enzyme System -- metabolism KW - Benzo(a)pyrene -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80672133?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+fluorescence+study+of+the+interactions+of+benzo%5Ba%5Dpyrene%2C+cytochrome+P450c+and+NADPH-cytochrome+P450+reductase.&rft.au=Omata%2C+Y%3BFriedman%2C+F+K&rft.aulast=Omata&rft.aufirst=Y&rft.date=1991-06-21&rft.volume=42&rft.issue=1&rft.spage=97&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 - 1991-08-09 N1 - Date created - 1991-08-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Monoclonal antibodies in diagnosis and therapy. AN - 80609891; 2047874 AB - Monoclonal antibodies have been applied clinically to the diagnosis and therapy of an array of human disorders, including cancer and infectious diseases, and have been used for the modulation of immune responses. Effective therapy using unmodified monoclonal antibodies has, however, been elusive. Recently, monoclonal antibody-mediated therapy has been revolutionized by advances such as the definition of cell-surface structures on abnormal cells as targets for effective monoclonal antibody action, genetic engineering to create less immunogenic and more effective monoclonal antibodies, and the arming of such antibodies with toxins or radionuclides to enhance their effector function. JF - Science (New York, N.Y.) AU - Waldmann, T A AD - Metabolism Branch, National Cancer Institute, National Institute of Health, Bethesda, MD 20892. Y1 - 1991/06/21/ PY - 1991 DA - 1991 Jun 21 SP - 1657 EP - 1662 VL - 252 IS - 5013 SN - 0036-8075, 0036-8075 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Surface KW - Immunotoxins KW - Radioisotopes KW - Index Medicus KW - Antibody Specificity KW - Genetic Engineering KW - Humans KW - Radioisotopes -- therapeutic use KW - Antigens, Surface -- immunology KW - Antibodies, Monoclonal -- genetics KW - Antibodies, Monoclonal -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80609891?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Monoclonal+antibodies+in+diagnosis+and+therapy.&rft.au=Waldmann%2C+T+A&rft.aulast=Waldmann&rft.aufirst=T&rft.date=1991-06-21&rft.volume=252&rft.issue=5013&rft.spage=1657&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 - 1991-07-16 N1 - Date created - 1991-07-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Levodopa replacement therapy alters enzyme activities in striatum and neuropeptide content in striatal output regions of 6-hydroxydopamine lesioned rats. AN - 72122592; 1717109 AB - The effects of striatal dopamine denervation and levodopa replacement therapy on neuronal populations in the rat striatum were assessed by measurement of glutamic acid decarboxylase (GAD) and choline acetyltransferase (CAT) activities in the striatum, dynorphin and substance P concentrations in the substantia nigra, and enkephalin concentration in the globus pallidus. Rats with a unilateral 6-hydroxydopamine (6-OHDA) lesion of the nigrostriatal pathway were treated for 21 days with levodopa (100 mg/kg/day, i.p., with 25 mg/kg benserazide) on either an intermittent (b.i.d.) or continuous (osmotic pump infusion) regimen and sacrificed following a three day drug washout. In saline-treated control rats, striatal GAD activity and globus pallidus enkephalin content were elevated and nigral substance P content was reduced ipsilateral to the 6-OHDA lesion. Intermittent levodopa treatment further increased GAD activity, decreased CAT activity, restored substance P to control levels, markedly increased dynorphin content, and had no effect on enkephalin. In contrast, continuous levodopa elevated globus pallidus enkephalin beyond the levels occurring with denervation, but had no effect on any of the other neurochemical measures. These results indicate that striatal neuronal populations are differentially affected by chronic levodopa therapy and by the continuous or intermittent nature of the treatment regimen. With the exception of substance P, levodopa did not reverse the effects of the 6-OHDA lesion but, rather, either exacerbated the lesion-induced changes (e.g. GAD and enkephalin) or altered neurochemical markers which had been unaffected by the lesion (e.g. CAT and dynorphin).(ABSTRACT TRUNCATED AT 250 WORDS) JF - Brain research AU - Engber, T M AU - Susel, Z AU - Kuo, S AU - Gerfen, C R AU - Chase, T N AD - Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892. Y1 - 1991/06/21/ PY - 1991 DA - 1991 Jun 21 SP - 113 EP - 118 VL - 552 IS - 1 SN - 0006-8993, 0006-8993 KW - Enkephalins KW - 0 KW - Substance P KW - 33507-63-0 KW - Levodopa KW - 46627O600J KW - Dynorphins KW - 74913-18-1 KW - Oxidopamine KW - 8HW4YBZ748 KW - Choline O-Acetyltransferase KW - EC 2.3.1.6 KW - Glutamate Decarboxylase KW - EC 4.1.1.15 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Drug Administration Schedule KW - Male KW - Functional Laterality KW - Globus Pallidus -- metabolism KW - Substance P -- metabolism KW - Substantia Nigra -- drug effects KW - Choline O-Acetyltransferase -- metabolism KW - Corpus Striatum -- enzymology KW - Glutamate Decarboxylase -- metabolism KW - Substantia Nigra -- metabolism KW - Levodopa -- pharmacology KW - Levodopa -- administration & dosage KW - Oxidopamine -- toxicity KW - Corpus Striatum -- drug effects KW - Enkephalins -- metabolism KW - Globus Pallidus -- drug effects KW - Corpus Striatum -- pathology KW - Dynorphins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72122592?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Levodopa+replacement+therapy+alters+enzyme+activities+in+striatum+and+neuropeptide+content+in+striatal+output+regions+of+6-hydroxydopamine+lesioned+rats.&rft.au=Engber%2C+T+M%3BSusel%2C+Z%3BKuo%2C+S%3BGerfen%2C+C+R%3BChase%2C+T+N&rft.aulast=Engber&rft.aufirst=T&rft.date=1991-06-21&rft.volume=552&rft.issue=1&rft.spage=113&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 - 1991-11-04 N1 - Date created - 1991-11-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Preneoplastic alterations in nuclear morphology that accompany loss of tumor suppressor phenotype. AN - 80652663; 2061946 AB - Alterations of nuclear shape are frequently observed in tumor cells, but the genes controlling these changes and the stage in the neoplastic process at which they occur are unknown. We have studied nuclear shape changes in chemically immortalized, nontumorigenic Syrian hamster embryo cell clones that had either retained (supB+) or lost (supB-) the ability to suppress the tumorigenic phenotype when they were hybridized with a tumor cell line (BP6T). Quantitative morphometric analysis of the nuclei of cells from each of two pairs of supB+/supB- variants indicated that the nuclei of supB- cells were significantly more out of round than those of their corresponding supB+ clones. These data indicate that modification of nuclear structure may represent an early, preneoplastic event in multistep chemical carcinogenesis and that loss of a tumor suppressor gene function may regulate alterations in nuclear morphology. JF - Journal of the National Cancer Institute AU - Boyd, J AU - Pienta, K J AU - Getzenberg, R H AU - Coffey, D S AU - Barrett, J C AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/06/19/ PY - 1991 DA - 1991 Jun 19 SP - 862 EP - 866 VL - 83 IS - 12 SN - 0027-8874, 0027-8874 KW - Index Medicus KW - Phenotype KW - Animals KW - Tumor Cells, Cultured KW - Cells, Cultured KW - Mesocricetus KW - Microscopy, Electron KW - Cricetinae KW - Neoplasms, Experimental -- etiology KW - Cell Nucleus -- ultrastructure KW - Neoplasms, Experimental -- genetics KW - Genes, Suppressor -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80652663?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Preneoplastic+alterations+in+nuclear+morphology+that+accompany+loss+of+tumor+suppressor+phenotype.&rft.au=Boyd%2C+J%3BPienta%2C+K+J%3BGetzenberg%2C+R+H%3BCoffey%2C+D+S%3BBarrett%2C+J+C&rft.aulast=Boyd&rft.aufirst=J&rft.date=1991-06-19&rft.volume=83&rft.issue=12&rft.spage=862&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-06 N1 - Date created - 1991-08-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Children's exposure to environmental cigarette smoke before and after birth. Health of our nation's children, United States, 1988. AN - 80675951; 10111692 JF - Advance data AU - Overpeck, M D AU - Moss, A J AD - National Institute of Child Health and Human Development. Y1 - 1991/06/18/ PY - 1991 DA - 1991 Jun 18 SP - 1 EP - 11 IS - 202 SN - 0147-3956, 0147-3956 KW - Tobacco Smoke Pollution KW - 0 KW - Health administration KW - Humans KW - Infant, Newborn KW - Ethnic Groups -- statistics & numerical data KW - Child, Preschool KW - Pregnancy KW - Infant KW - Socioeconomic Factors KW - Cross-Sectional Studies KW - Risk Factors KW - Adult KW - Surveys and Questionnaires KW - Adolescent KW - United States -- epidemiology KW - Female KW - Environmental Exposure -- statistics & numerical data KW - Tobacco Smoke Pollution -- statistics & numerical data KW - Smoking -- epidemiology KW - Pregnancy Complications -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80675951?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advance+data&rft.atitle=Children%27s+exposure+to+environmental+cigarette+smoke+before+and+after+birth.+Health+of+our+nation%27s+children%2C+United+States%2C+1988.&rft.au=Overpeck%2C+M+D%3BMoss%2C+A+J&rft.aulast=Overpeck&rft.aufirst=M&rft.date=1991-06-18&rft.volume=&rft.issue=202&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Advance+data&rft.issn=01473956&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-14 N1 - Date created - 1991-08-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Development of a highly efficient expression cDNA cloning system: application to oncogene isolation. AN - 80622042; 2052597 AB - We developed an expression cDNA cloning system capable of generating high-complexity libraries with unidirectionally inserted cDNA fragments and allowing efficient plasmid rescue. As an application of this system, a cDNA library was constructed from an NIH 3T3 transformant induced by mouse hepatocellular carcinoma DNA. Transfection of NIH 3T3 cells by the library DNA led to the detection of several transformed foci from which identical plasmids with transforming ability could be rescued. Structure and sequence analysis of the cDNA clones revealed that the oncogene was created by recombinational events involving an unknown gene and the mouse homologue of the B-raf protooncogene. Detection of the same genetic rearrangement in independent primary transformants implied that generation of the oncogene occurred within the tumor rather than during DNA transfection or cDNA library construction. The high frequency at which clones were identified and the large sizes of some of the transforming cDNA inserts isolated suggest wide applicability of this mammalian expression cloning system for isolating cDNAs of biologic interest. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Miki, T AU - Fleming, T P AU - Crescenzi, M AU - Molloy, C J AU - Blam, S B AU - Reynolds, S H AU - Aaronson, S A AD - Laboratory of Cellular and Molecular Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/06/15/ PY - 1991 DA - 1991 Jun 15 SP - 5167 EP - 5171 VL - 88 IS - 12 SN - 0027-8424, 0027-8424 KW - RNA, Messenger KW - 0 KW - DNA KW - 9007-49-2 KW - Furaldehyde KW - DJ1HGI319P KW - Index Medicus KW - Animals KW - Base Sequence KW - Tumor Cells, Cultured KW - Transfection KW - Furaldehyde -- pharmacology KW - Restriction Mapping KW - RNA, Messenger -- analysis KW - Molecular Sequence Data KW - Mice KW - Amino Acid Sequence KW - Plasmids KW - Oncogenes -- genetics KW - DNA -- genetics KW - Liver Neoplasms, Experimental -- chemically induced KW - Liver Neoplasms, Experimental -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80622042?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Development+of+a+highly+efficient+expression+cDNA+cloning+system%3A+application+to+oncogene+isolation.&rft.au=Miki%2C+T%3BFleming%2C+T+P%3BCrescenzi%2C+M%3BMolloy%2C+C+J%3BBlam%2C+S+B%3BReynolds%2C+S+H%3BAaronson%2C+S+A&rft.aulast=Miki&rft.aufirst=T&rft.date=1991-06-15&rft.volume=88&rft.issue=12&rft.spage=5167&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 - 1991-07-19 N1 - Date created - 1991-07-19 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M64653; GENBANK; M64652; M59226; M59225; M59224; M64649; M60611; M64651; M64650; M64429 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1989 Dec;86(23):9193-7 [2687875] Proc Natl Acad Sci U S A. 1986 May;83(10):3209-12 [3010283] Proc Natl Acad Sci U S A. 1990 Jun;87(12):4645-9 [2162051] Proc Natl Acad Sci U S A. 1990 Aug;87(15):5802-6 [2198571] Science. 1991 Jan 4;251(4989):72-5 [1846048] Proc Natl Acad Sci U S A. 1991 Jan 15;88(2):415-9 [1824873] J Virol. 1969 Nov;4(5):549-53 [4311790] Cell. 1977 May;11(1):223-32 [194704] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Mol Cell Biol. 1983 Feb;3(2):280-9 [6300662] Nature. 1984 Dec 6-12;312(5994):558-61 [6438534] Mol Cell Biol. 1986 Jul;6(7):2655-62 [3491291] Mol Cell Biol. 1987 Mar;7(3):1171-9 [3561413] Science. 1987 Sep 11;237(4820):1309-16 [3629242] Nucleic Acids Res. 1987 Oct 26;15(20):8125-48 [3313277] Proc Natl Acad Sci U S A. 1987 Dec;84(23):8573-7 [2825196] Mol Cell Biol. 1988 Jun;8(6):2651-4 [3043188] EMBO J. 1988 Nov;7(11):3369-73 [2850163] Proc Natl Acad Sci U S A. 1989 Jan;86(1):162-6 [2463620] Science. 1989 Feb 10;243(4892):800-4 [2536956] Cell. 1989 Apr 21;57(2):277-85 [2539263] Science. 1989 Aug 18;245(4919):752-5 [2475908] Gene. 1989 Nov 15;83(1):137-46 [2531695] Proc Natl Acad Sci U S A. 1985 Jul;82(13):4360-4 [3925454] Science. 1985 Dec 20;230(4732):1350-4 [2999980] Proc Natl Acad Sci U S A. 1989 Dec;86(23):9248-52 [2531896] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vitro efficacy of anti-HIV immunotoxins targeted by various antibodies to the envelope protein. AN - 80595967; 1710247 AB - Six different anti-HIV envelope antibodies and one irrelevant control antibody were coupled to ricin A chain and tested for their efficacy in inhibiting HIV tissue culture infections. The anti-HIV antibodies consisted of five monoclonals, three of murine and two of human origin, and one polyclonal preparation prepared by affinity purifying pooled serum antibodies from HIV-infected humans on rgp160. The binding specificity of the antibodies was defined by ELISA by using recombinant envelope proteins and synthetic peptides, and by flow cytometry on HIV-infected cells. The in vitro efficacy of the antibodies was tested by the abilities of the immunotoxins to inhibit protein synthesis in persistently infected cell lines and by their abilities to inhibit HIV production during both acute and persistent infection as measured with an HIV-specific focal immunoassay. The immunotoxins were tested against a panel of distinctly different HIV isolates. The results indicate the following: 1) A mAb to the immunodominant neutralizing loop was highly effective against homologous strains of HIV, but had no activity against heterologous HIV. 2) The efficacy of anti-gp41 mAb varied depending upon the epitope recognized and possibly the affinity of binding to gp41. 3) The polyclonal human anti-gp160 antibodies produced the immunotoxin with the broadest specificity for different HIV strains and the greatest specific activity. This is related to the polyclonal nature of the preparation rather than an increase in relative avidity of the antibody. 4) Activity of an immunotoxin is not a direct function of the binding of the antibody to the surface of infected cells. 5) The ability of an immunotoxin to halt the spread of infection through a tissue culture cell population is dependent upon the ability of the antibody to neutralize the virus as well as the activity of the toxin. Our data suggest that efficacious immunotoxins for the treatment of AIDS may be made with polyclonal anti-envelope antibodies derived from the serum of patients who have been infected with HIV or with appropriately chosen anti-gp41 antibodies. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Pincus, S H AU - Cole, R L AU - Hersh, E M AU - Lake, D AU - Masuho, Y AU - Durda, P J AU - McClure, J AD - Laboratory of Microbial Structure and Function, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840. Y1 - 1991/06/15/ PY - 1991 DA - 1991 Jun 15 SP - 4315 EP - 4324 VL - 146 IS - 12 SN - 0022-1767, 0022-1767 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, CD4 KW - Epitopes KW - Immunotoxins KW - Viral Envelope Proteins KW - Ricin KW - 9009-86-3 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Antigens, CD4 -- physiology KW - Epitopes -- analysis KW - Animals KW - Dose-Response Relationship, Drug KW - Humans KW - Acquired Immunodeficiency Syndrome -- drug therapy KW - Mice KW - Cell Line KW - Antibodies, Monoclonal -- immunology KW - HIV -- drug effects KW - Viral Envelope Proteins -- immunology KW - HIV -- immunology KW - Immunotoxins -- therapeutic use KW - Immunotoxins -- pharmacology KW - Ricin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80595967?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=In+vitro+efficacy+of+anti-HIV+immunotoxins+targeted+by+various+antibodies+to+the+envelope+protein.&rft.au=Pincus%2C+S+H%3BCole%2C+R+L%3BHersh%2C+E+M%3BLake%2C+D%3BMasuho%2C+Y%3BDurda%2C+P+J%3BMcClure%2C+J&rft.aulast=Pincus&rft.aufirst=S&rft.date=1991-06-15&rft.volume=146&rft.issue=12&rft.spage=4315&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 - 1991-07-10 N1 - Date created - 1991-07-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cytokine secretion by C3H-lpr and -gld T cells. Hypersecretion of IFN-gamma and tumor necrosis factor-alpha by stimulated CD4+ T cells. AN - 80594845; 1674953 AB - Mice homozygous for lpr and gld develop profound lymphadenopathy characterized by the expansion of two unusual T cell subsets, a predominant Ly-5(B220)+ CD4- CD8- double negative (DN) population and a minor CD4 dull+ Ly-5(B220)+ population. The mechanisms promoting lymphoproliferation are unknown, but one possibility is a abnormality in the production of cytokines that regulate T cell growth. In the present report, unfractionated LN cells and sorted T cell subsets from C3H-lpr, -gld, and -+/+ mice were compared for spontaneous and induced secretion of a spectrum of lymphokines. In addition, CD4+, CD4 dull+ Ly-5(B220)+, and DN T cells were examined for expression of CD3 epsilon, TCR-alpha/beta heterodimers, Ly-6C, and CD44 and for proliferative responses to immobilized anti-TCR mAb and cofactors. These studies revealed that sorted DN T cells did not secrete IL-3, IL-4, IL-5, IL-6, GM-CSF, TNF-alpha, or IFN-gamma spontaneously or after TCR-alpha/beta cross-linking. In contrast, stimulated unfractionated lpr and gld LN cells proliferated strongly and secreted high levels of IFN-gamma and TNF-alpha and low levels of IL-3, IL-4, and IL-6. Despite a 5- to 10-fold deficit in the frequency of CD4+ and CD8+ T cells, cytokine secretion by lpr and gld LN generally exceeded that of +/+ LN. Comparisons of cytokine secretion by stimulated CD4+ T cells revealed that +/+, lpr, and gld CD4+ Ly-5(B220)- T cells proliferated strongly, but only lpr and gld cells produced significant levels of IFN-gamma. The lpr and gld CD4+ T cells also produced higher levels of TNF-alpha and IL-2 than +/+ cells. In contrast to normal CD4+ T cells, lpr and gld CD4+ Ly-5(B220)+ T cells proliferated weakly and did not secrete TNF-alpha, IL-2, or, in most experiments, IFN-gamma after stimulation. Phenotypic studies of T cell subsets revealed that unstimulated lpr and gld CD4+ Ly-5(B220)- T cells express significantly higher levels of CD44 than +/+ CD4+ T cells. In addition, CD4 dull+ Ly-5(B220)+ cells closely resembled DN T cells in size and expression of TCR-alpha/beta, CD3epsilon, CD44, and Ly-6C. Since elevated CD44 expression is generally associated with T cell activation and only previously activated normal CD4+ T cells produce high levels of IFN-gamma in vitro, our data suggest that lpr and gld CD4+ Ly-5(B220)- T cells contain a higher than normal proportion of primed or memory T cells and thus may be polyclonally activated in vivo.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Journal of immunology (Baltimore, Md. : 1950) AU - Davidson, W F AU - Calkins, C AU - Hügins, A AU - Giese, T AU - Holmes, K L AD - Laboratory of Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/06/15/ PY - 1991 DA - 1991 Jun 15 SP - 4138 EP - 4148 VL - 146 IS - 12 SN - 0022-1767, 0022-1767 KW - Interleukin-2 KW - 0 KW - Receptors, Antigen, T-Cell KW - Receptors, Lymphocyte Homing KW - Tumor Necrosis Factor-alpha KW - Interferon-gamma KW - 82115-62-6 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Mice, Inbred C3H KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Receptors, Lymphocyte Homing -- analysis KW - Mice KW - Interleukin-2 -- secretion KW - Receptors, Antigen, T-Cell -- physiology KW - Lymphocyte Activation KW - Interferon-gamma -- secretion KW - CD4-Positive T-Lymphocytes -- secretion KW - CD4-Positive T-Lymphocytes -- immunology KW - Lymphoproliferative Disorders -- immunology KW - Tumor Necrosis Factor-alpha -- secretion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80594845?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cytokine+secretion+by+C3H-lpr+and+-gld+T+cells.+Hypersecretion+of+IFN-gamma+and+tumor+necrosis+factor-alpha+by+stimulated+CD4%2B+T+cells.&rft.au=Davidson%2C+W+F%3BCalkins%2C+C%3BH%C3%BCgins%2C+A%3BGiese%2C+T%3BHolmes%2C+K+L&rft.aulast=Davidson&rft.aufirst=W&rft.date=1991-06-15&rft.volume=146&rft.issue=12&rft.spage=4138&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 - 1991-07-10 N1 - Date created - 1991-07-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Okadaic acid stimulates the activity of the nerve growth factor-sensitive S6 kinase of PC12 cells. AN - 80616029; 1646606 AB - PC12 pheochromocytoma cells contain at least two different and separable kinases that phosphorylate the S6 protein of the ribosomes. The activity of one of these S6 kinases is increased by treatment of the cells with nerve growth factor and of the other by treatment with epidermal growth factor. Okadaic acid increases the activity of the nerve growth factor-sensitive S6 kinase. The data suggest that the nerve growth factor-sensitive S6 kinase is activated by phosphorylation on serine or threonine residues and is inactivated by either phosphatase 1 or phosphatase 2A, probably the latter. JF - Biochemical and biophysical research communications AU - Mogi, M AU - Guroff, G AD - Section on Growth Factors National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/06/14/ PY - 1991 DA - 1991 Jun 14 SP - 624 EP - 629 VL - 177 IS - 2 SN - 0006-291X, 0006-291X KW - Ethers, Cyclic KW - 0 KW - Glycerophosphates KW - Nerve Growth Factors KW - Ribosomal Protein S6 KW - Ribosomal Proteins KW - Okadaic Acid KW - 1W21G5Q4N2 KW - Egtazic Acid KW - 526U7A2651 KW - Protein Kinases KW - EC 2.7.- KW - Phosphoprotein Phosphatases KW - EC 3.1.3.16 KW - Protein Phosphatase 1 KW - Protein Phosphatase 2 KW - beta-glycerophosphoric acid KW - WWH06G87W6 KW - Index Medicus KW - Animals KW - Tumor Cells, Cultured KW - Phosphorylation KW - Phosphoprotein Phosphatases -- pharmacology KW - Dose-Response Relationship, Drug KW - Enzyme Activation -- drug effects KW - Glycerophosphates -- pharmacology KW - Egtazic Acid -- pharmacology KW - Protein Kinases -- metabolism KW - Ribosomal Proteins -- metabolism KW - Nerve Growth Factors -- pharmacology KW - Ethers, Cyclic -- administration & dosage KW - Ethers, Cyclic -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80616029?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+stimulates+the+activity+of+the+nerve+growth+factor-sensitive+S6+kinase+of+PC12+cells.&rft.au=Mogi%2C+M%3BGuroff%2C+G&rft.aulast=Mogi&rft.aufirst=M&rft.date=1991-06-14&rft.volume=177&rft.issue=2&rft.spage=624&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 - 1991-07-12 N1 - Date created - 1991-07-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Somatostatin stimulates Ca(2+)-activated K+ channels through protein dephosphorylation. AN - 80612444; 1710783 AB - The neuropeptide somatostatin inhibits secretion from electrically excitable cells in the pituitary, pancreas, gut and brain. In mammalian pituitary tumour cells somatostatin inhibits secretion through two distinct pertussis toxin-sensitive mechanisms. One involves inhibition of adenylyl cyclase, the other an unidentified cyclic AMP-independent mechanism that reduces Ca2+ influx by increasing membrane conductance to potassium. Here we demonstrate that the predominant electrophysiological effect of somatostatin on metabolically intact pituitary tumour cells is a large, sustained increase in the activity of the large-conductance Ca(2+)- and voltage-activated K+ channels (BK). This action of somatostatin does not involve direct effects of Ca2+, cAMP or G proteins on the channels. Our results indicate instead that somatostatin stimulates BK channel activity through protein dephosphorylation. JF - Nature AU - White, R E AU - Schonbrunn, A AU - Armstrong, D L AD - Laboratory of Cellular and Molecular Pharmacology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/06/13/ PY - 1991 DA - 1991 Jun 13 SP - 570 EP - 573 VL - 351 IS - 6327 SN - 0028-0836, 0028-0836 KW - Ethers, Cyclic KW - 0 KW - Phosphoproteins KW - Potassium Channels KW - Scorpion Venoms KW - Tetraethylammonium Compounds KW - Charybdotoxin KW - 115422-61-2 KW - Okadaic Acid KW - 1W21G5Q4N2 KW - Somatostatin KW - 51110-01-1 KW - Cyclic AMP KW - E0399OZS9N KW - Phosphoprotein Phosphatases KW - EC 3.1.3.16 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Rats KW - Animals KW - Scorpion Venoms -- pharmacology KW - Tumor Cells, Cultured KW - In Vitro Techniques KW - Tetraethylammonium Compounds -- pharmacology KW - Phosphoprotein Phosphatases -- metabolism KW - Ethers, Cyclic -- pharmacology KW - Cyclic AMP -- physiology KW - Pituitary Gland -- physiology KW - Somatostatin -- physiology KW - Calcium -- physiology KW - Potassium Channels -- physiology KW - Phosphoproteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80612444?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Somatostatin+stimulates+Ca%282%2B%29-activated+K%2B+channels+through+protein+dephosphorylation.&rft.au=White%2C+R+E%3BSchonbrunn%2C+A%3BArmstrong%2C+D+L&rft.aulast=White&rft.aufirst=R&rft.date=1991-06-13&rft.volume=351&rft.issue=6327&rft.spage=570&rft.isbn=&rft.btitle=&rft.title=Nature&rft.issn=00280836&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-12 N1 - Date created - 1991-07-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Recombinant human chromosomal proteins HMG-14 and HMG-17. AN - 80642487; 2057367 AB - Vectors for expressing human chromosomal proteins HMG-14 and HMG-17 in bacterial cultures under the control of the temperature-inducible lambda PL promoter have been constructed. The open reading frames of the cDNAs have been amplified by the polymerase chain reaction (PCR), utilizing amplimers containing desired restriction sites, thereby facilitating precise location of the initiation codon downstream from a ribosomal binding site. Expression of the recombinant proteins does not significantly affect bacterial growth. The rate of synthesis of the recombinant proteins is maximal during the initial stages of induction and slows down appreciably with time. After an initial burst of protein synthesis, the level of the recombinant protein in the bacterial extracts remains constant at different times following induction. Methods for rapid extraction and purification of the recombinant proteins are described. The recombinant proteins are compared to the proteins isolated from eucaryotic cells by electrophoretic mobility, Western analysis and nucleosome core mobility-shift assays. The ability of the proteins to shift the mobility of the nucleosome cores, but not that of DNA, can be used as a functional assay for these HMG proteins. A source for large quantities of human chromosomal proteins HMG-14 and HMG-17 will facilitate studies on their structure, cellular function and mechanism of interaction with nucleosomes. JF - Nucleic acids research AU - Bustin, M AU - Becerra, P S AU - Crippa, M P AU - Lehn, D A AU - Pash, J M AU - Shiloach, J AD - Laboratory of Molecular Carcinogenesis, NCI National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/06/11/ PY - 1991 DA - 1991 Jun 11 SP - 3115 EP - 3121 VL - 19 IS - 11 SN - 0305-1048, 0305-1048 KW - High Mobility Group Proteins KW - 0 KW - Recombinant Proteins KW - Index Medicus KW - Gene Expression Regulation, Bacterial KW - Recombinant Proteins -- isolation & purification KW - Genes, Bacterial KW - Base Sequence KW - Electrophoresis, Polyacrylamide Gel KW - Humans KW - Molecular Sequence Data KW - Escherichia coli -- genetics KW - Recombinant Proteins -- genetics KW - Plasmids KW - High Mobility Group Proteins -- isolation & purification KW - High Mobility Group Proteins -- genetics KW - Chromosomes, Human UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80642487?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+acids+research&rft.atitle=Recombinant+human+chromosomal+proteins+HMG-14+and+HMG-17.&rft.au=Bustin%2C+M%3BBecerra%2C+P+S%3BCrippa%2C+M+P%3BLehn%2C+D+A%3BPash%2C+J+M%3BShiloach%2C+J&rft.aulast=Bustin&rft.aufirst=M&rft.date=1991-06-11&rft.volume=19&rft.issue=11&rft.spage=3115&rft.isbn=&rft.btitle=&rft.title=Nucleic+acids+research&rft.issn=03051048&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-31 N1 - Date created - 1991-07-31 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1974 Apr;71(4):1342-6 [4598299] J Mol Biol. 1990 Aug 20;214(4):897-910 [2388273] J Biol Chem. 1980 Apr 25;255(8):3673-84 [7364765] Methods Enzymol. 1979;68:482-92 [232223] Science. 1980 Sep 26;209(4464):1534-6 [7433974] Nucleic Acids Res. 1980 Sep 11;8(17):3757-78 [6449690] Cell. 1981 Feb;23(2):391-400 [6258801] Nature. 1982 May 27;297(5864):289-95 [6210847] J Biol Chem. 1982 Oct 10;257(19):11448-54 [6214552] Proc Natl Acad Sci U S A. 1982 Sep;79(17):5258-62 [6215649] Eur J Biochem. 1982 Oct;127(2):429-36 [6216108] Nucleic Acids Res. 1983 Jan 25;11(2):387-401 [6298725] J Mol Biol. 1983 Jun 5;166(4):557-80 [6345791] J Biol Chem. 1983 Nov 10;258(21):13221-9 [6226664] Nucleic Acids Res. 1983 Oct 11;11(19):6803-19 [6226937] Proc Natl Acad Sci U S A. 1983 Nov;80(22):6735-9 [6196774] Chromosoma. 1984;90(5):355-65 [6439496] J Mol Biol. 1985 Sep 20;185(2):329-39 [4057250] Gene. 1985;38(1-3):31-8 [2998948] Nucleic Acids Res. 1986 Apr 25;14(8):3363-76 [3703677] J Biol Chem. 1986 Jun 5;261(16):7479-84 [3754870] Exp Cell Res. 1986 Oct;166(2):486-96 [3743668] J Biol Chem. 1986 Dec 5;261(34):16082-6 [3782107] EMBO J. 1987 Aug;6(8):2393-9 [3665881] J Biol Chem. 1989 Jan 25;264(3):1799-803 [2912984] J Mol Biol. 1989 Apr 5;206(3):451-63 [2716057] Appl Environ Microbiol. 1989 May;55(5):1305-7 [2667464] Methods Enzymol. 1989;170:214-51 [2770539] Annu Rev Biochem. 1989;58:799-839 [2673023] Nucleic Acids Res. 1990 Apr 25;18(8):2011-6 [1692412] Proc Natl Acad Sci U S A. 1990 May;87(10):3836-40 [2140193] Biochim Biophys Acta. 1990 Jul 30;1049(3):231-43 [2200521] J Biol Chem. 1978 Mar 10;253(5):1694-9 [75209] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Down-regulation of cystic fibrosis gene mRNA transcript levels and induction of the cystic fibrosis chloride secretory phenotype in epithelial cells by phorbol ester. AN - 80573232; 2037584 AB - To evaluate the hypothesis that phorbol myristate acetate (PMA) might modulate the expression of the cystic fibrosis (CF) gene in epithelial cells, we examined the effect of PMA on CF mRNA levels and regulation of Cl- secretion. Strikingly, PMA down-regulated CF mRNA transcript numbers in a dose- and time-dependent manner. Importantly, in parallel with the reduction of CF mRNA levels, PMA-treated cells were unable to up-regulate Cl- secretion in a normal fashion in response to forskolin, an effect which was also dose- and time-dependent. Thus, PMA is capable of modulating expression of the CF gene and induces T84 cells to adopt the "CF phenotype" in regard to regulation of Cl- ion transport. JF - The Journal of biological chemistry AU - Trapnell, B C AU - Zeitlin, P L AU - Chu, C S AU - Yoshimura, K AU - Nakamura, H AU - Guggino, W B AU - Bargon, J AU - Banks, T C AU - Dalemans, W AU - Pavirani, A AD - Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/06/05/ PY - 1991 DA - 1991 Jun 05 SP - 10319 EP - 10323 VL - 266 IS - 16 SN - 0021-9258, 0021-9258 KW - Chlorides KW - 0 KW - RNA, Messenger KW - Colforsin KW - 1F7A44V6OU KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Phenotype KW - Colforsin -- pharmacology KW - Blotting, Northern KW - Tumor Cells, Cultured KW - Epithelial Cells KW - Humans KW - Epithelium -- drug effects KW - Cystic Fibrosis -- metabolism KW - Down-Regulation KW - Cystic Fibrosis -- genetics KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Transcription, Genetic KW - Chlorides -- metabolism KW - RNA, Messenger -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80573232?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Down-regulation+of+cystic+fibrosis+gene+mRNA+transcript+levels+and+induction+of+the+cystic+fibrosis+chloride+secretory+phenotype+in+epithelial+cells+by+phorbol+ester.&rft.au=Trapnell%2C+B+C%3BZeitlin%2C+P+L%3BChu%2C+C+S%3BYoshimura%2C+K%3BNakamura%2C+H%3BGuggino%2C+W+B%3BBargon%2C+J%3BBanks%2C+T+C%3BDalemans%2C+W%3BPavirani%2C+A&rft.aulast=Trapnell&rft.aufirst=B&rft.date=1991-06-05&rft.volume=266&rft.issue=16&rft.spage=10319&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 - 1991-07-01 N1 - Date created - 1991-07-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Rapid secretagogue-induced activation of Na+H+ exchange in rat parotid acinar cells. Possible interrelationship between volume regulation and stimulus-secretion coupling. AN - 80571503; 1709927 AB - We demonstrate a rapid activation of the Na+/H+ exchanger in intact rat parotid acini in response to muscarinic (carbachol; K1/2 = 0.4 microM) and alpha-adrenergic (epinephrine; K1/2 = 0.1 microM) stimulation. This rapid activation is apparently distinct from the relatively "slow" activation of the exchanger (t1/2 greater than or equal to 5 min) reported previously (Manganel, M., and Turner, R. J. (1989) J. Membr. Biol. 111, 191-198). This rapid activation is not produced by treatment of acini with active diacylglycerol analogues nor prevented by protein kinase inhibitors, arguing against the involvement of protein kinase C-dependent processes. Stimulation of the exchanger is, however, produced by concentrations of ionomycin which yield intracellular calcium levels in the physiologic (secretagogue-induced) range. In addition, chelation of intracellular calcium with 1,2-bis(O-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid blocks the effect of carbachol, but calmodulin antagonists are without effect. The possibility that the rapid activation of the Na+/H+ exchanger may be associated with cell shrinkage arising from carbachol-induced calcium mobilization is explored. In support of this suggestion we present evidence that: (i) the Na+/H+ exchanger is stimulated by shrinkage of these cells, (ii) the carbachol dose dependence of Na+/H+ exchange activation correlates well with that of shrinkage (but not with that of intracellular calcium levels), and (iii) maneuvers which blunt carbachol- or calcium-induced shrinkage also blunt activation of the exchanger. We suggest that this osmoregulatory response may play an important role in maintaining ionic homeostasis during the acinar fluid secretory process. JF - The Journal of biological chemistry AU - Manganel, M AU - Turner, R J AD - Clinical Investigations and Patient Care Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/06/05/ PY - 1991 DA - 1991 Jun 05 SP - 10182 EP - 10188 VL - 266 IS - 16 SN - 0021-9258, 0021-9258 KW - Carrier Proteins KW - 0 KW - Scorpion Venoms KW - Sodium-Hydrogen Antiporter KW - Charybdotoxin KW - 115422-61-2 KW - Carbachol KW - 8Y164V895Y KW - Protein Kinase C KW - EC 2.7.11.13 KW - Calcium KW - SY7Q814VUP KW - Epinephrine KW - YKH834O4BH KW - Index Medicus KW - Animals KW - Scorpion Venoms -- pharmacology KW - Enzyme Activation KW - Hydrogen-Ion Concentration KW - Osmosis KW - Rats, Inbred Strains KW - Rats KW - Calcium -- metabolism KW - Protein Kinase C -- metabolism KW - Protein Kinase C -- antagonists & inhibitors KW - Epinephrine -- pharmacology KW - In Vitro Techniques KW - Up-Regulation KW - Carbachol -- pharmacology KW - Male KW - Carrier Proteins -- metabolism KW - Parotid Gland -- drug effects KW - Parotid Gland -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80571503?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Rapid+secretagogue-induced+activation+of+Na%2BH%2B+exchange+in+rat+parotid+acinar+cells.+Possible+interrelationship+between+volume+regulation+and+stimulus-secretion+coupling.&rft.au=Manganel%2C+M%3BTurner%2C+R+J&rft.aulast=Manganel&rft.aufirst=M&rft.date=1991-06-05&rft.volume=266&rft.issue=16&rft.spage=10182&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 - 1991-07-01 N1 - Date created - 1991-07-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interactions between calcium and protein kinase C in the control of signaling and secretion in pituitary gonadotrophs. AN - 80571393; 1645348 AB - Single pituitary gonadotrophs exhibit episodes of spontaneous fluctuations in cytoplasmic calcium concentration [( Ca2+]i) due to entry through voltage-sensitive calcium channels (VSCC) and show prominent agonist-induced oscillations in [Ca2+]i that are generated by periodic release of intracellular Ca2+. Gonadotropin releasing hormone (GnRH) elicited three types of Ca2+ responses: at low doses, subthreshold, with an increase in basal [Ca2+]i; at intermediate doses, oscillatory, with dose-dependent modulation of spiking frequency; and at high doses, biphasic, without oscillations. Elevation of [Ca2+]i or activation of protein kinase C (PKC) did not influence the frequency of agonist-induced [Ca2+]i spikes but caused dose-dependent reductions in amplitude for all types of Ca2+ response. Stimulation of transient Ca2+ spikes by GnRH was followed by inhibition of the spontaneous fluctuations. GnRH also reduced the ability of high extracellular K+ to promote Ca2+ influx through VSCC. Activation of PKC by phorbol esters stimulated Ca2+ influx in quiescent cells but inhibited influx when VSCC were already activated, either spontaneously or by high K+. In contrast to their biphasic actions on [Ca2+]i, phorbol esters exerted only stimulatory actions on gonadotropin release, even when Ca2+ influx was concomitantly reduced. However, pituitary cells had to be primed with an appropriate [Ca2+]i level before exocytosis could be amplified by PKC. In PKC-depleted cells, all actions of phorbol esters on Ca2+ entry and amplitude modulation, and on LH release, were abolished. GnRH-induced LH secretion was also significantly reduced, especially the plateau phase of the response. These data indicate that Ca2+ and PKC serve as interacting signals during the cascade of cellular events triggered by agonist stimulation, in which Ca2+ turns cell responses on or off, and PKC amplifies the positive and negative effects of Ca2+. JF - The Journal of biological chemistry AU - Stojilković, S S AU - Iida, T AU - Merelli, F AU - Torsello, A AU - Krsmanović, L Z 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 - 1991/06/05/ PY - 1991 DA - 1991 Jun 05 SP - 10377 EP - 10384 VL - 266 IS - 16 SN - 0021-9258, 0021-9258 KW - Alkaloids KW - 0 KW - Calcium Channels KW - Gonadotropin-Releasing Hormone KW - 33515-09-2 KW - Luteinizing Hormone KW - 9002-67-9 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Staurosporine KW - H88EPA0A3N KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Potassium KW - RWP5GA015D KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Calcium Channels -- metabolism KW - Enzyme Activation KW - Temperature KW - Biological Transport KW - Luteinizing Hormone -- metabolism KW - Rats, Inbred Strains KW - Rats KW - Gonadotropin-Releasing Hormone -- metabolism KW - Blotting, Western KW - Luteinizing Hormone -- antagonists & inhibitors KW - Cells, Cultured KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Potassium -- pharmacology KW - Alkaloids -- pharmacology KW - Membrane Potentials KW - Female KW - Protein Kinase C -- metabolism KW - Calcium -- metabolism KW - Pituitary Gland, Anterior -- metabolism KW - Pituitary Gland, Anterior -- physiology KW - Pituitary Gland, Anterior -- cytology KW - Signal Transduction UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80571393?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Interactions+between+calcium+and+protein+kinase+C+in+the+control+of+signaling+and+secretion+in+pituitary+gonadotrophs.&rft.au=Stojilkovi%C4%87%2C+S+S%3BIida%2C+T%3BMerelli%2C+F%3BTorsello%2C+A%3BKrsmanovi%C4%87%2C+L+Z%3BCatt%2C+K+J&rft.aulast=Stojilkovi%C4%87&rft.aufirst=S&rft.date=1991-06-05&rft.volume=266&rft.issue=16&rft.spage=10377&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 - 1991-07-01 N1 - Date created - 1991-07-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - From the National Institutes of Health. AN - 80567427; 2033726 JF - JAMA AU - Healy, B AD - National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/06/05/ PY - 1991 DA - 1991 Jun 05 SP - 2777 VL - 265 IS - 21 SN - 0098-7484, 0098-7484 KW - Antigens, CD4 KW - 0 KW - Bacterial Toxins KW - Exotoxins KW - Recombinant Proteins KW - Virulence Factors KW - Propafenone KW - 68IQX3T69U KW - Doxorubicin KW - 80168379AG KW - Amoxicillin KW - 804826J2HU KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Infant KW - Acute Disease KW - Amoxicillin -- therapeutic use KW - Propafenone -- therapeutic use KW - Humans KW - Monocytes -- microbiology KW - Child KW - Lymphocytes -- microbiology KW - Doxorubicin -- adverse effects KW - Arrhythmias, Cardiac -- drug therapy KW - Cardiomyopathies -- chemically induced KW - HIV-1 -- physiology KW - Otitis Media -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80567427?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=JAMA&rft.atitle=From+the+National+Institutes+of+Health.&rft.au=Healy%2C+B&rft.aulast=Healy&rft.aufirst=B&rft.date=1991-06-05&rft.volume=265&rft.issue=21&rft.spage=2777&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-06-26 N1 - Date created - 1991-06-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Caffeine and novelty: effects on electrodermal activity and performance. AN - 85263815; pmid-1896498 AB - Caffeine has been shown to affect both physiological functioning and certain aspects of performance. These effects are typically attributed to a simple increase in general arousal. The present study was based on the theory that the effects of caffeine are actually multidimensional. Specifically, we hypothesized that the drug raises arousal, acts to maintain elevated arousal under conditions otherwise conductive to habituation, and enhances the impact of situational and psychological sources of arousal. Subjects were given caffeine (300 mg) or placebo and white noise or no noise and exposed to a series of pure tones and two Backwards Recall Tasks, one novel, the other repetitive. Electrodermal activity (EDA) and task performance were recorded. Caffeine increased arousal as measured by EDA. It also acted to slow habituation during repetitive stimulation, thus maintaining heightened arousal. Finally, it enhanced the effects of novel stimulation, which also independently raised arousal. These results support a multidimensional theory of caffeine effects and provide some understanding of the popularity of caffeine as a psychotropic agent. JF - Physiology & Behavior AU - Davidson, R A AU - Smith, B D AD - National Institutes of Health, NINDS, Bethesda, MD 20892. PY - 1991 SP - 1169 EP - 1175 VL - 49 IS - 6 SN - 0031-9384, 0031-9384 KW - Galvanic Skin Response KW - Arousal KW - Human KW - Mental Recall KW - Serial Learning KW - Habituation (Psychophysiology) KW - Adult KW - Support, Non-U.S. Gov't KW - Acoustic Stimulation KW - Caffeine KW - Attention KW - Male KW - Female KW - Social Environment UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85263815?accountid=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=Physiology+%26+Behavior&rft.atitle=Caffeine+and+novelty%3A+effects+on+electrodermal+activity+and+performance.&rft.au=Davidson%2C+R+A%3BSmith%2C+B+D&rft.aulast=Davidson&rft.aufirst=R&rft.date=1991-06-01&rft.volume=49&rft.issue=6&rft.spage=1169&rft.isbn=&rft.btitle=&rft.title=Physiology+%26+Behavior&rft.issn=00319384&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Successful treatment of selected cases of abductor spasmodic dysphonia using botulinum toxin injection. AN - 85212319; pmid-1908979 AB - Ten patients with abductor spasmodic dysphonia, who exhibited spasmodic bursts and heightened activity of the cricothyroid muscle during speech, were selected for participation. Between 5 and 20 U of botulinum toxin type A were injected into both right and left cricothyroid muscles. Six patients benefited substantially, whereas four did not. Acoustic analyses of voice patterns showed similar changes to the clinical impressions. Significant group improvements were found in sentence duration while selected patients improved in the proportion of their speech that was voiced and the duration of their voiceless consonants. Those patients with abductor spasmodic dysphonia and other muscle abnormalities in addition to the cricothyroid and with constant breathiness did not benefit. JF - Otolaryngology--Head and Neck Surgery AU - Ludlow, Christy L AU - Naunton, R F AU - Terada, S AU - Anderson, B J AD - Laryngeal and Speech Section, National Institute of Neurological Disorders and Stroke PY - 1991 SP - 849 EP - 855 VL - 104 IS - 6 SN - 0194-5998, 0194-5998 KW - Laryngeal Muscles KW - Human KW - Injections, Intramuscular KW - Electromyography KW - Aged KW - Botulinum Toxins KW - Adult KW - Middle Age KW - Laryngismus KW - Voice Disorders KW - Phonation KW - Female KW - Male UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85212319?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Otolaryngology--Head+and+Neck+Surgery&rft.atitle=Successful+treatment+of+selected+cases+of+abductor+spasmodic+dysphonia+using+botulinum+toxin+injection.&rft.au=Ludlow%2C+Christy+L%3BNaunton%2C+R+F%3BTerada%2C+S%3BAnderson%2C+B+J&rft.aulast=Ludlow&rft.aufirst=Christy&rft.date=1991-06-01&rft.volume=104&rft.issue=6&rft.spage=849&rft.isbn=&rft.btitle=&rft.title=Otolaryngology--Head+and+Neck+Surgery&rft.issn=01945998&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Hypochloremic metabolic alkalosis from ingestion of a chloride-deficient infant formula: outcome 9 and 10 years later. AN - 85178363; pmid-2034484 AB - In 1978 and 1979 two infant formulas, Neo-Mull-Soy and Cho-Free, were found to be deficient in chloride. The Centers for Disease Control received reports that hypochloremic metabolic alkalosis (HMA) had developed in 141 children as a result of exposure to these formulas. Thirty-five of these children were examined at 9 and 10 years of age and compared with a group of 32 children who were exposed to the chloride-deficient formulas but were not reported to experience HMA and a group of 61 children who received chloride-sufficient soy formulas in infancy. The control children were matched to the HMA children on sex, race, age, and maternal education. Growth characteristics, performance on the Wechsler Intelligence Scale for Children-Revised (WISC-R), the Boston Naming Test, the Rey-Osterrieth Test, the Clinical Evaluation of Language Fundamentals-Revised (CELF-R), and subtests from several other speech and language tests were compared across the groups. After adjustment for family income and the level of the father's education, significantly lower scores were observed in the HMA children on the WISC-R Arithmetic subtest (mean = 10.5) compared with the soy control children (mean = 12.0, P less than .05) and on the WISC-R Coding subtest (mean = 9.0) compared with the soy control children (mean = 10.8, P less than .01). All the WISC-R subtest scores were, however, within the normal range. Although no significant differences occurred on the CELF-R between groups, the risk of an HMA child falling below the range expected for a standard population was increased on the CELF-R Composite Total, Receptive, and Expressive Language scores: risk ratios = 2.14, 2.14, and 3.03 respectively. Significant differences were observed between the children exposed, both HMA and non-HMA children, and the soy control children for behavioral problems as determined by the Achenbach Childhood Behavioral Checklist. It is concluded that as a group, children with documented HMA appear to have recovered from their growth failure and have normal cognitive development. They may, however, be at risk for deficits in language skills that require expressive language abilities. JF - Pediatrics AU - Malloy, M H AU - Graubard, B AU - Moss, H AU - McCarthy, M AU - Gwyn, S AU - Vietze, P AU - Willoughby, A AU - Rhoads, G G AU - Berendes, H AD - Epidemiology Branch/PRP, National Institute of Child Health and Human Development, Bethesda, MD 20892. PY - 1991 SP - 811 EP - 822 VL - 87 IS - 6 SN - 0031-4005, 0031-4005 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85178363?accountid=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=Pediatrics&rft.atitle=Hypochloremic+metabolic+alkalosis+from+ingestion+of+a+chloride-deficient+infant+formula%3A+outcome+9+and+10+years+later.&rft.au=Malloy%2C+M+H%3BGraubard%2C+B%3BMoss%2C+H%3BMcCarthy%2C+M%3BGwyn%2C+S%3BVietze%2C+P%3BWilloughby%2C+A%3BRhoads%2C+G+G%3BBerendes%2C+H&rft.aulast=Malloy&rft.aufirst=M&rft.date=1991-06-01&rft.volume=87&rft.issue=6&rft.spage=811&rft.isbn=&rft.btitle=&rft.title=Pediatrics&rft.issn=00314005&rft_id=info:doi/ LA - English DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Oral contraceptives and cervical neoplasia. AN - 80737798; 1868734 AB - Although initial studies examining the relationship of oral contraceptives to risk of cervical neoplasia were reassuring, more recent studies provide some evidence of a positive relationship, particularly for long-term usage. Results, however, are difficult to interpret, because of a variety of methodologic complexities, including potential sources of confounding and bias. Sexual behavior and Pap smear screening have been identified as important confounders, but in several well-controlled studies residual excess risks of nearly 2-fold persist for users of 5 or more years. A possible promotional effect of oral contraceptives is suggested by higher risks associated with recent usage. There also is some suggestion of a stronger effect for adenocarcinomas than for squamous cell tumors. A relationship is biologically possible, given findings of hormone receptors in cervical tissue and the fact that oral contraceptives have been found to induce cervical hyperplasia. In addition, oral contraceptives may induce proliferation of the human papillomaviruses, the leading suspect agent for cervical cancer. Although a number of lines of evidence support a relationship of oral contraceptives to cervical cancer risk, firm conclusions await the results of additional studies that specifically address some of the methodologic shortcomings of previous investigations. In particular, additional follow-up studies are needed to define the effect of oral contraceptives on the natural history of cervical lesions. JF - Contraception AU - Brinton, L A AD - Environmental Epidemiology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 581 EP - 595 VL - 43 IS - 6 SN - 0010-7824, 0010-7824 KW - Contraceptives, Oral KW - 0 KW - Index Medicus KW - Population KW - Uterus KW - Physiology KW - Contraceptive Methods--side effects KW - Genitalia KW - Oral Contraceptives--side effects KW - Cervical Effects KW - Cervical Cancer--etiology KW - Cancer KW - Genitalia, Female KW - Neoplasms KW - Contraception KW - Risk Factors KW - Urogenital System KW - Diseases KW - Literature Review KW - Family Planning KW - Cervix KW - Biology KW - Adenocarcinoma -- chemically induced KW - Humans KW - Cohort Studies KW - Female KW - Uterine Cervical Neoplasms -- etiology KW - Contraceptives, Oral -- adverse effects KW - Uterine Cervical Neoplasms -- prevention & control KW - Uterine Cervical Neoplasms -- epidemiology KW - Uterine Cervical Neoplasms -- diagnosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80737798?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Contraception&rft.atitle=Oral+contraceptives+and+cervical+neoplasia.&rft.au=Brinton%2C+L+A&rft.aulast=Brinton&rft.aufirst=L&rft.date=1991-06-01&rft.volume=43&rft.issue=6&rft.spage=581&rft.isbn=&rft.btitle=&rft.title=Contraception&rft.issn=00107824&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-19 N1 - Date created - 1991-09-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Measures of renal function in patients with cisplatin-related chronic renal disease. AN - 80731181; 1865503 AB - Twenty-seven patients with advanced stage refractory ovarian cancer were studied to determine if chronic stable cisplatin-related renal dysfunction was present. Medical histories were examined to determine the types of therapy previously received as well as the total previous platinum doses received that ranged from 200 to 2,100 mg/m2. Standard assessments of renal function were made prior to administering current chemotherapy or immunotherapy to the patient, which included 24-hour creatinine clearance, serum creatinine, and blood urea nitrogen (BUN). For patients with a 24-hour creatinine clearance of less than 60 mL/minute, serum creatinine was highly variable (range: 0.9 to 2.0 mg/dL) and was not related to the degree of diminution in the 24-hour creatinine clearance value. Conversely, for patients with a serum creatinine of less than 1.5, the 24-hour creatinine clearance values varied by almost three-fold, ranging between 46 and 120 mL/minute. Two patients with serum creatinines of less than 1 had creatinine clearances of less than 50 mL per minute. Similarly, BUN measurements did not correlate with 24-hour creatinine clearance values, and the 24-hour creatinine clearance value was not related to the total cumulative platinum dose. We conclude that patients who receive substantive doses of cisplatin may experience chronic stable cisplatin-related renal dysfunction and that serum creatinine cannot be relied on to assess the degree of renal compromise. In such patients, we recommended that the 24-hour creatinine clearance value should be used when medical management is influenced by renal function. JF - Journal of the National Medical Association AU - Reed, E AU - Jacob, J AU - Brawley, O AD - Medicine Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 522 EP - 526 VL - 83 IS - 6 SN - 1943-4693, 1943-4693 KW - Creatinine KW - AYI8EX34EU KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Blood Urea Nitrogen KW - Creatinine -- blood KW - Female KW - Kidney Failure, Chronic -- blood KW - Cisplatin -- adverse effects KW - Kidney Failure, Chronic -- chemically induced KW - Ovarian Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80731181?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Medical+Association&rft.atitle=Measures+of+renal+function+in+patients+with+cisplatin-related+chronic+renal+disease.&rft.au=Reed%2C+E%3BJacob%2C+J%3BBrawley%2C+O&rft.aulast=Reed&rft.aufirst=E&rft.date=1991-06-01&rft.volume=83&rft.issue=6&rft.spage=522&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Medical+Association&rft.issn=19434693&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-11 N1 - Date created - 1991-09-11 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Semin Oncol. 1987 Dec;14(4 Suppl 4):12-9 [3120317] Proc Natl Acad Sci U S A. 1987 Jul;84(14):5024-8 [3110781] Carcinogenesis. 1988 Oct;9(10):1909-11 [2458857] Cancer Treat Rep. 1985 Jun;69(6):731-3 [4040425] Cancer. 1983 Jun 1;51(11):2035-40 [6340821] Am J Physiol. 1981 Aug;241(2):F175-85 [7196698] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Common expression of melanoma tumor-associated antigens recognized by human tumor infiltrating lymphocytes: analysis by human lymphocyte antigen restriction. AN - 80730582; 1868040 AB - Major histocompatibility complex (MHC) class I antigens (Ag), particularly human lymphocyte antigen (HLA)-A2, have been shown to function as restriction elements in human cytotoxic T lymphocyte recognition of tumor. This study was undertaken to determine the function of non-A2 MHC class I Ag in tumor recognition by tumor-infiltrating lymphocytes (TILs) cultured from six melanomas, and to find evidence for shared or unique tumor-associated Ag. Four predominantly CD8+ and two mixed CD4+, CD8+ population TIL cultures were tested for lysis in short-term 51Cr-release assays against a panel of targets including 29 fresh melanomas, 2 fresh sarcomas, 11 cultured melanoma lines, and 14 nonmelanoma cell lines derived from HLA-typed patients. All six melanoma TILs lysed the autologous melanoma. Two of three TILs from HLA-A2+ patients lysed allogeneic melanomas matched for HLA-A2, giving evidence for shared tumor Ag; one of these TILs also used HLA-B44 as a restriction element. The third HLA-A2+ TIL lysed autologous melanoma but not autologous Epstein-Barr virus-transformed B cells nor 14 HLA-A2 matched allogeneic melanomas, suggesting the possibility of a unique tumor Ag in this system. The three HLA-A2- TILs each lysed multiple HLA-matched melanomas, using HLA-A24, HLA-A31, and HLA-Cw7 as restriction elements. Blocking of autologous and allogeneic melanoma lysis by TILs with mAb w6/32 (anti-MHC class I) and anti-CD3, as well as cold target inhibition assays, confirmed that specific interaction of the T-cell receptor with MHC class I Ag and the relevant tumor Ag on the target cell surface is required for tumor lysis. These data provide evidence for specific recognition of shared melanoma Ag by human TILs. JF - Journal of immunotherapy : official journal of the Society for Biological Therapy AU - Hom, S S AU - Topalian, S L AU - Simonis, T AU - Mancini, M AU - Rosenberg, S A AD - Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 153 EP - 164 VL - 10 IS - 3 SN - 1053-8550, 1053-8550 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Neoplasm KW - HLA Antigens KW - Index Medicus KW - Tumor Cells, Cultured KW - Cells, Cultured KW - Humans KW - Killer Cells, Lymphokine-Activated -- immunology KW - Cytotoxicity Tests, Immunologic KW - Immunophenotyping KW - Antibodies, Monoclonal -- immunology KW - Lymphocytes, Tumor-Infiltrating -- immunology KW - HLA Antigens -- immunology KW - Melanoma -- immunology KW - Antigens, Neoplasm -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80730582?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Common+expression+of+melanoma+tumor-associated+antigens+recognized+by+human+tumor+infiltrating+lymphocytes%3A+analysis+by+human+lymphocyte+antigen+restriction.&rft.au=Hom%2C+S+S%3BTopalian%2C+S+L%3BSimonis%2C+T%3BMancini%2C+M%3BRosenberg%2C+S+A&rft.aulast=Hom&rft.aufirst=S&rft.date=1991-06-01&rft.volume=10&rft.issue=3&rft.spage=153&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 - 1991-09-17 N1 - Date created - 1991-09-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Doxorubicin-induced cross-resistance to tumor necrosis factor (TNF) related to differential TNF processing. AN - 80728973; 1651105 AB - To evaluate whether cells selected for doxorubicin resistance were cross-resistant to tumor necrosis factor, the effects of doxorubicin and recombinant human tumor necrosis factor-alpha (TNF) on doxorubicin-sensitive (WT) and 40-fold doxorubicin-resistant (40F) MCF-7 cell proliferation were assessed. The median dose (MD) for doxorubicin was 14.5 nM for WT cells and 474 nM for 40F cells. The MD for TNF was 0.18 nM for WT cells, while 40F cells were highly resistant to TNF concentrations up to 60 nM. Doxorubicin and TNF in combination were synergistic against WT cells, but not 40F cells. Glutathione depletion by buthionine sulfoxamine sensitized WT cells threefold to TNF, with no change in their response to doxorubicin, while 40F cells showed a twofold increase in doxorubicin sensitivity, with no apparent change in their resistance to TNF. No significant differences in TNF receptor number, Kd, or capacity for TNF internalization were noted between the two cell types. WT cells produced a single 15 kDa TNF degradation product, while the 40F cells produced three lower molecular weight degradation products. We conclude that cross-resistance to TNF in doxorubicin-resistant MCF-7 cells may be explained in part by altered TNF degradation. JF - Journal of immunotherapy : official journal of the Society for Biological Therapy AU - Fruehauf, J P AU - Mimnaugh, E G AU - Sinha, B K AD - Biochemical and Molecular Pharmacology Section, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 165 EP - 173 VL - 10 IS - 3 SN - 1053-8550, 1053-8550 KW - Receptors, Cell Surface KW - 0 KW - Receptors, Tumor Necrosis Factor KW - Tumor Necrosis Factor-alpha KW - Methionine Sulfoximine KW - 1982-67-8 KW - Buthionine Sulfoximine KW - 5072-26-4 KW - Doxorubicin KW - 80168379AG KW - Glutathione KW - GAN16C9B8O KW - Index Medicus KW - Receptors, Cell Surface -- metabolism KW - Drug Screening Assays, Antitumor KW - Drug Resistance -- physiology KW - Tumor Cells, Cultured KW - Humans KW - Glutathione -- metabolism KW - Methionine Sulfoximine -- pharmacology KW - Methionine Sulfoximine -- analogs & derivatives KW - Drug Synergism KW - Doxorubicin -- pharmacology KW - Tumor Necrosis Factor-alpha -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80728973?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Doxorubicin-induced+cross-resistance+to+tumor+necrosis+factor+%28TNF%29+related+to+differential+TNF+processing.&rft.au=Fruehauf%2C+J+P%3BMimnaugh%2C+E+G%3BSinha%2C+B+K&rft.aulast=Fruehauf&rft.aufirst=J&rft.date=1991-06-01&rft.volume=10&rft.issue=3&rft.spage=165&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 - 1991-09-17 N1 - Date created - 1991-09-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - [A ras guanine nucleotide exchange factor and ras-mediated signal transduction]. AN - 80726060; 1907747 JF - Tanpakushitsu kakusan koso. Protein, nucleic acid, enzyme AU - Kamata, T AD - Biological Carcinogenesis Development Program, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland 21702. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 1497 EP - 1508 VL - 36 IS - 8 SN - 0039-9450, 0039-9450 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Index Medicus KW - Animals KW - Second Messenger Systems KW - Humans KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Molecular Weight KW - Cell Transformation, Neoplastic KW - Genes, ras KW - GTP-Binding Proteins -- chemistry KW - GTP-Binding Proteins -- physiology KW - GTP-Binding Proteins -- genetics KW - Signal Transduction UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80726060?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Tanpakushitsu+kakusan+koso.+Protein%2C+nucleic+acid%2C+enzyme&rft.atitle=%5BA+ras+guanine+nucleotide+exchange+factor+and+ras-mediated+signal+transduction%5D.&rft.au=Kamata%2C+T&rft.aulast=Kamata&rft.aufirst=T&rft.date=1991-06-01&rft.volume=36&rft.issue=8&rft.spage=1497&rft.isbn=&rft.btitle=&rft.title=Tanpakushitsu+kakusan+koso.+Protein%2C+nucleic+acid%2C+enzyme&rft.issn=00399450&rft_id=info:doi/ LA - Japanese DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-09 N1 - Date created - 1991-09-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparison of amantadine and desipramine combined with psychotherapy for treatment of cocaine dependence. AN - 80717601; 1862788 AB - We conducted a single-blind, random assignment, placebo-controlled, 12-week comparison of desipramine hydrochloride and amantadine hydrochloride as adjunctive treatments to counseling for cocaine dependence. Subjects were 54 outpatients who met DSM III-R criteria for active cocaine dependence and who completed a minimum of 2 weeks of treatment. Subjects treated with fixed doses of 200 mg/day desipramine (N = 17), 400 mg/day amantadine-placebo (N = 16), and placebo (N = 21) did not differ for lifetime cocaine use, lifetime histories of psychopathology, admission scores on psychometric assessments, and sociodemographics. All treatment groups demonstrated dramatic and persistent decreases in cocaine use, craving for cocaine, and psychiatric symptoms consequent to treatment. Although there was a trend for more dropouts by subjects taking desipramine, there were no significant differences among treatment groups regarding retention in treatment, craving for cocaine, and decreased cocaine use confirmed by urine toxicology. There was a trend for subjects treated with desipramine to maintain longer periods of cocaine abstinence. Mean plasma concentration of desipramine in a subsample of our subjects was less than that recommended for treatment of depression, thus the dosage of desipramine may have been subtherapeutic. JF - The American journal of drug and alcohol abuse AU - Weddington, W W AU - Brown, B S AU - Haertzen, C A AU - Hess, J M AU - Mahaffey, J R AU - Kolar, A F AU - Jaffe, J H AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, Maryland 21224. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 137 EP - 152 VL - 17 IS - 2 SN - 0095-2990, 0095-2990 KW - Amantadine KW - BF4C9Z1J53 KW - Cocaine KW - I5Y540LHVR KW - Desipramine KW - TG537D343B KW - Index Medicus KW - Single-Blind Method KW - Dose-Response Relationship, Drug KW - Combined Modality Therapy KW - Humans KW - Adult KW - Follow-Up Studies KW - Male KW - Female KW - Amantadine -- pharmacokinetics KW - Amantadine -- administration & dosage KW - Substance-Related Disorders -- blood KW - Psychotherapy KW - Desipramine -- administration & dosage KW - Desipramine -- pharmacokinetics KW - Substance-Related Disorders -- rehabilitation KW - Substance-Related Disorders -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80717601?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+journal+of+drug+and+alcohol+abuse&rft.atitle=Comparison+of+amantadine+and+desipramine+combined+with+psychotherapy+for+treatment+of+cocaine+dependence.&rft.au=Weddington%2C+W+W%3BBrown%2C+B+S%3BHaertzen%2C+C+A%3BHess%2C+J+M%3BMahaffey%2C+J+R%3BKolar%2C+A+F%3BJaffe%2C+J+H&rft.aulast=Weddington&rft.aufirst=W&rft.date=1991-06-01&rft.volume=17&rft.issue=2&rft.spage=137&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+drug+and+alcohol+abuse&rft.issn=00952990&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-30 N1 - Date created - 1991-08-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chronic carcinogenic and toxic effects of a single subcutaneous dose of cadmium in the male Fischer rat. AN - 80700423; 1855489 AB - The carcinogenic effects of cadmium have not been thoroughly assessed in the commonly used Fischer (F344) rat. This study determined tumor incidence in various tissues of male F344/NCr rats after a single dose of cadmium. Cadmium (as CdCl2) was given sc in the dorsal thoracic midline at 30 mumole/kg to 70 8-week old male F344 rats while controls (n = 50) received saline. Rats were observed during the next 90 weeks. Early deaths (less than or equal to 32 weeks), due mostly to acute cadmium-induced hepatotoxicity, accounted for 37 of the cadmium-treated rats while no control rats died in the same period. A high incidence of injection site sarcomas (ISS) occurred in the cadmium-treated group (21 ISS/32 rats at risk; 66%) while only 1/50 occurred in controls (2%). In fact, ISS were the major cause of morbidity after 35 weeks in cadmium-treated rats. These tumors were mostly fibrosarcomas, although histiocytic and osteogenic sarcomas also occurred. Testicular interstitial cell tumors, which show a very high spontaneous incidence in this strain (41/49; 84%), were not markedly affected by cadmium (30/31; 97%). This is in sharp contrast to other strains, such as the Wistar, in which cadmium treatment is reported to cause as much as an eightfold increase in interstitial cell (Leydig cell) tumor incidence. The incidence of large granular lymphocyte (LGL) leukemia, which also occurred frequently in control F344 rats (12/47; 26%) was markedly decreased (2/31; 7%) by cadmium. Our recent studies indicate acute lymphonecrotic effects occur with cadmium in lymphoid tissues of rats, and this may be related to the suppression of the leukemia. These results indicate that cadmium is very effective in inducing ISS in F344 rats, as is the case with other strains thus far tested, and also markedly reduces spontaneous leukemia incidence. JF - Environmental research AU - Waalkes, M P AU - Rehm, S AU - Sass, B AU - Konishi, N AU - Ward, J M AD - Inorganic Carcinogenesis and Tumor Pathology Section, National Cancer Institute, Frederick Cancer Research and Development Center, Maryland 21702. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 40 EP - 50 VL - 55 IS - 1 SN - 0013-9351, 0013-9351 KW - Cadmium KW - 00BH33GNGH KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Necrosis KW - Testis -- drug effects KW - Liver -- drug effects KW - Injections, Subcutaneous KW - Spleen -- drug effects KW - Lymph Nodes -- drug effects KW - Thymus Gland -- drug effects KW - Male KW - Osteosarcoma -- chemically induced KW - Cadmium -- administration & dosage KW - Sarcoma, Experimental -- chemically induced KW - Skin Neoplasms -- chemically induced KW - Fibrosarcoma -- chemically induced KW - Cadmium -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80700423?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+research&rft.atitle=Chronic+carcinogenic+and+toxic+effects+of+a+single+subcutaneous+dose+of+cadmium+in+the+male+Fischer+rat.&rft.au=Waalkes%2C+M+P%3BRehm%2C+S%3BSass%2C+B%3BKonishi%2C+N%3BWard%2C+J+M&rft.aulast=Waalkes&rft.aufirst=M&rft.date=1991-06-01&rft.volume=55&rft.issue=1&rft.spage=40&rft.isbn=&rft.btitle=&rft.title=Environmental+research&rft.issn=00139351&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-26 N1 - Date created - 1991-08-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Perinatal carcinogenesis: current directions. AN - 80676059; 2069840 JF - British journal of cancer AU - Anderson, L M AU - Jones, A B AU - Rice, J M AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 1025 EP - 1028 VL - 63 IS - 6 SN - 0007-0920, 0007-0920 KW - Carcinogens KW - 0 KW - Index Medicus KW - Fetus KW - Animals, Newborn KW - Animals KW - Humans KW - Infant, Newborn KW - Neoplasms, Experimental -- physiopathology KW - Female KW - Pregnancy KW - Neoplasms -- etiology KW - Neoplasms -- embryology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80676059?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+cancer&rft.atitle=Perinatal+carcinogenesis%3A+current+directions.&rft.au=Anderson%2C+L+M%3BJones%2C+A+B%3BRice%2C+J+M&rft.aulast=Anderson&rft.aufirst=L&rft.date=1991-06-01&rft.volume=63&rft.issue=6&rft.spage=1025&rft.isbn=&rft.btitle=&rft.title=British+journal+of+cancer&rft.issn=00070920&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-21 N1 - Date created - 1991-08-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Principles of clinically important drug interactions with carbamazepine. Part I. AN - 80662411; 2066459 JF - Journal of clinical psychopharmacology AU - Ketter, T A AU - Post, R M AU - Worthington, K AD - Biological Psychiatry Branch, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 198 EP - 203 VL - 11 IS - 3 SN - 0271-0749, 0271-0749 KW - Analgesics KW - 0 KW - Anesthetics KW - Anti-Bacterial Agents KW - Anticoagulants KW - Anticonvulsants KW - Antidepressive Agents KW - Antineoplastic Agents KW - Immunosuppressive Agents KW - Carbamazepine KW - 33CM23913M KW - Index Medicus KW - Anticonvulsants -- pharmacology KW - Drug Interactions KW - Antidepressive Agents -- pharmacology KW - Anesthetics -- pharmacology KW - Humans KW - Anticoagulants -- pharmacology KW - Anti-Bacterial Agents -- pharmacology KW - Analgesics -- pharmacology KW - Antineoplastic Agents -- pharmacology KW - Immunosuppressive Agents -- pharmacology KW - Carbamazepine -- pharmacokinetics KW - Carbamazepine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80662411?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Principles+of+clinically+important+drug+interactions+with+carbamazepine.+Part+I.&rft.au=Ketter%2C+T+A%3BPost%2C+R+M%3BWorthington%2C+K&rft.aulast=Ketter&rft.aufirst=T&rft.date=1991-06-01&rft.volume=11&rft.issue=3&rft.spage=198&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 - 1991-08-09 N1 - Date created - 1991-08-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The role of the nurse in clinical cancer research. AN - 80647516; 2059955 AB - Although advances have been made in the treatment of a number of cancers, no standard effective treatment exists for many forms of the disease. To answer remaining questions about cancer therapy, patients are encouraged to enter clinical trials that test new therapies or combinations of therapies. These trials take place not only in cancer centers and large university hospitals, but also in community hospitals and private offices throughout the country. The nurse can be an active participant in these trials as both the patient advocate and the liaison between the patient and the physician or the nurse researcher responsible for conducting the clinical investigation. Each protocol contains specific guidelines that include eligibility requirements, detailed treatment regimens, patient evaluations, and data collection schedules. The regulatory issues or Institutional Review Board (IRB) approval, informed consent, toxicity reporting, and maintenance of accurate records for investigational drug accountability are also part of the research process. A nurse who is well informed on these issues is an asset to the successful completion of any clinical study. JF - Cancer nursing AU - Cassidy, J AU - Macfarlane, D K AD - Clinical Oncology Program, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 124 EP - 131 VL - 14 IS - 3 SN - 0162-220X, 0162-220X KW - Index Medicus KW - Nursing KW - Clinical Protocols -- standards KW - Medical Records -- standards KW - Role KW - Informed Consent KW - Medical Audit KW - Neoplasms -- drug therapy KW - Neoplasms -- nursing KW - Nurse Administrators -- methods KW - Job Description KW - Clinical Trials as Topic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80647516?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+nursing&rft.atitle=The+role+of+the+nurse+in+clinical+cancer+research.&rft.au=Cassidy%2C+J%3BMacfarlane%2C+D+K&rft.aulast=Cassidy&rft.aufirst=J&rft.date=1991-06-01&rft.volume=14&rft.issue=3&rft.spage=124&rft.isbn=&rft.btitle=&rft.title=Cancer+nursing&rft.issn=0162220X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-08 N1 - Date created - 1991-08-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Fine-structure analysis of the P1 plasmid partition site. AN - 80621646; 2050624 AB - P1 plasmid partition requires two plasmid-encoded Par proteins and a cis-acting site. The site, parS, lies in a region consisting of a 13-bp palindrome and an adjacent AT-rich sequence. A series of point mutations were analyzed for their effects on partition site activity. The results indicated that only the left arm of the palindrome and some adjacent bases were needed. The limits of the functional site were further refined to a maximum of 22 bp, which includes binding sites for the P1 ParB protein. Mutations in the 22-bp site cause concomitant defects in partition and the ability to exert partition-mediated incompatibility. Like the region immediately to the left of the 22-bp region, the right arm of the palindrome is not essential for partition but does contain information that affects the specificity of incompatibility. JF - Journal of bacteriology AU - Martin, K A AU - Davis, M A AU - Austin, S AD - Laboratory of Chromosome Biology, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland 21702-1202. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 3630 EP - 3634 VL - 173 IS - 12 SN - 0021-9193, 0021-9193 KW - parS KW - Bacterial Proteins KW - 0 KW - chromosome partition proteins, bacterial KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Base Sequence KW - Bacterial Proteins -- genetics KW - Bacterial Proteins -- metabolism KW - Molecular Sequence Data KW - Mutation KW - Binding Sites KW - Escherichia coli -- genetics KW - Plasmids UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80621646?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Fine-structure+analysis+of+the+P1+plasmid+partition+site.&rft.au=Martin%2C+K+A%3BDavis%2C+M+A%3BAustin%2C+S&rft.aulast=Martin&rft.aufirst=K&rft.date=1991-06-01&rft.volume=173&rft.issue=12&rft.spage=3630&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 - 1991-07-19 N1 - Date created - 1991-07-19 N1 - Date revised - 2017-01-13 N1 - Gene symbol - parS N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1976 Jun;73(6):1959-63 [132662] Plasmid. 1978 Sep;1(4):421-34 [372974] Genetics. 1980 May;95(1):15-38 [7000617] Cell. 1981 Sep;25(3):729-36 [7026049] J Mol Biol. 1983 Sep 15;169(2):353-72 [6312056] J Mol Biol. 1983 Sep 15;169(2):373-87 [6225875] EMBO J. 1990 Apr;9(4):991-8 [2182325] Gene. 1986;46(2-3):145-52 [3803923] Proc Natl Acad Sci U S A. 1987 Dec;84(23):8544-7 [3317415] Proc Natl Acad Sci U S A. 1988 Sep;85(18):6657-61 [2842786] Plasmid. 1988 Mar;19(2):103-12 [3420178] EMBO J. 1988 Jun;7(6):1881-8 [3049080] J Mol Biol. 1985 Sep 20;185(2):261-72 [3903163] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phorbol ester and bryostatin differentially regulate the hydrolysis of phosphatidylethanolamine in Ha-ras- and raf-oncogene-transformed NIH 3T3 cells. AN - 80612967; 2049075 AB - Previously it was reported that transformation of NIH 3T3 fibroblast by the Ha-ras, v-src, v-fms, and A-raf oncogenes decreased the stimulatory effects of phorbol 12-myristate 13-acetate (PMA; 'TPA'), an activator of protein kinase C (PKC), on the phosphorylation of an endogenous 80 kDa substrate and on 86Rb uptake [Wolfman, Wingrove, Blackshear & Macara (1987) J. Biol. Chem. 262, 16546-16552], as well as on sphingomyelin synthesis [Kiss, Rapp & Anderson (1988) FEBS Lett. 240, 221-226]. Here, we investigated how transformation affects the PMA-stimulated hydrolysis of phosphatidylethanolamine (PtdEtn), a recently characterized mechanism which may contribute to the generation of the second messengers phosphatidic acid and 1,2-diacylglycerol. The effects of PMA were compared with those of bryostatin, a non-tumour-promoter activator of PKC. Transformation of NIH 3T3 cells with Ha-ras, v-raf, or A-raf enhanced the stimulatory effect of PMA on the phospholipase D-mediated hydrolysis of PtdEtn. On the other hand, the effects of bryostatin on PtdEtn hydrolysis were only slightly increased, if at all, in cells transformed with these oncogenes. In crude membrane preparations isolated from these transformed cells, PMA, but not bryostatin, enhanced the combined stimulatory effects of ATP and the GTP analogue guanosine 5'-[gamma-thio]triphosphate on phospholipase D-mediated PtdEtn hydrolysis. The PKC inhibitor 1-(5-isoquinolinesulphonyl)-2-methylpiperazine inhibited the stimulatory effect of PMA only in intact cells. These results indicate that transformation of cells by certain oncogenes differentially affects phospholipase D-mediated hydrolysis of PtdEtn induced by PMA and bryostatin, suggesting that the action of PMA might involve two different mechanisms. JF - The Biochemical journal AU - Kiss, Z AU - Rapp, U R AU - Pettit, G R AU - Anderson, W B AD - Laboratory of Cellular Oncology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/06/01/ PY - 1991 DA - 1991 Jun 01 SP - 505 EP - 509 VL - 276 ( Pt 2) SN - 0264-6021, 0264-6021 KW - Ha-ras KW - raf KW - Antineoplastic Agents KW - 0 KW - Bryostatins KW - Lactones KW - Macrolides KW - Phosphatidylethanolamines KW - Retroviridae Proteins, Oncogenic KW - Guanosine 5'-O-(3-Thiotriphosphate) KW - 37589-80-3 KW - bryostatin 1 KW - 37O2X55Y9E KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Oncogene Proteins v-raf KW - EC 2.7.11.1 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Phospholipase D KW - EC 3.1.4.4 KW - Rubidium KW - MLT4718TJW KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Rubidium -- metabolism KW - Animals KW - Phospholipase D -- metabolism KW - Mice KW - Guanosine 5'-O-(3-Thiotriphosphate) -- pharmacology KW - Hydrolysis KW - Protein Kinase C -- metabolism KW - Mice, Inbred Strains KW - Protein-Tyrosine Kinases -- genetics KW - Kinetics KW - Cell Line KW - Adenosine Triphosphate -- pharmacology KW - Genes, ras KW - Retroviridae Proteins, Oncogenic -- genetics KW - Oncogenes KW - Phosphatidylethanolamines -- metabolism KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Antineoplastic Agents -- pharmacology KW - Cell Transformation, Neoplastic KW - Lactones -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80612967?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Phorbol+ester+and+bryostatin+differentially+regulate+the+hydrolysis+of+phosphatidylethanolamine+in+Ha-ras-+and+raf-oncogene-transformed+NIH+3T3+cells.&rft.au=Kiss%2C+Z%3BRapp%2C+U+R%3BPettit%2C+G+R%3BAnderson%2C+W+B&rft.aulast=Kiss&rft.aufirst=Z&rft.date=1991-06-01&rft.volume=276+%28+Pt+2%29&rft.issue=&rft.spage=505&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 - 1991-07-17 N1 - Date created - 1991-07-17 N1 - Date revised - 2017-01-13 N1 - Gene symbol - Ha-ras; raf N1 - SuppNotes - Cited By: J Biol Chem. 1986 Jul 5;261(19):8597-600 [3013856] Science. 1986 Jul 18;233(4761):305-12 [3014651] J Biol Chem. 1986 Dec 15;261(35):16438-45 [3465725] Nature. 1987 Jan 22-28;325(6102):359-61 [3027568] Cancer Res. 1987 Mar 1;47(5):1302-7 [3469014] Nucleic Acids Res. 1987 Jan 26;15(2):595-609 [3029685] Biochem Biophys Res Commun. 1987 Jul 15;146(1):208-15 [3038105] Carcinogenesis. 1987 Sep;8(9):1343-6 [3621472] Nature. 1987 Nov 19-25;330(6145):269-72 [3313065] J Biol Chem. 1987 Dec 5;262(34):16546-52 [3680264] Mol Cell Biol. 1987 Nov;7(11):4146-9 [3323889] Cell. 1988 Feb 12;52(3):343-54 [3345563] Cell. 1988 Feb 12;52(3):447-58 [3162207] Nature. 1988 Aug 25;334(6184):661-5 [3045562] FEBS Lett. 1988 Nov 21;240(1-2):221-6 [3191996] J Biol Chem. 1989 Jan 25;264(3):1483-7 [2912968] J Biol Chem. 1989 May 25;264(15):9069-76 [2498324] Mol Cell Biol. 1989 Jun;9(6):2641-7 [2474757] Biochem J. 1989 Oct 15;263(2):581-7 [2597122] J Biol Chem. 1990 Jan 5;265(1):1-4 [2104616] Nature. 1989 Dec 14;342(6251):807-11 [2601739] J Cell Biochem. 1990 Feb;42(2):59-70 [2407742] J Biol Chem. 1990 May 5;265(13):7345-50 [2185245] Biochem Biophys Res Commun. 1990 Sep 28;171(3):955-62 [2222456] Biochem J. 1990 Nov 1;271(3):693-700 [2123096] Biochem Pharmacol. 1975 May 1;24(9):999-1002 [168904] Eur J Biochem. 1976 Aug 16;67(2):557-61 [823017] J Virol. 1980 Jul;35(1):76-92 [6251279] J Biol Chem. 1982 Jul 10;257(13):7847-51 [7085651] Biochem Biophys Res Commun. 1982 May 31;106(2):590-5 [6809006] J Biol Chem. 1982 Nov 25;257(22):13341-8 [7142151] FEBS Lett. 1982 Nov 1;148(1):131-4 [6816631] Proc Natl Acad Sci U S A. 1983 Jul;80(14):4218-22 [6308607] Biochemistry. 1984 Oct 9;23(21):5036-41 [6238627] Cell. 1985 Oct;42(3):849-57 [2996780] Science. 1986 Jan 24;231(4736):407-10 [3001936] Proc Natl Acad Sci U S A. 1986 Mar;83(5):1334-8 [3456591] J Biol Chem. 1986 Apr 15;261(11):4978-85 [3007485] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Residual damage to hematopoietic system in mice exposed to a mixture of groundwater contaminants. AN - 80608414; 2048155 AB - To assess the potential health effects of chemically contaminated groundwater, we initiated a toxicological program on a mixture of 25 frequently-detected groundwater contaminants derived from hazardous waste disposal sites. As part of this program, myelotoxicity studies were conducted. Bone marrow parameters were examined in mice exposed to 0, 1, 5 or 10% of a simulated chemical mixture stock solution of groundwater contaminants in drinking water for 108 days. Mice treated with 5 or 10% of chemical mixture stock solution for 108 days showed suppressed marrow granulocyte macrophage progenitors (CFU-GM); however, this suppression disappeared in 10 weeks following the cessation of treatment. The possible toxicological interaction of groundwater contaminants and radiation on hematopoiesis was investigated by using the number of bone marrow CFU-GM as an index. When mice were exposed to 200 rads whole body irradiation at 2 and 9 weeks during this 10-week recovery period, the combined treatment (i.e., chemical mixture followed by irradiation) group showed a significantly slower recovery of bone marrow progenitors as compared with the control group (i.e., radiation but without prior chemical mixture treatment). This study showed that even 10 weeks after the cessation of chemical mixture treatment when all hematological parameters were normal, a residual effect of the chemical mixture may still be demonstrated as lower progenitor cell numbers following irradiation. Thus, residual damage of hematopoiesis in mice exposed to groundwater contaminants for 108 days renders the mice more sensitive to subsequent irradiation-induced injury. JF - Toxicology letters AU - Hong, H L AU - Yang, R S AU - Boorman, G A AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 101 EP - 111 VL - 57 IS - 1 SN - 0378-4274, 0378-4274 KW - Hazardous Waste KW - 0 KW - Water Pollutants KW - Index Medicus KW - Animals KW - Whole-Body Irradiation KW - Body Weight -- drug effects KW - Mice, Inbred C57BL KW - Refuse Disposal KW - Mice KW - Female KW - Blood Cell Count KW - Organ Size -- drug effects KW - Hematopoietic Stem Cells -- drug effects KW - Water Pollutants -- toxicity KW - Water Pollutants -- analysis KW - Fresh Water -- chemistry KW - Hematopoietic System -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80608414?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+letters&rft.atitle=Residual+damage+to+hematopoietic+system+in+mice+exposed+to+a+mixture+of+groundwater+contaminants.&rft.au=Hong%2C+H+L%3BYang%2C+R+S%3BBoorman%2C+G+A&rft.aulast=Hong&rft.aufirst=H&rft.date=1991-06-01&rft.volume=57&rft.issue=1&rft.spage=101&rft.isbn=&rft.btitle=&rft.title=Toxicology+letters&rft.issn=03784274&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-18 N1 - Date created - 1991-07-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The antiproliferative and antimetastatic compound L651582 inhibits muscarinic acetylcholine receptor-stimulated calcium influx and arachidonic acid release. AN - 80603872; 1646332 AB - L651582, a carboxyamide-amino-imidazole, was shown previously to have antiproliferative and antimetastatic properties at low micromolar concentrations; yet little is known about its cellular mechanism(s) of action. L651582 was tested for its ability to block receptor-stimulated calcium influx, arachidonic acid release, inositol phosphate and cyclic AMP (cAMP) generation. These signal transduction pathways are activated by muscarinic receptors transfected and expressed in Chinese hamster ovary cells. L651582 blocked muscarinic m5 receptor-stimulated 45Ca++ influx and release of arachidonic acid at low micromolar concentrations. Muscarinic receptor-stimulated release of arachidonic acid was shown previously to be dependent on calcium influx and not intracellular calcium release suggesting L651582 may be useful as calcium channel blocker. At low micromolar concentrations, L651582 had little effect on muscarinic m5 receptor-stimulated release of inositol phosphates or cAMP accumulation. Moreover, L651582 had little effect on muscarinic m2 receptor-mediated inhibition of forskolin-stimulated cAMP accumulation. Above 10 microM, L651582 inhibited all second messenger pathways tested and inhibited cell growth, suggesting its action may be less specific and toxic at these concentrations. JF - The Journal of pharmacology and experimental therapeutics AU - Felder, C C AU - Ma, A L AU - Liotta, L A AU - Kohn, E C AD - Laboratory of Cell Biology, National Institute of Mental Health, Bethesda, Maryland. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 967 EP - 971 VL - 257 IS - 3 SN - 0022-3565, 0022-3565 KW - Antineoplastic Agents KW - 0 KW - Arachidonic Acids KW - Inositol Phosphates KW - Receptors, Muscarinic KW - Triazoles KW - Arachidonic Acid KW - 27YG812J1I KW - Aminoimidazole Carboxamide KW - 360-97-4 KW - Carbachol KW - 8Y164V895Y KW - carboxyamido-triazole KW - 99519-84-3 KW - Cyclic AMP KW - E0399OZS9N KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Cyclic AMP -- biosynthesis KW - Animals KW - Inositol Phosphates -- biosynthesis KW - Transfection KW - Kinetics KW - Cell Division -- drug effects KW - Carbachol -- pharmacology KW - Cell Line KW - Calcium -- metabolism KW - Aminoimidazole Carboxamide -- pharmacology KW - Aminoimidazole Carboxamide -- analogs & derivatives KW - Arachidonic Acids -- metabolism KW - Receptors, Muscarinic -- physiology KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80603872?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+antiproliferative+and+antimetastatic+compound+L651582+inhibits+muscarinic+acetylcholine+receptor-stimulated+calcium+influx+and+arachidonic+acid+release.&rft.au=Felder%2C+C+C%3BMa%2C+A+L%3BLiotta%2C+L+A%3BKohn%2C+E+C&rft.aulast=Felder&rft.aufirst=C&rft.date=1991-06-01&rft.volume=257&rft.issue=3&rft.spage=967&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 - 1991-07-12 N1 - Date created - 1991-07-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Endothelin- and sarafotoxin-induced phosphoinositide hydrolysis in cultured cerebellar granule cells: biochemical and pharmacological characterization. AN - 80601434; 1646318 AB - Endothelin (ET)-1, -2, -3, big ET-1 and sarafotoxin S6b (S6b) dose-dependently increased phosphoinositide (PI) hydrolysis by 6- to 10-fold in cultured cerebellar granule cells prelabeled with [3H] myoinositol. The PI response elicited by ET-1 was dependent on the presence of extracellular Ca++, but was not reduced by organic (nisoldipine, nimodipine) or inorganic (Co++, Mn++) calcium channel blockers. Pretreatment of granule cells with tetrodotoxin or amiloride failed to affect the response to ET-1. Extracellular sodium depletion resulted in a marked increase in basal PI turnover; however, the net increase of PI turnover induced by ET-1 was unchanged. ET-induced PI breakdown could be partially inhibited by short or long term treatment with phorbol dibutyrate but was unaffected by pertussis toxin. ET- and S6b-induced PI turnover were dependent on the culturing time of granule cells, with the maximal response in a 4-day culture. The ET- and S6b-induced PI turnover appeared to be additive to that induced by carbachol, histamine, norepinephrine, serotonin, glutamate and maitotoxin. However, the responses induced by ET and S6b were nonadditive. Prestimulation of cells with ET or S6b for 30 sec to 24 hr resulted in dramatic loss of the ability of ET and S6b to stimulate PI hydrolysis, without affecting subsequent responsiveness induced by other stimuli, indicating homologous desensitization for ET- and S6b-induced responses. Moreover, our results further support the notion that ET and S6b act on the same population of receptors in cerebellar granule cells. JF - The Journal of pharmacology and experimental therapeutics AU - Lin, W W AU - Lee, C Y AU - Chuang, D M AD - Unit on Molecular Neurobiology, Biological Psychiatry Branch, NIMH, Bethesda, Maryland. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 1053 EP - 1061 VL - 257 IS - 3 SN - 0022-3565, 0022-3565 KW - Endothelins KW - 0 KW - Phosphatidylinositols KW - Receptors, Cell Surface KW - Receptors, Endothelin KW - Vasoconstrictor Agents KW - Viper Venoms KW - Virulence Factors, Bordetella KW - sarafotoxins s6 KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Sodium KW - 9NEZ333N27 KW - Pertussis Toxin KW - EC 2.4.2.31 KW - Type C Phospholipases KW - EC 3.1.4.- KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Receptors, Cell Surface -- antagonists & inhibitors KW - Calcium -- pharmacology KW - Hydrolysis KW - Phorbol 12,13-Dibutyrate -- pharmacology KW - Sodium -- pharmacology KW - Type C Phospholipases -- metabolism KW - Rats KW - Rats, Inbred Strains KW - Virulence Factors, Bordetella -- pharmacology KW - Cells, Cultured KW - Phosphatidylinositols -- metabolism KW - Endothelins -- pharmacology KW - Vasoconstrictor Agents -- pharmacology KW - Cerebellum -- cytology KW - Viper Venoms -- pharmacology KW - Cerebellum -- drug effects KW - Cerebellum -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80601434?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Endothelin-+and+sarafotoxin-induced+phosphoinositide+hydrolysis+in+cultured+cerebellar+granule+cells%3A+biochemical+and+pharmacological+characterization.&rft.au=Lin%2C+W+W%3BLee%2C+C+Y%3BChuang%2C+D+M&rft.aulast=Lin&rft.aufirst=W&rft.date=1991-06-01&rft.volume=257&rft.issue=3&rft.spage=1053&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 - 1991-07-12 N1 - Date created - 1991-07-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Identification of (+) and (-) anti benzo[a]pyrene dihydrodiol epoxide-nucleic acid adducts by the 32P-postlabeling assay. AN - 80600127; 1904321 AB - Purine deoxyribonucleoside 3'-phosphates were reacted with the (+)- and (-)-enantiomers of the anti dihydrodiol epoxide of benzo[a]pyrene. Products from cis and trans opening of the epoxide ring were separated by HPLC and they were identified by comparison of their CD spectra with those known for the corresponding nucleoside adducts. Thereafter, the eight known benzo[a]pyrene-purine deoxyribonucleoside-3'-phosphate adducts were postlabeled with [32P]ATP and T4 kinase and the positions of these individual bisphosphates were mapped by TLC. Though all eight adducts migrated to the same general region of the thin layer plates, the four possible adducts from each enantiomeric dihydrodiol epoxide were resolved. JF - Carcinogenesis AU - Canella, K AU - Peltonen, K AU - Dipple, A AD - Chemistry of Carcinogenesis Laboratory, NCI-Frederick Cancer Research and Development Center, MD 21702-1201. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 1109 EP - 1114 VL - 12 IS - 6 SN - 0143-3334, 0143-3334 KW - Phosphorus Radioisotopes KW - 0 KW - 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide KW - 55097-80-8 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Stereoisomerism KW - Spectrophotometry, Ultraviolet KW - Circular Dichroism KW - Chromatography, High Pressure Liquid KW - 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide -- metabolism KW - DNA -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80600127?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Identification+of+%28%2B%29+and+%28-%29+anti+benzo%5Ba%5Dpyrene+dihydrodiol+epoxide-nucleic+acid+adducts+by+the+32P-postlabeling+assay.&rft.au=Canella%2C+K%3BPeltonen%2C+K%3BDipple%2C+A&rft.aulast=Canella&rft.aufirst=K&rft.date=1991-06-01&rft.volume=12&rft.issue=6&rft.spage=1109&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-12 N1 - Date created - 1991-07-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Tumor necrosis factor and interleukin-1 protection against the lethal effects of tumor necrosis factor. AN - 80599032; 2042087 AB - Based on the hypothesis that tumor necrosis factor (TNF) causes the lethality of gram-negative sepsis and previous work of tolerance to the lethal effects of TNF induced by repetitive exposure to sublethal intraperitoneal doses of human recombinant (r) TNF, we studied the protective role of a single sublethal intravenous dose of either rTNF (100 micrograms/kg) or recombinant interleukin-1 (rIL-1; 10(5) units/kg) or both before a subsequent lethal intravenous dose of rTNF (800 to 1000 micrograms/kg) in C3H/HEN mice. Mice were treated with a single intravenous dose of saline, rTNF, rIL-1 or both cytokines and challenged within 2 hours to 10 days with a lethal dose of rTNF. Mice treated with rTNF showed significant protection against the lethal effects of TNF when the treatment dose was given only 2 hours before the lethal dose, but maximal protection required a 24-hour interval and lasted as long as 8 days. The treatment dose of rTNF was toxic, and it resulted in occasional treatment deaths. Mice treated with rIL-1 showed maximal protection when treatment was given only 2 hours before challenge and protection lasted for 8 days. No toxicity was apparent secondary to IL-1 treatment. The combination of rIL-1 and rTNF was not as effective as either cytokine alone. The results suggest that rTNF or rIL-1 may be clinically useful in the prevention and treatment of sepsis lethality by the induction of tolerance to the lethal effects of TNF. The more promising cytokine appears to be rIL-1 because it has less toxicity and more rapid induction of full therapeutic effectiveness. JF - Surgery AU - Sheppard, B C AU - Norton, J A AD - Surgical Metabolism Section, National Cancer Institute, National Institutes of Health, Bethesda, Md. 20892. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 698 EP - 705 VL - 109 IS - 6 SN - 0039-6060, 0039-6060 KW - Interleukin-1 KW - 0 KW - Recombinant Proteins KW - Tumor Necrosis Factor-alpha KW - Abridged Index Medicus KW - Index Medicus KW - Recombinant Proteins -- toxicity KW - Animals KW - Recombinant Proteins -- pharmacology KW - Dose-Response Relationship, Drug KW - Mice, Inbred C3H KW - Mice KW - Time Factors KW - Female KW - Tumor Necrosis Factor-alpha -- toxicity KW - Interleukin-1 -- pharmacology KW - Tumor Necrosis Factor-alpha -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80599032?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Surgery&rft.atitle=Tumor+necrosis+factor+and+interleukin-1+protection+against+the+lethal+effects+of+tumor+necrosis+factor.&rft.au=Sheppard%2C+B+C%3BNorton%2C+J+A&rft.aulast=Sheppard&rft.aufirst=B&rft.date=1991-06-01&rft.volume=109&rft.issue=6&rft.spage=698&rft.isbn=&rft.btitle=&rft.title=Surgery&rft.issn=00396060&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-08 N1 - Date created - 1991-07-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A comparison of interfollicular and hair follicle derived cells as targets for the v-rasHa oncogene in mouse skin carcinogenesis. AN - 80597256; 2044193 AB - Methods to isolate and culture intact mouse hair follicles and interfollicular epidermal cells provide a model to test the potential of each to form tumors as a consequence of rasHa gene activation and to determine the risk for progression in the resultant tumors. The v-rasHa oncogene was introduced into intact or dissociated hair follicle cells or interfollicular epidermal cells from newborn mouse skin via a defective retroviral vector. Either immediately after infection or after an additional 6 days of culture, the v-rasHa cells were transferred to nude mice as a skin graft. Both cell populations formed squamous papillomas which were indistinguishable based on morphology and immunocytochemistry. All papillomas expressed epidermal specific markers whether derived from hair follicle or interfollicular cells, and many regressed. After 16 weeks in vivo, 20-30% of the benign skin tumors in all groups converted to malignancy. In addition to papillomas, hair follicle derived populations produced hemangiomas in many animals. None of the groups formed basal cell carcinomas, keratoacanthomas or tumors with characteristics of differentiating hair follicle cells. These studies indicate that ras gene activation can contribute to benign squamous neoplasia originating from several skin-derived cell types. The underlying factors which determine the variable risk for neoplastic progression of skin papillomas after ras gene activation is not simply the origin of the tumor cell from hair follicle or interfollicular epidermis. The activated ras oncogene can also transform skin endothelial cells but does not appear to directly contribute to transformation of the more differentiated cells of the hair follicle. JF - Carcinogenesis AU - Weinberg, W C AU - Morgan, D L AU - George, C AU - Yuspa, S H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 1119 EP - 1124 VL - 12 IS - 6 SN - 0143-3334, 0143-3334 KW - v-raHa KW - Index Medicus KW - Animals KW - Papilloma -- etiology KW - Mice KW - Gene Expression Regulation KW - Mice, Inbred BALB C KW - Transcriptional Activation KW - Genes, ras KW - Skin Neoplasms -- etiology KW - Skin -- pathology KW - Skin Neoplasms -- pathology KW - Hair -- pathology KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80597256?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+comparison+of+interfollicular+and+hair+follicle+derived+cells+as+targets+for+the+v-rasHa+oncogene+in+mouse+skin+carcinogenesis.&rft.au=Weinberg%2C+W+C%3BMorgan%2C+D+L%3BGeorge%2C+C%3BYuspa%2C+S+H&rft.aulast=Weinberg&rft.aufirst=W&rft.date=1991-06-01&rft.volume=12&rft.issue=6&rft.spage=1119&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-12 N1 - Date created - 1991-07-12 N1 - Date revised - 2017-01-13 N1 - Gene symbol - v-raHa N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pilocarpine treatment of salivary gland hypofunction and dry mouth (xerostomia). AN - 80596207; 2043017 AB - We studied the effects of pilocarpine hydrochloride, a para-sympathomimetic agent, on major salivary gland output and subjective responses in 31 patients with salivary hypofunction. Pilocarpine hydrochloride (5-mg capsules, three times daily) was given for 5 months and a placebo was randomly assigned for 1 month in a double-blind fashion. Objective measurements of major salivary gland output, subjective impressions of oral moisture, treatment-related side effects, and a number of physiologic measures were assessed monthly. Pilocarpine significantly increased salivary output in 21 of the 31 patients. Subjective improvement in the feeling of oral dryness, speaking, chewing, and swallowing were reported by 27 individuals. Side effects, while common, generally were mild and tolerable. There were no significant alterations in cardiovascular or other physiologic measures. We conclude that pilocarpine is an effective and safe treatment for salivary gland hypofunction and xerostomia in selected patients. The increase in major gland output provides beneficial natural secretions and relief of oral dryness. JF - Archives of internal medicine AU - Fox, P C AU - Atkinson, J C AU - Macynski, A A AU - Wolff, A AU - Kung, D S AU - Valdez, I H AU - Jackson, W AU - Delapenha, R A AU - Shiroky, J AU - Baum, B J AD - Clinical Investigations and Patient Care Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 1149 EP - 1152 VL - 151 IS - 6 SN - 0003-9926, 0003-9926 KW - Pilocarpine KW - 01MI4Q9DI3 KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Submandibular Gland -- drug effects KW - Aged KW - Monitoring, Physiologic KW - Heart Rate -- drug effects KW - Parotid Gland -- drug effects KW - Electrocardiography KW - Adult KW - Middle Aged KW - Blood Pressure -- drug effects KW - Adolescent KW - Female KW - Male KW - Salivation -- drug effects KW - Xerostomia -- drug therapy KW - Pilocarpine -- pharmacology KW - Pilocarpine -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80596207?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+internal+medicine&rft.atitle=Pilocarpine+treatment+of+salivary+gland+hypofunction+and+dry+mouth+%28xerostomia%29.&rft.au=Fox%2C+P+C%3BAtkinson%2C+J+C%3BMacynski%2C+A+A%3BWolff%2C+A%3BKung%2C+D+S%3BValdez%2C+I+H%3BJackson%2C+W%3BDelapenha%2C+R+A%3BShiroky%2C+J%3BBaum%2C+B+J&rft.aulast=Fox&rft.aufirst=P&rft.date=1991-06-01&rft.volume=151&rft.issue=6&rft.spage=1149&rft.isbn=&rft.btitle=&rft.title=Archives+of+internal+medicine&rft.issn=00039926&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-11 N1 - Date created - 1991-07-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Coronary vasoconstriction induced by vasopressin. Production of myocardial ischemia in dogs by constriction of nondiseased small vessels. AN - 80583488; 1904014 AB - We studied the effect of intracoronary administration of arginine-8-vasopressin on blood flow in nondiseased coronary arteries and determined whether this vasoconstriction was severe enough to produce ischemia in 30 dogs. In group 1 (n = 6), after vasopressin administration coronary blood flow was decreased by 41% (p less than 0.002) without changes in heart rate or aortic pressure, and left ventricular ejection fraction measured by radionuclide angiocardiography was decreased by 18% (p less than 0.0005). In group 2 (n = 6), ischemia was confirmed by measurement of transmural pH changes. Administration of vasopressin decreased subendocardial pH of the infused zone from 7.40 +/- 0.03 to 7.31 +/- 0.07 (p less than 0.01). The subendocardial pH of the zone not infused with vasopressin did not change. To overcome the intrinsic regulation of blood flow, operating primarily in small coronary arteries, we hypothesized that vasopressin must increase resistance primarily in large rather than small coronary arteries. After intracoronary infusion in group 3 (n = 6), however, most (94%) of the increase in resistance during vasopressin administration was explained by an increase of resistance in small coronary arteries. In group 4 (n = 9), vasopressin decreased coronary blood flow by 50% and decreased local shortening by 90% at a time when systemic hemodynamics were unchanged. Coronary constriction induced by vasopressin, or the recovery from it, also was not altered by cyclooxygenase blockade. Thus, vasopressin produces myocardial ischemia by constricting small, nondiseased coronary arteries severely enough to overcome the competition from normal coronary regulation, and this ischemic event is not mediated by prostaglandin products. JF - Circulation AU - Maturi, M F AU - Martin, S E AU - Markle, D AU - Maxwell, M AU - Burruss, C R AU - Speir, E AU - Greene, R AU - Ro, Y M AU - Vitale, D AU - Green, M V AD - Experimental Physiology and Pharmacology Section, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 2111 EP - 2121 VL - 83 IS - 6 SN - 0009-7322, 0009-7322 KW - Cyclooxygenase Inhibitors KW - 0 KW - Arginine Vasopressin KW - 113-79-1 KW - Abridged Index Medicus KW - Index Medicus KW - Ventricular Function, Left -- drug effects KW - Hemodynamics -- drug effects KW - Animals KW - Hydrogen-Ion Concentration KW - Dogs KW - Myocardium -- metabolism KW - Male KW - Female KW - Arginine Vasopressin -- pharmacology KW - Coronary Disease -- metabolism KW - Coronary Disease -- chemically induced KW - Vasoconstriction KW - Coronary Circulation -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80583488?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Coronary+vasoconstriction+induced+by+vasopressin.+Production+of+myocardial+ischemia+in+dogs+by+constriction+of+nondiseased+small+vessels.&rft.au=Maturi%2C+M+F%3BMartin%2C+S+E%3BMarkle%2C+D%3BMaxwell%2C+M%3BBurruss%2C+C+R%3BSpeir%2C+E%3BGreene%2C+R%3BRo%2C+Y+M%3BVitale%2C+D%3BGreen%2C+M+V&rft.aulast=Maturi&rft.aufirst=M&rft.date=1991-06-01&rft.volume=83&rft.issue=6&rft.spage=2111&rft.isbn=&rft.btitle=&rft.title=Circulation&rft.issn=00097322&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-08 N1 - Date created - 1991-07-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Increased endotoxin sensitivity following T-2 toxin treatment is associated with increased absorption of endotoxin. AN - 80581074; 2038749 AB - Oral exposure to T-2 Toxin (T-2) in experimental animals results in a syndrome similar to that observed in endotoxemia. Endotoxins are lipopolysaccharide, outer-membrane components of gram-negative bacteria which induce acute, inflammatory responses. In the present study, several aspects of endotoxin pathophysiology were investigated in mice following simultaneous exposure to T-2 and endotoxin, including mortality, hypothermia, tumor necrosis factor-alpha (TNF-alpha) and corticosterone production, and thymic weight. The disposition of endotoxin was also assessed, Acute, simultaneous exposure to T-2 (4 mg/kg, po) and endotoxin (3 micrograms/mouse, ip) resulted in increased mortality, hypothermia, TNF-alpha production, and thymic atrophy compared to treatment with either T-2 of endotoxin alone. Pretreatment of mice with endotoxin, a regime that renders the animals resistant to the effects of endotoxin, reduced many endotoxin effects in animals treated simultaneously with T-2 and endotoxin. Upon further investigation, it was observed that T-2 increased the absorption rate of endotoxin: as the peak height of serum endotoxin increased, the time-to-peak decreased, and the area under the curve was unchanged in animals treated simultaneously with T-2 and endotoxin. It was concluded that increased endotoxin absorption accounted for the increases in mortality, hypothermia, and TNF-alpha associated with T-2 exposure. JF - Toxicology and applied pharmacology AU - Taylor, M J AU - Lafarge-Frayssinet, C AU - Luster, M I AU - Frayssinet, C AD - National Institute of Environmental Health Sciences, Immunotoxicology Group, Research Triangle Park, North Carolina 27709. Y1 - 1991/06/01/ PY - 1991 DA - 1991 Jun 01 SP - 51 EP - 59 VL - 109 IS - 1 SN - 0041-008X, 0041-008X KW - Endotoxins KW - 0 KW - Tumor Necrosis Factor-alpha KW - T-2 Toxin KW - I3FL5NM3MO KW - Corticosterone KW - W980KJ009P KW - Index Medicus KW - Animals KW - Drug Interactions KW - Body Temperature -- drug effects KW - Corticosterone -- blood KW - Mice KW - Tumor Necrosis Factor-alpha -- metabolism KW - Male KW - Endotoxins -- pharmacokinetics KW - T-2 Toxin -- toxicity KW - Endotoxins -- toxicity KW - Endotoxins -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80581074?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Increased+endotoxin+sensitivity+following+T-2+toxin+treatment+is+associated+with+increased+absorption+of+endotoxin.&rft.au=Taylor%2C+M+J%3BLafarge-Frayssinet%2C+C%3BLuster%2C+M+I%3BFrayssinet%2C+C&rft.aulast=Taylor&rft.aufirst=M&rft.date=1991-06-01&rft.volume=109&rft.issue=1&rft.spage=51&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 - 1991-07-01 N1 - Date created - 1991-07-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Intelligence at six years in relation to neonatal bilirubin levels: follow-up of the National Institute of Child Health and Human Development Clinical Trial of Phototherapy. AN - 80575385; 2034482 AB - Results of the National Institute of Child Health and Human Development Randomized Controlled Trial of Phototherapy were examined for the relationship of neonatal bilirubin level to neurological and developmental outcome at 6-year follow-up. This analysis focused on 224 control children with birth weight of less than 2000 g. Bilirubin levels were maintained below previously specified levels by the use of exchange transfusion only (24%). Rates of cerebral palsy were not significantly higher for children with elevated maximum bilirubin level than for those whose level remained low. No association was evident between maximum bilirubin level and IQ (Full Scale, Verbal, or Performance) by simple correlation analysis (r = -.087, P = .2 for Full Scale) or by multiple linear regression adjusting for factors that covary with IQ (beta = -.15, P = .58). IQ was not associated with mean bilirubin level, time and duration of exposure to bilirubin, or measures of bilirubin-albumin binding. Thus, over the range of bilirubin levels permitted in this clinical trial, there was no evidence of bilirubin toxicity to the central nervous system. Measures used to control the level of bilirubin in low birth weight neonates appear to prevent effectively the risk of bilirubin-induced neurotoxicity. JF - Pediatrics AU - Scheidt, P C AU - Graubard, B I AU - Nelson, K B AU - Hirtz, D G AU - Hoffman, H J AU - Gartner, L M AU - Bryla, D A AD - Human Learning and Behavior Branch, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 797 EP - 805 VL - 87 IS - 6 SN - 0031-4005, 0031-4005 KW - Bilirubin KW - RFM9X3LJ49 KW - Abridged Index Medicus KW - Index Medicus KW - Wechsler Scales KW - Birth Weight KW - Humans KW - Infant, Newborn KW - Follow-Up Studies KW - Child KW - Bilirubin -- blood KW - Cerebral Palsy -- etiology KW - Jaundice, Neonatal -- blood KW - Intelligence KW - Jaundice, Neonatal -- complications KW - Jaundice, Neonatal -- therapy KW - Phototherapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80575385?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pediatrics&rft.atitle=Intelligence+at+six+years+in+relation+to+neonatal+bilirubin+levels%3A+follow-up+of+the+National+Institute+of+Child+Health+and+Human+Development+Clinical+Trial+of+Phototherapy.&rft.au=Scheidt%2C+P+C%3BGraubard%2C+B+I%3BNelson%2C+K+B%3BHirtz%2C+D+G%3BHoffman%2C+H+J%3BGartner%2C+L+M%3BBryla%2C+D+A&rft.aulast=Scheidt&rft.aufirst=P&rft.date=1991-06-01&rft.volume=87&rft.issue=6&rft.spage=797&rft.isbn=&rft.btitle=&rft.title=Pediatrics&rft.issn=00314005&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-06-25 N1 - Date created - 1991-06-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Radiation therapy versus combination chemotherapy in the treatment of early-stage Hodgkin's disease: seven-year results of a prospective randomized trial. AN - 80572826; 2033427 AB - The study population included 136 patients with stage IA, IB, IIA, IIB, or IIIA1 Hodgkin's disease. The median follow-up is 7.5 years. Among the 30 patients with peripheral IA disease, all patients achieved a complete response (CR) with radiation therapy, and no patient has relapsed. Patients of other stages were randomized to receive radiation therapy or mechlorethamine, vincristine, procarbazine, and prednisone (MOPP). Among the 51 patients randomized to receive radiation therapy, 49 (96%) achieved complete remission, 17 (35%) have relapsed, and 10 (20%) have died. Fifty-two of the 54 (96%) assessable patients randomized to receive MOPP obtained CRs, seven (13%) have relapsed, and four (7%) have died. The projected 10-year disease-free survival of patients randomized to receive radiation therapy is 60%; for those randomized to receive MOPP, it is 86% (P2 = .009 in favor of MOPP). The projected 10-year overall survival for patients randomized to radiation therapy is 76%, and for MOPP-treated patients it is 92% (P2 = .051 in favor of MOPP). When the randomized patients with massive mediastinal disease or stage IIIA1 disease were excluded from the analysis, the disease-free (67% for radiation v 82% for MOPP) and overall survival (85% for radiation v 90% for MOPP) were not significantly different between the two arms. Subset analysis showed significant superiority of MOPP in the treatment of the following patient groups: stage IIIA1 or massive mediastinal disease, no B symptoms, initial erythrocyte sedimentation rate greater than 20 mm, four or more sites of disease, and younger than age 40 years. Preliminary analysis of this ongoing study shows that MOPP chemotherapy is at least as effective as radiation therapy in the treatment of the specific groups of early-stage Hodgkin's disease patients randomized. The final assessment of these two diverse treatment options will depend largely on the long-term survival and the incidence of early- and late-treatment complications for which patients are continuing to be observed. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Longo, D L AU - Glatstein, E AU - Duffey, P L AU - Young, R C AU - Hubbard, S M AU - Urba, W J AU - Wesley, M N AU - Raubitschek, A AU - Jaffe, E S AU - Wiernik, P H AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, MD. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 906 EP - 917 VL - 9 IS - 6 SN - 0732-183X, 0732-183X KW - Procarbazine KW - 35S93Y190K KW - Mechlorethamine KW - 50D9XSG0VR KW - Vincristine KW - 5J49Q6B70F KW - Prednisone KW - VB0R961HZT KW - Index Medicus KW - Mechlorethamine -- administration & dosage KW - Neoplasm Staging KW - Humans KW - Vincristine -- administration & dosage KW - Aged KW - Procarbazine -- administration & dosage KW - Prospective Studies KW - Survival Rate KW - Adult KW - Infertility -- chemically induced KW - Follow-Up Studies KW - Middle Aged KW - Adolescent KW - Female KW - Male KW - Prednisone -- administration & dosage KW - Hodgkin Disease -- radiotherapy KW - Hodgkin Disease -- pathology KW - Hodgkin Disease -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Hodgkin Disease -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80572826?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Radiation+therapy+versus+combination+chemotherapy+in+the+treatment+of+early-stage+Hodgkin%27s+disease%3A+seven-year+results+of+a+prospective+randomized+trial.&rft.au=Longo%2C+D+L%3BGlatstein%2C+E%3BDuffey%2C+P+L%3BYoung%2C+R+C%3BHubbard%2C+S+M%3BUrba%2C+W+J%3BWesley%2C+M+N%3BRaubitschek%2C+A%3BJaffe%2C+E+S%3BWiernik%2C+P+H&rft.aulast=Longo&rft.aufirst=D&rft.date=1991-06-01&rft.volume=9&rft.issue=6&rft.spage=906&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 - 1991-06-26 N1 - Date created - 1991-06-26 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: J Clin Oncol. 1991 Jun;9(6):897-901 [2033425] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The juxtamembrane regions of the epidermal growth factor receptor and gp185erbB-2 determine the specificity of signal transduction. AN - 80572024; 1674818 AB - The epidermal growth factor receptor (EGFR) and gp185erbB-2 are closely related tyrosine kinases. Despite extensive sequence and structural homology, these two receptors display quantitative and qualitative differences in their ability to couple with mitogenic signalling pathways. By using chimeric molecules between EGFR and erbB-2, we found that the determinants responsible for the specificity of mitogenic signal transduction are located in the amino-terminal half of the tyrosine kinase domain of either receptor. In the EGFR, mutational analysis within this subdomain revealed that deletion of residues 660 to 667 impaired receptor mitogenic activity without affecting its tyrosine kinase properties. This sequence is therefore likely to contribute to the specificity of substrate recognition by the EGFR kinase. JF - Molecular and cellular biology AU - Segatto, O AU - Lonardo, F AU - Wexler, D AU - Fazioli, F AU - Pierce, J H AU - Bottaro, D P AU - White, M F AU - Di Fiore, P P AD - Laboratory of Molecular and Cellular Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 3191 EP - 3202 VL - 11 IS - 6 SN - 0270-7306, 0270-7306 KW - Proto-Oncogene Proteins KW - 0 KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Receptor, Epidermal Growth Factor KW - Receptor, ErbB-2 KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Genetic Variation KW - Animals KW - Transfection KW - Genetic Vectors KW - Molecular Sequence Data KW - Mice KW - Amino Acid Sequence KW - Cell Membrane -- physiology KW - Cell Line KW - Cell Division KW - Receptor, Epidermal Growth Factor -- genetics KW - Receptor, Epidermal Growth Factor -- physiology KW - Proto-Oncogene Proteins -- genetics KW - Signal Transduction KW - Proto-Oncogene Proteins -- physiology KW - Protein-Tyrosine Kinases -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80572024?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+juxtamembrane+regions+of+the+epidermal+growth+factor+receptor+and+gp185erbB-2+determine+the+specificity+of+signal+transduction.&rft.au=Segatto%2C+O%3BLonardo%2C+F%3BWexler%2C+D%3BFazioli%2C+F%3BPierce%2C+J+H%3BBottaro%2C+D+P%3BWhite%2C+M+F%3BDi+Fiore%2C+P+P&rft.aulast=Segatto&rft.aufirst=O&rft.date=1991-06-01&rft.volume=11&rft.issue=6&rft.spage=3191&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 - 1991-07-03 N1 - Date created - 1991-07-03 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nature. 1984 Oct 4-10;311(5985):483-5 [6090945] Science. 1985 Dec 6;230(4730):1132-9 [2999974] Proc Natl Acad Sci U S A. 1985 Jan;82(2):488-92 [3881765] Cell. 1990 Apr 6;61(1):125-33 [2156626] J Biol Chem. 1990 Jan 25;265(3):1750-4 [1688559] Science. 1990 Apr 6;248(4951):79-83 [2181668] Science. 1990 Mar 30;247(4950):1578-81 [2157284] Cell. 1990 Apr 20;61(2):203-12 [2158859] Mol Cell Biol. 1990 Jun;10(6):2749-56 [2188097] J Biol Chem. 1990 Feb 25;265(6):3407-16 [2105948] Nature. 1984 May 31-Jun 6;309(5967):418-25 [6328312] Proc Natl Acad Sci U S A. 1981 Apr;78(4):2072-6 [7017722] Proc Natl Acad Sci U S A. 1977 Sep;74(9):3918-21 [302945] Cell. 1977 May;11(1):223-32 [194704] J Virol. 1969 Nov;4(5):549-53 [4311790] Virology. 1973 Apr;52(2):456-67 [4705382] New Biol. 1990 Feb;2(2):187-95 [1982072] J Biol Chem. 1991 Jan 5;266(1):637-44 [1845983] Mol Cell Biol. 1991 Apr;11(4):2040-8 [1672440] Mol Cell Biol. 1988 Dec;8(12):5570-4 [2907606] Cell. 1989 Jun 30;57(7):1109-22 [2472219] Cell. 1989 Jun 30;57(7):1101-7 [2472218] Science. 1989 Mar 24;243(4898):1564-70 [2538922] Cell. 1989 Oct 6;59(1):33-43 [2790960] Cell. 1989 Aug 25;58(4):649-57 [2475255] Mol Cell Biol. 1989 Jul;9(7):2934-43 [2550789] Nature. 1989 Dec 7;342(6250):699-702 [2556641] EMBO J. 1989 Nov;8(11):3345-50 [2555162] Mol Cell Biol. 1988 Sep;8(9):3969-73 [2464744] Proc Natl Acad Sci U S A. 1989 Mar;86(5):1568-72 [2466293] Science. 1987 Jul 10;237(4811):178-82 [2885917] Annu Rev Biochem. 1987;56:881-914 [3039909] Science. 1988 Feb 5;239(4840):628-31 [3257584] Cell. 1987 Dec 24;51(6):1063-70 [3500791] Annu Rev Biochem. 1988;57:443-78 [3052279] Cell. 1988 Aug 26;54(5):641-9 [2842060] Mol Cell Biol. 1988 Jun;8(6):2302-8 [3136317] Arch Biochem Biophys. 1985 Oct;242(1):176-86 [2413806] Proc Natl Acad Sci U S A. 1985 Apr;82(7):1974-8 [2984676] Science. 1988 Jul 1;241(4861):42-52 [3291115] J Biol Chem. 1988 Oct 5;263(28):14497-504 [2459119] J Biol Chem. 1988 Sep 15;263(26):13152-8 [3138233] J Biol Chem. 1988 Jul 5;263(19):9462-9 [3379075] Nature. 1984 Oct 4-10;311(5985):480-3 [6090944] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A ras effector domain mutant which is temperature sensitive for cellular transformation: interactions with GTPase-activating protein and NF-1. AN - 80567929; 2038322 AB - A series of v-rasH effector domain mutants were analyzed for their ability to transform rat 2 cells at either low or high temperatures. Three mutants were found to be significantly temperature sensitive: Ile-36 changed to Leu, Ser-39 changed to Cys (S39C), and Arg-41 changed to Leu. Of these, the codon 39 mutant (S39C) showed the greatest degree of temperature sensitivity. When the same mutation was analyzed in the proto-oncogene form of ras(c-rasH), this gene was also found to be temperature sensitive for transformation. Biochemical analysis of the proteins encoded by v-rasH(S39C) and c-rasH(S39C) demonstrated that the encoded p21ras proteins were stable and bound guanine nucleotides in vivo at permissive and nonpermissive temperatures. On the basis of these findings, it is likely that the temperature-sensitive phenotype results from an inability of the mutant (S39C) p21ras to interact properly with the ras target effector molecule(s) at the nonpermissive temperature. We therefore analyzed the interaction between the c-rasH(S39C) protein and the potential target molecules GTPase-activating protein (GAP) and the GAP-related domain of NF-1, on the basis of stimulation of the mutant p21ras GTPase activity by these molecules in vitro. Assays conducted across a range of temperatures revealed no temperature sensitivity for stimulation of the mutant protein, compared with that of authentic c-rasH protein. We conclude that for this mutant, there is a dissociation between the stimulation of p21ras GTPase activity by GAP and the GAP-related domain NF-1 and their potential target function. Our results are also consistent with the existence of a distinct, as-yet-unidentified effector for mammalian ras proteins. JF - Molecular and cellular biology AU - DeClue, J E AU - Stone, J C AU - Blanchard, R A AU - Papageorge, A G AU - Martin, P AU - Zhang, K AU - Lowy, D R AD - Laboratory of Cellular Oncology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 3132 EP - 3138 VL - 11 IS - 6 SN - 0270-7306, 0270-7306 KW - ras KW - Codon KW - 0 KW - GTPase-Activating Proteins KW - Neurofibromin 1 KW - Proteins KW - ras GTPase-Activating Proteins KW - Proto-Oncogene Proteins p21(ras) KW - EC 3.6.5.2 KW - Index Medicus KW - Rats KW - Animals KW - Proto-Oncogene Proteins p21(ras) -- isolation & purification KW - Proto-Oncogene Proteins p21(ras) -- biosynthesis KW - Transfection KW - Temperature KW - Proto-Oncogenes KW - Cell Line KW - Proto-Oncogene Proteins p21(ras) -- genetics KW - Mutagenesis, Site-Directed KW - Genes, ras KW - Moloney murine leukemia virus -- genetics KW - Proteins -- metabolism KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80567929?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+ras+effector+domain+mutant+which+is+temperature+sensitive+for+cellular+transformation%3A+interactions+with+GTPase-activating+protein+and+NF-1.&rft.au=DeClue%2C+J+E%3BStone%2C+J+C%3BBlanchard%2C+R+A%3BPapageorge%2C+A+G%3BMartin%2C+P%3BZhang%2C+K%3BLowy%2C+D+R&rft.aulast=DeClue&rft.aufirst=J&rft.date=1991-06-01&rft.volume=11&rft.issue=6&rft.spage=3132&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 - 1991-07-03 N1 - Date created - 1991-07-03 N1 - Date revised - 2017-01-13 N1 - Gene symbol - ras N1 - SuppNotes - Cited By: Science. 1988 Apr 22;240(4851):518-21 [2833817] Nature. 1988 Apr 7;332(6164):548-51 [2833702] Nature. 1988 Sep 1;335(6185):90-3 [2842690] Mol Cell Biol. 1988 Aug;8(8):3565-9 [3062384] J Virol. 1989 Mar;63(3):1384-92 [2536840] Proteins. 1989;6(3):306-15 [2516318] Cell. 1990 Jun 1;61(5):769-76 [2188736] Science. 1990 Jul 13;249(4965):162-5 [2115210] Science. 1990 Jul 13;249(4965):169-71 [2164710] Oncogene. 1990 Jul;5(7):1099-101 [2115644] Proc Natl Acad Sci U S A. 1990 Aug;87(15):5993-7 [2198577] Science. 1990 Aug 10;249(4969):635-40 [2116664] Nature. 1990 Aug 23;346(6286):754-6 [2201922] Cell. 1990 Nov 16;63(4):835-41 [2121369] Cell. 1990 Nov 16;63(4):843-9 [2121370] Cell. 1990 Nov 16;63(4):851-9 [2121371] Nature. 1990 Nov 8;348(6297):125-32 [2122258] J Virol. 1979 Aug;31(2):546-6 [225570] Virology. 1981 Aug;113(1):408-11 [7269249] J Mol Appl Genet. 1982;1(4):327-41 [6286831] J Virol. 1982 Jul;43(1):294-304 [6287003] J Biol Chem. 1982 Oct 10;257(19):11767-73 [6288698] J Virol. 1982 Nov;44(2):509-19 [6292515] Gene. 1983 Dec;26(1):101-6 [6323249] Cell. 1983 May;33(1):153-9 [6678608] Proc Natl Acad Sci U S A. 1984 Sep;81(17):5305-9 [6089191] Proc Natl Acad Sci U S A. 1986 Feb;83(3):710-4 [3003746] Proc Natl Acad Sci U S A. 1986 Jul;83(13):4725-9 [2425352] J Virol. 1986 Nov;60(2):750-3 [3022007] Mol Cell Biol. 1986 Jul;6(7):2646-54 [3023943] Mol Cell Biol. 1987 Jun;7(6):2128-33 [3299060] J Biol Chem. 1987 Aug 5;262(22):10426-9 [3038880] Annu Rev Biochem. 1987;56:779-827 [3304147] Science. 1987 Oct 23;238(4826):542-5 [2821624] Mol Cell Biol. 1987 Dec;7(12):4553-6 [3325827] Mutat Res. 1988 May;195(3):255-71 [3283542] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Monoclonal antibody-based therapy of a human tumor xenograft with a 177lutetium-labeled immunoconjugate. AN - 80565198; 1851665 AB - 177Lutetium (177Lu) is a member of the family of elements known as lanthanides or rare earths. Monoclonal antibody (MAb) CC49, a murine IgG1, which is reactive with the tumor-associated antigen, TAG-72, has been shown previously to react with a wide range of human carcinomas; CC49 reacts to a different epitope on the TAG-72 molecule than MAb B72.3 and has a higher binding affinity. We report here the first use of a 177Lu-labeled immunoconjugate, 177Lu-CC49, in an experimental therapy model for human carcinoma. 177Lu-CC49 was shown to delay the growth of established LS-174T human colon carcinomas in athymic mice at a single dose of 50 microCi. Overt toxicity was observed with the administration of approximately 500 microCi of 177Lu-CC49 in which 5 of 9 mice died of apparent marrow toxicity. A single administration of 200 or 350 microCi of 177Lu-CC49, however, was shown to eliminate established tumors through the 77-day observation period after MAb administration. Dose fractionation experiments revealed that at least 750 microCi of 177Lu-CC49 (250 microCi/week for 3 consecutive weeks) was well tolerated in that 9 of 10 mice survived. Moreover, this dose schedule was able to eliminate the growth of relatively large (300 mm3) human colon tumor xenografts in 90% of the animals treated. Single-dose and dose fractionation studies were also carried out with an isotype-matched control MAb, 177Lu-MOPC-21. In all dose schedules, a large differential was seen between the therapeutic effects of the 177Lu-CC49 versus that of the 177Lu-control MAb. The merits and limitations of the use of 177Lu-labeled immunoconjugates (in particular, 177Lu-CC49) are discussed in terms of potential novel therapeutics for human carcinoma. JF - Cancer research AU - Schlom, J AU - Siler, K AU - Milenic, D E AU - Eggensperger, D AU - Colcher, D AU - Miller, L S AU - Houchens, D AU - Cheng, R AU - Kaplan, D AU - Goeckeler, W AD - Laboratory of Tumor Immunology and Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/06/01/ PY - 1991 DA - 1991 Jun 01 SP - 2889 EP - 2896 VL - 51 IS - 11 SN - 0008-5472, 0008-5472 KW - Antibodies, Monoclonal KW - 0 KW - Immunoglobulin G KW - Radioisotopes KW - Lutetium KW - 5H0DOZ21UJ KW - Index Medicus KW - Drug Screening Assays, Antitumor KW - Animals KW - Tumor Cells, Cultured KW - Radiotherapy Dosage KW - Humans KW - Mice, Nude KW - Mice KW - Tissue Distribution KW - Female KW - Adenocarcinoma, Mucinous -- radiotherapy KW - Colonic Neoplasms -- radiotherapy KW - Lutetium -- pharmacokinetics KW - Radioisotopes -- therapeutic use KW - Radioisotopes -- pharmacokinetics KW - Lutetium -- therapeutic use KW - Immunoglobulin G -- immunology KW - Colonic Neoplasms -- pathology KW - Adenocarcinoma, Mucinous -- pathology KW - Immunoglobulin G -- therapeutic use KW - Antibodies, Monoclonal -- therapeutic use KW - Antibodies, Monoclonal -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80565198?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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-based+therapy+of+a+human+tumor+xenograft+with+a+177lutetium-labeled+immunoconjugate.&rft.au=Schlom%2C+J%3BSiler%2C+K%3BMilenic%2C+D+E%3BEggensperger%2C+D%3BColcher%2C+D%3BMiller%2C+L+S%3BHouchens%2C+D%3BCheng%2C+R%3BKaplan%2C+D%3BGoeckeler%2C+W&rft.aulast=Schlom&rft.aufirst=J&rft.date=1991-06-01&rft.volume=51&rft.issue=11&rft.spage=2889&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 - 1991-06-21 N1 - Date created - 1991-06-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Antitumor activity of a transforming growth factor alpha-Pseudomonas exotoxin fusion protein (TGF-alpha-PE40). AN - 80565157; 2032221 AB - TGF-alpha-PE40 is a chimeric protein composed of transforming growth factor alpha (TGF-alpha) linked to a modified Pseudomonas toxin from which the cell recognition domain has been deleted (PE40). TGF-alpha-PE40 has been shown to have cytotoxic effects on human cancer cell lines that express the epidermal growth factor (EGF) receptor on their surface, and when given i.p., it prolongs the survival of nude mice bearing i.p. tumors. Because several normal tissues, including liver, express EGF receptors on their surfaces, it has not been clear that this agent can be used systemically to treat EGF receptor-bearing tumors. In this study, we have delivered TGF-alpha-PE40 for 7 days by continuous infusion through a miniosmotic pump placed in the peritoneal cavity of nude immunodeficient mice. Two different human cancer cell lines that express EGF receptors on their surface were implanted s.c. One was A431, an epidermoid carcinoma; the other was DU-145, a prostate carcinoma. By using this mode of continuous i.p. delivery, we were able to achieve a constant serum level of TGF-alpha-PE40 that was nontoxic to the mice and yet delayed the growth of both tumors implanted s.c. and caused partial regression of one. We conclude that it is possible to deliver TGF-alpha-PE40 systemically and achieve a therapeutic serum level in mice without major toxicity. Although side effects may be expected, this study establishes that there is a therapeutic window for this agent in the therapy of cancers with high numbers of EGF receptors. JF - Cancer research AU - Pai, L H AU - Gallo, M G AU - FitzGerald, D J AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1991/06/01/ PY - 1991 DA - 1991 Jun 01 SP - 2808 EP - 2812 VL - 51 IS - 11 SN - 0008-5472, 0008-5472 KW - Exotoxins KW - 0 KW - Recombinant Fusion Proteins KW - Transforming Growth Factor alpha KW - transforming growth factor type alpha-Pseudomonas exotoxin A KW - Index Medicus KW - Drug Stability KW - Drug Screening Assays, Antitumor KW - Animals KW - Infusion Pumps KW - Tumor Cells, Cultured -- drug effects KW - Mice, Nude KW - Mice KW - Prostatic Neoplasms -- drug therapy KW - Carcinoma, Squamous Cell -- drug therapy KW - Male KW - Female KW - Exotoxins -- pharmacology KW - Exotoxins -- administration & dosage KW - Transforming Growth Factor alpha -- administration & dosage KW - Transforming Growth Factor alpha -- pharmacology KW - Recombinant Fusion Proteins -- pharmacology KW - Recombinant Fusion Proteins -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80565157?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Antitumor+activity+of+a+transforming+growth+factor+alpha-Pseudomonas+exotoxin+fusion+protein+%28TGF-alpha-PE40%29.&rft.au=Pai%2C+L+H%3BGallo%2C+M+G%3BFitzGerald%2C+D+J%3BPastan%2C+I&rft.aulast=Pai&rft.aufirst=L&rft.date=1991-06-01&rft.volume=51&rft.issue=11&rft.spage=2808&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 - 1991-06-21 N1 - Date created - 1991-06-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - IL-8 gene expression and production in human peripheral blood lymphocyte subsets. AN - 80562873; 1827816 AB - We have investigated IL-8 mRNA expression and IL-8 production in highly purified subsets of peripheral blood lymphocytes. T cells stimulated with PHA, ionomycin, or PMA alone failed to express IL-8 mRNA. However T cells stimulated with a combination of PMA and ionomycin or PMA and PHA expressed IL-8 mRNA in a PMA dose-dependent manner and maximally after 3 to 6 h of culture. Induction of IL-8 mRNA appeared to be specifically in the CD4+ T cell subset. Surprisingly, however, T cells were not induced to secrete significant levels of IL-8 polypeptide, even in the presence of accessory monocytes. In addition, immunoprecipitation analysis of PMA/ionomycin-treated T cell lysates detected only minor levels of cellular IL-8 Ag thereby suggesting that in T cells, the production of IL-8 was inhibited at the posttranscriptional level. By contrast, CD3- large granular lymphocytes (LGL) were both induced to express IL-8 mRNA and secrete biologically active IL-8 upon specific stimulation with IL-2 and ligand (anti-CD16 mAb) for the NK cell receptor for IgG-Fc (CD16), or upon nonspecific stimulation with PMA. IL-2 and anti-CD16 mAb synergistically induced IL-8 expression in LGL. Other nonactivating LGL-specific mAb did not induce LGL IL-8 secretion. The amount of IL-8 produced by activated LGL was donor variable, but generally 5 to 10 times less than that secreted by monocytes. The ability of LGL to release IL-8 and a large number of other cytokines further supports the hypothesis that LGL may contribute to both inflammatory and immunologic responses. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Smyth, M J AU - Zachariae, C O AU - Norihisa, Y AU - Ortaldo, J R AU - Hishinuma, A AU - Matsushima, K AD - Laboratory of Experimental Immunology, NCI-FCRDC, Frederick, MD 21702-1201. Y1 - 1991/06/01/ PY - 1991 DA - 1991 Jun 01 SP - 3815 EP - 3823 VL - 146 IS - 11 SN - 0022-1767, 0022-1767 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Differentiation KW - Interleukin-2 KW - Interleukin-8 KW - Lipopolysaccharides KW - RNA, Messenger KW - Receptors, Fc KW - Receptors, IgG KW - Ionomycin KW - 56092-81-0 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Interleukin-2 -- pharmacology KW - Receptors, Fc -- physiology KW - Lipopolysaccharides -- pharmacology KW - Humans KW - In Vitro Techniques KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Ionomycin -- pharmacology KW - Antigens, Differentiation -- physiology KW - RNA, Messenger -- biosynthesis KW - Antibodies, Monoclonal -- immunology KW - T-Lymphocyte Subsets -- metabolism KW - Interleukin-8 -- biosynthesis KW - Gene Expression KW - Interleukin-8 -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80562873?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=IL-8+gene+expression+and+production+in+human+peripheral+blood+lymphocyte+subsets.&rft.au=Smyth%2C+M+J%3BZachariae%2C+C+O%3BNorihisa%2C+Y%3BOrtaldo%2C+J+R%3BHishinuma%2C+A%3BMatsushima%2C+K&rft.aulast=Smyth&rft.aufirst=M&rft.date=1991-06-01&rft.volume=146&rft.issue=11&rft.spage=3815&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 - 1991-06-25 N1 - Date created - 1991-06-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - T cell receptor activation induces rapid phosphorylation of prosolin, which mediates down-regulation of DNA synthesis in proliferating peripheral lymphocytes. AN - 80562653; 1903411 AB - Prosolin is a major cytosolic phosphoprotein expressed prominently in rapidly proliferating human peripheral lymphocytes but produced at very low levels in resting (G0) PBL. It undergoes rapid phosphorylation upon treatment of growing cells with tumor-producing phorbol esters (TPA) and this phosphorylation event is correlated with a rapid down-regulation of DNA synthesis. In the present report we have studied various agents that, like TPA, act as partial or complete mitogens for G0 PBL and have determined their effect on phosphorylation of prosolin and on DNA synthesis in rapidly proliferating (IL-2-dependent) human PBL. Agents that activate the TCR (OKT3 and PHA), as well as agents that by-pass the receptor but activate biochemical pathways associated with TCR activation (TPA and Ca2(+)-ionophore), all produced rapid phosphorylation of prosolin and prompt down-regulation of DNA synthesis. Four phosphorylated forms of prosolin were produced, indicating activation of a complex phosphorylation pathway. Down-regulation of DNA synthesis did not lead to cell death or to permanent arrest, but was reversed after 24 to 48 h, and was not associated with any reduction in overall protein synthesis. Agents that bind to determinants closely connected to the TCR but without activating it (OKT4 and OKT8) had no effect on either prosolin phosphorylation or DNA synthesis. The results indicate that prosolin is an early target of the protein kinase activities induced by activation of the TCR in proliferating PBL, and suggest that its phosphorylation mediates the TCR signal, transmitting it into a biochemical pathway leading specifically to down-regulation of DNA synthesis. In G0 PBL, in which the negligible expression of prosolin precludes significant production of phosphorylated species, this inhibitory pathway is effectively blocked. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Cooper, H L AU - Fuldner, R AU - McDuffie, E AU - Braverman, R AD - Cell and Molecular Physiology Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/06/01/ PY - 1991 DA - 1991 Jun 01 SP - 3689 EP - 3696 VL - 146 IS - 11 SN - 0022-1767, 0022-1767 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, CD4 KW - Antigens, CD8 KW - Antigens, Differentiation, T-Lymphocyte KW - Phosphoproteins KW - Receptors, Antigen, T-Cell KW - Calcimycin KW - 37H9VM9WZL KW - DNA KW - 9007-49-2 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Antigens, CD4 -- physiology KW - Phosphorylation KW - Down-Regulation KW - Humans KW - Antigens, Differentiation, T-Lymphocyte -- physiology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Lymphocytes -- metabolism KW - Calcimycin -- pharmacology KW - Antibodies, Monoclonal -- immunology KW - Lymphocyte Activation KW - DNA -- biosynthesis KW - Receptors, Antigen, T-Cell -- physiology KW - Phosphoproteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80562653?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=T+cell+receptor+activation+induces+rapid+phosphorylation+of+prosolin%2C+which+mediates+down-regulation+of+DNA+synthesis+in+proliferating+peripheral+lymphocytes.&rft.au=Cooper%2C+H+L%3BFuldner%2C+R%3BMcDuffie%2C+E%3BBraverman%2C+R&rft.aulast=Cooper&rft.aufirst=H&rft.date=1991-06-01&rft.volume=146&rft.issue=11&rft.spage=3689&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 - 1991-06-25 N1 - Date created - 1991-06-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Therapeutic radiation at a young age is linked to secondary thyroid cancer. The Late Effects Study Group. AN - 80560622; 1851664 AB - We estimated the risk of thyroid cancer among 9170 patients who had survived 2 or more years after the diagnosis of a cancer in childhood. As compared with the general population, patients had a 53-fold increased risk (95% confidence interval, 34-80). Risk increased significantly with time since treatment for the initial cancer (P = 0.03). Detailed treatment data were obtained for 23 cases and 89 matched controls from the childhood cancer cohort. Sixty-eight % of the thyroid cancers arose within the field of radiation. Radiation doses to the thyroid of greater than 200 cGy were associated with a 13-fold increased risk (95% confidence interval, 1.7-104). The risk of thyroid cancer rose with increasing dose (P less than 0.001), but this was derived almost entirely from the increase from less than 200 to greater than 200 cGy. The risk of thyroid cancer did not decrease, however, at radiation doses as high as 6000 cGy. JF - Cancer research AU - Tucker, M A AU - Jones, P H AU - Boice, J D AU - Robison, L L AU - Stone, B J AU - Stovall, M AU - Jenkin, R D AU - Lubin, J H AU - Baum, E S AU - Siegel, S E AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/06/01/ PY - 1991 DA - 1991 Jun 01 SP - 2885 EP - 2888 VL - 51 IS - 11 SN - 0008-5472, 0008-5472 KW - Index Medicus KW - Wilms Tumor -- radiotherapy KW - Kidney Neoplasms -- drug therapy KW - Age Factors KW - Hodgkin Disease -- radiotherapy KW - Neuroblastoma -- radiotherapy KW - Wilms Tumor -- drug therapy KW - Humans KW - Infant, Newborn KW - Child KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Child, Preschool KW - Infant KW - Lymphoma, Non-Hodgkin -- drug therapy KW - Neuroblastoma -- drug therapy KW - Radiotherapy Dosage KW - Lymphoma, Non-Hodgkin -- radiotherapy KW - Hodgkin Disease -- drug therapy KW - Case-Control Studies KW - Kidney Neoplasms -- radiotherapy KW - Follow-Up Studies KW - Adolescent KW - Male KW - Female KW - Neoplasms, Radiation-Induced -- etiology KW - Thyroid Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80560622?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Therapeutic+radiation+at+a+young+age+is+linked+to+secondary+thyroid+cancer.+The+Late+Effects+Study+Group.&rft.au=Tucker%2C+M+A%3BJones%2C+P+H%3BBoice%2C+J+D%3BRobison%2C+L+L%3BStone%2C+B+J%3BStovall%2C+M%3BJenkin%2C+R+D%3BLubin%2C+J+H%3BBaum%2C+E+S%3BSiegel%2C+S+E&rft.aulast=Tucker&rft.aufirst=M&rft.date=1991-06-01&rft.volume=51&rft.issue=11&rft.spage=2885&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 - 1991-06-21 N1 - Date created - 1991-06-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mouthwash use and oral conditions in the risk of oral and pharyngeal cancer. AN - 80560538; 2032242 AB - Interviews with 866 patients with cancer of the oral cavity and pharynx and 1249 controls of similar age and sex from the general population in four areas of the United States revealed increased risks associated with the regular use of mouthwash. Risks of oral cancer were elevated by 40% among male and 60% among female mouthwash users, after adjusting for tobacco and alcohol consumption. Risks among both sexes generally increased in proportion to duration and frequency of mouthwash use. The increased risks were confined to users of mouthwash high in alcohol content, consistent with the elevated risks associated with drinking alcoholic beverages. Except for a higher prevalence of leukoplakia among cases, little relationship was found with oral or dental conditions, although denture wearing was reported more often by patients with cancer of the gums. These findings, together with other studies, provide further incentive for clarifying the association between mouthwash use and oral cancer. JF - Cancer research AU - Winn, D M AU - Blot, W J AU - McLaughlin, J K AU - Austin, D F AU - Greenberg, R S AU - Preston-Martin, S AU - Schoenberg, J B AU - Fraumeni, J F AD - National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/06/01/ PY - 1991 DA - 1991 Jun 01 SP - 3044 EP - 3047 VL - 51 IS - 11 SN - 0008-5472, 0008-5472 KW - Mouthwashes KW - 0 KW - Index Medicus KW - Oral Health KW - Oral Hygiene KW - Humans KW - Adult KW - Case-Control Studies KW - Aged KW - Middle Aged KW - United States -- epidemiology KW - Time Factors KW - Male KW - Female KW - Pharyngeal Neoplasms -- epidemiology KW - Pharyngeal Neoplasms -- etiology KW - Mouth Neoplasms -- etiology KW - Mouthwashes -- adverse effects KW - Mouth Neoplasms -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80560538?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mouthwash+use+and+oral+conditions+in+the+risk+of+oral+and+pharyngeal+cancer.&rft.au=Winn%2C+D+M%3BBlot%2C+W+J%3BMcLaughlin%2C+J+K%3BAustin%2C+D+F%3BGreenberg%2C+R+S%3BPreston-Martin%2C+S%3BSchoenberg%2C+J+B%3BFraumeni%2C+J+F&rft.aulast=Winn&rft.aufirst=D&rft.date=1991-06-01&rft.volume=51&rft.issue=11&rft.spage=3044&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 - 1991-06-21 N1 - Date created - 1991-06-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Practical spontaneous metastasis model for in vivo therapeutic studies using a human melanoma. AN - 80560086; 2032224 AB - In vivo studies aimed at therapy of spontaneous human tumor metastases have been hampered by the lack of practical experimental models. The LOX amelanotic melanoma model described here represents a transplantation model which rapidly and reproducibly results in spontaneous pulmonary metastasis following s.c. inoculation into athymic mice. Pulmonary lesions can be detected using a simple bioassay procedure which is useful for estimation of metastatic cell killing. Using this model we demonstrate that systemic therapy with cyclophosphamide or dacarbazine can produce metastatic cell killing consistent with complete eradication of established pulmonary metastases. This model may also prove useful for future experimental therapeutic studies aimed at prevention of metastases by manipulating tumor staging interval and treatment schedule. JF - Cancer research AU - Shoemaker, R H AU - Dykes, D J AU - Plowman, J AU - Harrison, S D AU - Griswold, D P AU - Abbott, B J AU - Mayo, J G AU - Fodstad, O AU - Boyd, M R AD - Developmental Therapeutics Program, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland 21702. Y1 - 1991/06/01/ PY - 1991 DA - 1991 Jun 01 SP - 2837 EP - 2841 VL - 51 IS - 11 SN - 0008-5472, 0008-5472 KW - Dacarbazine KW - 7GR28W0FJI KW - Cyclophosphamide KW - 8N3DW7272P KW - Index Medicus KW - Neoplasm Transplantation KW - Dacarbazine -- therapeutic use KW - Animals KW - Cyclophosphamide -- therapeutic use KW - Tumor Cells, Cultured KW - Humans KW - Neoplasm Metastasis KW - Mice, Nude KW - Mice KW - Melanoma -- secondary KW - Lung Neoplasms -- secondary KW - Melanoma -- drug therapy KW - Lung Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80560086?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Practical+spontaneous+metastasis+model+for+in+vivo+therapeutic+studies+using+a+human+melanoma.&rft.au=Shoemaker%2C+R+H%3BDykes%2C+D+J%3BPlowman%2C+J%3BHarrison%2C+S+D%3BGriswold%2C+D+P%3BAbbott%2C+B+J%3BMayo%2C+J+G%3BFodstad%2C+O%3BBoyd%2C+M+R&rft.aulast=Shoemaker&rft.aufirst=R&rft.date=1991-06-01&rft.volume=51&rft.issue=11&rft.spage=2837&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 - 1991-06-21 N1 - Date created - 1991-06-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Oncogenes and tumor-suppressor genes. AN - 72623818; 1685442 AB - The functional role of oncogenes in human lung carcinogenesis has been investigated by transfer of activated oncogenes into normal cells or an immortalized bronchial epithelial cell line, BEAS-2B. Transfection of v-Ha-ras, Ki-ras, or the combination of myc and raf into BEAS-2B cells produced tumorigenic cell lines, while transfection of raf or myc alone produced nontumorigenic cell lines. In addition to studying the pathogenic role of oncogenes, we are attempting to define negative growth-regulating genes that have tumor-suppressive effects for human lung carcinomas. Our strategy to identify tumor-suppressor genes involves loss of heterozygosity studies, monochromosome-cell fusion, and cell-cell fusion studies. Loss of heterozygosity studies have revealed consistent allelic DNA sequence deletions on chromosome 17p in squamous cell carcinomas, while large cell carcinomas and adenocarcinomas retained this locus. Mutations in p53, a tumor-suppressor gene located on chromosome 17p, have been observed. Cell-cell hybrid clones produced from fusion of nontumorigenic BEAS-2B cells with tumorigenic HuT292DM cells generally are nontumorigenic. The mechanistic role of the known tumor-suppressor genes Rb-1 and p53 in the development of human lung carcinomas is being investigated in this epithelial cell model of human bronchogenic carcinogenesis. JF - Environmental health perspectives AU - Lehman, T A AU - Reddel, R AU - Peiifer, A M AU - Spillare, E AU - Kaighn, M E AU - Weston, A AU - Gerwin, B I AU - Harris, C C AD - Laboratory of Human Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 133 EP - 144 VL - 93 SN - 0091-6765, 0091-6765 KW - Ha-ras KW - Ki-ras KW - N-myc KW - N-ras KW - Rb-1 KW - c-myc KW - c-raf-1 KW - erb-B2 KW - fur KW - jun KW - myb KW - myc KW - neu KW - raf KW - ras KW - v-Ha-ras KW - Antigens, Polyomavirus Transforming KW - 0 KW - DNA, Neoplasm KW - Heat-Shock Proteins KW - Retinoblastoma Protein KW - Tumor Suppressor Protein p53 KW - Index Medicus KW - Eye Neoplasms -- genetics KW - Animals KW - Tumor Suppressor Protein p53 -- physiology KW - Humans KW - Chromosomes, Human, Pair 11 -- ultrastructure KW - Mice, Nude KW - Antigens, Polyomavirus Transforming -- metabolism KW - Chromosomes, Human, Pair 17 -- ultrastructure KW - Genes, p53 KW - Heterozygote KW - Retinoblastoma -- genetics KW - Genetic Complementation Test KW - Hybrid Cells KW - Cell Line, Transformed KW - Tumor Suppressor Protein p53 -- genetics KW - Retinoblastoma Protein -- genetics KW - Heat-Shock Proteins -- metabolism KW - Chromosome Deletion KW - Retinoblastoma Protein -- physiology KW - Mice KW - Epithelial Cells KW - Cell Fusion KW - Bronchi -- cytology KW - Transfection KW - Genes, Retinoblastoma KW - Polymorphism, Restriction Fragment Length KW - DNA, Neoplasm -- genetics KW - Oncogenes KW - Genes, Tumor Suppressor KW - Lung Neoplasms -- genetics KW - Cell Transformation, Neoplastic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72623818?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Oncogenes+and+tumor-suppressor+genes.&rft.au=Lehman%2C+T+A%3BReddel%2C+R%3BPeiifer%2C+A+M%3BSpillare%2C+E%3BKaighn%2C+M+E%3BWeston%2C+A%3BGerwin%2C+B+I%3BHarris%2C+C+C&rft.aulast=Lehman&rft.aufirst=T&rft.date=1991-06-01&rft.volume=93&rft.issue=&rft.spage=133&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 - 1992-03-03 N1 - Date created - 1992-03-03 N1 - Date revised - 2017-01-13 N1 - Gene symbol - Ha-ras; Ki-ras; N-myc; N-ras; Rb-1; c-myc; c-raf-1; erb-B2; fur; jun; myb; myc; neu; raf; ras; v-Ha-ras N1 - SuppNotes - Cited By: Nucleic Acids Res. 1986 Jan 24;14(2):843-52 [3945555] Nature. 1985 May 30-Jun 5;315(6018):382-5 [3923365] Adv Cancer Res. 1985;44:43-68 [3898739] Cancer Res. 1985 Dec;45(12 Pt 1):6005-9 [4063960] Science. 1985 May 10;228(4700):725-8 [4039465] Science. 1985 Mar 8;227(4691):1174-9 [3975607] Cancer Res. 1990 Mar 15;50(6):1890-6 [2306741] Science. 1990 Feb 9;247(4943):712-5 [2300823] Science. 1990 Feb 2;247(4942):568-71 [2300817] Nature. 1984 May 10-16;309(5964):172-4 [6325937] Proc Natl Acad Sci U S A. 1981 Jan;78(1):313-7 [6264437] Int J Cancer. 1981 May 15;27(5):625-35 [6169665] Nature. 1983 Aug 11-17;304(5926):507-13 [6308467] Nature. 1983 Aug 11-17;304(5926):497-500 [6308465] Nature. 1984 May 10-16;309(5964):176-8 [6325939] Nature. 1984 May 10-16;309(5964):174-6 [6325938] Nature. 1984 May 10-16;309(5964):170-2 [6325936] N Engl J Med. 1987 Oct 8;317(15):929-35 [3041218] Nature. 1987 Dec 10-16;330(6148):578-81 [2825033] Nature. 1987 Oct 1-7;329(6138):451-4 [2821400] N Engl J Med. 1987 Oct 29;317(18):1109-13 [2821398] Cancer Res. 1986 Mar;46(3):1530-4 [3002619] Cancer Res. 1987 Apr 15;47(8):2148-55 [3030544] Science. 1987 Apr 10;236(4798):175-80 [3031816] Proc Natl Acad Sci U S A. 1987 Apr;84(8):2372-6 [3031679] Oncogene. 1988 Nov;3(5):595-603 [2978869] Cancer Res. 1985 Apr;45(4):1437-43 [2983882] Nature. 1988 Jul 14;334(6178):124-9 [2968522] Nature. 1985 Nov 7-13;318(6041):69-73 [2997622] Nature. 1985 Jul 25-31;316(6026):330-4 [2991766] Proc Natl Acad Sci U S A. 1985 Sep;82(18):6216-20 [2994066] Oncogene. 1988 Sep;3(3):313-21 [3060794] Oncogene Res. 1988;3(4):401-8 [3067190] Cancer Res. 1988 Oct 15;48(20):5738-41 [3048648] Mol Cell Biol. 1989 Sep;9(9):3982-91 [2476668] Cancer Res. 1988 Apr 1;48(7):1904-9 [2450641] Cancer Res. 1987 Aug 15;47(16):4248-53 [2440561] Proc Natl Acad Sci U S A. 1989 Jul;86(13):5099-103 [2567993] Science. 1989 Oct 27;246(4929):491-4 [2554494] EMBO J. 1989 Dec 20;8(13):4099-105 [2556261] J Natl Cancer Inst. 1989 Apr 19;81(8):587-94 [2539488] Science. 1989 Feb 17;243(4893):934-7 [2537532] Proc Natl Acad Sci U S A. 1989 Nov;86(22):8763-7 [2530586] Oncogene. 1989 Dec;4(12):1483-8 [2531855] Proc Natl Acad Sci U S A. 1984 Jan;81(1):71-5 [6320174] Virology. 1983 Apr 15;126(1):19-31 [6302981] Cell. 1982 Feb;28(2):387-94 [6277513] Proc Natl Acad Sci U S A. 1982 Jun;79(11):3637-40 [6285355] Proc Natl Acad Sci U S A. 1982 Oct;79(20):6309-12 [6292898] Proc Natl Acad Sci U S A. 1984 Jun;81(12):3670-4 [6587382] J Natl Cancer Inst. 1983 Jan;70(1):3-8 [6571918] Proc Natl Acad Sci U S A. 1984 Jan;81(1):202-5 [6582476] Science. 1984 Feb 17;223(4637):661-4 [6695174] Nature. 1983 Nov 10-16;306(5939):194-6 [6646201] Nature. 1983 Oct 27-Nov 2;305(5937):779-84 [6633649] Nature. 1982 Dec 9;300(5892):539-42 [7144906] Science. 1982 Jan 15;215(4530):252-9 [7053574] J Pediatr. 1980 Jan;96(1):47-50 [7350313] Proc Natl Acad Sci U S A. 1977 Jan;74(1):319-23 [264685] Cell. 1979 May;17(1):43-52 [222475] Nature. 1979 Mar 15;278(5701):261-3 [218111] Methods Cell Biol. 1977;15:339-57 [327204] Am J Dis Child. 1978 Feb;132(2):161-3 [626181] Nature. 1969 Jul 26;223(5204):363-8 [5387828] Proc Natl Acad Sci U S A. 1971 Apr;68(4):820-3 [5279523] J Virol. 1989 Feb;63(2):739-46 [2642977] Mol Cell Biol. 1988 Sep;8(9):3740-7 [2851728] Proc Natl Acad Sci U S A. 1986 Jul;83(14):5209-13 [3523486] Nature. 1989 Dec 7;342(6250):705-8 [2531845] Proc Natl Acad Sci U S A. 1989 Dec;86(24):10075-9 [2557616] Oncogene Res. 1988;3(1):99-103 [2905034] Differentiation. 1988 Jun;38(1):60-6 [2846394] Nature. 1986 Oct 16-22;323(6089):643-6 [2877398] Oncogene. 1988 Oct;3(4):471-5 [2856251] Mol Carcinog. 1988;1(3):151-60 [2855021] EMBO J. 1986 Dec 20;5(13):3461-6 [2881780] Nature. 1988 Jan 21;331(6153):273-7 [2827040] Oncogene. 1987 Mar;1(1):71-8 [2830576] N Engl J Med. 1988 Sep 1;319(9):525-32 [2841597] Science. 1988 Jul 15;241(4863):353-7 [2838909] Cell. 1988 Jul 15;54(2):275-83 [2839300] Oncogene. 1989 Mar;4(3):383-8 [2523032] Cell. 1989 Jun 30;57(7):1083-93 [2525423] Cell. 1989 Sep 22;58(6):1193-8 [2673546] Cell. 1989 Sep 22;58(6):1097-105 [2673543] Cell. 1989 Sep 22;58(6):1085-95 [2673542] Science. 1989 Apr 14;244(4901):217-21 [2649981] Mol Cell Biol. 1989 Nov;9(11):4596-604 [2601691] Science. 1989 Dec 8;246(4935):1300-3 [2588006] Mol Carcinog. 1989;2(1):12-21 [2730761] Cell. 1989 Jan 13;56(1):57-65 [2910497] J Clin Invest. 1988 Aug;82(2):502-7 [2900253] Science. 1987 Oct 9;238(4824):193-7 [2889267] Proc Natl Acad Sci U S A. 1987 Dec;84(24):9252-6 [2892196] Cancer Res. 1988 Feb 1;48(3):682-5 [2891438] Science. 1987 Jun 26;236(4809):1657-61 [2885916] Nature. 1987 Jun 25-Jul 1;327(6124):721-4 [2885753] Nature. 1987 Aug 13-19;328(6131):616-9 [2886919] Science. 1988 Dec 16;242(4885):1563-6 [3201247] Science. 1988 Sep 30;241(4874):1797-800 [3175621] Cancer Res. 1988 Jun 15;48(12):3302-6 [3370633] Nature. 1984 Dec 13-19;312(5995):646-9 [6095116] Mol Biol Med. 1984 Aug;2(4):261-72 [6544917] Nature. 1986 Mar 6-12;320(6057):84-5 [3456488] Cancer. 1987 Dec 1;60(11):2669-74 [3677003] Nature. 1987 Oct 15-21;329(6140):645-7 [3657988] Science. 1987 Mar 13;235(4794):1394-9 [3823889] Int J Cancer. 1986 Mar 15;37(3):419-23 [3949423] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alterations in epidermal biochemistry as a consequence of stage-specific genetic changes in skin carcinogenesis. AN - 72619820; 1773799 AB - The induction of cancer on mouse skin by initiation-promotion protocols occurs through stages in which a benign squamous papilloma is an obligate precursor of squamous cell carcinoma. Activation of the Ha-ras gene is sufficient to produce the papilloma phenotype, while additional genetic changes are required for malignant conversion. The introduction of Ha-ras into normal keratinocytes suppresses the expression of differentiation markers, keratin K1 and K10, and loricrin (a cornified envelope precursor) and, to a lesser extent, filaggrin, at the level of transcription. However, cells initiated by Ha-ras express a nonepidermal keratin, K8. The transcription of K8 in these cells is sensitive to the level of medium Ca2+, being abundant in 0.5 mM Ca2+ and not detected in 0.05 mM Ca2+. Epidermal differentiation is regulated by signalling, which involves changes in phosphatidylinositol turnover and intracellular Ca2+. Cells initiated by Ha-ras do not differ from normal keratinocytes in their intracellular Ca2+ response patterns, at least in response to changes in extracellular Ca2+ and serum factors. However, c-Ha-ra keratinocytes have a high basal level of phosphatidylinositol (PI) turnover, which is additive with several other inducers of this pathway, including Ca2+ and aluminum fluoride. Additional studies suggest that high turnover of the PI pathway is incompatible with differentiation-specific gene expression in keratinocytes. We suggest this negative relationship is mediated through elevated diacylglycerol production and chronic down-modulation of protein kinase C. Protein kinase C is known to be essential for expression of differentiation-related genes in keratinocytes.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Environmental health perspectives AU - Yuspa, S H AU - Kilkenny, A AU - Cheng, C AU - Roop, D AU - Hennings, H AU - Kruszewski, F AU - Lee, E AU - Strickland, J AU - Greenhalgh, D A AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 3 EP - 10 VL - 93 SN - 0091-6765, 0091-6765 KW - E1A KW - Ha-ras KW - c-Ha-ras KW - c-fos KW - c-myc KW - fos KW - jun KW - myc KW - neoR KW - ras KW - v-fos KW - Biomarkers, Tumor KW - 0 KW - Carcinogens KW - Oncogene Proteins v-fos KW - Oncogene Protein p21(ras) KW - EC 3.6.5.2 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Keratinocytes -- drug effects KW - Retroviridae KW - Transduction, Genetic KW - Mice KW - Biomarkers, Tumor -- metabolism KW - Calcium -- metabolism KW - Phenotype KW - Transfection KW - Cells, Cultured KW - Keratinocytes -- metabolism KW - Cell Line, Transformed KW - Signal Transduction KW - Carcinogens -- pharmacology KW - Oncogene Protein p21(ras) -- genetics KW - Epidermis -- metabolism KW - Carcinoma, Squamous Cell -- chemically induced KW - Oncogene Proteins v-fos -- genetics KW - Skin Neoplasms -- genetics KW - Epidermis -- drug effects KW - Carcinoma, Squamous Cell -- pathology KW - Cell Transformation, Neoplastic -- chemically induced KW - Carcinoma, Squamous Cell -- genetics KW - Oncogene Protein p21(ras) -- physiology KW - Papilloma -- chemically induced KW - Cell Transformation, Neoplastic -- genetics KW - Papilloma -- metabolism KW - Genes, ras -- drug effects KW - Papilloma -- pathology KW - Oncogene Protein p21(ras) -- biosynthesis KW - Carcinogens -- toxicity KW - Skin Neoplasms -- pathology KW - Carcinoma, Squamous Cell -- metabolism KW - Papilloma -- genetics KW - Skin Neoplasms -- metabolism KW - Gene Expression Regulation, Neoplastic -- drug effects KW - Oncogene Proteins v-fos -- physiology KW - Skin Neoplasms -- chemically induced KW - Epidermis -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72619820?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Alterations+in+epidermal+biochemistry+as+a+consequence+of+stage-specific+genetic+changes+in+skin+carcinogenesis.&rft.au=Yuspa%2C+S+H%3BKilkenny%2C+A%3BCheng%2C+C%3BRoop%2C+D%3BHennings%2C+H%3BKruszewski%2C+F%3BLee%2C+E%3BStrickland%2C+J%3BGreenhalgh%2C+D+A&rft.aulast=Yuspa&rft.aufirst=S&rft.date=1991-06-01&rft.volume=93&rft.issue=&rft.spage=3&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 - 1992-03-03 N1 - Date created - 1992-03-03 N1 - Date revised - 2017-01-13 N1 - Gene symbol - E1A; Ha-ras; c-Ha-ras; c-fos; c-myc; fos; jun; myc; neoR; ras; v-fos N1 - SuppNotes - Cited By: Prog Histochem Cytochem. 1989;18(4):1-61 [2657864] Cancer Res. 1976 Apr;36(4):1422-7 [816464] Mol Carcinog. 1988;1(2):134-43 [2475137] Science. 1987 Oct 23;238(4826):533-6 [2821623] Carcinogenesis. 1987 Dec;8(12):1821-5 [2824083] Mol Cell Biol. 1987 Nov;7(11):4146-9 [3323889] Proc Natl Acad Sci U S A. 1986 Dec;83(24):9413-7 [3540938] Adv Cancer Res. 1985;44:139-266 [2930999] J Mol Recognit. 1989 Apr;1(4):166-71 [2631864] Science. 1986 Jan 24;231(4736):407-10 [3001936] Carcinogenesis. 1986 Jun;7(6):949-58 [2871947] Cancer Lett. 1986 Mar;30(3):269-74 [2870794] Nature. 1985 Apr 4-10;314(6010):459-62 [2858820] Adv Cancer Res. 1987;49:29-52 [2823543] Nature. 1986 Jul 3-9;322(6074):78-80 [3014349] Proc Natl Acad Sci U S A. 1986 Aug;83(16):6048-52 [3016738] Carcinog Compr Surv. 1985;10:201-10 [2998612] Cell. 1988 Feb 12;52(3):471-80 [3125983] Cancer Res. 1988 Jan 1;48(1):165-9 [3121168] Mol Carcinog. 1988;1(2):96-108 [3076454] J Biol Chem. 1988 Dec 5;263(34):17975-80 [3056934] J Cell Biol. 1989 Sep;109(3):1207-17 [2475508] Mol Carcinog. 1988;1(3):171-9 [2471536] Cancer Res. 1988 Jun 1;48(11):3253-7 [2452689] Cancer Res. 1988 Jun 1;48(11):3245-52 [2452688] Differentiation. 1987;35(2):143-50 [2450799] Carcinogenesis. 1988 Jun;9(6):1033-8 [2453303] Curr Top Dev Biol. 1987;22:127-51 [2443308] Eur J Cell Biol. 1987 Jun;43(3):459-68 [2441990] Mol Cell Biol. 1986 Sep;6(9):3144-9 [2431297] Nature. 1986 Oct 30-Nov 5;323(6091):822-4 [2430189] Proc Natl Acad Sci U S A. 1985 Dec;82(24):8498-502 [2417222] Cancer Res. 1985 Nov;45(11 Pt 2):5845-50 [2414001] Carcinogenesis. 1989 Apr;10(4):777-80 [2702726] Cancer Res. 1988 Jan 1;48(1):74-81 [2891434] Nature. 1988 Mar 10;332(6160):166-71 [3347253] Cancer Metastasis Rev. 1984;3(4):361-72 [6097355] Cancer Res. 1986 Mar;46(3):1458-64 [3510726] Cancer Res. 1985 Nov;45(11 Pt 1):5540-6 [3863706] Cancer Res. 1985 Oct;45(10):4864-70 [4027973] Proc Natl Acad Sci U S A. 1990 Jan;87(2):643-7 [2153961] Cell. 1990 Jun 15;61(6):1103-12 [2190691] Biochem Biophys Res Commun. 1984 Aug 16;122(3):1234-40 [6206852] Nature. 1983 Aug 18-24;304(5927):602-6 [6308473] Nature. 1983 Aug 18-24;304(5927):596-602 [6308472] Cancer Res. 1983 Dec;43(12 Pt 1):6021-30 [6315224] Cell. 1984 Feb;36(2):259-68 [6319013] Am J Pathol. 1984 Feb;114(2):309-21 [6320650] Nature. 1982 Oct 14;299(5884):640-4 [6289129] J Virol. 1982 Nov;44(2):674-82 [6292525] Cancer Res. 1984 Jun;44(6):2634-41 [6426783] Cell. 1984 Jan;36(1):51-60 [6607118] Nature. 1984 Feb 16-22;307(5952):658-60 [6694757] Cell. 1983 May;33(1):153-9 [6678608] Nature. 1983 Jul 7-13;304(5921):67-9 [6866091] Nature. 1981 Sep 3;293(5827):72-4 [6791032] J Biol Chem. 1989 May 5;264(13):7317-27 [2540185] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Activation of proto-oncogenes in human and mouse lung tumors. AN - 72619426; 1773785 AB - Lung cancer is a leading cause of cancer-related deaths in several nations. Epidemiological studies have indicated that 85% of all lung cancer deaths and 30% of all cancer deaths in the U.S. are associated with tobacco smoking. Various chemicals in tobacco smoke are thought to react with DNA and to ultimately yield heritable mutations. In an effort to understand the molecular mechanisms involved in lung tumorigenesis, we have analyzed proto-oncogene activation in a series of human lung tumors from smokers and spontaneously occurring and chemically induced lung tumors in mice. Approximately 86% of the human lung tumors and greater than 90% of the mouse lung tumors were found to contain activated oncogenes. ras Oncogenes activated by point mutations were detected in many of the human lung adenocarcinomas and virtually all of the mouse lung adenomas and adenocarcinomas. The mutation profiles of the activated K-ras genes detected in the chemically induced mouse lung tumors suggest that the observed mutations result from genotoxic effects of the chemicals. Comparison of the K-ras mutations observed in the human lung adenocarcinomas with mutation profiles observed in the mouse lung tumors suggest that bulky hydrophobic DNA adducts may be responsible for the majority of the mutations observed in the activated human K-ras genes. Other data indicate that approximately 20% of human lung tumors contain potentially novel transforming genes that may also be targets for mutagens in cigarette smoke. JF - Environmental health perspectives AU - Reynolds, S H AU - Anderson, M W AD - Laboratory of Molecular Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 145 EP - 148 VL - 93 SN - 0091-6765, 0091-6765 KW - H-ras KW - K-ras KW - N-ras KW - c-raf KW - raf KW - ras KW - DNA, Neoplasm KW - 0 KW - Index Medicus KW - Animals KW - 3T3 Cells KW - Oncogenes KW - DNA Damage KW - Humans KW - DNA Mutational Analysis KW - Smoking -- adverse effects KW - DNA, Neoplasm -- genetics KW - Mice, Nude KW - Mice KW - Gene Expression Regulation, Neoplastic KW - Lung Neoplasms -- etiology KW - Genes, ras -- drug effects KW - Lung Neoplasms -- genetics KW - Lung Neoplasms -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72619426?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Activation+of+proto-oncogenes+in+human+and+mouse+lung+tumors.&rft.au=Reynolds%2C+S+H%3BAnderson%2C+M+W&rft.aulast=Reynolds&rft.aufirst=S&rft.date=1991-06-01&rft.volume=93&rft.issue=&rft.spage=145&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 - 1992-03-03 N1 - Date created - 1992-03-03 N1 - Date revised - 2017-01-13 N1 - Gene symbol - H-ras; K-ras; N-ras; c-raf; raf; ras N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1989 May;86(9):3070-4 [2654935] Cancer. 1972 Nov;30(5):1332-9 [5083068] Cancer Res. 1988 Oct 15;48(20):5738-41 [3048648] Proc Natl Acad Sci U S A. 1989 Jul;86(13):5099-103 [2567993] Cancer Res. 1989 Oct 1;49(19):5305-11 [2670201] Cancer Res. 1989 Jul 15;49(14):3713-21 [2660980] J Natl Cancer Inst. 1989 Mar 1;81(5):341-7 [2915370] Nature. 1988 Dec 22-29;336(6201):790-2 [3205307] Science. 1987 Jan 16;235(4786):305-11 [3541204] Science. 1987 Sep 11;237(4820):1309-16 [3629242] Cancer Res. 1987 Jun 15;47(12):3212-9 [3581065] Nature. 1985 May 30-Jun 5;315(6018):382-5 [3923365] N Engl J Med. 1985 Aug 22;313(8):491-8 [3894970] Mol Cell Biol. 1990 Jan;10(1):405-8 [2403644] Oncogene. 1990 Jul;5(7):1037-43 [2197591] Cancer Res. 1990 Aug 1;50(15):4818-23 [2196119] Science. 1990 Jan 5;247(4938):12-3 [2403692] Mutat Res. 1983 Jan;114(1):59-89 [6219288] Mutat Res. 1982 Sep;102(2):123-36 [6755230] N Engl J Med. 1987 Oct 8;317(15):929-35 [3041218] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Gene regulation and genetic susceptibility to neoplastic transformation: AP-1 and p80 expression in JB6 cells. AN - 72615673; 1773784 AB - The mouse epidermal JB6 cell system consists of clonal genetic variants that are sensitive (P+) or resistant (P-) to the promotion of neoplastic transformation by phorbol esters and other tumor-promoting agents. P+ cells display AP-1-dependent phorbol-ester-inducible transactivation of gene expression, whereas P- cells have a defect in transactivation. Transfection of promotion sensitivity gene pro-1 into P- cells reconstituted both P+ phenotype and AP-1-dependent phorbol-ester-inducible transactivation. P- and P+ cells exhibited induction of c-jun and c-fos messenger RNA levels by phorbol ester, but P- cells had significantly lower basal and induced levels of jun mRNA than P+ cells. Basal and induced levels of c-jun protein were significantly lower in P- cells as well. Differences in levels the 80-kDa pI 4.5 protein p80 were also observed in JB6 cells as a function of preneoplastic progression; high levels of p80 protein and mRNA were observed in P- cells, intermediate levels in P+ cells, and negligible levels were observed in transformed derivatives of JB6 cells. Phorbol ester treatment induced phosphorylation but not synthesis of p80. These data are consistent with the hypotheses that AP-1 is required in the signal transduction pathway for promotion of neoplastic transformation by tumor promoter, that pro genes may control AP-1 activity, that threshold levels of Jun mRNA and protein may play a role in transactivation and promotion sensitivity, and that the p80 protein in JB6 cells may behave in vivo as a suppressor of cellular transformation. JF - Environmental health perspectives AU - Bernstein, L R AU - Ben-Ari, E T AU - Simek, S L AU - Colburn, N H AD - Cell Biology Section, National Cancer Institute-FCRDC, Frederick, MD 21702. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 111 EP - 119 VL - 93 SN - 0091-6765, 0091-6765 KW - c-fos KW - c-jun KW - fos KW - jun KW - pro 1 KW - pro 2 KW - Carcinogens KW - 0 KW - Neoplasm Proteins KW - Proto-Oncogene Proteins c-fos KW - Proto-Oncogene Proteins c-jun KW - RNA, Messenger KW - RNA, Neoplasm KW - Recombinant Fusion Proteins KW - protein p80 KW - Index Medicus KW - RNA, Neoplasm -- biosynthesis KW - Recombinant Fusion Proteins -- biosynthesis KW - Animals KW - Carcinogens -- pharmacology KW - Clone Cells -- pathology KW - Mice, Inbred BALB C -- genetics KW - Transcriptional Activation -- drug effects KW - Amino Acid Sequence KW - Mice KW - RNA, Messenger -- biosynthesis KW - Phosphorylation KW - Protein Binding -- drug effects KW - Enhancer Elements, Genetic KW - Molecular Sequence Data KW - Cell Line, Transformed KW - Genetic Predisposition to Disease KW - Clone Cells -- drug effects KW - Neoplasm Proteins -- biosynthesis KW - Proto-Oncogene Proteins c-fos -- metabolism KW - Proto-Oncogene Proteins c-fos -- genetics KW - Epidermis -- cytology KW - Neoplasm Proteins -- genetics KW - Cell Transformation, Neoplastic -- chemically induced KW - Proto-Oncogene Proteins c-jun -- genetics KW - Proto-Oncogene Proteins c-jun -- metabolism KW - Neoplasm Proteins -- metabolism KW - Gene Expression Regulation, Neoplastic -- drug effects KW - Cell Transformation, Neoplastic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72615673?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Gene+regulation+and+genetic+susceptibility+to+neoplastic+transformation%3A+AP-1+and+p80+expression+in+JB6+cells.&rft.au=Bernstein%2C+L+R%3BBen-Ari%2C+E+T%3BSimek%2C+S+L%3BColburn%2C+N+H&rft.aulast=Bernstein&rft.aufirst=L&rft.date=1991-06-01&rft.volume=93&rft.issue=&rft.spage=111&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 - 1992-03-03 N1 - Date created - 1992-03-03 N1 - Date revised - 2017-01-13 N1 - Gene symbol - c-fos; c-jun; fos; jun; pro 1; pro 2 N1 - SuppNotes - Cited By: Am J Physiol. 1988 Jul;255(1 Pt 1):E70-9 [2839039] Nature. 1970 Aug 15;227(5259):680-5 [5432063] Science. 1987 Dec 4;238(4832):1386-92 [2825349] Int J Cancer. 1986 Feb 15;37(2):293-302 [3002990] Mol Cell Biol. 1987 Jun;7(6):2256-66 [3037355] Cell. 1987 Jun 19;49(6):741-52 [3034433] Science. 1988 May 20;240(4855):1010-6 [3130660] Cell. 1988 Aug 12;54(4):553-60 [3135941] Cell. 1988 Aug 12;54(4):541-52 [3135940] Cell. 1988 Dec 2;55(5):907-15 [3142691] Cell. 1988 Dec 2;55(5):875-85 [3142689] Nature. 1988 Aug 18;334(6183):629-31 [2457172] Toxicology. 1989 Mar;54(3):241-71 [2650016] Proc Natl Acad Sci U S A. 1989 Apr;86(7):2257-61 [2648396] Proc Natl Acad Sci U S A. 1989 Oct;86(19):7410-4 [2798414] J Biol Chem. 1988 May 5;263(13):6424-31 [3360787] Carcinogenesis. 1988 Feb;9(2):239-45 [3338107] Nature. 1984 Oct 4-10;311(5985):433-8 [6090941] EMBO J. 1986 Jan;5(1):77-83 [3956481] J Biol Chem. 1985 Dec 5;260(28):15194-9 [3905792] Science. 1990 Jan 5;247(4938):12-3 [2403692] J Cell Physiol. 1984 Feb;118(2):133-42 [6319436] J Cell Biochem. 1982;18(3):261-70 [7068782] Proc Natl Acad Sci U S A. 1980 Sep;77(9):5201-5 [6159641] Teratog Carcinog Mutagen. 1980;1(1):87-96 [6119803] Carcinogenesis. 1984 Sep;5(9):1115-21 [6467502] Mol Cell Biol. 1983 Aug;3(8):1527-32 [6621538] J Cell Physiol. 1983 Feb;114(2):173-8 [6822609] J Natl Cancer Inst. 1982 Nov;69(5):1147-54 [6957659] Proc Natl Acad Sci U S A. 1982 Aug;79(16):4988-91 [6956909] J Natl Cancer Inst. 1982 Mar;68(3):469-73 [6950175] Proc Natl Acad Sci U S A. 1981 Nov;78(11):6912-6 [6947266] Ann N Y Acad Sci. 1981 Feb 27;359:251-9 [6942676] Carcinog Compr Surv. 1982;7:231-5 [7066919] Carcinogenesis. 1981;2(10):951-8 [7296762] Proc Natl Acad Sci U S A. 1979 Sep;76(9):4350-4 [388439] Nature. 1979 Oct 18;281(5732):589-91 [492322] Mol Cell Biol. 1989 Mar;9(3):1327-31 [2498646] Science. 1989 May 5;244(4904):566-9 [2541502] Science. 1988 Dec 9;242(4884):1424-7 [2462278] Cell. 1987 Jun 19;49(6):729-39 [3034432] Carcinogenesis. 1986 Dec;7(12):1949-56 [3096584] EMBO J. 1989 Sep;8(9):2567-74 [2511007] EMBO J. 1989 Sep;8(9):2559-66 [2511006] Mol Cell Biol. 1989 Sep;9(9):3727-35 [2789336] Science. 1989 Oct 13;246(4927):249-51 [2799385] Gene. 1988 Aug 15;68(1):63-72 [3146526] Nature. 1989 Feb 16;337(6208):661-3 [2537468] Cell. 1988 Mar 11;52(5):705-12 [2830989] Carcinogenesis. 1988 Feb;9(2):203-7 [2827903] J Biol Chem. 1977 Nov 25;252(22):8310-9 [914873] Nature. 1988 Jul 28;334(6180):314-9 [2839774] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Identification of genes associated with tumor suppression in Syrian hamster embryo cells. AN - 72615128; 1773782 AB - Loss of a tumor-suppressor gene function appears to play a critical role in the multistep process of neoplastic transformation of Syrian hamster embryo (SHE) cells in vitro. Clonal variants of two independent, preneoplastic cell lines have been isolated that have either retained (termed supB+) or lost (termed supB-) the ability to suppress the tumorigenicity of a highly malignant benzo[alpha]pyrene-transformed SHE cell line (BP6T) in cell hybrids. We have pursued several approaches in an attempt to identify genes that are responsible for tumor suppression in these cells. The only consistent differences detected in two-dimensional gel analyses of supB+ and supB- cellular proteins were decreases in the levels of two high molecular weight isoforms of tropomyosin in supB- cells. Differential screening of a supB+ cDNA library for genes that are preferentially expressed in supB+ cells yielded cDNA clones for four genes, i.e., collagen type II, collagen type IX, H19, and a previously unidentified gene (clone 5). Nuclear run-on assays suggested that higher transcription rates were responsible for the increased steady-state levels of some of these transcripts in supB+ cells. DNA sequence comparisons showed that two copies of a 9 bp element, previously identified in each of the mouse H19 enhancers, were also present in the 5' flanking region of the rat type II collagen gene. A transcription factor that controls expression of the collagen and H19 genes through binding to this conserved motif would be an attractive candidate for the supB+ gene or at least a mediator of the supB+ phenotype. JF - Environmental health perspectives AU - Wiseman, R W AU - Montgomery, J C AU - Hosoi, J AU - Hou, E W AU - Cochran, C J AU - Lamb, P W AU - Barrett, J C AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 105 EP - 109 VL - 93 SN - 0091-6765, 0091-6765 KW - supB+ KW - Biomarkers, Tumor KW - 0 KW - DNA, Neoplasm KW - Tropomyosin KW - Benzo(a)pyrene KW - 3417WMA06D KW - Collagen KW - 9007-34-5 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Collagen -- analysis KW - Transcription, Genetic KW - Tropomyosin -- analysis KW - Phenotype KW - Gene Expression Regulation, Neoplastic KW - Base Sequence KW - DNA -- genetics KW - Electrophoresis, Gel, Two-Dimensional KW - Molecular Sequence Data KW - Biomarkers, Tumor -- analysis KW - Hybrid Cells KW - DNA, Neoplasm -- genetics KW - Cell Line, Transformed KW - Cricetinae KW - Mesocricetus -- genetics KW - Genes, Tumor Suppressor KW - Mesocricetus -- embryology KW - Cell Transformation, Neoplastic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72615128?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Identification+of+genes+associated+with+tumor+suppression+in+Syrian+hamster+embryo+cells.&rft.au=Wiseman%2C+R+W%3BMontgomery%2C+J+C%3BHosoi%2C+J%3BHou%2C+E+W%3BCochran%2C+C+J%3BLamb%2C+P+W%3BBarrett%2C+J+C&rft.aulast=Wiseman&rft.aufirst=R&rft.date=1991-06-01&rft.volume=93&rft.issue=&rft.spage=105&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 - 1992-03-03 N1 - Date created - 1992-03-03 N1 - Date revised - 2017-01-13 N1 - Gene symbol - supB+ N1 - SuppNotes - Cited By: Science. 1990 Jan 5;247(4938):49-56 [2294591] Adv Cancer Res. 1990;54:25-62 [2404380] Cell. 1983 Sep;34(2):557-67 [6311432] J Biol Chem. 1983 Nov 25;258(22):13954-64 [6315714] Nucleic Acids Res. 1983 Sep 10;11(17):6021-39 [6310524] Proc Natl Acad Sci U S A. 1981 Sep;78(9):5633-7 [6272310] Cell. 1982 Sep;30(2):481-90 [6291771] Nature. 1983 Oct 27-Nov 2;305(5937):779-84 [6633649] Science. 1982 Jan 15;215(4530):252-9 [7053574] Cancer Res. 1980 Jan;40(1):91-4 [7349908] Proc Natl Acad Sci U S A. 1978 Aug;75(8):3761-5 [278986] Nature. 1988 Sep 29;335(6189):400-2 [3419514] Cancer Res. 1988 Mar 15;48(6):1623-32 [2449958] J Cell Biol. 1989 Jan;108(1):191-7 [2463256] Cell. 1989 Jan 13;56(1):77-84 [2642744] Nature. 1986 Oct 16-22;323(6089):643-6 [2877398] Cancer Res. 1985 Apr;45(4):1437-43 [2983882] Eur J Biochem. 1989 Jan 15;179(1):71-8 [2465149] Mol Cell Biol. 1988 Nov;8(11):4707-15 [2463463] J Biol Chem. 1989 Mar 25;264(9):5299-312 [2564397] Cell. 1989 Jun 30;57(7):1083-93 [2525423] Cancer Res. 1989 Jul 15;49(14):3713-21 [2660980] Science. 1989 Apr 14;244(4901):217-21 [2649981] Proc Natl Acad Sci U S A. 1989 Nov;86(22):8773-7 [2813423] J Biol Chem. 1989 Mar 25;264(9):5269-82 [2925692] Science. 1988 Dec 16;242(4885):1563-6 [3201247] EMBO J. 1988 Mar;7(3):673-81 [3396539] Cancer Res. 1988 Jun 15;48(12):3302-6 [3370633] Proc Natl Acad Sci U S A. 1986 Aug;83(16):5992-6 [3461473] Cell. 1987 Dec 24;51(6):987-1000 [3690668] Proc Natl Acad Sci U S A. 1985 May;82(9):2555-9 [3857598] Mol Cell Biol. 1985 May;5(5):972-83 [4000123] Nature. 1990 Aug 16;346(6285):668-71 [2117257] Mol Cell Biol. 1990 Jan;10(1):28-36 [1688465] Science. 1990 Jul 13;249(4965):181-6 [2134734] Cell. 1990 Jul 13;62(1):193-201 [2114220] Cell. 1990 Jun 1;61(5):759-67 [2188735] Nature. 1984 Mar 8-14;308(5955):149-53 [6199676] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Two simple indexes used to evaluate the impact of therapy on the quality of life of patients receiving primary chemotherapy for operable breast cancer. AN - 72609195; 1768628 AB - The psychometric characteristics of two indexes used to evaluate the subjective morbidity of chemotherapy regimens were analyzed. Both indexes assessed the duration of discomfort as perceived by the patient throughout therapy. The first index asked patients to state the number of days spent with 'discomfort', and the second index asked them which days they would like to eliminate altogether because of the unbearable symptoms experienced on those days. While the first index gives some idea of the duration of suffering, without defining it, the second highlights a specific time when the quality of her life was unacceptable to the patient. We studied these indexes in the form of a questionnaire completed by 168 women who had entered a cancer clinical trial. This trial evaluated the efficacy of primary chemotherapy in rendering conservative surgery feasible in women with operable breast cancer, but whose tumor size was greater than 3 cm. Four different treatment regimens were used: CMF, FAC, FEC, FNC (C = cyclophosphamide, M = methotrexate, F = fluorouracil, A = adriamycin, E = epirubicin, N = mitoxantrone). Seventy-nine patients were interviewed during chemotherapy and 89 during follow-up visits. Initial assessment of the reliability, discriminant and concurrent validity of the two indexes produced satisfactory results. Finally, we analyzed the responses given by 168 patients for a total of 600 treatment cycles. The average value of 'discomfort' was 3 days, whereas the average value of days 'to be eliminated' was 1. The range of subjective morbidity (for every cycle of treatment: 'discomfort = 0-30 days; 'to be eliminated' = 0-20 days) was very broad.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Annals of oncology : official journal of the European Society for Medical Oncology AU - Tamburini, M AU - Brambilla, C AU - Ferrari, L AU - Bombino, T AU - Gangeri, L AU - Rosso, S AD - Division of Psychological Research, National Cancer Institute, Milan. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 417 EP - 422 VL - 2 IS - 6 SN - 0923-7534, 0923-7534 KW - Epirubicin KW - 3Z8479ZZ5X KW - Doxorubicin KW - 80168379AG KW - Cyclophosphamide KW - 8N3DW7272P KW - Mitoxantrone KW - BZ114NVM5P KW - Fluorouracil KW - U3P01618RT KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - Cyclophosphamide -- administration & dosage KW - Discriminant Analysis KW - Reproducibility of Results KW - Lymphatic Metastasis KW - Humans KW - Mitoxantrone -- administration & dosage KW - Doxorubicin -- administration & dosage KW - Fluorouracil -- administration & dosage KW - Surveys and Questionnaires KW - Middle Aged KW - Epirubicin -- administration & dosage KW - Methotrexate -- administration & dosage KW - Chemotherapy, Adjuvant KW - Female KW - Breast Neoplasms -- drug therapy KW - Quality of Life KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Breast Neoplasms -- surgery KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72609195?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Two+simple+indexes+used+to+evaluate+the+impact+of+therapy+on+the+quality+of+life+of+patients+receiving+primary+chemotherapy+for+operable+breast+cancer.&rft.au=Tamburini%2C+M%3BBrambilla%2C+C%3BFerrari%2C+L%3BBombino%2C+T%3BGangeri%2C+L%3BRosso%2C+S&rft.aulast=Tamburini&rft.aufirst=M&rft.date=1991-06-01&rft.volume=2&rft.issue=6&rft.spage=417&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 - 1992-02-27 N1 - Date created - 1992-02-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Should the presence of carcinogens in breast milk discourage breast feeding? AN - 72466065; 1947235 AB - Pollutant chemicals are commonly found in human milk at levels that would prevent its sale as a commercial food for infants. The chemicals found most commonly are dichlorodiphenyl-dichloroethene, polychlorinated biphenyls, dieldrin, chlordane, heptachlor, and polychlorinated dibenzodioxins. In general, the regulatory levels for these chemicals have been set to prevent cancer in adult humans from lifetime exposure. We compared lives saved in the postneonatal period by breast feeding to the estimated excess cancer deaths attributable to the contaminants in breast milk. The results of this analysis suggest that only extreme levels of contaminants in breast milk represent more of a hazard than failure to breast feed, but clinical considerations in individual cases might override this conclusion. Our analysis depends on assumptions about how the chemicals might cause cancer in humans and on whether breast feeding prevents some postneonatal mortality. Noncarcinogenic hazards from chemical exposure, other hazards from breast feeding such as transmission of viruses, and benefits of breast feeding other than reduction in mortality were not considered. JF - Regulatory toxicology and pharmacology : RTP AU - Rogan, W J AU - Blanton, P J AU - Portier, C J AU - Stallard, E AD - Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 228 EP - 240 VL - 13 IS - 3 SN - 0273-2300, 0273-2300 KW - Carcinogens KW - 0 KW - Polychlorinated Biphenyls KW - DFC2HB4I0K KW - Index Medicus KW - United States KW - Infant KW - Neoplasms -- mortality KW - Humans KW - Neoplasms -- epidemiology KW - Life Expectancy KW - Infant, Newborn KW - Polychlorinated Biphenyls -- analysis KW - Female KW - Milk, Human -- chemistry KW - Breast Feeding KW - Carcinogens -- toxicity KW - Carcinogens -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72466065?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Should+the+presence+of+carcinogens+in+breast+milk+discourage+breast+feeding%3F&rft.au=Rogan%2C+W+J%3BBlanton%2C+P+J%3BPortier%2C+C+J%3BStallard%2C+E&rft.aulast=Rogan&rft.aufirst=W&rft.date=1991-06-01&rft.volume=13&rft.issue=3&rft.spage=228&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 - 1991-12-11 N1 - Date created - 1991-12-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Plasma pharmacokinetics and tissue penetration of a novel antifungal triazole, Bay R 3783, and its long-lasting active metabolite, Bay U 3625, in rabbits. AN - 72446490; 1938690 AB - The plasma pharmacokinetics and tissue penetration of Bay R 3783 (BR), a new antifungal triazole, and one of its active metabolites, Bay U 3625 (BU), were studied in rabbits. Plasma levels of BR and BU were determined simultaneously in five rabbits for six days after a single oral dose of 20 or 40 mg/kg BR. For BR, the mean Cmax was 1.9 +/- 0.4 mg/l, the Tmax 2.0 +/- 0.7 h, the AUC alpha 7.5 +/- 1.6 mg.h/l, and the terminal plasma T1/2 2.1 +/- 0.1 h. For BU, the mean Cmax was 0.84 +/- 0.09 mg/l, the Tmax 24 +/- 4 h, the AUC alpha 61.9 +/- 6.5 mg.h/l, and the plasma T1/2 was 48 +/- 3 h. In a multi-dose study, the plasma BR clearance during wash-out gradually diminished, suggesting possible metabolite inhibition of BRs biotransformation. No hepatic or renal toxicity was seen after 28 days of dosing with BR 40 mg/kg/d. Both BR and BU penetrated well into tissues, with tissue drug concentrations over three times higher than in plasma at multiple tissue sites. Persistence of BU in plasma, however, resulted in prolonged, higher tissue levels of BU than of BR. We conclude that BR is converted to a long-lasting active metabolite BU, that persistence of BU in tissue is prolonged, and that these properties may permit BU to contribute significantly to the antifungal activity of BR. JF - The Journal of antimicrobial chemotherapy AU - Lee, J W AU - Ritter, W AU - Lecciones, J AU - Kelly, P AU - Pizzo, P A AU - Walsh, T J AD - Infectious Disease Section, National Cancer Institute, Bethesda, MD. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 837 EP - 844 VL - 27 IS - 6 SN - 0305-7453, 0305-7453 KW - Antifungal Agents KW - 0 KW - Triazoles KW - Bay R 3783 KW - 126040-72-0 KW - Bay U 3625 KW - 126489-86-9 KW - Index Medicus KW - Animals KW - Drug Administration Schedule KW - Half-Life KW - Metabolic Clearance Rate KW - Rabbits KW - Tissue Distribution KW - Time Factors KW - Female KW - Antifungal Agents -- pharmacokinetics KW - Triazoles -- blood KW - Triazoles -- pharmacokinetics KW - Antifungal Agents -- blood KW - Triazoles -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72446490?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+antimicrobial+chemotherapy&rft.atitle=Plasma+pharmacokinetics+and+tissue+penetration+of+a+novel+antifungal+triazole%2C+Bay+R+3783%2C+and+its+long-lasting+active+metabolite%2C+Bay+U+3625%2C+in+rabbits.&rft.au=Lee%2C+J+W%3BRitter%2C+W%3BLecciones%2C+J%3BKelly%2C+P%3BPizzo%2C+P+A%3BWalsh%2C+T+J&rft.aulast=Lee&rft.aufirst=J&rft.date=1991-06-01&rft.volume=27&rft.issue=6&rft.spage=837&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+antimicrobial+chemotherapy&rft.issn=03057453&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-26 N1 - Date created - 1991-12-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential inhibition of 2'-deoxycytidine salvage as a possible mechanism for potentiation of the anti-human immunodeficiency virus activity of 2',3'-dideoxycytidine by dipyridamole. AN - 72167482; 1656858 AB - Dipyridamole, a commonly used coronary vasodilator and antithrombotic drug, was recently shown to potentiate the activity of 3'-azido-3'-deoxythymidine and 2',3'-dideoxycytidine against the human immunodeficiency virus type 1 (HIV-1) in human monocyte-macrophages in vitro. We report in the present paper that in uninfected monocyte-macrophages dipyridamole significantly inhibits cellular salvage of [3H]deoxycytidine, whereas it does not affect the salvage of [3H]dideoxycytidine. Similar differential inhibition by dipyridamole of the salvage of thymidine, as opposed to 3'-azido-3'-deoxythymidine, was reported previously (G. V. Betageri, J. Szebeni, K. Hung, S. S. Patel, L. M. Wahl, M. Corcoran, and J. N. Weinstein, Biochem. Pharmacol. 40:867-870, 1990). Taken together, these observations suggest that inhibition of the salvage of competing physiological nucleosides may explain or contribute to the potentiating effect of dipyridamole on these antiviral dideoxynucleoside drugs. JF - Antimicrobial agents and chemotherapy AU - Patel, S S AU - Szebeni, J AU - Wahl, L M AU - Weinstein, J N AD - National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 1250 EP - 1253 VL - 35 IS - 6 SN - 0066-4804, 0066-4804 KW - Antiviral Agents KW - 0 KW - Deoxycytidine KW - 0W860991D6 KW - Dipyridamole KW - 64ALC7F90C KW - Zalcitabine KW - 6L3XT8CB3I KW - Index Medicus KW - AIDS/HIV KW - Phosphorylation KW - Humans KW - Monocytes -- microbiology KW - Drug Synergism KW - Chromatography, High Pressure Liquid KW - HIV-1 -- metabolism KW - Deoxycytidine -- metabolism KW - Zalcitabine -- pharmacology KW - Dipyridamole -- pharmacology KW - Antiviral Agents -- metabolism KW - HIV-1 -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72167482?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antimicrobial+agents+and+chemotherapy&rft.atitle=Differential+inhibition+of+2%27-deoxycytidine+salvage+as+a+possible+mechanism+for+potentiation+of+the+anti-human+immunodeficiency+virus+activity+of+2%27%2C3%27-dideoxycytidine+by+dipyridamole.&rft.au=Patel%2C+S+S%3BSzebeni%2C+J%3BWahl%2C+L+M%3BWeinstein%2C+J+N&rft.aulast=Patel&rft.aufirst=S&rft.date=1991-06-01&rft.volume=35&rft.issue=6&rft.spage=1250&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+agents+and+chemotherapy&rft.issn=00664804&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-08 N1 - Date created - 1991-11-08 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Ann N Y Acad Sci. 1990;616:367-84 [2078029] Methods Cell Biol. 1978;20:211-36 [692430] J Exp Med. 1988 Sep 1;168(3):1111-25 [2844951] Proc Natl Acad Sci U S A. 1987 Apr;84(7):2033-7 [2436223] Proc Natl Acad Sci U S A. 1985 Oct;82(20):7096-100 [2413459] Biochem Pharmacol. 1989 Oct 15;38(20):3469-75 [2554924] Biochem Int. 1989 Aug;19(2):227-34 [2554906] Adv Exp Med Biol. 1989;253B:415-20 [2558543] Proc Natl Acad Sci U S A. 1989 May;86(10):3842-6 [2542948] Lancet. 1988 Jan 16;1(8577):76-81 [2891981] Antimicrob Agents Chemother. 1988 Jul;32(7):997-1001 [3190201] Adv Enzyme Regul. 1983;21:53-69 [6443595] N Engl J Med. 1987 May 14;316(20):1247-57 [3553945] Biochem Pharmacol. 1984 Nov 1;33(21):3325-31 [6497896] Am J Med. 1990 May 21;88(5B):31S-33S [2159708] J Acquir Immune Defic Syndr. 1990;3(1):28-31 [2152803] Biochem Pharmacol. 1990 Aug 15;40(4):867-70 [2386551] J Cell Physiol. 1983 Aug;116(2):236-46 [6306018] Cell Immunol. 1984 May;85(2):384-95 [6232003] Cell Immunol. 1984 May;85(2):373-83 [6232002] J Biol Chem. 1988 Sep 5;263(25):12391-6 [2842332] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Bacterial lipopolysaccharide acts synergistically with selected macromolecular polyanions to induce MHC-nonrestricted cytotoxic cells. AN - 72131944; 1916877 AB - We examined whether bacterial lipopolysaccharide, at a dose range extending to less than 1.0 ng/ml, would work with cofactors to induce MHC-nonrestricted cytotoxic cells. To this end, normal mouse splenocytes were cultured for 5 days with LPS and potential cofactors, after which the cells were tested for cytotoxic activity in short-term 51Cr-release assays. We found that LPS can act synergistically with the macromolecular polyanions, dextran sulfate and polyinosinic acid. The effector cells induced by LPS and polyanions showed characteristics of activated NK cells in that they were (1) cytotoxic for widely differing sources of tumor cells, (2) not inhibited by an anti-T cell receptor antibody, and (3) not removed by depletion of CD4+ or CD8+ cells. LPS was active at picogram concentrations when dextran sulfate was included. Exposure of splenocytes to LPS was necessary during the early phase of the 5-day culture, but as little as 1 h of exposure was required, whereas exposure to the macromolecular polyanions during either the first or the last 2 days of a 5-day culture with LPS was effective. As expected with LPS activity, the cytotoxic cell response was prevented by polymyxin B or by the use of splenocytes from LPS non-responder C3H/HeJ mice. Screening of the S. minnesota R mutants and other partial LPS structures revealed that lipid A was closely associated with LPS activity in this assay system and that at least one partially detoxified structure, a deacylated LPS, could substitute for native LPS. JF - Immunobiology AU - Winkler, D F AU - Myers, K R AU - Hochstein, H D AU - Ulrich, J T AU - Wunderlich, J R AD - Experimental Immunology Branch, DCBDC, NCI, NIH, Bethesda, Maryland. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 216 EP - 233 VL - 182 IS - 3-4 SN - 0171-2985, 0171-2985 KW - Antigens, CD4 KW - 0 KW - Antigens, CD8 KW - Lipid A KW - Lipopolysaccharides KW - Polymyxin B KW - 1404-26-8 KW - Dextran Sulfate KW - 9042-14-2 KW - Index Medicus KW - Animals KW - Lymphocytes -- immunology KW - Cells, Cultured KW - Mice, Inbred C57BL KW - Mice, Inbred C3H KW - Spleen -- immunology KW - Mice KW - Polymyxin B -- pharmacology KW - Drug Synergism KW - Lipid A -- pharmacology KW - Male KW - Antigens, CD4 -- immunology KW - Antigens, CD8 -- immunology KW - Cytotoxicity, Immunologic -- physiology KW - Dextran Sulfate -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72131944?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Immunobiology&rft.atitle=Bacterial+lipopolysaccharide+acts+synergistically+with+selected+macromolecular+polyanions+to+induce+MHC-nonrestricted+cytotoxic+cells.&rft.au=Winkler%2C+D+F%3BMyers%2C+K+R%3BHochstein%2C+H+D%3BUlrich%2C+J+T%3BWunderlich%2C+J+R&rft.aulast=Winkler&rft.aufirst=D&rft.date=1991-06-01&rft.volume=182&rft.issue=3-4&rft.spage=216&rft.isbn=&rft.btitle=&rft.title=Immunobiology&rft.issn=01712985&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-07 N1 - Date created - 1991-11-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Constant risk differences in the analysis of animal tumorigenicity data. AN - 72116087; 1912267 AB - In a typical tumorigenicity study, most tumors are not observable in live animals and only a single (terminal) sacrifice is performed. This paper proposes a nonparametric, survival-adjusted analysis for these data that focuses on tumor incidence and yet does not require data on cause of death or assumptions about the tumor's lethality. The tumor onset/death process is most naturally characterized in terms of the tumor incidence rate and the death rates for tumor-free and tumor-bearing animals. The proposed approach, however, reparameterizes the problem in terms of the incidence rate, the death rate for tumor-free animals, and the difference between the death rates for tumor-free and tumor-bearing animals (i.e., the risk difference). The advantage of this alternative formulation is that a full likelihood analysis is possible with as few as one sacrifice time if the risk difference is assumed to be constant with respect to time. Data from the large ED01 study suggest that reasonable results can be obtained under the assumption of constant risk differences. JF - Biometrics AU - Dinse, G E AD - Division of Biometry and Risk Assessment, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 681 EP - 700 VL - 47 IS - 2 SN - 0006-341X, 0006-341X KW - Carcinogens KW - 0 KW - Index Medicus KW - Regression Analysis KW - Animals KW - Carcinogens -- administration & dosage KW - Neoplasms, Experimental -- chemically induced KW - Risk Factors KW - Algorithms KW - Data Interpretation, Statistical KW - Likelihood Functions KW - Survival Analysis KW - Biometry KW - Carcinogenicity Tests -- statistics & numerical data UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72116087?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biometrics&rft.atitle=Constant+risk+differences+in+the+analysis+of+animal+tumorigenicity+data.&rft.au=Dinse%2C+G+E&rft.aulast=Dinse&rft.aufirst=G&rft.date=1991-06-01&rft.volume=47&rft.issue=2&rft.spage=681&rft.isbn=&rft.btitle=&rft.title=Biometrics&rft.issn=0006341X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-13 N1 - Date created - 1991-11-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modulation of the mitogenic activity of eukaryotic translation initiation factor-4E by protein kinase C. AN - 72113171; 1911648 AB - Eukaryotic initiation factor-4E (eIF-4E) binds to the cap structure of eukaryotic mRNAs and is a component of the cap-binding protein complex eIF-4F. eIF-4E is present in cells in limiting concentrations and is phosphorylated both in vivo and in vitro by protein kinase C (PKC). Recently, eIF-4E has been implicated as an intracellular transducer of extracellular growth signals; microinjection of recombinant eIF-4E into quiescent NIH 3T3 cells induced DNA synthesis. In the present report, the mitogenic activity of eIF-4E was examined after coinjection with PKC. Recombinant eIF-4E was phosphorylated by PKC at the same amino acid that is phosphorylated in cultured cells and reticulocytes in response to phorbol ester. At limiting concentrations of eIF-4E, coinjection with PKC induced a fivefold increase in the mitogenic activity of eIF-4E. Injection of PKC alone or coinjection of eIF-4E with cAMP-dependent protein kinase (PKA) or the Raf protein had no effect. These results suggest that the mitogenic activity of eIF-4E is enhanced by PKC-specific phosphorylation and that phosphate addition is a rate-limiting step in eIF-4E activity. JF - The New biologist AU - Smith, M R AU - Jaramillo, M AU - Tuazon, P T AU - Traugh, J A AU - Liu, Y L AU - Sonenberg, N AU - Kung, H F AD - Biological Carcinogenesis and Development Program, National Cancer Institute, Frederick Cancer Research and Development Center, MD 21702-1201. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 601 EP - 607 VL - 3 IS - 6 SN - 1043-4674, 1043-4674 KW - Eukaryotic Initiation Factor-4E KW - 0 KW - Mitogens KW - Peptide Initiation Factors KW - RNA, Messenger KW - DNA KW - 9007-49-2 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Index Medicus KW - Protein Biosynthesis -- drug effects KW - Animals KW - RNA, Messenger -- metabolism KW - Phosphorylation KW - Microinjections KW - RNA, Messenger -- genetics KW - Drug Synergism KW - DNA -- biosynthesis KW - Cell Line KW - Protein Kinase C -- metabolism KW - Peptide Initiation Factors -- metabolism KW - Protein Kinase C -- administration & dosage KW - Peptide Initiation Factors -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72113171?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+biologist&rft.atitle=Modulation+of+the+mitogenic+activity+of+eukaryotic+translation+initiation+factor-4E+by+protein+kinase+C.&rft.au=Smith%2C+M+R%3BJaramillo%2C+M%3BTuazon%2C+P+T%3BTraugh%2C+J+A%3BLiu%2C+Y+L%3BSonenberg%2C+N%3BKung%2C+H+F&rft.aulast=Smith&rft.aufirst=M&rft.date=1991-06-01&rft.volume=3&rft.issue=6&rft.spage=601&rft.isbn=&rft.btitle=&rft.title=The+New+biologist&rft.issn=10434674&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-01 N1 - Date created - 1991-11-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Biochemical and molecular epidemiology of cancer. AN - 72112839; 1910603 AB - Examples of practical approaches to molecular epidemiology of human cancer are described. Biomarkers of carcinogen exposure or inherited host factors for cancer susceptibility are discussed. Major advances have been made in the detection of carcinogenmacromolecular adducts through the use of high performance liquid chromatography, immunoaffinity chromatography, the 32P-postlabeling assay, enzyme immunoassays, gas chromatography/mass spectroscopy and synchronous spectrophotofluorimetry. The polycyclic aromatic hydrocarbon-DNA adducts are the most extensively studied in this field and together with antibodies to these adducts found in human serum, they have become useful indicators of exposure to carcinogens. Assays for various kinds of alkyl-DNA adducts have also been developed and the presence of these adducts have been documented in human tissues. Carcinogen-protein adducts have proven to be useful molecular dosimeters of carcinogen exposure. For example, 4-aminobiphenyl hemoglobin adducts are highly correlated with exposure to tobacco smoke. The study of the molecular aspects of interindividual differences in the metabolism and activation of xenobiotics and other genetic markers [DNA-restriction fragment length polymorphisms (RFLPs), mutations, and functional loss of specific genes in carcinogenesis] is an emerging new field that is discussed in the context of genetic susceptibility to cancer. The cytochrome P450 phenotypes and acetylation phenotype are examples of genetic markers that indicate an individual's potential for metabolism of exogenous substances. Further, inherited genetic polymorphic markers, e.g., DNA-RFLPs at protooncogene loci (HRAS-1 and L-myc) have been examined in a case-control study of lung cancer. Data concerning mutations of protooncogenes (H-, K-, and N-RAS) and tumor suppressor genes (retinoblastoma and p53 genes) in various common cancers are providing evidence of multiple genetic lesions that occur during the multistage process of carcinogenesis. JF - Biomedical and environmental sciences : BES AU - Sugimura, H AU - Weston, A AU - Caporaso, N E AU - Shields, P G AU - Bowman, E D AU - Metcalf, R A AU - Harris, C C AD - Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Rockville, Maryland 20892. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 73 EP - 92 VL - 4 IS - 1-2 SN - 0895-3988, 0895-3988 KW - Biomarkers KW - 0 KW - Carcinogens KW - Index Medicus KW - Disease Susceptibility KW - DNA Damage KW - Humans KW - Neoplasms -- epidemiology KW - Neoplasms -- genetics KW - Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72112839?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biomedical+and+environmental+sciences+%3A+BES&rft.atitle=Biochemical+and+molecular+epidemiology+of+cancer.&rft.au=Sugimura%2C+H%3BWeston%2C+A%3BCaporaso%2C+N+E%3BShields%2C+P+G%3BBowman%2C+E+D%3BMetcalf%2C+R+A%3BHarris%2C+C+C&rft.aulast=Sugimura&rft.aufirst=H&rft.date=1991-06-01&rft.volume=4&rft.issue=1-2&rft.spage=73&rft.isbn=&rft.btitle=&rft.title=Biomedical+and+environmental+sciences+%3A+BES&rft.issn=08953988&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-21 N1 - Date created - 1991-11-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Spontaneous electrical activity regulates vasoactive intestinal peptide expression in dissociated spinal cord cell cultures. AN - 72083835; 1715967 AB - Activity-dependent expression of vasoactive intestinal peptide (VIP) was investigated in spinal cord/dorsal root ganglia cultures derived from embryonic mice. Since all spinal cord neurons appear to exhibit spontaneous action potentials after one week in vitro, activity-dependent regulation of VIP-transcripts (mRNAVIP) could be studied with or without electrical blockade induced by tetrodotoxin (TTX). In 10-day-old cultures, a 50% decrease in mRNAVIP was observed after 3 days of treatment with TTX. The decrease in mRNAVIP was reversed upon removal of the TTX and was dependent on the age of the cultures: no decreases from control were observed in 5-day-old cultures and much smaller decrements were produced in one month old cultures treated with TTX. A variety of neuroactive substances were tested for effects on mRNAVIP in electrically active and electrically blocked cultures. Application of 8-bromo-cAMP (cAMP), N-methyl-D-aspartate (NMDA), substance P, muscimol, A23187 and VIP to electrically active cultures resulted in a 2- to 3-fold increase in mRNAVIP, while phorbol myristate 13-acetate (PMA) and 8-bromo-cGMP (cGMP) had no effect. In contrast, electrically inactive cultures exhibited a 3 to 4-fold increase in mRNAVIP after treatment with PMA, cAMP and VIP, while NMDA, substance P, muscimol, A23187 and cGMP produced no increases. In summary, the regulation of VIP gene expression in embryonic spinal cord neurons shows a temporal sensitivity to TTX-induced electrical blockade and may be mediated by multiple neurotransmitter inputs which converge on cAMP- and calcium-related processes in an activity-dependent manner. JF - Brain research. Molecular brain research AU - Agoston, D V AU - Eiden, L E AU - Brenneman, D E AU - Gozes, I AD - Laboratory of Cell Biology, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 235 EP - 240 VL - 10 IS - 3 SN - 0169-328X, 0169-328X KW - Actins KW - 0 KW - RNA, Messenger KW - 8-Bromo Cyclic Adenosine Monophosphate KW - 23583-48-4 KW - Muscimol KW - 2763-96-4 KW - Substance P KW - 33507-63-0 KW - Vasoactive Intestinal Peptide KW - 37221-79-7 KW - Calcimycin KW - 37H9VM9WZL KW - Tetrodotoxin KW - 4368-28-9 KW - N-Methylaspartate KW - 6384-92-5 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Blotting, Northern KW - RNA, Messenger -- analysis KW - Action Potentials -- drug effects KW - Mice KW - Calcimycin -- pharmacology KW - RNA, Messenger -- genetics KW - 8-Bromo Cyclic Adenosine Monophosphate -- pharmacology KW - Actins -- genetics KW - Substance P -- pharmacology KW - N-Methylaspartate -- pharmacology KW - Cells, Cultured KW - Kinetics KW - Second Messenger Systems -- drug effects KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Gene Expression Regulation -- drug effects KW - Time Factors KW - Embryo, Mammalian KW - Muscimol -- pharmacology KW - Vasoactive Intestinal Peptide -- pharmacology KW - Transcription, Genetic -- drug effects KW - Ganglia, Spinal -- physiology KW - Neurons -- drug effects KW - Spinal Cord -- drug effects KW - Neurons -- physiology KW - Spinal Cord -- physiology KW - Ganglia, Spinal -- drug effects KW - Tetrodotoxin -- pharmacology KW - Vasoactive Intestinal Peptide -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72083835?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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.+Molecular+brain+research&rft.atitle=Spontaneous+electrical+activity+regulates+vasoactive+intestinal+peptide+expression+in+dissociated+spinal+cord+cell+cultures.&rft.au=Agoston%2C+D+V%3BEiden%2C+L+E%3BBrenneman%2C+D+E%3BGozes%2C+I&rft.aulast=Agoston&rft.aufirst=D&rft.date=1991-06-01&rft.volume=10&rft.issue=3&rft.spage=235&rft.isbn=&rft.btitle=&rft.title=Brain+research.+Molecular+brain+research&rft.issn=0169328X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-10-07 N1 - Date created - 1991-10-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interaction of beta-funaltrexamine with [3H]cycloFOXY binding in rat brain: further evidence that beta-FNA alkylates the opioid receptor complex. AN - 72066621; 1652797 AB - beta-Funaltrexamine (beta-FNA) is an alkylating derivative of naltrexone. In addition to acting as an irreversible inhibitor of mu-receptor-mediated physiological effects, intracerebroventricular (i.c.v.) administration of beta-FNA to rat attenuates the ability of selective delta receptor antagonists and naloxone to reverse delta receptor-mediated effects. Moreover, recent work demonstrated that i.c.v. administration of beta-FNA alters the conformation of the opioid receptor complex, as inferred by a decrease in the Bmax of the lower affinity [3H][D-ala2,D-leu5]enkephalin binding site. Consistent with the decreased potency of naloxone as an inhibitor of delta receptor mediated effects, beta-FNA doubled the naloxone IC50 for displacing [3H][D-ala2,D-leu5]enkephalin from its lower affinity binding site. These data collectively support the hypothesis that the opioid receptor complex postulated to mediate mu-delta interactions in vivo is identical to the opioid receptor complex as defined by vitro ligand binding studies. A direct prediction of this hypothesis is that beta-FNA should increase the Kd of antagonists for the mu binding site (mu cx) of the receptor complex. The data reported in this paper demonstrate that beta-FNA doubled the IC50 of the potent narcotic antagonist, 6-desoxy-6 beta-fluoronaltrexone (cycloFOXY) for displacing [3H][D-ala2,D-leu5]enkephalin from its lower affinity binding site, and doubled the Kd of [3H]cycloFOXY for its mu binding site, providing additional data that the mu binding site labeled by [3H]cycloFOXY is the mu binding site of the opioid receptor complex. beta-FNA also altered the kappa binding site labeled by [3H]cycloFOXY, and when administered intrathecally to mice, beta-FNA produced a longlasting antinociception in the acetic acid writhing test. JF - Synapse (New York, N.Y.) AU - Rothman, R B AU - Bykov, V AU - Mahboubi, A AU - Long, J B AU - Jiang, Q AU - Porreca, F AU - de Costa, B R AU - Jacobson, A E AU - Rice, K C AU - Holaday, J W AD - Unit on Receptor Studies, Laboratory of Medicinal Chemistry, NIDDK, Bethesda, Maryland 20892. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 86 EP - 99 VL - 8 IS - 2 SN - 0887-4476, 0887-4476 KW - Alkylating Agents KW - 0 KW - Analgesics KW - Ligands KW - Receptors, Opioid KW - Receptors, Opioid, delta KW - Receptors, Opioid, kappa KW - Naltrexone KW - 5S6W795CQM KW - Enkephalin, Leucine-2-Alanine KW - 63631-40-3 KW - 6-deoxy-6-fluoronaltrexone KW - 669I3FR8VF KW - beta-funaltrexamine KW - 72782-05-9 KW - Index Medicus KW - Animals KW - Mice, Inbred ICR KW - Mice KW - Alkylation KW - Injections, Intraventricular KW - Rats KW - Rats, Inbred Strains KW - Kinetics KW - Enkephalin, Leucine-2-Alanine -- metabolism KW - Male KW - Surface Properties KW - Receptors, Opioid -- metabolism KW - Receptors, Opioid -- drug effects KW - Brain -- drug effects KW - Alkylating Agents -- pharmacology KW - Naltrexone -- analogs & derivatives KW - Naltrexone -- pharmacology KW - Naltrexone -- metabolism KW - Brain -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72066621?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Interaction+of+beta-funaltrexamine+with+%5B3H%5DcycloFOXY+binding+in+rat+brain%3A+further+evidence+that+beta-FNA+alkylates+the+opioid+receptor+complex.&rft.au=Rothman%2C+R+B%3BBykov%2C+V%3BMahboubi%2C+A%3BLong%2C+J+B%3BJiang%2C+Q%3BPorreca%2C+F%3Bde+Costa%2C+B+R%3BJacobson%2C+A+E%3BRice%2C+K+C%3BHoladay%2C+J+W&rft.aulast=Rothman&rft.aufirst=R&rft.date=1991-06-01&rft.volume=8&rft.issue=2&rft.spage=86&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 - 1991-09-30 N1 - Date created - 1991-09-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Tremor. AN - 72050068; 1678770 AB - Tremor is a rhythmic, involuntary muscular contraction with consistency of rate, amplitude and pattern. It is the most common of all involuntary movements. Several systems for classifying tremor exist with the most frequent system classed according to behavioral context, ie, resting, postural and action. Clinical recognition of tremor type is extremely important as type determines prognosis, treatment and need for genetic counseling. The most common forms are parkinsonian, physiological, cerebellar intention and essential tremor. Essential or hereditary tremor is the most common of all neurologic conditions with 3-4 million Americans affected. Nursing implications of caring for essential tremor patients are presented. JF - The Journal of neuroscience nursing : journal of the American Association of Neuroscience Nurses AU - Gillespie, M M AD - National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/06// PY - 1991 DA - June 1991 SP - 170 EP - 174 VL - 23 IS - 3 SN - 0888-0395, 0888-0395 KW - Adrenergic beta-Antagonists KW - 0 KW - Primidone KW - 13AFD7670Q KW - Index Medicus KW - Nursing KW - Adrenergic beta-Antagonists -- administration & dosage KW - Humans KW - Adrenergic beta-Antagonists -- adverse effects KW - Patient Care Planning KW - Primidone -- therapeutic use KW - Adrenergic beta-Antagonists -- therapeutic use KW - Primidone -- adverse effects KW - Primidone -- administration & dosage KW - Tremor -- drug therapy KW - Tremor -- classification KW - Tremor -- nursing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72050068?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+neuroscience+nursing+%3A+journal+of+the+American+Association+of+Neuroscience+Nurses&rft.atitle=Tremor.&rft.au=Gillespie%2C+M+M&rft.aulast=Gillespie&rft.aufirst=M&rft.date=1991-06-01&rft.volume=23&rft.issue=3&rft.spage=170&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+neuroscience+nursing+%3A+journal+of+the+American+Association+of+Neuroscience+Nurses&rft.issn=08880395&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-26 N1 - Date created - 1991-09-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pituitary-adrenal responses to oCRH and central neuropeptide levels in alcohol amnestic disorder. AN - 72044006; 1651774 JF - Biological psychiatry AU - Adinoff, B AU - Martin, P R AU - Eckardt, M J AU - Bone, G H AU - Gold, P W AU - Linnoila, M AD - Laboratory of Clinical Studies, DICBR, National Institute on Alcohol Abuse and Alcoholism Bethesda, MD 20892. Y1 - 1991/06/01/ PY - 1991 DA - 1991 Jun 01 SP - 1153 EP - 1155 VL - 29 IS - 11 SN - 0006-3223, 0006-3223 KW - Neuropeptides KW - 0 KW - Adrenocorticotropic Hormone KW - 9002-60-2 KW - Corticotropin-Releasing Hormone KW - 9015-71-8 KW - Hydrocortisone KW - WI4X0X7BPJ KW - Index Medicus KW - Hydrocortisone -- physiology KW - Adrenocorticotropic Hormone -- physiology KW - Humans KW - Adult KW - Blood-Brain Barrier -- physiology KW - Middle Aged KW - Male KW - Female KW - Neuropeptides -- physiology KW - Corticotropin-Releasing Hormone -- physiology KW - Alcohol Amnestic Disorder -- blood KW - Pituitary-Adrenal System -- physiopathology KW - Alcohol Amnestic Disorder -- diagnosis KW - Pituitary-Adrenal System -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72044006?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biological+psychiatry&rft.atitle=Pituitary-adrenal+responses+to+oCRH+and+central+neuropeptide+levels+in+alcohol+amnestic+disorder.&rft.au=Adinoff%2C+B%3BMartin%2C+P+R%3BEckardt%2C+M+J%3BBone%2C+G+H%3BGold%2C+P+W%3BLinnoila%2C+M&rft.aulast=Adinoff&rft.aufirst=B&rft.date=1991-06-01&rft.volume=29&rft.issue=11&rft.spage=1153&rft.isbn=&rft.btitle=&rft.title=Biological+psychiatry&rft.issn=00063223&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-26 N1 - Date created - 1991-09-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A rapid in vitro assay for HIV DNA integration. AN - 80591237; 2041748 AB - Retroviruses synthesize a double stranded DNA copy of their RNA genome after infection of a permissive cell and subsequent integration of this DNA copy into the host genome is necessary for normal viral replication. Integration occurs by a specialized DNA recombination reaction, mediated by the viral IN protein. Because this reaction has no known cellular counterpart, it is a particularly attractive target in the search for specific inhibitors with low toxicity that may serve as therapeutic antiviral agents. We present a simple assay system that is suitable for screening potential inhibitors of HIV DNA integration. Only short oligonucleotides matching one end of HIV DNA and purified HIV IN protein are required as substrates. Furthermore, since each step of the assay can be carried out in the wells of microtiter plates, large numbers of reactions can be processed simultaneously. JF - Nucleic acids research AU - Craigie, R AU - Mizuuchi, K AU - Bushman, F D AU - Engelman, A AD - Laboratory of Molecular Biology, National Institute of Diabetes, and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/05/25/ PY - 1991 DA - 1991 May 25 SP - 2729 EP - 2734 VL - 19 IS - 10 SN - 0305-1048, 0305-1048 KW - Antiviral Agents KW - 0 KW - DNA, Viral KW - Gene Products, pol KW - Viral Proteins KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Virus Replication -- genetics KW - Base Sequence KW - Gene Products, pol -- metabolism KW - Recombination, Genetic KW - Proviruses -- genetics KW - Molecular Sequence Data KW - Viral Proteins -- metabolism KW - Antiviral Agents -- isolation & purification KW - Drug Evaluation, Preclinical -- methods KW - Cell Line KW - HIV -- physiology KW - HIV -- genetics KW - DNA, Viral -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80591237?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+acids+research&rft.atitle=A+rapid+in+vitro+assay+for+HIV+DNA+integration.&rft.au=Craigie%2C+R%3BMizuuchi%2C+K%3BBushman%2C+F+D%3BEngelman%2C+A&rft.aulast=Craigie&rft.aufirst=R&rft.date=1991-05-25&rft.volume=19&rft.issue=10&rft.spage=2729&rft.isbn=&rft.btitle=&rft.title=Nucleic+acids+research&rft.issn=03051048&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-11 N1 - Date created - 1991-07-11 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cell. 1984 Jan;36(1):197-202 [6319007] Proc Natl Acad Sci U S A. 1986 Oct;83(20):7648-52 [2429313] J Virol. 1989 Mar;63(3):1455-9 [2915387] J Virol. 1989 Dec;63(12):5319-27 [2555556] Cell. 1990 Jan 12;60(1):3-4 [2403842] J Virol. 1990 Jun;64(6):2711-5 [2335814] Proc Natl Acad Sci U S A. 1991 Feb 15;88(4):1339-43 [1847518] Proc Natl Acad Sci U S A. 1990 Jul;87(13):5119-23 [2164223] Cell. 1990 Aug 24;62(4):829-37 [2167180] Cell. 1990 Oct 5;63(1):87-95 [2170022] J Virol. 1990 Nov;64(11):5656-9 [2214031] Science. 1990 Sep 28;249(4976):1533-44 [1699273] Science. 1990 Sep 28;249(4976):1555-8 [2171144] Proc Natl Acad Sci U S A. 1990 Jun;87(11):4164-8 [2349226] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inhibition of protein phosphatases by okadaic acid induces AP1 in human T cells. AN - 80561823; 1851743 AB - To examine the role of protein phosphatases in T cell activation, Jurkat cells were treated with okadaic acid, an inhibitor of type 1 and 2A phosphatases, and nuclear extracts were examined for the presence of AP1 as a measure of early T cell activation. Okadaic acid was found to be a potent inducer of AP1. In contrast to phorbol esters such as phorbol myristate acetate (PMA), the induction of AP1 by okadaic acid occurs predominantly by transcriptional activation of the jun and fos family of proto-oncogenes. Surprisingly, while the addition of phytohemagglutinin further enhanced the induction of AP1, the addition of PMA inhibited it. Okadaic acid treatment was found to dramatically increase mRNA transcripts of the jun family of proto-oncogenes including c-jun, junD, and junB and to a lesser extent the fos family including c-fos and fra-1. By comparison, PMA is a very inefficient inducer of the jun gene family in Jurkat cells. Similar to its effect on the induction of AP1 by okadaic acid, PMA inhibits the induction of c-jun mRNA by okadaic acid. Transfection of c-jun promoter constructs confirmed the marked difference between PMA and okadaic acid in inducing c-jun transcription. The induction of AP1 by okadaic acid suggests that protein phosphatases 1 and 2A (PP1 and PP2A) may be involved in T cell activation as important negative regulators of the transcription factor AP1. JF - The Journal of biological chemistry AU - Thévenin, C AU - Kim, S J AU - Kehrl, J H AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/05/25/ PY - 1991 DA - 1991 May 25 SP - 9363 EP - 9366 VL - 266 IS - 15 SN - 0021-9258, 0021-9258 KW - c-fos KW - c-jun KW - fra-1 KW - junB KW - junD KW - DNA-Binding Proteins KW - 0 KW - Ethers, Cyclic KW - Proto-Oncogene Proteins KW - Proto-Oncogene Proteins c-jun KW - RNA, Messenger KW - Transcription Factors KW - Okadaic Acid KW - 1W21G5Q4N2 KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Protein Kinases KW - EC 2.7.- KW - Phosphoprotein Phosphatases KW - EC 3.1.3.16 KW - Index Medicus KW - Protein Kinases -- metabolism KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Promoter Regions, Genetic KW - Base Sequence KW - Phosphorylation KW - Transfection KW - Humans KW - Molecular Sequence Data KW - Transcription, Genetic KW - RNA, Messenger -- genetics KW - Phosphoprotein Phosphatases -- antagonists & inhibitors KW - Proto-Oncogene Proteins -- biosynthesis KW - DNA-Binding Proteins -- biosynthesis KW - T-Lymphocytes -- drug effects KW - Ethers, Cyclic -- pharmacology KW - Transcription Factors -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80561823?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+by+okadaic+acid+induces+AP1+in+human+T+cells.&rft.au=Th%C3%A9venin%2C+C%3BKim%2C+S+J%3BKehrl%2C+J+H&rft.aulast=Th%C3%A9venin&rft.aufirst=C&rft.date=1991-05-25&rft.volume=266&rft.issue=15&rft.spage=9363&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 - 1991-06-25 N1 - Date created - 1991-06-25 N1 - Date revised - 2017-01-13 N1 - Gene symbol - c-fos; c-jun; fra-1; junB; junD N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Absolute configuration of 7,12-dimethylbenz[a]anthracene-DNA adducts in mouse epidermis. AN - 80564532; 1903326 AB - 32P-Postlabeling was used to monitor the formation of DMBA-DNA adducts in mouse epidermis from each enantiomer of the trans 3,4-dihydrodiol. It was shown that the (4R,3R)-dihydrodiol is converted to the anti (4R,3S)-dihydrodiol (2S,1R)-epoxide which reacts with deoxyguanosine and deoxyadenosine residues in epidermal DNA to yield two of the major adducts formed when DMBA itself binds to epidermal DNA. The third major DMBA-derived adduct with deoxyadenosine residues was shown to arise from the (4S,3R)-dihydrodiol through the intermediacy of the syn (4S,3R)-dihydrodiol (2S,1R)-epoxide. JF - Cancer letters AU - Vericat, J A AU - Cheng, S C AU - Dipple, A AD - ABL-Basic Research Program, NCI-Frederick Cancer Research and Development Center, MD 21702. Y1 - 1991/05/24/ PY - 1991 DA - 1991 May 24 SP - 237 EP - 242 VL - 57 IS - 3 SN - 0304-3835, 0304-3835 KW - Epoxy Compounds KW - 0 KW - Phosphates KW - 9,10-Dimethyl-1,2-benzanthracene KW - 57-97-6 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Stereoisomerism KW - In Vitro Techniques KW - Epidermis -- metabolism KW - Mice KW - Cell Line KW - DNA Damage KW - 9,10-Dimethyl-1,2-benzanthracene -- chemistry KW - DNA -- chemistry KW - 9,10-Dimethyl-1,2-benzanthracene -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80564532?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Absolute+configuration+of+7%2C12-dimethylbenz%5Ba%5Danthracene-DNA+adducts+in+mouse+epidermis.&rft.au=Vericat%2C+J+A%3BCheng%2C+S+C%3BDipple%2C+A&rft.aulast=Vericat&rft.aufirst=J&rft.date=1991-05-24&rft.volume=57&rft.issue=3&rft.spage=237&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 - 1991-06-26 N1 - Date created - 1991-06-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of high affinity GTPase activity correlated to beta-adrenergic receptor stimulation of adenylyl cyclase in rat parotid membranes. AN - 80614513; 1646644 AB - beta-Adrenergic receptor stimulation of adenylyl cyclase involves the activation of a GTP-binding regulatory protein (G-protein, termed here Gs). Inactivation of this G-protein is associated with the hydrolysis of bound GTP by an intrinsic high affinity GTPase activity. In the present study, we have characterized the GTPase activity in a Gs-enriched rat parotid gland membrane fraction. Two GTPase activities were resolved; a high affinity GTPase activity displaying Michaelis-Menten kinetics with increasing concentrations of GTP, and a low affinity GTPase activity which increased linearly with GTP concentrations up to 10 mM. The beta-adrenergic agonist isoproterenol (10 microM) increased the Vmax of the high affinity GTPase component approx. 50% from 90 to 140 pmol/mg protein per min, but did not change its Km value (approximately 450 nM). Isoproterenol also stimulated adenylyl cyclase activity in parotid membranes both in the absence or presence of GTP. In the presence of a non-hydrolyzable GTP analogue, guanosine 5'-(3-O-thio)triphosphate (GTP gamma S), isoproterenol increased cAMP formation to the same extent as that observed with AlF-4. Cholera toxin treatment of parotid membranes led to the ADP-ribosylation of two proteins (approximately 45 and 51 kDa). Cholera toxin also specifically decreased the high affinity GTPase activity in membranes and increased cAMP formation induced by GTP in the absence or the presence of isoproterenol. These data demonstrate that the high affinity GTPase characterized here is the 'turn-off' step for the adenylyl cyclase activation seen following beta-adrenergic stimulation of rat parotid glands. JF - Biochimica et biophysica acta AU - Hiramatsu, Y AU - Ambudkar, I S AU - Baum, B J AD - Clinical Investigations and Patient Care Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/05/17/ PY - 1991 DA - 1991 May 17 SP - 391 EP - 396 VL - 1092 IS - 3 SN - 0006-3002, 0006-3002 KW - Receptors, Adrenergic, beta KW - 0 KW - Guanosine Triphosphate KW - 86-01-1 KW - Cholera Toxin KW - 9012-63-9 KW - Propranolol KW - 9Y8NXQ24VQ KW - Cyclic AMP KW - E0399OZS9N KW - GTP Phosphohydrolases KW - EC 3.6.1.- KW - Adenylyl Cyclases KW - EC 4.6.1.1 KW - Isoproterenol KW - L628TT009W KW - Index Medicus KW - Animals KW - Cell Membrane -- enzymology KW - Electrophoresis, Polyacrylamide Gel KW - Propranolol -- pharmacology KW - Cholera Toxin -- pharmacology KW - Autoradiography KW - Isoproterenol -- pharmacology KW - Guanosine Triphosphate -- metabolism KW - Rats KW - Rats, Inbred Strains KW - Cyclic AMP -- metabolism KW - Signal Transduction KW - Male KW - Receptors, Adrenergic, beta -- metabolism KW - Adenylyl Cyclases -- drug effects KW - GTP Phosphohydrolases -- metabolism KW - Parotid Gland -- enzymology KW - Adenylyl Cyclases -- metabolism KW - Receptors, Adrenergic, beta -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80614513?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochimica+et+biophysica+acta&rft.atitle=Characterization+of+high+affinity+GTPase+activity+correlated+to+beta-adrenergic+receptor+stimulation+of+adenylyl+cyclase+in+rat+parotid+membranes.&rft.au=Hiramatsu%2C+Y%3BAmbudkar%2C+I+S%3BBaum%2C+B+J&rft.aulast=Hiramatsu&rft.aufirst=Y&rft.date=1991-05-17&rft.volume=1092&rft.issue=3&rft.spage=391&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+biophysica+acta&rft.issn=00063002&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-19 N1 - Date created - 1991-07-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of phosphatase inhibitors and a protein phosphatase on norepinephrine secretion by permeabilized bovine chromaffin cells. AN - 80612357; 1646643 AB - A protein phosphatase and phosphatase inhibitors were used to examine the role of protein phosphorylation in the regulation of norepinephrine secretion in digitonin-permeabilized bovine chromaffin cells. Addition of okadaic acid, a potent inhibitor of type 1 and type 2A protein phosphatases, or 1-naphthylphosphate, a more general phosphatase inhibitor, to digitonin-permeabilized chromaffin cells caused about a 100% increase in the amount of norepinephrine secreted in the absence of Ca2+ (in 5 mM EGTA) without affecting the amount of norepinephrine secreted in the presence of 10 microM free Ca2+. This stimulation of norepinephrine secretion by protein phosphatase inhibitors suggests that in the absence of Ca2+ there is a slow rate phosphorylation and that this phosphorylation triggers secretion. Addition of an exogenous type 2A protein phosphatase caused almost a 50% decrease in Ca(2+)-dependent norepinephrine secretion. Thus, the amounts of norepinephrine released both in the absence of Ca2+ and in the presence of Ca2+ appear to depend upon the level of protein phosphorylation. JF - Biochimica et biophysica acta AU - Wu, Y N AU - Wagner, P D AD - Laboratory of Biochemistry, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/05/17/ PY - 1991 DA - 1991 May 17 SP - 384 EP - 390 VL - 1092 IS - 3 SN - 0006-3002, 0006-3002 KW - Ethers, Cyclic KW - 0 KW - Imidazoles KW - Naphthalenes KW - Organophosphorus Compounds KW - Proteins KW - Okadaic Acid KW - 1W21G5Q4N2 KW - Trifluoperazine KW - 214IZI85K3 KW - naphthyl phosphate KW - 33881-88-8 KW - calmidazolium KW - 4R9H38JAWL KW - Phosphoprotein Phosphatases KW - EC 3.1.3.16 KW - Calcium KW - SY7Q814VUP KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Naphthalenes -- pharmacology KW - Animals KW - Cattle KW - Imidazoles -- pharmacology KW - Trifluoperazine -- pharmacology KW - Phosphorylation KW - Cell Membrane Permeability -- drug effects KW - Organophosphorus Compounds -- pharmacology KW - Calcium -- pharmacology KW - Ethers, Cyclic -- pharmacology KW - Phosphoprotein Phosphatases -- metabolism KW - Adrenal Medulla -- secretion KW - Adrenal Medulla -- cytology KW - Norepinephrine -- secretion KW - Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80612357?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochimica+et+biophysica+acta&rft.atitle=Effects+of+phosphatase+inhibitors+and+a+protein+phosphatase+on+norepinephrine+secretion+by+permeabilized+bovine+chromaffin+cells.&rft.au=Wu%2C+Y+N%3BWagner%2C+P+D&rft.aulast=Wu&rft.aufirst=Y&rft.date=1991-05-17&rft.volume=1092&rft.issue=3&rft.spage=384&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+biophysica+acta&rft.issn=00063002&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-19 N1 - Date created - 1991-07-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Intracerebroventricular pertussis toxin enhances sensitivity to N-methyl-D-aspartate-induced seizures in mice. AN - 72123509; 1655474 AB - The effect of pretreatment with pertussis toxin on N-methyl-D-aspartate (NMDA)-induced seizures was investigated in mice. In animals treated with pertussis toxin (0.5 micrograms/animal i.c.v) five days prior to testing the convulsant ED50 of NMDA was calculated to be 18 mg/kg whereas it was calculated to be 107 mg/kg in sham-treated animals. These results suggest the pertussis toxin enhances sensitivity to NMDA, possibly via its actions on inhibitory G-proteins. JF - European journal of pharmacology AU - Durcan, M J AU - Morgan, P F AD - Laboratory of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism, DICBR, Bethesda, MD 20892. Y1 - 1991/05/17/ PY - 1991 DA - 1991 May 17 SP - 209 EP - 211 VL - 197 IS - 2-3 SN - 0014-2999, 0014-2999 KW - Receptors, N-Methyl-D-Aspartate KW - 0 KW - Virulence Factors, Bordetella KW - N-Methylaspartate KW - 6384-92-5 KW - Pertussis Toxin KW - EC 2.4.2.31 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Index Medicus KW - Animals KW - GTP-Binding Proteins -- antagonists & inhibitors KW - Synaptic Transmission -- drug effects KW - Receptors, N-Methyl-D-Aspartate -- antagonists & inhibitors KW - Mice KW - Drug Synergism KW - Male KW - Injections, Intraventricular KW - Seizures -- chemically induced KW - Virulence Factors, Bordetella -- administration & dosage KW - Virulence Factors, Bordetella -- toxicity KW - N-Methylaspartate -- pharmacology KW - N-Methylaspartate -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72123509?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Intracerebroventricular+pertussis+toxin+enhances+sensitivity+to+N-methyl-D-aspartate-induced+seizures+in+mice.&rft.au=Durcan%2C+M+J%3BMorgan%2C+P+F&rft.aulast=Durcan&rft.aufirst=M&rft.date=1991-05-17&rft.volume=197&rft.issue=2-3&rft.spage=209&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 - 1991-10-31 N1 - Date created - 1991-10-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Apolipoprotein B upstream suppressor site: identification of an element which can decrease apolipoprotein B transcription. AN - 80589958; 2039496 AB - Elevated plasma levels of apolipoprotein B (apoB) may predispose to development of premature coronary atherosclerosis. We have identified the first well localized domain of the apoB gene which can effect negative regulation of its transcription. This region binds trans-activating factors present only in apoB producing cell lines. Mutagenesis of this region causes up-regulation of its transcriptional activity. We have termed this element apoB upstream suppressor site (aBUSS) and its trans-activators the apoB repressor proteins (ARP). aBUSS and ARP may play important roles in the transcriptional modulation of apoB. JF - Biochemical and biophysical research communications AU - Ross, R S AU - Li, A C AU - Hoeg, J M AU - Schumacher, U K AU - Demosky, S J AU - Brewer, H B AD - Molecular Disease Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 1991/05/15/ PY - 1991 DA - 1991 May 15 SP - 1116 EP - 1122 VL - 176 IS - 3 SN - 0006-291X, 0006-291X KW - Apolipoproteins B KW - 0 KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Index Medicus KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Animals KW - Promoter Regions, Genetic KW - Chromosome Deletion KW - Transfection KW - Cell Nucleus -- metabolism KW - Humans KW - Suppression, Genetic KW - Gene Expression Regulation KW - Plasmids KW - Chloramphenicol O-Acetyltransferase -- metabolism KW - Cell Line KW - Apolipoproteins B -- genetics KW - Transcription, Genetic KW - Genes, Suppressor UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80589958?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Apolipoprotein+B+upstream+suppressor+site%3A+identification+of+an+element+which+can+decrease+apolipoprotein+B+transcription.&rft.au=Ross%2C+R+S%3BLi%2C+A+C%3BHoeg%2C+J+M%3BSchumacher%2C+U+K%3BDemosky%2C+S+J%3BBrewer%2C+H+B&rft.aulast=Ross&rft.aufirst=R&rft.date=1991-05-15&rft.volume=176&rft.issue=3&rft.spage=1116&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 - 1991-07-03 N1 - Date created - 1991-07-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modulation of transcription factor NF-kappa B binding activity by oxidation-reduction in vitro. AN - 80574663; 1903539 AB - NF-kappa B is a widely used regulator of inducible and tissue-specific gene control. In the cytosol, when complexed to an inhibitory molecule, I kappa B, NF-kappa B is in an inactive form and cannot bind DNA. Activation of cells with appropriate stimuli results in the dissociation of NF-kappa B from I kappa B and its translocation to the nucleus as an active binding protein. We now demonstrate that NF-kappa B binding in vitro can be inhibited by agents that modify free sulfhydryls. Binding is eliminated after treatment with N-ethylmaleimide, an alkylating agent, and diamide, an oxidizing agent. The diamide effect can be reversed by 2-mercaptoethanol. Further, 2-mercaptoethanol acts synergistically with deoxycholate plus Nonidet P-40 in converting inactive cytosolic NF-kappa B to an active DNA-binding form. It is therefore possible that modulation of the redox state of NF-kappa B could represent a post-translational control mechanism for this factor. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Toledano, M B AU - Leonard, W J AD - Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesa, MD 20892. Y1 - 1991/05/15/ PY - 1991 DA - 1991 May 15 SP - 4328 EP - 4332 VL - 88 IS - 10 SN - 0027-8424, 0027-8424 KW - DNA-Binding Proteins KW - 0 KW - NF-kappa B KW - Nuclear Proteins KW - Proto-Oncogene Proteins c-jun KW - Serum Response Factor KW - Sulfhydryl Compounds KW - Transcription Factors KW - Deoxycholic Acid KW - 005990WHZZ KW - Diamide KW - 10465-78-8 KW - Polyethylene Glycols KW - 30IQX730WE KW - Mercaptoethanol KW - 60-24-2 KW - DNA KW - 9007-49-2 KW - Nonidet P-40 KW - 9036-19-5 KW - Ethylmaleimide KW - O3C74ACM9V KW - Index Medicus KW - Cytosol -- metabolism KW - Diamide -- pharmacology KW - Transcription Factors -- metabolism KW - Cell Nucleus -- metabolism KW - Humans KW - Mercaptoethanol -- pharmacology KW - Polyethylene Glycols -- pharmacology KW - Oxidation-Reduction KW - Deoxycholic Acid -- pharmacology KW - Tumor Cells, Cultured KW - Sulfhydryl Compounds -- chemistry KW - Drug Synergism KW - Ethylmaleimide -- pharmacology KW - Nuclear Proteins -- metabolism KW - DNA-Binding Proteins -- metabolism KW - NF-kappa B -- chemistry KW - DNA -- metabolism KW - NF-kappa B -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80574663?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Modulation+of+transcription+factor+NF-kappa+B+binding+activity+by+oxidation-reduction+in+vitro.&rft.au=Toledano%2C+M+B%3BLeonard%2C+W+J&rft.aulast=Toledano&rft.aufirst=M&rft.date=1991-05-15&rft.volume=88&rft.issue=10&rft.spage=4328&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 - 1991-06-25 N1 - Date created - 1991-06-25 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1988 Dec;85(23):8825-9 [2848241] J Am Chem Soc. 1976 May 12;98(10):3001-7 [1262629] Proc Natl Acad Sci U S A. 1988 Mar;85(5):1482-6 [3125549] Cell. 1988 Apr 22;53(2):211-7 [3129195] Eur J Biochem. 1988 May 2;173(3):507-15 [3131140] Science. 1988 Oct 28;242(4878):540-6 [3140380] EMBO J. 1987 Sep;6(9):2711-7 [3119326] Cell. 1988 Dec 2;55(5):917-24 [3142692] Cell. 1988 Dec 2;55(5):907-15 [3142691] Science. 1989 Apr 28;244(4903):466-9 [2497520] Genes Dev. 1989 Nov;3(11):1689-98 [2691328] Science. 1989 Nov 17;246(4932):870-2 [2683086] Cell. 1989 Jul 28;58(2):227-9 [2665943] EMBO J. 1989 Mar;8(3):757-64 [2785919] Biochem Biophys Res Commun. 1989 Sep 15;163(2):803-9 [2783121] Science. 1989 Apr 21;244(4902):357-9 [2711187] Science. 1988 Jul 8;241(4862):202-5 [3260404] Cell. 1988 Dec 23;55(6):989-1003 [3203386] New Biol. 1989 Oct;1(1):83-92 [2518691] Proc Natl Acad Sci U S A. 1990 Nov;87(21):8282-6 [2172979] Proc Natl Acad Sci U S A. 1990 Dec;87(24):9943-7 [2263644] Cell. 1987 Jun 19;49(6):729-39 [3034432] Nature. 1988 Aug 11;334(6182):494-8 [2900470] Proc Natl Acad Sci U S A. 1988 Jul;85(13):4700-4 [3133660] Cell. 1988 Jun 3;53(5):827-36 [2836068] Science. 1987 Dec 4;238(4832):1386-92 [2825349] Methods Enzymol. 1987;143:264-70 [3657543] EMBO J. 1987 Mar;6(3):667-73 [3582369] Mol Cell Biol. 1987 Mar;7(3):1217-25 [3561415] Cell. 1990 Sep 7;62(5):1019-29 [2203532] Cell. 1990 Sep 7;62(5):1007-18 [2203531] Science. 1990 Sep 7;249(4973):1157-61 [2118682] Proc Natl Acad Sci U S A. 1990 May;87(9):3343-7 [1970635] Science. 1990 Apr 13;248(4952):189-94 [2183352] Proc Natl Acad Sci U S A. 1990 Mar;87(5):1830-4 [2308942] Nucleic Acids Res. 1983 Mar 11;11(5):1475-89 [6828386] Proc Natl Acad Sci U S A. 1983 Jun;80(11):3183-7 [6574479] J Immunol. 1979 Apr;122(4):1433-9 [312842] J Cell Biol. 1976 Dec;71(3):921-32 [993272] Nature. 1987 Apr 16-22;326(6114):711-3 [3031512] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The 45 pocket of HLA-A2.1 plays a role in presentation of influenza virus matrix peptide and alloantigens. AN - 80548263; 2026879 AB - Amino acid substitutions were introduced into the 45 pocket of HLA-A2.1 to determine the potential role of this structurally defined feature of class I molecules in viral peptide and alloantigen presentation. The 45 pocket lies below the alpha 1-domain alpha-helix and is composed of five amino acids, three of which differ between HLA-A2.1 and HLA-B37. These two class I molecules have previously been shown to have largely non-overlapping peptide-binding specificities. Site-directed mutagenesis was used to replace the hydrophobic residues at positions 24, 45, and 67 in the 45 pocket of HLA-A2.1 with the hydrophilic amino acids found in these positions in HLA-B37. Thus, three single amino acid mutants were produced: 24A----S, 45 M----T, and 67V----S. These mutants were transfected into HMy2.C1R cells and assessed for their ability to present influenza virus matrix M1 57-68 peptide and HTLV-I Tax-1 2-25 peptide to HLA-A2.1-restricted, peptide-specific CTL and to present alloantigens to HLA-A2-allospecific CTL lines. Each of these substitutions in the 45 pocket produced a molecule that failed to present the M1 peptide to most M1 peptide-specific CTL lines. In contrast, none of these mutations affected presentation of the Tax-1 peptide to Tax-1-specific CTL lines, which indicates that these mutant HLA-A2 molecules can function in viral peptide presentation. Two of the three substitutions in the 45 pocket resulted in lack of recognition by a subset of HLA-A2 allospecific CTL lines. These results demonstrate that the amino acid side chains in the 45 pocket can strongly influence peptide presentation and suggest that the 45 pocket may play a role in determining peptide-binding specificity. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Winter, C C AU - Carreno, B M AU - Turner, R V AU - Koenig, S AU - Biddison, W E AD - Molecular Immunology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/05/15/ PY - 1991 DA - 1991 May 15 SP - 3508 EP - 3512 VL - 146 IS - 10 SN - 0022-1767, 0022-1767 KW - Gene Products, tax KW - 0 KW - HLA-A Antigens KW - Isoantigens KW - M-protein, influenza virus KW - M1 protein, Influenza A virus KW - Viral Matrix Proteins KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Base Sequence KW - Transfection KW - Models, Molecular KW - Humans KW - Molecular Sequence Data KW - T-Lymphocytes, Cytotoxic -- immunology KW - Gene Products, tax -- immunology KW - Mutation KW - Structure-Activity Relationship KW - Isoantigens -- immunology KW - Influenza A virus -- immunology KW - Viral Matrix Proteins -- immunology KW - HLA-A Antigens -- physiology KW - HLA-A Antigens -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80548263?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=The+45+pocket+of+HLA-A2.1+plays+a+role+in+presentation+of+influenza+virus+matrix+peptide+and+alloantigens.&rft.au=Winter%2C+C+C%3BCarreno%2C+B+M%3BTurner%2C+R+V%3BKoenig%2C+S%3BBiddison%2C+W+E&rft.aulast=Winter&rft.aufirst=C&rft.date=1991-05-15&rft.volume=146&rft.issue=10&rft.spage=3508&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 - 1991-06-11 N1 - Date created - 1991-06-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The cystic fibrosis gene has a "housekeeping"-type promoter and is expressed at low levels in cells of epithelial origin. AN - 80545692; 1709163 AB - Evaluation of the expression of the cystic fibrosis (CF) gene in human epithelial cell lines demonstrated active, but low level, transcription of the gene. Analysis of 3.8 kilobases of genomic sequences 5' to exon 1 of the CF gene demonstrated no TATA promoter element, but a high G + C content, multiple transcription start sites, and several potential Sp1 binding sites. Fragments of 5'-flanking sequences from 2.2 kilobases to as small as 102 base pairs 5' to the major transcription start site supported constitutive reporter gene expression in epithelial cells, but at low levels, and independent of the length of the 5' fragment. CF gene transcription was down-regulated by phorbol myristate acetate. Importantly, evaluation of freshly isolated normal human bronchial cells also demonstrated CF gene transcription at a relatively low rate. Together, these observations suggest that although the normal CF gene promoter has characteristics of a "housekeeping"-type gene, and the gene is expressed at low levels in cells of organs that manifest the clinical disorder "cystic fibrosis," its expression can be modulated transcriptionally, implying a possible therapeutic approach for the disease. JF - The Journal of biological chemistry AU - Yoshimura, K AU - Nakamura, H AU - Trapnell, B C 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 - 1991/05/15/ PY - 1991 DA - 1991 May 15 SP - 9140 EP - 9144 VL - 266 IS - 14 SN - 0021-9258, 0021-9258 KW - CFTR protein, human KW - 0 KW - Membrane Proteins KW - Oligonucleotides KW - Cystic Fibrosis Transmembrane Conductance Regulator KW - 126880-72-6 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Base Sequence KW - Transcription, Genetic -- drug effects KW - Oligonucleotides -- chemistry KW - Humans KW - In Vitro Techniques KW - Epithelium -- physiology KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Regulatory Sequences, Nucleic Acid KW - Promoter Regions, Genetic KW - Bronchi -- cytology KW - Gene Expression Regulation -- drug effects KW - Membrane Proteins -- genetics KW - Bronchi -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80545692?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=The+cystic+fibrosis+gene+has+a+%22housekeeping%22-type+promoter+and+is+expressed+at+low+levels+in+cells+of+epithelial+origin.&rft.au=Yoshimura%2C+K%3BNakamura%2C+H%3BTrapnell%2C+B+C%3BDalemans%2C+W%3BPavirani%2C+A%3BLecocq%2C+J+P%3BCrystal%2C+R+G&rft.aulast=Yoshimura&rft.aufirst=K&rft.date=1991-05-15&rft.volume=266&rft.issue=14&rft.spage=9140&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 - 1991-06-10 N1 - Date created - 1991-06-10 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M57623; GENBANK; M62403; M57624; M60204; M63262; M60203; M60205; M58478; M60206; M62780 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interaction of protein kinase C isozymes with phosphatidylinositol 4,5-bisphosphate. AN - 80545351; 1851155 AB - Interaction of protein kinase C (PKC) isozymes with phosphatidylinositol 4,5-bisphosphate (PIP2) was investigated by monitoring the changes in the intrinsic fluorescence of the enzyme, the kinase activity, and phorbol ester binding. Incubation of PKC I, II, and III with PIP2 resulted in different rates of quenching of PKC fluorescence and different degrees of inactivation of these enzymes. Other inositol-containing phospholipids such as phosphatidylinositol and phosphatidylinositol 4-phosphate also caused differential rates of quenching of the intrinsic fluorescence of these enzymes. These latter two phospholipids were, however, less potent in the inactivation of PKCs than PIP2. The IC50 of PIP2 were 2, 4, and 11 microM for PKC I, II, and III, respectively. Inactivation of PKCs by PIP2 cannot be reversed by extensive dilution of PIP2 with Nonidet P-40 nor by digestion of PIP2 with phospholipase C. Interaction of PIP2 with the various PKC isozymes was greatly facilitated in the presence of Mg2+ or Ca2+ as evidenced by the accelerated quenching of the PKC fluorescence, however, these divalent metal ions protected PKC from the PIP2-induced inactivation. Binding of PIP2 to PKC in the absence of divalent metal ion also caused a reduction of [3H]phorbol 12,13-dibutyrate binding as a result of reducing the affinity of the enzyme for phorbol ester. Based on gel filtration chromatography, it was estimated that one molecule of PKC interacted with one PIP2 micelle with an aggregation number of 80-90. The PIP2-bound PKC could further interact with phosphatidylserine in the presence of Ca2+ to form a larger complex. Binding of PKC to both PIP2 and phosphatidylserine in the presence of Ca2+ was also evident by changes in the intrinsic fluorescence of PKC. As the interaction of PKC with PIP2, but not with phosphatidylserine, could be enhanced by millimolar concentrations of Mg2+, we propose that PIP2 may be a component of the membrane anchor for PKC under basal physiological conditions when [Ca2+]i is low and Mg2+ is plentiful. Under the in vitro assay conditions, PIP2 could stimulate PKC activity to a level approximately 10-20% of that by diacylglycerol. The stimulatory effect of PIP2 on PKC apparently is not due to binding to the same site recognized by diacylglycerol or phorbol ester, because PIP2 cannot effectively compete with phorbol 12,13-dibutyrate in the binding assay. JF - The Journal of biological chemistry AU - Huang, F L AU - Huang, K P AD - Section on Metabolic Regulation, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/05/15/ PY - 1991 DA - 1991 May 15 SP - 8727 EP - 8733 VL - 266 IS - 14 SN - 0021-9258, 0021-9258 KW - Cations, Divalent KW - 0 KW - Diglycerides KW - Isoenzymes KW - Phosphatidylinositol 4,5-Diphosphate KW - Phosphatidylinositols KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Index Medicus KW - Rats KW - Isoenzymes -- antagonists & inhibitors KW - Animals KW - Diglycerides -- pharmacology KW - Chromatography, Gel KW - Phorbol 12,13-Dibutyrate -- metabolism KW - In Vitro Techniques KW - Spectrophotometry, Ultraviolet KW - Protein Binding KW - Isoenzymes -- metabolism KW - Structure-Activity Relationship KW - Protein Kinase C -- metabolism KW - Phosphatidylinositols -- metabolism KW - Protein Kinase C -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80545351?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Interaction+of+protein+kinase+C+isozymes+with+phosphatidylinositol+4%2C5-bisphosphate.&rft.au=Huang%2C+F+L%3BHuang%2C+K+P&rft.aulast=Huang&rft.aufirst=F&rft.date=1991-05-15&rft.volume=266&rft.issue=14&rft.spage=8727&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-06-10 N1 - Date created - 1991-06-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Toxicity of N-acetylaspartylglutamate and its protection by NMDA and non-NMDA receptor antagonists. AN - 80728626; 1830940 AB - N-Acetylaspartylglutamate (NAAG) is a dipeptide, and has been demonstrated to be a putative neurotransmitter in the brain. We hereby report the toxicity of NAAG in sagittal slices of mouse brain, in vitro, which is prevented by both N-methyl-D-aspartate (NMDA) and non-NMDA receptor antagonists. Incubation of mouse brain slices with NAAG resulted in dose-dependent leakage of lactate dehydrogenase (LDH) and potassium from the slices into the medium. Significant leakage of LDH was observed when the slices were incubated with 0.1 pM NAAG. Significant leakage of LDH from the slice was observed only when a very high concentration of L-glutamic acid (10 microM) was added to the incubatio medium. Prior incubation with NMDA (MK-801) or non-NMDA (glutamate diethyl ester, (GDEE] receptor antagonists protected the slices against NAAG-mediated neurotoxicity, indicating the possible involvement of both of these classes of receptors in the toxic action of NAAG. JF - Neuroscience letters AU - Pai, K S AU - Ravindranath, V AD - Department of Neurochemistry, National Institute of Mental Health and Neuro Sciences, Bangalore, India. Y1 - 1991/05/13/ PY - 1991 DA - 1991 May 13 SP - 49 EP - 51 VL - 126 IS - 1 SN - 0304-3940, 0304-3940 KW - Dipeptides KW - 0 KW - Excitatory Amino Acid Antagonists KW - Glutamates KW - Neurotoxins KW - Receptors, N-Methyl-D-Aspartate KW - glutamic acid diethyl ester KW - 16450-41-2 KW - isospaglumic acid KW - 1W8M12WXYL KW - N-Methylaspartate KW - 6384-92-5 KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - L-Lactate Dehydrogenase KW - EC 1.1.1.27 KW - Potassium KW - RWP5GA015D KW - Index Medicus KW - Animals KW - Kinetics KW - In Vitro Techniques KW - Mice KW - L-Lactate Dehydrogenase -- secretion KW - Potassium -- metabolism KW - Male KW - Receptors, N-Methyl-D-Aspartate -- physiology KW - Receptors, N-Methyl-D-Aspartate -- drug effects KW - N-Methylaspartate -- pharmacology KW - Glutamates -- pharmacology KW - Brain -- drug effects KW - Neurotoxins -- pharmacology KW - Dipeptides -- antagonists & inhibitors KW - Brain -- physiology KW - Dipeptides -- pharmacology KW - Dizocilpine Maleate -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80728626?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Toxicity+of+N-acetylaspartylglutamate+and+its+protection+by+NMDA+and+non-NMDA+receptor+antagonists.&rft.au=Pai%2C+K+S%3BRavindranath%2C+V&rft.aulast=Pai&rft.aufirst=K&rft.date=1991-05-13&rft.volume=126&rft.issue=1&rft.spage=49&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 - 1991-09-10 N1 - Date created - 1991-09-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Selective decrease in extracellular DOPAC concentrations in rat striatum following in vivo dialysis with low concentrations of MPP+. AN - 80735565; 1714336 AB - Using the technique of in vivo dialysis, 1-methyl-4-phenylpyridinium (MPP+), the neurotoxic metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), was applied to the rat striatum and the effects of this treatment on the efflux of striatal dopamine (DA) and metabolites were monitored. The inclusion of low concentrations of MPP+ (1 and 10 microM) in the dialysis solution caused a progressive decrease in the efflux of dihydroxyphenylacetic acid (DOPAC), the major deamination product of DA, while homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) remained unchanged. Unlike the effects of dialysis with millimolar concentrations of MPP+, a large increase in the efflux of striatal DA was not observed. The effect of dialysis with 1 microM MPP+ was blocked if 1 microM GBR 12909, a specific DA reuptake blocker, was included in the dialysis fluid, suggesting uptake of MPP+ into striatal DA terminals mediated this effect. JF - Brain research AU - Caliguri, E J AU - Johannessen, J N AD - National Institute of Mental Health, Laboratory of Clinical Science, Bethesda, MD 20892. Y1 - 1991/05/10/ PY - 1991 DA - 1991 May 10 SP - 94 EP - 99 VL - 548 IS - 1-2 SN - 0006-8993, 0006-8993 KW - 3,4-Dihydroxyphenylacetic Acid KW - 102-32-9 KW - Hydroxyindoleacetic Acid KW - 54-16-0 KW - 1-Methyl-4-phenylpyridinium KW - R865A5OY8J KW - Dopamine KW - VTD58H1Z2X KW - Homovanillic Acid KW - X77S6GMS36 KW - Index Medicus KW - Rats KW - Animals KW - Kinetics KW - Hydroxyindoleacetic Acid -- metabolism KW - Dopamine -- metabolism KW - Homovanillic Acid -- metabolism KW - Dialysis -- methods KW - 3,4-Dihydroxyphenylacetic Acid -- metabolism KW - Corpus Striatum -- metabolism KW - Corpus Striatum -- drug effects KW - 1-Methyl-4-phenylpyridinium -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80735565?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Selective+decrease+in+extracellular+DOPAC+concentrations+in+rat+striatum+following+in+vivo+dialysis+with+low+concentrations+of+MPP%2B.&rft.au=Caliguri%2C+E+J%3BJohannessen%2C+J+N&rft.aulast=Caliguri&rft.aufirst=E&rft.date=1991-05-10&rft.volume=548&rft.issue=1-2&rft.spage=94&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 - 1991-09-19 N1 - Date created - 1991-09-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential expression during development of ADP-ribosylation factors, 20-kDa guanine nucleotide-binding protein activators of cholera toxin. AN - 80537422; 1902473 AB - Cholera toxin exerts its effects on cells in large part through the ADP-ribosylation of guanine nucleotide-binding proteins. Toxin-catalyzed ADP-ribosylation is enhanced by approximately 20-kDa guanine nucleotide-binding proteins termed ADP-ribosylation factors (ARFs), which are allosteric activators of the toxin catalytic unit. Rabbit antiserum against a purified bovine brain ARF (sARF II) reacted on immunoblots with two approximately 20-kDa ARF-like proteins (sARF I and II) in tissue extracts from bovine, rat, frog, and chicken. Levels of ARF were higher in brain than in non-neural tissues. In rat brain, on the second postnatal day, amounts of sARF I and II were similar. By the 10th postnatal day and thereafter, sARF II predominated. Relative levels of ARF determined by immunoreactivity were in agreement with levels assessed in functional assays of cholera toxin-catalyzed ADP-ribosylation. Based on nucleotide and deduced amino acid sequences of human and bovine cDNAs, there appear to be at least six different ARF-like genes. Northern blots of rat brain poly(A)+ RNA were hybridized with cDNA and oligonucleotide probes specific for each of the human and bovine ARF genes. From the second to the 27th postnatal day, ARF 3 mRNA increased, whereas mRNAs for ARFs 2 and 4 decreased; and those for ARFs 1, 5, and 6 were apparently unchanged. Partial amino acid sequence of sARF II is consistent with it being either the ARF 1 or 3 gene product. The developmental changes in rat brain ARF parallel neuronal maturation and synapse formation. JF - The Journal of biological chemistry AU - Tsai, S C AU - Adamik, R AU - Tsuchiya, M AU - Chang, P P 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 - 1991/05/05/ PY - 1991 DA - 1991 May 05 SP - 8213 EP - 8219 VL - 266 IS - 13 SN - 0021-9258, 0021-9258 KW - Antibodies KW - 0 KW - Membrane Proteins KW - Adenosine Diphosphate KW - 61D2G4IYVH KW - DNA KW - 9007-49-2 KW - Cholera Toxin KW - 9012-63-9 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - ADP-Ribosylation Factors KW - EC 3.6.5.2 KW - Index Medicus KW - Immunoblotting KW - Animals KW - Blotting, Northern KW - Electrophoresis, Polyacrylamide Gel KW - Isoelectric Focusing KW - Cross Reactions KW - Rats KW - Base Sequence KW - Cattle KW - Chickens KW - Chromatography, Gel KW - Ranidae KW - Molecular Sequence Data KW - Adenosine Diphosphate -- metabolism KW - Membrane Proteins -- metabolism KW - Membrane Proteins -- immunology KW - GTP-Binding Proteins -- metabolism KW - Membrane Proteins -- biosynthesis KW - Membrane Proteins -- genetics KW - Cholera Toxin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80537422?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+expression+during+development+of+ADP-ribosylation+factors%2C+20-kDa+guanine+nucleotide-binding+protein+activators+of+cholera+toxin.&rft.au=Tsai%2C+S+C%3BAdamik%2C+R%3BTsuchiya%2C+M%3BChang%2C+P+P%3BMoss%2C+J%3BVaughan%2C+M&rft.aulast=Tsai&rft.aufirst=S&rft.date=1991-05-05&rft.volume=266&rft.issue=13&rft.spage=8213&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 - 1991-06-05 N1 - Date created - 1991-06-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of vanilloid receptors in the dorsal horn of pig spinal cord. AN - 72070790; 1884211 AB - Specific [3H]resiniferatoxin binding is thought to represent the postulated vanilloid (capsaicin) receptor. We have previously characterized [3H]resiniferatoxin binding to membranes from rat and pig dorsal root ganglia, which contain the cell bodies of capsaicin-sensitive primary afferent neurons. We now demonstrate specific binding of [3H]resiniferatoxin to particulate preparations from pig dorsal horn, which contains the central nerve endings of the capsaicin-sensitive primary afferent neurons. The Kd was 0.27 +/- 0.03 nM; the Bmax was 370 +/- 40 fmol/mg protein. Vanilloids of the capsaicin class (capsaicin, piperine, zingerone) and resiniferatoxin class (tinyatoxin, 12-deoxyphorbol 13-phenylacetate 20-homovanillate) inhibited binding with affinities consistent with their relative in vivo potencies. Given the interest in vanilloids as potential non-narcotic analgesic agents, this binding assay affords an attractive approach for characterization of structure-activity relations at spinal vanilloid receptors. JF - Brain research AU - Szallasi, A AU - Blumberg, P M AD - Molecular Mechanisms of Tumor Promotion Section, National Cancer Institute, NIH, Bethesda, MD 20892. Y1 - 1991/05/03/ PY - 1991 DA - 1991 May 03 SP - 335 EP - 338 VL - 547 IS - 2 SN - 0006-8993, 0006-8993 KW - Diterpenes KW - 0 KW - Phorbol Esters KW - resiniferatoxin KW - A5O6P1UL4I KW - Capsaicin KW - S07O44R1ZM KW - Index Medicus KW - Swine KW - Animals KW - Phorbol Esters -- metabolism KW - In Vitro Techniques KW - Binding, Competitive -- physiology KW - Capsaicin -- metabolism KW - Radioligand Assay KW - Capsaicin -- analogs & derivatives KW - Structure-Activity Relationship KW - Spinal Cord -- metabolism KW - Diterpenes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72070790?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Characterization+of+vanilloid+receptors+in+the+dorsal+horn+of+pig+spinal+cord.&rft.au=Szallasi%2C+A%3BBlumberg%2C+P+M&rft.aulast=Szallasi&rft.aufirst=A&rft.date=1991-05-03&rft.volume=547&rft.issue=2&rft.spage=335&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 - 1991-10-04 N1 - Date created - 1991-10-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Personality and cerebrospinal fluid monoamine metabolites in alcoholics and controls. AN - 85254421; pmid-1708656 AB - Alcoholics as a group have been consistently reported to show differences from controls on various personality inventories. Moreover, neurobiologic substrates have been postulated to underlie personality dimensions. Therefore, we compared alcoholics with controls on measures of personality and investigated relationships between measures of personality and cerebrospinal fluid monoamine metabolite concentrations. The alcoholics were significantly different from controls on many personality measurements. There were significant, negative correlations between interview-derived lifetime aggression scores and cerebrospinal fluid concentrations of both the serotonin metabolite 5-hydroxyindoleacetic acid and the dopamine metabolite homovanillic acid. However, there were no significant correlations between any cerebrospinal fluid monoamine metabolite concentrations and scores on personality inventories. JF - Archives of General Psychiatry AU - Limson, R AU - Goldman, D AU - Roy, A AU - Lamparski, D AU - Ravitz, B AU - Adinoff, B AU - Linnoila, M AD - Laboratory of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892. PY - 1991 SP - 437 EP - 441 VL - 48 IS - 5 SN - 0003-990X, 0003-990X KW - Hydroxyindoleacetic Acid KW - Human KW - Personality Inventory KW - 3,4-Dihydroxyphenylacetic Acid KW - Psychiatric Status Rating Scales KW - Adult KW - Alcoholism KW - MMPI KW - Norepinephrine KW - Methoxyhydroxyphenylglycol KW - Aggression KW - Homovanillic Acid KW - Male KW - Personality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85254421?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+General+Psychiatry&rft.atitle=Personality+and+cerebrospinal+fluid+monoamine+metabolites+in+alcoholics+and+controls.&rft.au=Limson%2C+R%3BGoldman%2C+D%3BRoy%2C+A%3BLamparski%2C+D%3BRavitz%2C+B%3BAdinoff%2C+B%3BLinnoila%2C+M&rft.aulast=Limson&rft.aufirst=R&rft.date=1991-05-01&rft.volume=48&rft.issue=5&rft.spage=437&rft.isbn=&rft.btitle=&rft.title=Archives+of+General+Psychiatry&rft.issn=0003990X&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Smell and taste disorders, a study of 750 patients from the University of Pennsylvania Smell and Taste Center. AN - 85228611; pmid-2021470 AB - Smell and taste disorders are common in the general population, yet little is known about their nature or cause. This article describes a study of 750 patients with complaints of abnormal smell or taste perception from the University of Pennsylvania Smell and Taste Center, Philadelphia. Major findings suggest that: chemosensory dysfunction influences quality of life; complaints of taste loss usually reflect loss of smell function; upper respiratory infection, head trauma, and chronic nasal and paranasal sinus disease are the most common causes of the diminution of the sense of smell, with head trauma having the greatest loss; depression frequently accompanies chemosensory distortion; low body weight accompanies burning mouth syndrome; estrogens protect against loss of the sense of smell in postmenopausal women; zinc therapy may provide no benefit to patients with chemosensory dysfunction; and thyroid hormone function is associated with oral sensory distortion. The findings are discussed in relation to management of patients with chemosensory disturbances. JF - Archives of Otolaryngology--Head and Neck Surgery AU - Deems, D A AU - Doty, R L AU - Settle, R G AU - Moore-Gillon, V AU - Shaman, P AU - Mester, A F AU - Kimmelman, C P AU - Brightman, V J AU - Snow, J B AD - Department of Otorhinolaryngology and Human Communication, School of Medicine, University of Pennsylvania, Philadelphia.; National Institute on Deafness and other Communication Disorders, Bethesda, Maryland 20892, USA. PY - 1991 SP - 519 EP - 528 VL - 117 IS - 5 SN - 0886-4470, 0886-4470 KW - Craniocerebral Trauma KW - Estrogen Replacement Therapy KW - Depression KW - Sex Factors KW - Drug Therapy KW - Dysgeusia KW - Paranasal Sinus Diseases KW - Humans KW - Taste KW - Smell KW - Sensation KW - Nose Diseases KW - Research Support, U.S. Gov't, P.H.S. KW - Taste Disorders KW - Olfaction Disorders KW - Respiratory Tract Infections KW - Middle Aged KW - Pennsylvania KW - Male KW - Female KW - Thyroid Diseases KW - Burning Mouth Syndrome UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85228611?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+Otolaryngology--Head+and+Neck+Surgery&rft.atitle=Smell+and+taste+disorders%2C+a+study+of+750+patients+from+the+University+of+Pennsylvania+Smell+and+Taste+Center.&rft.au=Deems%2C+D+A%3BDoty%2C+R+L%3BSettle%2C+R+G%3BMoore-Gillon%2C+V%3BShaman%2C+P%3BMester%2C+A+F%3BKimmelman%2C+C+P%3BBrightman%2C+V+J%3BSnow%2C+J+B&rft.aulast=Deems&rft.aufirst=D&rft.date=1991-05-01&rft.volume=117&rft.issue=5&rft.spage=519&rft.isbn=&rft.btitle=&rft.title=Archives+of+Otolaryngology--Head+and+Neck+Surgery&rft.issn=08864470&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Shock wave-induced pancreatic trauma. AN - 85223063; pmid-2028959 AB - A case is described of the appearance of a pancreatic or peripancreatic lesion after left renal calculus fragmentation by extracorporeal shock wave lithotripsy (ESWL). Its anatomical location and subsequent disappearance suggest it was related to trauma caused by the shock waves. The brief literature on pancreatic injury after ESWL is reviewed, and the role of the patient's underlying liver disease in the genesis of this complication is discussed. JF - The American Journal of Gastroenterology AU - Mullen, K D AU - Hoofnagle, J H AU - Jones, E A AD - Liver Disease Section, NIDDK, National Institutes of Health, Bethesda, Maryland. PY - 1991 SP - 630 EP - 632 VL - 86 IS - 5 SN - 0002-9270, 0002-9270 KW - Hematoma KW - Lithotripsy KW - Human KW - Pancreas KW - Adult KW - Hepatitis B KW - Pancreatic Diseases KW - Case Report KW - Chronic Disease KW - Kidney Pelvis KW - Kidney Calculi KW - Male UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85223063?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+Journal+of+Gastroenterology&rft.atitle=Shock+wave-induced+pancreatic+trauma.&rft.au=Mullen%2C+K+D%3BHoofnagle%2C+J+H%3BJones%2C+E+A&rft.aulast=Mullen&rft.aufirst=K&rft.date=1991-05-01&rft.volume=86&rft.issue=5&rft.spage=630&rft.isbn=&rft.btitle=&rft.title=The+American+Journal+of+Gastroenterology&rft.issn=00029270&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Planning for future actions. Workshop on residential and outpatient treatment modalities. AN - 80732430; 1868284 JF - Bulletin of the New York Academy of Medicine AU - Weissman, G AU - Mitchell, J AD - Division of Applied Research, National Institute on Drug Abuse, Rockville, Maryland. PY - 1991 SP - 311 EP - 314 VL - 67 IS - 3 SN - 0028-7091, 0028-7091 KW - Index Medicus KW - Humans KW - Female KW - Pregnancy KW - Substance-Related Disorders -- therapy KW - Pregnancy Complications -- therapy KW - Maternal Health Services KW - Ambulatory Care Facilities KW - Residential Facilities UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80732430?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bulletin+of+the+New+York+Academy+of+Medicine&rft.atitle=Planning+for+future+actions.+Workshop+on+residential+and+outpatient+treatment+modalities.&rft.au=Weissman%2C+G%3BMitchell%2C+J&rft.aulast=Weissman&rft.aufirst=G&rft.date=1991-05-01&rft.volume=67&rft.issue=3&rft.spage=311&rft.isbn=&rft.btitle=&rft.title=Bulletin+of+the+New+York+Academy+of+Medicine&rft.issn=00287091&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-17 N1 - Date created - 1991-09-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Is nicotine more addictive than cocaine? AN - 80710149; 1859920 AB - Is nicotine more addictive than cocaine? That claim is increasingly in vogue, often supported by data showing the high likelihood of progression to daily tobacco use following experimentation and the high percentage of cigarette smokers, compared with cocaine users who appear addicted. In the context of criteria for addiction of dependence presented by the World Health Organization, the American Psychiatric Association, and the US Surgeon General, we consider several lines of evidence, including patterns of mortality, physical dependence potential, and pharmacologic addiction liability measures. Within each line of evidence, we compare nicotine with cocaine. We conclude that on the current evidence nicotine cannot be considered more addicting than cocaine. Both are highly addicting drugs for which patterns of use and the development of dependence are strongly influenced by factors such as availability, price, social pressures, and regulations, as well as certain pharmacologic characteristics. JF - British journal of addiction AU - Henningfield, J E AU - Cohen, C AU - Slade, J D AD - Clinical Pharmacology Branch, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 565 EP - 569 VL - 86 IS - 5 SN - 0952-0481, 0952-0481 KW - Nicotine KW - 6M3C89ZY6R KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Euphoria -- drug effects KW - Cross-Sectional Studies KW - Animals KW - United Kingdom -- epidemiology KW - Humans KW - Incidence KW - Nicotine -- pharmacokinetics KW - Nicotine -- adverse effects KW - Cocaine -- pharmacokinetics KW - Smoking -- psychology KW - Substance-Related Disorders -- psychology KW - Cocaine -- adverse effects KW - Smoking -- epidemiology KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80710149?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Is+nicotine+more+addictive+than+cocaine%3F&rft.au=Henningfield%2C+J+E%3BCohen%2C+C%3BSlade%2C+J+D&rft.aulast=Henningfield&rft.aufirst=J&rft.date=1991-05-01&rft.volume=86&rft.issue=5&rft.spage=565&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 - 1991-09-05 N1 - Date created - 1991-09-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Positron emission imaging of cardiac sympathetic innervation and function using 18F-6-fluorodopamine: effects of chemical sympathectomy by 6-hydroxydopamine. AN - 80701983; 1649861 AB - Hypotheses concerning the pathophysiology of hypertension, cardiac failure and other cardiovascular disorders have imputed abnormal cardiac sympathoneural activity. Here we describe a technique to examine cardiac sympathetic innervation and function using positron emission tomographic (PET) scanning after systemic intravenous injection of 18F-6-fluorodopamine, and the effects of chemical sympathectomy by the neurotoxin, 6-hydroxydopamine (6-OHDA). Uptake of 18F-6-fluorodopamine by the heart of anesthetized dogs resulted in striking delineation of the left ventricular myocardium. Myocardial radioactivity declined bi-exponentially, with a half-life of approximately 2 h during the longer phase. In 6-OHDA-treated animals, the ventricular myocardium was barely distinguishable from the chamber; myocardial radioactivity declined rapidly and was virtually absent within 30 min after injection of 18F-6-fluorodopamine. The rates of decline in myocardial radioactivity in dogs treated with 6-OHDA were similar to those in dogs treated with reserpine, but the mechanisms of sympatholysis by these drugs were distinguished by arterial plasma levels of 6-fluorodihydroxyphenylacetic acid (6-FDOPAC). Plasma 6-FDOPAC levels were diminished in 6-OHDA-treated dogs and elevated in reserpinized dogs. The results confirm that, after injection of 18F-6-fluorodopamine, cardiac sympathetic nerve endings are radiolabeled, allowing visualization of sites of sympathetic innervation. Combined assessments of PET time-activity curves and plasma levels of metabolites of 18F-6-fluorodopamine constitute a new, potentially clinically applicable means by which to examine cardiac sympathetic function. JF - Journal of hypertension AU - Goldstein, D S AU - Grossman, E AU - Tamrat, M AU - Chang, P C AU - Eisenhofer, G AU - Bacher, J AU - Kirk, K L AU - Bacharach, S AU - Kopin, I J AD - Clinical Neuroscience Branch, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, Maryland 20892. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 417 EP - 423 VL - 9 IS - 5 SN - 0263-6352, 0263-6352 KW - Catechols KW - 0 KW - Fluorine Radioisotopes KW - Hydroxydopamines KW - Neurotoxins KW - 6-fluorodopamine KW - 59043-70-8 KW - Oxidopamine KW - 8HW4YBZ748 KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Animals KW - Half-Life KW - Dogs KW - Tomography, Emission-Computed KW - Hemodynamics KW - Catechols -- blood KW - Monitoring, Physiologic KW - Dopamine -- analogs & derivatives KW - Heart -- innervation KW - Sympathetic Nervous System -- physiology KW - Sympathectomy, Chemical KW - Sympathetic Nervous System -- diagnostic imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80701983?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+hypertension&rft.atitle=Positron+emission+imaging+of+cardiac+sympathetic+innervation+and+function+using+18F-6-fluorodopamine%3A+effects+of+chemical+sympathectomy+by+6-hydroxydopamine.&rft.au=Goldstein%2C+D+S%3BGrossman%2C+E%3BTamrat%2C+M%3BChang%2C+P+C%3BEisenhofer%2C+G%3BBacher%2C+J%3BKirk%2C+K+L%3BBacharach%2C+S%3BKopin%2C+I+J&rft.aulast=Goldstein&rft.aufirst=D&rft.date=1991-05-01&rft.volume=9&rft.issue=5&rft.spage=417&rft.isbn=&rft.btitle=&rft.title=Journal+of+hypertension&rft.issn=02636352&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-23 N1 - Date created - 1991-08-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Quinapril: a new second-generation ACE inhibitor. AN - 80675846; 2068835 AB - Quinapril is a new non-sulfhydryl angiotensin-converting enzyme (ACE) inhibitor. The drug undergoes hepatic hydrolysis into its major active diacid metabolite, quinaprilat, and two minor inactive metabolites. On a weight basis quinaprilat is three times as potent an ACE inhibitor as quinapril. Approximately 60 percent of an oral dose of quinapril is absorbed. In contrast with captopril, the absorption of quinapril is unaffected by food. Peak serum concentrations of quinapril and quinaprilat are achieved within one and two hours, respectively. Approximately 61 percent of an orally administered dose is excreted in the urine, principally as quinaprilat. The elimination half-life of quinaprilat is three hours, but is prolonged up to 11 hours in patients with renal dysfunction. Quinapril dose reduction is recommended in patients with a creatinine clearance of 0.50 mL/sec or less. In the elderly the elimination of quinaprilat is reduced and correlates well with renal function. In patients with cirrhosis the hydrolysis of quinapril to quinaprilat is impaired resulting in lower plasma quinaprilat concentrations and up to a two-fold increase in quinapril half-life. Quinaprilat has a strong binding capacity to tissue ACE allowing for once-daily dosing. The recommended starting dose for quinapril is 20 mg/d. The nature and incidence of adverse reactions to quinapril are similar to those of enalapril and captopril. Quinapril's antihypertensive efficacy is equal to that of captopril and enalapril. A small number of patients with congestive heart failure (CHF) have been treated with quinapril. Preliminary data indicate that quinapril is an equally effective therapeutic alternative to presently available ACE inhibitors in the treatment of CHF.(ABSTRACT TRUNCATED AT 250 WORDS) JF - DICP : the annals of pharmacotherapy AU - Cetnarowski-Cropp, A B AD - Cardiology Branch, National Heart, Lung, and Blood Institute, Warren Grant Magneson Clinical Center, Bethesda, MD 20892. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 499 EP - 504 VL - 25 IS - 5 SN - 1042-9611, 1042-9611 KW - Angiotensin-Converting Enzyme Inhibitors KW - 0 KW - Isoquinolines KW - Tetrahydroisoquinolines KW - quinapril KW - RJ84Y44811 KW - Index Medicus KW - Drug Interactions KW - Humans KW - Clinical Trials as Topic KW - Isoquinolines -- therapeutic use KW - Heart Failure -- drug therapy KW - Angiotensin-Converting Enzyme Inhibitors -- therapeutic use KW - Isoquinolines -- pharmacokinetics KW - Angiotensin-Converting Enzyme Inhibitors -- adverse effects KW - Heart Failure -- metabolism KW - Isoquinolines -- adverse effects KW - Hypertension -- metabolism KW - Angiotensin-Converting Enzyme Inhibitors -- pharmacokinetics KW - Hypertension -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80675846?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=DICP+%3A+the+annals+of+pharmacotherapy&rft.atitle=Quinapril%3A+a+new+second-generation+ACE+inhibitor.&rft.au=Cetnarowski-Cropp%2C+A+B&rft.aulast=Cetnarowski-Cropp&rft.aufirst=A&rft.date=1991-05-01&rft.volume=25&rft.issue=5&rft.spage=499&rft.isbn=&rft.btitle=&rft.title=DICP+%3A+the+annals+of+pharmacotherapy&rft.issn=10429611&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-13 N1 - Date created - 1991-08-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mortality among industrial workers exposed to phenol. AN - 80631202; 2054400 AB - We conducted a follow-up study to evaluate mortality among 14,861 workers employed in five facilities producing or using phenol and formaldehyde. More than 360,000 person-years of follow-up accrued. Mortality rates from all causes of death combined were similar to those in the general U.S. population. We observed excesses of cancer of the esophagus, cancer of the kidney, and Hodgkin's disease among workers exposed to phenol, but none of these excesses showed a dose-response relation with exposure to phenol. Excess lung cancer mortality (SMR = 1.2) showed no consistent pattern by any exposure index. Workers exposed to phenol had lower mortality ratios for cancer of the buccal cavity and pharynx, cancer of the stomach, cancer of the brain, arteriosclerotic heart disease, emphysema, disease of the digestive system, and cirrhosis of the liver. Of these, arteriosclerotic heart disease, emphysema, and cirrhosis of the liver were inversely related to duration of phenol exposure and to cumulative phenol exposure levels. Although these inverse associations may be due to chance or uncontrolled confounders, the ability of phenol to interfere with the generation of oxidants in experimental systems suggests that the pattern may have biologic plausibility. JF - Epidemiology (Cambridge, Mass.) AU - Dosemeci, M AU - Blair, A AU - Stewart, P A AU - Chandler, J AU - Trush, M A AD - Occupational Studies Section, National Cancer Institute, Bethesda, MD. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 188 EP - 193 VL - 2 IS - 3 SN - 1044-3983, 1044-3983 KW - Phenols KW - 0 KW - Formaldehyde KW - 1HG84L3525 KW - Phenol KW - 339NCG44TV KW - Index Medicus KW - Occupational Exposure KW - Emphysema -- mortality KW - Neoplasms -- mortality KW - Humans KW - Retrospective Studies KW - Aged KW - Liver Cirrhosis KW - Demography KW - Adult KW - Cohort Studies KW - Formaldehyde -- adverse effects KW - Middle Aged KW - Male KW - Coronary Artery Disease -- mortality KW - Phenols -- adverse effects KW - Occupational Diseases -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80631202?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Epidemiology+%28Cambridge%2C+Mass.%29&rft.atitle=Mortality+among+industrial+workers+exposed+to+phenol.&rft.au=Dosemeci%2C+M%3BBlair%2C+A%3BStewart%2C+P+A%3BChandler%2C+J%3BTrush%2C+M+A&rft.aulast=Dosemeci&rft.aufirst=M&rft.date=1991-05-01&rft.volume=2&rft.issue=3&rft.spage=188&rft.isbn=&rft.btitle=&rft.title=Epidemiology+%28Cambridge%2C+Mass.%29&rft.issn=10443983&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-01 N1 - Date created - 1991-08-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Detection of three rare frameshift mutations in the cystic fibrosis gene in an African-American (CF444delA), an Italian (CF2522insC), and a Soviet (CF3821delT). AN - 80605244; 1710600 AB - We have identified three new frameshift mutations in the CFTR gene in patients with cystic fibrosis (CF). The first one involves the deletion of an adenine nucleotide in exon 4 in an African-American patient (CF444delA), the second involves the insertion of a cytosine nucleotide in exon 13 in an Italian patient (CF2522insC), and the third results from the deletion of a thymidine nucleotide in exon 19 in a Soviet patient (CF3821delT). Each mutation is predicted to result in premature termination of the CFTR protein. JF - Genomics AU - White, M B AU - Krueger, L J AU - Holsclaw, D S AU - Gerrard, B C AU - Stewart, C AU - Quittell, L AU - Dolganov, G AU - Baranov, V AU - Ivaschenko, T AU - Kapronov, N I AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick Cancer Research and Development Center (FCRDC), Frederick, Maryland. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 266 EP - 269 VL - 10 IS - 1 SN - 0888-7543, 0888-7543 KW - CFTR KW - CFTR protein, human KW - 0 KW - Membrane Proteins KW - Cystic Fibrosis Transmembrane Conductance Regulator KW - 126880-72-6 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - United States KW - Exons KW - Humans KW - Amino Acid Sequence KW - Child KW - Child, Preschool KW - USSR -- ethnology KW - Italy -- ethnology KW - Base Sequence KW - Adult KW - Molecular Sequence Data KW - Africa -- ethnology KW - Frameshift Mutation KW - Cystic Fibrosis -- ethnology KW - Cystic Fibrosis -- genetics KW - Membrane Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80605244?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Genomics&rft.atitle=Detection+of+three+rare+frameshift+mutations+in+the+cystic+fibrosis+gene+in+an+African-American+%28CF444delA%29%2C+an+Italian+%28CF2522insC%29%2C+and+a+Soviet+%28CF3821delT%29.&rft.au=White%2C+M+B%3BKrueger%2C+L+J%3BHolsclaw%2C+D+S%3BGerrard%2C+B+C%3BStewart%2C+C%3BQuittell%2C+L%3BDolganov%2C+G%3BBaranov%2C+V%3BIvaschenko%2C+T%3BKapronov%2C+N+I&rft.aulast=White&rft.aufirst=M&rft.date=1991-05-01&rft.volume=10&rft.issue=1&rft.spage=266&rft.isbn=&rft.btitle=&rft.title=Genomics&rft.issn=08887543&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-18 N1 - Date created - 1991-07-18 N1 - Date revised - 2017-01-13 N1 - Gene symbol - CFTR N1 - Genetic sequence - M65281; GENBANK; M65280; M65279; M65198; M65277; M65278; M65282; M65197; M65283; M65196 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evidence for a common cell of origin for primitive epithelial cells isolated from rat liver and pancreas. AN - 80591993; 1710229 AB - The appearance of differentiated hepatocytes in the adult rat pancreas as well as pancreatic-type tissue in the adult rat liver can be experimentally induced (Reddy et al.: J. Cell Biol., 98:2082-2090, 1984; Rao et al., J. Histochem. Cytochem., 34:197-201, 1986). These observations suggest a lineage relationship between cell compartments present in rat liver and pancreas. The present data demonstrate that epithelial cell lines with almost identical phenotypes can be established from adult rat liver and pancreas. The established cell lines showed similar morphologies as established by light- and electron-microscopic studies. The cell lines showed a unique expression pattern of intermediate filament proteins. Vimentin, actin, and beta-tubulin were present in all cell lines. In addition, simple epithelial type II cytokeratins 7 and 8 were found to be coexpressed with the type I cytokeratin 14 in several of the cell lines. Neither the type I cytokeratins 18 and 19, which are the normal partners for cytokeratins 8 and 7 in filament formation, nor the type II cytokeratin 5 could be detected despite the fact that filaments were formed by both cytokeratins 8 and 14. This suggests that cytokeratin 14 acts as an indiscriminate type I cytokeratin in filament formation in the established cell lines. The cell lines expressed the same sets of LDH and aldolase isoenzymes and identical sets of glutathione transferase subunits. In addition, the epithelial cell lines from liver and pancreas were equally sensitive to the growth-inhibitory effects of TGF-beta 1. No expression of tissue- or cell-specific proteins such as alpha-fetoprotein, albumin, amylase, elastase, or gamma-glutamyl transpeptidase were detected. The almost identical phenotypes of the hepatic and pancreatic cell lines suggest that they may be derived from a common primitive epithelial cell type present in both rat liver and pancreas. In contrast to parenchymal cells, these cells have an extended capacity for proliferation in vitro and may represent a progeny from a "precursor" or "stem" cell compartment in vivo. JF - Journal of cellular physiology AU - Bisgaard, H C AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 333 EP - 343 VL - 147 IS - 2 SN - 0021-9541, 0021-9541 KW - Actins KW - 0 KW - Isoenzymes KW - Tubulin KW - Vimentin KW - Keratins KW - 68238-35-7 KW - L-Lactate Dehydrogenase KW - EC 1.1.1.27 KW - Glutathione Transferase KW - EC 2.5.1.18 KW - Fructose-Bisphosphate Aldolase KW - EC 4.1.2.13 KW - Index Medicus KW - Fructose-Bisphosphate Aldolase -- metabolism KW - Karyotyping KW - Keratins -- metabolism KW - Animals KW - Immunoblotting KW - Glutathione Transferase -- metabolism KW - Tubulin -- metabolism KW - Actins -- metabolism KW - Isoenzymes -- metabolism KW - Rats KW - Phenotype KW - Rats, Inbred F344 KW - Epithelial Cells KW - Vimentin -- metabolism KW - Microscopy, Electron KW - Epithelium -- metabolism KW - Epithelium -- ultrastructure KW - Male KW - L-Lactate Dehydrogenase -- metabolism KW - Cell Division KW - Liver -- cytology KW - Stem Cells -- cytology KW - Pancreas -- cytology KW - Pancreas -- metabolism KW - Pancreas -- ultrastructure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80591993?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Evidence+for+a+common+cell+of+origin+for+primitive+epithelial+cells+isolated+from+rat+liver+and+pancreas.&rft.au=Bisgaard%2C+H+C%3BThorgeirsson%2C+S+S&rft.aulast=Bisgaard&rft.aufirst=H&rft.date=1991-05-01&rft.volume=147&rft.issue=2&rft.spage=333&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 - 1991-07-10 N1 - Date created - 1991-07-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A toxin-resistant mouse L-cell mutant defective in protein transport along the secretory pathway. AN - 80591906; 1645740 AB - Using methods designed for isolation of mutants defective in receptor-mediated endocytosis, a novel L-cell mutant was obtained that exhibits resistance to three different protein toxins as well as alterations in secretion. This mutant, LEFIC, is resistant to modeccin, Pseudomonas exotoxin, and ricin. These toxins, which enter the cytoplasm via receptor-mediated endocytosis, are thought to penetrate into cells at the level of late endosomes or the trans Golgi network. Early endosomal acidification appears to be normal in the mutant based on its accumulation of iron from transferrin and its sensitivity to diphtheria toxin A chain-transferrin conjugate. Within the secretory pathway two delays in transport of vesicular stomatitis virus (VSV) G protein were observed in LEFIC: a 20-30 min delay in acquisition of Endo H resistance and a 1-2 hr delay in appearance of newly synthesized G protein on the cell surface. Movement of endogenous proteins along the secretory pathway was also affected in LEFIC. Fibronectin secretion was delayed by 15 min, and membrane proteins were delayed in arrival at the cell surface. The phenotype of LEFIC is consistent with a defect in a component or compartment shared by both the late endocytic and constitutive secretory pathways. JF - Journal of cellular physiology AU - Laurie, S M AU - Robbins, A R AD - Laboratory of Biochemistry and Metabolism, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 215 EP - 223 VL - 147 IS - 2 SN - 0021-9541, 0021-9541 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - Fibronectins KW - Lectins KW - Membrane Proteins KW - Plant Lectins KW - Proteins KW - Ribosome Inactivating Proteins, Type 2 KW - Toxins, Biological KW - Viral Proteins KW - Virulence Factors KW - modeccin KW - 65988-88-7 KW - Ricin KW - 9009-86-3 KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Index Medicus KW - Vesicular stomatitis Indiana virus KW - Animals KW - Drug Resistance -- genetics KW - Exotoxins -- pharmacology KW - Viral Proteins -- secretion KW - GTP-Binding Proteins -- secretion KW - Protein Processing, Post-Translational KW - Biological Transport KW - Mice KW - Fibronectins -- secretion KW - Membrane Proteins -- secretion KW - Ricin -- pharmacology KW - Lectins -- pharmacology KW - Phenotype KW - Proteins -- secretion KW - Endocytosis KW - L Cells (Cell Line) -- metabolism KW - Toxins, Biological -- pharmacology KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80591906?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+toxin-resistant+mouse+L-cell+mutant+defective+in+protein+transport+along+the+secretory+pathway.&rft.au=Laurie%2C+S+M%3BRobbins%2C+A+R&rft.aulast=Laurie&rft.aufirst=S&rft.date=1991-05-01&rft.volume=147&rft.issue=2&rft.spage=215&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 - 1991-07-10 N1 - Date created - 1991-07-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Spin trap protection from tumor necrosis factor cytotoxicity. AN - 80569999; 2038186 AB - Tumor necrosis factor (TNF) facilitates superoxide production, and spin traps may detoxify superoxide by acting as superoxide dismutase mimics. We investigated the ability of a stable nitroxide spin trap, TEMPOL, to protect TNF-sensitive cells from exogenously added TNF. WEHI or L929 cells were incubated with TNF (500 units/ml) for 18 hr either simultaneously with 0 to 8 mM TEMPOL or with the TEMPOL added at varying intervals after TNF exposure. A dose-dependent increase in survival was noted in the TEMPOL-treated cells, with 92 +/- 2% survival of WEHIs treated with 4 mM TEMPOL compared to 26 +/- 1% survival for non-TEMPOL-exposed cells (P2 less than 0.01). Significant increases in survival could be accomplished with as late as 15-hr delayed addition of the compound. The mechanism of protection does not seem to involve newly synthesized protein, and Northern blot analysis revealed that TEMPOL does not induce the genes for MnSOD or Cu-ZnSOD. The ability of TEMPOL to protect against TNF injury, even when exposure is delayed, may prove useful in conditions thought to be associated with free radical-lymphokine interactions such as ischemia-reperfusion, oxygen toxicity, or sepsis. JF - The Journal of surgical research AU - Pogrebniak, H AU - Matthews, W AU - Mitchell, J AU - Russo, A AU - Samuni, A AU - Pass, H AD - Thoracic Oncology Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 469 EP - 474 VL - 50 IS - 5 SN - 0022-4804, 0022-4804 KW - Cyclic N-Oxides KW - 0 KW - Cytotoxins KW - Spin Labels KW - Tumor Necrosis Factor-alpha KW - Cycloheximide KW - 98600C0908 KW - tempol KW - U78ZX2F65X KW - Index Medicus KW - Animals KW - Blotting, Northern KW - Tumor Cells, Cultured KW - Dose-Response Relationship, Drug KW - Kinetics KW - Cycloheximide -- pharmacology KW - Time Factors KW - Cell Line KW - Cyclic N-Oxides -- pharmacology KW - Tumor Necrosis Factor-alpha -- antagonists & inhibitors KW - Cytotoxins -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80569999?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+surgical+research&rft.atitle=Spin+trap+protection+from+tumor+necrosis+factor+cytotoxicity.&rft.au=Pogrebniak%2C+H%3BMatthews%2C+W%3BMitchell%2C+J%3BRusso%2C+A%3BSamuni%2C+A%3BPass%2C+H&rft.aulast=Pogrebniak&rft.aufirst=H&rft.date=1991-05-01&rft.volume=50&rft.issue=5&rft.spage=469&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+surgical+research&rft.issn=00224804&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-06-28 N1 - Date created - 1991-06-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human recombinant interleukin-1 alpha protection against the lethality of endotoxin and experimental sepsis in mice. AN - 80569943; 2038179 AB - Human recombinant interleukin-1 alpha (IL-1) has a diverse range of physiological activities which may be beneficial or deleterious to the host. Pretreatment with doses of IL-1 has been shown to protect mice against a subsequent lethal bacterial injection; however, the protective effects of a single intravenous (iv) dose of IL-1 have not been well characterized. The current experiments were performed to determine the best dose, timing, and duration of action of a single iv dose of IL-1 against a subsequent lethal challenge with intraperitoneal endotoxin (LPS) or experimental sepsis induced by cecal ligation and puncture (CLP). Female C57B1/6 mice treated with iv IL-1 24 hr prior to 30 mg/kg LPS ip had improved survival compared to saline-treated controls (P less than 0.01). IL-1 was also protective when given 6 to 72 hr, but not 2 or 96 hr, prior to LPS. IL-1 protection against LPS lethality was similar to protection seen with an iv dose of tumor necrosis factor (TNF). After CLP, survival was improved with IL-1 versus saline pretreatment (P = 0.02). Unlike previous work with TNF, no toxicity or lethality was observed at any dose of IL-1 administered. A single iv dose of IL-1 protects against the lethality of LPS and CLP in mice. IL-1 may be a useful treatment strategy in patients at risk for the development of life-threatening sepsis. JF - The Journal of surgical research AU - Alexander, H R AU - Doherty, G M AU - Fraker, D L AU - Block, M I AU - Swedenborg, J E AU - Norton, J A AD - Surgical Metabolism Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 421 EP - 424 VL - 50 IS - 5 SN - 0022-4804, 0022-4804 KW - Endotoxins KW - 0 KW - Interleukin-1 KW - Lipopolysaccharides KW - Recombinant Proteins KW - Tumor Necrosis Factor-alpha KW - Index Medicus KW - Animals KW - Lipopolysaccharides -- pharmacology KW - Tumor Necrosis Factor-alpha -- pharmacology KW - Punctures KW - Mice, Inbred C57BL KW - Ligation KW - Cecum KW - Mice KW - Female KW - Interleukin-1 -- pharmacology KW - Escherichia coli KW - Endotoxins -- antagonists & inhibitors KW - Bacterial Infections -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80569943?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+surgical+research&rft.atitle=Human+recombinant+interleukin-1+alpha+protection+against+the+lethality+of+endotoxin+and+experimental+sepsis+in+mice.&rft.au=Alexander%2C+H+R%3BDoherty%2C+G+M%3BFraker%2C+D+L%3BBlock%2C+M+I%3BSwedenborg%2C+J+E%3BNorton%2C+J+A&rft.aulast=Alexander&rft.aufirst=H&rft.date=1991-05-01&rft.volume=50&rft.issue=5&rft.spage=421&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+surgical+research&rft.issn=00224804&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-06-28 N1 - Date created - 1991-06-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vitro study of simultaneous infusion of incompatible drugs in multilumen catheters. AN - 80564972; 1903369 AB - Multilumen catheters are commonly used to simultaneously administer incompatible drugs to critically ill patients. Though there are no known documented reports that this practice has been responsible for harmful events in patients, likewise there are no published data to verify the safety and efficacy of this practice. This study utilized an in vitro model flow system to examine the physicochemical phenomena that occur when two incompatible drugs (phenytoin and total parenteral nutrition) are simultaneously administered through multilumen catheters. Flow conditions and drug infusions in the venous model were designed to mimic the in vivo clinical situation to evaluate two central venous catheter types, a double- and a triple-lumen catheter. Video recordings were made of drug interactions, and assays of phenytoin concentration were performed on samples of the circulating fluid. White clouds of phenytoin precipitation were observed near the tip of the double-lumen catheter but not the triple-lumen catheter. Infusion through the double-lumen catheter resulted in an average of 6% loss of phenytoin to precipitate, which, on microscopic examination, appeared as spindle-shaped crystals 25 to 50 microns in length and 5 to 10 microns wide. In some cases, millimeter-size fragments of phenytoin precipitate were seen to dislodge from the tip of the double-lumen catheter. The adjacent orifices at the tip of the end hole of the double-lumen catheter appeared to permit interaction of the two effusing streams of the incompatible drugs, whereas the staggered orifices of the triple-lumen catheter reduce this interaction.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Heart & lung : the journal of critical care AU - Collins, J L AU - Lutz, R J AD - Clinical Center, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 271 EP - 277 VL - 20 IS - 3 SN - 0147-9563, 0147-9563 KW - Phenytoin KW - 6158TKW0C5 KW - Abridged Index Medicus KW - Index Medicus KW - Parenteral Nutrition, Total KW - Phenytoin -- pharmacology KW - Catheterization, Central Venous -- adverse effects KW - Catheterization, Central Venous -- instrumentation KW - Infusions, Intravenous -- instrumentation KW - Drug Antagonism KW - Infusions, Intravenous -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80564972?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Heart+%26+lung+%3A+the+journal+of+critical+care&rft.atitle=In+vitro+study+of+simultaneous+infusion+of+incompatible+drugs+in+multilumen+catheters.&rft.au=Collins%2C+J+L%3BLutz%2C+R+J&rft.aulast=Collins&rft.aufirst=J&rft.date=1991-05-01&rft.volume=20&rft.issue=3&rft.spage=271&rft.isbn=&rft.btitle=&rft.title=Heart+%26+lung+%3A+the+journal+of+critical+care&rft.issn=01479563&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-06-21 N1 - Date created - 1991-06-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evidence that cyclosporine treatment during pregnancy predisposes offspring to develop autoantibodies. AN - 80563943; 1903221 AB - Cyclosporine was administered (11 mg/kg/day) to pregnant mice to study the effects of passively transferred CsA on the developing immune system. Placental transfer of CsA was shown by the detection of fetal-tissue levels ranging from 400 to 1500 ng CsA/g tissue. Treatment clearly altered the developing immune system. Thymuses from the day-18 embryos exposed to CsA were partially depleted of CD4+CD8- single positive cells. Eleven of 50 offspring born to CsA-treated mothers developed significant levels of IgG autoantibodies to gastric antigens. In addition, two animals that received CsA in utero developed an extensive mononuclear cell infiltrate in the gastric mucosa resembling autoimmune gastritis. These results raise the possibility that the administration of CsA during pregnancy may result in potential long-term effects on the developing immune system. Offspring of such pregnancies may suffer an increased incidence or severity of autoimmune diseases. JF - Transplantation AU - Classen, J B AU - Shevach, E M AD - Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 1052 EP - 1057 VL - 51 IS - 5 SN - 0041-1337, 0041-1337 KW - Antigens, CD4 KW - 0 KW - Antigens, CD8 KW - Antigens, Differentiation, T-Lymphocyte KW - Autoantibodies KW - Cyclosporins KW - Index Medicus KW - Animals KW - Mice KW - Gastric Mucosa -- pathology KW - Thymus Gland -- drug effects KW - Pregnancy KW - Antigens, Differentiation, T-Lymphocyte -- analysis KW - Antigens, CD4 -- analysis KW - Gastric Mucosa -- immunology KW - Mice, Inbred C3H KW - Autoimmune Diseases -- chemically induced KW - Flow Cytometry KW - Female KW - Gastritis -- chemically induced KW - Fetus -- drug effects KW - Cyclosporins -- toxicity KW - Autoantibodies -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80563943?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Transplantation&rft.atitle=Evidence+that+cyclosporine+treatment+during+pregnancy+predisposes+offspring+to+develop+autoantibodies.&rft.au=Classen%2C+J+B%3BShevach%2C+E+M&rft.aulast=Classen&rft.aufirst=J&rft.date=1991-05-01&rft.volume=51&rft.issue=5&rft.spage=1052&rft.isbn=&rft.btitle=&rft.title=Transplantation&rft.issn=00411337&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-06-17 N1 - Date created - 1991-06-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparison between DNA adduct formation and tumorigenesis in livers and bladders of mice chronically fed 2-acetylaminofluorene. AN - 80553947; 2029755 AB - Female BALB/c mice continuously fed 2-acetylaminofluorene (AAF) develop liver and bladder tumors. The incidence of liver tumors is linearly related to the carcinogen concentration in the diet, while the tumor response in the bladder is markedly non-linear. In the current experiments, liver and bladder DNA adducts were measured in female BALB/c mice fed several different concentrations of AAF for 28 days. The adduct concentrations were then compared to the previously reported incidences of neoplastic and preneoplastic lesions in these tissues. In initial experiments, mice were fed either 30 or 150 mg [ring-3H]AAF/kg diet for 21 days. Liver DNA adducts were identified by HPLC, which indicated the presence of one major adduct, N-(deoxyguanosin-8-yl)-2-aminofluorene (dG-C8-AF). This adduct was also the major product detected by 32P-postlabeling in liver and bladder DNA from mice fed the same concentrations of AAF for 28 days. Radioimmunoassays, conducted with an antibody specific for dG-C8-AF, showed that steady-state concentrations of dG-C8-AF were obtained at 28 days of AAF feeding; thus, this time point was used to determine the relationship between the dose of AAF and the adduct levels. In mice fed nine concentrations of AAF (5-150 mg AAF/kg diet), the adduct concentrations after 28 days of feeding were linearly related to dose in both the liver and bladder, with the adduct concentration being approximately 3-fold greater in the bladder. These results indicate that a linear correlation exists between the hepatic concentration of dG-C8-AF and the liver tumor incidence. In the bladder however, a linear relationship was not observed, which suggests that additional tissue-specific factors, such as toxicity, are essential components for tumorigenesis in this tissue. JF - Carcinogenesis AU - Poirier, M C AU - Fullerton, N F AU - Kinouchi, T AU - Smith, B A AU - Beland, F A AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 895 EP - 900 VL - 12 IS - 5 SN - 0143-3334, 0143-3334 KW - 2-Acetylaminofluorene KW - 9M98QLJ2DL KW - Index Medicus KW - Animals KW - Hyperplasia -- chemically induced KW - Adenoma -- chemically induced KW - Mice KW - Mice, Inbred BALB C KW - Autoradiography KW - Female KW - Chromatography, High Pressure Liquid KW - Carcinoma -- chemically induced KW - 2-Acetylaminofluorene -- toxicity KW - DNA Damage KW - Liver Neoplasms -- chemically induced KW - Urinary Bladder Neoplasms -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80553947?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Comparison+between+DNA+adduct+formation+and+tumorigenesis+in+livers+and+bladders+of+mice+chronically+fed+2-acetylaminofluorene.&rft.au=Poirier%2C+M+C%3BFullerton%2C+N+F%3BKinouchi%2C+T%3BSmith%2C+B+A%3BBeland%2C+F+A&rft.aulast=Poirier&rft.aufirst=M&rft.date=1991-05-01&rft.volume=12&rft.issue=5&rft.spage=895&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-06-19 N1 - Date created - 1991-06-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Acute effects of pulsatile levodopa administration on central dopamine pharmacodynamics. AN - 80550520; 2027476 AB - Inconsistencies in the response to individual levodopa doses occur in most patients with advanced Parkinson's disease (PD). To investigate the possible development of acute tachyphylaxis, we evaluated the effects of repeated injections of intravenous levodopa in 10 PD patients with motor fluctuations by administering, during a single day, a previously determined optimal levodopa dose repeatedly each time motor function returned to baseline. Peak antiparkinsonian response was lower by 20%, and peak plasma levodopa levels lower by 35% following the first dose compared with all subsequent doses. Neither peak dyskinesia scores nor the duration of motor response changed significantly with successive levodopa doses. These data suggest that pulsatile levodopa administration does not acutely alter dopamine receptor responsiveness, and that other pharmacokinetic and pharmacodynamic factors contribute to the dose-to-dose variability in response to levodopa. JF - Neurology AU - Davis, T L AU - Brughitta, G AU - Baronti, F AU - Mouradian, M M AD - Experimental Therapeutics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 630 EP - 633 VL - 41 IS - 5 SN - 0028-3878, 0028-3878 KW - Levodopa KW - 46627O600J KW - Dopamine KW - VTD58H1Z2X KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Middle Aged KW - Dyskinesia, Drug-Induced -- physiopathology KW - Time Factors KW - Male KW - Levodopa -- pharmacology KW - Parkinson Disease -- blood KW - Dopamine -- physiology KW - Levodopa -- therapeutic use KW - Motor Activity -- drug effects KW - Parkinson Disease -- physiopathology KW - Parkinson Disease -- drug therapy KW - Levodopa -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80550520?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurology&rft.atitle=Acute+effects+of+pulsatile+levodopa+administration+on+central+dopamine+pharmacodynamics.&rft.au=Davis%2C+T+L%3BBrughitta%2C+G%3BBaronti%2C+F%3BMouradian%2C+M+M&rft.aulast=Davis&rft.aufirst=T&rft.date=1991-05-01&rft.volume=41&rft.issue=5&rft.spage=630&rft.isbn=&rft.btitle=&rft.title=Neurology&rft.issn=00283878&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-06-07 N1 - Date created - 1991-06-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Kinetic analysis of interactions between kainate and AMPA: evidence for activation of a single receptor in mouse hippocampal neurons. AN - 80544742; 1673850 AB - AMPA but not kainate produces a rapidly desensitizing response in mouse hippocampal neurons. The characteristic action of these agonists appears to arise from activation of a single receptor with active and desensitized states, for which AMPA and kainate have different relative affinity. The equilibrium potency of a series of five agonists that produce rapidly desensitizing responses at non-NMDA receptors (EC50 1 microM to 4 mM) was similar to their equilibrium potency for block of kainate responses. Increasing the concentration of kainate overcame such block, but in the presence of AMPA the rate of activation of responses to kainate was slowed. Conversely, in the presence of kainate the amplitude of rapidly desensitizing responses evoked by AMPA was reduced, and the rate of onset of desensitization was slowed. JF - Neuron AU - Patneau, D K AU - Mayer, M L AD - Laboratory of Developmental Neurobiology, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 785 EP - 798 VL - 6 IS - 5 SN - 0896-6273, 0896-6273 KW - Glutamates KW - 0 KW - Receptors, Kainic Acid KW - Receptors, Neurotransmitter KW - Ibotenic Acid KW - 2552-55-8 KW - Glutamic Acid KW - 3KX376GY7L KW - alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid KW - 77521-29-0 KW - Quisqualic Acid KW - 8OC22C1B99 KW - domoic acid KW - M02525818H KW - Kainic Acid KW - SIV03811UC KW - Index Medicus KW - Quisqualic Acid -- pharmacology KW - Animals KW - Glutamates -- pharmacology KW - Dose-Response Relationship, Drug KW - Cells, Cultured KW - Mice KW - Electrophysiology KW - Drug Antagonism KW - Kainic Acid -- pharmacology KW - Kainic Acid -- analogs & derivatives KW - Hippocampus -- physiology KW - Ibotenic Acid -- analogs & derivatives KW - Neurons -- drug effects KW - Neurons -- physiology KW - Receptors, Neurotransmitter -- drug effects KW - Hippocampus -- embryology KW - Ibotenic Acid -- pharmacology KW - Hippocampus -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80544742?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuron&rft.atitle=Kinetic+analysis+of+interactions+between+kainate+and+AMPA%3A+evidence+for+activation+of+a+single+receptor+in+mouse+hippocampal+neurons.&rft.au=Patneau%2C+D+K%3BMayer%2C+M+L&rft.aulast=Patneau&rft.aufirst=D&rft.date=1991-05-01&rft.volume=6&rft.issue=5&rft.spage=785&rft.isbn=&rft.btitle=&rft.title=Neuron&rft.issn=08966273&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-06-12 N1 - Date created - 1991-06-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inhalation of tetranitromethane causes nasal passage irritation and pulmonary carcinogenesis in rodents. AN - 80542826; 1851054 AB - Fischer 344 rats and B6C3F1 mice were exposed for 2 years to vapors of tetranitromethane at concentrations below (0.5 ppm) and slightly above (2 or 5 ppm) the current U.S. recommended occupational exposure limit. Under the conditions of exposure of 6 h/day, 5 days/week, tetranitromethane was found to cause mild irritation and hyperplastic lesions in the nasal passages, but not nasal cavity neoplasms were observed. In contrast, nearly all animals exposed to the higher TNM concentrations, and the majority of animals exposed to the lower concentrations developed alveolar/bronchiolar adenoma or carcinoma; squamous cell neoplasms of the lung also occurred in exposed rats. The extent of the lung tumor response, and the low concentrations of tetranitromethane required for this response, are unprecedented in National Toxicology Program (NTP) studies. JF - Cancer letters AU - Bucher, J R AU - Huff, J E AU - Jokinen, M P AU - Haseman, J K AU - Stedham, M AU - Cholakis, J M AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/05/01/ PY - 1991 DA - 1991 May 01 SP - 95 EP - 101 VL - 57 IS - 2 SN - 0304-3835, 0304-3835 KW - Tetranitromethane KW - K1G7CKU98F KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Hyperplasia -- chemically induced KW - Dose-Response Relationship, Drug KW - Bronchi -- drug effects KW - Bronchi -- pathology KW - Administration, Inhalation KW - Male KW - Female KW - Rhinitis -- chemically induced KW - Adenocarcinoma, Bronchiolo-Alveolar -- chemically induced KW - Tetranitromethane -- administration & dosage KW - Carcinoma, Squamous Cell -- chemically induced KW - Lung Neoplasms -- chemically induced KW - Tetranitromethane -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80542826?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Inhalation+of+tetranitromethane+causes+nasal+passage+irritation+and+pulmonary+carcinogenesis+in+rodents.&rft.au=Bucher%2C+J+R%3BHuff%2C+J+E%3BJokinen%2C+M+P%3BHaseman%2C+J+K%3BStedham%2C+M%3BCholakis%2C+J+M&rft.aulast=Bucher&rft.aufirst=J&rft.date=1991-05-01&rft.volume=57&rft.issue=2&rft.spage=95&rft.isbn=&rft.btitle=&rft.title=Cancer+letters&rft.issn=03043835&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-06-13 N1 - Date created - 1991-06-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Activation of Escherichia coli heat-labile enterotoxins by native and recombinant adenosine diphosphate-ribosylation factors, 20-kD guanine nucleotide-binding proteins. AN - 80540034; 1902492 AB - Escherichia coli heat-labile enterotoxins (LT) are responsible in part for "traveler's diarrhea" and related diarrheal illnesses. The family of LTs comprises two serogroups termed LT-I and LT-II; each serogroup includes two or more antigenic variants. The effects of LTs result from ADP ribosylation of Gs alpha, a stimulatory component of adenylyl cyclase; the mechanism of action is identical to that of cholera toxin (CT). The ADP-ribosyltransferase activity of CT is enhanced by 20-kD guanine nucleotide-binding proteins, known as ADP-ribosylation factors or ARFs. These proteins directly activate the CTA1 catalytic unit and stimulate its ADP ribosylation of Gs alpha, other proteins, and simple guanidino compounds (e.g., agmatine). Because of the similarities between CT and LTs, we investigated the effects of purified bovine brain ARF and a recombinant form of bovine ARF synthesized in Escherichia coli on LT activity. ARF enhanced the LT-I-, LT-IIa-, and LT-IIb-catalyzed ADP ribosylation of agmatine, as well as the auto-ADP ribosylation of the toxin catalytic unit. Stimulation of ADP-ribosylagmatine formation by LTs and CT in the presence of ARF was GTP dependent and enhanced by sodium dodecyl sulfate. With agmatine as substrate, LT-IIa and LT-IIb exhibited less than 1% the activity of CT and LT-Ih. CT and LTs catalyzed ADP-ribosyl-Gs alpha formation in a reaction dependent on ARF, GTP, and dimyristoyl phosphatidylcholine/cholate. With Gs alpha as substrate, the ADP-ribosyltransferase activities of the toxins were similar, although CT and LT-Ih appeared to be slightly more active than LT-IIa and LT-IIb. Thus, LT-IIa and LT-IIb appear to differ somewhat from CT and LT-Ih in substrate specificity. Responsiveness to stimulation by ARF, GTP, and phospholipid/detergent as well as the specificity of ADP-ribosyltransferase activity are functions of LTs from serogroups LT-I and LT-II that are shared with CT. JF - The Journal of clinical investigation AU - Lee, C M AU - Chang, P P AU - Tsai, S C AU - Adamik, R AU - Price, S R AU - Kunz, B C AU - Moss, J AU - Twiddy, E M AU - Holmes, R K AD - Laboratory of Cellular Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 1780 EP - 1786 VL - 87 IS - 5 SN - 0021-9738, 0021-9738 KW - Bacterial Toxins KW - 0 KW - Enterotoxins KW - Escherichia coli Proteins KW - Membrane Proteins KW - Recombinant Proteins KW - heat-labile enterotoxin, E coli KW - Adenosine Diphosphate Ribose KW - 20762-30-5 KW - Guanosine Triphosphate KW - 86-01-1 KW - Cholera Toxin KW - 9012-63-9 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - ADP-Ribosylation Factors KW - EC 3.6.5.2 KW - Abridged Index Medicus KW - Index Medicus KW - Recombinant Proteins -- pharmacology KW - Cholera Toxin -- pharmacology KW - Adenosine Diphosphate Ribose -- metabolism KW - Guanosine Triphosphate -- pharmacology KW - Escherichia coli -- metabolism KW - Membrane Proteins -- pharmacology KW - Enterotoxins -- pharmacology KW - Bacterial Toxins -- pharmacology KW - GTP-Binding Proteins -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80540034?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Activation+of+Escherichia+coli+heat-labile+enterotoxins+by+native+and+recombinant+adenosine+diphosphate-ribosylation+factors%2C+20-kD+guanine+nucleotide-binding+proteins.&rft.au=Lee%2C+C+M%3BChang%2C+P+P%3BTsai%2C+S+C%3BAdamik%2C+R%3BPrice%2C+S+R%3BKunz%2C+B+C%3BMoss%2C+J%3BTwiddy%2C+E+M%3BHolmes%2C+R+K&rft.aulast=Lee&rft.aufirst=C&rft.date=1991-05-01&rft.volume=87&rft.issue=5&rft.spage=1780&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 - 1991-05-31 N1 - Date created - 1991-05-31 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Gene. 1985;38(1-3):31-8 [2998948] Nature. 1970 Aug 15;227(5259):680-5 [5432063] Infect Immun. 1988 Jul;56(7):1748-53 [3290106] Proc Natl Acad Sci U S A. 1988 Jul;85(13):4667-71 [2455296] Infect Immun. 1986 Nov;54(2):529-36 [2429930] Ann Intern Med. 1984 Nov;101(5):653-66 [6148909] Infect Immun. 1986 Nov;54(2):587-9 [3533784] Pediatr Infect Dis. 1986 Jan-Feb;5(1 Suppl):S101-5 [3511458] J Bacteriol. 1986 Feb;165(2):348-52 [3511028] Science. 1986 Jun 6;232(4755):1258-64 [3704651] Gastroenterology. 1985 Jul;89(1):27-35 [3891496] Biochemistry. 1990 Jan 30;29(4):855-61 [2111167] Biochim Biophys Acta. 1990 May 16;1034(2):195-9 [2112955] Nature. 1983 Dec 8-14;306(5943):551-7 [6646234] J Biol Chem. 1984 May 25;259(10):6235-40 [6327672] Proc Natl Acad Sci U S A. 1981 Aug;78(8):4809-12 [6272274] J Biol Chem. 1981 Dec 25;256(24):12861-5 [6273411] Nature. 1981 Jan 22;289(5795):319-21 [6256663] Proc Natl Acad Sci U S A. 1981 Jan;78(1):50-4 [7017718] Nature. 1980 Dec 4;288(5790):499-501 [7003397] Infect Immun. 1982 Nov;38(2):424-33 [7141703] Am J Clin Nutr. 1979 Jan;32(1):189-96 [32766] Proc Natl Acad Sci U S A. 1977 Aug;74(8):3307-11 [198781] Infect Immun. 1978 Dec;22(3):709-13 [83301] J Clin Invest. 1979 Aug;64(2):381-4 [222809] J Biol Chem. 1979 Jul 10;254(13):5855-61 [221485] Gene. 1979 Jan;5(1):59-76 [372049] Proc Natl Acad Sci U S A. 1986 Jul;83(13):4631-5 [2873570] Infect Immun. 1987 Aug;55(8):1854-8 [3112012] Annu Rev Biochem. 1987;56:615-49 [3113327] J Biol Chem. 1988 Feb 5;263(4):1768-72 [3123477] Adv Enzymol Relat Areas Mol Biol. 1988;61:303-79 [3128060] Biochem J. 1986 Sep 1;238(2):313-22 [3541910] Proc Natl Acad Sci U S A. 1988 Aug;85(15):5488-91 [3135549] J Biol Chem. 1986 Jun 15;261(17):7906-11 [3086320] Infect Immun. 1988 May;56(5):1158-61 [2833443] J Bacteriol. 1987 Nov;169(11):5180-7 [2822667] Infect Immun. 1986 Sep;53(3):464-73 [3017862] J Biol Chem. 1984 May 25;259(10):6228-34 [6327671] J Biol Chem. 1982 Jan 10;257(1):32-4 [6273433] J Biol Chem. 1981 Nov 25;256(22):11517-26 [6271754] J Biol Chem. 1979 Jul 10;254(13):5849-54 [447682] J Biol Chem. 1977 Oct 25;252(20):7249-56 [903362] Biochemistry. 1976 Mar 23;15(6):1242-8 [3214] J Infect Dis. 1974 Mar;129(3):277-83 [4131518] Infect Immun. 1973 Dec;8(6):851-9 [4206342] J Exp Med. 1973 Apr 1;137(4):1009-23 [4571325] Proc Natl Acad Sci U S A. 1987 Aug;84(15):5139-42 [3110784] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Antibiotic magainins exert cytolytic activity against transformed cell lines through channel formation. AN - 80537416; 1708887 AB - Magainins are an ionophoric class of vertebrate peptides with antibiotic activity against various microorganisms. Here we show that magainin 2 and synthetic analogues can rapidly and irreversibly lyse hematopoietic tumor and solid tumor target cells with a relative cytotoxic potency that parallels their antibacterial efficacy and at concentrations that are relatively nontoxic to well-differentiated cells. The cytotoxicity is prevented by cell depolarization. Magainins represent a natural cytolytic agent in vertebrates and may provide another therapeutic strategy for certain tumors. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Cruciani, R A AU - Barker, J L AU - Zasloff, M AU - Chen, H C AU - Colamonici, O AD - Laboratory of Neurophysiology, National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/05/01/ PY - 1991 DA - 1991 May 01 SP - 3792 EP - 3796 VL - 88 IS - 9 SN - 0027-8424, 0027-8424 KW - Anti-Bacterial Agents KW - 0 KW - Antimicrobial Cationic Peptides KW - Chlorides KW - Ion Channels KW - Ionophores KW - Peptides KW - Xenopus Proteins KW - magainin 1 peptide, Xenopus KW - 108433-99-4 KW - Gramicidin KW - 1405-97-6 KW - Sodium KW - 9NEZ333N27 KW - Potassium KW - RWP5GA015D KW - Index Medicus KW - Potassium -- physiology KW - Cell Survival -- drug effects KW - Sodium -- physiology KW - Humans KW - In Vitro Techniques KW - Membrane Potentials -- drug effects KW - Gramicidin -- pharmacology KW - Chlorides -- physiology KW - Tumor Cells, Cultured -- drug effects KW - Peptides -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80537416?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Antibiotic+magainins+exert+cytolytic+activity+against+transformed+cell+lines+through+channel+formation.&rft.au=Cruciani%2C+R+A%3BBarker%2C+J+L%3BZasloff%2C+M%3BChen%2C+H+C%3BColamonici%2C+O&rft.aulast=Cruciani&rft.aufirst=R&rft.date=1991-05-01&rft.volume=88&rft.issue=9&rft.spage=3792&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 - 1991-05-31 N1 - Date created - 1991-05-31 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Pept Res. 1989 Mar-Apr;2(2):157-60 [2520751] FEBS Lett. 1988 Aug 29;236(2):462-6 [3410055] FEBS Lett. 1989 Jun 5;249(2):219-23 [2544449] FEBS Lett. 1988 Jan 18;227(1):21-6 [3338566] Biophys J. 1989 Nov;56(5):1017-21 [2481510] Proc Natl Acad Sci U S A. 1987 Aug;84(15):5449-53 [3299384] J Clin Invest. 1988 Feb;81(2):449-54 [2448342] J Cell Physiol. 1985 Oct;125(1):72-81 [2413058] Proc Natl Acad Sci U S A. 1989 Sep;86(17):6597-601 [2671997] Biochim Biophys Acta. 1989 May 19;981(1):130-4 [2719968] FEBS Lett. 1989 Apr 10;247(1):17-21 [2707446] Proc Natl Acad Sci U S A. 1988 Jul;85(14):5072-6 [2455891] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Properties of murine pelage hair follicles in monolayer and collagen matrix cultures. AN - 80535708; 2022891 JF - The Journal of investigative dermatology AU - Lichti, U AU - Weinberg, W C AU - Yuspa, S H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 81S EP - 82S VL - 96 IS - 5 SN - 0022-202X, 0022-202X KW - Transforming Growth Factor beta KW - 0 KW - Epidermal Growth Factor KW - 62229-50-9 KW - Collagen KW - 9007-34-5 KW - Index Medicus KW - Transforming Growth Factor beta -- pharmacology KW - Animals KW - Cells, Cultured KW - Mice KW - Epidermal Growth Factor -- pharmacology KW - Hair -- growth & development UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80535708?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Properties+of+murine+pelage+hair+follicles+in+monolayer+and+collagen+matrix+cultures.&rft.au=Lichti%2C+U%3BWeinberg%2C+W+C%3BYuspa%2C+S+H&rft.aulast=Lichti&rft.aufirst=U&rft.date=1991-05-01&rft.volume=96&rft.issue=5&rft.spage=81S&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 - 1991-05-31 N1 - Date created - 1991-05-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Depression among alcoholics. Relationship to clinical and cerebrospinal fluid variables. AN - 80528360; 2021295 AB - Although depression is common among alcoholics, its determinants are poorly understood. Among 339 alcoholics, 111 (33%) had a history of major depression. Depressed, compared with never-depressed alcoholics, had a higher daily alcohol intake, more lifetime diagnoses of other anxiety and affective disorders and drug abuse, more had attempted suicide, and more reported alcoholism in both parents. Depressed alcoholics also had significantly lower cerebrospinal fluid levels of the dopamine metabolite homovanillic acid and of gamma-aminobutyric acid. Among subgroups of depressed alcoholics, secondary compared with primary depressives were more often divorced, of lower social status, with an earlier onset of alcoholism, and higher Michigan Alcohol Screening Test scores. Secondary depressives also had significantly lower cerebrospinal fluid concentrations of homovanillic acid than never depressed alcoholics. These results suggest that certain psychosocial variables, alcohol consumption, and neurochemical variables may be specifically associated with depression in alcoholics. JF - Archives of general psychiatry AU - Roy, A AU - DeJong, J AU - Lamparski, D AU - George, T AU - Linnoila, M AD - Laboratory of Clinical Studies, DICBR, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Md. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 428 EP - 432 VL - 48 IS - 5 SN - 0003-990X, 0003-990X KW - Neuropeptides KW - 0 KW - Methoxyhydroxyphenylglycol KW - 534-82-7 KW - gamma-Aminobutyric Acid KW - 56-12-2 KW - Dopamine KW - VTD58H1Z2X KW - Homovanillic Acid KW - X77S6GMS36 KW - Abridged Index Medicus KW - Index Medicus KW - Mood Disorders -- diagnosis KW - Age Factors KW - Divorce KW - Neuropeptides -- cerebrospinal fluid KW - Anxiety Disorders -- diagnosis KW - Humans KW - Mood Disorders -- complications KW - Dopamine -- metabolism KW - Alcohol Drinking KW - gamma-Aminobutyric Acid -- cerebrospinal fluid KW - Anxiety Disorders -- complications KW - Homovanillic Acid -- cerebrospinal fluid KW - Methoxyhydroxyphenylglycol -- cerebrospinal fluid KW - Social Class KW - Adult KW - Middle Aged KW - Female KW - Male KW - Alcoholism -- diagnosis KW - Alcoholism -- cerebrospinal fluid KW - Depressive Disorder -- diagnosis KW - Depressive Disorder -- cerebrospinal fluid KW - Alcoholism -- complications KW - Depressive Disorder -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80528360?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Depression+among+alcoholics.+Relationship+to+clinical+and+cerebrospinal+fluid+variables.&rft.au=Roy%2C+A%3BDeJong%2C+J%3BLamparski%2C+D%3BGeorge%2C+T%3BLinnoila%2C+M&rft.aulast=Roy&rft.aufirst=A&rft.date=1991-05-01&rft.volume=48&rft.issue=5&rft.spage=428&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 - 1991-05-24 N1 - Date created - 1991-05-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mental disorders among alcoholics. Relationship to age of onset and cerebrospinal fluid neuropeptides. AN - 80527664; 1673594 AB - Eighty-one percent of 339 alcoholics participating in a research program were found to have associated mental disorders. Alcoholics with onset of heavy drinking before 20 years of age had significantly more antisocial personality traits, drug abuse, bipolar disorder, panic disorder, suicide attempts, and paternal alcoholism than alcoholics with onset after age 20 years. Alcoholics with onset before and after 20 years of age also differed significantly from each other for cerebrospinal fluid concentrations of diazepam-binding inhibitor and somatostatin. These results support the notion that age of onset may delineate subgroups of alcoholics with significant clinical and neurochemical differences. JF - Archives of general psychiatry AU - Roy, A AU - DeJong, J AU - Lamparski, D AU - Adinoff, B AU - George, T AU - Moore, V AU - Garnett, D AU - Kerich, M AU - Linnoila, M AD - Laboratory of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Md. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 423 EP - 427 VL - 48 IS - 5 SN - 0003-990X, 0003-990X KW - Diazepam Binding Inhibitor KW - 0 KW - Neuropeptides KW - Somatostatin KW - 51110-01-1 KW - Abridged Index Medicus KW - Index Medicus KW - Somatostatin -- cerebrospinal fluid KW - Bipolar Disorder -- diagnosis KW - Age Factors KW - Anxiety Disorders -- diagnosis KW - Humans KW - Bipolar Disorder -- complications KW - Anxiety Disorders -- complications KW - Substance-Related Disorders -- diagnosis KW - Antisocial Personality Disorder -- complications KW - Psychiatric Status Rating Scales KW - Suicide, Attempted -- statistics & numerical data KW - Adult KW - Substance-Related Disorders -- complications KW - Antisocial Personality Disorder -- diagnosis KW - Panic KW - Female KW - Male KW - Mental Disorders -- diagnosis KW - Neuropeptides -- cerebrospinal fluid KW - Alcoholism -- diagnosis KW - Alcoholism -- cerebrospinal fluid KW - Mental Disorders -- complications KW - Alcoholism -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80527664?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mental+disorders+among+alcoholics.+Relationship+to+age+of+onset+and+cerebrospinal+fluid+neuropeptides.&rft.au=Roy%2C+A%3BDeJong%2C+J%3BLamparski%2C+D%3BAdinoff%2C+B%3BGeorge%2C+T%3BMoore%2C+V%3BGarnett%2C+D%3BKerich%2C+M%3BLinnoila%2C+M&rft.aulast=Roy&rft.aufirst=A&rft.date=1991-05-01&rft.volume=48&rft.issue=5&rft.spage=423&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 - 1991-05-24 N1 - Date created - 1991-05-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Disposition and excretion of intravenous 2,3,7,8-tetrabromodibenzo-p-dioxin (TBDD) in rats. AN - 80526632; 2020967 AB - Polybrominated dibenzodioxins and dibenzofurans are of toxicologic interest due to potential occupational and environmental exposure and because of their structural similarity to the highly toxic chlorinated analogues. The excretion and terminal tissue distribution of [3H]TBDD was studied in male F344 rats for 56 days following single iv doses of .001 or 0.1 mumol/kg. The major tissue depots of radioactivity were liver, adipose tissue, and skin, and tissue distribution was dose-dependent. At 56 days, liver concentrations in the high dose group were disproportionately increased compared to those of the low dose group. Liver:adipose tissue concentration ratios were 0.2 and 2.6 at the low and high doses, respectively. Elimination of radioactivity in the feces, the major route of excretion, and urine was also nonlinear with respect to dose. By Day 56, feces accounted for approximately 50% of the administered dose at the low dose versus 70% at the high dose. Based on fecal excretion, the apparent terminal whole body half-life was estimated to be 18 days for both dose groups. The time-dependent pattern of tissue disposition was characterized at the low dose over a 56-day period. Blood levels of radioactivity declined rapidly with 2% remaining in the blood by 24 hr. Radioactivity levels in the liver peaked by 7 hr and then gradually declined concomitant with a slow accumulation in adipose tissue. The terminal excretion half-life of radioactivity in adipose tissue was estimated to be 60 days. Liver:adipose tissue concentration ratios declined with time. Thus, the overall disposition of TBDD appears similar to that observed for the chlorinated analogue, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). The results of these studies are consistent with the hypothesis that TBDD, like TCDD, induces a binding species in the liver which accounts for higher liver:adipose tissue concentration ratios at the high dose. The dose-dependent tissue disposition and excretion kinetics of these compounds suggest important considerations for extrapolations from high to low doses. JF - Toxicology and applied pharmacology AU - Kedderis, L B AU - Diliberto, J J AU - Birnbaum, L S AD - Experimental Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 397 EP - 406 VL - 108 IS - 3 SN - 0041-008X, 0041-008X KW - Dioxins KW - 0 KW - 2,3,7,8-tetrabromodibenzo-4-dioxin KW - 04PL7F455E KW - Index Medicus KW - Rats KW - Weight Gain -- drug effects KW - Skin -- chemistry KW - Animals KW - Rats, Inbred F344 KW - Body Weight -- drug effects KW - Tissue Distribution KW - Liver -- chemistry KW - Feces -- chemistry KW - Adipose Tissue -- chemistry KW - Male KW - Dioxins -- urine KW - Dioxins -- pharmacokinetics KW - Dioxins -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80526632?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Disposition+and+excretion+of+intravenous+2%2C3%2C7%2C8-tetrabromodibenzo-p-dioxin+%28TBDD%29+in+rats.&rft.au=Kedderis%2C+L+B%3BDiliberto%2C+J+J%3BBirnbaum%2C+L+S&rft.aulast=Kedderis&rft.aufirst=L&rft.date=1991-05-01&rft.volume=108&rft.issue=3&rft.spage=397&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 - 1991-05-30 N1 - Date created - 1991-05-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effect of chronic dietary zinc deficiency on cadmium toxicity and carcinogenesis in the male Wistar [Hsd: (WI)BR] rat. AN - 80525401; 2020969 AB - Though it is known that excess zinc will prevent cadmium carcinogenesis, the impact of zinc deficiency on cadmium carcinogenesis has not been defined. This study assessed the effect of dietary zinc deficiency on the carcinogenic potential of cadmium in rats. Groups (n = 28 each) of male Wistar [Hsd: (WI)BR] rats were fed diets adequate (60 ppm) or deficient (7 ppm) in zinc and received a single sc dose of cadmium (5, 10, or 30 mumol Cd/kg). Lesions were assessed over the next 92 weeks. All cadmium doses increased the incidence of testicular interstitial cell tumors. The incidence of cadmium-induced testicular tumors was unaffected by dietary zinc status. However, when multiplicity of testicular lesions was considered, zinc-deficient diets markedly increased the number of testicular interstitial cell adenomas generated by cadmium exposure while significantly reducing the number of preneoplastic lesions (interstitial cell hyperplasias). The combined total number of neoplastic and preneoplastic lesions of the testes was independent of zinc status clearly indicating a shift from hyperplasia to neoplasia within the testes of zinc-deficient rats. The highest cadmium dose (30 mumol/kg) increased injection site sarcomas in zinc-deficient rats (7 tumors/27 rats at risk) but not zinc-adequate rats (3/26) when compared to control (0/49). Chronic progressive renal nephropathy was accelerated by cadmium in zinc-deficient rats. Results indicate that dietary zinc deficiency enhances carcinogenic response at the injection site of cadmium, promotes the neoplastic progression of cadmium-induced testicular lesions, and enhances chronic progressive nephropathy. Thus, dietary zinc deficiency appears to cause a generalized increase in the chronic toxic effects of cadmium. JF - Toxicology and applied pharmacology AU - Waalkes, M P AU - Kovatch, R AU - Rehm, S AD - Inorganic Carcinogenesis, Section, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 448 EP - 456 VL - 108 IS - 3 SN - 0041-008X, 0041-008X KW - Cadmium KW - 00BH33GNGH KW - Zinc KW - J41CSQ7QDS KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Hyperplasia -- chemically induced KW - Kidney -- drug effects KW - Diet KW - Male KW - Sarcoma, Experimental -- chemically induced KW - Cadmium -- toxicity KW - Testicular Neoplasms -- chemically induced KW - Zinc -- deficiency UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80525401?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+applied+pharmacology&rft.atitle=Effect+of+chronic+dietary+zinc+deficiency+on+cadmium+toxicity+and+carcinogenesis+in+the+male+Wistar+%5BHsd%3A+%28WI%29BR%5D+rat.&rft.au=Waalkes%2C+M+P%3BKovatch%2C+R%3BRehm%2C+S&rft.aulast=Waalkes&rft.aufirst=M&rft.date=1991-05-01&rft.volume=108&rft.issue=3&rft.spage=448&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 - 1991-05-30 N1 - Date created - 1991-05-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effect of modulators of glutathione synthesis on the hepatotoxicity of 2-methylfuran. AN - 80521315; 2018563 AB - Treatment of male Sprague-Dawley rats with buthionine sulfoximine (BSO), prior to administration of carbon-14(14C)-labelled 2-methylfuran (2MF) caused a marked decrease in the covalent binding of 14C-labelled 2MF metabolites to both DNA and protein, although there was no apparent change in the distribution of the labelled parent 2MF. BSO pretreatment also protected against hepatotoxicity of 2MF, as indicated by lower serum glutamic pyruvic transaminase (GPT) levels. Pretreatment with BSO offered protection only if administered 1.5 hr before 2MF dosage. Administration of 2MF, 4 and 6 hr after BSO resulted in manifestation of the hepatotoxicity of 2MF. Prior treatment with diethylmaleate (DEM), increased covalent binding of [14C]2MF to liver proteins and also elevated serum GPT levels. Thus, depletion of tissue glutathione (GSH) by two different chemicals acting by different mechanisms produced opposite effects on the covalent binding and toxicity of 2MF. Pretreatment with L-2-oxothiazolidine-4-carboxylate (OTZ), a promoter of GSH biosynthesis, increased the hepatic covalent binding of [14C]2MF and potentiated hepatotoxicity. However, administration of OTZ and BSO prior to an i.p. dose of 100 mg/kg of 2MF, decreased the hepatic covalent binding of [14C]2MF and decreased the hepatoxicity. The marked instability of the GSH conjugate of the reactive metabolite of 2MF may account for the potentiation of hepatotoxicity of 2MF by OTZ. A single s.c. dose of BSO, caused a transient increase in plasma cystine levels concurrent with the depletion of liver GSH. Administration of 2MF, 1.5 hr after BSO, significantly decreased plasma cystine levels as compared to control animals that received vehicle alone. Pretreatment with BSO also resulted in increased excretion of urinary metabolites in 2MF treated animals as compared to animals receiving 2MF alone. Thus, BSO probably protects against hepatoxicity of 2MF by indirectly causing more detoxification of the reactive metabolite of 2MF, as it does not alter the distribution of unmetabolized 2MF and does not have any apparent effect on the microsomal mixed-function oxidase which mediates the activation of 2MF. The enhanced detoxification of 2MF in BSO treated animals appears independent of the depleted GSH levels; it may result from increased availability of a better alternative nucleophile (i.e. cysteine), capable of conjugating with acetyl acrolein. Acetyl acrolein (AA) appears to be the principal reactive metabolite of 2MF which binds covalently to tissues. Previous in vitro studies have shown that cysteine is a better trapping agent of AA than GSH or N-acetyl-cysteine. JF - Biochemical pharmacology AU - Ravindranath, V AU - Boyd, M R AD - Division of Cancer Treatment, National Cancer Institute, National Institutes of Health, Frederick, MD 21702-1013. Y1 - 1991/05/01/ PY - 1991 DA - 1991 May 01 SP - 1311 EP - 1318 VL - 41 IS - 9 SN - 0006-2952, 0006-2952 KW - Antimetabolites KW - 0 KW - Furans KW - Maleates KW - Thiazoles KW - Thiazolidines KW - Methionine Sulfoximine KW - 1982-67-8 KW - Cystine KW - 48TCX9A1VT KW - Buthionine Sulfoximine KW - 5072-26-4 KW - 2-methylfuran KW - 51O3BGW3F2 KW - diethyl maleate KW - AK5N1DQX7U KW - Alanine Transaminase KW - EC 2.6.1.2 KW - Glutathione KW - GAN16C9B8O KW - Pyrrolidonecarboxylic Acid KW - SZB83O1W42 KW - 2-oxothiazolidine-4-carboxylic acid KW - X7063P804E KW - Index Medicus KW - Thiazoles -- pharmacology KW - Rats, Inbred Strains KW - Rats KW - Maleates -- pharmacology KW - Animals KW - Drug Interactions KW - Alanine Transaminase -- blood KW - Cystine -- blood KW - Male KW - Antimetabolites -- pharmacology KW - Chemical and Drug Induced Liver Injury -- etiology KW - Methionine Sulfoximine -- administration & dosage KW - Furans -- toxicity KW - Furans -- antagonists & inhibitors KW - Antimetabolites -- administration & dosage KW - Methionine Sulfoximine -- pharmacology KW - Methionine Sulfoximine -- analogs & derivatives KW - Chemical and Drug Induced Liver Injury -- metabolism KW - Glutathione -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80521315?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Effect+of+modulators+of+glutathione+synthesis+on+the+hepatotoxicity+of+2-methylfuran.&rft.au=Ravindranath%2C+V%3BBoyd%2C+M+R&rft.aulast=Ravindranath&rft.aufirst=V&rft.date=1991-05-01&rft.volume=41&rft.issue=9&rft.spage=1311&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 - 1991-05-17 N1 - Date created - 1991-05-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Not all that moves is tardive dyskinesia. AN - 80516641; 1673323 AB - Because tardive dyskinesia and spontaneous dyskinesia appear the same, it is difficult to determine whether an individual patient's abnormal movements are induced by medication or have developed spontaneously. Therefore, estimates of the prevalence of tardive dyskinesia that are based on observations not adjusted for spontaneous dyskinesia are inflated. In addition, age is thought to be an important risk factor in the development of both tardive and spontaneous dyskinesias. The authors estimate the prevalence of both disorders for specific age groups. The authors reviewed nine reports on dyskinesia prevalence that included history of neuroleptic treatment and related prevalence to age. A rating of 2 or more on the Abnormal Involuntary Movement Scale or an equivalent score on another scale was considered an indication of dyskinesia. If the subject had taken neuroleptics for more than 3 months, the movement disorder was classified as neuroleptic-associated dyskinesia; other dyskinesias were considered spontaneous. The prevalence of tardive dyskinesia was defined as the rate of neuroleptic-associated dyskinesia minus the rate of spontaneous dyskinesia. The true rate of tardive dyskinesia was below 20% for all age groups except 70-79 years. The correlation between the rate of neuroleptic-associated dyskinesia and the rate of spontaneous dyskinesia was low. After age 40 the prevalence of spontaneous dyskinesia is sufficiently high to conclude that many patients with diagnoses of tardive dyskinesia have abnormal movements attributable to causes other than neuroleptics. JF - The American journal of psychiatry AU - Khot, V AU - Wyatt, R J AD - Neuropsychiatry Branch, NIMH Neuroscience Center, St. Elizabeths Hospital, Washington, DC 20032. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 661 EP - 666 VL - 148 IS - 5 SN - 0002-953X, 0002-953X KW - Antipsychotic Agents KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Age Factors KW - Diagnosis, Differential KW - Aged, 80 and over KW - Humans KW - Adult KW - Neurologic Examination KW - Aged KW - Antipsychotic Agents -- adverse effects KW - Adolescent KW - Prevalence KW - Movement Disorders -- epidemiology KW - Movement Disorders -- etiology KW - Movement Disorders -- diagnosis KW - Dyskinesia, Drug-Induced -- epidemiology KW - Dyskinesia, Drug-Induced -- diagnosis KW - Dyskinesia, Drug-Induced -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80516641?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+journal+of+psychiatry&rft.atitle=Not+all+that+moves+is+tardive+dyskinesia.&rft.au=Khot%2C+V%3BWyatt%2C+R+J&rft.aulast=Khot&rft.aufirst=V&rft.date=1991-05-01&rft.volume=148&rft.issue=5&rft.spage=661&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+psychiatry&rft.issn=0002953X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-05-20 N1 - Date created - 1991-05-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Am J Psychiatry. 1992 Aug;149(8):1123-4 [1353319] Am J Psychiatry. 1992 Jan;149(1):141 [1558561] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Murine tumor cells transduced with the gene for tumor necrosis factor-alpha. Evidence for paracrine immune effects of tumor necrosis factor against tumors. AN - 80514897; 2016545 AB - Studies of the anti-tumor activity of TNF-alpha in vivo have been hampered by the need to administer systemically toxic doses of the cytokine to obtain a curative response. To facilitate studies of the effect of high local concentrations of TNF-alpha on tumor growth and host immunity, a newly induced murine sarcoma was transduced with the gene for human TNF-alpha and the biologic characteristics of these cells were examined. We identified high and low TNF-producing tumor clones which exhibited stable TNF secretion over time. Significant amounts of membrane associated TNF were found in a high-TNF producing clone as well. No difference in the in vitro growth rates between TNF-producing and nonproducing cell lines was observed. In contrast, in vivo studies demonstrate that although unmodified parental tumor cells grew progressively when implanted s.c. in animals, tumor cells transduced with the TNF gene were found to regress in a significant number of animals after an initial phase of growth. This effect correlated with the amount of TNF produced and could be blocked with a specific anti-TNF antibody. Regressions of TNF-producing cells occurred in the absence of any demonstrable toxicity in the animals bearing these tumors. TNF-producing tumor cells could function in a paracrine fashion by inhibiting the growth of unmodified, parental tumor cells implanted at the same site. The ability of tumor cells to regress was abrogated by in vivo depletion of CD4+ or CD8+ T cell subsets and animals that had experienced regression of TNF-producing tumors rejected subsequent challenges of parental tumor. Our studies thus show that tumor cells elaborating high local concentrations of TNF regress in the absence of toxicity in the host and that this process requires the existence of intact host immunity. Studies of the lymphocytes infiltrating the gene modified tumors and attempts to use TNF gene modified tumor infiltrating lymphocytes to deliver high local concentrations of TNF to the tumor site without inducing systemic toxicity are underway. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Asher, A L AU - Mulé, J J AU - Kasid, A AU - Restifo, N P AU - Salo, J C AU - Reichert, C M AU - Jaffe, G AU - Fendly, B AU - Kriegler, M AU - Rosenberg, S A AD - Division of Cancer Treatment, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/05/01/ PY - 1991 DA - 1991 May 01 SP - 3227 EP - 3234 VL - 146 IS - 9 SN - 0022-1767, 0022-1767 KW - Tumor Necrosis Factor-alpha KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Tumor Cells, Cultured KW - Transfection KW - Humans KW - T-Lymphocyte Subsets -- immunology KW - Mice KW - Cell Membrane -- physiology KW - Mice, Inbred BALB C KW - Cell Division KW - Neoplasms, Experimental -- immunology KW - Neoplasms, Experimental -- therapy KW - Tumor Necrosis Factor-alpha -- physiology KW - Neoplasms, Experimental -- pathology KW - Tumor Necrosis Factor-alpha -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80514897?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Murine+tumor+cells+transduced+with+the+gene+for+tumor+necrosis+factor-alpha.+Evidence+for+paracrine+immune+effects+of+tumor+necrosis+factor+against+tumors.&rft.au=Asher%2C+A+L%3BMul%C3%A9%2C+J+J%3BKasid%2C+A%3BRestifo%2C+N+P%3BSalo%2C+J+C%3BReichert%2C+C+M%3BJaffe%2C+G%3BFendly%2C+B%3BKriegler%2C+M%3BRosenberg%2C+S+A&rft.aulast=Asher&rft.aufirst=A&rft.date=1991-05-01&rft.volume=146&rft.issue=9&rft.spage=3227&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 - 1991-05-23 N1 - Date created - 1991-05-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Exp Med. 1990 Mar 1;171(3):629-36 [2307930] Proc Natl Acad Sci U S A. 1990 Feb;87(4):1486-90 [2137615] Nature. 1975 Dec 25;258(5537):731-2 [1207755] Proc Natl Acad Sci U S A. 1975 Sep;72(9):3666-70 [1103152] J Immunol. 1990 Jun 15;144(12):4555-61 [2161875] Exp Cell Biol. 1979;47(1):53-60 [437245] Proc Natl Acad Sci U S A. 1979 Mar;76(3):1373-6 [286319] J Natl Cancer Inst. 1979 Dec;63(6):1393-5 [292810] Jpn J Exp Med. 1981 Jun;51(3):191-4 [7300034] J Mol Appl Genet. 1982;1(4):327-41 [6286831] Int J Cancer. 1984 Aug 15;34(2):263-7 [6469400] Nature. 1984 Dec 6-12;312(5994):548-51 [6150440] J Immunol. 1985 Sep;135(3):2069-73 [3926894] Science. 1985 Nov 22;230(4728):943-5 [3933111] Nature. 1986 Sep 4-10;323(6083):86-9 [3092113] Nature. 1986 Sep 11-17;323(6084):164-6 [3528866] Cancer Res. 1986 Nov;46(11):5687-90 [3756916] J Immunol. 1987 Feb 1;138(3):963-74 [3805720] J Immunol. 1987 Mar 15;138(6):1786-90 [3029221] J Immunol. 1987 Jun 1;138(11):4023-32 [3295044] J Immunol. 1987 Jul 1;139(1):285-94 [3108401] Cell. 1987 Aug 14;50(4):555-63 [3607879] J Immunol Methods. 1987 Aug 24;102(1):127-41 [3305708] J Exp Med. 1987 Oct 1;166(4):991-8 [3498791] Hybridoma. 1987 Oct;6(5):489-507 [2445655] Cancer Res. 1988 Feb 1;48(3):544-50 [3257167] Cancer Res. 1988 Feb 15;48(4):788-92 [3257408] Cell. 1988 Apr 8;53(1):45-53 [3349526] J Exp Med. 1988 Mar 1;167(3):1067-85 [3351434] J Immunol. 1988 Apr 15;140(8):2639-44 [2965728] Cancer Immunol Immunother. 1988;26(3):202-8 [3383204] Cancer Res. 1988 Oct 15;48(20):5818-24 [3139284] Cancer Immunol Immunother. 1989;28(2):153-6 [2783890] Proc Natl Acad Sci U S A. 1989 May;86(9):3286-90 [2654942] Cell. 1989 May 5;57(3):503-12 [2785856] J Immunol. 1989 Jul 1;143(1):162-7 [2499626] Ann Surg. 1989 Oct;210(4):474-84; discussion 484-5 [2679456] Proc Natl Acad Sci U S A. 1989 Dec;86(23):9456-60 [2512580] Proc Natl Acad Sci U S A. 1990 Jan;87(1):473-7 [2404283] Cell. 1990 Feb 9;60(3):397-403 [2137372] J Exp Med. 1990 Mar 1;171(3):941-6 [2307938] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cerebral metabolic effects of monoamine oxidase inhibition in normal and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine acutely treated monkeys. AN - 80506525; 2013759 AB - The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induces dopaminergic cell death in the substantia nigra pars compacta (SNpc) and clinical parkinsonism in humans and experimental animals. Pretreatment with monoamine oxidase inhibitors prevents this cell death and associated parkinsonism by blocking the oxidation of MPTP to a toxic intermediate. The 2-deoxyglucose method was used to study the acute effects of MPTP in the monkey brain and the effects of monoamine oxidase inhibition on local cerebral glucose utilization in both normal and MPTP-treated monkeys. MPTP administration alone caused a major increase in glucose utilization in the SNpc and smaller increases in some subnuclei within the ventral tegmental area in which eventual dopaminergic cell loss also occurs. Pretreatment with pargyline abolished these metabolic increases, a finding suggesting both that the oxidized product of MPTP generates the metabolic increases and that the increased glucose consumption may contribute to cell toxicity. On the other hand, in most cortical, thalamic, striatal, brainstem, and cerebellar areas MPTP alone caused reductions in glucose utilization, and pargyline failed to prevent these effects. Pargyline alone depressed metabolism in the locus coeruleus and a few other monoaminergic structures. JF - Journal of neurochemistry AU - Palombo, E AU - Porrino, L J AU - Crane, A M AU - Bankiewicz, K S AU - Kopin, I J AU - Sokoloff, L AD - Laboratory of Cerebral Metabolism, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 1639 EP - 1646 VL - 56 IS - 5 SN - 0022-3042, 0022-3042 KW - Monoamine Oxidase Inhibitors KW - 0 KW - Pargyline KW - 9MV14S8G3E KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Glucose KW - IY9XDZ35W2 KW - Index Medicus KW - Behavior, Animal -- drug effects KW - Animals KW - Reference Values KW - Glucose -- metabolism KW - Macaca mulatta KW - Male KW - Female KW - Pargyline -- pharmacology KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- pharmacology KW - Brain -- metabolism KW - Monoamine Oxidase Inhibitors -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80506525?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cerebral+metabolic+effects+of+monoamine+oxidase+inhibition+in+normal+and+1-methyl-4-phenyl-1%2C2%2C3%2C6-tetrahydropyridine+acutely+treated+monkeys.&rft.au=Palombo%2C+E%3BPorrino%2C+L+J%3BCrane%2C+A+M%3BBankiewicz%2C+K+S%3BKopin%2C+I+J%3BSokoloff%2C+L&rft.aulast=Palombo&rft.aufirst=E&rft.date=1991-05-01&rft.volume=56&rft.issue=5&rft.spage=1639&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 - 1991-05-16 N1 - Date created - 1991-05-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Classification according to chemical structure, mutagenicity to Salmonella and level of carcinogenicity of a further 39 chemicals tested for carcinogenicity by the U.S. National Toxicology Program. AN - 80504540; 2014033 AB - This paper is an extension of compilations published previously in this journal. (Ashby and Tennant, 1988; Ashby et al., 1989). A summary of the rodent carcinogenicity bioassay data on a further 39 chemicals tested by the U.S. National Toxicology Program (NTP) is presented. An evaluation of each chemical for structural alerts to DNA-reactivity is also provided, together with a summary of its mutagenicity to Salmonella. Chemicals with an aliphatic nitro group (-C-NO2) have been added to the composite structure of DNA-reactive sub-groups. The 39 chemicals were numbered and evaluated as an extension of the earlier analysis of 264 NTP chemicals. The activity patterns and conclusions derived from the earlier studies are followed by these 39 chemicals, albeit a detailed analysis of the total database of 301 chemicals is reserved for the succeeding paper. JF - Mutation research AU - Tennant, R W AU - Ashby, J AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 209 EP - 227 VL - 257 IS - 3 SN - 0027-5107, 0027-5107 KW - Carcinogens KW - 0 KW - Mutagens KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Information Systems KW - Mutagenicity Tests KW - Carcinogenicity Tests KW - Structure-Activity Relationship KW - DNA -- drug effects KW - Salmonella typhimurium -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80504540?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Classification+according+to+chemical+structure%2C+mutagenicity+to+Salmonella+and+level+of+carcinogenicity+of+a+further+39+chemicals+tested+for+carcinogenicity+by+the+U.S.+National+Toxicology+Program.&rft.au=Tennant%2C+R+W%3BAshby%2C+J&rft.aulast=Tennant&rft.aufirst=R&rft.date=1991-05-01&rft.volume=257&rft.issue=3&rft.spage=209&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 - 1991-05-14 N1 - Date created - 1991-05-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Selenocysteyl-tRNA occurs in the diatom Thalassiosira and in the ciliate Tetrahymena. AN - 72495579; 1835508 AB - Selenocysteyl-tRNAs that decode UGA were identified previously in animal and bacterial cells and the genes for these tRNAs have been shown to be widespread in animals and eubacteria. In the present study, we identify a selenocysteyl-tRNA that codes for UGA in Thalassiosira pseudonana, which is a diatom, and in Tetrahymena borealis, which is a ciliate. The fact that these very diverse unicellular organisms also contain a selenocysteyl-tRNA suggests that selenocysteine-containing proteins and the use of UGA as a codon for selenocysteine are widespread, if not ubiquitous, in nature. JF - Molecular microbiology AU - Hatfield, D L AU - Lee, B J AU - Price, N M AU - Stadtman, T C AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 1183 EP - 1186 VL - 5 IS - 5 SN - 0950-382X, 0950-382X KW - Codon KW - 0 KW - Organoselenium Compounds KW - Selenocysteine KW - 0CH9049VIS KW - Cysteine KW - K848JZ4886 KW - Index Medicus KW - Animals KW - Enterobacteriaceae -- genetics KW - Fungi -- genetics KW - Species Specificity KW - Tetrahymena -- genetics KW - Tetrahymena -- chemistry KW - Eukaryota -- chemistry KW - Genetic Code KW - Eukaryota -- genetics KW - Cysteine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72495579?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Selenocysteyl-tRNA+occurs+in+the+diatom+Thalassiosira+and+in+the+ciliate+Tetrahymena.&rft.au=Hatfield%2C+D+L%3BLee%2C+B+J%3BPrice%2C+N+M%3BStadtman%2C+T+C&rft.aulast=Hatfield&rft.aufirst=D&rft.date=1991-05-01&rft.volume=5&rft.issue=5&rft.spage=1183&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 - 1991-12-30 N1 - Date created - 1991-12-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Taxinine M, a new tetracyclic taxane from Taxus brevifolia. AN - 72486897; 1955887 JF - Journal of natural products AU - Beutler, J A AU - Chmurny, G M AU - Look, S A AU - Witherup, K M AD - Chemical Synthesis and Analysis Laboratory, PRI/DynCorp. NCI-Frederick Cancer Research and Development Center, Maryland 21702-1201. PY - 1991 SP - 893 EP - 897 VL - 54 IS - 3 SN - 0163-3864, 0163-3864 KW - Bridged-Ring Compounds KW - 0 KW - Taxoids KW - taxinine M KW - 135730-55-1 KW - Index Medicus KW - Molecular Structure KW - Animals KW - Artemia -- drug effects KW - Magnetic Resonance Spectroscopy KW - Bridged-Ring Compounds -- chemistry KW - Bridged-Ring Compounds -- toxicity KW - Bridged-Ring Compounds -- isolation & purification KW - Plants UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72486897?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+natural+products&rft.atitle=Taxinine+M%2C+a+new+tetracyclic+taxane+from+Taxus+brevifolia.&rft.au=Beutler%2C+J+A%3BChmurny%2C+G+M%3BLook%2C+S+A%3BWitherup%2C+K+M&rft.aulast=Beutler&rft.aufirst=J&rft.date=1991-05-01&rft.volume=54&rft.issue=3&rft.spage=893&rft.isbn=&rft.btitle=&rft.title=Journal+of+natural+products&rft.issn=01633864&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-30 N1 - Date created - 1991-12-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - [A case of conversion disorder analyzed from a psychodynamic, psychophysiologic, and morphodynamic perspective]. TT - Un caso de trastorno de conversión analizado desde una perspectiva psicodinámica, psicofisiológica y morfodinámica. AN - 72485948; 1953308 AB - This paper presents a case of conversion disorder characterized by sensory paralysis that involved the right half of the body, a motor deficit consisting of permanent contracture in flexion of fingers 2-5 of the right hand (clenched fist syndrome), and a visual alteration compatible with homonymous hemianopia and amblyopia. The patient initially presented a clinical picture of depression as well as frequent gynecological disorders. The author evaluates important aspects of the psychogenesis of the clinical picture and emphasizes the identifying aspects and primary and secondary gains. Consideration is given to the distinct therapeutic strategies used (psychotherapy, autogenous training, hypnosis), and the case is analyzed from a morphodynamic point of view. The author concludes that the organic basis of the clinical picture would be localized in the posterior nuclei of the thalamus. JF - Archivos de neurobiologia AU - Oregón García, F AD - Unit on Dissociative Disorders, National Institute of Mental Health Bethesda, MD. PY - 1991 SP - 111 EP - 121 VL - 54 IS - 3 SN - 0004-0576, 0004-0576 KW - Index Medicus KW - Occupational Diseases -- diagnosis KW - Diagnosis, Differential KW - Nerve Compression Syndromes -- diagnosis KW - Cerebrovascular Disorders -- diagnosis KW - Psychotherapy KW - Humans KW - Adult KW - Female KW - Thalamic Nuclei -- physiopathology KW - Hemianopsia -- psychology KW - Hypesthesia -- diagnosis KW - Conversion Disorder -- therapy KW - Hand Deformities, Acquired -- psychology KW - Hypesthesia -- physiopathology KW - Hemianopsia -- physiopathology KW - Conversion Disorder -- diagnosis KW - Conversion Disorder -- physiopathology KW - Hand Deformities, Acquired -- physiopathology KW - Hypesthesia -- psychology KW - Conversion Disorder -- psychology KW - Hand Deformities, Acquired -- diagnosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72485948?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archivos+de+neurobiologia&rft.atitle=%5BA+case+of+conversion+disorder+analyzed+from+a+psychodynamic%2C+psychophysiologic%2C+and+morphodynamic+perspective%5D.&rft.au=Oreg%C3%B3n+Garc%C3%ADa%2C+F&rft.aulast=Oreg%C3%B3n+Garc%C3%ADa&rft.aufirst=F&rft.date=1991-05-01&rft.volume=54&rft.issue=3&rft.spage=111&rft.isbn=&rft.btitle=&rft.title=Archivos+de+neurobiologia&rft.issn=00040576&rft_id=info:doi/ LA - Spanish DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-02 N1 - Date created - 1991-12-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Arch Neurobiol (Madr). 1992 Sep-Oct;55(5):241-4 [1482277] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Development of chemotherapy treatment for pediatric brain tumors. AN - 72453872; 1944105 AB - Until relatively recently the standard treatment for the child diagnosed with a brain tumor was surgical resection followed by radiation therapy. If initial treatment failed patients were rarely referred for chemotherapy. This, in large part, was owing to the therapeutic nihilism that resulted from the disappointing experience with chemotherapy in the treatment of adults with glioblastoma multiforme. Following encouraging reports of clinical responses to chemotherapy in children with recurrent medulloblastoma, however, the value of adjuvant chemotherapy has become more accepted. JF - Neurologic clinics AU - Horowitz, M E AU - Poplack, D G AD - Pediatric Branch, National Cancer Institute, Bethesda, Maryland. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 363 EP - 373 VL - 9 IS - 2 SN - 0733-8619, 0733-8619 KW - Antineoplastic Agents KW - 0 KW - Index Medicus KW - Combined Modality Therapy KW - Humans KW - Child KW - Brain Neoplasms -- drug therapy KW - Brain Neoplasms -- surgery KW - Brain Neoplasms -- radiotherapy KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Antineoplastic Agents -- therapeutic use KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72453872?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurologic+clinics&rft.atitle=Development+of+chemotherapy+treatment+for+pediatric+brain+tumors.&rft.au=Horowitz%2C+M+E%3BPoplack%2C+D+G&rft.aulast=Horowitz&rft.aufirst=M&rft.date=1991-05-01&rft.volume=9&rft.issue=2&rft.spage=363&rft.isbn=&rft.btitle=&rft.title=Neurologic+clinics&rft.issn=07338619&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-17 N1 - Date created - 1991-12-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A simple and inexpensive slicer for preparation of brain slices. AN - 72453577; 1719306 AB - A simple and inexpensive slicer has been developed for the preparation of slices of mouse or rat brain. The instrument consists of razor blades, separated by an 0.5 mm thick polyethylene sheet (1 x 1 cm), mounted on metal screws through a hole in the center of the polyethylene sheet. Using this slicer, 6-8 uniform slices of 500 microns thickness were obtained from mouse or rat brain. These brain slices were incubated in a medium consisting of artificial cerebrospinal fluid for 1 h at 37 degrees C under an oxygen atmosphere and the activities of various subcellular marker enzymes were assayed. The slice weights and the activities of the enzymes did not vary significantly in different batches of slices. Morphological evaluation of the slices revealed well-preserved neurons. Histochemical staining for mitochondrial enzymes revealed intense staining of neuronal cells and lighter staining of the white matter in all the regions examined. These slices could serve as a useful in vitro model for studying brain function and the effect of various toxicants on the brain. JF - Journal of neuroscience methods AU - Pai, K S AU - Shankar, S K AU - Ravindranath, V AD - Department of Neurochemistry, National Institute of Mental Health and Neuro Sciences, Bangalore, India. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 209 EP - 214 VL - 37 IS - 3 SN - 0165-0270, 0165-0270 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Cerebrospinal Fluid -- chemistry KW - Mice KW - Histocytochemistry KW - Cerebrospinal Fluid -- physiology KW - Tissue Fixation KW - Staining and Labeling KW - Brain -- enzymology KW - Brain -- anatomy & histology KW - Tomography -- instrumentation KW - Brain -- ultrastructure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72453577?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+methods&rft.atitle=A+simple+and+inexpensive+slicer+for+preparation+of+brain+slices.&rft.au=Pai%2C+K+S%3BShankar%2C+S+K%3BRavindranath%2C+V&rft.aulast=Pai&rft.aufirst=K&rft.date=1991-05-01&rft.volume=37&rft.issue=3&rft.spage=209&rft.isbn=&rft.btitle=&rft.title=Journal+of+neuroscience+methods&rft.issn=01650270&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-27 N1 - Date created - 1991-11-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential effects of antidepressant treatments on fenfluramine-induced increases in plasma prolactin and corticosterone in rats. AN - 72154043; 1924518 AB - Intravenous administration of 5-HT releasing agent, fenfluramine, to rats produced increases in plasma prolactin and corticosterone concentrations. Short-term or long-term treatment with either clorgyline or imipramine did not affect baseline levels of prolactin or corticosterone. On the other hand, short-term but not long-term lithium treatment significantly increased baseline levels of corticosterone but not of prolactin. Short-term treatment with lithium but not clorgyline or imipramine potentiated fenfluramine-induced increases in plasma prolactin but not corticosterone. On the other hand, long-term treatment with clorgyline but not imipramine or lithium attenuated fenfluramine's effect on plasma prolactin but not on corticosterone. These findings demonstrate differential effects of antidepressant treatments on fenfluramine-induced increases in plasma prolactin and corticosterone in rats and are consistent with several other clinical and animal studies demonstrating dissimilar actions of different antidepressant treatments on two different 5-HT-mediated neuroendocrine functions. JF - Pharmacology, biochemistry, and behavior AU - Aulakh, C S AU - Zohar, J AU - Wozniak, K M AU - Hill, J L AU - Haass, M AU - Murphy, D L AD - Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 91 EP - 95 VL - 39 IS - 1 SN - 0091-3057, 0091-3057 KW - Antidepressive Agents KW - 0 KW - Fenfluramine KW - 2DS058H2CF KW - Prolactin KW - 9002-62-4 KW - Lithium KW - 9FN79X2M3F KW - Clorgyline KW - LYJ16FZU9Q KW - Imipramine KW - OGG85SX4E4 KW - Corticosterone KW - W980KJ009P KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Drug Interactions KW - Injections, Intravenous KW - Imipramine -- pharmacology KW - Clorgyline -- pharmacology KW - Male KW - Lithium -- pharmacology KW - Fenfluramine -- administration & dosage KW - Prolactin -- blood KW - Antidepressive Agents -- pharmacology KW - Corticosterone -- blood KW - Fenfluramine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72154043?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacology%2C+biochemistry%2C+and+behavior&rft.atitle=Differential+effects+of+antidepressant+treatments+on+fenfluramine-induced+increases+in+plasma+prolactin+and+corticosterone+in+rats.&rft.au=Aulakh%2C+C+S%3BZohar%2C+J%3BWozniak%2C+K+M%3BHill%2C+J+L%3BHaass%2C+M%3BMurphy%2C+D+L&rft.aulast=Aulakh&rft.aufirst=C&rft.date=1991-05-01&rft.volume=39&rft.issue=1&rft.spage=91&rft.isbn=&rft.btitle=&rft.title=Pharmacology%2C+biochemistry%2C+and+behavior&rft.issn=00913057&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-01 N1 - Date created - 1991-11-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A 20-year-old man with persistent aminotransferase elevations. AN - 72081684; 1887257 AB - Through intravenous drug abuse, this 20-year-old man contracted chronic active hepatitis due to hepatitis D superinfection of hepatitis B. The correct diagnosis, made after a hiatus of 20 years, awaited advances in the understanding of viral hepatitis, the discovery of the hepatitis D virus, and the development of immunostaining techniques that could be applied to his liver biopsy specimen. The case illustrates how immunoperoxidase staining may be done retrospectively and may be particularly useful in diagnosis of individual cases where serologic testing is not available or possible, as well as in scientific surveys of HBV and HDV infection. Since staining for HBcAg and HDAg can provide clinically useful information not available by other methods, it should be considered as a part of the assessment of the liver biopsy in every patient with HBV infection. JF - Seminars in liver disease AU - Di Bisceglie, A M AU - Goodman, Z D AD - Liver Diseases Section, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD 20895. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 175 EP - 181 VL - 11 IS - 2 SN - 0272-8087, 0272-8087 KW - Aspartate Aminotransferases KW - EC 2.6.1.1 KW - Alanine Transaminase KW - EC 2.6.1.2 KW - Index Medicus KW - Diagnosis, Differential KW - Humans KW - Adult KW - Time Factors KW - Male KW - Liver -- microbiology KW - Immunoenzyme Techniques KW - Substance Abuse, Intravenous KW - Hepatitis D -- diagnosis KW - Aspartate Aminotransferases -- blood KW - Alanine Transaminase -- blood KW - Hepatitis, Chronic -- diagnosis KW - Hepatitis, Chronic -- microbiology KW - Hepatitis B -- transmission KW - Hepatitis B -- diagnosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72081684?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Seminars+in+liver+disease&rft.atitle=A+20-year-old+man+with+persistent+aminotransferase+elevations.&rft.au=Di+Bisceglie%2C+A+M%3BGoodman%2C+Z+D&rft.aulast=Di+Bisceglie&rft.aufirst=A&rft.date=1991-05-01&rft.volume=11&rft.issue=2&rft.spage=175&rft.isbn=&rft.btitle=&rft.title=Seminars+in+liver+disease&rft.issn=02728087&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-10-04 N1 - Date created - 1991-10-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The effects of ethylene dibromide on semen quality and fertility in the rabbit: evaluation of a model for human seminal characteristics. AN - 72081017; 1884910 AB - Mature (12 months old) male New Zealand White rabbits (8-10/group) were dosed subcutaneously with ethylene dibromide (EDB) in corn oil (untreated and vehicle controls, 15, 30, or 45 mg/kg body wt/day for 5 days). Weekly semen samples (for 6 weeks preexposure, during treatment, and 12 weeks postdosing [pd]) were analyzed for sperm concentration, number, morphology, viability, and motion parameters (velocity, linearity, beat cross-frequency, amplitude of lateral head displacement (ALH), and circularity), and semen pH, osmolality, volume, fructose, citric acid, carnitine, protein, and acid phosphatase (AP). Male fertility was assessed preexposure and at 4 and 12 weeks pd by artificial insemination of three females/male/time point with one million motile sperm. The percentage pregnant females, litter size, fetal body weights, and structural development were assessed. In the 45 mg/kg dose group of males there was 30% mortality and liver damage in 43% of the survivors as evidenced by increased levels of serum enzymes. Also in this group, EDB produced significant decreases in sperm velocity, percentage motility, and ALH (up to 25% at various times pd). There were also dose-related decreases in semen pH (up to 2%) and total ejaculate volume (up to 23%, 15 and 30 mg/kg dose groups only). AP activities were significantly elevated (up to 116%) 2 weeks pd in the 45 mg/kg dose group. All other semen parameters evaluated were unaffected. Male fertility and fetal structural development were also unaffected. Of the seven semen parameters perturbed by EDB in humans (Schrader et al., 1988), four were also affected in the rabbit (sperm velocity, percentage motility, pH, and volume), whereas sperm number, viability, and morphology were not. Thus, some of the male reproductive effects of EDB in the human have been modelled in the rabbit, although the rabbit appears not to be as sensitive, since semen parameters were affected only at doses close to the LD50 (55 mg/kg). The present study (together with other published data) suggests that the rabbit appears to be a potential model for male reproductive toxicity in humans, warranting further evaluation. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Williams, J AU - Gladen, B C AU - Turner, T W AU - Schrader, S M AU - Chapin, R E AD - Developmental and Reproductive Toxicology Group Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 687 EP - 700 VL - 16 IS - 4 SN - 0272-0590, 0272-0590 KW - Ethylene Dibromide KW - 1N41638RNO KW - Acid Phosphatase KW - EC 3.1.3.2 KW - Index Medicus KW - Eating -- drug effects KW - Animals KW - Sperm Head -- drug effects KW - Genitalia, Male -- drug effects KW - Humans KW - Hydrogen-Ion Concentration KW - Exocrine Glands -- drug effects KW - Predictive Value of Tests KW - Rabbits KW - Sperm Motility -- drug effects KW - Acid Phosphatase -- metabolism KW - Spermatozoa -- drug effects KW - Species Specificity KW - Male KW - Semen -- enzymology KW - Ethylene Dibromide -- toxicity KW - Models, Biological KW - Semen -- drug effects KW - Fertility -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72081017?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fundamental+and+applied+toxicology+%3A+official+journal+of+the+Society+of+Toxicology&rft.atitle=The+effects+of+ethylene+dibromide+on+semen+quality+and+fertility+in+the+rabbit%3A+evaluation+of+a+model+for+human+seminal+characteristics.&rft.au=Williams%2C+J%3BGladen%2C+B+C%3BTurner%2C+T+W%3BSchrader%2C+S+M%3BChapin%2C+R+E&rft.aulast=Williams&rft.aufirst=J&rft.date=1991-05-01&rft.volume=16&rft.issue=4&rft.spage=687&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 - 1991-10-10 N1 - Date created - 1991-10-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Lung cancer: rational strategies for early detection and intervention. AN - 72076467; 1832003 AB - The current mortality rate for lung cancer, which approaches 90% at two years, is not decreasing despite intensive clinical trials attempting to improve systemic therapy. New drug discoveries and dose intensification approaches have not resulted in more effective anti-tumor control. An alternative approach using sputum immunocytology for early lung cancer detection was recently reported. The proposed basis for this early detection reflects the underlying biology of immunodominant carbohydrate tumor-associated antigens, which are recognized as a class of oncofetal antigens. The process of bronchial epithelial carcinogenesis is associated with an evolution of carbohydrate display which reverses the sequence originally associated with fetal organ development. By elucidating this pattern of fetal carbohydrate display, a precise map of stage of bronchial carcinogenesis may emerge. JF - Oncology (Williston Park, N.Y.) AU - Mulshine, J L AU - Treston, A M AU - Scott, F M AU - Avis, I AU - Boland, C AU - Phelps, R AU - Kasprzyk, P G AU - Nakanishi, Y AU - Cuttitta, F AD - NCI-Navy Medical Oncology Branch, National Naval Medical Center, Bethesda. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 25 EP - 32; discussion 32-3, 37 VL - 5 IS - 5 SN - 0890-9091, 0890-9091 KW - Antigens, Neoplasm KW - 0 KW - Antigens, Tumor-Associated, Carbohydrate KW - Biomarkers, Tumor KW - Growth Substances KW - Tretinoin KW - 5688UTC01R KW - Index Medicus KW - Humans KW - Biomarkers, Tumor -- analysis KW - Antigens, Neoplasm -- analysis KW - Growth Substances -- analysis KW - Antigens, Tumor-Associated, Carbohydrate -- analysis KW - Time Factors KW - Tretinoin -- therapeutic use KW - Lung Neoplasms -- diagnosis KW - Lung Neoplasms -- drug therapy KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72076467?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncology+%28Williston+Park%2C+N.Y.%29&rft.atitle=Lung+cancer%3A+rational+strategies+for+early+detection+and+intervention.&rft.au=Mulshine%2C+J+L%3BTreston%2C+A+M%3BScott%2C+F+M%3BAvis%2C+I%3BBoland%2C+C%3BPhelps%2C+R%3BKasprzyk%2C+P+G%3BNakanishi%2C+Y%3BCuttitta%2C+F&rft.aulast=Mulshine&rft.aufirst=J&rft.date=1991-05-01&rft.volume=5&rft.issue=5&rft.spage=25&rft.isbn=&rft.btitle=&rft.title=Oncology+%28Williston+Park%2C+N.Y.%29&rft.issn=08909091&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-10-07 N1 - Date created - 1991-10-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A quantitative model for translational control of the GCN4 gene of Saccharomyces cerevisiae. AN - 72070379; 1883814 AB - Expression of the GCN4 gene of Saccharomyces cerevisiae is regulated at the translational level by short open reading frames (uORFs) present in the leader sequence of its mRNA. Under conditions of amino acid sufficiency, these sequences restrict the flow of initiating ribosomes to the GCN4 AUG start codon. Mutational analysis of GCN4 has led to a model in which ribosomes must translate the 5'-proximal uORF1 and reassemble an initiation complex in order to translate GCN4. This reassembly process is thought to be rapid when amino acids are abundant, such that reinitiation occurs at uORF2, uORF3, or uORF4. Reinitiation at these sites prevents translation of GCN4, presumably because ribosomes dissociate from the mRNA following termination at uORFs 2 to 4. Because of reduced initiation factor activity under starvation conditions, a substantial fraction of ribosomal subunits scanning downstream from uORF1 are not ready to reinitiate when they reach uORFs 2 to 4, but become competent to do so while scanning the additional sequences between uORF4 and GCN4. Examination of the effects of point mutations in the ATG codons of the different uORFs suggests a quantitative model for this control mechanism that describes the probability of reinitiation as a function of the distance scanned downstream from uORF1. This model accounts for the phenotypes of a number of deletion and insertion mutations that alter the intercistronic spacing between the uORFs and GCN4. The correspondence between observed and predicted results implies that the differential rates of reinitiation at GCN4 versus uORFs 2 to 4 are determined largely by the different scanning times required to reach each of these start sites following translation of uORF1. In addition, it supports the notion that an increased scanning-time requirement for reinitiation in amino acid-starved cells forms the basis for translational derepression of GCN4 expression. JF - The New biologist AU - Abastado, J P AU - Miller, P F AU - Hinnebusch, A G AD - Section on Molecular Genetics of Lower Eukaryotes, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 511 EP - 524 VL - 3 IS - 5 SN - 1043-4674, 1043-4674 KW - GCN4 KW - Amino Acids KW - 0 KW - DNA-Binding Proteins KW - Fungal Proteins KW - RNA, Messenger KW - Saccharomyces cerevisiae Proteins KW - Transcription Factors KW - Protein Kinases KW - EC 2.7.- KW - Index Medicus KW - Ribosomes -- metabolism KW - Peptide Chain Initiation, Translational KW - Open Reading Frames KW - Amino Acids -- metabolism KW - Mutagenesis, Insertional KW - Saccharomyces cerevisiae -- genetics KW - Protein Biosynthesis KW - Gene Expression Regulation, Enzymologic KW - Genes, Fungal KW - Models, Genetic KW - Fungal Proteins -- genetics KW - RNA, Messenger -- genetics KW - Transcription Factors -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72070379?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+biologist&rft.atitle=A+quantitative+model+for+translational+control+of+the+GCN4+gene+of+Saccharomyces+cerevisiae.&rft.au=Abastado%2C+J+P%3BMiller%2C+P+F%3BHinnebusch%2C+A+G&rft.aulast=Abastado&rft.aufirst=J&rft.date=1991-05-01&rft.volume=3&rft.issue=5&rft.spage=511&rft.isbn=&rft.btitle=&rft.title=The+New+biologist&rft.issn=10434674&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-10-09 N1 - Date created - 1991-10-09 N1 - Date revised - 2017-01-13 N1 - Gene symbol - GCN4 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Estrogen receptor stereochemistry: ligand binding and hormonal responsiveness. AN - 72053600; 1877066 AB - Estrogen stimulation of the uterus produces a spectrum of biochemical responses that are customarily linked together. This report is an overview of a series of studies by our laboratory investigating the role of different ligand structures in eliciting hormonal responses. Diethylstilbestrol (DES) and certain structural analogs, indenestrol A (IA), indenestrol B (IB), and pseudo-DES, were used as probes to segregate various genomic responses previously considered interrelated, most notably the events of specific protein synthesis and DNA synthesis. These compounds have weak uterotrophic activity; however, they interact with high affinity specifically with mouse uterine estrogen receptors (ERs). All of them produce stoichiometrically similar amounts of ER complex in the nucleus. Indenestrol A and IB possess a single chiral carbon atom and exist as a mixture of enantiomers (ENTs). Competitive binding assays of pure ENTs and cytosolic ERs demonstrated a stereochemical chiral preference for the IA isomer but not IB. This preference was also evident from nuclear ER occupancy experiments. Biologic activity of the IA ENTs also demonstrated differences as seen by receptor binding. Ornithine decarboxylase (ODC) activity was stimulated 600% by DES and partially by IA (rac). All of the ODC activity produced by IA (rac) was due to the IA(C3)-S ENT. Uterine DNA synthesis was measured after treatment with the IA compounds. Indenestrol A (rac) increased DNA synthesis to 40% of the level seen with DES. The weak ENTs showed no activity and the active ENTs were weaker than the IA racemic. These compounds should be useful probes for studying the individual responses involved in estrogen-induced uterine growth.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Steroids AU - Korach, K S AU - Chae, K AU - Gibson, M AU - Curtis, S AD - Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. Y1 - 1991/05// PY - 1991 DA - May 1991 SP - 263 EP - 270 VL - 56 IS - 5 SN - 0039-128X, 0039-128X KW - DNA-Binding Proteins KW - 0 KW - Receptors, Estrogen KW - Diethylstilbestrol KW - 731DCA35BT KW - Index Medicus KW - Molecular Structure KW - Animals KW - Mice KW - Female KW - Structure-Activity Relationship KW - Protein Conformation KW - DNA-Binding Proteins -- metabolism KW - Diethylstilbestrol -- metabolism KW - Receptors, Estrogen -- chemistry KW - Diethylstilbestrol -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72053600?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Steroids&rft.atitle=Estrogen+receptor+stereochemistry%3A+ligand+binding+and+hormonal+responsiveness.&rft.au=Korach%2C+K+S%3BChae%2C+K%3BGibson%2C+M%3BCurtis%2C+S&rft.aulast=Korach&rft.aufirst=K&rft.date=1991-05-01&rft.volume=56&rft.issue=5&rft.spage=263&rft.isbn=&rft.btitle=&rft.title=Steroids&rft.issn=0039128X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-24 N1 - Date created - 1991-09-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Extra lethal damage due to residual incompletely repaired sublethal damage in hyperfractionated and continuous radiation treatment. AN - 72033863; 1870493 AB - In the conventional linear-quadratic model of single-dose response, the alpha and beta terms reflect lethal damage created during the delivery of a dose, from two different presumed molecular processes, one linear with dose, the other quadratic. With the conventional one-fraction-per-day (or less) regimens, the sublethal damage (SLD), presumably repairing exponentially over time, is essentially completely fixed by the time of the next dose of radiation. If this assumption is true, the effects of subsequent fractions of radiation should be independent, that is, there should be little, if any, reversible damage left from previous fractions, at the time of the next dose. For multiple daily fractions, or for the limiting case, continuous radiation, this simplification may overlook damaged cells that have had insufficient time for repair. A generalized method is presented for accounting for extra lethal damage (ELD) arising from such residual SLD for hyperfractionation and continuous irradiation schemes. It may help to predict differences in toxicity and tumor control, if any, obtained with "unconventional" treatment regimens. A key element in the present model is the finite size and the dynamic character of the pool of sublethal damage. Besides creating the usual linear and quadratic components of lethal damage, each new fraction converts a certain fraction of the existing SLD into ELD, and creates some new SLD. The expressions developed by Thames [Int. J. Radiat. Biol. 47, 319-339 (1987)] for fractionated treatment (the IR model) and by Dale [Br. J. Radiol. 58, 515-528 (1985); 59, 919-927 (1986)] for protracted and fractionated treatment are found to be similar to our results in the limiting case where the pool of SLD is very large (infinite).(ABSTRACT TRUNCATED AT 250 WORDS) JF - Medical physics AU - Chen, J AU - van de Geijn, J AU - Goffman, T AD - ROB, DCT, NCI, NIH, Bethesda, Maryland 20892. PY - 1991 SP - 488 EP - 496 VL - 18 IS - 3 SN - 0094-2405, 0094-2405 KW - Index Medicus KW - Humans KW - Cell Survival -- radiation effects KW - Time Factors KW - DNA Repair KW - Neoplasms -- radiotherapy KW - DNA Damage KW - Radiotherapy Dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72033863?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+physics&rft.atitle=Extra+lethal+damage+due+to+residual+incompletely+repaired+sublethal+damage+in+hyperfractionated+and+continuous+radiation+treatment.&rft.au=Chen%2C+J%3Bvan+de+Geijn%2C+J%3BGoffman%2C+T&rft.aulast=Chen&rft.aufirst=J&rft.date=1991-05-01&rft.volume=18&rft.issue=3&rft.spage=488&rft.isbn=&rft.btitle=&rft.title=Medical+physics&rft.issn=00942405&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-19 N1 - Date created - 1991-09-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Brain regional specificity and time-course of changes in the NMDA receptor-ionophore complex during ethanol withdrawal. AN - 80709221; 1830510 AB - Previous work, using membrane receptor binding techniques, demonstrated an increase in hippocampal MK-801 binding sites in mice after chronic ethanol ingestion. The current studies, using quantitative autoradiography, demonstrate that chronic ethanol ingestion also produces increases in MK-801 binding in cerebral cortex, striatum and thalamus, as well as in hippocampus. The persistence of changes in MK-801 binding paralleled the time-course for ethanol withdrawal seizure susceptibility. These results support the hypothesis that an increase in the number of NMDA receptor/channel complexes in hippocampus, and possibly other brain regions, plays a role in the generation or expression of ethanol withdrawal seizures. JF - Brain research AU - Gulya, K AU - Grant, K A AU - Valverius, P AU - Hoffman, P L AU - Tabakoff, B AD - Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20852. Y1 - 1991/04/26/ PY - 1991 DA - 1991 Apr 26 SP - 129 EP - 134 VL - 547 IS - 1 SN - 0006-8993, 0006-8993 KW - Receptors, N-Methyl-D-Aspartate KW - 0 KW - Ethanol KW - 3K9958V90M KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - Index Medicus KW - Membranes -- drug effects KW - Animals KW - Dizocilpine Maleate -- metabolism KW - Seizures -- physiopathology KW - Brain -- pathology KW - Mice, Inbred C57BL KW - Membranes -- metabolism KW - Mice KW - Autoradiography KW - Time Factors KW - Male KW - Substance Withdrawal Syndrome -- pathology KW - Substance Withdrawal Syndrome -- metabolism KW - Receptors, N-Methyl-D-Aspartate -- drug effects KW - Ethanol -- pharmacology KW - Brain Chemistry -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80709221?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Brain+regional+specificity+and+time-course+of+changes+in+the+NMDA+receptor-ionophore+complex+during+ethanol+withdrawal.&rft.au=Gulya%2C+K%3BGrant%2C+K+A%3BValverius%2C+P%3BHoffman%2C+P+L%3BTabakoff%2C+B&rft.aulast=Gulya&rft.aufirst=K&rft.date=1991-04-26&rft.volume=547&rft.issue=1&rft.spage=129&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 - 1991-09-05 N1 - Date created - 1991-09-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Site-directed mutagenesis of the beta subunit of tryptophan synthase from Salmonella typhimurium. Role of active site glutamic acid 350. AN - 80523448; 1673461 AB - To investigate the functional role of glutamic acid 350 in the active site of the beta subunit of tryptophan synthase from Salmonella typhimurium, we have replaced this residue by glutamine or alanine by use of site-directed mutagenesis. The mutant alpha 2 beta 2 complexes were expressed, purified, crystallized, and characterized by spectroscopic and kinetic studies with several substrates. We find large alterations in the substrate and reaction specificity of each mutant form of the alpha 2 beta 2 complex. Since the two mutant enzymes are virtually inactive in reactions with L-serine but are active in reactions with beta-chloro-L-alanine, glutamic acid 350 may facilitate the beta-elimination of the weak hydroxyl leaving group of L-serine. The mutant alpha 2 beta 2 complexes are more active than the wild type enzyme in the beta-elimination reaction with beta-chloro-L-alanine. These enzymes are irreversibly inactivated by beta-chloro-L-alanine, whereas the wild type enzyme is not. These altered properties may result from a change in the conformation of the active site, from a change in the orientation of the coenzyme relative to active site residues, or from a change in the solvent accessibility of the active site. The alteration in the active site may enhance the release of amino acrylate from the Schiff base intermediate by hydrolysis or by transamination. JF - The Journal of biological chemistry AU - Kayastha, A M AU - Sawa, Y AU - Nagata, S AU - Miles, E W AD - Laboratory of Biochemical Pharmacology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/04/25/ PY - 1991 DA - 1991 Apr 25 SP - 7618 EP - 7625 VL - 266 IS - 12 SN - 0021-9258, 0021-9258 KW - Amino Acids KW - 0 KW - Glutamates KW - Glutamic Acid KW - 3KX376GY7L KW - Tryptophan Synthase KW - EC 4.2.1.20 KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Spectrum Analysis KW - Fluorescence Polarization KW - Circular Dichroism KW - Amino Acids -- metabolism KW - Mutation KW - Binding Sites KW - Glutamates -- metabolism KW - Glutamates -- genetics KW - Tryptophan Synthase -- genetics KW - Salmonella typhimurium -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80523448?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Site-directed+mutagenesis+of+the+beta+subunit+of+tryptophan+synthase+from+Salmonella+typhimurium.+Role+of+active+site+glutamic+acid+350.&rft.au=Kayastha%2C+A+M%3BSawa%2C+Y%3BNagata%2C+S%3BMiles%2C+E+W&rft.aulast=Kayastha&rft.aufirst=A&rft.date=1991-04-25&rft.volume=266&rft.issue=12&rft.spage=7618&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 - 1991-05-29 N1 - Date created - 1991-05-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Guanine nucleotide dependent formation of a complex between choleragen (cholera toxin) a subunit and bovine brain ADP-ribosylation factor. AN - 80508824; 1901726 AB - Cholera toxin activates adenylyl cyclase by catalyzing the ADP-ribosylation of Gs alpha, the stimulatory guanine nucleotide binding protein of the cyclase system. This toxin-catalyzed reaction, as well as the ADP-ribosylation of guanidino compounds and auto-ADP-ribosylation of the toxin A1 protein (CTA1), is stimulated, in the presence of GTP (or GTP analogue), by 19-21-kDa proteins, termed ADP-ribosylation factors or ARFs. These proteins directly activate CTA1 in a reaction enhanced by sodium dodecyl sulfate (SDS) or dimyristoylphosphatidylcholine (DMPC)/cholate. To determine whether ARF stimulation of ADP-ribosylation is associated with formation of a toxin-ARF complex, these proteins were incubated with guanine nucleotides and/or detergents and then subjected to gel permeation chromatography. An active ARF-toxin complex was observed in the presence of SDS and GTP gamma S [guanosine 5'-O-(3-thiotriphosphate)] but not GDP beta S [guanosine 5'-O-(2-thiodiphosphate)]. Only a fraction of the ARF was capable of complex formation. The substrate specificities of complexed and noncomplexed CTA differed; complexed CTA exhibited markedly enhanced auto-ADP-ribosylation. In the presence of GTP gamma S and DMPC/cholate, an ARF-CTA complex was not detected. A GTP gamma S-dependent ARF aggregate was observed, however, exhibiting a different substrate specificity from monomeric ARF. These studies support the hypothesis that in the presence of guanine nucleotide and either SDS or DMPC/cholate, ARF and toxin exist as multiple species which exhibit different substrate specificities. JF - Biochemistry AU - Tsai, S C AU - Adamik, R AU - Moss, J AU - Vaughan, M AD - Laboratory of Cellular Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/04/16/ PY - 1991 DA - 1991 Apr 16 SP - 3697 EP - 3703 VL - 30 IS - 15 SN - 0006-2960, 0006-2960 KW - Cholic Acids KW - 0 KW - Membrane Proteins KW - Thionucleotides KW - Guanosine Diphosphate KW - 146-91-8 KW - Sodium Dodecyl Sulfate KW - 368GB5141J KW - Guanosine 5'-O-(3-Thiotriphosphate) KW - 37589-80-3 KW - guanosine 5'-O-(2-thiodiphosphate) KW - 71376-97-1 KW - Cholera Toxin KW - 9012-63-9 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - ADP-Ribosylation Factors KW - EC 3.6.5.2 KW - Cholic Acid KW - G1JO7801AE KW - Dimyristoylphosphatidylcholine KW - U86ZGC74V5 KW - Index Medicus KW - Thionucleotides -- pharmacology KW - Animals KW - Sodium Dodecyl Sulfate -- pharmacology KW - Cattle KW - Chromatography, Gel KW - Dimyristoylphosphatidylcholine -- pharmacology KW - Cholic Acids -- pharmacology KW - Guanosine Diphosphate -- analogs & derivatives KW - Guanosine Diphosphate -- pharmacology KW - Guanosine 5'-O-(3-Thiotriphosphate) -- pharmacology KW - Membrane Proteins -- metabolism KW - GTP-Binding Proteins -- metabolism KW - Brain -- drug effects KW - Brain -- metabolism KW - Cholera Toxin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80508824?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Guanine+nucleotide+dependent+formation+of+a+complex+between+choleragen+%28cholera+toxin%29+a+subunit+and+bovine+brain+ADP-ribosylation+factor.&rft.au=Tsai%2C+S+C%3BAdamik%2C+R%3BMoss%2C+J%3BVaughan%2C+M&rft.aulast=Tsai&rft.aufirst=S&rft.date=1991-04-16&rft.volume=30&rft.issue=15&rft.spage=3697&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-05-17 N1 - Date created - 1991-05-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Induction of cytochrome P-450IA1 in fetal rat liver by a single dose of 3-methylcholanthrene. AN - 80522640; 1708245 AB - Pregnant Sprague-Dawley rats were treated with a single ip dose of either olive oil or 40 mg/kg of 3-methylcholanthrene on gestation day 20 and sacrificed at various times after injection. Determination of aryl hydrocarbon hydroxylase activity 24 hr after injection revealed that treatment with 3-methylcholanthrene resulted in a 10.5-fold stimulation of enzymatic activity in liver 800 x g supernatants. Western blot analysis with monoclonal antibody 1-7-1 confirmed these results and demonstrated the presence of a 3-methylcholanthrene-inducible P-450 isozyme. Using Northern and slot blot techniques, the induction of steady-state levels of CYPIA1 RNA was shown to occur as early as 4 hr following 3-methylcholanthrene injection. CYPIA1 RNA levels were induced 31.6-fold over values obtained from oil-treated tissues at this time. This appears to be the optimal time to study changes in the levels of CYPIA1 RNA gene expression in the fetus following transplacental exposure to polycyclic aromatic hydrocarbons. By 12 to 24 hr postinjection, the induction of CYPIA1 RNA levels declined to 3.5- to 8.5-fold above control values. These results demonstrate that the kinetics of induction of the CYPIA1 gene during the fetal period differed from that seen in adults. JF - Biochemical and biophysical research communications AU - Miller, M S AU - Jones, A B AU - Chauhan, D P AU - Park, S S AU - Anderson, L M AD - Perinatal Carcinogenesis Section, National Cancer Institute, Frederick, Maryland 21702. Y1 - 1991/04/15/ PY - 1991 DA - 1991 Apr 15 SP - 280 EP - 287 VL - 176 IS - 1 SN - 0006-291X, 0006-291X KW - Methylcholanthrene KW - 56-49-5 KW - RNA KW - 63231-63-0 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Animals KW - Fetus KW - Gestational Age KW - Cloning, Molecular KW - Pregnancy KW - Rats, Inbred Strains KW - Rats KW - Blotting, Western KW - Genes KW - RNA -- isolation & purification KW - Enzyme Induction KW - Female KW - RNA -- genetics KW - Liver -- enzymology KW - Methylcholanthrene -- pharmacology KW - Liver -- drug effects KW - Cytochrome P-450 Enzyme System -- genetics KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Liver -- embryology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80522640?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Induction+of+cytochrome+P-450IA1+in+fetal+rat+liver+by+a+single+dose+of+3-methylcholanthrene.&rft.au=Miller%2C+M+S%3BJones%2C+A+B%3BChauhan%2C+D+P%3BPark%2C+S+S%3BAnderson%2C+L+M&rft.aulast=Miller&rft.aufirst=M&rft.date=1991-04-15&rft.volume=176&rft.issue=1&rft.spage=280&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 - 1991-05-20 N1 - Date created - 1991-05-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Increases in cytosolic Ca++ down regulate thyrotropin receptor gene expression by a mechanism different from the cAMP signal. AN - 80521263; 1708253 AB - Thyrotropin (TSH) receptor mRNA levels in rat FRTL-5 thyroid cells are decreased by treatment with the calcium ionophores, A23187 or ionomycin, as well as with TSH, cholera toxin, forskolin, and 8-bromo-cAMP. Down regulation is, in each case, associated with a decrease in [125I]TSH binding and a decreased ability of TSH to increase cAMP levels. The ionophore does not alter cAMP levels and ethylene glycol-bis-(beta-aminoethyl ether) N, N'-tetraacetic acid (EGTA) in the medium prevents down regulation of TSH receptor mRNA levels by the ionophore, but not by TSH; the EGTA action is reversed by the simultaneous addition of Ca++. Whereas down regulation by TSH and its cAMP signal requires the presence of insulin and/or serum in the medium; down regulation by a calcium ionophore is still evident in their absence. Down regulation of TSH receptor mRNA levels and receptor desensitization by TSH/cAMP or an ionophore is lost in cells transfected with a full length TSH receptor cDNA devoid of regulatory elements, but able to reconstitute TSH receptor signal generation. JF - Biochemical and biophysical research communications AU - Saji, M AU - Ikuyama, S AU - Akamizu, T AU - Kohn, L D AD - Section on Cell Regulation, National Institute of Diabetes and Kidney and Digestive Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/04/15/ PY - 1991 DA - 1991 Apr 15 SP - 94 EP - 101 VL - 176 IS - 1 SN - 0006-291X, 0006-291X KW - Calmodulin KW - 0 KW - Receptors, Thyrotropin KW - Sulfonamides KW - Colforsin KW - 1F7A44V6OU KW - 8-Bromo Cyclic Adenosine Monophosphate KW - 23583-48-4 KW - Egtazic Acid KW - 526U7A2651 KW - Ionomycin KW - 56092-81-0 KW - RNA KW - 63231-63-0 KW - W 7 KW - 65595-90-6 KW - Cholera Toxin KW - 9012-63-9 KW - Edetic Acid KW - 9G34HU7RV0 KW - Cyclic AMP KW - E0399OZS9N KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Cytosol -- physiology KW - Animals KW - Calmodulin -- antagonists & inhibitors KW - Cholera Toxin -- pharmacology KW - Ionomycin -- pharmacology KW - Thyroid Gland KW - 8-Bromo Cyclic Adenosine Monophosphate -- pharmacology KW - Cloning, Molecular KW - Rats KW - Colforsin -- pharmacology KW - Transfection KW - Sulfonamides -- pharmacology KW - Kinetics KW - RNA -- isolation & purification KW - Down-Regulation -- drug effects KW - Egtazic Acid -- pharmacology KW - Cell Line KW - Edetic Acid -- pharmacology KW - RNA -- genetics KW - Receptors, Thyrotropin -- drug effects KW - Calcium -- physiology KW - Calcium -- pharmacology KW - Cyclic AMP -- physiology KW - Signal Transduction KW - Receptors, Thyrotropin -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80521263?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Increases+in+cytosolic+Ca%2B%2B+down+regulate+thyrotropin+receptor+gene+expression+by+a+mechanism+different+from+the+cAMP+signal.&rft.au=Saji%2C+M%3BIkuyama%2C+S%3BAkamizu%2C+T%3BKohn%2C+L+D&rft.aulast=Saji&rft.aufirst=M&rft.date=1991-04-15&rft.volume=176&rft.issue=1&rft.spage=94&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 - 1991-05-20 N1 - Date created - 1991-05-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Genetic mapping of the chloroquine-resistance locus on Plasmodium falciparum chromosome 7. AN - 80508001; 1673031 AB - The resurgence of malaria in recent decades has been accompanied by the worldwide spread of resistance to chloroquine, a drug once uncontested as the first-line antimalarial agent because of its efficacy and low toxicity. Chloroquine-resistant strains of Plasmodium falciparum counter the drug by expelling it rapidly via an unknown mechanism. In the absence of explicit biochemical knowledge of this efflux mechanism, reverse genetics provides a powerful approach to the molecular basis of chloroquine resistance. Here we report genetic linkage analysis in which 85 restriction fragment length polymorphism markers were used to examine inheritance of the 14 P. falciparum chromosomes in a laboratory cross between a chloroquine-resistant and a chloroquine-sensitive parasite. Inheritance data from 16 independent recombinant progeny show that the rapid efflux, chloroquine-resistant phenotype is governed by a single locus within an approximately 400-kilobase region of chromosome 7. Identification and characterization of genes within this region should lead to an understanding of the chloroquine-resistance mechanism. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Wellems, T E AU - Walker-Jonah, A AU - Panton, L J AD - Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/04/15/ PY - 1991 DA - 1991 Apr 15 SP - 3382 EP - 3386 VL - 88 IS - 8 SN - 0027-8424, 0027-8424 KW - Oligonucleotides KW - 0 KW - Chloroquine KW - 886U3H6UFF KW - Index Medicus KW - Genetic Linkage KW - Polymerase Chain Reaction KW - Animals KW - Base Sequence KW - Genes KW - Polymorphism, Restriction Fragment Length KW - Oligonucleotides -- chemistry KW - DNA Mutational Analysis KW - Molecular Sequence Data KW - Chromosome Mapping KW - Drug Resistance -- genetics KW - Chloroquine -- pharmacology KW - Plasmodium falciparum -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80508001?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Genetic+mapping+of+the+chloroquine-resistance+locus+on+Plasmodium+falciparum+chromosome+7.&rft.au=Wellems%2C+T+E%3BWalker-Jonah%2C+A%3BPanton%2C+L+J&rft.aulast=Wellems&rft.aufirst=T&rft.date=1991-04-15&rft.volume=88&rft.issue=8&rft.spage=3382&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 - 1991-05-15 N1 - Date created - 1991-05-15 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Biol Sci. 1990 Dec 22;242(1305):205-16 [1983036] Science. 1976 Aug 20;193(4254):673-5 [781840] Nature. 1988 May 5;333(6168):74-6 [3283563] Cell. 1986 Dec 26;47(6):845-50 [2430724] Proc Natl Acad Sci U S A. 1988 Dec;85(23):9114-8 [2904149] Nature. 1988 Sep 1;335(6185):79-82 [3045563] Mol Biochem Parasitol. 1988 Sep;30(3):279-88 [2847041] EMBO J. 1987 Feb;6(2):485-91 [2438130] Science. 1987 Jun 26;236(4809):1661-6 [3299700] Cell. 1987 Jun 5;49(5):633-42 [2884039] Proc Natl Acad Sci U S A. 1986 Aug;83(16):6065-9 [3016741] Proc Natl Acad Sci U S A. 1988 Sep;85(17):6277-81 [3045815] Genomics. 1988 Nov;3(4):287-95 [3072285] Proc Natl Acad Sci U S A. 1988 Jul;85(14):5195-9 [3293051] Mol Biochem Parasitol. 1987 Nov;26(1-2):203-14 [2448620] Mol Cell Biol. 1989 Jul;9(7):3151-4 [2701947] Cell. 1989 Jun 16;57(6):921-30 [2701941] Trends Genet. 1989 Oct;5(10):337-42 [2692241] Science. 1989 Jun 9;244(4909):1184-6 [2658061] Science. 1989 Sep 29;245(4925):1434-5 [2781285] Science. 1987 Nov 27;238(4831):1283-5 [3317830] Nature. 1987 Sep 10-16;329(6135):164-7 [3306406] Science. 1987 Feb 20;235(4791):899-901 [3544220] Nucleic Acids Res. 1986 Nov 11;14(21):8265-77 [3537955] Mol Biol Med. 1986 Aug;3(4):351-68 [3534513] Mol Biochem Parasitol. 1986 Sep;20(3):265-77 [3531849] Proc Natl Acad Sci U S A. 1986 Apr;83(8):2677-81 [3517875] Nucleic Acids Res. 1986 Apr 25;14(8):3311-23 [3517809] Cell. 1986 Mar 14;44(5):689-96 [3512098] Proc Natl Acad Sci U S A. 1985 Jan;82(2):543-7 [3881769] J Biol Chem. 1990 Jul 25;265(21):12337-41 [2197273] Nature. 1990 May 17;345(6272):253-5 [1970614] Nature. 1990 May 17;345(6272):255-8 [2185424] Nature. 1990 May 17;345(6272):202-3 [2185423] Science. 1984 Aug 10;225(4662):593-9 [6204383] J Biol Chem. 1983 Jun 10;258(11):6984-90 [6304071] Science. 1984 Aug 10;225(4662):625-8 [6330899] Am J Hum Genet. 1980 May;32(3):314-31 [6247908] Cell. 1985 Apr;40(4):775-83 [3886159] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Anti-tumor activities of immunotoxins made of monoclonal antibody B3 and various forms of Pseudomonas exotoxin. AN - 80507964; 2014255 AB - B3 is a monoclonal antibody that reacts with a carbohydrate epitope present on a variety of proteins located on the surface of many cancer cells and a limited number of normal tissues. We evaluated the cytotoxic activity of immunotoxins composed of monoclonal antibody B3 coupled to native Pseudomonas exotoxin (PE) or two recombinant forms of Pseudomonas exotoxin, PEArg57 or LysPE40, a form of PE with a deletion of the cell binding domain. All three conjugates were cytotoxic to human cell lines expressing the B3 antigen on their surface. The survival of each of the three immunotoxins in the circulation of mice was determined after administering the immunotoxin i.v. The half-life in blood of B3-PE and B3-PEArg57 was 20 hr, whereas the half-life of B3-LysPE40 was 4 hr. The short half-life of B3-LysPE40 may be due to the absence of domain I of PE. To determine the therapeutic effects of the three immunotoxins, they were given intraperitoneally to nude mice bearing subcutaneous A431 tumors. All three immunotoxins caused complete regression of 50-mm3 tumors with no toxic effects to the animals at therapeutic doses. Furthermore, substantial regression was also noted with much larger tumors. Our data indicate that the monoclonal antibody B3, when coupled to PE or recombinant forms of PE, may be useful for the treatment of tumors expressing B3 antigen. The therapeutic window was largest with B3-LysPE40, which can be administered in higher doses because it lacks sequences in domain I of PE that enable PE to bind to nontarget cells. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Pai, L H AU - Batra, J K AU - FitzGerald, D J AU - Willingham, M C AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/04/15/ PY - 1991 DA - 1991 Apr 15 SP - 3358 EP - 3362 VL - 88 IS - 8 SN - 0027-8424, 0027-8424 KW - Antibodies, Monoclonal KW - 0 KW - Antibodies, Neoplasm KW - Bacterial Toxins KW - Exotoxins KW - Immunotoxins 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 - Neoplasm Transplantation KW - Breast Neoplasms -- immunology KW - Cytotoxicity, Immunologic KW - Animals KW - Carcinoma, Squamous Cell -- immunology KW - Neoplasms, Experimental -- immunology KW - Neoplasms, Experimental -- therapy KW - Humans KW - Pseudomonas -- pathogenicity KW - Mice, Nude KW - Mice KW - Carcinoma, Squamous Cell -- therapy KW - Immunotoxins -- pharmacokinetics KW - Carcinoma -- therapy KW - Exotoxins -- administration & dosage KW - Immunotoxins -- immunology KW - Antibodies, Monoclonal -- pharmacokinetics KW - Antibodies, Neoplasm -- administration & dosage KW - Carcinoma -- immunology KW - Antibodies, Monoclonal -- administration & dosage KW - Antibodies, Monoclonal -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80507964?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Anti-tumor+activities+of+immunotoxins+made+of+monoclonal+antibody+B3+and+various+forms+of+Pseudomonas+exotoxin.&rft.au=Pai%2C+L+H%3BBatra%2C+J+K%3BFitzGerald%2C+D+J%3BWillingham%2C+M+C%3BPastan%2C+I&rft.aulast=Pai&rft.aufirst=L&rft.date=1991-04-15&rft.volume=88&rft.issue=8&rft.spage=3358&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 - 1991-05-15 N1 - Date created - 1991-05-15 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1986 Mar;83(5):1320-4 [3006045] Cell. 1987 Jan 16;48(1):129-36 [3098436] Proc Natl Acad Sci U S A. 1987 Apr;84(8):2474-8 [3104916] Science. 1987 Nov 20;238(4830):1098-104 [3317828] J Biol Chem. 1988 Jul 5;263(19):9470-5 [3132465] J Biol Chem. 1988 Sep 15;263(26):13203-7 [2901411] Nature. 1988 Sep 22;335(6188):369-72 [2843774] Proc Natl Acad Sci U S A. 1989 Nov;86(21):8545-9 [2510169] Blood. 1990 Apr 1;75(7):1426-32 [2180494] Cancer Res. 1990 Apr 1;50(7):2183-90 [1690595] Biotechniques. 1990 Mar;8(3):320-4 [2184853] Erratum In: Proc Natl Acad Sci U S A 1991 Jun 1;88(11):5066 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Negative regulation of the major histocompatibility complex class I promoter in embryonal carcinoma cells. AN - 80507761; 2014233 AB - Transcription of major histocompatibility complex (MHC) class I genes is negatively regulated in undifferentiated F9 mouse embryonal carcinoma cells via the conserved upstream regulatory region. This region contains constitutive enhancers and an inducible enhancer, the interferon consensus sequence (ICS), that is responsible for interferon-induced transcription. A series of mutations in the ICS, but not in the enhancer elements, resulted in an increase in expression of the MHC class I promoter in F9 cells. However, these ICS mutants did not increase promoter activity in F9 cells differentiated after retinoic acid treatment. Results of mobility-shift DNA-binding assays and methylation interference experiments showed that undifferentiated F9 cells contained a factor(s) that bound to a sequence within the 5' and central part of the ICS. This binding site, termed the MHC negative regulatory element (NRE), coincided with the site of mutations that increased promoter activity in F9 cells and was distinct from the element to which interferon-response factors bind. The factor(s) that binds to the MHC NRE was not detected in differentiated F9 cells treated with retinoic acid or in other cells expressing MHC class I genes. Finally, introduction of concatenated, double-stranded NRE oligomers, but not oligomers of unrelated sequences, into F9 cells abolished negative regulation of the MHC class I promoter activity, providing evidence that the NRE binding factor is responsible for repression of the MHC class I genes in F9 cells. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Flanagan, J R AU - Murata, M AU - Burke, P A AU - Shirayoshi, Y AU - Appella, E AU - Sharp, P A AU - Ozato, K AD - Laboratory of Developmental and Molecular Immunity, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/04/15/ PY - 1991 DA - 1991 Apr 15 SP - 3145 EP - 3149 VL - 88 IS - 8 SN - 0027-8424, 0027-8424 KW - DNA-Binding Proteins KW - 0 KW - Histocompatibility Antigens Class I KW - Nuclear Proteins KW - Repressor Proteins KW - Index Medicus KW - Regulatory Sequences, Nucleic Acid KW - Animals KW - Base Sequence KW - Tumor Cells, Cultured KW - DNA Mutational Analysis KW - Molecular Sequence Data KW - Mice KW - DNA-Binding Proteins -- physiology KW - Teratoma KW - Nuclear Proteins -- physiology KW - Methylation KW - Binding Sites KW - Promoter Regions, Genetic KW - Histocompatibility Antigens Class I -- genetics KW - Gene Expression Regulation KW - Major Histocompatibility Complex UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80507761?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Negative+regulation+of+the+major+histocompatibility+complex+class+I+promoter+in+embryonal+carcinoma+cells.&rft.au=Flanagan%2C+J+R%3BMurata%2C+M%3BBurke%2C+P+A%3BShirayoshi%2C+Y%3BAppella%2C+E%3BSharp%2C+P+A%3BOzato%2C+K&rft.aulast=Flanagan&rft.aufirst=J&rft.date=1991-04-15&rft.volume=88&rft.issue=8&rft.spage=3145&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 - 1991-05-15 N1 - Date created - 1991-05-15 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Methods Enzymol. 1983;101:582-98 [6888276] Nature. 1983 Jan 6;301(5895):32-7 [6296681] Cell. 1984 Dec;39(3 Pt 2):653-62 [6096017] Proc Natl Acad Sci U S A. 1985 Apr;82(8):2427-31 [2581247] Cell. 1985 Sep;42(2):519-26 [2992802] J Virol. 1986 Sep;59(3):761-3 [3016339] Cell. 1986 Nov 7;47(3):391-9 [3768959] Mol Cell Biol. 1986 Sep;6(9):3200-6 [3023967] Proc Natl Acad Sci U S A. 1986 Dec;83(24):9537-41 [3467324] Mol Cell Biol. 1987 Jan;7(1):305-13 [3561391] Proc Natl Acad Sci U S A. 1987 May;84(9):2653-7 [3554244] Nucleic Acids Res. 1987 May 26;15(10):4307-24 [3035489] EMBO J. 1987 Aug;6(8):2297-303 [3665875] Mol Cell Biol. 1987 Oct;7(10):3548-53 [2824991] Science. 1989 Jan 27;243(4890):544-6 [2536195] J Exp Med. 1989 Apr 1;169(4):1309-21 [2926327] Mol Cell Biol. 1989 Feb;9(2):739-46 [2540425] EMBO J. 1989 Apr;8(4):1139-44 [2501084] Cell. 1989 Aug 25;58(4):729-39 [2475256] Cell. 1989 Nov 3;59(3):405-8 [2572326] Mol Cell Biol. 1989 Nov;9(11):4670-6 [2601693] EMBO J. 1990 Jan;9(1):127-35 [2136829] Proc Natl Acad Sci U S A. 1990 May;87(10):3743-7 [2111015] Cell Growth Differ. 1990 Mar;1(3):135-47 [1964077] Cell. 1988 Mar 11;52(5):685-95 [3345568] Oncogene Res. 1987 Jul;1(2):113-9 [2835729] Genes Dev. 1988 Apr;2(4):383-93 [3371658] Proc Natl Acad Sci U S A. 1988 Aug;85(16):5884-8 [2457903] Proc Natl Acad Sci U S A. 1988 Nov;85(21):7952-6 [2847148] Nucleic Acids Res. 1988 Nov 25;16(22):10575-92 [3205717] Proc Natl Acad Sci U S A. 1973 Dec;70(12):3581-4 [4587255] Transplantation. 1974 Jun;17(6):632-4 [4829671] Science. 1980 Aug 15;209(4458):768-76 [6250214] Cell. 1980 Sep;21(2):347-55 [6250719] Dev Biol. 1982 Feb;89(2):503-8 [7056443] J Biol Chem. 1982 Apr 10;257(7):3414-21 [6174520] Biochim Biophys Acta. 1982 Apr 29;651(2-3):105-41 [6284213] Nature. 1984 Mar 29-Apr 4;308(5958):470-2 [6323996] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Exonucleolytic proofreading of leading and lagging strand DNA replication errors. AN - 80506056; 1901658 AB - We have asked whether exonucleolytic proofreading occurs during simian virus 40 origin-dependent, bidirectional DNA replication in extracts of human HeLa cells. In addition, we have compared the fidelity of leading and lagging strand DNA synthesis. In a fidelity assay that scores single-base substitution errors that revert a TGA codon in the lacZ alpha gene in an M13mp vector, providing an excess of a single dNTP substrate over the other three dNTP substrates in a replication reaction generates defined, strand-specific errors. Fidelity measurements with two vectors having the origin of replication on opposite sides of the opal codon demonstrate that error rates for two different A.dCTP and T.dGTP mispairs increase when deoxyguanosine monophosphate is added to replication reaction mixtures or when the concentration of deoxynucleoside triphosphates is increased. The data suggest that exonucleolytic proofreading occurs on both strands during bidirectional replication. Measurements using the two simian virus 40 origin-containing vectors suggest that base substitution error rates are similar for replication of the leading and lagging strands. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Roberts, J D AU - Thomas, D C AU - Kunkel, T A AD - Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/04/15/ PY - 1991 DA - 1991 Apr 15 SP - 3465 EP - 3469 VL - 88 IS - 8 SN - 0027-8424, 0027-8424 KW - Antigens, Polyomavirus Transforming KW - 0 KW - Deoxyribonucleotides KW - DNA-Directed DNA Polymerase KW - EC 2.7.7.7 KW - Exodeoxyribonucleases KW - EC 3.1.- KW - beta-Galactosidase KW - EC 3.2.1.23 KW - Index Medicus KW - DNA Repair KW - HeLa Cells KW - Humans KW - In Vitro Techniques KW - Deoxyribonucleotides -- metabolism KW - beta-Galactosidase -- genetics KW - Templates, Genetic KW - Antigens, Polyomavirus Transforming -- genetics KW - Exodeoxyribonucleases -- metabolism KW - DNA Replication KW - Mutagenesis KW - DNA-Directed DNA Polymerase -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80506056?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Exonucleolytic+proofreading+of+leading+and+lagging+strand+DNA+replication+errors.&rft.au=Roberts%2C+J+D%3BThomas%2C+D+C%3BKunkel%2C+T+A&rft.aulast=Roberts&rft.aufirst=J&rft.date=1991-04-15&rft.volume=88&rft.issue=8&rft.spage=3465&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 - 1991-05-15 N1 - Date created - 1991-05-15 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Biochimie. 1975;57(5):587-95 [1182215] J Biol Chem. 1984 May 10;259(9):5567-73 [6325441] J Biol Chem. 1991 Feb 25;266(6):3744-51 [1995629] J Biol Chem. 1990 Oct 25;265(30):18043-6 [1976634] Nature. 1987 May 14-20;327(6118):169-70 [3574477] Proc Natl Acad Sci U S A. 1988 Oct;85(19):7064-8 [3174620] J Biol Chem. 1989 Feb 15;264(5):2801-9 [2536723] Cell. 1988 Jun 17;53(6):837-40 [2838173] Proc Natl Acad Sci U S A. 1987 Jul;84(14):4865-9 [3474631] J Biol Chem. 1981 Oct 10;256(19):9883-9 [6456268] Cell. 1982 Apr;28(4):767-79 [6178514] Cell. 1983 Jun;33(2):455-64 [6305512] Proc Natl Acad Sci U S A. 1979 Oct;76(10):4946-50 [159450] J Biol Chem. 1979 Jul 10;254(13):5718-25 [376517] J Biol Chem. 1979 Mar 25;254(6):1902-12 [422561] Biochemistry. 1978 May 2;17(9):1603-6 [350269] Biochemistry. 1977 Aug 23;16(17):3740-6 [332220] Annu Rev Genet. 1975;9:245-84 [55095] Proc Natl Acad Sci U S A. 1987 Aug;84(16):5635-9 [3112771] FEBS Lett. 1988 Feb 29;229(1):6-10 [3345838] Biochemistry. 1986 Jan 14;25(1):26-36 [3954990] Proc Natl Acad Sci U S A. 1988 Apr;85(8):2523-7 [2833742] J Biol Chem. 1987 Dec 5;262(34):16267-70 [2824485] J Biol Chem. 1988 Dec 5;263(34):17889-92 [2848017] Mol Cell Biol. 1988 Aug;8(8):3267-71 [2850485] Nucleic Acids Res. 1985 Jan 11;13(1):261-74 [2987791] Mol Cell Biol. 1985 Jun;5(6):1238-46 [2993858] J Biol Chem. 1988 Jun 25;263(18):8953-7 [3288626] Annu Rev Cell Biol. 1989;5:197-245 [2557059] Proc Natl Acad Sci U S A. 1989 Jun;86(11):3949-52 [2657730] Cell. 1988 Apr 8;53(1):117-26 [2894900] Proc Natl Acad Sci U S A. 1984 Dec;81(24):7747-51 [6393125] Proc Natl Acad Sci U S A. 1984 Nov;81(22):6973-7 [6095264] Methods Enzymol. 1987;154:367-82 [3323813] Eur J Biochem. 1990 Aug 17;191(3):617-8 [2390988] Biochemistry. 1990 Jun 5;29(22):5226-31 [2166556] Nature. 1990 Aug 9;346(6284):534-9 [2165567] Cell. 1990 Sep 21;62(6):1143-51 [2169349] Proc Natl Acad Sci U S A. 1990 Aug;87(15):5837-41 [2116007] J Biol Chem. 1990 Aug 15;265(23):13878-87 [2199444] J Mol Biol. 1983 Apr 25;165(4):669-82 [6222198] Biochim Biophys Acta. 1991 Jan 17;1088(1):11-24 [1846563] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cardiopulmonary toxicity after liposomal amphotericin B infusion. AN - 80474578; 2003714 JF - Annals of internal medicine AU - Levine, S J AU - Walsh, T J AU - Martinez, A AU - Eichacker, P Q AU - Lopez-Berestein, G AU - Natanson, C AD - National Institutes of Health, Bethesda, Maryland. Y1 - 1991/04/15/ PY - 1991 DA - 1991 Apr 15 SP - 664 EP - 666 VL - 114 IS - 8 SN - 0003-4819, 0003-4819 KW - Drug Carriers KW - 0 KW - Liposomes KW - Amphotericin B KW - 7XU7A7DROE KW - Abridged Index Medicus KW - Index Medicus KW - Lung -- blood supply KW - Drug Administration Schedule KW - Infusions, Intravenous KW - Dose-Response Relationship, Drug KW - Pulmonary Gas Exchange -- drug effects KW - Humans KW - Adult KW - Female KW - Hemodynamics -- drug effects KW - Lung Diseases -- chemically induced KW - Lung Diseases -- physiopathology KW - Amphotericin B -- adverse effects KW - Amphotericin B -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80474578?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+internal+medicine&rft.atitle=Cardiopulmonary+toxicity+after+liposomal+amphotericin+B+infusion.&rft.au=Levine%2C+S+J%3BWalsh%2C+T+J%3BMartinez%2C+A%3BEichacker%2C+P+Q%3BLopez-Berestein%2C+G%3BNatanson%2C+C&rft.aulast=Levine&rft.aufirst=S&rft.date=1991-04-15&rft.volume=114&rft.issue=8&rft.spage=664&rft.isbn=&rft.btitle=&rft.title=Annals+of+internal+medicine&rft.issn=00034819&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-17 N1 - Date created - 1991-04-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modulation of an ultraviolet mutational hotspot in a shuttle vector Xeroderma cells. AN - 80553067; 2027767 AB - Ultraviolet mutagenesis of the shuttle vector plasmid pZ189 in Xeroderma Pigmentosum cells yields a mutational pattern marked by hotspots at photoproduct sites on both strands of the supF marker gene. In order to test the influence of strand orientation on the appearance of hotspots the mutagenesis study was repeated on a vector with the supF gene in the inverted orientation. We recovered a pattern the same as that in the earlier work and conclude that the nature of the DNA polymerase involved in the replication of specific strands is not a primary determinant of hotspot occurrence in this system. One of the hotspots lies in an 8 base palindrome while the corresponding site on the other strand was not a hotspot. These results were obtained with calcium phosphate transfection of the UV treated vector. When DEAE dextran was used as a transfection agent both sites in the palindrome were hotspots. In a mixing experiment the calcium phosphate pattern was recovered. Our data suggest that the sequence determinants of mutational probability at these two sites lie outside the 8 bases of the palindrome and that mutagenesis at one, but not the other, site is sensitive to perturbation of cellular calcium levels. JF - Nucleic acids research AU - Seetharam, S AU - Seidman, M M AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/04/11/ PY - 1991 DA - 1991 Apr 11 SP - 1601 EP - 1604 VL - 19 IS - 7 SN - 0305-1048, 0305-1048 KW - supF KW - Calcium Phosphates KW - 0 KW - alpha-tricalcium phosphate KW - tetracalcium phosphate KW - calcium phosphate, monobasic, anhydrous KW - 701EKV9RMN KW - DEAE-Dextran KW - 9015-73-0 KW - calcium phosphate KW - 97Z1WI3NDX KW - calcium phosphate, dibasic, anhydrous KW - L11K75P92J KW - Index Medicus KW - Ultraviolet Rays KW - Base Sequence KW - Transfection KW - Molecular Sequence Data KW - Xeroderma Pigmentosum -- pathology KW - Genetic Vectors KW - Xeroderma Pigmentosum -- genetics KW - Plasmids KW - Mutagenesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80553067?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+acids+research&rft.atitle=Modulation+of+an+ultraviolet+mutational+hotspot+in+a+shuttle+vector+Xeroderma+cells.&rft.au=Seetharam%2C+S%3BSeidman%2C+M+M&rft.aulast=Seetharam&rft.aufirst=S&rft.date=1991-04-11&rft.volume=19&rft.issue=7&rft.spage=1601&rft.isbn=&rft.btitle=&rft.title=Nucleic+acids+research&rft.issn=03051048&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-06-11 N1 - Date created - 1991-06-11 N1 - Date revised - 2017-01-13 N1 - Gene symbol - supF N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1986 Nov;83(21):8273-7 [3464953] Gene. 1985;38(1-3):233-7 [2998945] Mol Cell Biol. 1987 May;7(5):2031-4 [3037341] J Clin Invest. 1987 Dec;80(6):1613-7 [3680516] Cell. 1988 Apr 8;53(1):117-26 [2894900] J Mol Biol. 1988 Apr 20;200(4):665-80 [2842508] Mol Cell Biol. 1989 Mar;9(3):1277-83 [2725498] Proc Natl Acad Sci U S A. 1989 Jun;86(11):4147-51 [2657743] Biochemistry. 1989 May 30;28(11):4601-7 [2669960] Cancer Res. 1989 Nov 1;49(21):5918-21 [2790806] J Mol Biol. 1990 Apr 5;212(3):433-6 [2182882] J Mol Biol. 1964 Aug;9:372-5 [14202273] J Natl Cancer Inst. 1968 Aug;41(2):351-7 [4299537] Proc Natl Acad Sci U S A. 1982 Jan;79(2):422-6 [6952193] Biochimie. 1982 Aug-Sep;64(8-9):829-38 [6215955] J Mol Biol. 1984 Jul 25;177(1):173-80 [6748082] Proc Natl Acad Sci U S A. 1987 Jun;84(11):3782-6 [3473483] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evidence that specific high mannose structures directly regulate multiple cellular activities. AN - 72060431; 1881387 AB - Previous studies have demonstrated that much of the immunomodulatory activity of the glycoprotein uromodulin can be attributed to attached oligosaccharides. Structural studies of isolated and purified saccharides derived from uromodulin suggest that the structure Man6GlcNAc2-asn can inhibit in vitro assays of antigen driven T cell proliferation. Based on these observations, we isolated a series of high mannose glycopeptides from a variety of natural sources and tested them for biological activity in a number of assays. We found that purified mannose rich glycopeptides are able to activate the hexose monophosphate (HMP) shunt, induce prostaglandin synthesis, and directly stimulate IL-1 synthesis. These in vitro effects appear to have in vivo counterparts. Thus in a species-restricted fashion, high mannose compounds are able to directly activate a delayed mononuclear cell infiltrate after intradermal injection. Our data suggest that specific mannose oligosaccharides may activate as well as inhibit cellular immune responses at several different levels. These findings support the hypothesis that specific saccharide structures could participate in the physiologic regulation of the immune response. JF - Molecular and cellular biochemistry AU - Sathyamoorthy, N AU - Decker, J M AU - Sherblom, A P AU - Muchmore, A AD - Metabolism Branch, NCI, NIH, Bethesda, MD. Y1 - 1991/04/10/ PY - 1991 DA - 1991 Apr 10 SP - 139 EP - 147 VL - 102 IS - 2 SN - 0300-8177, 0300-8177 KW - Glycoproteins KW - 0 KW - Interleukin-1 KW - Mucoproteins KW - Oligosaccharides KW - UMOD protein, human KW - Uromodulin KW - Dinoprostone KW - K7Q1JQR04M KW - Mannose KW - PHA4727WTP KW - Index Medicus KW - Swine KW - Animals KW - Hypersensitivity, Delayed -- chemically induced KW - Interleukin-1 -- biosynthesis KW - Dinoprostone -- biosynthesis KW - Guinea Pigs KW - Humans KW - Leukocytes, Mononuclear -- immunology KW - Swine, Miniature KW - Stimulation, Chemical KW - Pentose Phosphate Pathway -- drug effects KW - Oligosaccharides -- metabolism KW - Mucoproteins -- physiology KW - Immunocompetence KW - Carbohydrate Sequence KW - Molecular Sequence Data KW - Oligosaccharides -- pharmacology KW - Leukocytes, Mononuclear -- drug effects KW - Immunity, Cellular KW - Glycoproteins -- pharmacology KW - Mannose -- physiology KW - Glycoproteins -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72060431?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Evidence+that+specific+high+mannose+structures+directly+regulate+multiple+cellular+activities.&rft.au=Sathyamoorthy%2C+N%3BDecker%2C+J+M%3BSherblom%2C+A+P%3BMuchmore%2C+A&rft.aulast=Sathyamoorthy&rft.aufirst=N&rft.date=1991-04-10&rft.volume=102&rft.issue=2&rft.spage=139&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 - 1991-09-27 N1 - Date created - 1991-09-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Identification and localization of a kainate binding protein in the frog inner ear by electron microscopy immunocytochemistry. AN - 85230123; pmid-1650275 AB - A kainate binding protein (KBP) was studied in Rana pipiens inner ear using monoclonal and polyclonal antibodies against affinity purified KBP from frog brain. The KBP identified and analyzed in inner ear tissue homogenates, with one- and two-dimensional immunoblots, was similar to the affinity purified KBP and to the antibody-identified frog brain KBP. As brain KBP, inner ear KBP had 5 main components in the molecular weight dimension, centered at Mr = 48,000; however, inner ear KBP had a greater abundance of the higher molecular weight components. Light and electron microscopy observations showed KBP immunostaining at two locations: (1) in the dendrites of the eight nerve afferent fibers contacting sensory hair cells, with the postsynaptic density being more intensely stained; and (2) on the cytoplasmic membrane of fibroblasts present in the inner ear connective tissue which displayed intense immunostaining. The presence of kainate (KA) binding sites in the inner ear was assessed using in vitro receptor autoradiography. [3H]KA binding sites were found in connective tissue areas confirming the immunocytochemistry results. The postsynaptic localization of the KBP in afferent endings, strongly supports it as being a component of the KA receptor complex. However, its presence on fibroblasts situated in the inner ear connective tissue makes its function hypothetical. The dual presence of the KBP on non-neuronal cells as well as at postsynaptic membrane sites suggests the existence of a family of proteins involved in KA binding and KA receptors with a complex organization. JF - Brain Research AU - Dechesne, C J AU - Hampson, D R AU - Goping, G AU - Wheaton, K D AU - Wenthold, R J AD - Neurochemistry Section, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD 20892. PY - 1991 SP - 223 EP - 233 VL - 545 IS - 1-2 SN - 0006-8993, 0006-8993 KW - Rana pipiens KW - Labyrinth KW - Immunoblotting KW - Synapses KW - Hair Cells KW - Electrophoresis, Polyacrylamide Gel KW - Animal KW - Brain KW - Autoradiography KW - Molecular Weight KW - Kainic Acid KW - Tritium KW - Electrophoresis, Gel, Two-Dimensional KW - Receptors, Neurotransmitter KW - Support, Non-U.S. Gov't KW - Receptors, Kainic Acid KW - Microscopy, Immunoelectron KW - Afferent Pathways KW - Immunoenzyme Techniques UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85230123?accountid=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=Identification+and+localization+of+a+kainate+binding+protein+in+the+frog+inner+ear+by+electron+microscopy+immunocytochemistry.&rft.au=Dechesne%2C+C+J%3BHampson%2C+D+R%3BGoping%2C+G%3BWheaton%2C+K+D%3BWenthold%2C+R+J&rft.aulast=Dechesne&rft.aufirst=C&rft.date=1991-04-01&rft.volume=545&rft.issue=1-2&rft.spage=223&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 - Imaging the tongue and vocal tract. AN - 85181234; pmid-1954111 AB - The internal structures of the vocal tract are difficult to measure without impinging upon their normal movement patterns. Imaging techniques overcome that difficulty because they measure internal movement indirectly, without direct contact with the structures. This paper examines four well-known imaging techniques: X-ray, computed tomography (CT), magnetic resonance imaging (MRI) and ultrasound. Tongue and vocal tract researchers have employed all of these techniques. Imaging systems provide very different articulatory information from flesh point tracking systems. They provide information about the shape and position of the entire imaged structure, rather than a single point on the structure. In addition, images usually can be made in multiple planes, providing midsagittal, parasagittal, coronal, transverse and oblique sections of the structure. However, these systems have several limitations. CT and MRI create static images only. Ultrasound cannot image hard tissue. Radiation exposure limits the duration of X-ray imaging. This paper discusses the advantages and limitations of imaging systems, as well as the uniqueness of the measurements made with them. JF - The British Journal of Disorders of Communication AU - Stone, M AD - National Institutes of Health, Department of Rehabilitation Medicine, Bethesda, MD 20892. PY - 1991 SP - 11 EP - 23 VL - 26 IS - 1 SN - 0007-098X, 0007-098X KW - Magnetic Resonance Imaging KW - Oropharynx KW - Human KW - Larynx KW - Tomography, X-Ray Computed KW - Tongue KW - Speech UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85181234?accountid=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+British+Journal+of+Disorders+of+Communication&rft.atitle=Imaging+the+tongue+and+vocal+tract.&rft.au=Stone%2C+M&rft.aulast=Stone&rft.aufirst=M&rft.date=1991-04-01&rft.volume=26&rft.issue=1&rft.spage=11&rft.isbn=&rft.btitle=&rft.title=The+British+Journal+of+Disorders+of+Communication&rft.issn=0007098X&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Efficacy of desipramine in painful diabetic neuropathy: a placebo-controlled trial. AN - 80718925; 1861872 AB - Although amitriptyline relieves pain in many patients with painful diabetic neuropathy, side effects often preclude effective treatment. Desipramine has the least anticholinergic and sedative effects of the first generation tricyclic antidepressants. We compared a 6 week course of desipramine (mean dose, 201 mg/day) to active placebo in 20 patients with painful diabetic neuropathy in a double-blind crossover trial. Pain relief with desipramine was statistically significant in weeks 5 and 6. Eleven patients reported at least moderate relief with desipramine, compared to 2 with placebo. Pain relief tended to be greater in depressed patients, but relief was also observed in patients who did not show an antidepressant effect. We conclude that desipramine relieves pain in many patients with painful diabetic neuropathy, offering an alternative for patients unable to tolerate amitriptyline. Blockade of norepinephrine reuptake, an action shared by desipramine, amitriptyline, and other antidepressants proven effective in neuropathic pain, may mediate this analgesic effect. JF - Pain AU - Max, M B AU - Kishore-Kumar, R AU - Schafer, S C AU - Meister, B AU - Gracely, R H AU - Smoller, B AU - Dubner, R AD - Neurobiology and Anesthesiology Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 3 EP - 9; discussion 1-2 VL - 45 IS - 1 SN - 0304-3959, 0304-3959 KW - Benztropine KW - 1NHL2J4X8K KW - Desipramine KW - TG537D343B KW - Index Medicus KW - Double-Blind Method KW - Humans KW - Depression -- complications KW - Adult KW - Aged KW - Middle Aged KW - Benztropine -- therapeutic use KW - Male KW - Female KW - Emotions -- drug effects KW - Pain -- etiology KW - Pain -- drug therapy KW - Diabetic Neuropathies -- complications KW - Desipramine -- therapeutic use KW - Desipramine -- adverse effects KW - Diabetic Neuropathies -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80718925?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Efficacy+of+desipramine+in+painful+diabetic+neuropathy%3A+a+placebo-controlled+trial.&rft.au=Max%2C+M+B%3BKishore-Kumar%2C+R%3BSchafer%2C+S+C%3BMeister%2C+B%3BGracely%2C+R+H%3BSmoller%2C+B%3BDubner%2C+R&rft.aulast=Max&rft.aufirst=M&rft.date=1991-04-01&rft.volume=45&rft.issue=1&rft.spage=3&rft.isbn=&rft.btitle=&rft.title=Pain&rft.issn=03043959&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-30 N1 - Date created - 1991-08-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Geophysical variables and behavior: LXV. Seasonal changes in mood in opioid addicts on the Addiction Research Center Inventory. AN - 80716258; 1862167 AB - Seasonal changes in mood using the Addiction Research Center Inventory (ARCI) were tested in 243 male opioid addicts when they were free of drug and withdrawal effects. No significant changes were found on scales which measure euphoria (MBG), tension-anxiety (LSD), excitement (Ex), or dysphoric effects (SOW). A significant difference between seasons was found for lowered motivation (PCAG) in the summer and spring relative to winter, but these effects were not consistent with a winter seasonal affective disorder. Significant changes were more common for spring-fall and summer seasons relative to winter on items of the inventory. JF - Psychological reports AU - Haertzen, C A AD - National Institute on Drug Abuse, Addiction Research Center, Baltimore, MD 21224. Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 360 EP - 362 VL - 68 IS - 2 SN - 0033-2941, 0033-2941 KW - Index Medicus KW - Humans KW - Adult KW - Prisoners -- psychology KW - Psychometrics KW - Male KW - Opioid-Related Disorders -- psychology KW - Personality Inventory -- statistics & numerical data KW - Depressive Disorder -- psychology KW - Anxiety Disorders -- psychology KW - Anxiety Disorders -- diagnosis KW - Seasons KW - Depressive Disorder -- diagnosis KW - Opioid-Related Disorders -- rehabilitation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80716258?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychological+reports&rft.atitle=Geophysical+variables+and+behavior%3A+LXV.+Seasonal+changes+in+mood+in+opioid+addicts+on+the+Addiction+Research+Center+Inventory.&rft.au=Haertzen%2C+C+A&rft.aulast=Haertzen&rft.aufirst=C&rft.date=1991-04-01&rft.volume=68&rft.issue=2&rft.spage=360&rft.isbn=&rft.btitle=&rft.title=Psychological+reports&rft.issn=00332941&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-04 N1 - Date created - 1991-09-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Detection of hantavirus RNA in tissues of experimentally infected mice using reverse transcriptase-directed polymerase chain reaction. AN - 80701553; 1713266 AB - Detection of hantaviruses, the etiological agents of hemorrhagic fever with renal syndrome (HFRS), by virus isolation using experimental animals or cell culture is time-consuming. A more rapid but equally specific method is needed. We used a reverse transcriptase-directed polymerase chain reaction (RT-PCR) to detect hantavirus genomic sequences and compared its sensitivity with conventional virus isolation. RNA, extracted by the guanidinium isothiocyanate-cesium chloride method from hantavirus-infected Vero E6 cells and from tissues of infant mice inoculated intracerebrally with 100 LD50 of hantavirus, was initially reverse transcribed using avian myeloblastosis virus reverse transcriptase. The resulting complementary DNA (cDNA) was used as template to amplify the glycoprotein 2-encoding region of the hantavirus M segment. With this method, Vero E6 cell cultures infected with Hantaan virus strains 76-118 (prototype) and HV114 (an isolate from the urine of an HFRS patient in China) were positive, while control cultures were negative. Brain, lung, and heart tissues from hantavirus-infected mice were positive by RT-PCR at 5, 8, and 11 days after intracerebral inoculation. The specificity of the positive results was confirmed by restriction endonuclease digestion of the amplified fragments with AluI and HpaI. The sensitivity of the RT-PCR was equal to cell culture amplification but required less time. This method is being adapted for detection of hantavirus genomic sequences in clinical specimens and postmortem tissues from patients with HFRS. JF - Journal of medical virology AU - Xiao, S Y AU - Yanagihara, R AU - Godec, M S AU - Eldadah, Z A AU - Johnson, B K AU - Gajdusek, D C AU - Asher, D M AD - Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland 20892. Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 277 EP - 282 VL - 33 IS - 4 SN - 0146-6615, 0146-6615 KW - DNA, Viral KW - 0 KW - RNA, Viral KW - RNA-Directed DNA Polymerase KW - EC 2.7.7.49 KW - Index Medicus KW - Sensitivity and Specificity KW - Animals, Newborn KW - Animals KW - DNA, Viral -- chemistry KW - Lethal Dose 50 KW - Brain -- microbiology KW - Heart -- microbiology KW - Vero Cells KW - Mice KW - Lung -- microbiology KW - Hemorrhagic Fever with Renal Syndrome -- diagnosis KW - Polymerase Chain Reaction KW - Hantavirus -- genetics KW - Hantavirus -- pathogenicity KW - RNA, Viral -- analysis KW - Hemorrhagic Fever with Renal Syndrome -- microbiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80701553?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+medical+virology&rft.atitle=Detection+of+hantavirus+RNA+in+tissues+of+experimentally+infected+mice+using+reverse+transcriptase-directed+polymerase+chain+reaction.&rft.au=Xiao%2C+S+Y%3BYanagihara%2C+R%3BGodec%2C+M+S%3BEldadah%2C+Z+A%3BJohnson%2C+B+K%3BGajdusek%2C+D+C%3BAsher%2C+D+M&rft.aulast=Xiao&rft.aufirst=S&rft.date=1991-04-01&rft.volume=33&rft.issue=4&rft.spage=277&rft.isbn=&rft.btitle=&rft.title=Journal+of+medical+virology&rft.issn=01466615&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-27 N1 - Date created - 1991-08-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Codeine: developmental toxicity in hamsters and mice. AN - 80701443; 1855614 AB - Timed-pregnant LVG Syrian hamsters and Swiss CD-1 mice were dosed orally twice daily (b.i.d.) with codeine in water on Gestational Days (gd) 5-13 (0, 10, 50, or 150 mg/kg, b.i.d.--hamsters) or 6-15 (0, 37.5, 75, 150, or 300 mg/kg, b.i.d.--mice). Dams were necropsied on gd 14 (hamsters) or 17 (mice), and fetuses were weighed, sexed, and examined for external, visceral, and skeletal malformations. No maternal deaths were observed in hamsters, while 19% of the pregnant mice in the high-dose group died. Maternal weight gain (gestational and treatment periods) and gravid uterine weights were significantly depressed in hamsters (150 mg/kg, b.i.d.) and in mice (300 mg/kg, b.i.d.). However, the corrected weight gain for both species, although decreased, was not significantly different from that of the controls. In both species, maternal liver weights (relative) were significantly increased in the high-dose groups. There were increases in the percentage resorptions per pregnant dam and in the proportion of litters with 100% resorptions in the high-dose groups of both species. Considering only live litters, the number of live fetuses per litter and the sex ratio were unaffected in both species. Mean fetal body weights were also significantly decreased in the 50 and 150 mg/kg, b.i.d. (hamsters), and the 150 and 300 mg/kg, b.i.d. (mice), groups. The no-observed-adverse-effect levels (NOAELs) for developmental toxicity were 10 (hamsters) and 75 (mice) mg/kg, b.i.d., whereas the NOAELs for maternal toxicity were 50 (hamsters) and 150 (mice) mg/kg, b.i.d. The predominant structural malformation in hamsters was meningoencephalocele (high-dose group only), affecting 3% of fetuses and 19% of litters (neither statistically significant). Codeine did not induce any increase in structural malformations in mice. Thus, codeine produced developmental toxicity (as indicated by decreased fetal body weight) at doses below those producing maternal toxicity in both hamsters and mice. In the hamster, the more sensitive species to codeine developmental toxicity, effects were observed at a total daily dose of 100 mg/kg, which is only 11 times the maximum human therapeutic oral dose. JF - Fundamental and applied toxicology : official journal of the Society of Toxicology AU - Williams, J AU - Price, C J AU - Sleet, R B AU - George, J D AU - Marr, M C AU - Kimmel, C A AU - Morrissey, R E AD - Developmental and Reproductive Toxicology Group, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 401 EP - 413 VL - 16 IS - 3 SN - 0272-0590, 0272-0590 KW - Teratogens KW - 0 KW - Codeine KW - Q830PW7520 KW - Index Medicus KW - Abnormalities, Drug-Induced -- pathology KW - Administration, Oral KW - Animals KW - Fetus -- drug effects KW - Mice, Inbred ICR KW - Random Allocation KW - Gestational Age KW - Mice KW - Pregnancy KW - Body Weight -- drug effects KW - Mesocricetus KW - Female KW - Male KW - Organ Size -- drug effects KW - Cricetinae KW - Codeine -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80701443?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Codeine%3A+developmental+toxicity+in+hamsters+and+mice.&rft.au=Williams%2C+J%3BPrice%2C+C+J%3BSleet%2C+R+B%3BGeorge%2C+J+D%3BMarr%2C+M+C%3BKimmel%2C+C+A%3BMorrissey%2C+R+E&rft.aulast=Williams&rft.aufirst=J&rft.date=1991-04-01&rft.volume=16&rft.issue=3&rft.spage=401&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 - 1991-08-29 N1 - Date created - 1991-08-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Rescue of experimental intrathecal methotrexate overdose with carboxypeptidase-G2. AN - 80667069; 2066764 AB - The carboxypeptidase G class of enzymes rapidly hydrolyze methotrexate (MTX) into the inactive metabolites 4-deoxy-4-amino-N10-methylpteroic acid (DAMPA) and glutamate. This study evaluated the use of carboxypeptidase-G2 (CPDG2) as a potential intrathecal (IT) rescue agent for massive IT MTX overdose. The CSF pharmacokinetics of MTX with and without CPDG2 rescue was studied in adult rhesus monkeys (Macaca mulatta) using a nontoxic IT 5 mg dose (equivalent to 50 mg in humans). Without CPDG2 rescue, peak CSF MTX concentration was 2,904 +/- 340 mumol/L. Within 5 minutes of administration of 30 U IT CPDG2, CSF MTX concentrations decreased greater than 400-fold to 6.55 +/- 6.7 microM. Subsequently, groups of three monkeys received either 25 mg IT MTX (equivalent to 250 mg in humans) followed by 150 U IT CPDG2 or 50 mg IT MTX (equivalent to 500 mg in humans) followed by 300 U IT CPDG2. All animals survived without neurotoxicity. Our studies suggest that CPDG2 may prove to be an important addition to the currently recommended strategy for the management of IT MTX overdose. 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 - Bacher, J D AU - Walsh, T J AU - Poplack, D G AD - Pediatric Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 670 EP - 674 VL - 9 IS - 4 SN - 0732-183X, 0732-183X KW - gamma-Glutamyl Hydrolase KW - EC 3.4.19.9 KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - Animals KW - Injections, Spinal KW - Macaca mulatta KW - Drug Overdose -- drug therapy KW - Methotrexate -- pharmacokinetics KW - gamma-Glutamyl Hydrolase -- therapeutic use KW - Methotrexate -- poisoning KW - Methotrexate -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80667069?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Rescue+of+experimental+intrathecal+methotrexate+overdose+with+carboxypeptidase-G2.&rft.au=Adamson%2C+P+C%3BBalis%2C+F+M%3BMcCully%2C+C+L%3BGodwin%2C+K+S%3BBacher%2C+J+D%3BWalsh%2C+T+J%3BPoplack%2C+D+G&rft.aulast=Adamson&rft.aufirst=P&rft.date=1991-04-01&rft.volume=9&rft.issue=4&rft.spage=670&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 - 1991-08-15 N1 - Date created - 1991-08-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of Raf-1 serine/threonine protein kinase in growth factor signal transduction. AN - 80558839; 2030909 JF - Oncogene AU - Rapp, U R AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick, Maryland 21702-1201. Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 495 EP - 500 VL - 6 IS - 4 SN - 0950-9232, 0950-9232 KW - Growth Substances KW - 0 KW - Proto-Oncogene Proteins 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 - Second Messenger Systems -- physiology KW - Humans KW - Cell Division -- physiology KW - Gene Expression Regulation KW - Signal Transduction -- physiology KW - Growth Substances -- physiology KW - Proto-Oncogene Proteins -- physiology KW - Protein-Tyrosine Kinases -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80558839?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Role+of+Raf-1+serine%2Fthreonine+protein+kinase+in+growth+factor+signal+transduction.&rft.au=Rapp%2C+U+R&rft.aulast=Rapp&rft.aufirst=U&rft.date=1991-04-01&rft.volume=6&rft.issue=4&rft.spage=495&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=09509232&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-06-18 N1 - Date created - 1991-06-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Fluorouracil, doxorubicin, and cyclophosphamide versus fluorouracil, doxorubicin, and cyclophosphamide plus lonidamine for the treatment of advanced breast cancer: a multicentric randomized clinical study. AN - 80557759; 2031201 AB - Experimental models have demonstrated the Adriamycin (doxorubicin; Adria Laboratories, Columbus, OH)-potentiating activity of lonidamine. Phase II clinical trials on advanced breast cancer have shown that this drug induced a 16% objective response rate. Present multicentric randomized trial was conducted to verify whether lonidamine can potentiate the antineoplastic effects of conventional fluorouacil, Adriamycin, cyclophosphamide (FAC) chemotherapy in advanced breast cancer. From January 1987 to December 1989, 265 patients were enrolled in this study, and 231 are evaluable for response. After stratification according to institution and ECOG performance status (PS), the patients were randomly allocated to receive either standard FAC therapy (group A) or FAC plus lonidamine (600 mg orally daily three times a day) (group B). After three FAC courses, the patients with no progressive disease were further randomized to either receive continuous treatment up to the time of tumor progression (maximum: 10 courses) or to discontinue therapy when a response "plateau" was reached. In this latter group, the same therapy was restarted at relapse or disease progression. Objective response (complete response plus partial response) was significantly higher in group B (66.3%) compared to group A (42.3%). The actuarial median times to disease progression was also significantly longer (P less than 0.0001) in group B (median 9 months) than in group A (median 6 months). Other than myalgia and gastric pain, no increased toxicity was observed in the lonidamine. The analysis of second randomization are yet available because of the longer follow-up time required. Present findings suggest an interesting additive effect of lonidamine when combined with FAC chemotherapy and warrant further investigation in other therapeutic regimens and in other neoplastic diseases. JF - Seminars in oncology AU - Calabresi, F AU - Di Lauro, L AU - Marolla, P AU - Curcio, C G AU - Paoletti, G AU - Calabró, A AU - Giannarelli, D AU - Ballatore, P AU - Foggi, C M AU - Di Palma, M AD - Regina Elena National Cancer Institute, Rome, Italy. Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 66 EP - 72 VL - 18 IS - 2 Suppl 4 SN - 0093-7754, 0093-7754 KW - Antineoplastic Agents KW - 0 KW - Indazoles KW - Doxorubicin KW - 80168379AG KW - Cyclophosphamide KW - 8N3DW7272P KW - Fluorouracil KW - U3P01618RT KW - lonidamine KW - U78804BIDR KW - Index Medicus KW - Drug Administration Schedule KW - Prospective Studies KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Follow-Up Studies KW - Time Factors KW - Female KW - Remission Induction KW - Breast Neoplasms -- drug therapy KW - Cyclophosphamide -- administration & dosage KW - Doxorubicin -- adverse effects KW - Antineoplastic Agents -- administration & dosage KW - Doxorubicin -- administration & dosage KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Agents -- adverse effects KW - Cyclophosphamide -- adverse effects KW - Fluorouracil -- administration & dosage KW - Fluorouracil -- adverse effects KW - Indazoles -- adverse effects KW - Indazoles -- administration & dosage KW - Breast Neoplasms -- pathology KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80557759?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Seminars+in+oncology&rft.atitle=Fluorouracil%2C+doxorubicin%2C+and+cyclophosphamide+versus+fluorouracil%2C+doxorubicin%2C+and+cyclophosphamide+plus+lonidamine+for+the+treatment+of+advanced+breast+cancer%3A+a+multicentric+randomized+clinical+study.&rft.au=Calabresi%2C+F%3BDi+Lauro%2C+L%3BMarolla%2C+P%3BCurcio%2C+C+G%3BPaoletti%2C+G%3BCalabr%C3%B3%2C+A%3BGiannarelli%2C+D%3BBallatore%2C+P%3BFoggi%2C+C+M%3BDi+Palma%2C+M&rft.aulast=Calabresi&rft.aufirst=F&rft.date=1991-04-01&rft.volume=18&rft.issue=2+Suppl+4&rft.spage=66&rft.isbn=&rft.btitle=&rft.title=Seminars+in+oncology&rft.issn=00937754&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-06-17 N1 - Date created - 1991-06-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - 1990 Sir Henry Wellcome medal and prize winner. Leukoregulin: a new biotherapeutic cytokine in the search for more effective anti-viral pharmacologic agents. AN - 80555927; 1851546 AB - This investigation examines whether cytokines, as exemplified by leukoregulin, with their immense potential for biorecognition and target cell modulation as a result of their complex three-dimensional structure, have the potential to provide new directions for biotherapy of infectious disease. Leukoregulin is a naturally occurring immunologic cytokine, secreted by stimulated lymphocytes, which increases membrane permeability and drug uptake in tumor but not in normal cells. This study demonstrates that leukoregulin also increases the plasma membrane permeability of cells acutely infected with herpes simplex type 1 virus and that the increase in membrane permeability is accompanied by a 10- to 100-fold increase in the ability of acyclovir to inhibit the release of infectious virus when the cells are treated with leukoregulin 3 hours after infection with the virus. This is the first demonstration that a cytokine, alone or in combination with anti-viral chemotherapy, can effectively inhibit virus replication in human cells following acute virus infection, which indicates that combination immunotherapy and chemotherapy have the potential to completely inhibit the production of infectious virus by acutely infected human cells. JF - Military medicine AU - Evans, C H AU - Hooks, J J AU - Detrick, B AD - National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 155 EP - 159 VL - 156 IS - 4 SN - 0026-4075, 0026-4075 KW - Antineoplastic Agents KW - 0 KW - Antiviral Agents KW - Cytokines KW - Lymphokines KW - leukoregulin KW - Acyclovir KW - X4HES1O11F KW - Index Medicus KW - Animals KW - Guinea Pigs KW - Tumor Cells, Cultured -- drug effects KW - Acyclovir -- therapeutic use KW - Humans KW - Tumor Cells, Cultured -- microbiology KW - Drug Therapy, Combination KW - Simplexvirus -- drug effects KW - Virus Replication -- drug effects KW - Cell Membrane Permeability -- drug effects KW - Adolescent KW - Drug Synergism KW - Female KW - Antiviral Agents -- therapeutic use KW - Cytokines -- therapeutic use KW - Lymphokines -- pharmacology KW - Virus Diseases -- drug therapy KW - Lymphokines -- therapeutic use KW - Antineoplastic Agents -- therapeutic use KW - Antineoplastic Agents -- pharmacology KW - Virus Diseases -- microbiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80555927?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Military+medicine&rft.atitle=1990+Sir+Henry+Wellcome+medal+and+prize+winner.+Leukoregulin%3A+a+new+biotherapeutic+cytokine+in+the+search+for+more+effective+anti-viral+pharmacologic+agents.&rft.au=Evans%2C+C+H%3BHooks%2C+J+J%3BDetrick%2C+B&rft.aulast=Evans&rft.aufirst=C&rft.date=1991-04-01&rft.volume=156&rft.issue=4&rft.spage=155&rft.isbn=&rft.btitle=&rft.title=Military+medicine&rft.issn=00264075&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-06-19 N1 - Date created - 1991-06-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Hematologic effects of AIDS therapies. AN - 80536541; 1708759 AB - Hematologic abnormalities remain an important feature of HIV infection, and they often limit the therapy of this disorder. This is currently a field of intense research, and some progress has already been made. The current development of newer, less myelosuppressive therapies for HIV infection is encouraging. In addition, as more is learned about the biochemistry, molecular biology, and pathophysiology of HIV and its effects upon its host, more effective, HIV-specific, and less toxic therapies may be developed. Finally, the use of various cytokines to ameliorate toxicities and possibly stimulate the functioning of myeloid cells is a promising area of research and should be pursued further. However, in spite of these efforts, much more needs to be done. In particular, therapy of HIV-associated lymphoma, which is likely to be increasingly observed as AIDS patients live longer, is often entirely unsatisfactory, in part because patients cannot tolerate the hematologic toxicity of the regimens employed. As in the general field of oncology, hematologic toxicities in AIDS remains a major limitation of therapy, and advances in this area have the potential to markedly improve both survival and quality of life. JF - Hematology/oncology clinics of North America AU - Pluda, J M AU - Mitsuya, H AU - Yarchoan, R AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, Maryland. Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 229 EP - 248 VL - 5 IS - 2 SN - 0889-8588, 0889-8588 KW - Dideoxynucleosides KW - 0 KW - Granulocyte Colony-Stimulating Factor KW - 143011-72-7 KW - Zidovudine KW - 4B9XT59T7S KW - Zalcitabine KW - 6L3XT8CB3I KW - Macrophage Colony-Stimulating Factor KW - 81627-83-0 KW - Granulocyte-Macrophage Colony-Stimulating Factor KW - 83869-56-1 KW - Index Medicus KW - AIDS/HIV KW - Sarcoma, Kaposi -- drug therapy KW - Zidovudine -- adverse effects KW - Macrophage Colony-Stimulating Factor -- therapeutic use KW - Granulocyte Colony-Stimulating Factor -- therapeutic use KW - Humans KW - Dideoxynucleosides -- adverse effects KW - Granulocyte-Macrophage Colony-Stimulating Factor -- therapeutic use KW - Zalcitabine -- adverse effects KW - Bone Marrow -- drug effects KW - Acquired Immunodeficiency Syndrome -- complications KW - Acquired Immunodeficiency Syndrome -- blood KW - Acquired Immunodeficiency Syndrome -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80536541?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hematology%2Foncology+clinics+of+North+America&rft.atitle=Hematologic+effects+of+AIDS+therapies.&rft.au=Pluda%2C+J+M%3BMitsuya%2C+H%3BYarchoan%2C+R&rft.aulast=Pluda&rft.aufirst=J&rft.date=1991-04-01&rft.volume=5&rft.issue=2&rft.spage=229&rft.isbn=&rft.btitle=&rft.title=Hematology%2Foncology+clinics+of+North+America&rft.issn=08898588&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-06-06 N1 - Date created - 1991-06-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Childhood cancer mortality and radon concentration in drinking water in North Carolina. AN - 80529955; 2021549 AB - We explored the association between groundwater radon levels and childhood cancer mortality in North Carolina. Using data from two state-wide surveys of public drinking water supplies, counties were ranked according to average groundwater radon concentration. Age and sex-adjusted 1950-79 cancer death rates among children under age 15 were calculated for counties with high, medium, and low radon levels. Overall cancer mortality was increased in counties with medium and high radon levels. The strongest association was for the leukaemias, but risks were also suggested for other sites. These associations could be due to confounding or other biases, but the findings are consistent with other recent reports. JF - British journal of cancer AU - Collman, G W AU - Loomis, D P AU - Sandler, D P AD - Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 626 EP - 629 VL - 63 IS - 4 SN - 0007-0920, 0007-0920 KW - Water Pollutants, Radioactive KW - 0 KW - Radon KW - Q74S4N8N1G KW - Index Medicus KW - Risk Factors KW - Humans KW - Leukemia, Radiation-Induced -- mortality KW - Child KW - North Carolina -- epidemiology KW - Adolescent KW - Neoplasms, Radiation-Induced -- mortality KW - Water Pollutants, Radioactive -- adverse effects KW - Radon -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80529955?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+cancer&rft.atitle=Childhood+cancer+mortality+and+radon+concentration+in+drinking+water+in+North+Carolina.&rft.au=Collman%2C+G+W%3BLoomis%2C+D+P%3BSandler%2C+D+P&rft.aulast=Collman&rft.aufirst=G&rft.date=1991-04-01&rft.volume=63&rft.issue=4&rft.spage=626&rft.isbn=&rft.btitle=&rft.title=British+journal+of+cancer&rft.issn=00070920&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-06-04 N1 - Date created - 1991-06-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Scand J Work Environ Health. 1988 Oct;14(5):286-92 [3201187] Int Arch Occup Environ Health. 1988;61(1-2):13-8 [3198278] Lancet. 1989 Jul 8;2(8654):99-100 [2567891] BMJ. 1989 Jul 29;299(6694):289-93 [2504406] Lancet. 1990 Apr 28;335(8696):1008-12 [1970069] Nature. 1990 May 31;345(6274):389-90 [2188139] J Natl Cancer Inst. 1990 Jun 20;82(12):1025-30 [2348467] Pediatr Hematol Oncol. 1987;4(1):55-61 [2856360] Health Phys. 1969 May;16(5):571-8 [5795875] Health Phys. 1978 Jun;34(6):667-71 [730518] Scand J Work Environ Health. 1979 Mar;5(1):10-5 [441704] Health Phys. 1980 Jul;39(1):108-11 [7419400] Arch Environ Health. 1983 Jul-Aug;38(4):248-51 [6615007] N Engl J Med. 1984 Jun 7;310(23):1485-94 [6325913] Scand J Work Environ Health. 1984 Feb;10(1):25-34 [6740274] Health Phys. 1986 Jan;50(1):33-47 [3943972] Health Phys. 1986 May;50(5):605-18 [3700112] Health Phys. 1986 Jun;50(6):823-7 [3011707] Br Med J (Clin Res Ed). 1987 Mar 7;294(6572):597-602 [3103819] Int Arch Occup Environ Health. 1987;59(2):123-31 [3557623] Int J Epidemiol. 1987 Mar;16(1):7-12 [3570624] Arch Environ Health. 1987 Mar-Apr;42(2):87-91 [3579371] Cancer Res. 1989 Apr 1;49(7):1861-5 [2924324] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Induction of cytochrome P450 and other drug metabolizing enzymes in rat liver following dietary exposure to Aroclor 1254. AN - 80522385; 1902007 AB - Selected drug metabolizing activities were measured in female F344/NCr rats exposed to graded dietary concentrations of Aroclor 1254 (1 to 1000 ppm) for 7 days or to lower concentrations of Aroclor (1 to 10 ppm) for up to 28 days. Following the 7-day exposure, the hepatic O-dealkylation of ethoxyresorufin (ETR), mediated primarily by cytochrome P450IA, was increased 60-, 10-, and 4-fold by 33, 10, and 3 ppm Aroclor, respectively. In rats exposed to 10 and 3 ppm Aroclor for 28 days, this activity was increased approximately 30- and 10-fold, respectively. Hepatic ETR O-dealkylase activities correlated with Aroclor concentrations in the livers of exposed rats (r = 0.99, p less than 0.01). Although the O-dealkylation of benzyloxyresorufin was highly increased by 7-days dietary exposure to 1000 ppm Aroclor, the levels of Aroclor necessary for detection of induction were substantially higher than those required for detection of ETR O-dealkylase induction. Examination of the non-P450-mediated drug metabolizing activities, epoxide hydrolase and DT-diaphorase, similarly showed limited (approximately 10-fold) increases. In contrast, aldehyde dehydrogenase (benzaldehyde, NADP+) activity was highly increased (greater than 40-fold) at 1000 ppm, however this activity was increased to only a limited extent at lower Aroclor concentrations (e.g. approximately 3-fold at 33 ppm). These results support the potential use of cytochrome P450 activities as potential biomarkers for environmental exposure to PCBs and related compounds. JF - Toxicology and applied pharmacology AU - Lubet, R A AU - Jones, C R AU - Stockus, D L AU - Fox, S D AU - Nims, R W AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick, Maryland 21702. Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 355 EP - 365 VL - 108 IS - 2 SN - 0041-008X, 0041-008X KW - Aroclors KW - 0 KW - Chlorodiphenyl (54% Chlorine) KW - 11097-69-1 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Oxidoreductases KW - EC 1.- KW - Cytochrome P-450 CYP1A1 KW - EC 1.14.14.1 KW - Cytochrome P-450 CYP2B1 KW - Aldehyde Dehydrogenase KW - EC 1.2.1.3 KW - NAD(P)H Dehydrogenase (Quinone) KW - EC 1.6.5.2 KW - Quinone Reductases KW - EC 1.6.99.- KW - Index Medicus KW - Animals KW - Dose-Response Relationship, Drug KW - Quinone Reductases -- biosynthesis KW - Aldehyde Dehydrogenase -- biosynthesis KW - Rats KW - Kinetics KW - Body Weight -- drug effects KW - Enzyme Induction KW - Female KW - Oxidoreductases -- biosynthesis KW - Organ Size -- drug effects KW - Liver -- anatomy & histology KW - Liver -- enzymology KW - Liver -- drug effects KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Aroclors -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80522385?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Induction+of+cytochrome+P450+and+other+drug+metabolizing+enzymes+in+rat+liver+following+dietary+exposure+to+Aroclor+1254.&rft.au=Lubet%2C+R+A%3BJones%2C+C+R%3BStockus%2C+D+L%3BFox%2C+S+D%3BNims%2C+R+W&rft.aulast=Lubet&rft.aufirst=R&rft.date=1991-04-01&rft.volume=108&rft.issue=2&rft.spage=355&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 - 1991-05-17 N1 - Date created - 1991-05-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - 2,3,7,8-Tetrachlorodibenzo-p-dioxin stimulation of tyrosine phosphorylation in B lymphocytes: potential role in immunosuppression. AN - 80517521; 1850092 AB - The prototype halogenated aromatic hydrocarbon 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is carcinogenic and toxic in experimental animals. At the cellular level, TCDD toxicity is often expressed as an inhibition or alteration in normal cell maturation. In this respect, we and others have demonstrated that exposure of experimental animals to TCDD causes immunosuppression, including inhibition of B lymphocyte maturation and antibody synthesis. Although the immunological effects of TCDD are well described, little is known about its mechanism of action. In the present studies, it was found that TCDD increases membrane protein phosphorylation, which is, in part, associated with tyrosine-specific phosphorylation in B lymphocytes. This increase in phosphorylation occurred within minutes following TCDD treatment and was not associated with protein kinase C. The increase in tyrosine kinase by TCDD appears to be primarily due to de novo synthesis of new protein, because the protein synthesis inhibitors puromycin and cycloheximide, as well as the transcriptional inhibitor actinomycin D, partially inhibited the effect, although increased activity of preexisting protein cannot be fully dismissed. The dose response for increased phosphorylation by TCDD was identical to that we previously reported for inhibition of antibody synthesis, suggesting that immunosuppression by TCDD may be expressed through alterations in regulatory processes controlled by tyrosine kinases. These studies are discussed in terms of the potential role of TCDD-induced tyrosine phosphorylation in immunosuppression. JF - Molecular pharmacology AU - Clark, G C AU - Blank, J A AU - Germolec, D R AU - Luster, M I AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 495 EP - 501 VL - 39 IS - 4 SN - 0026-895X, 0026-895X KW - Membrane Proteins KW - 0 KW - Polychlorinated Dibenzodioxins KW - Receptors, Aryl Hydrocarbon KW - Receptors, Drug KW - Tyrosine KW - 42HK56048U KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Index Medicus KW - Stimulation, Chemical KW - Mice, Inbred Strains KW - Animals KW - Receptors, Drug -- metabolism KW - Membrane Proteins -- blood KW - Phosphorylation KW - Enzyme Activation KW - Mice KW - Tyrosine -- blood KW - Time Factors KW - Antibody Formation -- drug effects KW - Immunosuppression KW - B-Lymphocytes -- drug effects KW - Protein-Tyrosine Kinases -- genetics KW - Polychlorinated Dibenzodioxins -- toxicity KW - Protein-Tyrosine Kinases -- blood KW - B-Lymphocytes -- immunology KW - B-Lymphocytes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80517521?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=2%2C3%2C7%2C8-Tetrachlorodibenzo-p-dioxin+stimulation+of+tyrosine+phosphorylation+in+B+lymphocytes%3A+potential+role+in+immunosuppression.&rft.au=Clark%2C+G+C%3BBlank%2C+J+A%3BGermolec%2C+D+R%3BLuster%2C+M+I&rft.aulast=Clark&rft.aufirst=G&rft.date=1991-04-01&rft.volume=39&rft.issue=4&rft.spage=495&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 - 1991-05-21 N1 - Date created - 1991-05-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The effects of tri-o-cresyl phosphate and metabolites on rat Sertoli cell function in primary culture. AN - 80515820; 1902005 AB - A neurotoxic organophosphate, tri-o-cresyl phosphate (TOCP) is also a testicular toxicant. Histopathologic damage in the testis is first seen in Sertoli cells. TOCP and its activated metabolite saligenin cyclic-o-tolyl phosphate (SCOTP) were evaluated for effects on rat Sertoli cells in primary culture. SCOTP, but not TOCP, caused minor morphologic effects on the cells and increased levels of lactate in the spent medium with no change in pyruvate levels, synthesis of cellular or secreted proteins, or the cyclic AMP response to FSH stimulation. SCOTP was the metabolite of TOCP that produced the largest decrease in nonspecific esterase activity in Sertoli cells (up to 80%), when tested in the concentration range found in vivo. This decrease is consistent with previous in vivo evidence. These in vitro experiments replicate previously observed in vivo biochemical effects and suggest that SCOTP is the metabolite responsible for at least some of the biochemical effects seen in the testis after TOCP exposure. JF - Toxicology and applied pharmacology AU - Chapin, R E AU - Phelps, J L AU - Burka, L T AU - Abou-Donia, M B AU - Heindel, J J AD - Developmental and Reproductive Toxicology Group, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 194 EP - 204 VL - 108 IS - 2 SN - 0041-008X, 0041-008X KW - Androgen-Binding Protein KW - 0 KW - Lactates KW - Organophosphorus Compounds KW - Pyruvates KW - Tritolyl Phosphates KW - Vimentin KW - 2-(2-cresyl)-4H-1-3-2-benzodioxaphosphorin-2-oxide KW - 1222-87-3 KW - Pyruvic Acid KW - 8558G7RUTR KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Follicle Stimulating Hormone KW - 9002-68-0 KW - Carboxylic Ester Hydrolases KW - EC 3.1.1.- KW - Carboxylesterase KW - EC 3.1.1.1 KW - tri-o-cresyl phosphate KW - X8II18JD0A KW - Index Medicus KW - Protein Biosynthesis KW - Androgen-Binding Protein -- secretion KW - Animals KW - Carboxylic Ester Hydrolases -- metabolism KW - Intermediate Filaments -- metabolism KW - Lactates -- metabolism KW - Microtubules -- drug effects KW - Pyruvates -- metabolism KW - Intermediate Filaments -- drug effects KW - Rats KW - Cells, Cultured KW - Adenosine Triphosphate -- metabolism KW - Vimentin -- metabolism KW - Organophosphorus Compounds -- toxicity KW - Follicle Stimulating Hormone -- pharmacology KW - Male KW - Microscopy, Electron, Scanning KW - Sertoli Cells -- drug effects KW - Sertoli Cells -- cytology KW - Tritolyl Phosphates -- toxicity KW - Tritolyl Phosphates -- metabolism KW - Sertoli Cells -- metabolism KW - Sertoli Cells -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80515820?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+effects+of+tri-o-cresyl+phosphate+and+metabolites+on+rat+Sertoli+cell+function+in+primary+culture.&rft.au=Chapin%2C+R+E%3BPhelps%2C+J+L%3BBurka%2C+L+T%3BAbou-Donia%2C+M+B%3BHeindel%2C+J+J&rft.aulast=Chapin&rft.aufirst=R&rft.date=1991-04-01&rft.volume=108&rft.issue=2&rft.spage=194&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 - 1991-05-17 N1 - Date created - 1991-05-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Anti-HIV activity of CD4-Pseudomonas exotoxin on infected primary human lymphocytes and monocyte/macrophages. AN - 80500349; 2010626 AB - CD4(178)-PE40 is a recombinant protein consisting of a portion of human CD4 linked to active domains of Pseudomonas aeruginosa exotoxin A. In previous experiments with human T cell lines, the hybrid toxin was found to selectively kill cells infected with human immunodeficiency virus type 1 (HIV-1), and to inhibit HIV-1 spread in mixtures of infected and uninfected cells. CD4(178)-PE40 inhibits HIV-1 spread in cultured primary human lymphocytes. Moreover, the hybrid toxin selectively kills HIV-1 chronically infected monocyte/macrophage cell lines and inhibits HIV-1 spread in primary macrophage cultures. Control experiments indicate that the protective effects of CD4(178)-PE40 against HIV-1 spread are due to selective killing of the infected cells rather than simply to neutralization by the CD4 moiety. Thus, for the major cell types susceptible to HIV infection in vivo, surface envelope glycoprotein is expressed at sufficient levels to enable binding and internalization of CD4(178)-PE40 and consequent selective cell killing. JF - The Journal of infectious diseases AU - Ashorn, P AU - Englund, G AU - Martin, M A AU - Moss, B AU - Berger, E A AD - Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 703 EP - 709 VL - 163 IS - 4 SN - 0022-1899, 0022-1899 KW - Antigens, CD4 KW - 0 KW - Bacterial Proteins KW - CD4-Pseudomonas toxin KW - Exotoxins KW - Immunotoxins KW - Recombinant Proteins KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Cell Survival -- drug effects KW - Cell Count KW - Bacterial Proteins -- pharmacology KW - Dose-Response Relationship, Drug KW - Cells, Cultured KW - Humans KW - Flow Cytometry KW - Cell Line KW - Exotoxins -- pharmacology KW - Recombinant Proteins -- pharmacology KW - Macrophages -- microbiology KW - Monocytes -- drug effects KW - Monocytes -- microbiology KW - Macrophages -- drug effects KW - Lymphocytes -- microbiology KW - Immunotoxins -- pharmacology KW - Lymphocytes -- drug effects KW - HIV-1 -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80500349?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+infectious+diseases&rft.atitle=Anti-HIV+activity+of+CD4-Pseudomonas+exotoxin+on+infected+primary+human+lymphocytes+and+monocyte%2Fmacrophages.&rft.au=Ashorn%2C+P%3BEnglund%2C+G%3BMartin%2C+M+A%3BMoss%2C+B%3BBerger%2C+E+A&rft.aulast=Ashorn&rft.aufirst=P&rft.date=1991-04-01&rft.volume=163&rft.issue=4&rft.spage=703&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+infectious+diseases&rft.issn=00221899&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-05-06 N1 - Date created - 1991-05-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Detection of direct mutagenicity of cigarette smoke condensate in mammalian cells. AN - 80499872; 2013132 AB - Mutagenicity of cigarette smoke condensate (CSC) and the acidic, basic and neutral fractions of CSC was examined in the AL hybrid cell, a Chinese hamster ovary cell containing one human chromosome 11. Since the human chromosome 11 is not necessary for survival of the AL cells, mutations involving large deletions and chromosomal loss by non-dysjunction are non-lethal events that are detectable by loss of human cell surface antigens (a1, a2 and a3) encoded by genes on chromosome 11p (a1 and a3) and 11q (a2) through an antibody-complement lysis assay. Exposure of AL cells to CSC without exogenous metabolic activation caused a dose-dependent cytotoxicity and mutagenicity. Mutagenicity also increased with time of incubation up to 3 h with a maximum of 300 a1- mutants/10(5) survivors (250% above background; P less than 0.0005) after incubation with 100 micrograms/ml CSC. Cytotoxicity and mutagenicity of CSC were inversely proportional to cell density. Fifty percent lethal doses for the acidic, basic and neutral fractions of CSC after 3 h of incubation were 30, 100 and 240 micrograms/ml respectively, and the acidic fraction at a concentration of 25 micrograms/ml induced 350 a1- mutants/10(5) survivors (230% above background; P less than 0.0005); the basic and neutral fractions were less mutagenic. These results indicate that CSC and fractions of CSC can directly produce a spectrum of mutations, through both deletional and non-dysjunctional mechanisms of a kind known to lead to inactivation of tumor suppressor genes. JF - Carcinogenesis AU - Matsukura, N AU - Willey, J AU - Miyashita, M AU - Taffe, B AU - Hoffmann, D AU - Waldren, C AU - Puck, T T AU - Harris, C C AD - Laboratory of Human Carcinogenesis, NCI, Bethesda, MD 20892. Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 685 EP - 689 VL - 12 IS - 4 SN - 0143-3334, 0143-3334 KW - Mutagens KW - 0 KW - Smoke KW - Methylnitronitrosoguanidine KW - 12H3O2UGSF KW - Index Medicus KW - Animals KW - Methylnitronitrosoguanidine -- toxicity KW - Cricetulus KW - Cell Survival -- drug effects KW - Mutagenicity Tests -- methods KW - Dose-Response Relationship, Drug KW - Cells, Cultured KW - Hydrogen-Ion Concentration KW - Humans KW - Hybrid Cells -- drug effects KW - Time Factors KW - Cricetinae KW - Smoke -- adverse effects KW - Mutagens -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80499872?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Detection+of+direct+mutagenicity+of+cigarette+smoke+condensate+in+mammalian+cells.&rft.au=Matsukura%2C+N%3BWilley%2C+J%3BMiyashita%2C+M%3BTaffe%2C+B%3BHoffmann%2C+D%3BWaldren%2C+C%3BPuck%2C+T+T%3BHarris%2C+C+C&rft.aulast=Matsukura&rft.aufirst=N&rft.date=1991-04-01&rft.volume=12&rft.issue=4&rft.spage=685&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-05-14 N1 - Date created - 1991-05-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Anti-Tac-H, a humanized antibody to the interleukin 2 receptor, prolongs primate cardiac allograft survival. AN - 80497877; 2011577 AB - High-affinity interleukin 2 receptors (IL-2Rs) are expressed by T cells activated in response to foreign histocompatibility antigens but not by normal resting T cells. To exploit this difference in IL-2R expression, anti-Tac-M, a murine monoclonal antibody specific for the IL-2R alpha chain, was used to inhibit organ allograft rejection. However, the use of murine anti-Tac as an immunosuppressive agent was limited by neutralization by human anti-murine antibodies and by weak recruitment of effector functions. To circumvent these difficulties, a humanized antibody to the IL-2R, anti-Tac-H, was prepared. This molecule is human with the exception of the hypervariable segments, which are retained from the mouse. In vivo survival of anti-Tac-H is 2.5-fold longer than simultaneously administered anti-Tac-M (terminal t1/2, 103 hr vs. 38 hr). In addition, anti-Tac-H is less immunogenic than anti-Tac-M when administered to cynomolgus monkeys undergoing heterotopic cardiac allografting. Specifically, all monkeys treated with anti-Tac-M developed measurable anti-anti-Tac-M levels by day 15 (mean onset, 11 days). In contrast, none of the animals receiving anti-Tac-H produced measurable antibodies to this monoclonal antibody before day 33. Finally, there was a prolongation of graft survival in the cynomolgus heterotopic cardiac allograft model in animals receiving anti-Tac. In animals that received anti-Tac-M, the allograft survival was prolonged compared to that of the control group (mean survival, 14 +/- 1.98 days compared to 9.2 +/- 0.48 days; P less than 0.025). Graft survival was further prolonged by anti-Tac-H with a mean survival of 20.0 +/- 0.55 days (compared to controls, P less than 0.001; compared to anti-Tac-M, P less than 0.02). There was no toxicity attributable to the administration of either form of anti-Tac. Thus, anti-Tac-H significantly prolonged allograft survival in primates, without toxic side effects, and may be of value as an adjunct to standard immunosuppressive therapy in humans. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Brown, P S AU - Parenteau, G L AU - Dirbas, F M AU - Garsia, R J AU - Goldman, C K AU - Bukowski, M A AU - Junghans, R P AU - Queen, C AU - Hakimi, J AU - Benjamin, W R AD - Surgery Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/04/01/ PY - 1991 DA - 1991 Apr 01 SP - 2663 EP - 2667 VL - 88 IS - 7 SN - 0027-8424, 0027-8424 KW - Antibodies, Monoclonal KW - 0 KW - Receptors, Interleukin-2 KW - Index Medicus KW - Animals KW - Macaca fascicularis KW - Enzyme-Linked Immunosorbent Assay KW - Transplantation, Homologous KW - Heart Transplantation -- immunology KW - Antibodies, Monoclonal -- pharmacokinetics KW - Antibodies, Monoclonal -- metabolism KW - Graft Survival KW - Receptors, Interleukin-2 -- immunology KW - Antibodies, Monoclonal -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80497877?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Anti-Tac-H%2C+a+humanized+antibody+to+the+interleukin+2+receptor%2C+prolongs+primate+cardiac+allograft+survival.&rft.au=Brown%2C+P+S%3BParenteau%2C+G+L%3BDirbas%2C+F+M%3BGarsia%2C+R+J%3BGoldman%2C+C+K%3BBukowski%2C+M+A%3BJunghans%2C+R+P%3BQueen%2C+C%3BHakimi%2C+J%3BBenjamin%2C+W+R&rft.aulast=Brown&rft.aufirst=P&rft.date=1991-04-01&rft.volume=88&rft.issue=7&rft.spage=2663&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 - 1991-05-06 N1 - Date created - 1991-05-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Prog Allergy. 1969;13:1-110 [4186070] Transplantation. 1990 Nov;50(5):760-5 [2238051] J Immunol. 1976 Feb;116(2):518-26 [814165] J Immunol. 1981 Apr;126(4):1393-7 [6970774] J Immunol. 1983 Aug;131(2):690-6 [6408186] Hybridoma. 1985 Summer;4(2):91-102 [2408992] J Exp Med. 1985 Jul 1;162(1):358-62 [3925068] J Med Primatol. 1985;14(6):357-62 [3908687] Science. 1986 May 9;232(4751):727-32 [3008337] Lancet. 1987 Jun 13;1(8546):1339-42 [2884454] J Biol Chem. 1987 Dec 25;262(36):17336-41 [3121594] Am J Kidney Dis. 1988 Feb;11(2):101-6 [3124608] Curr Surg. 1988 Jan-Feb;45(1):28-30 [3126026] Blood. 1988 Nov;72(5):1805-16 [2846094] Lancet. 1988 Dec 17;2(8625):1394-9 [2904526] Proc Natl Acad Sci U S A. 1989 Jun;86(11):4220-4 [2726771] Annu Rev Biochem. 1989;58:875-911 [2673025] Proc Natl Acad Sci U S A. 1989 Dec;86(24):10029-33 [2513570] Cancer Res. 1990 Mar 1;50(5):1495-502 [2406013] J Clin Invest. 1970 Apr;49(4):673-80 [5443170] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Amphotericin B vs high-dose ketoconazole for empirical antifungal therapy among febrile, granulocytopenic cancer patients. A prospective, randomized study. AN - 80497671; 2012462 AB - We compared high-dose ketoconazole (800 mg/kg per day, orally) with amphotericin B (0.5 mg/kg per day, intravenously) for empirical antifungal therapy in a prospective, randomized study of persistently or recurrently febrile granulocytopenic cancer patients. Among 97 patients eligible for empirical antifungal therapy, 20 (21%) of these patients were ineligible for randomization to ketoconazole treatment because of their inability to tolerate oral medications. Among 72 patients eligible for randomization, 64 were assessable (32 in each arm of the study). Five of six patients with proved fungal infections who were randomized to receive ketoconazole treatment required crossover to amphotericin B treatment because of progressive infection. The conditions of three of these five patients improved after receiving amphotericin B. The frequency of transaminase elevation was higher in those receiving ketoconazole, while the frequency of azotemia was higher in those receiving amphotericin B. Bioavailability of ketoconazole was unpredictable. Amphotericin B remains the drug of choice for empirical antifungal therapy in granulocytopenic patients; whereas, lack of a parenteral formulation, ineffectiveness against proved mycoses, and unreliable bioavailability preclude high-dose ketoconazole from being an appropriate compound for this purpose. JF - Archives of internal medicine AU - Walsh, T J AU - Rubin, M AU - Hathorn, J AU - Gress, J AU - Thaler, M AU - Skelton, J AU - McKnight, J AU - Browne, M AU - Marshall, D AU - Cotton, D AD - Pediatric Branche, National Cancer Institute, National Institutes of Health, Bethesda, Md. 20892. Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 765 EP - 770 VL - 151 IS - 4 SN - 0003-9926, 0003-9926 KW - Amphotericin B KW - 7XU7A7DROE KW - Ketoconazole KW - R9400W927I KW - Abridged Index Medicus KW - Index Medicus KW - Prospective Studies KW - Humans KW - Adult KW - Immune Tolerance KW - Ketoconazole -- pharmacokinetics KW - Fever -- etiology KW - Agranulocytosis -- complications KW - Neoplasms -- complications KW - Mycoses -- complications KW - Ketoconazole -- therapeutic use KW - Ketoconazole -- administration & dosage KW - Amphotericin B -- adverse effects KW - Mycoses -- drug therapy KW - Amphotericin B -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80497671?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+internal+medicine&rft.atitle=Amphotericin+B+vs+high-dose+ketoconazole+for+empirical+antifungal+therapy+among+febrile%2C+granulocytopenic+cancer+patients.+A+prospective%2C+randomized+study.&rft.au=Walsh%2C+T+J%3BRubin%2C+M%3BHathorn%2C+J%3BGress%2C+J%3BThaler%2C+M%3BSkelton%2C+J%3BMcKnight%2C+J%3BBrowne%2C+M%3BMarshall%2C+D%3BCotton%2C+D&rft.aulast=Walsh&rft.aufirst=T&rft.date=1991-04-01&rft.volume=151&rft.issue=4&rft.spage=765&rft.isbn=&rft.btitle=&rft.title=Archives+of+internal+medicine&rft.issn=00039926&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-05-07 N1 - Date created - 1991-05-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Use of omeprazole in patients with Zollinger-Ellison syndrome. AN - 80489431; 2007355 AB - Omeprazole, a substituted benzimidazole, has been shown to be a potent inhibitor of gastric acid secretion in patients with Zollinger-Ellison syndrome (ZES). We review our experience, as well as the published data on 210 patients with ZES who have required omeprazole for control of gastric acid hypersecretion over the past seven years. The dose of omeprazole required in individual patients ranged from 10 to 180 mg/24 hr with 20-60% requiring a split dosage regimen. Omeprazole was effective in approximately 99% of the patients over a period ranging from 0.5 to 54 months. Twenty-four percent of patients required an increase in omeprazole dose, while 26% required a decrease in dose. Adverse effects attributable to omeprazole were reported in 2% of patients, and in all cases, they were mild (ie, rash, constipation, headache). There was no effect of omeprazole on serum gastrin concentration or on gastric endocrine cells in three studies. Although one patient with multiple endocrine neoplasia, type-I syndrome (MEN-I) in this series developed a gastric carcinoid while taking omeprazole, evidence is presented that suggests the presence of MEN-I per se may be important in determining the development of gastric carcinoid in patients with ZES. It is concluded that omeprazole is safe and effective in patients with ZES, and in these patients, it is the drug of choice for the management of gastric acid hypersecretion. However, yearly assessment is indicated to clearly evaluate the long-term risk of gastric carcinoid as well as therapy directed at the gastrinoma itself. JF - Digestive diseases and sciences AU - Frucht, H AU - Maton, P N AU - Jensen, R T AD - Digestive Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 394 EP - 404 VL - 36 IS - 4 SN - 0163-2116, 0163-2116 KW - Omeprazole KW - KG60484QX9 KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Zollinger-Ellison Syndrome -- drug therapy KW - Omeprazole -- adverse effects KW - Omeprazole -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80489431?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Digestive+diseases+and+sciences&rft.atitle=Use+of+omeprazole+in+patients+with+Zollinger-Ellison+syndrome.&rft.au=Frucht%2C+H%3BMaton%2C+P+N%3BJensen%2C+R+T&rft.aulast=Frucht&rft.aufirst=H&rft.date=1991-04-01&rft.volume=36&rft.issue=4&rft.spage=394&rft.isbn=&rft.btitle=&rft.title=Digestive+diseases+and+sciences&rft.issn=01632116&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-05-02 N1 - Date created - 1991-05-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Dig Dis Sci. 1992 Aug;37(8):1308-9 [1354155] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A recombinant human receptor antagonist to interleukin 1 improves survival after lethal endotoxemia in mice. AN - 80487093; 1826127 AB - Interleukin 1 (IL-1) is an endogenously produced cytokine that mediates a variety of physiological effects that may be beneficial or deleterious to the host. C57Bl/6 mice treated intravenously with a recently characterized human recombinant receptor antagonist protein to IL-1 (IL-1ra) had improved survival when treated after a lethal Escherichia coli endotoxin (lipopolysaccharide [LPS]) challenge. IL-1ra was effective when treatment was initiated after LPS, and intravenous administration every 4 h for 24 h was required. Serum levels of tumor necrosis factor (TNF) activity after LPS and in vitro TNF cytotoxicity were not altered by treatment with IL-1ra. These experiments provide direct evidence that the lethal effects of LPS may be mediated through the action of IL-1 and that the IL-1ra can provide a new treatment strategy for disease processes mediated via this cytokine. JF - The Journal of experimental medicine AU - Alexander, H R AU - Doherty, G M AU - Buresh, C M AU - Venzon, D J AU - Norton, J A AD - Surgical Metabolism Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/04/01/ PY - 1991 DA - 1991 Apr 01 SP - 1029 EP - 1032 VL - 173 IS - 4 SN - 0022-1007, 0022-1007 KW - Endotoxins KW - 0 KW - IL1RN protein, human KW - Il1rn protein, mouse KW - Interleukin 1 Receptor Antagonist Protein KW - Lipopolysaccharides KW - Proteins KW - Receptors, Immunologic KW - Receptors, Interleukin-1 KW - Sialoglycoproteins KW - Tumor Necrosis Factor-alpha KW - Index Medicus KW - Animals KW - Lipopolysaccharides -- antagonists & inhibitors KW - Mice, Inbred C57BL KW - Escherichia coli KW - Mice KW - Tumor Necrosis Factor-alpha -- metabolism KW - Time Factors KW - Female KW - Proteins -- pharmacology KW - Endotoxins -- toxicity KW - Endotoxins -- blood KW - Receptors, Immunologic -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80487093?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+recombinant+human+receptor+antagonist+to+interleukin+1+improves+survival+after+lethal+endotoxemia+in+mice.&rft.au=Alexander%2C+H+R%3BDoherty%2C+G+M%3BBuresh%2C+C+M%3BVenzon%2C+D+J%3BNorton%2C+J+A&rft.aulast=Alexander&rft.aufirst=H&rft.date=1991-04-01&rft.volume=173&rft.issue=4&rft.spage=1029&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 - 1991-04-26 N1 - Date created - 1991-04-26 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Lab Invest. 1987 Mar;56(3):234-48 [3029503] J Immunol Methods. 1984 Mar 30;68(1-2):167-75 [6707477] J Immunol Methods. 1987 May 4;99(1):47-52 [3106502] Immunol Lett. 1988 Nov;19(3):183-91 [3069706] J Exp Med. 1988 Jun 1;167(6):1987-92 [3290384] Clin Immunol Immunopathol. 1989 Dec;53(3):400-21 [2680192] J Exp Med. 1989 Nov 1;170(5):1627-33 [2809510] J Clin Invest. 1989 Jul;84(1):228-35 [2786888] J Exp Med. 1989 Sep 1;170(3):1015-20 [2788701] Infect Immun. 1988 Sep;56(9):2255-63 [3261716] J Clin Invest. 1988 Apr;81(4):1162-72 [3258319] Nature. 1987 Dec 17-23;330(6149):662-4 [3317066] J Clin Invest. 1986 Mar;77(3):1020-7 [3512598] Nature. 1990 Jan 25;343(6256):341-6 [2137201] Nature. 1990 Jan 25;343(6256):336-40 [2137200] Surg Gynecol Obstet. 1988 Feb;166(2):147-53 [3122336] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Macrophage- and astrocyte-derived transforming growth factor beta as a mediator of central nervous system dysfunction in acquired immune deficiency syndrome. AN - 80486956; 2007861 AB - The multifunctional cytokine, transforming growth factor beta (TGF-beta), was identified by immunocytochemistry in the brain tissues of four patients with acquired immune deficiency syndrome (AIDS), but not in control brain tissue. The TGF-beta staining was localized to cells of monocytic lineage as well as astrocytes, especially in areas of brain pathology. In addition, the brain tissues from the AIDS patients contained transcripts for human immunodeficiency virus 1 (HIV-1) by in situ hybridization, suggesting a correlation between the presence of HIV-1 in the brain and the expression of TGF-beta. However, the expression of TGF-beta was not limited to HIV-1-positive cells, raising the possibility of alternative mechanisms for the induction of TGF-beta in these AIDS patients' brains. To investigate these mechanisms, purified human monocytes were infected in vitro with HIV-1 and were shown to secrete increased levels of TGF-beta. In addition, HIV-1-infected monocytes released a factor(s) capable of triggering cultured astrocytes that are not infected with HIV-1 to secrete TGF-beta. The release of TGF-beta, which is an extremely potent chemotactic factor, may contribute to the recruitment of HIV-1-infected monocytic cells, enabling viral spread to and within the central nervous system (CNS). Moreover, TGF-beta augments cytokine production, including cytokines known to be neurotoxic. The identification of TGF-beta within the CNS implicates this cytokine in the immunopathologic processes responsible for AIDS-related CNS dysfunction. JF - The Journal of experimental medicine AU - Wahl, S M AU - Allen, J B AU - McCartney-Francis, N AU - Morganti-Kossmann, M C AU - Kossmann, T AU - Ellingsworth, L AU - Mai, U E AU - Mergenhagen, S E AU - Orenstein, J M AD - Laboratory of Immunology, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/04/01/ PY - 1991 DA - 1991 Apr 01 SP - 981 EP - 991 VL - 173 IS - 4 SN - 0022-1007, 0022-1007 KW - RNA, Messenger KW - 0 KW - Transforming Growth Factor beta KW - Index Medicus KW - AIDS/HIV KW - Blotting, Northern KW - Humans KW - Monocytes -- metabolism KW - In Vitro Techniques KW - Brain -- microbiology KW - HIV-1 -- growth & development KW - RNA, Messenger -- genetics KW - Male KW - Transforming Growth Factor beta -- physiology KW - Astrocytes -- physiology KW - Macrophages -- physiology KW - AIDS Dementia Complex -- physiopathology KW - Transforming Growth Factor beta -- genetics KW - Astrocytes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80486956?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Macrophage-+and+astrocyte-derived+transforming+growth+factor+beta+as+a+mediator+of+central+nervous+system+dysfunction+in+acquired+immune+deficiency+syndrome.&rft.au=Wahl%2C+S+M%3BAllen%2C+J+B%3BMcCartney-Francis%2C+N%3BMorganti-Kossmann%2C+M+C%3BKossmann%2C+T%3BEllingsworth%2C+L%3BMai%2C+U+E%3BMergenhagen%2C+S+E%3BOrenstein%2C+J+M&rft.aulast=Wahl&rft.aufirst=S&rft.date=1991-04-01&rft.volume=173&rft.issue=4&rft.spage=981&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 - 1991-04-26 N1 - Date created - 1991-04-26 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Brain Res. 1989 Jul 10;491(2):394-7 [2765895] J Clin Invest. 1989 Sep;84(3):733-7 [2474573] Immunol Today. 1989 Aug;10(8):258-61 [2478145] J Immunol. 1989 Nov 15;143(10):3222-9 [2809198] J Clin Invest. 1990 Jan;85(1):192-9 [2295695] J Immunol. 1990 Jan 15;144(2):480-4 [2295799] Ann N Y Acad Sci. 1990;593:188-96 [1695824] Science. 1990 Aug 3;249(4968):549-53 [2200125] Growth Factors. 1990;3(2):139-46 [2206556] Proc Natl Acad Sci U S A. 1990 Nov;87(21):8321-5 [1700428] Growth Factors. 1990;4(1):27-35 [1707635] Am J Pathol. 1987 Mar;126(3):403-10 [3548405] J Immunol. 1982 Dec;129(6):2413-9 [6982921] Ann Neurol. 1983 Oct;14(4):403-18 [6314874] Cell Immunol. 1984 May;85(2):373-83 [6232002] J Biol Chem. 1984 Aug 10;259(15):9756-61 [6086646] Am J Clin Pathol. 1984 Dec;82(6):678-82 [6095642] J Clin Invest. 1984 Dec;74(6):2121-8 [6511917] Science. 1985 Jan 11;227(4683):177-82 [2981429] Mol Cell Biol. 1985 Jan;5(1):242-7 [3856735] Nature. 1985 Aug 22-28;316(6030):701-5 [3861940] Clin Chim Acta. 1986 Mar 16;155(2):143-50 [2421949] Science. 1986 Jul 11;233(4760):215-9 [3014648] Science. 1986 Sep 5;233(4768):1089-93 [3016903] J Biol Chem. 1986 Sep 15;261(26):12362-7 [3528157] Proc Natl Acad Sci U S A. 1986 Sep;83(18):7089-93 [3018755] JAMA. 1986 Nov 7;256(17):2365-71 [3490587] J Clin Invest. 1987 Jul;80(1):101-6 [3496359] Anal Biochem. 1987 Apr;162(1):156-9 [2440339] Proc Natl Acad Sci U S A. 1987 Aug;84(16):5788-92 [2886992] Proc Natl Acad Sci U S A. 1987 Sep;84(17):6020-4 [2888109] J Immunol. 1987 Oct 15;139(8):2593-7 [3116087] J Cell Biol. 1987 Dec;105(6 Pt 2):2861-76 [3320058] J Leukoc Biol. 1988 Jan;43(1):91-7 [3275735] Hum Pathol. 1988 Mar;19(3):350-61 [3346011] J Exp Med. 1988 Apr 1;167(4):1428-41 [3258626] J Immunol. 1988 May 1;140(9):3026-32 [3129508] Ann Neurol. 1988 Apr;23(4):339-46 [3132891] J Neurosci. 1988 Jun;8(6):1901-4 [2455024] J Exp Med. 1988 Oct 1;168(4):1403-17 [2971758] Proc Natl Acad Sci U S A. 1989 Jan;86(2):621-5 [2536171] Oncogene Res. 1988;2(2):135-48 [3217109] J Infect Dis. 1989 Mar;159(3):467-71 [2915167] Arch Intern Med. 1989 Apr;149(4):941-3 [2705847] J Immunol. 1989 May 15;142(10):3553-9 [2541200] J Virol. 1989 Oct;63(10):4404-8 [2789293] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Principles of treatment of pediatric solid tumors. AN - 80484205; 2006077 AB - Great strides have been made in the treatment of pediatric solid tumors over the last three decades. A multimodality approach involving a combination of surgery, radiation therapy, and chemotherapy is now used in the treatment of these diseases. This article reviews the principles that guide the use of these modalities and the multidisciplinary approach used to integrate them into a coordinated treatment plan. The role of each modality in the control of local and systemic disease is described. Radiation treatment planning, dose fractionation, and toxicity are also discussed. JF - Pediatric clinics of North America AU - Berg, S L AU - Grisell, D L AU - DeLaney, T F AU - Balis, F M AD - Pediatric Branch, National Cancer Institute, Bethesda, Maryland. Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 249 EP - 267 VL - 38 IS - 2 SN - 0031-3955, 0031-3955 KW - Antineoplastic Agents KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Combined Modality Therapy KW - Radiotherapy Dosage KW - Humans KW - Antineoplastic Agents -- pharmacokinetics KW - Drug Resistance KW - Child KW - Antineoplastic Agents -- therapeutic use KW - Antineoplastic Agents -- adverse effects KW - Neoplasms -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80484205?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pediatric+clinics+of+North+America&rft.atitle=Principles+of+treatment+of+pediatric+solid+tumors.&rft.au=Berg%2C+S+L%3BGrisell%2C+D+L%3BDeLaney%2C+T+F%3BBalis%2C+F+M&rft.aulast=Berg&rft.aufirst=S&rft.date=1991-04-01&rft.volume=38&rft.issue=2&rft.spage=249&rft.isbn=&rft.btitle=&rft.title=Pediatric+clinics+of+North+America&rft.issn=00313955&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-22 N1 - Date created - 1991-04-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Threshold dose for peripheral neuropathy following intraoperative radiotherapy (IORT) in a large animal model. AN - 80484119; 2004946 AB - Radiation injury to peripheral nerve is a dose-limiting toxicity in the clinical application of intraoperative radiotherapy, particularly for pelvic and retroperitoneal tumors. Intraoperative radiotherapy-related peripheral neuropathy in humans receiving doses of 20-25 Gy is manifested as a mixed motor-sensory deficit beginning 6-9 months following treatment. In a previous experimental study of intraoperative radiotherapy-related neuropathy of the lumbro-sacral plexus, an approximate inverse linear relationship was reported between the intraoperative dose (20-75 Gy range) and the time to onset of hind limb paresis (1-12 mos following intraoperative radiotherapy). The principal histological lesion in irradiated nerve was loss of large nerve fibers and perineural fibrosis without significant vascular injury. Similar histological changes in irradiated nerves were found in humans. To assess peripheral nerve injury to lower doses of intraoperative radiotherapy in this same large animal model, groups of four adult American Foxhounds (wt 20-25 kg) received doses of 10, 15, or 20 Gy to the right lumbro-sacral plexus and sciatic nerve using 9 MeV electrons. The left lumbro-sacral plexus and sciatic nerve were excluded from the intraoperative field to allow each animal to serve as its own control. Following treatment, a complete neurological exam, electromyogram, and nerve conduction studies were performed monthly for 1 year. Monthly neurological exams were performed in years 2 and 3 whereas electromyogram and nerve conduction studies were performed every 3 months during this follow-up period. With follow-up of greater than or equal to 42 months, no dog receiving 10 or 15 Gy IORT shows any clinical or laboratory evidence of peripheral nerve injury. However, all four dogs receiving 20 Gy developed right hind limb paresis at 8, 9, 9, and 12 mos following intraoperative radiotherapy. These experimental data suggest that intraoperative doses of less than 20 Gy may not result in clinically significant peripheral nerve injury with follow-up of 3.5 years. Longer (5 yrs) follow-up with planned sacrifice of the remaining dogs is scheduled to assess any late peripheral nerve damage. JF - International journal of radiation oncology, biology, physics AU - Kinsella, T J AU - DeLuca, A M AU - Barnes, M AU - Anderson, W AU - Terrill, R AU - Sindelar, W F AD - Radiation Oncology Branch, National Cancer Institute, Bethesda, MD 20205. Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 697 EP - 701 VL - 20 IS - 4 SN - 0360-3016, 0360-3016 KW - Index Medicus KW - Sciatic Nerve -- radiation effects KW - Animals KW - Radiotherapy Dosage KW - Muscles -- innervation KW - Neural Conduction -- radiation effects KW - Electromyography KW - Dogs KW - Intraoperative Period KW - Peripheral Nerves -- radiation effects KW - Radiation Injuries, Experimental -- physiopathology KW - Radiotherapy -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80484119?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+radiation+oncology%2C+biology%2C+physics&rft.atitle=Threshold+dose+for+peripheral+neuropathy+following+intraoperative+radiotherapy+%28IORT%29+in+a+large+animal+model.&rft.au=Kinsella%2C+T+J%3BDeLuca%2C+A+M%3BBarnes%2C+M%3BAnderson%2C+W%3BTerrill%2C+R%3BSindelar%2C+W+F&rft.aulast=Kinsella&rft.aufirst=T&rft.date=1991-04-01&rft.volume=20&rft.issue=4&rft.spage=697&rft.isbn=&rft.btitle=&rft.title=International+journal+of+radiation+oncology%2C+biology%2C+physics&rft.issn=03603016&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-19 N1 - Date created - 1991-04-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - New insights into the causes of cancer. AN - 80483288; 2006074 AB - Recent advances in molecular biologic analysis have led to major new insights concerning the genetic mechanisms underlying the development of cancer. This article examines the current state of our understanding of the genetic basis underlying the possible mechanisms of carcinogenesis and metastasis. The nature of the genetic lesions found in some cancer-causing genes, cancer-inhibiting genes, growth factor genes, and metastasis genes is discussed, as is the impact that these may have on clinical oncology. JF - Pediatric clinics of North America AU - Helman, L J AU - Thiele, C J AD - Molecular Genetics Section, National Cancer Institute, Bethesda, Maryland. Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 201 EP - 221 VL - 38 IS - 2 SN - 0031-3955, 0031-3955 KW - Carcinogens KW - 0 KW - Genetic Markers KW - Growth Substances KW - Abridged Index Medicus KW - Index Medicus KW - Oncogenes KW - Genes, Tumor Suppressor KW - Neoplasm Metastasis KW - Carcinogens -- toxicity KW - Mutation -- genetics KW - Ploidies KW - Neoplasms -- therapy KW - Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80483288?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pediatric+clinics+of+North+America&rft.atitle=New+insights+into+the+causes+of+cancer.&rft.au=Helman%2C+L+J%3BThiele%2C+C+J&rft.aulast=Helman&rft.aufirst=L&rft.date=1991-04-01&rft.volume=38&rft.issue=2&rft.spage=201&rft.isbn=&rft.btitle=&rft.title=Pediatric+clinics+of+North+America&rft.issn=00313955&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-22 N1 - Date created - 1991-04-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Single-chain immunotoxins directed at the human transferrin receptor containing Pseudomonas exotoxin A or diphtheria toxin: anti-TFR(Fv)-PE40 and DT388-anti-TFR(Fv). AN - 80481537; 2005905 AB - Two single-chain immunotoxins directed at the human transferrin receptor have been constructed by using polymerase chain reaction-based methods. Anti-TFR(Fv)-PE40 is encoded by a gene fusion between the DNA sequence encoding the antigen-binding portion (Fv) of a monoclonal antibody directed at the human transferrin receptor and that encoding a 40,000-molecular-weight fragment of Pseudomonas exotoxin (PE40). The other fusion protein, DT388-anti-TFR(Fv), is encoded by a gene fusion between the DNA encoding a truncated form of diphtheria toxin and that encoding the antigen-binding portion of antibody to human transferrin receptor. These gene fusions were expressed in Escherichia coli, and fusion proteins were purified by conventional chromatography techniques to near homogeneity. In anti-TFR(Fv)-PE40, the antigen-binding portion is placed at the amino terminus of the toxin, while in DT388-anti-TFR(Fv), it is at the carboxyl end of the toxin. Both these single-chain immunotoxins kill cells bearing the human transferrin receptors. However, anti-TFR(Fv)-PE40 was usually more active than DT388-anti-TFR(Fv), and in some cases it was several-hundred-fold more active. Anti-TFR(Fv)-PE40 was also more active on cell lines than a conjugate made by chemically coupling the native antibody to PE40, and in some cases it was more than 100-fold more active. JF - Molecular and cellular biology AU - Batra, J K AU - Fitzgerald, D J AU - Chaudhary, V K AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 2200 EP - 2205 VL - 11 IS - 4 SN - 0270-7306, 0270-7306 KW - Bacterial Toxins KW - 0 KW - Diphtheria Toxin KW - Exotoxins KW - Immunotoxins KW - Receptors, Transferrin KW - Recombinant Fusion Proteins KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - Animals KW - Electrophoresis, Polyacrylamide Gel KW - Humans KW - Escherichia coli -- genetics KW - Amino Acid Sequence KW - Mice KW - Plasmids KW - Cell Survival KW - Cloning, Molecular KW - Polymerase Chain Reaction KW - Base Sequence KW - Tumor Cells, Cultured KW - Binding, Competitive KW - Molecular Sequence Data KW - Exotoxins -- genetics KW - Immunotoxins -- toxicity KW - Diphtheria Toxin -- toxicity KW - Immunotoxins -- metabolism KW - Diphtheria Toxin -- genetics KW - Receptors, Transferrin -- metabolism KW - Receptors, Transferrin -- genetics KW - Exotoxins -- toxicity KW - Immunotoxins -- genetics KW - Receptors, Transferrin -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80481537?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Single-chain+immunotoxins+directed+at+the+human+transferrin+receptor+containing+Pseudomonas+exotoxin+A+or+diphtheria+toxin%3A+anti-TFR%28Fv%29-PE40+and+DT388-anti-TFR%28Fv%29.&rft.au=Batra%2C+J+K%3BFitzgerald%2C+D+J%3BChaudhary%2C+V+K%3BPastan%2C+I&rft.aulast=Batra&rft.aufirst=J&rft.date=1991-04-01&rft.volume=11&rft.issue=4&rft.spage=2200&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 - 1991-04-22 N1 - Date created - 1991-04-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nature. 1989 Jun 1;339(6223):394-7 [2498664] J Biol Chem. 1988 Jul 5;263(19):9470-5 [3132465] Proc Natl Acad Sci U S A. 1989 Nov;86(21):8545-9 [2510169] Proc Natl Acad Sci U S A. 1990 Jan;87(1):308-12 [2104981] Proc Natl Acad Sci U S A. 1990 Feb;87(3):1066-70 [2105495] J Biol Chem. 1990 May 5;265(13):7331-7 [2332431] J Biol Chem. 1990 Sep 5;265(25):15198-202 [2118522] Cancer Treat Res. 1988;37:113-22 [2908621] Cancer Treat Res. 1988;37:123-40 [2908622] J Biol Chem. 1990 Nov 25;265(33):20678-85 [2122978] J Natl Cancer Inst. 1989 Oct 4;81(19):1455-63 [2550658] Nature. 1970 Aug 15;227(5259):680-5 [5432063] Science. 1972 Feb 25;175(4024):901-3 [4621498] J Biol Chem. 1973 Jun 10;248(11):3838-44 [4196584] Anal Biochem. 1976 May 7;72:248-54 [942051] J Immunol. 1981 Jul;127(1):347-51 [6787129] Cancer Res. 1985 Feb;45(2):751-7 [2981613] Proc Natl Acad Sci U S A. 1986 Mar;83(5):1320-4 [3006045] Cell. 1986 Dec 5;47(5):641-8 [3536124] Cell. 1987 Jan 16;48(1):129-36 [3098436] Proc Natl Acad Sci U S A. 1987 Jul;84(13):4538-42 [3299371] Science. 1987 Nov 20;238(4830):1098-104 [3317828] J Biol Chem. 1988 Feb 15;263(5):2518-25 [3339019] J Biol Chem. 1989 Sep 15;264(26):15709-13 [2768283] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Second cancers following non-Hodgkin's lymphoma. AN - 80478753; 2004317 AB - The risk of second malignancies following non-Hodgkin's lymphoma (NHL) was estimated in 29,153 patients diagnosed with NHL between 1973 and 1987 in one of nine areas participating in the National Cancer Institute's Surveillance, Epidemiology, and End Results Program. Compared with the general population, NHL patients were at a significantly increased risk of developing second cancers (observed/expected [O/E] = 1.18; O = 1231). The O/E ratio increased significantly with time to reach 1.77 in 10-year survivors. Significant excesses were noted for acute nonlymphocytic leukemia (O/E = 2.88), cancers of the bladder (O/E = 1.30), kidney (O/E = 1.47), and lung (O/E = 1.57), malignant melanoma (O/E = 2.44), and Hodgkin's disease (O/E = 4.16). Chemotherapy appeared related to subsequent acute nonlymphocytic leukemia (ANLL) and bladder cancer. Radiation therapy was associated with ANLL and possibly cancers of the lung, bladder, and bone. Malignant melanoma was not clearly related to initial NHL treatment. JF - Cancer AU - Travis, L B AU - Curtis, R E AU - Boice, J D AU - Hankey, B F AU - Fraumeni, J F AD - Epidemiology and Biostatistics Program, National Cancer Institute, National Institutes of Health, U.S. Department of Health and Human Services, Bethesda, Maryland 20892. Y1 - 1991/04/01/ PY - 1991 DA - 1991 Apr 01 SP - 2002 EP - 2009 VL - 67 IS - 7 SN - 0008-543X, 0008-543X KW - Antineoplastic Agents KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Neoplasm Staging KW - Neoplasms, Radiation-Induced -- pathology KW - Combined Modality Therapy KW - Risk Factors KW - Neoplasms, Radiation-Induced -- epidemiology KW - Humans KW - Incidence KW - Middle Aged KW - Follow-Up Studies KW - Male KW - Female KW - Antineoplastic Agents -- adverse effects KW - Neoplasms, Multiple Primary -- etiology KW - Neoplasms, Multiple Primary -- pathology KW - Neoplasms, Multiple Primary -- epidemiology KW - Lymphoma, Non-Hodgkin -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80478753?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Second+cancers+following+non-Hodgkin%27s+lymphoma.&rft.au=Travis%2C+L+B%3BCurtis%2C+R+E%3BBoice%2C+J+D%3BHankey%2C+B+F%3BFraumeni%2C+J+F&rft.aulast=Travis&rft.aufirst=L&rft.date=1991-04-01&rft.volume=67&rft.issue=7&rft.spage=2002&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-22 N1 - Date created - 1991-04-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Diethylstilbestrol metabolites and analogs: differential ligand effects on estrogen receptor interactions with nuclear matrix sites. AN - 80475291; 2004602 AB - Estradiol (E), diethylstilbestrol (DES), and three structurally similar DES derivatives and analogs, consisting of racemic mixtures of indenestrol-A (IA; rac), indenestrol-B (IB; rac), and the Z-isomer of pseudo-DES (PD) were used as probes to determine the effect of ligand on receptor-nuclear acceptor site interactions. IA (rac), IB (rac), and Z-PD have been previously shown to interact with the mouse uterine estrogen receptor with high affinity (Kd, approximately 1.5-2.2 x 10(-10) M), occupy similar levels of receptor in the nucleus in vivo, and have nuclear retention times similar to those of E and DES. However, in spite of these similarities, they differentially stimulate estrogenic responses that were previously thought to be interrelated and obligatory for full estrogenic action. In an attempt to elucidate the mechanism of differential stimulation of estrogen-regulated responses, the temporal pattern of KCl-resistant receptor sites was examined after a single injection of E, DES, IA (rac), IB (rac), Z-PD, or saline. Z-PD displayed lower levels of KCl-resistant receptor than the other compounds, whereas IA (rac) and IB (rac) had patterns similar to those of E and DES. In cell-free binding assays, all of the different receptor-ligand complexes were equally effective at competitively inhibiting the binding of receptor-[3H]E complexes to mouse uterine nuclear matrix with a Ki of 1.1 x 10(-10) M. Direct binding analysis showed no difference in the number of nuclear binding sites (range, 40.4-63.9 fmol/100 micrograms DNA) or Kd (range, 1.3-1.8 x 10(-10) M) among the different receptor-ligand complexes. Dissociation studies performed at 4 C showed no differences among the different complexes. In contrast, Z-PD-receptor complexes dissociated much faster from matrix sites at 22 C than any of the other complexes. Significant differences were noted in the proportion of complexes that were resistant to extraction with 0.6 M KCl. Forty-three percent of receptor-E complexes and 44% of receptor-DES complexes were resistant to KCl extraction, while 61% of receptor-IA and 29% of receptor-PD complexes were resistant to extraction, paralleling their activity in eliciting some estrogenic responses. In contrast, no difference was seen by gel shift assays in the ability of the ligand-receptor complexes to bind to a specific PS2 estrogen-responsive DNA sequence. These results demonstrate that the ligand may significantly affect the interaction of the estrogen receptor with nuclear acceptor sites. JF - Endocrinology AU - Metzger, D A AU - Curtis, S AU - Korach, K S AD - Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 1785 EP - 1791 VL - 128 IS - 4 SN - 0013-7227, 0013-7227 KW - Indenes KW - 0 KW - Receptors, Estrogen KW - pseudodiethylstilbestrol KW - 39011-86-4 KW - indenestrol KW - 4A464K3BSI KW - Estradiol KW - 4TI98Z838E KW - Potassium Chloride KW - 660YQ98I10 KW - Diethylstilbestrol KW - 731DCA35BT KW - DNA KW - 9007-49-2 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Mice, Inbred ICR KW - DNA -- metabolism KW - Potassium Chloride -- pharmacology KW - Estradiol -- pharmacology KW - Mice KW - Estradiol -- metabolism KW - Uterus -- metabolism KW - Indenes -- pharmacology KW - Kinetics KW - Nuclear Matrix -- metabolism KW - Binding, Competitive KW - Indenes -- metabolism KW - Female KW - Diethylstilbestrol -- metabolism KW - Receptors, Estrogen -- drug effects KW - Diethylstilbestrol -- pharmacology KW - Diethylstilbestrol -- analogs & derivatives KW - Receptors, Estrogen -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80475291?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Diethylstilbestrol+metabolites+and+analogs%3A+differential+ligand+effects+on+estrogen+receptor+interactions+with+nuclear+matrix+sites.&rft.au=Metzger%2C+D+A%3BCurtis%2C+S%3BKorach%2C+K+S&rft.aulast=Metzger&rft.aufirst=D&rft.date=1991-04-01&rft.volume=128&rft.issue=4&rft.spage=1785&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=00137227&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-23 N1 - Date created - 1991-04-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The National Institute on Drug Abuse and methadone maintenance treatment. AN - 72594401; 1765885 JF - Journal of psychoactive drugs AU - Schuster, C R AD - National Institute on Drug Abuse, Rockville, Maryland 20857. PY - 1991 SP - 111 EP - 112 VL - 23 IS - 2 SN - 0279-1072, 0279-1072 KW - Methadone KW - UC6VBE7V1Z KW - Index Medicus KW - United States KW - Humans KW - Cost-Benefit Analysis KW - National Institutes of Health (U.S.) KW - Opioid-Related Disorders -- rehabilitation KW - Opioid-Related Disorders -- economics KW - Methadone -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72594401?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+psychoactive+drugs&rft.atitle=The+National+Institute+on+Drug+Abuse+and+methadone+maintenance+treatment.&rft.au=Schuster%2C+C+R&rft.aulast=Schuster&rft.aufirst=C&rft.date=1991-04-01&rft.volume=23&rft.issue=2&rft.spage=111&rft.isbn=&rft.btitle=&rft.title=Journal+of+psychoactive+drugs&rft.issn=02791072&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-14 N1 - Date created - 1992-02-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Kinetics of superoxide production by stimulated neutrophils. AN - 72113128; 1654777 AB - Oxygen-derived active species and superoxide radical in particular are generated and excreted upon granulocyte activation and are instrumental in host defense against bacterial and fungal infections. Associated with the activation of neutrophils is an apparent transitory oxy-radical production. Evidence from independent methods has previously suggested that radical production peaks shortly following neutrophil stimulation and decays within minutes. However, since neutrophil function in the body might reasonably be expected to last beyond the few minutes following stimulation, cessation of the production of oxy-radicals is unexpected. In an attempt to reconcile this discrepancy, the formation kinetics of superoxide by stimulated human neutrophils was reinvestigated by three independent methods: electron spin resonance, chemiluminescence, and ferricytochrome c reduction. The present results demonstrate that under appropriate experimental conditions stimulated neutrophils have the capacity to produce superoxide for several hours. The reasons for the previously reported "apparent" ephemeral nature of oxy-radical formation are discussed. JF - Archives of biochemistry and biophysics AU - Black, C D AU - Samuni, A AU - Cook, J A AU - Krishna, C M AU - Kaufman, D C AU - Malech, H L AU - Russo, A AD - Radiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 126 EP - 131 VL - 286 IS - 1 SN - 0003-9861, 0003-9861 KW - Superoxides KW - 11062-77-4 KW - Peroxidase KW - EC 1.11.1.7 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Luminescent Measurements KW - Granulocytes -- metabolism KW - Kinetics KW - Humans KW - Electron Spin Resonance Spectroscopy KW - In Vitro Techniques KW - Granulocytes -- drug effects KW - Peroxidase -- blood KW - Neutrophils -- metabolism KW - Neutrophils -- drug effects KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Superoxides -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72113128?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Kinetics+of+superoxide+production+by+stimulated+neutrophils.&rft.au=Black%2C+C+D%3BSamuni%2C+A%3BCook%2C+J+A%3BKrishna%2C+C+M%3BKaufman%2C+D+C%3BMalech%2C+H+L%3BRusso%2C+A&rft.aulast=Black&rft.aufirst=C&rft.date=1991-04-01&rft.volume=286&rft.issue=1&rft.spage=126&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 - 1991-10-24 N1 - Date created - 1991-10-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - On the significance of Lhermitte's sign in oncology. AN - 72101674; 1895161 AB - We present three cases of Lhermitte's sign out of twenty consecutive cases of epidural spinal cord compression due to metastatic cancer. The three patients were diagnosed with epidural thoracic compressions. The literature on Lhermitte's sign is reviewed with emphasis on the differential diagnosis of this symptom in oncological patients. JF - Journal of neuro-oncology AU - Ventafridda, V AU - Caraceni, A AU - Martini, C AU - Sbanotto, A AU - De Conno, F AD - Pain Therapy and Palliative Care Division, National Cancer Institute of Milan, Italy. Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 133 EP - 137 VL - 10 IS - 2 SN - 0167-594X, 0167-594X KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Demyelinating Diseases -- complications KW - Diagnosis, Differential KW - Lung Neoplasms KW - Humans KW - Adult KW - Breast Neoplasms KW - Middle Aged KW - Cisplatin -- adverse effects KW - Male KW - Female KW - Radiotherapy -- adverse effects KW - Spinal Cord Neoplasms -- secondary KW - Paresthesia -- etiology KW - Spinal Cord Neoplasms -- diagnosis KW - Spinal Cord Compression -- etiology KW - Spinal Cord Compression -- diagnosis KW - Spinal Cord Neoplasms -- complications KW - Paresthesia -- diagnosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72101674?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+neuro-oncology&rft.atitle=On+the+significance+of+Lhermitte%27s+sign+in+oncology.&rft.au=Ventafridda%2C+V%3BCaraceni%2C+A%3BMartini%2C+C%3BSbanotto%2C+A%3BDe+Conno%2C+F&rft.aulast=Ventafridda&rft.aufirst=V&rft.date=1991-04-01&rft.volume=10&rft.issue=2&rft.spage=133&rft.isbn=&rft.btitle=&rft.title=Journal+of+neuro-oncology&rft.issn=0167594X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-10-22 N1 - Date created - 1991-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - T cell receptor beta-chain usage in experimental autoimmune uveoretinitis. AN - 72070319; 1652969 AB - Genomic rearrangements to the T-cell receptor (TCR) V beta 8 gene locus were examined in T cells derived from the lymph nodes of Lewis rats immunized with either S-Antigen or peptides derived from interphotoreceptor retinoid binding protein (IRBP). The cells used in these studies are from T-cell lines that have been selected by several cycles of antigen/IL-2 stimulations, or clones isolated from these lines. No apparent rearrangement of the V beta 8 gene was observed by Southern analysis, suggesting that if indeed there are T cells using V beta 8 gene elements they represent small proportions of the cells in these T-cell lines that induce EAU (uveitogenic T cells) and that the lines may consist of large numbers of clones. On the other hand, we have demonstrated V beta 8 gene expression in uveitogenic T-cell populations by Northern analysis and by polymerase chain reaction (PCR). Although V beta 8 gene transcripts were detectable in pathogenic, but not in non-pathogenic, T-cell lines using a V beta 8 cDNA probe, RNA from pathogenic T cell lines did not hybridize to another probe specific for rat V beta 8.2. Taken together, these results suggest that, unlike the T-cell lines that mediate experimental allergic encephalomyelitis (EAE), some T-cell lines that induce EAU do not predominantly express V beta 8.2 gene but other member(s) of the V beta 8 family. JF - Journal of autoimmunity AU - Egwuagu, C E AU - Chow, C AU - Beraud, E AU - Caspi, R R AU - Mahdi, R M AU - Brézin, A P AU - Nussenblatt, R B AU - Gery, I AD - Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 315 EP - 324 VL - 4 IS - 2 SN - 0896-8411, 0896-8411 KW - V&bgr;8 KW - Antigens KW - 0 KW - Arrestin KW - Eye Proteins KW - Receptors, Antigen, T-Cell KW - Receptors, Antigen, T-Cell, alpha-beta KW - Retinol-Binding Proteins KW - interstitial retinol-binding protein KW - Index Medicus KW - Animals KW - Eye Proteins -- toxicity KW - Retinol-Binding Proteins -- toxicity KW - Multigene Family KW - Rats, Inbred Lew -- genetics KW - Antigens -- toxicity KW - Immunization KW - Rats, Inbred Lew -- immunology KW - Rats KW - Base Sequence KW - Retinol-Binding Proteins -- immunology KW - Eye Proteins -- immunology KW - Immunotherapy, Adoptive KW - Molecular Sequence Data KW - Antigens -- immunology KW - Cell Line KW - Uveitis, Posterior -- immunology KW - T-Lymphocytes, Cytotoxic -- transplantation KW - Uveitis, Posterior -- etiology KW - Uveitis, Posterior -- genetics KW - Gene Rearrangement, beta-Chain T-Cell Antigen Receptor KW - T-Lymphocytes, Cytotoxic -- immunology KW - Receptors, Antigen, T-Cell -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72070319?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+autoimmunity&rft.atitle=T+cell+receptor+beta-chain+usage+in+experimental+autoimmune+uveoretinitis.&rft.au=Egwuagu%2C+C+E%3BChow%2C+C%3BBeraud%2C+E%3BCaspi%2C+R+R%3BMahdi%2C+R+M%3BBr%C3%A9zin%2C+A+P%3BNussenblatt%2C+R+B%3BGery%2C+I&rft.aulast=Egwuagu&rft.aufirst=C&rft.date=1991-04-01&rft.volume=4&rft.issue=2&rft.spage=315&rft.isbn=&rft.btitle=&rft.title=Journal+of+autoimmunity&rft.issn=08968411&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-10-08 N1 - Date created - 1991-10-08 N1 - Date revised - 2017-01-13 N1 - Gene symbol - V&bgr;8 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transfer of 45Ca and 36Cl at the blood-nerve barrier of the sciatic nerve in rats fed low or high calcium diets. AN - 72034208; 1908025 AB - Unidirectional fluxes of 45Ca, 36Cl, and of [3H]mannitol from blood into the sciatic nerve and cerebral cortex were determined from 5- and 15-min uptakes of these tracers after an intravenous (i.v.) bolus injection in awake rats. Rats were fed diets for 8 wk, that had either a low (0.01% wt/wt), normal (0.67%), or high (3%) Ca content. Plasma [Ca] was 32% less and 11% more in rats fed low (LOCA) and high Ca diets (HICA), respectively, than in rats fed a normal Ca diet (CONT). The mean permeability-surface area product (PA) of 45Ca at the blood-nerve barrier was about eightfold higher than at the blood-brain barrier in the same animals and did not differ significantly between groups (greater than 0.05). Mean PA ratios of 45Ca/36Cl for the blood-nerve and blood-brain barriers in CONT rats, 0.52 +/- 0.04 and 0.40 +/- 0.02, respectively, were not significantly different from corresponding ratios in LOCA and HICA groups, and corresponded to the aqueous limiting diffusion ratio (0.45). Our results show no evidence for concentration-dependent transport of Ca over a plasma [Ca] range of 0.8-1.4 mmol/liter at the blood-nerve barrier of the rat peripheral nerve, and suggest that Ca and Cl exchange slowly between nerve and blood via paracellular pathways. JF - Journal of neuroscience research AU - Wadhwani, K C AU - Murphy, V A AU - Rapoport, S I AD - Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 563 EP - 566 VL - 28 IS - 4 SN - 0360-4012, 0360-4012 KW - Calcium Radioisotopes KW - 0 KW - Calcium, Dietary KW - Chlorides KW - Radioisotopes KW - Mannitol KW - 3OWL53L36A KW - Chlorine KW - 4R7X1O2820 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Blood-Brain Barrier -- drug effects KW - Permeability -- drug effects KW - Animals KW - Body Weight -- drug effects KW - Mannitol -- metabolism KW - Homeostasis -- drug effects KW - Male KW - Calcium -- metabolism KW - Calcium -- blood KW - Calcium, Dietary -- pharmacology KW - Calcium -- cerebrospinal fluid KW - Sciatic Nerve -- metabolism KW - Chlorides -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72034208?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Transfer+of+45Ca+and+36Cl+at+the+blood-nerve+barrier+of+the+sciatic+nerve+in+rats+fed+low+or+high+calcium+diets.&rft.au=Wadhwani%2C+K+C%3BMurphy%2C+V+A%3BRapoport%2C+S+I&rft.aulast=Wadhwani&rft.aufirst=K&rft.date=1991-04-01&rft.volume=28&rft.issue=4&rft.spage=563&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 - 1991-09-19 N1 - Date created - 1991-09-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differentiation of PC12 cells with K-ras: comparison with nerve growth factor. AN - 72034158; 1651400 AB - The cell line PC12, derived from a rat pheochromocytoma, has served as a model for studies on the mechanism of action of nerve growth factor, as well as for the exploration of neuronal differentiation in general. When treated with nanomolar concentrations of nerve growth factor, these neoplastic chromaffin-like cells stop dividing and acquire, for all intents and purposes, the phenotype of mature sympathetic neurons. This phenotype is characterized by the extensive outgrowth of electrically excitable neurites, the ability to form functional synapses, and the acquisition of a number of biochemical markers. Treatment of PC12 cells with retroviral vectors encoding the K-ras, the N-ras, or the v-src oncogenes also produces a marked morphological differentiation very similar to that seen upon treatment with nerve growth factor. Treated cells stop dividing and develop an extensive network of neurites. It has recently been shown that PC12 cells differentiated with v-src, while resembling, morphologically, those treated with nerve growth factor, differ substantially in the biochemical characteristics normally associated with nerve growth factor-induced differentiation. Cells infected with K-ras also develop a neurite network similar to that seen after treatment with nerve growth factor. In addition, such cells develop tetanus toxin-binding sites and saxitoxin-binding sites, as do cells treated with nerve growth factor. Decreases in the binding of epidermal growth factor and in the activity of calpain also occur and these, as well, are characteristic of nerve growth factor-treated cells. But the adhesive properties of cells infected with K-ras are different than those of nerve growth factor-treated cells, and the former do not show an increase in the NILE glycoprotein. Finally, K-252a, an inhibitor of the actions of nerve growth factor on PC12 cells, has no effect on the neurite outgrowth produced by infection with K-ras. Thus, many of the key markers of nerve growth factor-induced differentiation of PC12 cells also appear upon differentiation with K-ras, but there are, nevertheless, some crucial differences in the properties of these two sets of cells. JF - Journal of neuroscience research AU - Simpson, D L AU - Dickens, G AU - Doll, S AU - Koizumi, S AU - Tocco, M AU - Okuda, O AU - Oshima, M AU - Rudkin, B B AU - Brightman, M AU - Guroff, G AD - National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 486 EP - 496 VL - 28 IS - 4 SN - 0360-4012, 0360-4012 KW - K-ras KW - Amphibian Proteins KW - 0 KW - Carbazoles KW - Carrier Proteins KW - Indole Alkaloids KW - Membrane Glycoproteins KW - Nerve Growth Factors KW - Neural Cell Adhesion Molecule L1 KW - Sodium Channels KW - Tetanus Toxin KW - saxitoxin-binding protein, Rana catesbeiana KW - staurosporine aglycone KW - 97161-97-2 KW - Sodium KW - 9NEZ333N27 KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Calpain KW - EC 3.4.22.- KW - Index Medicus KW - Animals KW - Receptor, Epidermal Growth Factor -- metabolism KW - Carrier Proteins -- metabolism KW - Sarcoma Viruses, Murine KW - Neurons -- drug effects KW - Sodium Channels -- metabolism KW - Calpain -- metabolism KW - Rats KW - Protein Kinase C -- antagonists & inhibitors KW - Transfection KW - Tetanus Toxin -- metabolism KW - Carbazoles -- pharmacology KW - Down-Regulation -- drug effects KW - Sodium Channels -- drug effects KW - Cell Line KW - Sodium -- metabolism KW - Membrane Glycoproteins -- metabolism KW - Genes, ras KW - Nerve Growth Factors -- pharmacology KW - Cell Differentiation -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72034158?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Differentiation+of+PC12+cells+with+K-ras%3A+comparison+with+nerve+growth+factor.&rft.au=Simpson%2C+D+L%3BDickens%2C+G%3BDoll%2C+S%3BKoizumi%2C+S%3BTocco%2C+M%3BOkuda%2C+O%3BOshima%2C+M%3BRudkin%2C+B+B%3BBrightman%2C+M%3BGuroff%2C+G&rft.aulast=Simpson&rft.aufirst=D&rft.date=1991-04-01&rft.volume=28&rft.issue=4&rft.spage=486&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 - 1991-09-19 N1 - Date created - 1991-09-19 N1 - Date revised - 2017-01-13 N1 - Gene symbol - K-ras N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Script Generation as an Indicator of Knowledge Representation in Patients with Alzheimer's Disease AN - 58259680; 9107493 AB - Activation of script memory was examined in Dementia-Alzheimer's type (DAT) patients, elderly depressed patients, & normal controls (N = 29, 14, & 31, respectively) in closely age- & education-matched samples. Analysis of results indicates that DAT patients were impaired on word generation & sentence cloze tasks; they scored poorly on free-associates & letter fluency. Depressed patients were impaired only on free-associate word generation. When asked to name events that occurred between getting up in the morning & leaving the house, DAT patients produced significantly fewer events than did depressed patients or controls. For all groups, the earliest events named were rated most central to the script, especially for the first six events produced. DAT patients produced more "beyond-script-boundary" events (implausible events given the context of the script) compared to depressed & normal Ss. Findings support the idea that script event productions, like category-based lexical production, are impaired in DAT patients. It is suggested that scripts are a separate representational system stored in prefrontal cortex devoted to memory of sequential events with a typical thematic structure. Dissociations of knowledge production is discussed. 1 Table, 7 Figures, 35 References. M. Lemons JF - Brain and Language AU - Grafman, Jordan AU - Thompson, Karen AU - Weingartner, Herbert AU - Martinez, Rick AU - Lawlor, Brian A AU - Sunderland, Trey AD - Cognitive Neuroscience Section Medical Neurology Branch NINDS/NIH, Bethesda MD 20892 Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 344 EP - 358 VL - 40 IS - 3 SN - 0093-934X, 0093-934X KW - script memory activation, Dementia-Alzheimer's vs elderly depressed vs normal subjects KW - empirical data KW - Brain Anatomy (br1) KW - Memory (me3) KW - Nervous System Pathology (ne3) KW - article KW - 6410: language-pathological and normal; language-pathological and normal UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/58259680?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Allba&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+and+Language&rft.atitle=Script+Generation+as+an+Indicator+of+Knowledge+Representation+in+Patients+with+Alzheimer%27s+Disease&rft.au=Grafman%2C+Jordan%3BThompson%2C+Karen%3BWeingartner%2C+Herbert%3BMartinez%2C+Rick%3BLawlor%2C+Brian+A%3BSunderland%2C+Trey&rft.aulast=Grafman&rft.aufirst=Jordan&rft.date=1991-04-01&rft.volume=40&rft.issue=3&rft.spage=344&rft.isbn=&rft.btitle=&rft.title=Brain+and+Language&rft.issn=0093934X&rft_id=info:doi/ LA - English DB - Linguistics and Language Behavior Abstracts (LLBA) N1 - Date revised - 2003-10-01 N1 - Last updated - 2016-09-27 N1 - CODEN - BRLGAZ N1 - SubjectsTermNotLitGenreText - Nervous System Pathology (ne3); Brain Anatomy (br1); Memory (me3) ER - TY - JOUR T1 - Geological characteristics and origin of the Hadamio gold-bearing cryptoexplosion breccia zone, Inner Mongolia AN - 50395388; 1992-059699 JF - Bulletin of the Chinese Academy of Geological Sciences AU - Nie, Fengjun AU - Zhang, Hongtao AU - Sun, Hao AU - Fan, Jianting Y1 - 1991/04// PY - 1991 DA - April 1991 SP - 81 EP - 90 PB - Chinese Academy of Geological Sciences, Beijing VL - 22 SN - 0254-3176, 0254-3176 KW - mineral deposits, genesis KW - Inner Mongolia China KW - petrology KW - Far East KW - Northern China KW - igneous processes KW - economic geology KW - pipes KW - Hadamio KW - breccia pipes KW - intrusions KW - metal ores KW - gold ores KW - Asia KW - China KW - 27A:Economic geology, geology of ore deposits KW - 05A:Igneous and metamorphic petrology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/50395388?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ageorefmodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bulletin+of+the+Chinese+Academy+of+Geological+Sciences&rft.atitle=Geological+characteristics+and+origin+of+the+Hadamio+gold-bearing+cryptoexplosion+breccia+zone%2C+Inner+Mongolia&rft.au=Nie%2C+Fengjun%3BZhang%2C+Hongtao%3BSun%2C+Hao%3BFan%2C+Jianting&rft.aulast=Nie&rft.aufirst=Fengjun&rft.date=1991-04-01&rft.volume=22&rft.issue=&rft.spage=81&rft.isbn=&rft.btitle=&rft.title=Bulletin+of+the+Chinese+Academy+of+Geological+Sciences&rft.issn=02543176&rft_id=info:doi/ LA - Chinese DB - GeoRef N1 - Copyright - GeoRef, Copyright 2012, American Geosciences Institute. N1 - Date revised - 1992-01-01 N1 - Number of references - 7 N1 - Document feature - charts, 2 tables, geol. sketch maps N1 - Last updated - 2012-06-07 N1 - SubjectsTermNotLitGenreText - Asia; breccia pipes; China; economic geology; Far East; gold ores; Hadamio; igneous processes; Inner Mongolia China; intrusions; metal ores; mineral deposits, genesis; Northern China; petrology; pipes ER - TY - JOUR T1 - Parachloroamphetamine selectively alters regional cerebral metabolic responses to the serotonergic agonist metachlorophenylpiperazine in rats. AN - 80701771; 1713115 AB - To determine if reported reductions of regional cerebral metabolic rates for glucose (rCMRglc) induced by the 5-HT agent metachlorophenylpiperazine (MCPP) (2.5 mg/kg) are due to a presynaptic action, 3-month old Fischer-344 rats were given parachloroamphetamine (PCA), a serotonin neurotoxin, and rCMRglc was measured 1 or 3 weeks later with the quantitative autoradiographic [14C]2-deoxyglucose procedure in 74 brain regions after administering saline, MCPP or other drugs. PCA alone increased rCMRglc significantly only in the raphe nuclei and in visual structures (visual cortex, lateral geniculate, superior colliculus). MCPP alone reduced rCMRglc in 75% of the regions studied. In PCA-lesioned rats, metabolic responses to MCPP 2.5 mg/kg were virtually abolished and rCMRglc was increased in interanteromedial and centrolateral thalamic nuclei. rCMRglc responses to quipazine, a postsynaptic serotonin agonist, and to arecoline and bromocriptine, cholinergic and dopaminergic agonists, were unchanged by PCA-pretreatment. Selective abolition by PCA of the metabolic response to MCPP confirms that MCPP, at the dose studied, reduces rCMRglc in the forebrain via a presynaptic mechanism and that postsynaptic serotonergic function is not altered by PCA. JF - Brain research AU - Freo, U AU - Larson, D M AU - Tolliver, T AU - Rapoport, S I AU - Soncrant, T T AD - Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/03/22/ PY - 1991 DA - 1991 Mar 22 SP - 17 EP - 25 VL - 544 IS - 1 SN - 0006-8993, 0006-8993 KW - Biogenic Amines KW - 0 KW - Piperazines KW - Serotonin KW - 333DO1RDJY KW - Bromocriptine KW - 3A64E3G5ZO KW - Arecoline KW - 4ALN5933BH KW - Quipazine KW - 4WCY05C0SJ KW - Hydroxyindoleacetic Acid KW - 54-16-0 KW - p-Chloroamphetamine KW - 64-12-0 KW - Deoxyglucose KW - 9G2MP84A8W KW - 1-(3-chlorophenyl)piperazine KW - REY0CNO998 KW - Index Medicus KW - Rats KW - Biogenic Amines -- metabolism KW - Animals KW - Rats, Inbred F344 KW - Quipazine -- pharmacology KW - Arecoline -- pharmacology KW - Kinetics KW - Hydroxyindoleacetic Acid -- metabolism KW - Bromocriptine -- pharmacology KW - Organ Specificity KW - Male KW - p-Chloroamphetamine -- pharmacology KW - Brain -- drug effects KW - Brain -- metabolism KW - Serotonin -- metabolism KW - Piperazines -- pharmacology KW - Deoxyglucose -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80701771?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Parachloroamphetamine+selectively+alters+regional+cerebral+metabolic+responses+to+the+serotonergic+agonist+metachlorophenylpiperazine+in+rats.&rft.au=Freo%2C+U%3BLarson%2C+D+M%3BTolliver%2C+T%3BRapoport%2C+S+I%3BSoncrant%2C+T+T&rft.aulast=Freo&rft.aufirst=U&rft.date=1991-03-22&rft.volume=544&rft.issue=1&rft.spage=17&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 - 1991-08-29 N1 - Date created - 1991-08-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cancer in populations living near nuclear facilities. A survey of mortality nationwide and incidence in two states. AN - 80467716; 1999880 AB - Reports from the United Kingdom have described increases in leukemia and lymphoma among young persons living near certain nuclear installations. Because of concerns raised by these reports, a mortality survey was conducted in populations living near nuclear facilities in the United States. All facilities began service before 1982. Over 900,000 cancer deaths occurred from 1950 through 1984 in 107 counties with or near nuclear installations. Each study county was matched for comparison to three "control counties" in the same region. There were 1.8 million cancer deaths in the 292 control counties during the 35 years studied. Deaths due to leukemia or other cancers were not more frequent in the study counties than in the control counties. For childhood leukemia mortality, the relative risk comparing the study counties with their controls before plant start-up was 1.08, while after start-up it was 1.03. For leukemia mortality at all ages, the relative risks were 1.02 before start-up and 0.98 after. For counties in two states, cancer incidence data were also available. For one facility, the standardized registration ratio for childhood leukemia was increased significantly after start-up. However, the increase also antedated the operation of this facility. The study is limited by the correlational approach and the large size of the geographic areas (counties) used. It does not prove the absence of any effect. If, however, any excess cancer risk was present in US counties with nuclear facilities, it was too small to be detected with the methods employed. JF - JAMA AU - Jablon, S AU - Hrubec, Z AU - Boice, J D AD - Radiation Epidemiology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/03/20/ PY - 1991 DA - 1991 Mar 20 SP - 1403 EP - 1408 VL - 265 IS - 11 SN - 0098-7484, 0098-7484 KW - Abridged Index Medicus KW - Index Medicus KW - Leukemia, Radiation-Induced -- epidemiology KW - Risk Factors KW - Humans KW - Adult KW - Leukemia, Radiation-Induced -- mortality KW - Environmental Exposure KW - Incidence KW - Child KW - United States -- epidemiology KW - Male KW - Female KW - Neoplasms, Radiation-Induced -- epidemiology KW - Neoplasms, Radiation-Induced -- mortality KW - Nuclear Reactors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80467716?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cancer+in+populations+living+near+nuclear+facilities.+A+survey+of+mortality+nationwide+and+incidence+in+two+states.&rft.au=Jablon%2C+S%3BHrubec%2C+Z%3BBoice%2C+J+D&rft.aulast=Jablon&rft.aufirst=S&rft.date=1991-03-20&rft.volume=265&rft.issue=11&rft.spage=1403&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-10 N1 - Date created - 1991-04-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: JAMA. 1991 Aug 7;266(5):652-5 [2072473] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Increased toxicity of anthracycline antibiotics induced by calcium entry blockers in cultured cardiomyocytes. AN - 80486682; 2006501 AB - Calcium channel blocking drugs have been reported to reduce survival rate of laboratory animals treated with cardiotoxic antitumor anthracyclines. In order to elucidate the mechanisms of this drug interaction, cell toxicity of the anthracyclines, doxorubicin and daunorubicin, was evaluated in primary cultures of cardiac myocytes isolated from neonatal rats. Low concentrations of extracellular calcium ([Ca2+]0) and addition of calcium entry blockers (nifedipine or flunarizine) potentiated myocardial toxicity of anthracyclines as assessed by the release of lactate dehydrogenase from the cells. Accumulation of anthracyclines in the cardiomyocytes was increased by calcium entry blockers (nifedipine, flunarizine, and verapamil) and by low [Ca2+]0; efflux of [3H]daunorubicin from myocardial cells was inhibited by nifedipine. At a dose that exerts only modest calcium channel activity, R-verapamil failed to affect doxorubicin accumulation in cardiomyocytes, whereas the calcium channel activator, (+/-)-Bay K-8644, reduced the retention of anthracyclines; the calcium channel activity is thus required in order to increase the accumulation of anthracyclines in myocardial cells. Calcium channel blockers are also known to increase intracellular retention and toxicity of chemotherapeutic drugs in multidrug resistant tumor cells by inhibiting the efflux of cytotoxic agents from cells; however, the ability of the interacting drugs to inhibit the efflux of chemotherapeutic agents from tumor cells is not dependent on the calcium channel blocking activity. Therefore, the mechanism(s) by which calcium channel blocking drugs increase the accumulation of anthracyclines in resistant tumor cells and myocardial cells may be different. In accordance with previous investigations, the present in vitro study confirmed that anthracycline-induced cardiotoxicity may be potentiated by calcium channel blocking drugs. This indicates that, in the association of antineoplastic drugs with agents that reverse multidrug resistance, the potential exists for enhanced damage of normal cells and tissues; further studies are needed to evaluate the relevance of this adverse interaction. JF - Toxicology and applied pharmacology AU - Santostasi, G AU - Kutty, R K AU - Krishna, G AD - Section on Drug-Tissue Interaction, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/03/15/ PY - 1991 DA - 1991 Mar 15 SP - 140 EP - 149 VL - 108 IS - 1 SN - 0041-008X, 0041-008X KW - Antibiotics, Antineoplastic KW - 0 KW - Calcium Channel Blockers KW - Doxorubicin KW - 80168379AG KW - Nifedipine KW - I9ZF7L6G2L KW - Flunarizine KW - R7PLA2DM0J KW - Daunorubicin KW - ZS7284E0ZP KW - Index Medicus KW - Rats KW - Nifedipine -- pharmacology KW - Doxorubicin -- pharmacokinetics KW - Animals KW - Doxorubicin -- pharmacology KW - Cells, Cultured KW - Drug Resistance KW - Drug Synergism KW - Flunarizine -- pharmacology KW - Daunorubicin -- pharmacokinetics KW - Heart -- drug effects KW - Calcium Channel Blockers -- toxicity KW - Antibiotics, Antineoplastic -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80486682?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Increased+toxicity+of+anthracycline+antibiotics+induced+by+calcium+entry+blockers+in+cultured+cardiomyocytes.&rft.au=Santostasi%2C+G%3BKutty%2C+R+K%3BKrishna%2C+G&rft.aulast=Santostasi&rft.aufirst=G&rft.date=1991-03-15&rft.volume=108&rft.issue=1&rft.spage=140&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 - 1991-04-25 N1 - Date created - 1991-04-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the hepatic estrogen and glucocorticoid receptors in congenic strains of Ah responsive and Ah nonresponsive C57BL/6J mice. AN - 80484749; 1672475 AB - The present study examines the role of the Ah receptor in the effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the binding capacity of the hepatic glucocorticoid (GC) and estrogen (E) receptors in female congenic C57BL/6J mice differing only at the Ah (aromatic hydrocarbon responsiveness) locus. The Ah locus is thought to encode the Ah receptor, which regulates the effects of TCDD and related compounds on cytochrome P450IA1 and appears to mediate most of the toxic effects of TCDD. The differences between Ah responsive (Ahb/b) and nonresponsive (Ahd/d) mice appear to reflect differences in the affinity of the Ah receptor in the two strains for ligands such as TCDD. Administration of a single oral dose of TCDD (30 micrograms/kg) to Ahb/b mice produced approximately a 30% decrease in the maximum binding capacities of both the hepatic GC and E receptors, as well as 50-fold induction of a P450IA1-mediated enzymatic activity, ethoxyresorufin-O-deethylase (EROD). Tyrosine aminotransferase (TAT) activity, which is mediated by the GC receptor, was also decreased approximately 30% by TCDD. Dose-response curves indicated that Ah responsive mice are 10-fold more sensitive to induction of EROD than Ah nonresponsive mice (ED50 1.6 vs 15 micrograms/kg), as would be expected for an effect mediated by the Ah receptor. Dose-response curves also indicated that there was a statistical difference in the responsiveness of the hepatic E receptor to TCDD in the two congenic strains of mice (p less than 0.01). Surprisingly, no significant differences in the dose-response curves for the effect of TCDD on hepatic GC receptor binding or TAT activity were observed in the two strains of mice in two separate experiments. These results indicate that the Ah receptor regulates the effects of TCDD on the binding of estrogen to the hepatic estrogen receptor, but suggest that the decrease in the binding capacity of the hepatic GC receptor does not appear to be mediated directly by the Ah locus. JF - Toxicology and applied pharmacology AU - Lin, F H AU - Stohs, S J AU - Birnbaum, L S AU - Clark, G AU - Lucier, G W AU - Goldstein, J A AD - Laboratory of Biochemical Risk Analysis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/03/15/ PY - 1991 DA - 1991 Mar 15 SP - 129 EP - 139 VL - 108 IS - 1 SN - 0041-008X, 0041-008X KW - Polychlorinated Dibenzodioxins KW - 0 KW - Receptors, Aryl Hydrocarbon KW - Receptors, Drug KW - Receptors, Estrogen KW - Receptors, Glucocorticoid KW - Tyrosine Transaminase KW - EC 2.6.1.5 KW - Corticosterone KW - W980KJ009P KW - Index Medicus KW - Animals KW - Tyrosine Transaminase -- analysis KW - Dose-Response Relationship, Drug KW - Corticosterone -- blood KW - Mice, Inbred C57BL KW - Mice KW - Receptors, Glucocorticoid -- drug effects KW - Receptors, Estrogen -- drug effects KW - Liver -- drug effects KW - Polychlorinated Dibenzodioxins -- toxicity KW - Receptors, Glucocorticoid -- analysis KW - Receptors, Estrogen -- analysis KW - Liver -- chemistry KW - Receptors, Drug -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80484749?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+effects+of+2%2C3%2C7%2C8-tetrachlorodibenzo-p-dioxin+%28TCDD%29+on+the+hepatic+estrogen+and+glucocorticoid+receptors+in+congenic+strains+of+Ah+responsive+and+Ah+nonresponsive+C57BL%2F6J+mice.&rft.au=Lin%2C+F+H%3BStohs%2C+S+J%3BBirnbaum%2C+L+S%3BClark%2C+G%3BLucier%2C+G+W%3BGoldstein%2C+J+A&rft.aulast=Lin&rft.aufirst=F&rft.date=1991-03-15&rft.volume=108&rft.issue=1&rft.spage=129&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 - 1991-04-25 N1 - Date created - 1991-04-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Suppression of the immune response to immunotoxins with anti-CD4 monoclonal antibodies. AN - 80481138; 1672333 AB - Treatment of normal mice with a mAb to CD4 (GK1.5) was explored as a means of inhibiting the antibody response to an immunotoxin. Three days of pretreatment with 200 micrograms of GK1.5 completely abrogated the primary antibody response to a 3-micrograms dose of a mutant diphtheria toxin conjugated to an anti-transferrin receptor antibody. The same dose and schedule of anti-CD4 antibody significantly reduced and delayed, but did not prevent, the anamnestic antitoxin response in animals that had been previously primed to the immunotoxin. Three daily injections of anti-CD4 antibodies followed by weekly doses of immunotoxin resulted in a 3-wk delay in the development of antitoxin antibodies, and the kinetics of the antitoxin response correlated with the kinetics of recovery of CD4+ T cells in the spleen and lymph nodes. The antitoxin response to repeated doses of immunotoxin was completely abrogated when anti-CD4 antibodies were given every 2 wk throughout the course of immunotoxin treatment. Thus, transient depletion of Th cells during treatment can block the immune response to an immunotoxin. There was no evidence of tolerance induction with this regimen. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Jin, F S AU - Youle, R J AU - Johnson, V G AU - Shiloach, J AU - Fass, R AU - Longo, D L AU - Bridges, S H AD - Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/03/15/ PY - 1991 DA - 1991 Mar 15 SP - 1806 EP - 1811 VL - 146 IS - 6 SN - 0022-1767, 0022-1767 KW - Antibodies, Anti-Idiotypic KW - 0 KW - Antibodies, Monoclonal KW - Antigens, CD4 KW - Immunotoxins KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Kinetics KW - Mice, Inbred C57BL KW - CD4-Positive T-Lymphocytes -- immunology KW - Mice, Nude KW - Mice KW - Mice, Inbred BALB C KW - Antibodies, Anti-Idiotypic -- biosynthesis KW - Immunotoxins -- immunology KW - Immunotoxins -- administration & dosage KW - Immunosuppression -- methods KW - Antigens, CD4 -- immunology KW - Antibodies, Monoclonal -- therapeutic use KW - Antibodies, Monoclonal -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80481138?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Suppression+of+the+immune+response+to+immunotoxins+with+anti-CD4+monoclonal+antibodies.&rft.au=Jin%2C+F+S%3BYoule%2C+R+J%3BJohnson%2C+V+G%3BShiloach%2C+J%3BFass%2C+R%3BLongo%2C+D+L%3BBridges%2C+S+H&rft.aulast=Jin&rft.aufirst=F&rft.date=1991-03-15&rft.volume=146&rft.issue=6&rft.spage=1806&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 - 1991-04-22 N1 - Date created - 1991-04-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Glutathione modulates activation-dependent proliferation of human peripheral blood lymphocyte populations without regulating their activated function. AN - 80479235; 2005386 AB - L-Buthionine-(S,R)-sulfoximine (BSO) specifically depletes GSH synthesis by inactivating gamma-glutamylcysteine synthetase, whereas 2-ME augments intracellular GSH concentration. These reagents were used to examine GSH regulation of the proliferation and function of human PBL in response to IL-2 or OKT-3 mAb directed at the CD3 T cell Ag. 2-ME enhanced both IL-2-induced proliferation of PBL and CD3- large granular lymphocytes (LGL) and OKT-3 mAb-induced proliferation of CD3+ T cells. BSO partially suppressed activation-induced proliferation in CD3- LGL and CD3+ T cells and totally inhibited the positive co-proliferative regulation by 2-ME in these cells. By contrast, neither BSO nor 2-ME appeared to affect the activation-dependent differentiation of cytotoxic lymphocytes. The absence of effect of 2-ME or BSO on activation-induced PBL NK activity and T cell cytotoxic potential was supported by their negligible effect on the induction of two different markers of activated cytotoxic lymphocytes, namely pore-forming protein gene expression and benzoyloxycarbonyl-1-L-lysine thiobenzylester-esterase activity. BSO inhibition of CD3- LGL proliferation accounted for the inhibitory effects of BSO on both IFN-gamma production in IL-2-stimulated PBL cultures and IL-2-induced PBL lymphokine activated killer activity. The modulatory effects of 2-ME and BSO on lymphocyte proliferation regardless of phenotype (LGL vs T cell) or stimulation (IL-2, via CD3, lectin, etc.) and the functional differentiation of cytotoxic lymphocytes independent of proliferation suggests that these cells share a common site of GSH regulation close to or at the level of DNA synthesis. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Smyth, M J AD - Laboratory of Experimental Immunology, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702-1201. Y1 - 1991/03/15/ PY - 1991 DA - 1991 Mar 15 SP - 1921 EP - 1927 VL - 146 IS - 6 SN - 0022-1767, 0022-1767 KW - Antimetabolites KW - 0 KW - Interleukin-2 KW - Methionine Sulfoximine KW - 1982-67-8 KW - Buthionine Sulfoximine KW - 5072-26-4 KW - Mercaptoethanol KW - 60-24-2 KW - Glutathione KW - GAN16C9B8O KW - Abridged Index Medicus KW - Index Medicus KW - Killer Cells, Lymphokine-Activated -- physiology KW - Humans KW - Cell Division -- drug effects KW - T-Lymphocytes -- physiology KW - Mercaptoethanol -- pharmacology KW - Methionine Sulfoximine -- analogs & derivatives KW - Interleukin-2 -- physiology KW - Antimetabolites -- pharmacology KW - Lymphocyte Activation -- drug effects KW - In Vitro Techniques KW - Methionine Sulfoximine -- pharmacology KW - Killer Cells, Natural -- physiology KW - Glutathione -- physiology KW - Lymphocytes -- physiology KW - Lymphocytes -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80479235?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Glutathione+modulates+activation-dependent+proliferation+of+human+peripheral+blood+lymphocyte+populations+without+regulating+their+activated+function.&rft.au=Smyth%2C+M+J&rft.aulast=Smyth&rft.aufirst=M&rft.date=1991-03-15&rft.volume=146&rft.issue=6&rft.spage=1921&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 - 1991-04-22 N1 - Date created - 1991-04-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Induction of transforming growth factor-beta 1 (TGF-beta 1), receptor expression and TGF-beta 1 protein production in retinoic acid-treated HL-60 cells: possible TGF-beta 1-mediated autocrine inhibition. AN - 80468645; 1848114 AB - Treatment of HL-60 cells, a human promyelocytic leukemia cell line, with the vitamin A derivative retinoic acid (RA) for 7 days resulted in a dose-dependent decrease in proliferation and increase in granulocytic differentiation. The role of transforming growth factor-beta 1 (TGF-beta 1), a protein with pleiotropic effects on the proliferation and differentiation of various cell types, was examined during RA-induced differentiation of HL-60 cells. Although TGF-beta 1 alone had little effect on proliferation or differentiation of HL-60 cells, addition of TGF-beta 1 to HL-60 cells treated with a suboptimum concentration of RA (1.0 nmol/L) resulted in a marked decrease in proliferation with no effect on granulocytic differentiation. Studies of the mechanism of RA-induced TGF-beta sensitivity showed that although untreated HL-60 cells expressed low levels of TGF-beta 1 binding proteins on the cell surface, the levels were increased in a dose-dependent manner after RA treatment. Maximum induction was achieved after treatment with 10 nmol/L RA and consisted predominantly of the 65-Kd TGF-beta 1 receptor type. Moreover, RA treatment also resulted in a dose-dependent increase in both TGF-beta 1 steady-state mRNA expression and production of active TGF-beta with maximum induction at 10 nmol/LRA. RA treatment of HL-60 cells had no effect on TGF-beta 2 and TGF-beta 3 mRNA expression. These data suggest that the effects of RA may be mediated by a TGF-beta 1-mediated autocrine antiproliferative loop during differentiation of HL-60 cells. JF - Blood AU - Falk, L A AU - De Benedetti, F AU - Lohrey, N AU - Birchenall-Roberts, M C AU - Ellingsworth, L W AU - Faltynek, C R AU - Ruscetti, F W AD - Biological Carcinogenesis and Development Program, Program Resources, Inc, Dyn Corp, NCI-Frederick Cancer Research and Development Center, MD 21702. Y1 - 1991/03/15/ PY - 1991 DA - 1991 Mar 15 SP - 1248 EP - 1255 VL - 77 IS - 6 SN - 0006-4971, 0006-4971 KW - RNA, Messenger KW - 0 KW - Receptors, Cell Surface KW - Receptors, Transforming Growth Factor beta KW - Transforming Growth Factor beta KW - Tretinoin KW - 5688UTC01R KW - Abridged Index Medicus KW - Index Medicus KW - Hematopoiesis -- physiology KW - Tumor Cells, Cultured -- ultrastructure KW - Tumor Cells, Cultured -- drug effects KW - Dose-Response Relationship, Drug KW - Humans KW - Cell Division -- drug effects KW - Cell Division -- physiology KW - RNA, Messenger -- analysis KW - RNA, Messenger -- genetics KW - Cell Differentiation -- physiology KW - RNA, Messenger -- metabolism KW - Hematopoiesis -- drug effects KW - Tumor Cells, Cultured -- pathology KW - Cell Differentiation -- drug effects KW - Receptors, Cell Surface -- metabolism KW - Tretinoin -- pharmacology KW - Transforming Growth Factor beta -- physiology KW - Gene Expression Regulation, Leukemic -- physiology KW - Receptors, Cell Surface -- genetics KW - Transforming Growth Factor beta -- genetics KW - Transforming Growth Factor beta -- metabolism KW - Receptors, Cell Surface -- drug effects KW - Gene Expression Regulation, Leukemic -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80468645?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+transforming+growth+factor-beta+1+%28TGF-beta+1%29%2C+receptor+expression+and+TGF-beta+1+protein+production+in+retinoic+acid-treated+HL-60+cells%3A+possible+TGF-beta+1-mediated+autocrine+inhibition.&rft.au=Falk%2C+L+A%3BDe+Benedetti%2C+F%3BLohrey%2C+N%3BBirchenall-Roberts%2C+M+C%3BEllingsworth%2C+L+W%3BFaltynek%2C+C+R%3BRuscetti%2C+F+W&rft.aulast=Falk&rft.aufirst=L&rft.date=1991-03-15&rft.volume=77&rft.issue=6&rft.spage=1248&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=00064971&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-17 N1 - Date created - 1991-04-17 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 metastatic renal cell carcinoma. AN - 80466047; 2001538 AB - Suramin sodium is an aromatic polysulfonated compound that was originally introduced as an antiparasitic agent in the 1920s. Recently, in view of its ability to bind and disrupt the function of multiple growth factors and cellular enzyme systems, the authors have been evaluating the role of suramin as an antitumor agent. In this study, 12 patients with metastatic renal cell carcinoma received parenteral suramin by continuous infusion to a peak plasma suramin level greater than 200 micrograms/ml. No objective radiographic responses were observed, although greater than 90% necrosis of multiple tumor sites was documented at autopsy in one patient and normalization of tumor-related hypercalcemia occurred in another patient. Two patients had stable disease of 10 and 28 weeks' duration, respectively. Significant toxicities included hypotension related to sepsis and resulting in renal insufficiency (one patient), development of liver function abnormalities (one patient) marked thrombocytopenia (one patient), prothrombin time prolongation (all patients), vortex keratopathy (two patients), and Grade 1 sensory neuropathy (two patients). On the basis of the current results, suramin does not appear to be an active single agent against metastatic renal cell carcinoma when administered by this dosing schedule. JF - Cancer AU - La Rocca, R V AU - Stein, C A AU - Danesi, R AU - Cooper, M R AU - Uhrich, M AU - Myers, C E AD - Medicine Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/03/15/ PY - 1991 DA - 1991 Mar 15 SP - 1509 EP - 1513 VL - 67 IS - 6 SN - 0008-543X, 0008-543X KW - Suramin KW - 6032D45BEM KW - Abridged Index Medicus KW - Index Medicus KW - Fever -- chemically induced KW - Hematologic Diseases -- chemically induced KW - Humans KW - Adult KW - Gastrointestinal Diseases -- chemically induced KW - Aged KW - Pilot Projects KW - Middle Aged KW - Radiography KW - Nervous System Diseases -- chemically induced KW - Male KW - Female KW - Proteinuria -- chemically induced KW - Kidney Neoplasms -- drug therapy KW - Suramin -- adverse effects KW - Carcinoma, Renal Cell -- secondary KW - Carcinoma, Renal Cell -- drug therapy KW - Kidney Neoplasms -- diagnostic imaging KW - Suramin -- blood KW - Suramin -- therapeutic use KW - Carcinoma, Renal Cell -- diagnostic imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80466047?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=A+pilot+study+of+suramin+in+the+treatment+of+metastatic+renal+cell+carcinoma.&rft.au=La+Rocca%2C+R+V%3BStein%2C+C+A%3BDanesi%2C+R%3BCooper%2C+M+R%3BUhrich%2C+M%3BMyers%2C+C+E&rft.aulast=La+Rocca&rft.aufirst=R&rft.date=1991-03-15&rft.volume=67&rft.issue=6&rft.spage=1509&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-18 N1 - Date created - 1991-04-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The multidrug resistance phenotype: 31P nuclear magnetic resonance characterization and 2-deoxyglucose toxicity. AN - 80455672; 1998955 AB - In order to identify changes in 31P nuclear magnetic resonance (NMR) spectra associated with multiple drug resistance (MDR), a number of wild type and drug-resistant cancer cell lines were studied. The resistant cells included cells selected with various drugs, mainly Adriamycin, as well as cells transfected with the human multidrug resistance gene (MDR1 gene), which encodes P-glycoprotein. In most cases, 31P NMR spectra were significantly different from those of parental, drug-sensitive lines. The spectra of resistant cells generally indicated increased levels of ATP and phosphocreatine in the cytoplasm. These changes are compatible with the increased glucose utilization rate previously described for resistant cells. Major changes were also observed in the levels of glycerophosphocholine and glycerophosphoethanolamine. Changes in cellular metabolism reflected by 31P NMR spectra depend on the drug used to select the cells for MDR. The direction of these changes was not consistent for all cell lines studied and could not be directly attributed to expression of P-glycoprotein, suggesting that the changes may be related to alterations in metabolism and membrane function associated with other mechanisms of MDR. The results demonstrate the suitability of 31P NMR for studies of biochemical changes associated with MDR. The toxicity of 2-deoxyglucose, a glucose antimetabolite, was investigated in addition to the NMR studies and was found to be consistently higher in multidrug-resistant cells than in the parental drug-sensitive lines. For MCF-7 breast cancer cells, where several sublines with different levels of resistance were available, the toxicity was highest for the most resistant lines. JF - Cancer research AU - Kaplan, O AU - Jaroszewski, J W AU - Clarke, R AU - Fairchild, C R AU - Schoenlein, P AU - Goldenberg, S AU - Gottesman, M M AU - Cohen, J S AD - Medicine Branch, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1991/03/15/ PY - 1991 DA - 1991 Mar 15 SP - 1638 EP - 1644 VL - 51 IS - 6 SN - 0008-5472, 0008-5472 KW - Doxorubicin KW - 80168379AG KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Deoxyglucose KW - 9G2MP84A8W KW - Index Medicus KW - Phenotype KW - Tumor Cells, Cultured KW - Doxorubicin -- pharmacology KW - Cell Survival -- drug effects KW - Transfection KW - Humans KW - Adenosine Triphosphate -- analysis KW - Magnetic Resonance Spectroscopy KW - Drug Resistance -- genetics KW - Deoxyglucose -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80455672?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=The+multidrug+resistance+phenotype%3A+31P+nuclear+magnetic+resonance+characterization+and+2-deoxyglucose+toxicity.&rft.au=Kaplan%2C+O%3BJaroszewski%2C+J+W%3BClarke%2C+R%3BFairchild%2C+C+R%3BSchoenlein%2C+P%3BGoldenberg%2C+S%3BGottesman%2C+M+M%3BCohen%2C+J+S&rft.aulast=Kaplan&rft.aufirst=O&rft.date=1991-03-15&rft.volume=51&rft.issue=6&rft.spage=1638&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 - 1991-04-09 N1 - Date created - 1991-04-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Diagnostic x-ray procedures and risk of leukemia, lymphoma, and multiple myeloma. AN - 80450007; 2053936 AB - Exposure to diagnostic x-rays and the risk of leukemia, non-Hodgkin's lymphoma (NHL), and multiple myeloma were studied within two prepaid health plans. Adult patients with leukemia (n = 565), NHL (n = 318), and multiple myeloma (n = 208) were matched to controls (n = 1390), and over 25,000 x-ray procedures were abstracted from medical records. Dose response was evaluated by assigning each x-ray procedure a score based on estimated bone marrow dose. X-ray exposure was not associated with chronic lymphocytic leukemia, one of the few malignant conditions never linked to radiation (relative risk [RR], 0.66). For all other forms of leukemia combined (n = 358), there was a slight elevation in risk (RR, 1.17) but no evidence of a dose-response relationship when x-ray procedures near the time of diagnosis were excluded. Similarly, patients with NHL were exposed to diagnostic x-ray procedures more often than controls (RR, 1.32), but the RR fell to 0.99 when the exposure to diagnostic x-ray procedures within 2 years of diagnosis was ignored. For multiple myeloma, overall risk was not significantly high (RR, 1.14), but there was consistent evidence of increasing risk with increasing numbers of diagnostic x-ray procedures. These data suggest that persons with leukemia and NHL undergo x-ray procedures frequently just prior to diagnosis for conditions related to the development or natural history of their disease. There was little evidence that diagnostic x-ray procedures were causally associated with leukemia or NHL. The risk for multiple myeloma, however, was increased among those patients who were frequently exposed to x-rays. JF - JAMA AU - Boice, J D AU - Morin, M M AU - Glass, A G AU - Friedman, G D AU - Stovall, M AU - Hoover, R N AU - Fraumeni, J F AD - Epidemiology and Biostatistics Program, National Cancer Institute, Bethesda, MD 20852. Y1 - 1991/03/13/ PY - 1991 DA - 1991 Mar 13 SP - 1290 EP - 1294 VL - 265 IS - 10 SN - 0098-7484, 0098-7484 KW - Abridged Index Medicus KW - Index Medicus KW - California KW - Regression Analysis KW - Radiation Dosage KW - Oregon KW - Risk Factors KW - Humans KW - Adult KW - Case-Control Studies KW - Leukemia, Lymphocytic, Chronic, B-Cell -- etiology KW - Middle Aged KW - Male KW - Female KW - Multiple Myeloma -- etiology KW - Neoplasms, Radiation-Induced -- etiology KW - Leukemia, Radiation-Induced -- etiology KW - Lymphoma, Non-Hodgkin -- etiology KW - Radiography -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80450007?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Diagnostic+x-ray+procedures+and+risk+of+leukemia%2C+lymphoma%2C+and+multiple+myeloma.&rft.au=Boice%2C+J+D%3BMorin%2C+M+M%3BGlass%2C+A+G%3BFriedman%2C+G+D%3BStovall%2C+M%3BHoover%2C+R+N%3BFraumeni%2C+J+F&rft.aulast=Boice&rft.aufirst=J&rft.date=1991-03-13&rft.volume=265&rft.issue=10&rft.spage=1290&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-03-25 N1 - Date created - 1991-03-25 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: JAMA 1991 Jun 5;265(21):2810 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Neoglycolipid analogues of ganglioside GM1 as functional receptors of cholera toxin. AN - 80468901; 1848091 AB - We synthesized several lipid analogues of ganglioside GM1 by attaching its oligosaccharide moiety (GM1OS) to aminophospholipids, aliphatic amines, and cholesteryl hemisuccinate. We incubated GM1-deficient rat glioma C6 cells with each of the derivatives as well as native GM1 and assayed the cells for their ability to bind and respond to cholera toxin. On the basis of the observed increase in binding of 125I-labeled cholera toxin, it was apparent that the cells took up and initially incorporated most of the derivatives into the plasma membrane. In the case of the aliphatic amine derivatives, the ability to generate new toxin binding sites was dependent on chain length; whereas the C10 derivative was ineffective, C12 and higher analogues were effective. Increased binding was dependent on both the concentration of the neoglycolipid in the medium and the time of exposure. Cells pretreated with the various derivatives accumulated cyclic AMP in response to cholera toxin, but there were differences in their effectiveness. The cholesterol and long-chain aliphatic amine derivatives were more effective than native GM1, whereas the phospholipid derivatives were less effective. The distance between GM1OS and the phospholipid also appeared to influence its functional activity. The neoglycolipid formed by cross-linking the amine of GM1OS to phosphatidylethanolamine (PE) with disuccinimidyl suberate was less effective than the neoglycolipid formed by directly attaching GM1OS to PE by reductive amination. Furthermore, insertion of a C8 spacer in the former neoglycolipid rendered it even less effective.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Biochemistry AU - Pacuszka, T AU - Bradley, R M AU - Fishman, P H AD - Membrane Biochemistry Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/03/12/ PY - 1991 DA - 1991 Mar 12 SP - 2563 EP - 2570 VL - 30 IS - 10 SN - 0006-2960, 0006-2960 KW - Glycolipids KW - 0 KW - G(M1) Ganglioside KW - 37758-47-7 KW - Chloroquine KW - 886U3H6UFF KW - Cholera Toxin KW - 9012-63-9 KW - Cyclic AMP KW - E0399OZS9N KW - Adenylyl Cyclases KW - EC 4.6.1.1 KW - Index Medicus KW - Rats KW - Animals KW - Tumor Cells, Cultured KW - Chloroquine -- pharmacology KW - Binding, Competitive KW - Cyclic AMP -- metabolism KW - Adenylyl Cyclases -- metabolism KW - Chromatography, Thin Layer KW - G(M1) Ganglioside -- metabolism KW - Glycolipids -- metabolism KW - G(M1) Ganglioside -- analogs & derivatives KW - Cholera Toxin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80468901?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Neoglycolipid+analogues+of+ganglioside+GM1+as+functional+receptors+of+cholera+toxin.&rft.au=Pacuszka%2C+T%3BBradley%2C+R+M%3BFishman%2C+P+H&rft.aulast=Pacuszka&rft.aufirst=T&rft.date=1991-03-12&rft.volume=30&rft.issue=10&rft.spage=2563&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-17 N1 - Date created - 1991-04-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparative acute nephrotoxicity of salicylic acid, 2,3-dihydroxybenzoic acid, and 2,5-dihydroxybenzoic acid in young and middle aged Fischer 344 rats. AN - 80499038; 2011854 AB - Experimental evidence suggests that the oxidative metabolites 2,3- and 2,5-dihydroxybenzoic acid (DIOH) may be responsible for the nephrotoxicity of salicylic acid (SAL). In the present study, enzymuria in conjunction with glucose (GLU) and protein (PRO) excretion were used as endpoints to compare the relative nephrotoxicity of SAL with 2,3- and 2,5-DIOH. In addition, the effect of age on enzymuria and GLU and PRO excretion following treatment with SAL or 2,3- and 2,5-DIOH was investigated because the elderly are at greater risk for SAL-induced nephrotoxicity. Three and 12-month male Fischer 344 rats were administered either no treatment, vehicle, SAL, 2,3-DIOH, or 2,5-DIOH at 500 mg/kg p.o. in 5 ml/kg corn oil/DMSO (5:1). Effects of these treatments on functional integrity of renal tissue was assessed from 0--72 h after dosing by measurement of urinary creatinine, GLU, and PRO, as well as excretion of proximal and distal tubular renal enzymes. Enzymes measured as indicators of proximal tubular damage were N-acetyl-beta-glucosaminidase (NAG), gamma glutamyltransferase (GGT), alanine aminotransferase (ALT), and alkaline phosphatase (AP), while urinary lactate dehydrogenase (LD) and aspartate aminotransferase (AST) were measured as indicators of distal tubular damage. In comparison to 3-month vehicle-treated rats, 2,3- and 2,5-DIOH caused a significant increase between 0-8 h in excretion of urinary GLU and activities of AST, NAG, and LD, with peak effects occurring between 4-8 h. Toxic effects of either metabolite were not evident beyond 24 h, and toxicity of 2,5-DIOH was significantly greater in comparison to 2,3-DIOH. SAL treatment resulted in similar effects on enzymuria as well as GLU and PRO excretion, but peak effects did not occur until 16-24 h, and often persisted until 72 h after dosing. Maximal enzymuria in response to SAL treatment was significantly greater in 12- vs. 3-month rats for AST, NAG, and LD. In response to 2,3-DIOH treatment, the maximal response was significantly greater in 12- vs. 3-month rats for LD and AST, and for NAG in response to 2,5-DIOH treatment. The results of this study suggest that both 2,3- and 2,5-DIOH are nephrotoxic metabolites of SAL, but implicate 2,5-DIOH as the more potent nephrotoxic metabolite. The relative lack of an age effect for 2,3- and 2,5-DIOH vs. SAL supports the hypothesis [2] that age-related differences in biotransformation of SAL, and not increased tissue sensitivity to 2,3- or 2,5-DIOH, contribute to the age-related increase in susceptibility to SAL-induced nephrotoxicity. JF - Toxicology AU - McMahon, T F AU - Stefanski, S A AU - Wilson, R E AU - Blair, P C AU - Clark, A M AU - Birnbaum, L S AD - Experimental Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/03/11/ PY - 1991 DA - 1991 Mar 11 SP - 297 EP - 311 VL - 66 IS - 3 SN - 0300-483X, 0300-483X KW - Gentisates KW - 0 KW - Hydroxybenzoates KW - Salicylates KW - 2,3-dihydroxybenzoic acid KW - 70D5FBB392 KW - Alanine Transaminase KW - EC 2.6.1.2 KW - Alkaline Phosphatase KW - EC 3.1.3.1 KW - Acetylglucosaminidase KW - EC 3.2.1.52 KW - Salicylic Acid KW - O414PZ4LPZ KW - 2,5-dihydroxybenzoic acid KW - VP36V95O3T KW - Index Medicus KW - Rats KW - Administration, Oral KW - Animals KW - Alanine Transaminase -- urine KW - Rats, Inbred F344 KW - Alkaline Phosphatase -- urine KW - Acetylglucosaminidase -- urine KW - Glycosuria -- chemically induced KW - Male KW - Salicylates -- toxicity KW - Aging -- metabolism KW - Hydroxybenzoates -- toxicity KW - Kidney -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80499038?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Comparative+acute+nephrotoxicity+of+salicylic+acid%2C+2%2C3-dihydroxybenzoic+acid%2C+and+2%2C5-dihydroxybenzoic+acid+in+young+and+middle+aged+Fischer+344+rats.&rft.au=McMahon%2C+T+F%3BStefanski%2C+S+A%3BWilson%2C+R+E%3BBlair%2C+P+C%3BClark%2C+A+M%3BBirnbaum%2C+L+S&rft.aulast=McMahon&rft.aufirst=T&rft.date=1991-03-11&rft.volume=66&rft.issue=3&rft.spage=297&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=0300483X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-05-07 N1 - Date created - 1991-05-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Spinal opioid analgesic effects are enhanced in a model of unilateral inflammation/hyperalgesia: possible involvement of noradrenergic mechanisms. AN - 80649331; 1676373 AB - We have examined the spinal analgesic activity of opioid agonists and antagonists in a model of short term, unilateral, carrageenan-induced inflammation/hyperalgesia. Rats received a single s.c. injection of carrageenan (2-6 mg in saline) 3-24 h prior to testing hindpaw withdrawal latencies to noxious thermal stimuli. Dose-response curves for intrathecally administered agonists with mu- and/or delta-opioid activity were shifted to the left for inflamed hindpaws when compared to contralateral non-inflamed paws. The selective kappa-receptor agonist U-50,488H had no activity in this analgesic assay on either inflamed or non-inflamed paws when administered intrathecally. However, systemic administration of U-50,488H did produce significant elevations of paw withdrawal latencies in inflamed paws. The alpha 2-adrenoceptor agonist clonidine also produced dose-dependent antinociception in the paw withdrawal assay after systemic or intrathecal administration. Inflamed hindpaws were significantly more sensitive to the antinociceptive effect of morphine on inflamed hindpaws was blocked by the opioid antagonist naloxone or the alpha 2-adrenoceptor antagonist idazoxan. The effect of clonidine was only blocked by idazoxan. Antagonists alone had no significant effect on withdrawal latencies. The data indicate that the analgesic action of opioids during conditions of inflammation may depend on an interaction with spinal noradrenergic pathways. JF - European journal of pharmacology AU - Hylden, J L AU - Thomas, D A AU - Iadarola, M J AU - Nahin, R L AU - Dubner, R AD - Neurobiology and Anesthesiology Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/03/05/ PY - 1991 DA - 1991 Mar 05 SP - 135 EP - 143 VL - 194 IS - 2-3 SN - 0014-2999, 0014-2999 KW - Adrenergic alpha-Antagonists KW - 0 KW - Enkephalins KW - Narcotic Antagonists KW - Receptors, Opioid KW - Morphine KW - 76I7G6D29C KW - Carrageenan KW - 9000-07-1 KW - Clonidine KW - MN3L5RMN02 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Enkephalins -- pharmacology KW - Clonidine -- pharmacology KW - Male KW - Nociceptors -- drug effects KW - Morphine -- pharmacology KW - Adrenergic alpha-Antagonists -- pharmacology KW - Receptors, Opioid -- drug effects KW - Spinal Cord -- drug effects KW - Inflammation -- chemically induced KW - Inflammation -- drug therapy KW - Hyperalgesia -- chemically induced KW - Hyperalgesia -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80649331?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Spinal+opioid+analgesic+effects+are+enhanced+in+a+model+of+unilateral+inflammation%2Fhyperalgesia%3A+possible+involvement+of+noradrenergic+mechanisms.&rft.au=Hylden%2C+J+L%3BThomas%2C+D+A%3BIadarola%2C+M+J%3BNahin%2C+R+L%3BDubner%2C+R&rft.aulast=Hylden&rft.aufirst=J&rft.date=1991-03-05&rft.volume=194&rft.issue=2-3&rft.spage=135&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 - 1991-08-02 N1 - Date created - 1991-08-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A colorimetric assay for a pyridoxal phosphate-dependent beta-replacement reaction with L-cysteine: application to studies of wild-type and mutant tryptophan synthase alpha 2 beta 2 complexes. AN - 72042348; 1872468 AB - We present an improved and simple direct assay for formation of inorganic sulfide from L-cysteine in a beta-replacement reaction catalyzed by tryptophan synthase. This method provides a useful enzymatic assay for pyridoxal phosphate-dependent beta-replacement reactions in which the amino acid substrate is L-cysteine and the cosubstrate is 2-mercaptoethanol. The assay should be applicable to similar reactions with L-cysteine and other cosubstrates. The method has several advantages over other methods which have been used to assay similar beta-replacement reactions. The assay is highly reproducible and sensitive and is conveniently carried out in disposable 1.5-ml centrifuge tubes. The color remains stable for several hours. The thiol compounds L-cysteine and 2-mercaptoethanol do not interfere at the concentrations used. The method has useful applications to studies of the rates and reaction specificities of several other pyridoxal phosphate enzymes which catalyze beta-replacement reactions. We demonstrate the use of the method to study the effects of site-directed mutagenesis on the reaction specificity and mechanism of the tryptophan synthase alpha 2 beta 2 complex. JF - Analytical biochemistry AU - Kayastha, A M AU - Miles, E W AD - Laboratory of Biochemical Pharmacology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/03/02/ PY - 1991 DA - 1991 Mar 02 SP - 200 EP - 203 VL - 193 IS - 2 SN - 0003-2697, 0003-2697 KW - Phenylenediamines KW - 0 KW - Sulfides KW - Pyridoxal Phosphate KW - 5V5IOJ8338 KW - dimethyl-4-phenylenediamine KW - 7GZH2FMK7X KW - Tryptophan Synthase KW - EC 4.2.1.20 KW - Cysteine KW - K848JZ4886 KW - Methylene Blue KW - T42P99266K KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Phenylenediamines -- chemistry KW - Tryptophan Synthase -- chemistry KW - Methylene Blue -- chemistry KW - Colorimetry -- methods KW - Sulfides -- chemistry KW - Escherichia coli -- enzymology KW - Salmonella typhimurium -- enzymology KW - Cysteine -- chemistry KW - Pyridoxal Phosphate -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72042348?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+colorimetric+assay+for+a+pyridoxal+phosphate-dependent+beta-replacement+reaction+with+L-cysteine%3A+application+to+studies+of+wild-type+and+mutant+tryptophan+synthase+alpha+2+beta+2+complexes.&rft.au=Kayastha%2C+A+M%3BMiles%2C+E+W&rft.aulast=Kayastha&rft.aufirst=A&rft.date=1991-03-02&rft.volume=193&rft.issue=2&rft.spage=200&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 - 1991-09-19 N1 - Date created - 1991-09-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Precision and accuracy considerations of physiological quantitation in PET. AN - 85278225; pmid-1997487 AB - The ability to differentiate regional patterns of flow and metabolism between various patient populations depends upon the signal-to-noise characteristics of the data. The approach chosen for producing quantitative data will affect the detection sensitivity of a method. Methods based on mathematical models can reduce intersubject variability by accounting for factors unrelated to the physiological measure of interest, in particular, differences in the input function. However, errors in the model and in the implementation of a model-based method can increase variability compared to simpler, empirical methods. Normalization of physiological measures can significantly reduce intersubject variation; however, interpretation of normalized results can be more complex. The advantages and disadvantages of various approaches for physiological quantitation are considered. JF - Journal of Cerebral Blood Flow and Metabolism AU - Carson, R E AD - Department of Nuclear Medicine, National Institutes of Health, Bethesda, MD 20892. PY - 1991 SP - A45 EP - A50 VL - 11 IS - 2 SN - 0271-678X, 0271-678X KW - Human KW - Brain KW - Glucose KW - Tomography, Emission-Computed KW - Cerebrovascular Circulation KW - Models, Biological KW - Mathematics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85278225?accountid=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+Cerebral+Blood+Flow+and+Metabolism&rft.atitle=Precision+and+accuracy+considerations+of+physiological+quantitation+in+PET.&rft.au=Carson%2C+R+E&rft.aulast=Carson&rft.aufirst=R&rft.date=1991-03-01&rft.volume=11&rft.issue=2&rft.spage=A45&rft.isbn=&rft.btitle=&rft.title=Journal+of+Cerebral+Blood+Flow+and+Metabolism&rft.issn=0271678X&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - The role of chronic viral hepatitis in hepatocellular carcinoma in the United States. AN - 85224557; pmid-1847790 AB - Although hepatocellular carcinoma is a relatively uncommon tumor in the United States, it is quite common in sub-Saharan Africa and the Far East, where most cases are associated with infection with the hepatitis B virus. We have studied 99 American patients with hepatocellular carcinoma for evidence of hepatitis B or hepatitis C viral infection and compared these findings to those in a group of matched controls with other cancers. The two groups differed in proportion, with hepatitis B surface antigen in serum being significantly higher in patients with hepatocellular carcinoma (7% vs. 0%, p = 0.009). Antibody to hepatitis C virus was also found more frequently in patients with hepatocellular carcinoma (13% vs. 2%, p = 0.002). The relative risk for hepatocellular carcinoma in hepatitis B surface antigen-positive patients was calculated to be 17.3 and for antibody to hepatitis C virus to be 7.3. The attributable fraction of cases related to the hepatitis B surface antigen carrier state was 6.7% and for patients infected with the hepatitis C virus was 11.4%. Approximately three quarters of cases of hepatocellular carcinoma did not have evidence of either hepatitis C or hepatitis B virus infection. These findings provide strong evidence that hepatitis C virus infection is associated with the development of hepatocellular carcinoma, and in the United States may even play a more important role than the hepatitis B virus. JF - The American Journal of Gastroenterology AU - Di Bisceglie A M AU - Order S E AU - Klein, J L AU - Waggoner, J G AU - Sjogren, M H AU - Kuo, G AU - Houghton, M AU - Choo, Q L AU - Hoofnagle, J H AD - Liver Diseases Section, Digestive Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland. PY - 1991 SP - 335 EP - 338 VL - 86 IS - 3 SN - 0002-9270, 0002-9270 KW - United States KW - Hepatitis B Surface Antigens KW - Carcinoma, Hepatocellular KW - Human KW - Aged KW - Child KW - Radioimmunoassay KW - Liver Neoplasms KW - Aged, 80 and over KW - Adult KW - Hepatitis B KW - Middle Age KW - Hepatitis C KW - Adolescent KW - Male KW - Female UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85224557?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+Journal+of+Gastroenterology&rft.atitle=The+role+of+chronic+viral+hepatitis+in+hepatocellular+carcinoma+in+the+United+States.&rft.au=Di+Bisceglie+A+M%3BOrder+S+E%3BKlein%2C+J+L%3BWaggoner%2C+J+G%3BSjogren%2C+M+H%3BKuo%2C+G%3BHoughton%2C+M%3BChoo%2C+Q+L%3BHoofnagle%2C+J+H&rft.aulast=Di+Bisceglie+A+M&rft.aufirst=&rft.date=1991-03-01&rft.volume=86&rft.issue=3&rft.spage=335&rft.isbn=&rft.btitle=&rft.title=The+American+Journal+of+Gastroenterology&rft.issn=00029270&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Effect of nerve growth factor on C-1300 murine neuroblastoma tumor growth and catecholamine content in neonatally sympathectomized mice. AN - 80701218; 1906944 AB - The in situ C-1300 murine neuroblastoma (MNB) tumor model was used to investigate the influence of exogenously administered nerve growth factor (NGF) on tumor growth and tissue catecholamine concentration in mice sympathectomized with 6-hydroxy-dopamine (6-OHDA) on postnatal days 4-10. Mice were implanted with 1 x 10(6) disaggregated MNB cells 3 days after termination of 6-OHDA administration. NGF (12-15 micrograms/mouse/day) treatment was initiated at the time of MNB cell implantation and continued until sacrifice of the animal. The time interval between tumor cell implantation and detection of palpable tumor (tumor onset time), transverse tumor diameter, tumor weight, tumor weight to body weight ratio, and tumor catecholamine concentration were determined. Neonatal sympathectomy caused a decrease in myocardial norepinephrine concentration of 88% compared with vehicle-treated animals as well as a significant reduction in total body and organ weight. Average body, brain, heart, and spleen weights were decreased 31%, 16%, 25%, and 42%, respectively, below control values. The daily injection of NGF, from the time of MNB tumor implantation to sacrifice, did not prevent these effects of chemical sympathectomy from being expressed. Tumor onset time following implantation of MNB cells was significantly increased in neonatally sympathectomized mice and was not altered by treatment with NGF. In contrast, the decrease in MNB tumor growth rate observed in sympathectomized mice was reversed by administration of NGF. Mean tumor weight and mean tumor to body weight ratio were 89% and 115% of comparable control values, respectively, in sympathectomized mice receiving exogenous NGF.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Journal of neuroscience research AU - Fink, D W AU - Mirkin, B L AD - NIGMS/NICHD, National Institutes of Health, Bethesda, Maryland. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 343 EP - 351 VL - 28 IS - 3 SN - 0360-4012, 0360-4012 KW - Hydroxydopamines KW - 0 KW - Nerve Growth Factors KW - Oxidopamine KW - 8HW4YBZ748 KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Neoplasm Transplantation KW - Mice, Inbred A KW - Animals, Newborn KW - Animals KW - Myocardium -- chemistry KW - Sympathectomy, Chemical KW - Mice KW - Hydroxydopamines -- toxicity KW - Norepinephrine -- analysis KW - Neuroblastoma -- pathology KW - Nerve Growth Factors -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80701218?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Effect+of+nerve+growth+factor+on+C-1300+murine+neuroblastoma+tumor+growth+and+catecholamine+content+in+neonatally+sympathectomized+mice.&rft.au=Fink%2C+D+W%3BMirkin%2C+B+L&rft.aulast=Fink&rft.aufirst=D&rft.date=1991-03-01&rft.volume=28&rft.issue=3&rft.spage=343&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 - 1991-08-29 N1 - Date created - 1991-08-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Brain distribution and fate of tris(2-chloroethyl) phosphate in Fischer 344 rats. AN - 80666698; 1676650 AB - Tris(2-chloroethyl) phosphate (TRCP) is a flame retardant that has a wide variety of industrial applications. In subchronic studies, oral administration of TRCP to rats and mice has been reported to produce dose-, sex-, and species-dependent lesions in the hippocampal brain region. The present investigation has examined the metabolism, elimination, and regional brain distribution of [14C]TRCP in male and female rats. [14C]TRCP was administered by gavage (0, 175, 350, or 700 mg/kg) and urine, feces, exhaled volatiles, CO2, and selected tissues were collected. Regional brain distribution of 14C was determined 2 hr following single doses of TRCP to male and female rats, and 24 hr after a single dose and the last of 14 daily doses of TRCP to female rats. Results of these studies indicate that TRCP is readily absorbed from the gastrointestinal tract, distributed to all brain regions, and that metabolism and excretion are nearly complete in 72 hr. Most of the TRCP-derived radioactivity was excreted in urine (up to 85%), with feces, volatiles, and CO2 combined accounting for less than 10% of the dose. Predominant signs of toxicity associated with TRCP administration (350 and 700 mg/kg) were seizures within 2 hr of treatment, when most of the TRCP-derived radioactivity present in brain tissue was in the form of the parent compound. Traces of inextractable 14C were detected at later times, but this material was not concentrated in brain relative to other tissues.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Drug metabolism and disposition: the biological fate of chemicals AU - Herr, D W AU - Sanders, J M AU - Matthews, H B AD - Experimental Toxicology Branch, National Institute of Environmental Health Sciences Research Triangle Park, NC 27709. PY - 1991 SP - 436 EP - 442 VL - 19 IS - 2 SN - 0090-9556, 0090-9556 KW - Flame Retardants KW - 0 KW - Organophosphates KW - tris(chloroethyl)phosphate KW - 115-96-8 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Sex Factors KW - Cerebral Cortex -- metabolism KW - Liver -- metabolism KW - Feces -- chemistry KW - Male KW - Female KW - Chromatography, High Pressure Liquid KW - Organophosphates -- pharmacokinetics KW - Organophosphates -- toxicity KW - Brain -- metabolism KW - Flame Retardants -- pharmacokinetics KW - Flame Retardants -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80666698?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Brain+distribution+and+fate+of+tris%282-chloroethyl%29+phosphate+in+Fischer+344+rats.&rft.au=Herr%2C+D+W%3BSanders%2C+J+M%3BMatthews%2C+H+B&rft.aulast=Herr&rft.aufirst=D&rft.date=1991-03-01&rft.volume=19&rft.issue=2&rft.spage=436&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 - 1991-08-14 N1 - Date created - 1991-08-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Metabolism of tris(2-chloroethyl) phosphate in rats and mice. AN - 80663535; 1676651 AB - Tris(2-chloroethyl) phosphate (TRCP), a flame retardant, produces a dose-, sex-, and species-dependent lesion in the hippocampal region of the brain following subchronic oral administration. This lesion is more common and more severe in female F344 rats than in male F344 rats, and is not observed in B6C3F1 mice. The present investigation of the metabolism of TRCP was designed to detect sex and species variations that might account for differences in toxicity. Elimination of TRCP-derived radioactivity was more rapid in mice, which excreted greater than 70% of an oral dose of 175 mg/kg in urine in 8 hr vs. approximately 40% for male or female rats. However, the metabolic profile of TRCP-derived radioactivity in urine was similar for both species. The major metabolite in female rat urine was identified as bis(2-chloroethyl) carboxymethyl phosphate. This metabolite co-chromatographed with the major metabolite found in both male rat and mouse urine. Two additional metabolites identified in female rat urine were bis(2-chloroethyl) hydrogen phosphate and the glucuronide of bis(2-chloroethyl) 2-hydroxyethyl phosphate. These metabolites also cochromatographed with metabolites found in male rat and mouse urine. TRCP metabolism in rats was not induced or inhibited by nine daily 175 mg/kg doses. Toxicity, as evidenced by seizures, was potentiated in male rats pretreated with inhibitors of aldehyde dehydrogenase. JF - Drug metabolism and disposition: the biological fate of chemicals AU - Burka, L T AU - Sanders, J M AU - Herr, D W AU - Matthews, H B AD - Experimental Toxicology Branch, National Institute of Environmental Health Sciences Research Triangle Park, NC 27709. PY - 1991 SP - 443 EP - 447 VL - 19 IS - 2 SN - 0090-9556, 0090-9556 KW - Enzyme Inhibitors KW - 0 KW - Flame Retardants KW - Organophosphates KW - tris(chloroethyl)phosphate KW - 115-96-8 KW - Index Medicus KW - Rats KW - Mice, Inbred Strains KW - Animals KW - Rats, Inbred F344 KW - Sex Factors KW - Biotransformation KW - Enzyme Inhibitors -- pharmacology KW - Mice KW - Male KW - Female KW - Chromatography, High Pressure Liquid KW - Organophosphates -- metabolism KW - Flame Retardants -- metabolism KW - Organophosphates -- toxicity KW - Flame Retardants -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80663535?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Drug+metabolism+and+disposition%3A+the+biological+fate+of+chemicals&rft.atitle=Metabolism+of+tris%282-chloroethyl%29+phosphate+in+rats+and+mice.&rft.au=Burka%2C+L+T%3BSanders%2C+J+M%3BHerr%2C+D+W%3BMatthews%2C+H+B&rft.aulast=Burka&rft.aufirst=L&rft.date=1991-03-01&rft.volume=19&rft.issue=2&rft.spage=443&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 - 1991-08-14 N1 - Date created - 1991-08-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparative disposition and metabolism of 1,2,3-trichloropropane in rats and mice. AN - 80663030; 1676646 AB - 1,2,3-Trichloropropane (TCP) has been used as a solvent and degreasing agent and as an intermediate in pesticide manufacture. TCP is currently the subject of a National Toxicology Program chronic toxicity study. The present study is part of a larger effort to characterize the toxicity of TCP. Following acute oral exposure of male and female F344 rats (30 mg/kg) and male B6C3F1 mice (30 and 60 mg/kg), TCP was rapidly absorbed, metabolized, and excreted. The major route of excretion of TCP was in the urine. By 60 hr postdosing, rats had excreted 50% and mice 65% of the administered dose by this route. Exhalation as 14CO2 and excretion in the feces each accounted for 20% of the total dose in 60 hr rats and 20 and 15%, respectively, in mice. No apparent sex-related differences were observed in the ability of the rats to excrete TCP-derived radioactivity. At 60 hr, TCP-derived radioactivity was most concentrated in the liver, kidney, and forestomach in both rats and male mice. Male mice eliminated TCP-derived radioactivity more rapidly than rats and lower concentrations of radioactivity were found in tissues 60 hr after dosing in mice. Two urinary metabolites were isolated and identified by NMR, mass spectroscopy, and comparison with synthetic standards, as N-acetyl- and S-(3-chloro-2-hydroxypropyl)cysteine. Analyses of the early urine (0-6 hr) showed this mercapturic acid to be the major metabolite in rat urine and was only a minor component in mouse urine. 2-(S-Glutathionyl)malonic acid was identified by NMR and mass spectrometry and by chemical synthesis as the major biliary metabolite in rats.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Drug metabolism and disposition: the biological fate of chemicals AU - Mahmood, N A AU - Overstreet, D AU - Burka, L T AD - Experimental Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. PY - 1991 SP - 411 EP - 418 VL - 19 IS - 2 SN - 0090-9556, 0090-9556 KW - Carbon Dioxide KW - 142M471B3J KW - 1,2,3-trichloropropane KW - 3MJ7QCK0Z0 KW - Propane KW - T75W9911L6 KW - Index Medicus KW - Rats KW - Oxidation-Reduction KW - Mice, Inbred Strains KW - Animals KW - Rats, Inbred F344 KW - Biotransformation KW - Mice KW - Intestinal Absorption KW - Bile -- metabolism KW - Tissue Distribution KW - Carbon Dioxide -- metabolism KW - Male KW - Chromatography, High Pressure Liquid KW - Propane -- metabolism KW - Propane -- analogs & derivatives KW - Propane -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80663030?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Comparative+disposition+and+metabolism+of+1%2C2%2C3-trichloropropane+in+rats+and+mice.&rft.au=Mahmood%2C+N+A%3BOverstreet%2C+D%3BBurka%2C+L+T&rft.aulast=Mahmood&rft.aufirst=N&rft.date=1991-03-01&rft.volume=19&rft.issue=2&rft.spage=411&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 - 1991-08-14 N1 - Date created - 1991-08-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Use of a focal infectivity assay for testing susceptibility of HIV to antiviral agents. AN - 80659949; 2064772 AB - A highly sensitive and quantitative focal immunoassay has been developed for detecting the human immunodeficiency virus (HIV). The assay can be used to measure cell-free virus or the production of HIV by virus-infected cells. Both laboratory-adapted strains of HIV and patient isolates can be studied with this assay. In this communication, we demonstrate the utility of this assay for measuring the effects of anti-HIV agents on viral isolates. We show that the anti-viral effects of such diverse agents as azidothymidine, interferon-alpha, immunotoxins, soluble CD4 and antibody can be accurately quantified. This assay may be used in the discovery and evaluation of new anti-HIV therapies or may be adapted for use in testing the sensitivity of patient isolates to standard therapeutic agents. JF - BioTechniques AU - Pincus, S H AU - Wehrly, K AU - Chesebro, B AD - NIAID Rocky Mountain Laboratories. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 336 EP - 342 VL - 10 IS - 3 SN - 0736-6205, 0736-6205 KW - Antiviral Agents KW - 0 KW - Gene Products, env KW - HIV Antibodies KW - HIV Envelope Protein gp120 KW - HIV Envelope Protein gp160 KW - Immunoglobulin G KW - Immunotoxins KW - Interferon Type I KW - Protein Precursors KW - Recombinant Proteins KW - Zidovudine KW - 4B9XT59T7S KW - Ricin KW - 9009-86-3 KW - Index Medicus KW - AIDS/HIV KW - Ricin -- administration & dosage KW - HeLa Cells KW - Humans KW - Zidovudine -- pharmacology KW - Immunoglobulin G -- pharmacology KW - Acquired Immunodeficiency Syndrome -- microbiology KW - Ricin -- pharmacology KW - HIV Envelope Protein gp120 -- immunology KW - Protein Precursors -- immunology KW - Interferon Type I -- pharmacology KW - Gene Products, env -- immunology KW - Immunotoxins -- pharmacology KW - HIV Antibodies -- pharmacology KW - HIV -- drug effects KW - Antiviral Agents -- pharmacology KW - HIV -- isolation & purification KW - Immunoenzyme Techniques UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80659949?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BioTechniques&rft.atitle=Use+of+a+focal+infectivity+assay+for+testing+susceptibility+of+HIV+to+antiviral+agents.&rft.au=Pincus%2C+S+H%3BWehrly%2C+K%3BChesebro%2C+B&rft.aulast=Pincus&rft.aufirst=S&rft.date=1991-03-01&rft.volume=10&rft.issue=3&rft.spage=336&rft.isbn=&rft.btitle=&rft.title=BioTechniques&rft.issn=07366205&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-14 N1 - Date created - 1991-08-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Immunological correlates of seasonal fluctuations in mood and behavior and their relationship to phototherapy. AN - 80658030; 2062967 AB - Immunological parameters were studied before and after phototherapy, with bright and dim light, in 38 individuals with a range of retrospectively reported seasonal changes in mood and behavior. There was a significant negative correlation between the degree of mood and behavioral difficulties in fall and winter (seasonality) and the total number of circulating natural killer cells. Changes in the numbers of circulating helper T cells correlated significantly with changes in mood following phototherapy. Moreover, mitogen-induced lymphocyte blastogenesis increased significantly after phototherapy, but there was no significant difference between the bright and dim light treatments. The results suggest that cellular immune function is associated with both seasonality and response to phototherapy. JF - Psychiatry research AU - Kasper, S AU - Rosenthal, N E AU - Barberi, S AU - Williams, A AU - Tamarkin, L AU - Rogers, S L AU - Pillemer, S R AD - Clinical Psychobiology Branch, National Institute of Mental Health (NIMH), Bethesda, MD. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 253 EP - 264 VL - 36 IS - 3 SN - 0165-1781, 0165-1781 KW - Index Medicus KW - Leukocyte Count -- radiation effects KW - Personality Tests KW - Lymphocyte Activation -- immunology KW - Lymphocyte Activation -- radiation effects KW - Humans KW - Adult KW - Retrospective Studies KW - Middle Aged KW - Dose-Response Relationship, Radiation KW - Killer Cells, Natural -- radiation effects KW - Male KW - Killer Cells, Natural -- immunology KW - Female KW - Depressive Disorder -- psychology KW - Depressive Disorder -- immunology KW - T-Lymphocyte Subsets -- radiation effects KW - T-Lymphocyte Subsets -- immunology KW - Seasons KW - Depressive Disorder -- therapy KW - Phototherapy -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80658030?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Immunological+correlates+of+seasonal+fluctuations+in+mood+and+behavior+and+their+relationship+to+phototherapy.&rft.au=Kasper%2C+S%3BRosenthal%2C+N+E%3BBarberi%2C+S%3BWilliams%2C+A%3BTamarkin%2C+L%3BRogers%2C+S+L%3BPillemer%2C+S+R&rft.aulast=Kasper&rft.aufirst=S&rft.date=1991-03-01&rft.volume=36&rft.issue=3&rft.spage=253&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 - 1991-08-08 N1 - Date created - 1991-08-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Intravenous vs intraperitoneal sensitizer: implications for intraperitoneal photodynamic therapy. AN - 80651623; 1829531 AB - Photodynamic therapy (PDT) is a potential treatment for peritoneal carcinomatosis. However, little data is available regarding the relative distribution of sensitizer to tumor and intra-abdominal organs, optimal route of sensitizer administration, and maximal tolerated light dose. Tumor and normal tissue sensitizer levels were measured by tissue extraction 3, 24, 48 and 72 h after 10 mg/kg of Photofrin II was given intraperitoneally (IP) or intravenously (IV) in a mouse peritoneal tumor model, and the maximal tolerated PDT light dose determined. Equivalent tumor sensitizer levels were obtained regardless of the route of sensitizer administration. Route of administration, however, did affect the kinetics of tumor sensitizer elimination, with the half-time for elimination (T1/2) 113.6 h for IP drug and 60.6 h for IV drug. Route of administration also affected sensitizer levels in several intra-abdominal organs, resulting in somewhat higher tumor to liver and kidney levels at 24 and 72 h after IP sensitizer administration. Despite these tissue distribution differences, route of sensitizer administration did not significantly affect PDT toxicity or mortality when mice were treated with 630 nm light. The maximum tolerated light dose was 1.04 J/cm2. These parameters will prove helpful in designing large scale animal trials assessing the efficacy and safety of intra-abdominal PDT. JF - Photochemistry and photobiology AU - Perry, R R AU - Smith, P D AU - Evans, S AU - Pass, H I AD - Thoracic Oncology Section, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 335 EP - 340 VL - 53 IS - 3 SN - 0031-8655, 0031-8655 KW - Antineoplastic Agents KW - 0 KW - Hematoporphyrins KW - Radiation-Sensitizing Agents KW - Dihematoporphyrin Ether KW - 97067-70-4 KW - Index Medicus KW - Injections, Intraperitoneal KW - Animals KW - Injections, Intravenous KW - Mice, Inbred C57BL KW - Mice KW - Tissue Distribution KW - Sarcoma, Experimental -- drug therapy KW - Antineoplastic Agents -- administration & dosage KW - Hematoporphyrins -- pharmacokinetics KW - Hematoporphyrins -- administration & dosage KW - Photochemotherapy KW - Hematoporphyrins -- therapeutic use KW - Radiation-Sensitizing Agents -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80651623?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Photochemistry+and+photobiology&rft.atitle=Intravenous+vs+intraperitoneal+sensitizer%3A+implications+for+intraperitoneal+photodynamic+therapy.&rft.au=Perry%2C+R+R%3BSmith%2C+P+D%3BEvans%2C+S%3BPass%2C+H+I&rft.aulast=Perry&rft.aufirst=R&rft.date=1991-03-01&rft.volume=53&rft.issue=3&rft.spage=335&rft.isbn=&rft.btitle=&rft.title=Photochemistry+and+photobiology&rft.issn=00318655&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-02 N1 - Date created - 1991-08-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evidence for calcitonin gene-related peptide contacts on a population of lamina I projection neurons. AN - 80649325; 1711858 AB - Using double-labeling techniques, we evaluated small diameter primary afferent input, as indicated by calcitonin gene-related peptide-immunoreactive varicosities, to a population of lamina I projection neurons in the rat lumbar spinal cord. About one third of the lamina I neurons labeled after injections of a retrograde tracer into the region surrounding the brachium conjunctivum received contacts from immunoreactive varicosities. Significantly fewer immunoreactive varicosities were in apposition to fusiform neurons than pyramidal or flattened neurons. A positive correlation was found between the size of the retrogradely labeled neuron and the number of contacts received. This study demonstrates that a known population of nociceptive lamina I neurons received direct input from presumed nociceptive primary afferents. JF - Journal of chemical neuroanatomy AU - Nahin, R L AU - Humphrey, E AU - Hylden, J L AD - Neurobiology and Anesthesiology Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892. PY - 1991 SP - 123 EP - 129 VL - 4 IS - 2 SN - 0891-0618, 0891-0618 KW - Wheat Germ Agglutinin-Horseradish Peroxidase Conjugate KW - 0 KW - Wheat Germ Agglutinins KW - Calcitonin Gene-Related Peptide KW - 83652-28-2 KW - Cholera Toxin KW - 9012-63-9 KW - Horseradish Peroxidase KW - EC 1.11.1.- KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Immunohistochemistry KW - Male KW - Immunoenzyme Techniques KW - Axonal Transport KW - Afferent Pathways -- cytology KW - Brain -- cytology KW - Afferent Pathways -- anatomy & histology KW - Calcitonin Gene-Related Peptide -- analysis KW - Neurons -- cytology KW - Brain -- anatomy & histology KW - Neurons -- physiology KW - Afferent Pathways -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80649325?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+chemical+neuroanatomy&rft.atitle=Evidence+for+calcitonin+gene-related+peptide+contacts+on+a+population+of+lamina+I+projection+neurons.&rft.au=Nahin%2C+R+L%3BHumphrey%2C+E%3BHylden%2C+J+L&rft.aulast=Nahin&rft.aufirst=R&rft.date=1991-03-01&rft.volume=4&rft.issue=2&rft.spage=123&rft.isbn=&rft.btitle=&rft.title=Journal+of+chemical+neuroanatomy&rft.issn=08910618&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-02 N1 - Date created - 1991-08-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The partial opioid agonist, buprenorphine, protects against lethal effects of cocaine. AN - 80632869; 1647294 AB - Buprenorphine (0.3-3.0 mg/kg) produced dose-dependent protection against the lethal effects of cocaine in mice. The (+)-enantiomer of buprenorphine did not protect up to doses over 100 times greater than the lowest effective dose of its (-)-enantiomer. The protective effects were also produced by the opioid agonists morphine and methadone, but not by the opioid antagonist, naltrexone. Low doses of naltrexone (0.3-1.0 mg/kg) blocked the protective effects of buprenorphine. Protection conferred by buprenorphine was not observed in CXBK mice, a recombinant inbred strain relatively devoid of mu-opioid receptors. Thus, buprenorphine appears to protect against the lethal effects of cocaine by a process mediated by mu-opioid receptors. The present results should provide some additional safety assurance in future clinical trials with buprenorphine, especially in outpatient trials where cocaine abuse may continue along with treatment. JF - Drug and alcohol dependence AU - Witkin, J M AU - Johnson, R E AU - Jaffe, J H AU - Goldberg, S R AU - Grayson, N A AU - Rice, K C AU - Katz, J L AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 177 EP - 184 VL - 27 IS - 2 SN - 0376-8716, 0376-8716 KW - Receptors, Opioid KW - 0 KW - Receptors, Opioid, mu KW - Buprenorphine KW - 40D3SCR4GZ KW - Naltrexone KW - 5S6W795CQM KW - Morphine KW - 76I7G6D29C KW - Cocaine KW - I5Y540LHVR KW - Methadone KW - UC6VBE7V1Z KW - Index Medicus KW - Seizures -- chemically induced KW - Mice, Inbred Strains KW - Animals KW - Dose-Response Relationship, Drug KW - Receptors, Opioid -- drug effects KW - Brain -- drug effects KW - Naltrexone -- pharmacology KW - Mice KW - Seizures -- prevention & control KW - Morphine -- pharmacology KW - Methadone -- pharmacology KW - Buprenorphine -- pharmacology KW - Cocaine -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80632869?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Drug+and+alcohol+dependence&rft.atitle=The+partial+opioid+agonist%2C+buprenorphine%2C+protects+against+lethal+effects+of+cocaine.&rft.au=Witkin%2C+J+M%3BJohnson%2C+R+E%3BJaffe%2C+J+H%3BGoldberg%2C+S+R%3BGrayson%2C+N+A%3BRice%2C+K+C%3BKatz%2C+J+L&rft.aulast=Witkin&rft.aufirst=J&rft.date=1991-03-01&rft.volume=27&rft.issue=2&rft.spage=177&rft.isbn=&rft.btitle=&rft.title=Drug+and+alcohol+dependence&rft.issn=03768716&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-01 N1 - Date created - 1991-08-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Promotion of mouse lung tumors by bioaccumulated polychlorinated aromatic hydrocarbons. AN - 80618393; 1904809 AB - Lung tumors initiated in infant Swiss mice by N-nitrosodimethylamine (NDMA) were promoted by a single dose of a mixture of polychlorinated biphenyls (PCBs), Aroclor 1254 (250 or 500 mg/kg) given 4 days later. The tumors were typical alveologenic adenomas, and their number increased gradually over the course of 1 year to a maximum 4-fold enhancement in average tumor number compared with those given NDMA alone. The time course pattern suggested continuous tumor stimulation by the nonmetabolized PCB congeners retained in the tissues. Content of the nine major bioretained PCB congeners in carcass, liver, and lung was determined at intervals after treatment. Several showed tissue-specific retention patterns: 2,3,3',4,4'-PCB was selectively retained in lung and liver, and 2,2',3,4,4', 5'-HCB in lung. In tests of the tumor-promoting ability of individual congeners, the 2,2',3,4,4',5'-HCB, an Ah receptor agonist, promoted lung tumors when given singly, whereas another prominent bioretained congener, the 2,2',4,4',5,5'-HCB, an Ah receptor antagonist, did not promote, and in fact abrogated the positive effect of the 2,2',3,4,4',5'-HCB. In a parallel examination of persistent biochemical effects, a single low dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (5 nmole/kg) resulted in significant elevation of immunochemically detected protein and enzymatic activity of cytochrome P450 IA1 in lung for at least 12 weeks; these parameters were elevated for at least 30 weeks after a single dose of Aroclor 1254 (500 mg/kg). Taken together these results suggest that Ah-receptor-dependent induction of cytochrome P450 IA1 in mouse lung is correlated with and possibly causally involved in promotion of tumors by retained congeners. JF - Experimental lung research AU - Anderson, L M AU - Beebe, L E AU - Fox, S D AU - Issaq, H J AU - Kovatch, R M AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick, MD 21701. PY - 1991 SP - 455 EP - 471 VL - 17 IS - 2 SN - 0190-2148, 0190-2148 KW - Carcinogens KW - 0 KW - N-Methylaspartate KW - 6384-92-5 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Polychlorinated Biphenyls KW - DFC2HB4I0K KW - Index Medicus KW - Animals KW - Cocarcinogenesis KW - Enzyme Induction -- drug effects KW - Organ Specificity -- physiology KW - N-Methylaspartate -- toxicity KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Mice KW - Polychlorinated Biphenyls -- toxicity KW - Carcinogens -- pharmacokinetics KW - Lung Neoplasms -- chemically induced KW - Polychlorinated Biphenyls -- pharmacokinetics KW - Lung Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80618393?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+lung+research&rft.atitle=Promotion+of+mouse+lung+tumors+by+bioaccumulated+polychlorinated+aromatic+hydrocarbons.&rft.au=Anderson%2C+L+M%3BBeebe%2C+L+E%3BFox%2C+S+D%3BIssaq%2C+H+J%3BKovatch%2C+R+M&rft.aulast=Anderson&rft.aufirst=L&rft.date=1991-03-01&rft.volume=17&rft.issue=2&rft.spage=455&rft.isbn=&rft.btitle=&rft.title=Experimental+lung+research&rft.issn=01902148&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-25 N1 - Date created - 1991-07-25 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Exp Lung Res 1992 May-Jun;18(3):433 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Correlation of data from the strain A mouse bioassay with long-term bioassays. AN - 80618284; 2050041 AB - Fifty-nine chemicals that had completed National Cancer Institute rat and mouse 2-year carcinogenicity tests were tested in the strain A mouse pulmonary tumor assay. Without knowledge of chemical identity, 53 chemicals were tested in strain A mice in one laboratory and 30 were tested in a second independent laboratory. Strain A tests on 24 of these chemicals were conducted in both laboratories. The strain A results were generally not predictive of the 2-year rat and mouse carcinogenicity test results. Furthermore, there was poor agreement of strain A results between the two laboratories. Although a variety of explanations may be invoked to explain the lack of concordance between the strain A tests and the 2-year rat and mouse tests, no one factor is sufficient to rationalize the poor concordance between strain A and 2-year carcinogenicity bioassay results. JF - Experimental lung research AU - Maronpot, R R AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. PY - 1991 SP - 425 EP - 431 VL - 17 IS - 2 SN - 0190-2148, 0190-2148 KW - Index Medicus KW - Animals KW - Biological Assay KW - Mice KW - Time Factors KW - Mice, Inbred A KW - Carcinogenicity Tests -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80618284?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+lung+research&rft.atitle=Correlation+of+data+from+the+strain+A+mouse+bioassay+with+long-term+bioassays.&rft.au=Maronpot%2C+R+R&rft.aulast=Maronpot&rft.aufirst=R&rft.date=1991-03-01&rft.volume=17&rft.issue=2&rft.spage=425&rft.isbn=&rft.btitle=&rft.title=Experimental+lung+research&rft.issn=01902148&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-25 N1 - Date created - 1991-07-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Histologic characterization of mouse bronchiolar cell hyperplasia, metaplasia, and neoplasia induced intratracheally by 3-methylcholanthrene. AN - 80618245; 1646707 AB - Female B6C3F1 mice were treated intratracheally with 3-methylcholanthrene (MCA) at intervals of once every 2 weeks for a total of six doses each of 222 micrograms or 457 micrograms/mouse per dose. Animals were necropsied when found dead, moribund, or at the end of the study 43 weeks after the first treatment. Controls were treated with the vehicle (0.2% gelatin saline) only. Lungs were fixed in neutral buffered formalin and processed for light microscopic evaluation. Proliferative and metaplastic bronchiolar cell alterations were seen both within bronchioles and in the alveolar parenchyma. In both locations, changes included hyperplasia of nonciliated cells, squamous cell metaplasia, presence of ciliated cells, and mucous cell metaplasia. Mucous cells were either positive for alcian blue or the periodic-acid Schiff's reaction (PAS), or appeared eosinophilic with hematoxylin and eosin (H&E) but colorless with PAS. Tumors seemed to develop from both extra- and intrabronchiolar areas of cellular proliferation and invaded pulmonary structures. The majority were squamous cell carcinomas and adenosquamous carcinomas, accompanied by a few mucinous cell tumors and some rare tumors that were largely composed of ciliated cells. Combinations of the different metaplastic changes were frequently present in these neoplasms. In summary, it appears that tumors originating from bronchiolar cells in mice show the same morphologic variability that is observed in hyperplastic and metaplastic bronchiolar cells within airways. JF - Experimental lung research AU - Rehm, S AU - Kelloff, G J AD - Tumor Pathology and Pathogenesis Section, National Cancer Institute, Frederick, Maryland 21702-1201. PY - 1991 SP - 229 EP - 244 VL - 17 IS - 2 SN - 0190-2148, 0190-2148 KW - Methylcholanthrene KW - 56-49-5 KW - Index Medicus KW - Mice, Inbred Strains KW - Animals KW - Hyperplasia -- chemically induced KW - Intubation, Intratracheal KW - Mice KW - Metaplasia -- chemically induced KW - Female KW - Adenocarcinoma, Bronchiolo-Alveolar -- chemically induced KW - Adenocarcinoma, Bronchiolo-Alveolar -- pathology KW - Lung Neoplasms -- chemically induced KW - Bronchi -- pathology KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80618245?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+lung+research&rft.atitle=Histologic+characterization+of+mouse+bronchiolar+cell+hyperplasia%2C+metaplasia%2C+and+neoplasia+induced+intratracheally+by+3-methylcholanthrene.&rft.au=Rehm%2C+S%3BKelloff%2C+G+J&rft.aulast=Rehm&rft.aufirst=S&rft.date=1991-03-01&rft.volume=17&rft.issue=2&rft.spage=229&rft.isbn=&rft.btitle=&rft.title=Experimental+lung+research&rft.issn=01902148&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-25 N1 - Date created - 1991-07-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Proliferative lesions of the mouse lung: progression studies in strain A mice. AN - 80618212; 2050022 AB - The progression of pulmonary neoplasia was examined in strain A/J male mice treated with a single dose of vinyl carbamate (60 mg/kg, i.p.) 6 weeks after birth. Interim sacrifices were performed at 7, 8, 10, 12, or 14 months. Proliferative lesions of the lung were divided into four categories: hyperplasias, adenomas, carcinomas arising within adenomas, and carcinomas. Grossly visible surface tumor counts, histologic diagnoses, and morphometric measurements of histologic lesions were used to evaluate progression. Vinyl carbamate-treated mice showed increased mean surface tumor counts at all time points. Diagnostic evaluation suggested that as a function of time, the relative frequency of hyperplasias decreased and the relative frequency of adenomas increased. The relative frequency of adenomas subsequently decreased, whereas the relative frequency of carcinomas increased. At all time points, carcinomas arising within adenomas were present. As time progressed, the number of carcinomas arising within adenomas decreased, whereas the number of "pure" carcinomas increased. Morphometric analysis of lesions indicated hyperplasias to be small, that adenomas were larger than hyperplasias, and carcinomas were larger than adenomas and hyperplasias, suggesting that few adenomas or carcinomas arise de novo. Collectively, these data suggest that the majority of pulmonary tumors in A/J mice treated with vinyl carbamate arise as hyperplasias, progress to adenomas, and ultimately result in carcinomas. JF - Experimental lung research AU - Foley, J F AU - Anderson, M W AU - Stoner, G D AU - Gaul, B W AU - Hardisty, J F AU - Maronpot, R R AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. PY - 1991 SP - 157 EP - 168 VL - 17 IS - 2 SN - 0190-2148, 0190-2148 KW - Urethane KW - 3IN71E75Z5 KW - vinyl carbamate KW - 7Y2431GOM5 KW - Index Medicus KW - Animals KW - Urethane -- analogs & derivatives KW - Cell Division -- physiology KW - Disease Models, Animal KW - Mice KW - Male KW - Mice, Inbred A KW - Lung Neoplasms -- genetics KW - Lung Neoplasms -- chemically induced KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80618212?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+lung+research&rft.atitle=Proliferative+lesions+of+the+mouse+lung%3A+progression+studies+in+strain+A+mice.&rft.au=Foley%2C+J+F%3BAnderson%2C+M+W%3BStoner%2C+G+D%3BGaul%2C+B+W%3BHardisty%2C+J+F%3BMaronpot%2C+R+R&rft.aulast=Foley&rft.aufirst=J&rft.date=1991-03-01&rft.volume=17&rft.issue=2&rft.spage=157&rft.isbn=&rft.btitle=&rft.title=Experimental+lung+research&rft.issn=01902148&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-25 N1 - Date created - 1991-07-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of Clara cells and type II cells in the development of pulmonary tumors in rats and mice following exposure to a tobacco-specific nitrosamine. AN - 80615086; 2050030 AB - The role of the Clara and type II cell in the development of pulmonary tumors in the A/J mouse and Fischer rat was investigated by determining the relationship of DNA methylation and repair in pulmonary cells to oncogene activation and by characterizing the morphology of pulmonary tumors induced by treatment with 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). Marked differences in the formation of the promutagenic adduct O6-methylguanine (O6MG) were observed in pulmonary cells following treatment of rats with NNK. Concentrations of this adduct in Clara cells greatly exceeded (3- to 30-fold) those detected in type II cells and whole lung with doses of NNK ranging from 0.1 to 50 mg/kg. In addition, very low rates of repair of this adduct were detected in Clara cells, whereas efficient adduct removal occurred in type II cells. The importance of this adduct and the role of cell specificity was suggested by the fact that a strong correlation was observed between the concentration of O6MG in Clara cells and tumor incidence in the Fischer rat with doses of NNK ranging from 0.03-50 mg/kg. In contrast, no differences in adduct concentration between type II and Clara cells from A/J mice were observed under conditions resulting in pulmonary tumor formation. Activation of the K-ras gene was detected in lung tumors from A/J mice. This gene was activated by a mutation in codon 12 involving a GC to AT transition (GGT to GAT) and is consistent with base mispairing produced by the formation of O6MG. Activation of this gene was not associated with lung tumor formation in the Fischer rat. DNA from rat lung tumors did induce tumors in the nude mouse carcinogenicity assay. In addition, rat repetitive sequences were detected in DNA isolated from these nude mouse tumors. In spite of the cell selectivity for DNA methylation in Clara cells from rat and the relationship between O6MG formation and tumorigenicity, early proliferative lesions observed in both mice and rats involved the alveolar areas. Ultrastructural examination of these lesions and adenomas revealed morphologic features characteristic of the type II cell. Thus the lack of agreement between biochemical and morphological findings makes it difficult to hypothesize a cell of origin for the pulmonary neoplasms induced by NNK. However, these studies indicate that the concentration of O6MG in Clara cells is an excellent indicator of the carcinogenic potency of NNK in the rat.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Experimental lung research AU - Belinsky, S A AU - Devereux, T R AU - White, C M AU - Foley, J F AU - Maronpot, R R AU - Anderson, M W AD - Laboratory of Molecular Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina. PY - 1991 SP - 263 EP - 278 VL - 17 IS - 2 SN - 0190-2148, 0190-2148 KW - Carcinogens KW - 0 KW - DNA, Neoplasm KW - Nitrosamines KW - Guanine KW - 5Z93L87A1R KW - 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone KW - 7S395EDO61 KW - O-(6)-methylguanine KW - 9B710FV2AE KW - Methyltransferases KW - EC 2.1.1.- KW - O(6)-Methylguanine-DNA Methyltransferase KW - EC 2.1.1.63 KW - Index Medicus KW - Animals KW - Cell Division -- drug effects KW - Mice KW - DNA, Neoplasm -- isolation & purification KW - Gene Expression Regulation, Neoplastic -- drug effects KW - Guanine -- metabolism KW - Rats KW - Rats, Inbred F344 KW - Oncogenes -- genetics KW - Base Sequence KW - Gene Amplification -- genetics KW - Transfection -- genetics KW - Molecular Sequence Data KW - Guanine -- analogs & derivatives KW - Methyltransferases -- metabolism KW - Male KW - Plants, Toxic KW - Nitrosamines -- pharmacology KW - Carcinogens -- pharmacology KW - Tobacco -- analysis KW - Lung Neoplasms -- genetics KW - Lung Neoplasms -- chemically induced KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80615086?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+lung+research&rft.atitle=Role+of+Clara+cells+and+type+II+cells+in+the+development+of+pulmonary+tumors+in+rats+and+mice+following+exposure+to+a+tobacco-specific+nitrosamine.&rft.au=Belinsky%2C+S+A%3BDevereux%2C+T+R%3BWhite%2C+C+M%3BFoley%2C+J+F%3BMaronpot%2C+R+R%3BAnderson%2C+M+W&rft.aulast=Belinsky&rft.aufirst=S&rft.date=1991-03-01&rft.volume=17&rft.issue=2&rft.spage=263&rft.isbn=&rft.btitle=&rft.title=Experimental+lung+research&rft.issn=01902148&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-25 N1 - Date created - 1991-07-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pulmonary carcinogenesis in transgenic mice. AN - 80614930; 2050033 AB - Use of genetically engineered mice offers a unique approach to identifying and investigating factors that may influence tumor development. We have used conventional histopathologic and ultrastructural techniques to characterize lung tumors in three lines of transgenic mice bearing an albumin enhancer/promoter linked to a mutated human H-ras gene. Mice in all three lines developed multiple alveolar-bronchiolar (A/B) adenocarcinomas that are eventually lethal. The large diversity in tumor morphological features and differential tumor growth rates suggests that secondary events contribute to tumor phenotype and biological behavior. Two of the transgenic lines developed numerous A/B neoplasms within 6 to 8 weeks and thus may be useful animal models for testing potential anticancer chemotherapeutic agents. The other line lived for approximately 10 months, had fewer A/B tumors, but also developed bronchiogenic tumors. All three transgenic lines may be useful models for studying factors that affect lung tumor development. JF - Experimental lung research AU - Maronpot, R R AU - Palmiter, R D AU - Brinster, R L AU - Sandgren, E P AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina. PY - 1991 SP - 305 EP - 320 VL - 17 IS - 2 SN - 0190-2148, 0190-2148 KW - H-ras KW - Albumins KW - 0 KW - Index Medicus KW - Animals KW - Albumins -- genetics KW - Enhancer Elements, Genetic -- genetics KW - Promoter Regions, Genetic -- genetics KW - Microscopy, Electron KW - Mice KW - Mice, Transgenic KW - Mutation KW - Female KW - Genes, ras -- genetics KW - Lung Neoplasms -- genetics KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80614930?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+lung+research&rft.atitle=Pulmonary+carcinogenesis+in+transgenic+mice.&rft.au=Maronpot%2C+R+R%3BPalmiter%2C+R+D%3BBrinster%2C+R+L%3BSandgren%2C+E+P&rft.aulast=Maronpot&rft.aufirst=R&rft.date=1991-03-01&rft.volume=17&rft.issue=2&rft.spage=305&rft.isbn=&rft.btitle=&rft.title=Experimental+lung+research&rft.issn=01902148&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-25 N1 - Date created - 1991-07-25 N1 - Date revised - 2017-01-13 N1 - Gene symbol - H-ras N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Origin of spontaneous and transplacentally induced mouse lung tumors from alveolar type II cells. AN - 80614759; 2050024 AB - Mouse lung tumors were induced transplacentally in offspring by treating C3H/HeNCrMTV- and Swiss Webster [Tac:(SW)fBR] mice during different periods of gestation with a single i.p. injection of N-nitrosoethylurea (ENU) at 0.5 mmol or 0.74 mmol/kg. Quantitative and qualitative evaluation of the lung tumors in the offspring at ages ranging from 1 week to 52 weeks was carried out by light microscopic study of hematoxylin and eosin-stained (H&E) serial and step sections. By nitroblue tetrazolium enzyme histochemistry, 3-hydroxybutyrate dehydrogenase (seen predominantly in Clara cells) was localized in frozen tissue sections. By avidin-biotin peroxidase complex immunohistochemistry, various specific cellular and nuclear markers were investigated on paraffin sections (antisera against surfactant apoprotein, Clara cell antigen, lysozyme, and 5-bromo-2' deoxyuridine). Normal lung and lung tumors were also studied by electron microscopy. A histological method was developed to assess all lesions present in the entire lung. It was shown that solid and papillary tumor types arose individually and that mixed solid/papillary forms represented a progression of the benign solid adenoma to the malignant papillary carcinoma. Immunocytochemical localization of DNA synthesis with 5-bromo-2' deoxyuridine gave the highest labeling indices at early stages of tumor growth. As the size of the papillary tumors increased, fewer nuclei were labeled/mm2 of tumor section. Lack of both specific Clara cell antigen and 3-hydroxybutyrate dehydrogenase and the absence of typical nonosmiophilic Clara cell granules indicated a cell of origin other than Clara cells. Evidence for alveolar type II cell origin of both solid and papillary neoplasms in spontaneous and induced tumors was found in the expression of surfactant apoprotein, the presence of mature lamellar bodies (solid tumors) or small lamellar bodies, and immature stages of lamellar bodies (papillary tumors). Lysozyme was present in mature alveolar type II cells and solid tumors but absent in fetal lung and papillary neoplasms. Tumors induced on gestation day 14 or day 16 had all developed by 2 weeks of age and generally did not increase in multiplicity with age, whereas those induced on day 18 showed a protracted development with regard to frequency, growth (size), and progression. The multiplicity of mouse lung tumors induced at different stages of fetal development paralleled the number of alveolar type II precursor cells (i.e., followed a bell-shaped pattern peaking on day 16 of gestation). JF - Experimental lung research AU - Rehm, S AU - Devor, D E AU - Henneman, J R AU - Ward, J M AD - Tumor Pathology and Pathogenesis Section, National Cancer Institute, Frederick, MD 21702-1201. PY - 1991 SP - 181 EP - 195 VL - 17 IS - 2 SN - 0190-2148, 0190-2148 KW - Ethylnitrosourea KW - P8M1T4190R KW - Index Medicus KW - Animals KW - Mice, Inbred C3H KW - Mice KW - Rodent Diseases -- pathology KW - Female KW - Pregnancy KW - Lung Neoplasms -- veterinary KW - Pulmonary Alveoli -- drug effects KW - Pulmonary Alveoli -- cytology KW - Lung Neoplasms -- genetics KW - Lung Neoplasms -- chemically induced KW - Prenatal Exposure Delayed Effects KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80614759?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+lung+research&rft.atitle=Origin+of+spontaneous+and+transplacentally+induced+mouse+lung+tumors+from+alveolar+type+II+cells.&rft.au=Rehm%2C+S%3BDevor%2C+D+E%3BHenneman%2C+J+R%3BWard%2C+J+M&rft.aulast=Rehm&rft.aufirst=S&rft.date=1991-03-01&rft.volume=17&rft.issue=2&rft.spage=181&rft.isbn=&rft.btitle=&rft.title=Experimental+lung+research&rft.issn=01902148&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-25 N1 - Date created - 1991-07-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Applications of mouse lung tumor models: carcinogenesis studies. AN - 80614332; 2050039 JF - Experimental lung research AU - Griesemer, R A AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. PY - 1991 SP - 403 EP - 404 VL - 17 IS - 2 SN - 0190-2148, 0190-2148 KW - Index Medicus KW - Mice, Inbred A KW - Animals KW - Disease Models, Animal KW - Mice KW - Lung Neoplasms -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80614332?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+lung+research&rft.atitle=Applications+of+mouse+lung+tumor+models%3A+carcinogenesis+studies.&rft.au=Griesemer%2C+R+A&rft.aulast=Griesemer&rft.aufirst=R&rft.date=1991-03-01&rft.volume=17&rft.issue=2&rft.spage=403&rft.isbn=&rft.btitle=&rft.title=Experimental+lung+research&rft.issn=01902148&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-25 N1 - Date created - 1991-07-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - O-specific side-chain toxin-protein conjugates as parenteral vaccines for the prevention of shigellosis and related diseases. AN - 80611765; 2047664 AB - Only indirect evidence has been cited to document that lipopolysaccharide-mediated virulence at the bacterial level and serum antibodies to the O-specific side chain of the lipopolysaccharide molecule may prevent shigellosis. Our proposed use of the B subunit of Shiga toxin as a carrier protein is based upon evidence (even more indirect) that serum antitoxin may reduce the severity of dysentery and diarrhea. Because animal models of disease may provide information inapplicable to the prediction of vaccine-induced protective immunity, we suggest that clinical trials in the population at risk should be started after successful completion of the safety and immunogenicity phases of vaccine development in laboratory animals and in the target population. Clinical studies of shigella vaccines are difficult because of the many causes of dysentery in a population with a high rate of intestinal disease. JF - Reviews of infectious diseases AU - Robbins, J B AU - Chu, C AU - Watson, D C AU - Szu, S C AU - Daniels, E M AU - Lowe, C U AU - Schneerson, R AD - National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland. PY - 1991 SP - S362 EP - S365 VL - 13 Suppl 4 SN - 0162-0886, 0162-0886 KW - Bacterial Toxins KW - 0 KW - Bacterial Vaccines KW - Cytotoxins KW - Enterotoxins KW - Shiga Toxins KW - Index Medicus KW - Virulence KW - Enterotoxins -- immunology KW - Animals KW - Humans KW - Cytotoxins -- immunology KW - Dysentery, Bacillary -- prevention & control KW - Shigella -- immunology KW - Bacterial Toxins -- immunology KW - Shigella -- pathogenicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80611765?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Reviews+of+infectious+diseases&rft.atitle=O-specific+side-chain+toxin-protein+conjugates+as+parenteral+vaccines+for+the+prevention+of+shigellosis+and+related+diseases.&rft.au=Robbins%2C+J+B%3BChu%2C+C%3BWatson%2C+D+C%3BSzu%2C+S+C%3BDaniels%2C+E+M%3BLowe%2C+C+U%3BSchneerson%2C+R&rft.aulast=Robbins&rft.aufirst=J&rft.date=1991-03-01&rft.volume=13+Suppl+4&rft.issue=&rft.spage=S362&rft.isbn=&rft.btitle=&rft.title=Reviews+of+infectious+diseases&rft.issn=01620886&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-17 N1 - Date created - 1991-07-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In utero PCB/PCDF exposure: relation of developmental delay to dysmorphology and dose. AN - 80605064; 1710764 AB - In 1979, there was an outbreak of food poisoning in central Taiwan due to cooking oil contaminated with polychlorinated biphenyls and their thermal degradation products. Starting in 1985, we studied 128 children born to exposed women after the oil was removed from the market; the exposure of these children was transplacental or through breast milk. We also studied matched controls. The exposed children exhibited developmental delays as measured by parental report, by neurologic examination, and by standard cognitive tests; delay was seen at all ages and persisted over time. Delay was greater in children who were smaller in size and in children who had exhibited neonatal symptoms of intoxication. Children with a history of nail deformity also were delayed. However, there was little relationship between other physical findings or measures of maternal exposure and developmental delay. There was some indication that the child's prenatal exposure was more important to developmental delay than was exposure through breast milk. JF - Neurotoxicology and teratology AU - Yu, M L AU - Hsu, C C AU - Gladen, B C AU - Rogan, W J AD - Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. PY - 1991 SP - 195 EP - 202 VL - 13 IS - 2 SN - 0892-0362, 0892-0362 KW - Benzofurans KW - 0 KW - Dibenzofurans, Polychlorinated KW - Teratogens KW - Polychlorinated Biphenyls KW - DFC2HB4I0K KW - Index Medicus KW - Taiwan KW - Abnormalities, Drug-Induced KW - Humans KW - Skin Pigmentation -- drug effects KW - Infant, Newborn KW - Child KW - Child, Preschool KW - Pregnancy KW - Infant KW - Nails, Malformed KW - Foodborne Diseases KW - Female KW - Male KW - Developmental Disabilities -- chemically induced KW - Maternal-Fetal Exchange KW - Polychlorinated Biphenyls -- poisoning KW - Benzofurans -- poisoning KW - Benzofurans -- administration & dosage KW - Polychlorinated Biphenyls -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80605064?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurotoxicology+and+teratology&rft.atitle=In+utero+PCB%2FPCDF+exposure%3A+relation+of+developmental+delay+to+dysmorphology+and+dose.&rft.au=Yu%2C+M+L%3BHsu%2C+C+C%3BGladen%2C+B+C%3BRogan%2C+W+J&rft.aulast=Yu&rft.aufirst=M&rft.date=1991-03-01&rft.volume=13&rft.issue=2&rft.spage=195&rft.isbn=&rft.btitle=&rft.title=Neurotoxicology+and+teratology&rft.issn=08920362&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-15 N1 - Date created - 1991-07-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of tixocortol pivalate on gastrointestinal disease in systemic mastocytosis: a preliminary study. AN - 80604617; 2043986 AB - Tixocortol pivalate is a steroid reportedly without significant adrenal-pituitary axis suppression when administered via the gastrointestinal tract. To determine whether this steroid would suppress the gastrointestinal manifestations of systemic mastocytosis, we performed an open clinical trial for safety and efficacy with tixocortal pivalate in four patients for periods of 8-15 weeks. All patients showed a decrease in the symptoms of abdominal pain and frequency of stools. Laboratory parameters of malabsorption improved in parallel with symptom relief. Histopathologic abnormalities of the small bowel improved in one patient. There was no significant suppression of the pituitary-adrenal axis. Two patients developed fluid retention while on tixocortol pivalate, which was attributed to a mineralocorticoid effect. One patient had a fall in AM cortisol. In summary, this study strongly suggests that tixocortol pivalate, when administered orally, has gastrointestinal anti-inflammatory activity comparable to conventional steroids, but may not be entirely without adrenal-suppressive effect and may lead to fluid retention in some patients. Further studies are warranted to assess the value of tixocortol pivalate in the therapy of inflammatory diseases of the upper gastrointestinal tract. JF - Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology AU - Friedman, B S AU - Metcalfe, D D AD - Mast Cell Physiology Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 183 EP - 188 VL - 21 IS - 2 SN - 0954-7894, 0954-7894 KW - Anti-Inflammatory Agents KW - 0 KW - tixocortol pivalate KW - 6K28E35M3B KW - Hydrocortisone KW - WI4X0X7BPJ KW - Index Medicus KW - Humans KW - Adult KW - Anti-Inflammatory Agents -- therapeutic use KW - Aged KW - Middle Aged KW - Malabsorption Syndromes -- etiology KW - Pituitary-Adrenal System -- drug effects KW - Male KW - Female KW - Malabsorption Syndromes -- drug therapy KW - Mastocytosis -- drug therapy KW - Gastrointestinal Diseases -- drug therapy KW - Gastrointestinal Diseases -- etiology KW - Hydrocortisone -- adverse effects KW - Mastocytosis -- complications KW - Hydrocortisone -- analogs & derivatives KW - Hydrocortisone -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80604617?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+and+experimental+allergy+%3A+journal+of+the+British+Society+for+Allergy+and+Clinical+Immunology&rft.atitle=Effects+of+tixocortol+pivalate+on+gastrointestinal+disease+in+systemic+mastocytosis%3A+a+preliminary+study.&rft.au=Friedman%2C+B+S%3BMetcalfe%2C+D+D&rft.aulast=Friedman&rft.aufirst=B&rft.date=1991-03-01&rft.volume=21&rft.issue=2&rft.spage=183&rft.isbn=&rft.btitle=&rft.title=Clinical+and+experimental+allergy+%3A+journal+of+the+British+Society+for+Allergy+and+Clinical+Immunology&rft.issn=09547894&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-15 N1 - Date created - 1991-07-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Metergoline blocks the behavioral and neuroendocrine effects of orally administered m-chlorophenylpiperazine in patients with obsessive-compulsive disorder. AN - 80520963; 2018816 AB - The pharmacological probe, meta-chlorophenylpiperazine (m-CPP), administered orally to patients with obsessive-compulsive disorder (OCD) has been shown to induce an acute exacerbation in OCD symptoms as well as an exaggerated anxiogenic response in comparison with controls. The mechanism of m-CPP's behavioral effects in humans remains controversial. To further study m-CPP's actions in OCD patients, we completed a series of double-blind pharmacological challenges in 12 OCD patients. Six OCD patients received four separate challenges: placebo, metergoline, m-CPP, and metergoline plus m-CPP; the second group (n = 6) received metergoline and metergoline plus m-CPP in separate challenges. OCD patients receiving placebo or metergoline alone failed to show evidence of significant changes on any of the behavioral rating scales, in contrast to the patients who received m-CPP alone who exhibited significant increases in anxiety and OCD symptoms. However, the 12 OCD patients who received pretreatment with metergoline before m-CPP experienced no significant changes from baseline OCD symptoms or other behavioral changes. m-CPP's ability to elicit elevations in plasma prolactin was blocked by metergoline pretreatment. Metergoline's ability to block m-CPP's effects on behavior and plasma prolactin lends further support to a serotonergic mediation of m-CPP's effects, including its elicitation of OCD symptoms. JF - Biological psychiatry AU - Pigott, T A AU - Zohar, J AU - Hill, J L AU - Bernstein, S E AU - Grover, G N AU - Zohar-Kadouch, R C AU - Murphy, D L AD - Section on Clinical Neuropharmacology, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1991/03/01/ PY - 1991 DA - 1991 Mar 01 SP - 418 EP - 426 VL - 29 IS - 5 SN - 0006-3223, 0006-3223 KW - Piperazines KW - 0 KW - Placebos KW - Receptors, Serotonin KW - Metergoline KW - 1501393LY5 KW - Serotonin KW - 333DO1RDJY KW - Prolactin KW - 9002-62-4 KW - 1-(3-chlorophenyl)piperazine KW - REY0CNO998 KW - Hydrocortisone KW - WI4X0X7BPJ KW - Index Medicus KW - Receptors, Serotonin -- physiology KW - Administration, Oral KW - Receptors, Serotonin -- drug effects KW - Drug Interactions KW - Prolactin -- blood KW - Serotonin -- physiology KW - Double-Blind Method KW - Humans KW - Hydrocortisone -- blood KW - Stimulation, Chemical KW - Psychiatric Status Rating Scales KW - Adult KW - Female KW - Male KW - Piperazines -- pharmacokinetics KW - Piperazines -- antagonists & inhibitors KW - Obsessive-Compulsive Disorder -- blood KW - Metergoline -- pharmacology KW - Obsessive-Compulsive Disorder -- physiopathology KW - Obsessive-Compulsive Disorder -- psychology KW - Piperazines -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80520963?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biological+psychiatry&rft.atitle=Metergoline+blocks+the+behavioral+and+neuroendocrine+effects+of+orally+administered+m-chlorophenylpiperazine+in+patients+with+obsessive-compulsive+disorder.&rft.au=Pigott%2C+T+A%3BZohar%2C+J%3BHill%2C+J+L%3BBernstein%2C+S+E%3BGrover%2C+G+N%3BZohar-Kadouch%2C+R+C%3BMurphy%2C+D+L&rft.aulast=Pigott&rft.aufirst=T&rft.date=1991-03-01&rft.volume=29&rft.issue=5&rft.spage=418&rft.isbn=&rft.btitle=&rft.title=Biological+psychiatry&rft.issn=00063223&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-05-30 N1 - Date created - 1991-05-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mechanism of action of food-associated polycyclic aromatic hydrocarbon carcinogens. AN - 80517624; 2017212 AB - The polycyclic aromatic hydrocarbon carcinogens are formed in the inefficient combustion of organic matter and contaminate foods through direct deposition from the atmosphere or during cooking or smoking of foods. These potent carcinogens and mutagens require metabolism to dihydrodiol epoxide metabolites in order to express their biological activities. In vitro studies show that these reactive metabolites can react with the bases in DNA with different specificities depending upon the hydrocarbon from which they are derived. Thus, the more potent carcinogens react more extensively with adenine residues in DNA than do the less potent carcinogens, with the result that mutation at A . T base pairs is enhanced for the more potent carcinogens. In the past few years, considerable clarification of the mechanism of metabolic activation have been achieved and the focus for the immediate future is expected to be on how the reactive metabolites actually bring about biological responses. JF - Mutation research AU - Dipple, A AU - Bigger, C A AD - NCI-Frederick Cancer Research and Development Center, ABL-Basic Research Program, MD 21702-1201. PY - 1991 SP - 263 EP - 276 VL - 259 IS - 3-4 SN - 0027-5107, 0027-5107 KW - Carcinogens KW - 0 KW - Epoxy Compounds KW - Mutagens KW - Polycyclic Compounds KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Molecular Structure KW - Animals KW - Base Sequence KW - Cooking KW - Molecular Sequence Data KW - Epoxy Compounds -- toxicity KW - DNA -- drug effects KW - Carcinogens -- metabolism KW - Mutagens -- metabolism KW - Polycyclic Compounds -- toxicity KW - Food Contamination KW - Carcinogens -- toxicity KW - Mutagens -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80517624?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mechanism+of+action+of+food-associated+polycyclic+aromatic+hydrocarbon+carcinogens.&rft.au=Dipple%2C+A%3BBigger%2C+C+A&rft.aulast=Dipple&rft.aufirst=A&rft.date=1991-03-01&rft.volume=259&rft.issue=3-4&rft.spage=263&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 - 1991-05-21 N1 - Date created - 1991-05-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The formation and occurrence of polynuclear aromatic hydrocarbons associated with food. AN - 80516839; 2017211 AB - Polynuclear aromatic hydrocarbons are common contaminants of processed food, usually at trace levels. These hydrocarbons are products of combustion and pyrolysis, and are present in petroleum and coal, and in products derived from them. Most polynuclear aromatic hydrocarbons are not carcinogenic, but some of them are, and a few are potent inducers of skin and lung tumors in mice. Their carcinogenic properties have not been fully explored, but they seem to be less potent by ingestion or inhalation, and they are known as a group to produce cancer in humans. The most effective carcinogens among them are those with 5 or 6 fused rings, and these tend to be less prevalent in mixtures than the 3- and 4-ring hydrocarbons, most of which are not carcinogenic. Sophisticated analytical methods, using solvent extraction and chromatography have been developed to detect and measure polynuclear aromatic hydrocarbons at levels of 1 in 10(9) (1 part per billion) or less, and these have been applied to the measurement of individual compounds in foods, as well as in products of combustion and pyrolysis. Wood smoke and smoked foods contain the carcinogenic benzo[a]pyrene at levels of 1 ppb, and other hydrocarbons; liquid smoke has lower levels. Crude vegetable oils have higher concentrations, but purified 'deodorized' oils have benzo[a]pyrene levels near 1 ppb. Sausages cooked over burning logs had as much as 200 ppb benzo[a]pyrene. Charcoal-broiled steaks and ground meat had benzo[a]pyrene concentrations up to 50 micrograms/kg, while less fatty pork and chicken had lower concentrations (up to 10 micrograms/kg). It was probable that the rendered fat dripped on to the hot charcoal and pyrolyzed to form quantities of polynuclear aromatic hydrocarbons, which rose with the smoke to deposit on the meat. Therefore, oven cooking or cooking with a heat source above the meat, or segregation of the meat from the smoke resulted in food containing negligible amounts of polynuclear aromatic hydrocarbons. Modifications of cookings practices accordingly would greatly reduce exposure to this group of carcinogens. JF - Mutation research AU - Lijinsky, W AD - NCI-Frederick Cancer Research Facility, BRI-Basic Research, Program, MD 21701. PY - 1991 SP - 251 EP - 261 VL - 259 IS - 3-4 SN - 0027-5107, 0027-5107 KW - Polycyclic Compounds KW - 0 KW - Index Medicus KW - Swine KW - Meat KW - Hot Temperature KW - Animals KW - Cattle KW - Cooking KW - Carcinogenicity Tests KW - Polycyclic Compounds -- analysis KW - Polycyclic Compounds -- toxicity KW - Food Contamination KW - Polycyclic Compounds -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80516839?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+formation+and+occurrence+of+polynuclear+aromatic+hydrocarbons+associated+with+food.&rft.au=Lijinsky%2C+W&rft.aulast=Lijinsky&rft.aufirst=W&rft.date=1991-03-01&rft.volume=259&rft.issue=3-4&rft.spage=251&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 - 1991-05-21 N1 - Date created - 1991-05-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - From science to social policy: an uncertain road. AN - 80514914; 2016869 JF - Journal of studies on alcohol AU - Gordis, E AD - National Institute on Alcohol Abuse and Alcoholism, Rockville, Md. 20857. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 101 EP - 109 VL - 52 IS - 2 SN - 0096-882X, 0096-882X KW - Methadone KW - UC6VBE7V1Z KW - Index Medicus KW - Methadone -- therapeutic use KW - Insurance Benefits -- legislation & jurisprudence KW - Genetic Testing -- trends KW - Humans KW - Substance Abuse Detection -- trends KW - Opioid-Related Disorders -- rehabilitation KW - Health Policy -- legislation & jurisprudence KW - Substance Abuse Detection -- legislation & jurisprudence KW - Health Policy -- trends KW - Insurance Benefits -- trends KW - Patient Advocacy -- legislation & jurisprudence KW - Science -- trends KW - Public Policy KW - Public Opinion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80514914?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=From+science+to+social+policy%3A+an+uncertain+road.&rft.au=Gordis%2C+E&rft.aulast=Gordis&rft.aufirst=E&rft.date=1991-03-01&rft.volume=52&rft.issue=2&rft.spage=101&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 - 1991-05-22 N1 - Date created - 1991-05-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Xeroderma pigmentosum: review and report of a case. AN - 80499154; 2011352 AB - Xeroderma pigmentosum is a rare inherited dermatosis that provides insight into the basic mechanism of carcinogenesis. It is a model disorder linking defective DNA repair with clinical abnormalities and neoplasia. UV light-induced damage to the skin begins early and results in multiple benign and malignant skin tumors, especially in sun-exposed areas of the head and neck. Oral cancers, primarily squamous cell carcinomas of the anterior third of the tongue, occur with greatly increased frequency. A patient with multiple facial neoplasia and oral manifestations of xeroderma pigmentosum is presented. The role of the dentist in surveillance of oral and perioral structures is emphasized. The dentist is advised against the use of UV light-curing units in these patients because UV-induced epithelial damage may cause dysplasia when DNA repair mechanisms are dysfunctional. JF - Oral surgery, oral medicine, and oral pathology AU - Patton, L L AU - Valdez, I H AD - National Institute of Dental Research, National Institutes of Health, Bethesda, Md. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 297 EP - 300 VL - 71 IS - 3 SN - 0030-4220, 0030-4220 KW - Composite Resins KW - 0 KW - Dentistry KW - Index Medicus KW - Carcinoma, Basal Cell -- physiopathology KW - Neoplasms, Radiation-Induced -- etiology KW - Humans KW - Carcinoma, Squamous Cell -- physiopathology KW - Adult KW - Ultraviolet Rays -- adverse effects KW - Melanoma -- physiopathology KW - Female KW - Mouth Neoplasms -- physiopathology KW - Xeroderma Pigmentosum -- pathology KW - DNA Repair -- radiation effects KW - Composite Resins -- contraindications KW - Xeroderma Pigmentosum -- genetics KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80499154?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oral+surgery%2C+oral+medicine%2C+and+oral+pathology&rft.atitle=Xeroderma+pigmentosum%3A+review+and+report+of+a+case.&rft.au=Patton%2C+L+L%3BValdez%2C+I+H&rft.aulast=Patton&rft.aufirst=L&rft.date=1991-03-01&rft.volume=71&rft.issue=3&rft.spage=297&rft.isbn=&rft.btitle=&rft.title=Oral+surgery%2C+oral+medicine%2C+and+oral+pathology&rft.issn=00304220&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-05-09 N1 - Date created - 1991-05-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Estrogen receptor, epidermal growth factor receptor and cellular ploidy in elutriated subpopulations of hepatocytes during liver tumor promotion by 17 alpha-ethinylestradiol in rats. AN - 80493556; 1672626 AB - 17 alpha-Ethinylestradiol (EE2)-mediated promotion of diethylnitrosamine (DEN)-initiated liver tumors was evaluated in distinct hepatocyte subpopulations. Our initiation-promotion regime consisted of a single dose of DEN (200 mg/kg) to ovariectomized rats, followed by chronic exposure to EE2 (90 micrograms/kg/day for 30 weeks). We observed significant increases in liver and uterine organ wts which were associated with liver tumor formation. Isolated hepatocytes were separated by elutriation into seven subpopulations. The early eluting subpopulations consisted of a greater proportion of diploid cells and they exhibited a preferential uptake of acridine orange, which is characteristic of periportal cells. With the increasing order of elutriated fractions, hepatocyte subpopulations of tetraploid and octaploid cells were obtained. Elutriation revealed that EE2 promotion enhanced nuclear estrogen receptor levels (3-fold) and gamma-glutamyltranspeptidase activity (5-fold) to a greater extent in the early eluting diploid subpopulations (1 and 2), even though total estrogen receptor (ER) levels were higher in the later eluting subpopulations. The stimulatory effect of EE2 on ER levels was associated with an increased ER occupancy in all subpopulations, although the effect was greatest in the later eluting fractions. Chronic EE2 exposure induced the emergence of new hepatocyte populations within fractions 6 and 7. Enhanced cell growth was observed in the DEN/EE2-derived hepatocytes by flow cytometric measurements of DNA synthesis. The new populations of altered cells expressed high levels of epidermal growth factor receptor (EGFR), with 90% of the cells positive for EGFR-antibody. In summary, our data demonstrate that many effects of EE2 on hepatocyte pathways involved in growth control occur in nearly all populations of cells, derived by elutriation although some effects such as the emergence of an EGFR-enriched population of hepatocytes are localized in specific populations. JF - Carcinogenesis AU - Vickers, A E AU - Lucier, G W AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 391 EP - 399 VL - 12 IS - 3 SN - 0143-3334, 0143-3334 KW - Receptors, Estradiol KW - 0 KW - Receptors, Estrogen KW - Diethylnitrosamine KW - 3IQ78TTX1A KW - Ethinyl Estradiol KW - 423D2T571U KW - gamma-Glutamyltransferase KW - EC 2.3.2.2 KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Index Medicus KW - Animals KW - gamma-Glutamyltransferase -- metabolism KW - Cell Division -- drug effects KW - Cell Separation KW - Uterus -- anatomy & histology KW - Cell Fractionation KW - Diethylnitrosamine -- toxicity KW - Rats KW - Rats, Inbred Strains KW - Cell Count -- drug effects KW - Body Weight -- drug effects KW - Mitosis -- drug effects KW - Ovariectomy KW - Time Factors KW - Female KW - Liver -- ultrastructure KW - Liver -- anatomy & histology KW - Liver -- cytology KW - Receptor, Epidermal Growth Factor -- metabolism KW - Liver Neoplasms, Experimental -- chemically induced KW - Ethinyl Estradiol -- toxicity KW - Receptors, Estrogen -- metabolism KW - Ploidies KW - Receptors, Estradiol -- toxicity KW - Liver -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80493556?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Estrogen+receptor%2C+epidermal+growth+factor+receptor+and+cellular+ploidy+in+elutriated+subpopulations+of+hepatocytes+during+liver+tumor+promotion+by+17+alpha-ethinylestradiol+in+rats.&rft.au=Vickers%2C+A+E%3BLucier%2C+G+W&rft.aulast=Vickers&rft.aufirst=A&rft.date=1991-03-01&rft.volume=12&rft.issue=3&rft.spage=391&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-05-07 N1 - Date created - 1991-05-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inhibition of the myeloperoxidase-H2O2-Cl- system of neutrophils by indomethacin and other non-steroidal anti-inflammatory drugs. AN - 80490387; 1848981 AB - The results presented herein demonstrate that the non-steroidal anti-inflammatory drug (NSAID) indomethacin is a strong inhibitor of the formation of HOCl by murine neutrophils (50% inhibition at 15 microM). Addition of 40 microM indomethacin to activated neutrophils caused 80% inhibition of HOCl formation throughout a 60-min time course while slightly increasing the levels of O2- and H2O2 produced. Comparable degrees of inhibition were achieved when the cells were stimulated with phorbol myristate acetate and with opsonized zymosan. Control experiments indicated that the drug did not act by scavenging HOCl. Direct inhibition of the chlorinating activity of myeloperoxidase (MPO) was confirmed using highly purified human enzyme in vitro. Kinetic analysis of the mechanism of inhibition showed that the drug was competitive with respect to Cl- and uncompetitive with respect to H2O2, showing a Ki of 37 microM. In contrast to its inhibition of the oxidation of Cl- by MPO, indomethacin had no effect on the peroxidative activity of the enzyme (oxidation of 4-aminoantipyrene), nor did it inhibit the activity of several other enzymes involved in H2O2 metabolism, including horseradish peroxidase, catalase, xanthine oxidase, and superoxide dismutase. Finally, it was found that inhibition of HOCl formation was a shared but non-uniform property of many NSAIDs; piroxicam, salicylate, sulindac, ibuprofen, and aspirin were all inhibitory but at widely different concentrations [Ki(app) values of 0.05, 0.18, 0.18, greater than 1, and 3 mM respectively] that correlated only partially with their therapeutic dose range. The results encourage further studies into the possibility that inhibition of HOCl formation may constitute an additional mechanism whereby NSAIDs reduce tissue destruction in chronically inflamed tissues. JF - Biochemical pharmacology AU - Shacter, E AU - Lopez, R L AU - Pati, S AD - Laboratory of Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. PY - 1991 SP - 975 EP - 984 VL - 41 IS - 6-7 SN - 0006-2952, 0006-2952 KW - Anti-Inflammatory Agents, Non-Steroidal KW - 0 KW - Chlorides KW - Superoxides KW - 11062-77-4 KW - Hypochlorous Acid KW - 712K4CDC10 KW - Hydrogen Peroxide KW - BBX060AN9V KW - Peroxidase KW - EC 1.11.1.7 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Indomethacin KW - XXE1CET956 KW - Index Medicus KW - Animals KW - Superoxides -- metabolism KW - Hypochlorous Acid -- metabolism KW - Oxidation-Reduction -- drug effects KW - Dose-Response Relationship, Drug KW - Kinetics KW - Hydrogen Peroxide -- metabolism KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Mice KW - Chlorides -- metabolism KW - Mice, Inbred BALB C KW - Female KW - Neutrophils -- drug effects KW - Peroxidase -- antagonists & inhibitors KW - Neutrophils -- enzymology KW - Anti-Inflammatory Agents, Non-Steroidal -- blood KW - Indomethacin -- analogs & derivatives KW - Indomethacin -- pharmacology KW - Anti-Inflammatory Agents, Non-Steroidal -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80490387?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Inhibition+of+the+myeloperoxidase-H2O2-Cl-+system+of+neutrophils+by+indomethacin+and+other+non-steroidal+anti-inflammatory+drugs.&rft.au=Shacter%2C+E%3BLopez%2C+R+L%3BPati%2C+S&rft.aulast=Shacter&rft.aufirst=E&rft.date=1991-03-01&rft.volume=41&rft.issue=6-7&rft.spage=975&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 - 1991-04-30 N1 - Date created - 1991-04-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Influence of the Ah locus on the effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on the hepatic epidermal growth factor receptor. AN - 80485858; 1848654 AB - The present studies examine whether the Ah receptor mediates the effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the binding capacity of the hepatic epidermal growth factor (EGF) receptor in congenic strains of C57BL/6J mice that differ only at the Ah locus. The Ah locus is believed to encode the Ah receptor, which mediates the induction of cytochrome P4501A1 by TCDD and appears to mediate many of the toxic effects of TCDD. TCDD produced an 80-90% decrease in the maximum binding capacity (both high and low affinity sites) of the hepatic EGF receptor in female Ah-responsive (Ahb/b) and Ah-nonresponsive (Ahd/d) C57BL/6 mice. However, the ED50 for the effects of TCDD on the binding capacity of the EGF receptor was 10-fold higher in the Ah-nonresponsive mice, compared with the Ah-responsive mice (7 versus 0.7 micrograms/kg). TCDD did not affect the hepatic content of two EGF receptor mRNA transcripts (10 and 6 kb), indicating that the effects on the EGF receptor are not pretranslational. Similarly, TCDD did not affect the hepatic content of mRNA for transforming growth factor-alpha, an alternate ligand for the EGF receptor that is synthesized in the liver. In contrast, TCDD markedly increased the hepatic content of the mRNA for cytochrome P4501A1, which is known to be regulated transcriptionally by TCDD. The ED50 for this effect was 10-fold higher in Ah-nonresponsive mice than in Ah-responsive mice (13 versus 1.3 micrograms/kg). This study indicates that the effects of TCDD on EGF receptor ligand binding are mediated by the Ah receptor. However, unlike the effect of TCDD on cytochrome P4501A1, the effects of TCDD on the EGF receptor do not involve changes in the levels of the mRNA for this protein or changes in the mRNA for transforming growth factor-alpha, an alternate ligand for the EGF receptor. JF - Molecular pharmacology AU - Lin, F H AU - Clark, G AU - Birnbaum, L S AU - Lucier, G W AU - Goldstein, J A AD - Laboratory of Biochemical Risk Analysis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 307 EP - 313 VL - 39 IS - 3 SN - 0026-895X, 0026-895X KW - Ah KW - Polychlorinated Dibenzodioxins KW - 0 KW - RNA, Messenger KW - Receptors, Aryl Hydrocarbon KW - Receptors, Drug KW - Transforming Growth Factor alpha KW - Epidermal Growth Factor KW - 62229-50-9 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Index Medicus KW - Gene Expression -- drug effects KW - Animals KW - Mice, Mutant Strains KW - Blotting, Northern KW - Transforming Growth Factor alpha -- genetics KW - Dose-Response Relationship, Drug KW - Cytochrome P-450 Enzyme System -- genetics KW - Mice KW - RNA, Messenger -- genetics KW - Epidermal Growth Factor -- metabolism KW - Receptor, Epidermal Growth Factor -- metabolism KW - Receptor, Epidermal Growth Factor -- genetics KW - Liver -- drug effects KW - Polychlorinated Dibenzodioxins -- toxicity KW - Liver -- metabolism KW - Receptors, Drug -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80485858?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Influence+of+the+Ah+locus+on+the+effects+of+2%2C3%2C7%2C8-tetrachlorodibenzo-p-dioxin+on+the+hepatic+epidermal+growth+factor+receptor.&rft.au=Lin%2C+F+H%3BClark%2C+G%3BBirnbaum%2C+L+S%3BLucier%2C+G+W%3BGoldstein%2C+J+A&rft.aulast=Lin&rft.aufirst=F&rft.date=1991-03-01&rft.volume=39&rft.issue=3&rft.spage=307&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 - 1991-04-22 N1 - Date created - 1991-04-22 N1 - Date revised - 2017-01-13 N1 - Gene symbol - Ah N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Analysis of Fv-1 restriction in two murine embryonal carcinoma cell lines and a series of differentiated derivatives. AN - 80484410; 1848595 AB - We have used antibiotic-resistant retrovirus vectors rescued by Fv-1-sensitive murine leukaemia viruses (MuLV) to examine the Fv-1 phenotype of two undifferentiated embryonal carcinoma (EC) cell lines derived from teratocarcinomas of mouse strain 129. In addition, a set of EC cell-derived differentiated cell lines was analysed. Restriction of both B-tropic and endogenous N-tropic virus is characteristic of the Nr-type restriction reported in mouse strain 129. However, results indicate that Fv-1 restriction is not expressed in the PCC4.aza1R EC cell line. In contrast, the F9 EC cell line showed a strong restriction of the B-tropic pseudotyped vector but failed to restrict endogenous N-tropic pseudotypes. The Fv-1 gene thus seems to be differentially expressed in two EC cell lines derived from the same mouse strain. Furthermore, the selective restriction of B-tropic but not endogenous N-tropic MuLV in F9 cells suggests that these activities function independently of each other. Analysis of PCC4.aza1R-derived differentiated cell lines revealed that three fibroblast cell lines derived by retinoic acid-induced differentiation were also phenotypically silent for Fv-1. However, a pre-adipocyte line established following simultaneous exposure to retinoic acid and 5-azacytidine showed strong restriction of both B-tropic and endogenous N-tropic MuLV. Although additional data suggest that there is no correlation between the differentiated pre-adipocyte phenotype and Fv-1 expression, our results nonetheless show that Nr restriction can be observed in some derivatives of PCC4.aza1R cells, presumably by activating expression of the Fv-1 gene. JF - The Journal of general virology AU - Heitman, C K AU - Innes, C L AU - Jetten, A M AU - Boone, L R AD - Cellular and Genetic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 609 EP - 616 VL - 72 ( Pt 3) SN - 0022-1317, 0022-1317 KW - Fv-1 KW - Index Medicus KW - Phenotype KW - Animals KW - Virus Replication -- genetics KW - Tumor Cells, Cultured KW - Genetic Vectors KW - Mice KW - Embryonal Carcinoma Stem Cells KW - Gene Expression Regulation, Neoplastic KW - Neoplastic Stem Cells -- microbiology KW - Leukemia Virus, Murine -- physiology KW - Genes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80484410?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+general+virology&rft.atitle=Analysis+of+Fv-1+restriction+in+two+murine+embryonal+carcinoma+cell+lines+and+a+series+of+differentiated+derivatives.&rft.au=Heitman%2C+C+K%3BInnes%2C+C+L%3BJetten%2C+A+M%3BBoone%2C+L+R&rft.aulast=Heitman&rft.aufirst=C&rft.date=1991-03-01&rft.volume=72+%28+Pt+3%29&rft.issue=&rft.spage=609&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+general+virology&rft.issn=00221317&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-22 N1 - Date created - 1991-04-22 N1 - Date revised - 2017-01-13 N1 - Gene symbol - Fv-1 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transfected D2 dopamine receptors mediate the potentiation of arachidonic acid release in Chinese hamster ovary cells. AN - 80484061; 1848657 AB - A rat D2L dopamine receptor, a splice variant of the D2 receptor, has recently been cloned. When transfected into and stably expressed in Chinese hamster ovary cells, these receptors mediate the inhibition of both basal and forskolin-stimulated cAMP production, as previously described. We examined what role this receptor might play in the production of the second messenger arachidonic acid. The calcium ionophore A23187 stimulated the release of arachidonic acid, and this release of arachidonic acid was potentiated by dopamine in a concentration-dependent manner. Dopamine alone, however, had no effect on arachidonic acid release. Quinpirole, a D2-selective agonist, augmented A23187-stimulated arachidonic acid release, and sulpiride, a D2-selective antagonist, blocked this augmentation. cAMP analogs and agents that activate adenylyl cyclase were utilized in an attempt to overcome this dopamine effect. Forskolin, prostaglandin E2, dibutyryl-cAMP, 8-(4-chlorophenylthio)-cAMP, and pertussis toxin all had no appreciable effect on either A23187-stimulated arachidonic acid release or the dopamine enhancement. Inhibition of protein kinase C using long term phorbol ester desensitization and pharmacological inhibitors diminished the dopamine potentiation of arachidonic acid release. These results suggest that the D2 receptor may be increasing the release of arachidonic acid by a mechanism involving protein kinase C but independent of the D2 receptor's inhibition of adenylyl cyclase. JF - Molecular pharmacology AU - Kanterman, R Y AU - Mahan, L C AU - Briley, E M AU - Monsma, F J AU - Sibley, D R AU - Axelrod, J AU - Felder, C C AD - Laboratory of Cell Biology, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 364 EP - 369 VL - 39 IS - 3 SN - 0026-895X, 0026-895X KW - Adenylate Cyclase Toxin KW - 0 KW - Arachidonic Acids KW - Ergolines KW - Receptors, Dopamine KW - Virulence Factors, Bordetella KW - Melitten KW - 20449-79-0 KW - Quinpirole KW - 20OP60125T KW - Arachidonic Acid KW - 27YG812J1I KW - Calcimycin KW - 37H9VM9WZL KW - Sulpiride KW - 7MNE9M8287 KW - Cyclic AMP KW - E0399OZS9N KW - Pertussis Toxin KW - EC 2.4.2.31 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Adenylyl Cyclases KW - EC 4.6.1.1 KW - Haloperidol KW - J6292F8L3D KW - Apomorphine KW - N21FAR7B4S KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Animals KW - Sulpiride -- pharmacology KW - Cricetulus KW - Apomorphine -- pharmacology KW - Ergolines -- pharmacology KW - Calcimycin -- pharmacology KW - Melitten -- pharmacology KW - Adenylyl Cyclases -- physiology KW - Virulence Factors, Bordetella -- pharmacology KW - Transfection KW - In Vitro Techniques KW - Haloperidol -- pharmacology KW - Cyclic AMP -- metabolism KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Protein Kinase C -- physiology KW - Drug Synergism KW - Cricetinae KW - Receptors, Dopamine -- physiology KW - Dopamine -- pharmacology KW - Arachidonic Acids -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80484061?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Transfected+D2+dopamine+receptors+mediate+the+potentiation+of+arachidonic+acid+release+in+Chinese+hamster+ovary+cells.&rft.au=Kanterman%2C+R+Y%3BMahan%2C+L+C%3BBriley%2C+E+M%3BMonsma%2C+F+J%3BSibley%2C+D+R%3BAxelrod%2C+J%3BFelder%2C+C+C&rft.aulast=Kanterman&rft.aufirst=R&rft.date=1991-03-01&rft.volume=39&rft.issue=3&rft.spage=364&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 - 1991-04-22 N1 - Date created - 1991-04-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mortality among aerial pesticide applicators and flight instructors: a reprint. AN - 80482940; 2006895 AB - A cohort mortality study was conducted of male aerial pesticide applicators and flight instructors identified from computerized Federal Aviation Administration medical examination records from 1965-1979. Vital status of 9,677 applicators and 9,727 instructors was determined through January 1, 1980, and standardized mortality ratios (SMRs) were calculated. The overall SMR was 127 for applicators (699 deaths) and 93 for instructors (454 deaths). Fatalities from nonmotor vehicle accidents, mostly aircraft crashes, were in notable excess (SMR = 1,168 among applicators, 630 among instructors), whereas deaths from most chronic diseases, including all cancer, was below expectation (e.g., for arteriosclerotic heart disease, SMR = 52 among applicators and 50 among instructors). The ability of the study to assess cancer risk among applicators was limited by a relatively brief follow-up period. However, 8 applicators (SMR = 171), but only 1 flight instructor (SMR = 24), died of leukemia, and small, nonsignificant risk elevations for some other cancer sites among applicators were observed and warrant continued follow-up. JF - Archives of environmental health AU - Cantor, K P AU - Booze, C F AD - National Cancer Institute, Bethesda, Maryland. PY - 1991 SP - 110 EP - 116 VL - 46 IS - 2 SN - 0003-9896, 0003-9896 KW - Pesticides KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Space life sciences KW - Aviation -- education KW - Certification -- standards KW - Humans KW - Aged KW - Cause of Death KW - Health Status Indicators KW - Prospective Studies KW - Risk Factors KW - Adult KW - Follow-Up Studies KW - Middle Aged KW - Adolescent KW - United States -- epidemiology KW - Male KW - Agriculture KW - Neoplasms -- pathology KW - Neoplasms -- mortality KW - Accidents, Aviation -- mortality KW - Neoplasms -- epidemiology KW - Aerospace Medicine KW - Pesticides -- adverse effects KW - Accidents, Aviation -- statistics & numerical data UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80482940?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+environmental+health&rft.atitle=Mortality+among+aerial+pesticide+applicators+and+flight+instructors%3A+a+reprint.&rft.au=Cantor%2C+K+P%3BBooze%2C+C+F&rft.aulast=Cantor&rft.aufirst=K&rft.date=1991-03-01&rft.volume=46&rft.issue=2&rft.spage=110&rft.isbn=&rft.btitle=&rft.title=Archives+of+environmental+health&rft.issn=00039896&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-19 N1 - Date created - 1991-04-19 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Republished From: Arch Environ Health 1990 Sep-Oct;45(5):295-302 N1 - Last updated - 2017-01-19 ER - TY - JOUR T1 - The role of prostaglandin synthetase in the rate depressant effects and narcosis caused by ethanol. AN - 80481005; 1900890 AB - Ethanol is proposed to exert its pharmacological effects by increasing membrane fluidity. Support for this hypothesis comes from strong correlations between in vitro effects of ethanol and pharmacological effects and genetic variation seen in vivo. Because arachidonate acid (AA) cascade is a membrane-bound system activated by disruptions in the cell membrane, it is possible that ethanol-induced membrane fluidization increases the formation of AA metabolites such as prostaglandins. The studies reported here were designed to characterize systematically the ability of various prostaglandin endoperoxide synthetase (PES; prostaglandin synthetase or cyclooxygenase) inhibitors to antagonize the effects of ethanol. A wide range of chemically diverse PES inhibitors significantly antagonized the rate-depressant effects and acute narcosis caused by ethanol. The ability of these compounds to antagonize the effects of ethanol was significantly correlated with two measures of PES activity; in vitro inhibition of the PES enzyme and in vivo anti-inflammatory activity. These significant potency correlations between the ability of PES inhibitors to antagonize in vivo acute ethanol hypnosis and their ability to inhibit in vitro and in vivo conversion of AA to AA metabolites strongly suggest an underlying functional relationship. These results obtained from two divergent dependent measures of the effects of ethanol, duration of loss of the righting reflex and rate depressant effects, extend the range of ethanol-related behaviors that PES inhibitors effectively antagonize and provide substantive evidence in support of a mechanistic role for PES and related metabolites in the central effects of ethanol. JF - The Journal of pharmacology and experimental therapeutics AU - Elmer, G I AU - George, F R AD - Preclinical Pharmacology Branch, National Institute on Drug Abuse, Baltimore, Maryland. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 1139 EP - 1146 VL - 256 IS - 3 SN - 0022-3565, 0022-3565 KW - Anti-Inflammatory Agents, Non-Steroidal KW - 0 KW - Ethanol KW - 3K9958V90M KW - Prostaglandin-Endoperoxide Synthases KW - EC 1.14.99.1 KW - Index Medicus KW - Animals KW - Analysis of Variance KW - Reflex -- drug effects KW - Mice, Inbred C57BL KW - Mice KW - Male KW - Mice, Inbred DBA KW - Prostaglandin-Endoperoxide Synthases -- physiology KW - Ethanol -- antagonists & inhibitors KW - Ethanol -- toxicity KW - Anti-Inflammatory Agents, Non-Steroidal -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80481005?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+role+of+prostaglandin+synthetase+in+the+rate+depressant+effects+and+narcosis+caused+by+ethanol.&rft.au=Elmer%2C+G+I%3BGeorge%2C+F+R&rft.aulast=Elmer&rft.aufirst=G&rft.date=1991-03-01&rft.volume=256&rft.issue=3&rft.spage=1139&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 - 1991-04-24 N1 - Date created - 1991-04-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Eosinophil cationic protein stimulates and major basic protein inhibits airway mucus secretion. AN - 80479231; 2005321 AB - Possible roles of eosinophil (EO) products in modulating the release of mucus from airway explants were investigated. Cell- and membrane-free lysates from purified human EOs (1 to 20 x 10(5)) caused a dose-dependent release of respiratory glycoconjugates (RGC) from cultured feline tracheal explants. Crude extracts from isolated EO granules also stimulated RGC release, suggesting that a granular protein might be responsible. Three proteins derived from EO granules, EO-derived neurotoxin, EO cationic protein (ECP), and major basic protein (MBP) were separated by sequential sizing and affinity chromatography. ECP (0.025 to 25 micrograms/ml) caused a dose-dependent increase in RGC release from both feline and human airway explants and also stimulated the release of the serous cell-marker, lactoferrin, from human bronchial explants. EO-derived neurotoxin (0.025 to 50 micrograms/ml) failed to affect RGC release, whereas MBP (50 micrograms/ml) significantly inhibited RGC release from feline explants. Thus, ECP stimulates RGC and lactoferrin release from airway explants, whereas MBP inhibits RGC release. JF - The Journal of allergy and clinical immunology AU - Lundgren, J D AU - Davey, R T AU - Lundgren, B AU - Mullol, J AU - Marom, Z AU - Logun, C AU - Baraniuk, J AU - Kaliner, M A AU - Shelhamer, J H AD - Critical Care Medicine Department, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Md. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 689 EP - 698 VL - 87 IS - 3 SN - 0091-6749, 0091-6749 KW - Blood Proteins KW - 0 KW - Eosinophil Granule Proteins KW - Neurotoxins KW - Eosinophil-Derived Neurotoxin KW - EC 3.1.- KW - Ribonucleases KW - Lactoferrin KW - EC 3.4.21.- KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Lactoferrin -- physiology KW - Airway Obstruction -- physiopathology KW - Dose-Response Relationship, Drug KW - Humans KW - Cats KW - Neurotoxins -- pharmacology KW - Enzyme-Linked Immunosorbent Assay KW - Eosinophils -- secretion KW - Organ Culture Techniques KW - Asthma -- physiopathology KW - Trachea -- drug effects KW - Blood Proteins -- pharmacology KW - Mucus -- secretion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80479231?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+allergy+and+clinical+immunology&rft.atitle=Eosinophil+cationic+protein+stimulates+and+major+basic+protein+inhibits+airway+mucus+secretion.&rft.au=Lundgren%2C+J+D%3BDavey%2C+R+T%3BLundgren%2C+B%3BMullol%2C+J%3BMarom%2C+Z%3BLogun%2C+C%3BBaraniuk%2C+J%3BKaliner%2C+M+A%3BShelhamer%2C+J+H&rft.aulast=Lundgren&rft.aufirst=J&rft.date=1991-03-01&rft.volume=87&rft.issue=3&rft.spage=689&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+allergy+and+clinical+immunology&rft.issn=00916749&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-22 N1 - Date created - 1991-04-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Separate neural mechanisms mediate sufentanil-induced pupillary responses in the cat. AN - 80478361; 1672378 AB - The pharmacologic characteristics of a highly selective mu receptor agonist, sufentanil, were studied on the cat's pupillary responses (size, light reflex and fluctuations) measured with an infrared video pupillometer. The pupillary effects of sufentanil were also compared with those of morphine and clonidine, known mydriatics in the cat. Sufentanil (0.3-10 micrograms/kg i.v.) dose-dependently increased pupillary size and decreased light reflex and fluctuations. Naltrexone (10 micrograms/kg i.v.) pretreatment shifted the dose-response curve to the right by a factor of 26 for pupillary size, 9.5 for light reflex and 7.2 for fluctuations (nonvalid bioassay). Equivalent mydriatic doses of sufentanil (1 micrograms/kg), morphine (0.5 mg/kg) and clonidine (10 micrograms/kg) produced divergent effects on the light reflex and fluctuations. At these doses, morphine was more effective than sufentanil in inhibiting fluctuations. Clonidine was a more potent inhibitor of fluctuations but significantly enhanced the light reflex. Sufentanil (compared with morphine in a previous study) was 298 times more potent than morphine as a mydriatic, 100 times more potent in inhibiting the light reflex, and only slightly more potent in inhibiting fluctuations. These results indicate that separate neural mechanisms control the three pupillary components and that mu opioid receptors are more involved in mediating opiate-induced mydriasis than in inhibiting the light reflex and fluctuations in the cat. JF - The Journal of pharmacology and experimental therapeutics AU - Sharpe, L G AD - National Institute on Drug Abuse, Addiction Research Center, Baltimore, Maryland. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 845 EP - 849 VL - 256 IS - 3 SN - 0022-3565, 0022-3565 KW - Analgesics, Opioid KW - 0 KW - Receptors, Opioid KW - Receptors, Opioid, mu KW - Naltrexone KW - 5S6W795CQM KW - Morphine KW - 76I7G6D29C KW - Sufentanil KW - AFE2YW0IIZ KW - Clonidine KW - MN3L5RMN02 KW - Fentanyl KW - UF599785JZ KW - Index Medicus KW - Animals KW - Drug Interactions KW - Receptors, Opioid -- drug effects KW - Cats KW - Naltrexone -- pharmacology KW - Clonidine -- pharmacology KW - Male KW - Morphine -- pharmacology KW - Pupil -- drug effects KW - Analgesics, Opioid -- pharmacology KW - Fentanyl -- pharmacology KW - Fentanyl -- analogs & derivatives KW - Mydriasis -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80478361?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Separate+neural+mechanisms+mediate+sufentanil-induced+pupillary+responses+in+the+cat.&rft.au=Sharpe%2C+L+G&rft.aulast=Sharpe&rft.aufirst=L&rft.date=1991-03-01&rft.volume=256&rft.issue=3&rft.spage=845&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 - 1991-04-24 N1 - Date created - 1991-04-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alpha-adrenergic regulation of phosphoinositide metabolism and protein kinase C in isolated cardiac myocytes. AN - 80475297; 1848404 AB - alpha 1-Adrenergic regulation of phosphoinositide metabolism and protein kinase C translocation was studied in isolated rat cardiac myocytes. Exposure of [3H]inositol-labeled myocytes to norepinephrine in the presence of propranolol caused a dose-dependent increase in [3H]inositol phosphates. Norepinephrine also increased the level of membrane-associated protein kinase C from approximately 10% of total activity to 18%, with a dose response similar to that for generation of inositol phosphates. Depolarization of myocytes with 30 mM KCl had no effect on inositol phosphates or membrane-associated protein kinase C but potentiated the effect of submaximal norepinephrine on both parameters. The potentiation of protein kinase C translocation was amplified when extracellular Ca2+ was increased to 4 mM, resulting in membrane association of one-third of the total cellular activity. These data show that activation of protein kinase C occurs during alpha 1-adrenergic stimulation of cardiac myocytes and that elevation of intracellular Ca2+ amplifies this effect at least in part through increased phosphoinositide metabolism. JF - The American journal of physiology AU - Kaku, T AU - Lakatta, E AU - Filburn, C AD - Laboratory of Cardiovascular Science, National Institute on Aging, Baltimore, Maryland 21224. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - C635 EP - C642 VL - 260 IS - 3 Pt 1 SN - 0002-9513, 0002-9513 KW - Detergents KW - 0 KW - Inositol Phosphates KW - Phosphatidylinositols KW - Polyethylene Glycols KW - 30IQX730WE KW - Inositol KW - 4L6452S749 KW - Ionomycin KW - 56092-81-0 KW - Octoxynol KW - 9002-93-1 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Calcium Chloride KW - M4I0D6VV5M KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Norepinephrine KW - X4W3ENH1CV KW - Prazosin KW - XM03YJ541D KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Cells, Cultured KW - Kinetics KW - Prazosin -- pharmacology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Ionomycin -- pharmacology KW - Detergents -- pharmacology KW - Calcium Chloride -- pharmacology KW - Polyethylene Glycols -- pharmacology KW - Inositol -- metabolism KW - Protein Kinase C -- metabolism KW - Phosphatidylinositols -- metabolism KW - Norepinephrine -- pharmacology KW - Inositol Phosphates -- metabolism KW - Myocardium -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80475297?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+physiology&rft.atitle=Alpha-adrenergic+regulation+of+phosphoinositide+metabolism+and+protein+kinase+C+in+isolated+cardiac+myocytes.&rft.au=Kaku%2C+T%3BLakatta%2C+E%3BFilburn%2C+C&rft.aulast=Kaku&rft.aufirst=T&rft.date=1991-03-01&rft.volume=260&rft.issue=3+Pt+1&rft.spage=C635&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+physiology&rft.issn=00029513&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-12 N1 - Date created - 1991-04-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Relationship of DNA strand breakage produced by bromodeoxyuridine to topoisomerase II activity in Bloom-syndrome fibroblasts. AN - 80474156; 1848352 AB - Cells from patients with Bloom syndrome, a cancer-prone disorder with cutaneous photosensitivity and spontaneous chromosome breakage, exhibit an abnormally increased number of sister-chromatid exchanges following treatment with 5-bromodeoxyuridine (BrdU). This effect has been postulated to be mediated by abnormal topoisomerase II activity. We used alkaline elution to measure DNA single-strand breakage following prolonged exposure to BrdU. Five-day exposure to BrdU produced equal numbers of alkali-labile sites in normal and Bloom-syndrome fibroblasts. These breaks were not protein-associated but were produced by alkali. Treatment with topoisomerase II inhibitors induced similar frequencies of DNA single-strand breaks in normal and Bloom-syndrome fibroblasts. These findings imply that BrdU incorporation into cellular DNA induces alkali-labile DNA lesions that are independent of topoisomerase II activity in Bloom and normal cells. JF - Mutation research AU - Pommier, Y AU - Rünger, T M AU - Kerrigan, D AU - Kraemer, K H AD - Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 185 EP - 190 VL - 254 IS - 2 SN - 0027-5107, 0027-5107 KW - DNA KW - 9007-49-2 KW - DNA Topoisomerases, Type II KW - EC 5.99.1.3 KW - Bromodeoxyuridine KW - G34N38R2N1 KW - Index Medicus KW - Gamma Rays -- adverse effects KW - Fibroblasts -- enzymology KW - Dose-Response Relationship, Drug KW - Cells, Cultured KW - Hydrogen-Ion Concentration KW - Humans KW - In Vitro Techniques KW - Bromodeoxyuridine -- adverse effects KW - X-Rays -- adverse effects KW - DNA Damage KW - DNA Topoisomerases, Type II -- metabolism KW - Bloom Syndrome -- genetics KW - DNA -- radiation effects KW - DNA -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80474156?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Relationship+of+DNA+strand+breakage+produced+by+bromodeoxyuridine+to+topoisomerase+II+activity+in+Bloom-syndrome+fibroblasts.&rft.au=Pommier%2C+Y%3BR%C3%BCnger%2C+T+M%3BKerrigan%2C+D%3BKraemer%2C+K+H&rft.aulast=Pommier&rft.aufirst=Y&rft.date=1991-03-01&rft.volume=254&rft.issue=2&rft.spage=185&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 - 1991-04-15 N1 - Date created - 1991-04-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - DNA-expressed human cytochrome P450s: a new age of molecular toxicology and human risk assessment. AN - 80471898; 2002797 AB - It has long been recognized that a large degree of species differences exists among drug and carcinogen metabolizing enzymes. In particular, differences in cytochrome P450s, the principal enzymes of metabolic activation of procarcinogens, are widespread and may determine species and individual susceptibility to cancer causing chemicals. Although species differences in both the regulation and catalytic activities of P450s are quite large, roden-based systems are mainly used as the means to determine the degree of hazard of environmental pollutants, pesticides, drugs and other environmental chemicals to humans. During recent years, a large effort has been expended on analyzing directly the structure, properties and catalytic activities of P450s from human tissues. In vitro mutagen testing systems, based on activation by human P450s, are being developed that will supplement other test systems in order to more accurately predict human risk to chemical exposure. JF - Mutation research AU - Gonzalez, F J AU - Crespi, C L AU - Gelboin, H V AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institute of Health, Bethesda, MD 20892. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 113 EP - 127 VL - 247 IS - 1 SN - 0027-5107, 0027-5107 KW - Carcinogens KW - 0 KW - Mutagens KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Animals KW - Mutagenicity Tests KW - Biotransformation KW - Risk Factors KW - Humans KW - DNA -- genetics KW - Gene Expression KW - Carcinogens -- metabolism KW - Cytochrome P-450 Enzyme System -- genetics KW - Carcinogens -- toxicity KW - Cytochrome P-450 Enzyme System -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80471898?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=DNA-expressed+human+cytochrome+P450s%3A+a+new+age+of+molecular+toxicology+and+human+risk+assessment.&rft.au=Gonzalez%2C+F+J%3BCrespi%2C+C+L%3BGelboin%2C+H+V&rft.aulast=Gonzalez&rft.aufirst=F&rft.date=1991-03-01&rft.volume=247&rft.issue=1&rft.spage=113&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 - 1991-04-17 N1 - Date created - 1991-04-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evaluation of the persistence of hydronephrosis induced in mice following in utero and/or lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin. AN - 80470514; 2000631 AB - 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is an extremely potent teratogen in mice, inducing structural malformations in the kidney and secondary palate. Maternal depots of TCDD, stored primarily in adipose tissue, are mobilized during the nursing period. Thus, lactation serves as a significant route of exposure for the developing neonate. The objective of this present investigation was to assess whether hydronephrosis persisted postnatally, as well as to determine if the renal lesion could be induced lactationally. Pregnant C57BL/6N mice were treated once by gavage with 0, 3, or 12 micrograms TCDD/kg body wt on Gestation Day (GD) 6. All dams were allowed to litter, and each litter was standardized at random to a size of six pups. Standardized litters were then reciprocally cross-fostered on the day of birth. Postnatal Day (PND) 0, resulting in the establishment of four experimental groups: pups not exposed by either route, pups exposed only in utero, pups exposed only lactationally, and pups exposed by both routes. Pups were euthanized at one of two time points, either at weaning (PND 25) or at puberty (PND 67). TCDD was not overtly toxic to the dams or neonates with the dosing regime used in this study. Hydronephrotic incidence and severity, while greatest for pups receiving dual exposure, were essentially the same for pups exposed in utero only vs lactationally only. Lactational exposure induced hydronephrosis (HN), as well as exacerbated the severity of existing HN which was induced in utero. Regardless of the exposure group, the severity of the renal lesion was always greater in the right kidney than in the left. There were no sex-related differences in either the incidence or the severity of HN, nor was there any difference in response between PNDs 25 and 67. These data suggest that the renal lesion persists from weaning through puberty, despite the cessation of exposure. However, the data indicate that partial recovery from HN induced in utero occurs during the early postnatal period, as both hydronephrotic incidence and severity decreased with increasing age between GD 18 and PND 25. Recovery was most pronounced in the left kidney regardless of dose, thus suggesting that the ability to recover may in part be dependent upon the extent of renal damage. JF - Toxicology and applied pharmacology AU - Couture-Haws, L AU - Harris, M W AU - Lockhart, A C AU - Birnbaum, L S AD - Experimental Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/03/01/ PY - 1991 DA - 1991 Mar 01 SP - 402 EP - 412 VL - 107 IS - 3 SN - 0041-008X, 0041-008X KW - Polychlorinated Dibenzodioxins KW - 0 KW - Index Medicus KW - Animals, Suckling KW - Urinary Tract -- abnormalities KW - Animals KW - Abnormalities, Drug-Induced KW - Urinary Tract -- drug effects KW - Kidney -- drug effects KW - Mice KW - Kidney -- abnormalities KW - Pregnancy KW - Urinary Tract -- growth & development KW - Mice, Inbred Strains KW - Kidney -- growth & development KW - Incidence KW - Time Factors KW - Female KW - Male KW - Prenatal Exposure Delayed Effects KW - Lactation -- drug effects KW - Polychlorinated Dibenzodioxins -- toxicity KW - Hydronephrosis -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80470514?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Evaluation+of+the+persistence+of+hydronephrosis+induced+in+mice+following+in+utero+and%2For+lactational+exposure+to+2%2C3%2C7%2C8-tetrachlorodibenzo-p-dioxin.&rft.au=Couture-Haws%2C+L%3BHarris%2C+M+W%3BLockhart%2C+A+C%3BBirnbaum%2C+L+S&rft.aulast=Couture-Haws&rft.aufirst=L&rft.date=1991-03-01&rft.volume=107&rft.issue=3&rft.spage=402&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 - 1991-04-08 N1 - Date created - 1991-04-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differentiation of HL-60 leukemia by type I regulatory subunit antisense oligodeoxynucleotide of cAMP-dependent protein kinase. AN - 80465993; 2000408 AB - A marked decrease in the type I cAMP-dependent protein kinase regulatory subunit (RI alpha) and an increase in the type II protein kinase regulatory subunit (RII beta) correlate with growth inhibition and differentiation induced in a variety of types of human cancer cells, in vitro and in vivo, by site-selective cAMP analogs. To directly determine whether RI alpha is a growth-inducing protein essential for neoplastic cell growth, human HL-60 promyelocytic leukemia cells were exposed to 21-mer RI alpha antisense oligodeoxynucleotide, and the effects on cell replication and differentiation were examined. The RI alpha antisense oligomer brought about growth inhibition and monocytic differentiation, bypassing the effects of an exogenous cAMP analog. These effects of RI alpha antisense oligodeoxynucleotide correlated with a decrease in RI alpha receptor and an increase in RII beta receptor level. The growth inhibition and differentiation were abolished, however, when these cells were exposed simultaneously to both RI alpha and RII beta antisense oligodeoxynucleotides. The RII beta antisense oligodeoxynucleotide alone has been previously shown to specifically block the differentiation inducible by cAMP analogs. These results provide direct evidence that RI alpha cAMP receptor plays a critical role in neoplastic cell growth and that cAMP receptor isoforms display specific roles in cAMP regulation of cell growth and differentiation. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Tortora, G AU - Yokozaki, H AU - Pepe, S AU - Clair, T AU - Cho-Chung, Y S AD - Cellular Biochemistry Section, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/03/01/ PY - 1991 DA - 1991 Mar 01 SP - 2011 EP - 2015 VL - 88 IS - 5 SN - 0027-8424, 0027-8424 KW - Macromolecular Substances KW - 0 KW - Oligonucleotides, Antisense KW - 8-Bromo Cyclic Adenosine Monophosphate KW - 23583-48-4 KW - 8-chloro-cyclic adenosine monophosphate KW - 41941-56-4 KW - Protein Kinases KW - EC 2.7.- KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - 8-Bromo Cyclic Adenosine Monophosphate -- analogs & derivatives KW - Base Sequence KW - Kinetics KW - Humans KW - Molecular Sequence Data KW - Leukemia, Promyelocytic, Acute KW - Cell Division -- drug effects KW - Tetradecanoylphorbol Acetate -- pharmacology KW - 8-Bromo Cyclic Adenosine Monophosphate -- pharmacology KW - Cell Line KW - Protein Kinases -- metabolism KW - Protein Kinases -- genetics KW - Oligonucleotides, Antisense -- pharmacology KW - Cell Differentiation -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80465993?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Differentiation+of+HL-60+leukemia+by+type+I+regulatory+subunit+antisense+oligodeoxynucleotide+of+cAMP-dependent+protein+kinase.&rft.au=Tortora%2C+G%3BYokozaki%2C+H%3BPepe%2C+S%3BClair%2C+T%3BCho-Chung%2C+Y+S&rft.aulast=Tortora&rft.aufirst=G&rft.date=1991-03-01&rft.volume=88&rft.issue=5&rft.spage=2011&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 - 1991-04-11 N1 - Date created - 1991-04-11 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 1975 Jan 10;250(1):218-25 [166986] Proc Natl Acad Sci U S A. 1990 Jan;87(2):705-8 [1689049] J Biol Chem. 1977 Feb 25;252(4):1441-7 [190233] J Biol Chem. 1977 Jul 25;252(14):4888-94 [194899] Biochemistry. 1979 Nov 27;18(24):5294-9 [518835] Proc Natl Acad Sci U S A. 1980 Sep;77(9):5201-5 [6159641] Cell. 1980 Nov;22(2 Pt 2):329-30 [6256078] Leuk Res. 1981;5(6):491-5 [6948980] J Immunol. 1983 Jan;130(1):145-52 [6183346] Cell Immunol. 1983 May;78(1):83-99 [6342816] Proc Natl Acad Sci U S A. 1983 Jun;80(12):3608-12 [6190178] J Immunol. 1983 Dec;131(6):2757-61 [6227665] Methods Enzymol. 1983;99:3-6 [6316096] CRC Crit Rev Biochem. 1984;15(2):93-124 [6365450] Adv Cyclic Nucleotide Protein Phosphorylation Res. 1984;18:63-117 [6093482] J Biol Chem. 1985 Mar 25;260(6):3393-401 [2982859] J Biol Chem. 1985 May 25;260(10):6296-303 [2581952] Biochem J. 1985 Nov 1;231(3):655-61 [3000357] Proc Natl Acad Sci U S A. 1986 Mar;83(5):1300-4 [3456589] J Biol Chem. 1986 Sep 15;261(26):12352-61 [2427518] J Biol Chem. 1986 Nov 25;261(33):15360-3 [3023318] J Biol Chem. 1986 Dec 15;261(35):16288-91 [3023347] Proc Natl Acad Sci U S A. 1987 Aug;84(15):5192-6 [3037538] J Biol Chem. 1987 Nov 5;262(31):15202-7 [3667630] Blood. 1988 Jan;71(1):230-3 [2825845] Biochem Biophys Res Commun. 1987 Dec 31;149(3):939-45 [3426618] Cancer Res. 1988 May 15;48(10):2659-68 [3282648] Proc Natl Acad Sci U S A. 1988 Jun;85(11):3703-7 [3375237] Anal Biochem. 1988 Aug 1;172(2):289-95 [3056098] Mol Endocrinol. 1988 Dec;2(12):1364-73 [2851102] Proc Natl Acad Sci U S A. 1989 Apr;86(8):2849-52 [2539602] FEBS Lett. 1989 Mar 27;246(1-2):57-64 [2540040] J Natl Cancer Inst. 1989 Jul 5;81(13):982-7 [2659804] Cancer Invest. 1989;7(2):161-77 [2551468] J Biol Chem. 1989 Dec 5;264(34):20255-60 [2584216] J Biol Chem. 1975 Oct 10;250(19):7795-801 [170270] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Hydronephrosis in mice exposed to TCDD-contaminated breast milk: identification of the peak period of sensitivity and assessment of potential recovery. AN - 80465823; 2000632 AB - 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a potent inducer of hydronephrosis in both fetal and neonatal mice. A critical period of sensitivity to TCDD could not be identified for prenatally induced hydronephrosis since the urinary tract appeared equally sensitive throughout organogenesis. To identify the critical period of susceptibility for development of lactationally induced hydronephrosis in neonatal mice, as well as to characterize the potential for recovery from this renal lesion, dose-response and time-course studies were conducted in the postnatal period. Pregnant C57BL/6N mice were allowed natural delivery. In the dose-response phase of this investigation, mothers were administered 0, 3, 6, or 12 micrograms TCDD/kg once by gavage on Postnatal Day (PND) 1, 4, 8, or 14, and dams and pups were euthanized on PND 26. The kidneys were examined, and hydronephrotic severity was scored. The incidence and severity of hydronephrosis were significantly increased above controls only following treatment on PND 1 or 4, while on PND 8 the increase was marginal and pairwise tests were nonsignificant. Following treatment of dams on PND 1, the hydronephrotic response detected in 26-day-old pups was significantly greater than that for all later exposure days. In the time-course study, dams were given a single oral dose of 0 or 9 micrograms TCDD/kg on PND 1, and mothers and litters were subsequently euthanized on PND 7, 13, 19, or 26. Both hydronephrotic incidence and severity increased with time to euthanization following treatment on PND 1. Thus with the dosing regimen used in this study, recovery does not appear to occur between PNDs 7 and 26. Sex-related differences were observed, as the hydronephrotic response in males was generally greater than in females. In conclusion, the postnatal window of sensitivity during which TCDD can induce hydronephrosis is very narrow. Nonetheless, the hydronephrotic response induced during this early postnatal time is dramatic. Finally, PND 1 is the peak postnatal period of susceptibility for development of TCDD-induced hydronephrosis. JF - Toxicology and applied pharmacology AU - Couture-Haws, L AU - Harris, M W AU - McDonald, M M AU - Lockhart, A C AU - Birnbaum, L S AD - Experimental Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/03/01/ PY - 1991 DA - 1991 Mar 01 SP - 413 EP - 428 VL - 107 IS - 3 SN - 0041-008X, 0041-008X KW - Polychlorinated Dibenzodioxins KW - 0 KW - Index Medicus KW - Animals, Suckling KW - Animals KW - Liver -- anatomy & histology KW - Kidney -- pathology KW - Urinary Tract -- drug effects KW - Dose-Response Relationship, Drug KW - Kidney -- drug effects KW - Mice KW - Urinary Tract -- growth & development KW - Mice, Inbred Strains KW - Lactation -- drug effects KW - Body Weight -- drug effects KW - Time Factors KW - Female KW - Male KW - Organ Size -- drug effects KW - Kidney -- anatomy & histology KW - Milk -- drug effects KW - Polychlorinated Dibenzodioxins -- administration & dosage KW - Polychlorinated Dibenzodioxins -- toxicity KW - Hydronephrosis -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80465823?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Hydronephrosis+in+mice+exposed+to+TCDD-contaminated+breast+milk%3A+identification+of+the+peak+period+of+sensitivity+and+assessment+of+potential+recovery.&rft.au=Couture-Haws%2C+L%3BHarris%2C+M+W%3BMcDonald%2C+M+M%3BLockhart%2C+A+C%3BBirnbaum%2C+L+S&rft.aulast=Couture-Haws&rft.aufirst=L&rft.date=1991-03-01&rft.volume=107&rft.issue=3&rft.spage=413&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 - 1991-04-08 N1 - Date created - 1991-04-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Absence of modulation of monokine production via endogenous cyclooxygenase or 5-lipoxygenase metabolites: MK-886 (3-[1-(4-chlorobenzyl)-3-t-butyl-thio-5-isopropylindol-2-yl]-2,2- dimethylpropanoic acid), indomethacin, or arachidonate fail to alter immunoreactive interleukin-1 beta, or TNF-alpha production by human monocytes in vitro. AN - 80465630; 1900463 AB - Human peripheral blood monocytes exposed to MK-886 (3-[1-(4-chlorobenzyl)-3-t-butyl-thio-5-isopropylindol-2-yl]-2,2- dimethylpropanoic acid) at doses which abolish formation of 5-lipoxygenase metabolites showed unaltered interleukin-1 beta (IL-1 beta) or tumor necrosis factor-alpha (TNF-alpha) levels in response to phorbol ester, concanavalin A, serum-treated zymosan, or lipopolysaccharide. Indomethacin (10 microM), alone or in combination with MK-886, also failed to modulate monokine production in response to any stimulus. Exogenous arachidonate (3-30 microM) which augmented the formation of PGE2 and LTB4 in the absence of stimulation, also had no effect on monokine production. LPS-induced IL-1 and TNF production occurred despite stimulation of PGE2 synthesis. The results make a role for endogenous prostaglandins and leukotrienes in the regulation of monocyte IL-1 beta and TNF-alpha production unlikely. These data also indicate that MK-886, a novel inhibitor of 5-lipoxygenase product formation, is a potentially useful leukotriene inhibitor which does not affect monokine production. JF - Clinical immunology and immunopathology AU - Hoffman, T AU - Lee, Y L AU - Lizzio, E F AU - Tripathi, A K AU - Jessop, J J AU - Taplits, M AU - Abrahamsen, T G AU - Carter, C S AU - Puri, J AD - Pediatric Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 399 EP - 408 VL - 58 IS - 3 SN - 0090-1229, 0090-1229 KW - Arachidonic Acids KW - 0 KW - Indoles KW - Interleukin-1 KW - Leukotriene Antagonists KW - Lipopolysaccharides KW - Tumor Necrosis Factor-alpha KW - MK-886 KW - 080626SQ8C KW - Concanavalin A KW - 11028-71-0 KW - Arachidonic Acid KW - 27YG812J1I KW - Zymosan KW - 9010-72-4 KW - Arachidonate 5-Lipoxygenase KW - EC 1.13.11.34 KW - Prostaglandin-Endoperoxide Synthases KW - EC 1.14.99.1 KW - Dinoprostone KW - K7Q1JQR04M KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Indomethacin KW - XXE1CET956 KW - Index Medicus KW - Analysis of Variance KW - Dinoprostone -- pharmacology KW - Zymosan -- pharmacology KW - Dose-Response Relationship, Drug KW - Humans KW - Lipopolysaccharides -- pharmacology KW - Radioimmunoassay KW - In Vitro Techniques KW - Enzyme-Linked Immunosorbent Assay KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Concanavalin A -- pharmacology KW - Prostaglandin-Endoperoxide Synthases -- physiology KW - Arachidonate 5-Lipoxygenase -- metabolism KW - Interleukin-1 -- biosynthesis KW - Prostaglandin-Endoperoxide Synthases -- metabolism KW - Monocytes -- metabolism KW - Tumor Necrosis Factor-alpha -- biosynthesis KW - Indoles -- pharmacology KW - Arachidonate 5-Lipoxygenase -- physiology KW - Indomethacin -- pharmacology KW - Arachidonic Acids -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80465630?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+immunology+and+immunopathology&rft.atitle=Absence+of+modulation+of+monokine+production+via+endogenous+cyclooxygenase+or+5-lipoxygenase+metabolites%3A+MK-886+%283-%5B1-%284-chlorobenzyl%29-3-t-butyl-thio-5-isopropylindol-2-yl%5D-2%2C2-+dimethylpropanoic+acid%29%2C+indomethacin%2C+or+arachidonate+fail+to+alter+immunoreactive+interleukin-1+beta%2C+or+TNF-alpha+production+by+human+monocytes+in+vitro.&rft.au=Hoffman%2C+T%3BLee%2C+Y+L%3BLizzio%2C+E+F%3BTripathi%2C+A+K%3BJessop%2C+J+J%3BTaplits%2C+M%3BAbrahamsen%2C+T+G%3BCarter%2C+C+S%3BPuri%2C+J&rft.aulast=Hoffman&rft.aufirst=T&rft.date=1991-03-01&rft.volume=58&rft.issue=3&rft.spage=399&rft.isbn=&rft.btitle=&rft.title=Clinical+immunology+and+immunopathology&rft.issn=00901229&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-17 N1 - Date created - 1991-04-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Radiation-induced skin carcinomas of the head and neck. AN - 80464893; 2000456 AB - Radiation exposures to the scalp during childhood for tinea capitis were associated with a fourfold increase in skin cancer, primarily basal cell carcinomas, and a threefold increase in benign skin tumors. Malignant melanoma, however, was not significantly elevated. Overall, 80 neoplasms were identified from an extensive search of the pathology logs of all major hospitals in Israel and computer linkage with the national cancer registry. Radiation dose to the scalp was computed for over 10,000 persons irradiated for ringworm (mean 7 Gy), and incidence rates were contrasted with those observed in 16,000 matched comparison subjects. The relative risk of radiogenic skin cancer did not differ significantly between men or women or by time since exposure; however, risk was greatest following exposures in early childhood. After adjusting for sex, ethnic origin, and attained age, the estimated excess relative risk was 0.7 per Gy and the average excess risk over the current follow-up was 0.31/10(4) PY-Gy. The risk per Gy of radiation-induced skin cancer was intermediate between the high risk found among whites and no risk found among blacks in a similar study conducted in New York City (Shore et al., Radiat. Res. 100, 192-204, 1984). This finding suggests the role that subsequent exposure to uv radiation likely plays in the expression of a potential radiation-induced skin malignancy. JF - Radiation research AU - Ron, E AU - Modan, B AU - Preston, D AU - Alfandary, E AU - Stovall, M AU - Boice, J D AD - Radiation Epidemiology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 318 EP - 325 VL - 125 IS - 3 SN - 0033-7587, 0033-7587 KW - Index Medicus KW - Space life sciences KW - Age Factors KW - Israel -- epidemiology KW - Sex Factors KW - Carcinoma, Basal Cell -- etiology KW - Melanoma -- etiology KW - Humans KW - Retrospective Studies KW - Carcinoma, Basal Cell -- epidemiology KW - Child KW - Child, Preschool KW - Melanoma -- epidemiology KW - Infant KW - Risk KW - Adolescent KW - Female KW - Male KW - Tinea Capitis -- radiotherapy KW - Neoplasms, Radiation-Induced -- etiology KW - Head and Neck Neoplasms -- etiology KW - Skin Neoplasms -- etiology KW - Neoplasms, Radiation-Induced -- epidemiology KW - Skin Neoplasms -- epidemiology KW - Scalp -- radiation effects KW - Head and Neck Neoplasms -- epidemiology KW - Radiotherapy -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80464893?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Radiation+research&rft.atitle=Radiation-induced+skin+carcinomas+of+the+head+and+neck.&rft.au=Ron%2C+E%3BModan%2C+B%3BPreston%2C+D%3BAlfandary%2C+E%3BStovall%2C+M%3BBoice%2C+J+D&rft.aulast=Ron&rft.aufirst=E&rft.date=1991-03-01&rft.volume=125&rft.issue=3&rft.spage=318&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 - 1991-04-05 N1 - Date created - 1991-04-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Repression of the Drosophila fushi tarazu (ftz) segmentation gene. AN - 80464116; 2001679 AB - The striped expression of the Drosophila segmentation gene fushi tarazu in alternate parasegments of the early embryo is controlled by the 740 bp zebra element. Among multiple protein factors that bind to the zebra element, FTZ-F2 behaves as a transcriptional repressor of ftz. Point mutations in the zebra element which disrupt FTZ-F2 binding to DNA cause ectopic expression of zebra-lacZ activity in transformed embryos. The mutant constructs are expressed from the zygotic genome in preblastoderm embryos as early as the third nuclear division cycle. This unprecedented early transcription suggests that ftz requires active repression during initial nuclear division cycles, a novel type of embryonic gene regulation. A putative FTZ-F2 cDNA clone isolated by recognition site screening of an expression library was found to be identical in sequence with the zinc finger protein tramtrack (Harrison and Travers, 1990). JF - The EMBO journal AU - Brown, J L AU - Sonoda, S AU - Ueda, H AU - Scott, M P AU - Wu, C AD - Laboratory of Biochemistry, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 665 EP - 674 VL - 10 IS - 3 SN - 0261-4189, 0261-4189 KW - ftz KW - Drosophila Proteins KW - 0 KW - Fushi Tarazu Transcription Factors KW - Homeodomain Proteins KW - Insect Hormones KW - ftz protein, Drosophila KW - Deoxyribonuclease I KW - EC 3.1.21.1 KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Animals KW - Base Sequence KW - Embryo, Nonmammalian -- physiology KW - Molecular Sequence Data KW - Transcription, Genetic KW - Methylation KW - Gene Library KW - Cloning, Molecular KW - Cell Division KW - Genes KW - Insect Hormones -- genetics KW - Drosophila -- genetics KW - Drosophila -- anatomy & histology KW - Drosophila -- embryology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80464116?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Repression+of+the+Drosophila+fushi+tarazu+%28ftz%29+segmentation+gene.&rft.au=Brown%2C+J+L%3BSonoda%2C+S%3BUeda%2C+H%3BScott%2C+M+P%3BWu%2C+C&rft.aulast=Brown&rft.aufirst=J&rft.date=1991-03-01&rft.volume=10&rft.issue=3&rft.spage=665&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 - 1991-04-15 N1 - Date created - 1991-04-15 N1 - Date revised - 2017-01-13 N1 - Gene symbol - ftz N1 - Genetic sequence - UNKNOWN; GENBANK N1 - SuppNotes - Cited By: Nature. 1980 Oct 30;287(5785):795-801 [6776413] Development. 1989 Mar;105(3):605-12 [2612367] Cell. 1982 Oct;30(3):675-86 [6183003] Cell. 1982 Oct;30(3):687-96 [7139712] Cell. 1984 Jul;37(3):833-41 [6430568] Nature. 1985 Dec 5-11;318(6045):433-9 [4069216] Cell. 1985 Nov;43(1):47-57 [3000605] Cell. 1985 Dec;43(3 Pt 2):603-13 [3935327] Nature. 1985 Dec 19-1986 Jan 1;318(6047):677-80 [4079981] Cell. 1986 Jan 31;44(2):365-72 [3080248] J Biol Chem. 1986 Jan 25;261(3):1398-408 [3003068] Cell. 1986 Mar 28;44(6):871-7 [2420468] Cell. 1986 Mar 28;44(6):949-57 [3955654] Cell. 1986 Apr 11;45(1):113-26 [3082519] Cell. 1986 Dec 5;47(5):747-54 [3096577] Nature. 1987 Jul 30-Aug 5;328(6129):440-2 [2886916] Cell. 1987 Sep 11;50(6):963-74 [2887293] Cell. 1987 Nov 6;51(3):405-15 [3664640] Cell. 1987 Dec 4;51(5):689-98 [2890437] Science. 1987 Dec 18;238(4834):1675-81 [3686007] Science. 1988 Jan 8;239(4836):170-5 [2892267] Genes Dev. 1987 Nov;1(9):981-95 [2892761] Development. 1989 Nov;107(3):489-504 [2612375] Development. 1989 May;106(1):95-103 [2697548] Cell. 1990 Apr 20;61(2):309-17 [2331752] Genes Dev. 1990 Apr;4(4):624-35 [2113881] Genes Dev. 1990 Jul;4(7):1224-39 [1976571] Cell. 1988 Feb 12;52(3):415-23 [2964277] Development. 1987 Sep;101(1):1-22 [2896587] Nature. 1988 Sep 1;335(6185):25-34 [2901040] Genes Dev. 1988 Aug;2(8):1021-36 [3049237] EMBO J. 1988 Sep;7(9):2881-7 [2846287] Genes Dev. 1988 Jul;2(7):801-6 [3061875] Genes Dev. 1988 Jul;2(7):883-90 [3209072] Nucleic Acids Res. 1988 Dec 23;16(24):11403-16 [2905442] Cell. 1989 Apr 21;57(2):223-32 [2495181] Cell. 1976 Jun;8(2):305-19 [822943] Dev Biol. 1976 Aug;52(1):31-42 [823060] Dev Biol. 1979 May;70(1):217-31 [110635] Methods Enzymol. 1980;65(1):499-560 [6246368] Genes Dev. 1989 Mar;3(3):384-98 [2498165] Nature. 1989 Sep 28;341(6240):340-3 [2571934] Cell. 1990 Jan 12;60(1):9-16 [2403844] EMBO J. 1990 Jan;9(1):207-16 [2104801] Dev Biol. 1981 Jan 15;81(1):51-64 [6780397] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transforming growth factor beta 1 suppresses acute and chronic arthritis in experimental animals. AN - 80462906; 1999490 AB - Systemic administration of the cytokine, TGF beta 1, profoundly antagonized the development of polyarthritis in susceptible rats. TGF beta 1 administration (1 or 5 micrograms/animal), initiated one day before an arthritogenic dose of streptococcal cell wall (SCW) fragments, virtually eliminated the joint swelling and distortion typically observed during both the acute phase (articular index, AI = 2.5 vs. 11; P less than 0.025) and the chronic phase (AI = 0 vs. 12.5) of the disease. Moreover, TGF beta 1 suppressed the evolution of arthritis even when administration was begun after the acute phase of the disease. Histopathological examination of the joint revealed the systemic TGF beta 1 treatment greatly reduced inflammatory cell infiltration, pannus formation, and joint erosion. Consistent with the inhibition of inflammatory cell recruitment into the synovium, TGF beta 1 reversed the leukocytosis associated with the chronic phase of the arthritis. Control animals subjected to the same TGF beta 1 dosing regimen displayed no discernable immunosuppressive or toxic effects even after 4 wk of treatment. These observations not only provide insight into the immunoregulatory effects of TGF beta, but also implicate this cytokine as a potentially important therapeutic agent. JF - The Journal of clinical investigation AU - Brandes, M E AU - Allen, J B AU - Ogawa, Y AU - Wahl, S M AD - Cellular Immunology Section, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 1108 EP - 1113 VL - 87 IS - 3 SN - 0021-9738, 0021-9738 KW - Transforming Growth Factor beta KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Rats KW - Acute Disease KW - Leukocyte Count -- drug effects KW - Animals KW - Streptococcus -- immunology KW - Rats, Inbred Lew KW - Cell Wall -- immunology KW - Chronic Disease KW - Arthritis -- prevention & control KW - Arthritis -- pathology KW - Transforming Growth Factor beta -- adverse effects KW - Arthritis -- drug therapy KW - Transforming Growth Factor beta -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80462906?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Transforming+growth+factor+beta+1+suppresses+acute+and+chronic+arthritis+in+experimental+animals.&rft.au=Brandes%2C+M+E%3BAllen%2C+J+B%3BOgawa%2C+Y%3BWahl%2C+S+M&rft.aulast=Brandes&rft.aufirst=M&rft.date=1991-03-01&rft.volume=87&rft.issue=3&rft.spage=1108&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 - 1991-04-10 N1 - Date created - 1991-04-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Exp Med. 1977 Dec 1;146(6):1585-602 [336836] Science. 1988 Oct 7;242(4875):97-9 [3175638] Proc Natl Acad Sci U S A. 1985 Apr;82(8):2267-71 [3857579] J Clin Invest. 1985 Sep;76(3):1042-56 [3876354] J Immunol. 1986 May 15;136(10):3916-20 [2871107] Biochem Biophys Res Commun. 1988 Dec 30;157(3):1352-9 [3144973] J Cell Biochem. 1989 Feb;39(2):175-84 [2654150] J Immunol. 1989 Aug 1;143(3):877-80 [2745976] Immunol Today. 1989 Aug;10(8):258-61 [2478145] J Immunol. 1989 Nov 15;143(10):3230-4 [2809199] J Exp Med. 1990 Jan 1;171(1):231-47 [2295877] Science. 1990 Jul 6;249(4964):61-4 [2164258] J Exp Med. 1990 Sep 1;172(3):737-44 [2143773] Methods Enzymol. 1991;198:317-27 [1857225] Bull Johns Hopkins Hosp. 1964 Sep;115:265-74 [14209047] J Exp Med. 1986 May 1;163(5):1037-50 [2871125] Proc Natl Acad Sci U S A. 1986 Aug;83(15):5531-3 [3488549] J Immunol. 1986 Dec 15;137(12):3855-60 [2878044] Proc Natl Acad Sci U S A. 1987 Aug;84(16):5788-92 [2886992] J Cell Biol. 1987 Aug;105(2):965-75 [2887577] J Clin Invest. 1987 Sep;80(3):750-7 [3476497] J Biol Chem. 1987 Oct 15;262(29):14090-9 [2443501] Nature. 1987 Oct 8-14;329(6139):539-41 [2889143] J Immunol. 1988 Apr 15;140(8):2645-51 [3258617] J Immunol. 1988 May 1;140(9):3026-32 [3129508] J Immunol. 1988 Jun 15;140(12):4217-23 [3131428] Nature. 1988 Jul 21;334(6179):260-2 [3041283] Proc Natl Acad Sci U S A. 1988 Aug;85(15):5683-7 [3165196] J Clin Invest. 1988 Aug;82(2):680-5 [3165385] J Exp Med. 1988 Aug 1;168(2):737-50 [3261777] J Exp Med. 1988 Oct 1;168(4):1403-17 [2971758] Arthritis Rheum. 1983 Dec;26(12):1442-51 [6360180] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Acquired cisplatin resistance in human ovarian cancer cells is associated with enhanced repair of cisplatin-DNA lesions and reduced drug accumulation. AN - 80462138; 1999494 AB - Studies were undertaken to investigate acquired resistance to cisplatin in human ovarian cancer cells. The cell lines A2780 and A2780/CP70 were studied to assess their respective characteristics of drug accumulation and efflux, cytosolic inactivation of drug, and DNA repair. All experiments were performed using 1-h drug exposures. The A2780/CP70 cell line was 13-fold more resistant to cisplatin than A2780 cells. When studied at their respective IC50 doses, drug accumulation rates were similar for the two cell lines. However, the resistant cell line was twofold more efficient at effluxing drug, which was associated with reduced total drug accumulation for equivalent micromolar drug exposures. At equivalent levels of total cellular drug accumulation, the two cell lines formed the same levels of cisplatin-DNA damage, suggesting that cytosolic inactivation of drug does not contribute to the differential in resistance between these cell lines. Resistant cells were also twofold more efficient at repairing cisplatin-DNA lesions in cellular DNA and in transfected plasmid DNA. We conclude that in these paired cell lines, alterations in drug uptake/efflux and in DNA repair are the major contributing factors to acquired resistance to cisplatin. JF - The Journal of clinical investigation AU - Parker, R J AU - Eastman, A AU - Bostick-Bruton, F AU - Reed, E AD - Medicine Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 772 EP - 777 VL - 87 IS - 3 SN - 0021-9738, 0021-9738 KW - DNA KW - 9007-49-2 KW - Cisplatin KW - Q20Q21Q62J KW - Abridged Index Medicus KW - Index Medicus KW - Tumor Cells, Cultured KW - Transfection KW - DNA Damage KW - Humans KW - DNA -- metabolism KW - In Vitro Techniques KW - Biological Transport KW - Plasmids KW - Female KW - Cell Survival KW - Ovarian Neoplasms -- metabolism KW - DNA Repair KW - Ovarian Neoplasms -- genetics KW - Cisplatin -- toxicity KW - Drug Resistance KW - Cisplatin -- metabolism KW - Ovarian Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80462138?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Acquired+cisplatin+resistance+in+human+ovarian+cancer+cells+is+associated+with+enhanced+repair+of+cisplatin-DNA+lesions+and+reduced+drug+accumulation.&rft.au=Parker%2C+R+J%3BEastman%2C+A%3BBostick-Bruton%2C+F%3BReed%2C+E&rft.aulast=Parker&rft.aufirst=R&rft.date=1991-03-01&rft.volume=87&rft.issue=3&rft.spage=772&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 - 1991-04-10 N1 - Date created - 1991-04-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Somatic Cell Genet. 1981 Mar;7(2):161-70 [6170119] Cancer Res. 1979 Feb;39(2 Pt 1):365-9 [570092] Proc Natl Acad Sci U S A. 1985 Oct;82(19):6622-6 [2995975] J Clin Invest. 1986 Feb;77(2):545-50 [3944268] Cancer Res. 1986 Apr;46(4 Pt 2):1972-9 [3512077] Cancer Chemother Pharmacol. 1987;19(2):149-54 [3568272] Proc Natl Acad Sci U S A. 1987 Jul;84(14):5024-8 [3110781] Pharmacol Ther. 1987;34(2):155-66 [3317449] Cancer Res. 1988 Jun 1;48(11):3019-24 [3365691] Biochemistry. 1988 Jun 28;27(13):4730-4 [3167012] IARC Sci Publ. 1988;(89):313-20 [3058599] Biochem Pharmacol. 1988 Dec 15;37(24):4597-600 [3144285] J Natl Cancer Inst. 1989 Apr 5;81(7):535-9 [2493524] Biochemistry. 1989 Apr 4;28(7):3120-4 [2742829] Cancer Res. 1990 Mar 15;50(6):1863-6 [2306738] Cancer Res. 1990 Apr 15;50(8):2256-60 [2180564] Photochem Photobiol. 1974 Jan;19(1):9-13 [4811564] Mutat Res. 1975 Dec;33(2-3):311-20 [1214823] Mutat Res. 1978 Jun;50(3):383-94 [672921] Biochemistry. 1983 Aug 2;22(16):3927-33 [6225458] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Polyamines can protect against ischemia-induced nerve cell death in gerbil forebrain. AN - 80460240; 1999235 AB - We have previously demonstrated that administration of the polyamines putrescine, spermidine, or spermine can prevent neuronal degeneration in rats during naturally occurring cell death or after injurious treatments such as nerve injury or monosodium glutamate neurotoxicity. The present study demonstrates that also in adult gerbils polyamine treatment can protect forebrain neurons from degeneration after ischemia. Neurons in the hippocampus and striatum were rescued from delayed cell death after brief (5 min) global ischemia in gerbils which were treated with daily injections (10 mg/kg) of polyamines. The evidence accrued, so far, indicates that systemic polyamines can protect a wide variety of central and peripheral neurons from natural or induced degeneration. JF - Experimental neurology AU - Gilad, G M AU - Gilad, V H AD - Neuropsychiatry Branch, NIMH Neuroscience Center, Saint Elizabeths, Washington, D.C. 20032. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 349 EP - 355 VL - 111 IS - 3 SN - 0014-4886, 0014-4886 KW - Polyamines KW - 0 KW - Eflornithine KW - ZQN1G5V6SR KW - Index Medicus KW - Body Weight KW - Nerve Degeneration -- drug effects KW - Gerbillinae KW - Animals KW - Reference Values KW - Analysis of Variance KW - Body Temperature KW - Pyramidal Tracts -- drug effects KW - Pyramidal Tracts -- pathology KW - Eflornithine -- pharmacology KW - Male KW - Ischemic Attack, Transient -- prevention & control KW - Polyamines -- pharmacology KW - Neurons -- drug effects KW - Brain -- pathology KW - Brain -- drug effects KW - Ischemic Attack, Transient -- pathology KW - Neurons -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80460240?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+neurology&rft.atitle=Polyamines+can+protect+against+ischemia-induced+nerve+cell+death+in+gerbil+forebrain.&rft.au=Gilad%2C+G+M%3BGilad%2C+V+H&rft.aulast=Gilad&rft.aufirst=G&rft.date=1991-03-01&rft.volume=111&rft.issue=3&rft.spage=349&rft.isbn=&rft.btitle=&rft.title=Experimental+neurology&rft.issn=00144886&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-08 N1 - Date created - 1991-04-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transforming growth factor beta suppresses human immunodeficiency virus expression and replication in infected cells of the monocyte/macrophage lineage. AN - 80458887; 1705278 AB - The pleiotropic immunoregulatory cytokine transforming growth factor beta (TGF-beta) potently suppresses production of the human immunodeficiency virus (HIV), the causative agent of the acquired immunodeficiency syndrome, in the chronically infected promonocytic cell line U1. TGF-beta significantly (50-90%) inhibited HIV reverse transcriptase production and synthesis of viral proteins in U1 cells stimulated with phorbol myristate acetate (PMA) or interleukin 6 (IL-6). Furthermore, TGF-beta suppressed PMA induction of HIV transcription in U1 cells. In contrast, TGF-beta did not significantly affect the expression of HIV induced by tumor necrosis factor alpha (TNF-alpha). These suppressive effects were not mediated via the induction of interferon alpha (IFN-alpha). TGF-beta also suppressed HIV replication in primary monocyte-derived macrophages infected in vitro, both in the absence of exogenous cytokines and in IL-6-stimulated cultures. In contrast, no significant effects of TGF-beta were observed in either a chronically infected T cell line (ACH-2) or in primary T cell blasts infected in vitro. Therefore, TGF-beta may play a potentially important role as a negative regulator of HIV expression in infected monocytes or tissue macrophages in infected individuals. JF - The Journal of experimental medicine AU - Poli, G AU - Kinter, A L AU - Justement, J S AU - Bressler, P AU - Kehrl, J H AU - Fauci, A S AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/03/01/ PY - 1991 DA - 1991 Mar 01 SP - 589 EP - 597 VL - 173 IS - 3 SN - 0022-1007, 0022-1007 KW - Antiviral Agents KW - 0 KW - Interleukin-6 KW - Recombinant Proteins KW - Reverse Transcriptase Inhibitors KW - Transforming Growth Factor beta KW - Viral Proteins KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - AIDS/HIV KW - Macrophages KW - Recombinant Proteins -- pharmacology KW - Monocytes -- cytology KW - Cells, Cultured KW - Kinetics KW - Humans KW - Viral Proteins -- biosynthesis KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Monocytes -- drug effects KW - Interleukin-6 -- pharmacology KW - Cell Line KW - Transforming Growth Factor beta -- pharmacology KW - HIV-1 -- genetics KW - Transcription, Genetic -- drug effects KW - Virus Replication -- drug effects KW - HIV-1 -- enzymology KW - HIV-1 -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80458887?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Transforming+growth+factor+beta+suppresses+human+immunodeficiency+virus+expression+and+replication+in+infected+cells+of+the+monocyte%2Fmacrophage+lineage.&rft.au=Poli%2C+G%3BKinter%2C+A+L%3BJustement%2C+J+S%3BBressler%2C+P%3BKehrl%2C+J+H%3BFauci%2C+A+S&rft.aulast=Poli&rft.aufirst=G&rft.date=1991-03-01&rft.volume=173&rft.issue=3&rft.spage=589&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 - 1991-04-02 N1 - Date created - 1991-04-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Immunol. 1986 Dec 15;137(12):3855-60 [2878044] Lancet. 1985 Mar 16;1(8429):602-4 [2857946] J Virol. 1986 Aug;59(2):284-91 [3016298] Science. 1985 Dec 6;230(4730):1126-32 [2999973] Nature. 1987 Apr 16-22;326(6114):711-3 [3031512] Cell Immunol. 1988 Apr 1;112(2):343-50 [2965617] Clin Exp Immunol. 1986 Apr;64(1):166-72 [2942321] J Immunol. 1988 May 1;140(9):3026-32 [3129508] J Exp Med. 1987 Aug 1;166(2):571-6 [3110354] Science. 1988 Sep 23;241(4873):1673-5 [3047875] Immunol Today. 1989 Aug;10(8):258-61 [2478145] J Immunol. 1989 Jan 15;142(2):431-8 [2463307] J Immunol. 1988 Feb 15;140(4):1117-22 [2449497] J Immunol. 1986 Jun 1;136(11):4049-53 [2422271] J Immunol. 1989 Jun 15;142(12):4295-300 [2542408] Virology. 1989 Feb;168(2):399-405 [2492697] Proc Natl Acad Sci U S A. 1989 Apr;86(7):2336-40 [2494664] Cell. 1989 Jul 28;58(2):227-9 [2665943] J Neuroimmunol. 1989 Jul;23(2):109-16 [2656753] J Cell Biochem. 1989 Feb;39(2):175-84 [2654150] J Immunol. 1989 Jun 15;142(12):4339-45 [2786029] Proc Natl Acad Sci U S A. 1989 Apr;86(7):2365-8 [2784570] Proc Natl Acad Sci U S A. 1989 Aug;86(15):5974-8 [2762307] Proc Natl Acad Sci U S A. 1987 Sep;84(17):6020-4 [2888109] Proc Natl Acad Sci U S A. 1990 Nov;87(21):8321-5 [1700428] Am J Med. 1988 Sep;85(3):289-91 [3414726] Science. 1989 May 5;244(4904):575-7 [2470148] Adv Cancer Res. 1988;51:107-45 [2906217] J Acquir Immune Defic Syndr. 1988;1(5):436-40 [3146635] AIDS Res Hum Retroviruses. 1989 Apr;5(2):131-8 [2713164] Clin Exp Immunol. 1985 Oct;62(1):136-42 [2998656] Clin Exp Immunol. 1985 Oct;62(1):128-35 [2415279] J Exp Med. 1986 May 1;163(5):1037-50 [2871125] J Immunol. 1986 May 15;136(10):3916-20 [2871107] Proc Natl Acad Sci U S A. 1987 Aug;84(16):5788-92 [2886992] J Virol. 1988 Jan;62(1):139-47 [3257102] J Clin Invest. 1984 Dec;74(6):2121-8 [6511917] Science. 1987 Nov 6;238(4828):800-2 [3313729] J Clin Immunol. 1985 Jan;5(1):21-5 [3872310] J Immunol. 1990 Aug 15;145(4):1120-6 [1696294] J Biol Chem. 1990 May 15;265(14):8339-43 [2186042] J Exp Med. 1990 Jul 1;172(1):253-61 [2193097] J Exp Med. 1990 Jul 1;172(1):151-8 [2193094] Immunol Today. 1990 Jun;11(6):217-23 [2191685] Immunol Today. 1990 Mar;11(3):81-2 [2186744] Cell. 1990 Jun 29;61(7):1271-6 [2364429] Proc Natl Acad Sci U S A. 1990 Jan;87(2):782-5 [2300561] Science. 1984 May 4;224(4648):497-500 [6200935] Science. 1983 May 20;220(4599):868-71 [6189183] J Gen Virol. 1979 Mar;42(3):467-80 [85689] Virology. 1977 Mar;77(1):135-48 [65834] Proc Natl Acad Sci U S A. 1974 Sep;71(9):3542-4 [4139716] J Virol. 1971 May;7(5):625-34 [4326752] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Risk factors for emphysema. Cigarette smoking is associated with a reduction in the association rate constant of lung alpha 1-antitrypsin for neutrophil elastase. AN - 80458778; 1999486 AB - The increased risk of developing emphysema among individuals who smoke cigarettes and who have normal levels of alpha 1-antitrypsin (alpha 1AT) is hypothesized to result from a decrease in the antineutrophil elastase capacity of the lower respiratory tract alpha 1AT of smokers compared with nonsmokers. To evaluate this hypothesis we compared the time-dependent kinetics of the inhibition of neutrophil elastase by lung alpha 1AT from healthy, young cigarette smokers (n = 8) and nonsmokers (n = 12). alpha 1-antitrypsin was purified from lavage fluid using affinity and molecular sieve chromatography, and the association rate constant (k assoc) for neutrophil elastase quantified. The k assoc of smoker plasma alpha 1AT (9.5 +/- 0.5 X 10(6) M-1s-1) was similar to that of nonsmoker plasma (9.3 +/- 0.7 X 10(6) M-1s-1, P greater than 0.5). In marked contrast, the k assoc of smoker lower respiratory tract alpha 1AT was significantly lower than that of nonsmoker alpha 1AT (6.5 +/- 0.4 X 10(6) M-1s-1 vs. 8.1 +/- 0.5 X 10(6) M-1s-1, P less than 0.01). Furthermore, the smoker lower respiratory tract alpha 1AT k assoc was significantly less than that of autologous plasma (P less than 0.01). When considered in the context of the concentration of alpha 1AT in the lower respiratory tract epithelial lining fluid, the inhibition time for neutrophil elastase of smoker lung alpha 1AT was twofold greater than that of nonsmoker lung alpha 1AT (smoker: 0.34 +/- 0.05 s vs. nonsmoker: 0.17 +/- 0.05 s, P less than 0.01). Consequently, for concentrations of alpha 1AT in the lower respiratory tract it takes twice as long for an equivalent amount of neutrophil elastase to be inhibited in the smoker's lung compared with the nonsmoker's lung. These observations support the concept that cigarette smoking is associated with a decrease in the lower respiratory tract neutrophil elastase inhibitory capacity, thus increasing the vulnerability of the lung to elastolytic destruction and thereby increasing the risk for the development of emphysema. JF - The Journal of clinical investigation AU - Ogushi, F AU - Hubbard, R C AU - Vogelmeier, C AU - Fells, G A AU - Crystal, R G AD - Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 1060 EP - 1065 VL - 87 IS - 3 SN - 0021-9738, 0021-9738 KW - alpha 1-Antitrypsin KW - 0 KW - Pancreatic Elastase KW - EC 3.4.21.36 KW - Abridged Index Medicus KW - Index Medicus KW - Plants, Toxic KW - Risk Factors KW - Kinetics KW - Humans KW - Tobacco KW - Protein Binding KW - Pancreatic Elastase -- metabolism KW - alpha 1-Antitrypsin -- metabolism KW - Emphysema -- etiology KW - Smoking -- metabolism KW - Neutrophils -- enzymology KW - Lung -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80458778?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Risk+factors+for+emphysema.+Cigarette+smoking+is+associated+with+a+reduction+in+the+association+rate+constant+of+lung+alpha+1-antitrypsin+for+neutrophil+elastase.&rft.au=Ogushi%2C+F%3BHubbard%2C+R+C%3BVogelmeier%2C+C%3BFells%2C+G+A%3BCrystal%2C+R+G&rft.aulast=Ogushi&rft.aufirst=F&rft.date=1991-03-01&rft.volume=87&rft.issue=3&rft.spage=1060&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 - 1991-04-10 N1 - Date created - 1991-04-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: N Engl J Med. 1972 Apr 20;286(16):853-7 [5061068] Am Rev Respir Dis. 1983 Nov;128(5):833-8 [6556892] N Engl J Med. 1974 Oct 10;291(15):755-8 [4414996] Biochemistry. 1974 Dec 17;13(26):5439-45 [4547976] N Engl J Med. 1975 Feb 6;292(6):278-81 [1078596] J Clin Invest. 1975 Feb;55(2):427-30 [1079211] Eur J Biochem. 1975 Sep 1;57(1):107-13 [809280] Am Rev Respir Dis. 1975 Nov;112(5):657-711 [1103668] Am Rev Respir Dis. 1977 Jul;116(1):65-72 [301725] Eur J Biochem. 1978 Feb 1;83(1):143-53 [304805] Am Rev Respir Dis. 1978 Feb;117(2):343-78 [345898] Am Rev Respir Dis. 1978 Jun;117(6):1109-33 [352207] N Engl J Med. 1978 Nov 9;299(19):1045-8 [360063] J Biol Chem. 1979 May 25;254(10):4022-6 [312289] J Clin Invest. 1979 Apr;63(4):793-7 [220283] Am J Pathol. 1979 Oct;97(1):111-36 [495691] Science. 1979 Dec 14;206(4424):1313-4 [316187] Science. 1979 Dec 14;206(4424):1315-6 [316188] Hum Genet. 1980;53(3):429-33 [6102963] Clin Chest Med. 1983 Sep;4(3):405-12 [6196148] Am Rev Respir Dis. 1984 Sep;130(3):386-90 [6332562] Hoppe Seylers Z Physiol Chem. 1984 Jul;365(7):731-6 [6332770] Am Rev Respir Dis. 1984 Oct;130(4):650-8 [6385789] Am Rev Respir Dis. 1985 Jan;131(1):79-85 [3871315] Biochem Med. 1984 Dec;32(3):387-97 [6517881] Proc Natl Acad Sci U S A. 1985 Feb;82(3):795-9 [3871944] Am Rev Respir Dis. 1985 Jun;131(6):828-30 [4003931] Am Rev Respir Dis. 1985 Jul;132(1):182-5 [4014865] Am Rev Respir Dis. 1985 Aug;132(2):417-33 [3896082] Biochem Biophys Res Commun. 1985 Aug 15;130(3):1177-84 [3896239] Am Rev Respir Dis. 1985 Oct;132(4):913-4 [3876796] J Appl Physiol (1985). 1986 Feb;60(2):532-8 [3512509] Am Rev Respir Dis. 1986 Mar;133(3):353-6 [3006558] J Clin Invest. 1986 Jun;77(6):1952-61 [3486887] J Clin Invest. 1986 Aug;78(2):482-93 [3525610] Lung. 1986;164(4):233-42 [3018387] Bull Eur Physiopathol Respir. 1986 Jul-Aug;22(4):359-63 [3094607] Am J Respir Cell Mol Biol. 1989 Nov;1(5):423-9 [2637756] Arch Environ Health. 1965 Jul;11:50-8 [14312390] J Biol Chem. 1980 May 10;255(9):3931-4 [6989830] Anal Biochem. 1980 May 1;104(1):205-14 [6992646] J Clin Invest. 1980 Nov;66(5):987-95 [6253528] Am Rev Respir Dis. 1981 Jan;123(1):85-9 [6257154] J Biol Chem. 1981 Apr 10;256(7):3348-53 [6162845] Bull Eur Physiopathol Respir. 1980;16 Suppl:183-97 [7225632] J Clin Invest. 1981 Oct;68(4):889-98 [6169740] J Biochem Biophys Methods. 1981 Dec;5(5):243-9 [7037919] Proc Natl Acad Sci U S A. 1982 Mar;79(6):2041-5 [6979049] Nature. 1982 Jul 22;298(5872):329-34 [7045697] Am Rev Respir Dis. 1982 Jul;126(1):25-30 [6979963] Am Rev Respir Dis. 1983 May;127(5):540-4 [6552150] Science. 1983 Sep 16;221(4616):1187-9 [6612333] Am Rev Respir Dis. 1983 Sep;128(3):434-9 [6311062] Annu Rev Biochem. 1983;52:655-709 [6193754] Clin Chim Acta. 1983 Aug 31;132(3):309-15 [6604594] Am Rev Respir Dis. 1974 Aug;110(2):176-94 [4212922] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ovarian hormones enhance 2,3,7,8-tetrachlorodibenzo-p-dioxin-mediated increases in cell proliferation and preneoplastic foci in a two-stage model for rat hepatocarcinogenesis. AN - 80456419; 1671757 AB - 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a potent hepatocarcinogen in rodents. However, liver tumor incidence is increased by TCDD in female Sprague-Dawley rats but not male rats in chronic carcinogen bioassays. Our studies have investigated this finding by evaluating histological and biochemical parameters in a two-stage model for hepatocarcinogenesis in female Sprague-Dawley rats (intact and ovariectomized), using diethylnitrosamine (DEN) as the initiating agent and TCDD as the promoting agent. Increases in gamma-glutamyl transpeptidase-positive foci were greater in intact female rats than in ovariectomized (OVX) animals. For example, in intact rats receiving both DEN and TCDD, the percentage of liver occupied by gamma-glutamyl transpeptidase-positive foci was 0.37, compared to 0.08 in OVX rats. Values for intact or OVX rats receiving either DEN or TCDD only were 0.04 or less. Similar results were obtained when using placental glutathione S-transferase to detect hepatic preneoplastic lesions. Cell proliferation data, obtained using bromodeoxyuridine in osmotic minipumps, were consistent with preneoplastic foci data in that the hepatocyte labeling index was increased in DEN/TCDD intact rats but not in DEN/TCDD OVX rats. Analysis of data from individual animals revealed a strong correlation (P less than 0.01) between cell proliferation and placental glutathione S-transferase-positive foci/cm3 in liver. These findings did not reflect effects of ovariectomy on TCDD tissue distribution, since livers of OVX rats contained more TCDD than livers of intact rats, although both groups of rats received a dose of 1.4 micrograms TCDD/kg once every 2 weeks for 30 weeks. Hepatic cytochrome P-450d (IA2) was induced approximately 6-8-fold in all TCDD-treated groups, and the magnitude of induction was not influenced by ovariectomy. This cytochrome efficiently catalyzes metabolism of 17 beta-estradiol to catechol estrogens. Our data suggest that ovarian hormones (probably estrogen) play a significant role in the hepatocarcinogenic actions of TCDD. JF - Cancer research AU - Lucier, G W AU - Tritscher, A AU - Goldsworthy, T AU - Foley, J AU - Clark, G AU - Goldstein, J AU - Maronpot, R AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/03/01/ PY - 1991 DA - 1991 Mar 01 SP - 1391 EP - 1397 VL - 51 IS - 5 SN - 0008-5472, 0008-5472 KW - Estrogens KW - 0 KW - Polychlorinated Dibenzodioxins KW - Receptors, Estrogen KW - Diethylnitrosamine KW - 3IQ78TTX1A KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - gamma-Glutamyltransferase KW - EC 2.3.2.2 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Cytochrome P-450 Enzyme System -- analysis KW - Animals KW - gamma-Glutamyltransferase -- analysis KW - Cell Division -- drug effects KW - Receptors, Estrogen -- analysis KW - Ovariectomy KW - Female KW - Precancerous Conditions -- chemically induced KW - Polychlorinated Dibenzodioxins -- toxicity KW - Liver Neoplasms, Experimental -- chemically induced KW - Estrogens -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80456419?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Ovarian+hormones+enhance+2%2C3%2C7%2C8-tetrachlorodibenzo-p-dioxin-mediated+increases+in+cell+proliferation+and+preneoplastic+foci+in+a+two-stage+model+for+rat+hepatocarcinogenesis.&rft.au=Lucier%2C+G+W%3BTritscher%2C+A%3BGoldsworthy%2C+T%3BFoley%2C+J%3BClark%2C+G%3BGoldstein%2C+J%3BMaronpot%2C+R&rft.aulast=Lucier&rft.aufirst=G&rft.date=1991-03-01&rft.volume=51&rft.issue=5&rft.spage=1391&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 - 1991-03-29 N1 - Date created - 1991-03-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Asbestos-induced alveolar injury. Evidence for macrophage-derived PDGF as a mediator of the fibrogenic response. AN - 80456179; 1997275 JF - Chest AU - Bonner, J C AU - Brody, A R AD - Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 54S EP - 55S VL - 99 IS - 3 Suppl SN - 0012-3692, 0012-3692 KW - Platelet-Derived Growth Factor KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Rats KW - Animals KW - Asbestosis -- pathology KW - Asbestosis -- metabolism KW - Pulmonary Alveoli -- pathology KW - Pulmonary Fibrosis -- pathology KW - Platelet-Derived Growth Factor -- biosynthesis KW - Pulmonary Fibrosis -- metabolism KW - Platelet-Derived Growth Factor -- physiology KW - Macrophages -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80456179?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chest&rft.atitle=Asbestos-induced+alveolar+injury.+Evidence+for+macrophage-derived+PDGF+as+a+mediator+of+the+fibrogenic+response.&rft.au=Bonner%2C+J+C%3BBrody%2C+A+R&rft.aulast=Bonner&rft.aufirst=J&rft.date=1991-03-01&rft.volume=99&rft.issue=3+Suppl&rft.spage=54S&rft.isbn=&rft.btitle=&rft.title=Chest&rft.issn=00123692&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-04 N1 - Date created - 1991-04-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Substitution of foreign protein sequences into a chimeric toxin composed of transforming growth factor alpha and Pseudomonas exotoxin. AN - 80450775; 1671711 AB - TGF alpha-PE40 is a chimeric toxin made by replacing domain Ia of Pseudomonas exotoxin (PE) with transforming growth factor alpha (TGF alpha). We have now replaced a portion of domain Ib of PE with different polypeptides or an extra domain III of PE in transforming growth factor alpha-PE40 and maintained cell killing. Thus, TGF alpha-PE40 can be used to transport foreign protein sequences into the cytosol of cells. JF - Molecular and cellular biology AU - Debinski, W AU - Siegall, C B AU - Fitzgerald, D AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 1751 EP - 1753 VL - 11 IS - 3 SN - 0270-7306, 0270-7306 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - Recombinant Fusion Proteins KW - Transforming Growth Factor alpha KW - Virulence Factors KW - Adenosine Diphosphate Ribose KW - 20762-30-5 KW - Somatostatin KW - 51110-01-1 KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - Somatostatin -- genetics KW - Protein Biosynthesis KW - Blotting, Western KW - Humans KW - In Vitro Techniques KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Adenosine Diphosphate Ribose -- metabolism KW - Structure-Activity Relationship KW - Recombinant Fusion Proteins -- metabolism KW - Exotoxins -- genetics KW - Transforming Growth Factor alpha -- genetics KW - Recombinant Fusion Proteins -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80450775?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Substitution+of+foreign+protein+sequences+into+a+chimeric+toxin+composed+of+transforming+growth+factor+alpha+and+Pseudomonas+exotoxin.&rft.au=Debinski%2C+W%3BSiegall%2C+C+B%3BFitzgerald%2C+D%3BPastan%2C+I&rft.aulast=Debinski&rft.aufirst=W&rft.date=1991-03-01&rft.volume=11&rft.issue=3&rft.spage=1751&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 - 1991-03-27 N1 - Date created - 1991-03-27 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 1990 Nov 25;265(33):20678-85 [2122978] J Biol Chem. 1971 Mar 10;246(5):1496-503 [5545092] FASEB J. 1989 Dec;3(14):2647-52 [2556314] Proc Natl Acad Sci U S A. 1987 Jul;84(13):4538-42 [3299371] Proc Natl Acad Sci U S A. 1988 Dec;85(24):9738-42 [3264406] J Bacteriol. 1987 Nov;169(11):4967-71 [2889718] J Mol Biol. 1986 May 5;189(1):113-30 [3537305] Nature. 1988 Sep 22;335(6188):369-72 [2843774] Proc Natl Acad Sci U S A. 1986 Mar;83(5):1320-4 [3006045] Proc Natl Acad Sci U S A. 1988 Mar;85(6):1922-6 [3126499] Cell. 1987 Jan 16;48(1):129-36 [3098436] Nature. 1989 Jun 1;339(6223):394-7 [2498664] Proc Natl Acad Sci U S A. 1989 Jun;86(11):4215-9 [2657746] Cell. 1986 Dec 5;47(5):641-8 [3536124] Proc Natl Acad Sci U S A. 1990 Jan;87(1):308-12 [2104981] J Biol Chem. 1989 Aug 25;264(24):14256-61 [2503515] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chromosomal protein HMG-14 is overexpressed in Down syndrome. AN - 80450424; 1825298 AB - The physical phenotype of Down syndrome, one of the most prevalent genetic disorders, results from an extra copy of regions q22.1 to q22.3 of chromosome 21 in cells of affected individuals. The gene coding for chromosomal protein HMG-14 is among the limited number of genes, coding for known functions, which has been mapped to this region of chromosome 21. Here we report a gene dosage effect on the expression of HMG-14 in both cultured cells and brain tissue samples obtained from Down syndrome patients. The putative role of HMG-14 in the structure of active chromatin raises the possibility that elevated levels of this protein may be a contributing factor in the etiology of Down syndrome. JF - Experimental cell research AU - Pash, J AU - Smithgall, T AU - Bustin, M AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 232 EP - 235 VL - 193 IS - 1 SN - 0014-4827, 0014-4827 KW - High Mobility Group Proteins KW - 0 KW - Index Medicus KW - Humans KW - Brain -- embryology KW - Gene Expression Regulation KW - Brain -- metabolism KW - Cell Line KW - High Mobility Group Proteins -- biosynthesis KW - High Mobility Group Proteins -- genetics KW - Down Syndrome -- metabolism KW - Down Syndrome -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80450424?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Chromosomal+protein+HMG-14+is+overexpressed+in+Down+syndrome.&rft.au=Pash%2C+J%3BSmithgall%2C+T%3BBustin%2C+M&rft.aulast=Pash&rft.aufirst=J&rft.date=1991-03-01&rft.volume=193&rft.issue=1&rft.spage=232&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 - 1991-03-27 N1 - Date created - 1991-03-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Intake of tapwater and total water by pregnant and lactating women. AN - 80450336; 1994741 AB - Despite theoretically higher requirements for water due to physiologic demands of pregnancy and lactation, little is known of actual ranges of intake in pregnant and lactating women. Population-based estimates of total water and tapwater intake in women of reproductive age were derived using data from the 1977-78 USDA Nationwide Food Consumption Survey. Three-day average intakes were calculated for 188 pregnant women, 77 lactating women, and 6,201 non-pregnant, non-lactating control women. Total water intake (mean +/- SD) was 1,940 +/- 686 g/day (median 1,835) for control women, 2,076 +/- 743 g/day (median 1,928) for pregnant women and 2,242 +/- 658 g/day (median 2,164) for lactating women. Tapwater intake was 1,157 +/- 635 g/day (median 1,065) for control women, 1,189 +/- 699 g/day (median 1,063) for pregnant women, and 1,310 +/- 591 g/day (median 1,330) for lactating women. Total water intake was equal to or greater than 3,000 g/day among 7 percent of control women, 11 percent of pregnant women, and 13 percent of lactating women. Tapwater intake was equal to or greater than 2,000 g/day among 10 percent of control women, 15 percent of pregnant women, and 8 percent of lactating women. These results should be useful in estimating amounts of nutrients and toxic substances that women of reproductive age obtain through the water supply. JF - American journal of public health AU - Ershow, A G AU - Brown, L M AU - Cantor, K P AD - Lipid Metabolism-Atherogenesis Branch, National Heart, Lung and Blood Institute, Bethesda, MD 20892. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 328 EP - 334 VL - 81 IS - 3 SN - 0090-0036, 0090-0036 KW - Abridged Index Medicus KW - Index Medicus KW - United States KW - Educational Status KW - Humans KW - Adult KW - Water Supply KW - Diet Surveys KW - Middle Aged KW - Adolescent KW - Female KW - Drinking KW - Diet KW - Pregnancy KW - Lactation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80450336?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Intake+of+tapwater+and+total+water+by+pregnant+and+lactating+women.&rft.au=Ershow%2C+A+G%3BBrown%2C+L+M%3BCantor%2C+K+P&rft.aulast=Ershow&rft.aufirst=A&rft.date=1991-03-01&rft.volume=81&rft.issue=3&rft.spage=328&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 - 1991-03-20 N1 - Date created - 1991-03-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Am Diet Assoc. 1989 May;89(5):671-6 [2723291] Annu Rev Nutr. 1983;3:413-32 [6357240] J Pediatr. 1985 Feb;106(2):207-11 [3968608] Am J Clin Nutr. 1985 Nov;42(5):870-6 [4061348] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Sequence-specific toxicity of transfected retroviral DNA. AN - 80449396; 1847335 AB - Experimental gene transfer and viral infections can result in the accumulation of unintegrated DNA in target cells. The effects of such accumulation on target cell metabolism have not been directly studied. The experiments reported in this paper show that transfection of cloned retroviral long-terminal-repeat (LTR) DNA, or of a variety of eukaryotic promoters, into proliferating HeLa cells results in rapid, sequence-specific, and dose-dependent cell death. Plasmids containing the Rous sarcoma virus LTR or the human immunodeficiency virus LTR cloned in pUC-related plasmids are 5 to 10 times more toxic than pUC19. The demonstrated sensitivity of eukaryotic cells to exogenously introduced DNA has important implications for the interpretation of gene transfer experiments and may be relevant to the pathogenic mechanisms in the course of retroviral infections such as AIDS. JF - Experimental cell research AU - Holter, W AU - Rabson, A B AU - Corsico, C D AU - Howard, B H AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 54 EP - 58 VL - 193 IS - 1 SN - 0014-4827, 0014-4827 KW - DNA, Viral KW - 0 KW - Receptors, Interleukin-2 KW - Index Medicus KW - AIDS/HIV KW - HIV Long Terminal Repeat KW - Transfection KW - HeLa Cells KW - Humans KW - Transcription, Genetic KW - Promoter Regions, Genetic -- genetics KW - Cytopathogenic Effect, Viral KW - Repetitive Sequences, Nucleic Acid KW - Avian Sarcoma Viruses -- genetics KW - Receptors, Interleukin-2 -- genetics KW - HIV -- genetics KW - Cell Survival KW - DNA, Viral -- physiology KW - Retroviridae -- genetics KW - DNA, Viral -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80449396?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Sequence-specific+toxicity+of+transfected+retroviral+DNA.&rft.au=Holter%2C+W%3BRabson%2C+A+B%3BCorsico%2C+C+D%3BHoward%2C+B+H&rft.aulast=Holter&rft.aufirst=W&rft.date=1991-03-01&rft.volume=193&rft.issue=1&rft.spage=54&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 - 1991-03-27 N1 - Date created - 1991-03-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Elevated nicotine levels in cervical lavages from passive smokers. AN - 80448345; 1994747 AB - One hundred forty-five nonsmokers found to have normal cytologic diagnoses on routine Pap smears were interviewed regarding environmental exposure to tobacco smoke, and a 3 ml saline lavage of the cervix was collected for measurement of cervical nicotine levels by gas chromatography-mass spectroscopy. Nicotine levels tended to be highest among women exposed to tobacco smoke in the home, intermediate in women exposed only outside the home, and lowest in women recalling no exposure (p = 0.001). JF - American journal of public health AU - Jones, C J AU - Schiffman, M H AU - Kurman, R AU - Jacob, P AU - Benowitz, N L AD - Environmental Epidemiology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 378 EP - 379 VL - 81 IS - 3 SN - 0090-0036, 0090-0036 KW - Tobacco Smoke Pollution KW - 0 KW - Nicotine KW - 6M3C89ZY6R KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Adult KW - Surveys and Questionnaires KW - Aged KW - Middle Aged KW - Adolescent KW - Female KW - Nicotine -- analysis KW - Cervix Uteri -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80448345?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Elevated+nicotine+levels+in+cervical+lavages+from+passive+smokers.&rft.au=Jones%2C+C+J%3BSchiffman%2C+M+H%3BKurman%2C+R%3BJacob%2C+P%3BBenowitz%2C+N+L&rft.aulast=Jones&rft.aufirst=C&rft.date=1991-03-01&rft.volume=81&rft.issue=3&rft.spage=378&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 - 1991-03-20 N1 - Date created - 1991-03-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Am J Public Health. 1988 Jun;78(6):699-701 [3369604] Am J Obstet Gynecol. 1988 Apr;158(4):910-3 [3364502] Cancer Res. 1987 Jul 15;47(14):3886-8 [3594446] N Engl J Med. 1985 Jan 31;312(5):315-6 [3965965] J Chromatogr. 1981 Jan 2;222(1):61-70 [6783675] Pharmacol Biochem Behav. 1988 May;30(1):249-53 [3174750] JAMA. 1989 Mar 17;261(11):1593-8 [2918652] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Variable role of the long terminal repeat Sp1-binding sites in human immunodeficiency virus replication in T lymphocytes. AN - 80447893; 1995951 AB - The long terminal repeat (LTR) of the human immunodeficiency virus (HIV) contains three binding sites for the transcriptional factor Sp1. In order to investigate the role that the Sp1-binding sites play in regulation of HIV replication, we have introduced a deletion of all three Sp1-binding sites into the LTR of an infectious molecular clone of HIV. Viral stocks have been prepared from this mutant virus, designated dl-Sp, and these stocks have been used to study its replicative ability in human T cells. The dl-Sp virus replicated efficiently in MT4 cells and in phytohemagglutinin-stimulated human peripheral blood lymphocytes, but it replicated poorly and with delayed kinetics in A3.01 (CEM) T cells unless those cells had been treated with the cytokine tumor necrosis factor alpha. Gel retardation assays to study the levels of DNA-binding proteins present in these cells showed that NF-kappa B activity could be detected in the nuclei of MT4 cells but not in A3.01 cells unless they had been treated with tumor necrosis factor alpha. Thus, the presence of NF-kappa B activity appeared to be required for efficient replication of an HIV whose LTR Sp1-binding sites had been deleted. This suggests that NF-kappa B can functionally compensate for Sp1 in activating HIV replication. The HIV LTR is therefore similar to the promoter-enhancer units of other viruses in that it is composed of multiple functional elements that may contribute differently to viral replication depending on the levels of DNA-binding proteins present in the target cells. JF - Journal of virology AU - Parrott, C AU - Seidner, T AU - Duh, E AU - Leonard, J AU - Theodore, T S AU - Buckler-White, A AU - Martin, M A AU - Rabson, A B AD - Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 1414 EP - 1419 VL - 65 IS - 3 SN - 0022-538X, 0022-538X KW - NF-kappa B KW - 0 KW - Sp1 Transcription Factor KW - Transcription Factors KW - Index Medicus KW - AIDS/HIV KW - Mutagenesis, Site-Directed KW - Animals KW - Chromosome Deletion KW - Base Sequence KW - Kinetics KW - Restriction Mapping KW - Molecular Sequence Data KW - Cell Line KW - T-Lymphocytes KW - NF-kappa B -- metabolism KW - Binding Sites KW - Virus Replication KW - HIV Long Terminal Repeat KW - HIV -- physiology KW - Transcription Factors -- metabolism KW - Sp1 Transcription Factor -- metabolism KW - HIV -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80447893?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Variable+role+of+the+long+terminal+repeat+Sp1-binding+sites+in+human+immunodeficiency+virus+replication+in+T+lymphocytes.&rft.au=Parrott%2C+C%3BSeidner%2C+T%3BDuh%2C+E%3BLeonard%2C+J%3BTheodore%2C+T+S%3BBuckler-White%2C+A%3BMartin%2C+M+A%3BRabson%2C+A+B&rft.aulast=Parrott&rft.aufirst=C&rft.date=1991-03-01&rft.volume=65&rft.issue=3&rft.spage=1414&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 - 1991-03-27 N1 - Date created - 1991-03-27 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cell. 1987 Feb 27;48(4):691-701 [3643816] J Virol. 1989 Jun;63(6):2504-9 [2470917] AIDS Res Hum Retroviruses. 1987 Spring;3(1):41-55 [3040054] Proc Natl Acad Sci U S A. 1987 Oct;84(19):6845-9 [3498942] EMBO J. 1986 Feb;5(2):387-97 [3011406] Cell. 1986 Sep 26;46(7):973-82 [3530501] Science. 1986 Nov 21;234(4779):988-92 [3490693] Proc Natl Acad Sci U S A. 1986 Dec;83(24):9734-8 [3025848] Mol Cell Biol. 1987 Aug;7(8):2735-44 [3670291] Science. 1987 Nov 6;238(4828):800-2 [3313729] J Virol. 1988 Jan;62(1):139-47 [3257102] J Virol. 1988 Jan;62(1):218-25 [3257103] Mol Cell Biol. 1987 Oct;7(10):3759-66 [3500398] Nature. 1987 Nov 26-Dec 2;330(6146):391-5 [2825023] Science. 1987 Dec 11;238(4833):1575-8 [2825351] EMBO J. 1987 Dec 20;6(13):4067-71 [3443102] Nature. 1988 May 5;333(6168):40-5 [2834649] Proc Natl Acad Sci U S A. 1988 Jul;85(13):4700-4 [3133660] Cell. 1988 Sep 23;54(7):943-53 [2843294] EMBO J. 1988 Jul;7(7):2117-30 [3138113] J Virol. 1988 Nov;62(11):4104-12 [2845125] Genes Dev. 1988 Sep;2(9):1055-62 [2847958] Proc Natl Acad Sci U S A. 1988 Dec;85(23):8825-9 [2848241] J Virol. 1989 Jan;63(1):328-37 [2783259] J Virol. 1989 Jun;63(6):2585-91 [2657100] Cell. 1989 Jul 14;58(1):1-4 [2665940] Cell. 1989 Aug 11;58(3):423-6 [2569361] J Virol. 1989 Sep;63(9):3595-600 [2547987] Proc Natl Acad Sci U S A. 1989 Aug;86(15):5974-8 [2762307] J Virol. 1989 Oct;63(10):4210-23 [2778872] J Virol. 1989 Nov;63(11):4919-24 [2795721] Cell. 1989 Oct 20;59(2):229-30 [2680105] Cell. 1989 Dec 1;59(5):827-36 [2512012] Genes Dev. 1990 Feb;4(2):233-42 [2338244] Cell. 1990 Aug 24;62(4):757-67 [2201451] New Biol. 1989 Nov;1(2):127-35 [2562218] J Mol Biol. 1967 Jun 14;26(2):365-9 [4291934] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] J Virol. 1983 Oct;48(1):218-28 [6310145] DNA. 1984 Dec;3(6):479-88 [6096101] Science. 1985 Feb 1;227(4686):538-40 [2981438] Proc Natl Acad Sci U S A. 1985 Jan;82(2):488-92 [3881765] Cell. 1985 Jul;41(3):813-23 [2988790] Proc Natl Acad Sci U S A. 1985 Jul;82(13):4539-43 [2989831] Science. 1985 Jul 5;229(4708):69-73 [2990040] Science. 1985 Jul 5;229(4708):74-7 [2990041] Science. 1986 May 9;232(4751):755-9 [3008338] Cell. 1986 May 9;45(3):461-70 [3009027] Proc Natl Acad Sci U S A. 1989 Apr;86(7):2331-5 [2494663] Proc Natl Acad Sci U S A. 1989 Apr;86(7):2365-8 [2784570] AIDS Res Hum Retroviruses. 1989 Apr;5(2):131-8 [2713164] Nature. 1987 Apr 16-22;326(6114):711-3 [3031512] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Introduction of new genetic markers on human chromosomes. AN - 80446660; 1995301 AB - The purpose of this study was to use DNA transfection and microcell chromosome transfer techniques to engineer a human chromosome containing multiple biochemical markers for which selectable growth conditions exist. The starting chromosome was a t(X;3)(3pter----3p12::Xq26----Xpter) chromosome from a reciprocal translocation in the normal human fibroblast cell line GM0439. This chromosome was transferred to a HPRT (hypoxanthine phosphoribosyltransferase)-deficient mouse A9 cell line by microcell fusion and selected under growth conditions (HAT medium) for the HPRT gene on the human t(X;3) chromosome. A resultant HAT-resistant cell line (A9(GM0439)-1) contained a single human t(X;3) chromosome. In order to introduce a second selectable genetic marker to the t(X;3) chromosome, A9(GM0439)-1 cells were transfected with pcDneo plasmid DNA. Colonies resistant to both G418 and HAT medium (G418r/HATr) were selected. To obtain A9 cells that contained a t(X;3) chromosome with an integrated neo gene, the microcell transfer step was repeated and doubly resistant cells were selected. G418r/HATr colonies arose at a frequently of 0.09 to 0.23 x 10(-6) per recipient cell. Of seven primary microcell hybrid clones, four yielded G418r/HATr clones at a detectable frequency (0.09 to 3.4 x 10(-6)) after a second round of microcell transfer. Doubly resistant cells were not observed after microcell chromosome transfers from three clones, presumably because the markers were on different chromosomes. The secondary G418r/HATr microcell hybrids contained at least one copy of the human t(X;3) chromosome and in situ hybridization with one of these clones confirmed the presence of a neo-tagged t(X;3) human chromosome. These results demonstrate that microcell chromosome transfer can be used to select chromosomes containing multiple markers. JF - Experimental cell research AU - Satoh, H AU - Barrett, J C AU - Oshimura, M AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 5 EP - 11 VL - 193 IS - 1 SN - 0014-4827, 0014-4827 KW - hprt KW - neo KW - Genetic Markers KW - 0 KW - Neomycin KW - 1404-04-2 KW - Hypoxanthine Phosphoribosyltransferase KW - EC 2.4.2.8 KW - Index Medicus KW - Drug Resistance -- genetics KW - Hypoxanthine Phosphoribosyltransferase -- genetics KW - Humans KW - Hybrid Cells KW - Neomycin -- pharmacology KW - Cell Line KW - Genetic Markers -- genetics KW - Genetic Techniques KW - Chromosome Mapping -- methods KW - Chromosomes, Human -- ultrastructure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80446660?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Introduction+of+new+genetic+markers+on+human+chromosomes.&rft.au=Satoh%2C+H%3BBarrett%2C+J+C%3BOshimura%2C+M&rft.aulast=Satoh&rft.aufirst=H&rft.date=1991-03-01&rft.volume=193&rft.issue=1&rft.spage=5&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 - 1991-03-27 N1 - Date created - 1991-03-27 N1 - Date revised - 2017-01-13 N1 - Gene symbol - hprt; neo N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Induction of the HTLV-I LTR by Jun occurs through the Tax-responsive 21-bp elements. AN - 80445155; 1899734 AB - The HTLV-I LTR is known to be induced by a variety of cellular signals. Tax protein is one potent viral trans-activator of LTR-directed transcription. We demonstrate here that Jun is another transcription factor that can strongly modulate the activity of this LTR. Using deletion and competition studies, the minimal portion of the LTR for Jun activation was found to coincide with the Tax-responsive 21-bp elements. In binding experiments, nuclear factors that bound to the HTLV-I 21-bp sequence were competed by an excess of AP-1 motif oligonucleotide. Although the Tax-responsive elements do not contain a strictly conserved AP-1 motif, these findings suggest that they function as AP-1 sites. We found, however, that in cells depleted for AP-1 activity (F9 teratocarcinoma), Tax activation of the HTLV-I LTR was maintained. Thus while Jun/AP-1 may be involved in the basal expression of the HTLV-I LTR, it may not be essential for Tax-mediated activation. JF - Virology AU - Jeang, K T AU - Chiu, R AU - Santos, E AU - Kim, S J AD - Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/03// PY - 1991 DA - March 1991 SP - 218 EP - 227 VL - 181 IS - 1 SN - 0042-6822, 0042-6822 KW - DNA-Binding Proteins KW - 0 KW - Gene Products, tax KW - Proto-Oncogene Proteins c-jun KW - Transcription Factors KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Index Medicus KW - AIDS/HIV KW - HeLa Cells -- metabolism KW - Animals KW - Base Sequence KW - Gene Expression Regulation, Viral KW - Kinetics KW - Humans KW - Restriction Mapping KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Protein-Tyrosine Kinases -- metabolism KW - Plasmids KW - Cell Line KW - Human T-lymphotropic virus 1 -- genetics KW - Gene Products, tax -- metabolism KW - Transcription Factors -- metabolism KW - Transcription, Genetic KW - Repetitive Sequences, Nucleic Acid KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80445155?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Virology&rft.atitle=Induction+of+the+HTLV-I+LTR+by+Jun+occurs+through+the+Tax-responsive+21-bp+elements.&rft.au=Jeang%2C+K+T%3BChiu%2C+R%3BSantos%2C+E%3BKim%2C+S+J&rft.aulast=Jeang&rft.aufirst=K&rft.date=1991-03-01&rft.volume=181&rft.issue=1&rft.spage=218&rft.isbn=&rft.btitle=&rft.title=Virology&rft.issn=00426822&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-03-15 N1 - Date created - 1991-03-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Relation of alcohol intake to left ventricular mass: The Framingham Study. AN - 80441901; 1825213 AB - Alcohol has direct toxic effects on the myocardium and is associated with elevated blood pressure, but its relation to left ventricular mass independent of blood pressure level has not been assessed. Reported alcohol intake and left ventricular mass measured by echocardiography were evaluated in 1,980 men and 2,511 women 17 to 90 years of age and free of cardiovascular disease in the Framingham offspring and cohort study. The relation of reported alcohol intake to left ventricular mass was assessed by gender-specific multivariate regression analysis adjusting for age, height, body mass index, systolic blood pressure, history of hypertension and cigarette smoking. Alcohol intake was positively associated with left ventricular mass in men (p less than 0.01) but not in women (p = 0.64). When stratified by beverage type, beer and wine in both men and women and liquor in men were positively related to left ventricular mass. The lack of association of total alcohol intake to left ventricular mass in women appeared to be due to a negative association (p less than 0.01) with liquor. The strongest positive associations were with wine in men (p less than 0.001) and beer in women (p less than 0.05). Alcohol use is independently associated with left ventricular mass; this association may vary by beverage type. In persons with unexplained left ventricular hypertrophy, excessive alcohol intake should be considered. JF - Journal of the American College of Cardiology AU - Manolio, T A AU - Levy, D AU - Garrison, R J AU - Castelli, W P AU - Kannel, W B AD - Division of Epidemiology and Clinical Applications, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/03/01/ PY - 1991 DA - 1991 Mar 01 SP - 717 EP - 721 VL - 17 IS - 3 SN - 0735-1097, 0735-1097 KW - Abridged Index Medicus KW - Index Medicus KW - Stroke Volume -- physiology KW - Aged, 80 and over KW - Humans KW - Echocardiography KW - Adult KW - Heart -- drug effects KW - Aging -- pathology KW - Aged KW - Middle Aged KW - Adolescent KW - Male KW - Female KW - Alcohol Drinking -- adverse effects KW - Cardiomegaly -- pathology KW - Cardiomegaly -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80441901?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+American+College+of+Cardiology&rft.atitle=Relation+of+alcohol+intake+to+left+ventricular+mass%3A+The+Framingham+Study.&rft.au=Manolio%2C+T+A%3BLevy%2C+D%3BGarrison%2C+R+J%3BCastelli%2C+W+P%3BKannel%2C+W+B&rft.aulast=Manolio&rft.aufirst=T&rft.date=1991-03-01&rft.volume=17&rft.issue=3&rft.spage=717&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+American+College+of+Cardiology&rft.issn=07351097&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-03-21 N1 - Date created - 1991-03-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - [A case of methemoglobinemia due to 4-nitrobenzonitrile exposure]. TT - Un caso di metaemoglobinemia da esposizione a 4-nitrobenzonitrile. AN - 72609201; 1770871 AB - The paper describes a singular case of acute intoxication by 4-nitrobenzonitrile, a rare intermediate compound produced by pharmaceutical synthesis. The patients subsequently showed an increase in triglycerides and fatty alterations of the liver. JF - La Medicina del lavoro AU - Monechi, G AU - Fabrizi de Biani, G AU - Colasanti, L AD - Servizio di Prevenzione Igiene e Sicurezza nei Luoghi di Lavoro U.S.L. 20/B, Valdarno, Firenze. PY - 1991 SP - 137 EP - 141 VL - 82 IS - 2 SN - 0025-7818, 0025-7818 KW - Nitriles KW - 0 KW - Nitrobenzenes KW - 4-nitrobenzonitrile KW - 619-72-7 KW - benzonitrile KW - 9V9APP5H5S KW - Index Medicus KW - Drug Industry KW - Humans KW - Emergencies KW - Poisoning -- diagnosis KW - Male KW - Italy KW - Occupational Diseases -- diagnosis KW - Methemoglobinemia -- chemically induced KW - Methemoglobinemia -- diagnosis KW - Occupational Diseases -- chemically induced KW - Nitrobenzenes -- poisoning KW - Nitriles -- poisoning UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72609201?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=La+Medicina+del+lavoro&rft.atitle=%5BA+case+of+methemoglobinemia+due+to+4-nitrobenzonitrile+exposure%5D.&rft.au=Monechi%2C+G%3BFabrizi+de+Biani%2C+G%3BColasanti%2C+L&rft.aulast=Monechi&rft.aufirst=G&rft.date=1991-03-01&rft.volume=82&rft.issue=2&rft.spage=137&rft.isbn=&rft.btitle=&rft.title=La+Medicina+del+lavoro&rft.issn=00257818&rft_id=info:doi/ LA - Italian DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-21 N1 - Date created - 1992-02-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Carcinogenesis in rats by substituted dialkylnitrosamines given by gavage. AN - 72608418; 1768792 AB - A number of nitrosamines that have been studied by administration to rats as solutions in drinking water have been examined by gavage administration of similar doses, for assessment of the role of pharmacokinetics in organ-specific carcinogenesis. Methylnitrosoethylamine was more effective as a liver carcinogen by gavage than in drinking water and gave rise to tumors of the lung and nasal mucosa by the former route, but not the latter. By gavage, methylnitroso-2-oxopropylamine and methylnitroso-2-hydroxypropylamine induced mainly tumors of the esophagus, as they did when given to rats in drinking water, but the potency was greater by gavage. At a higher dose rate (85 micromoles per week) methylnitrosohydroxypropylamine induced a high incidence of mesenchymal tumors of the kidney and lung tumors, in addition to esophageal tumors, but methylnitrosooxopropylamine did not. The tobacco-specific carcinogen NNK induced tumors of the liver, and to a lesser extent, of the lung and nasal mucosa when given by gavage to rats, as it did by other routes of administration. The similarly basic nitrosamine methylnitroso-N, N-dimethylaminoethylamine was equally potent, whether administered by gavage or in drinking water to rats, and gave rise only to tumors of the esophagus. The cyclic nitrosamine nitrosomorpholine was equally effective by gavage and in drinking water, but induced in rats more esophageal tumors by gavage in addition to a high incidence of liver tumors. Its 2-hydroxy derivative, a postulated metabolic intermediate of nitrosodiethanolamine, was a very much weaker carcinogen than either the latter or nitrosomorpholine, and induced low incidences of liver and lung tumors toward the end of the lifespan of the rats. JF - In vivo (Athens, Greece) AU - Lijinsky, W AU - Saavedra, J E AU - Kovatch, R M AD - Laboratory of Chemical and Physical Carcinogenesis, NCI-Frederick Cancer Research and Development Center, MD 21702. PY - 1991 SP - 85 EP - 89 VL - 5 IS - 2 SN - 0258-851X, 0258-851X KW - Nitrosamines KW - 0 KW - Index Medicus KW - Rats KW - Esophageal Neoplasms -- chemically induced KW - Administration, Oral KW - Thyroid Neoplasms -- chemically induced KW - Animals KW - Rats, Inbred F344 KW - Kidney Neoplasms -- chemically induced KW - Nose Neoplasms -- chemically induced KW - Lung Neoplasms -- chemically induced KW - Male KW - Female KW - Structure-Activity Relationship KW - Nitrosamines -- administration & dosage KW - Nitrosamines -- toxicity KW - Neoplasms, Experimental -- chemically induced KW - Neoplasms, Experimental -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72608418?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=unknown&rft.jtitle=Chronicle+-+Herald&rft.atitle=Stag+%26amp%3BDoe+en+route+to+altar%3B+Comedy+at+Neptune+Theatre+inspired+by+rural+ritual+of+party%2Ffundraiser+for+a+couple&rft.au=&rft.aulast=&rft.aufirst=&rft.date=2016-01-21&rft.volume=&rft.issue=&rft.spage=D1&rft.isbn=&rft.btitle=&rft.title=Chronicle+-+Herald&rft.issn=08281807&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-25 N1 - Date created - 1992-02-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The human costs of cancer and the response of the national cancer program AN - 1622611812; 20885875 AB - The three foundations of the National Cancer Program are basic research, clinical trials (in prevention and treatment), and cancer centers. These foundations have supported a great deal of progress against cancer over the past 20 years. Nevertheless, a number of challenges remain, and continued progress will depend on the speed with which research advances can be translated into practical realities. Poverty is a risk factor for cancer incidence and mortality. Thus, a lack of access to the technologies generated by the National Cancer Program can be a force for bringing about differential burdens of cancer in underserved populations. JF - Cancer AU - Broder, Samuel AD - National Cancer Institute, Bethesda, Maryland. Y1 - 1991/03// PY - 1991 DA - Mar 1991 SP - 1716 EP - 1717 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 67 IS - S6 SN - 0008-543X, 0008-543X KW - Risk Abstracts KW - Health risks KW - Mortality KW - Prevention KW - Risk factors KW - Poverty KW - Clinical trials KW - Cancer KW - Technology KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1622611812?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=The+human+costs+of+cancer+and+the+response+of+the+national+cancer+program&rft.au=Broder%2C+Samuel&rft.aulast=Broder&rft.aufirst=Samuel&rft.date=1991-03-01&rft.volume=67&rft.issue=S6&rft.spage=1716&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/10.1002%2Fcncr.2820671802 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-01 N1 - Last updated - 2015-08-05 N1 - SubjectsTermNotLitGenreText - Mortality; Health risks; Prevention; Poverty; Risk factors; Clinical trials; Cancer; Technology DO - http://dx.doi.org/10.1002/cncr.2820671802 ER - TY - JOUR T1 - Chronic exposure of C6 glioma cells to desipramine desensitizes beta-adrenoceptors, but increases KL/KH ratio. AN - 80659860; 1648502 AB - Incubation of rat glioma C6 cells with 10 microM desipramine for five days in vitro resulted in a 31% reduction of beta-adrenoceptors and a 38% reduction in isoproterenol-stimulated cyclic AMP accumulation. In contrast, forskolin or cholera toxin-stimulated cyclic AMP was unaffected by desipramine. Surprisingly, the beta-adrenoceptor desensitization was accompanied by an increase in the ratio of dissociation constants (KL/KH) for the low and high affinity states of the beta-adrenoceptor respectively and supports the concept of a complex interaction between the receptor and Gs protein. JF - European journal of pharmacology AU - Manji, H K AU - Chen, G A AU - Bitran, J A AU - Gusovsky, F AU - Potter, W Z AD - Section on Clinical Pharmacology, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1991/02/25/ PY - 1991 DA - 1991 Feb 25 SP - 159 EP - 162 VL - 206 IS - 2 SN - 0014-2999, 0014-2999 KW - Receptors, Adrenergic, beta KW - 0 KW - Colforsin KW - 1F7A44V6OU KW - Cholera Toxin KW - 9012-63-9 KW - Cyclic AMP KW - E0399OZS9N KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Isoproterenol KW - L628TT009W KW - Desipramine KW - TG537D343B KW - Index Medicus KW - Animals KW - Colforsin -- pharmacology KW - Tumor Cells, Cultured -- metabolism KW - Tumor Cells, Cultured -- drug effects KW - Kinetics KW - GTP-Binding Proteins -- metabolism KW - Cyclic AMP -- metabolism KW - Cholera Toxin -- pharmacology KW - Isoproterenol -- pharmacology KW - Receptors, Adrenergic, beta -- metabolism KW - Desipramine -- pharmacology KW - Receptors, Adrenergic, beta -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80659860?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Chronic+exposure+of+C6+glioma+cells+to+desipramine+desensitizes+beta-adrenoceptors%2C+but+increases+KL%2FKH+ratio.&rft.au=Manji%2C+H+K%3BChen%2C+G+A%3BBitran%2C+J+A%3BGusovsky%2C+F%3BPotter%2C+W+Z&rft.aulast=Manji&rft.aufirst=H&rft.date=1991-02-25&rft.volume=206&rft.issue=2&rft.spage=159&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 - 1991-08-09 N1 - Date created - 1991-08-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Selenium induces changes in the selenocysteine tRNA[Ser]Sec population in mammalian cells. AN - 80519048; 2017375 AB - Two isoacceptors of selenocysteine tRNA[Ser]Sec are present in higher vertebrates which are responsible for donating selenocysteine to protein. One such selenocysteine containing protein, glutathione peroxidase, requires selenium for its translation and transcription. Since tRNA[Ser]Sec is a critical component of the glutathione peroxidase translational machinery, the levels and distributions of its isoacceptors were examined from both human and rat cells grown in chemically defined media with and without selenium. Not only did the level of the selenocysteine tRNA[Ser]Sec population increase approximately 20% in cells grown in the presence of selenium, but the distributions of the two isoacceptors also changed relative to each other. JF - Nucleic acids research AU - Hatfield, D AU - Lee, B J AU - Hampton, L AU - Diamond, A M AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/02/25/ PY - 1991 DA - 1991 Feb 25 SP - 939 EP - 943 VL - 19 IS - 4 SN - 0305-1048, 0305-1048 KW - Culture Media KW - 0 KW - RNA, Transfer, Amino Acid-Specific KW - RNA, Transfer, Ser KW - tRNA, selenocysteine- KW - Glutathione Peroxidase KW - EC 1.11.1.9 KW - Selenium KW - H6241UJ22B KW - Index Medicus KW - Rats KW - Protein Biosynthesis KW - Animals KW - RNA, Transfer, Ser -- analysis KW - Blotting, Northern KW - Tumor Cells, Cultured KW - Humans KW - Electrophoresis, Agar Gel KW - Chromatography, Liquid KW - Glutathione Peroxidase -- genetics KW - Selenium -- pharmacology KW - RNA, Transfer, Amino Acid-Specific -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80519048?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+acids+research&rft.atitle=Selenium+induces+changes+in+the+selenocysteine+tRNA%5BSer%5DSec+population+in+mammalian+cells.&rft.au=Hatfield%2C+D%3BLee%2C+B+J%3BHampton%2C+L%3BDiamond%2C+A+M&rft.aulast=Hatfield&rft.aufirst=D&rft.date=1991-02-25&rft.volume=19&rft.issue=4&rft.spage=939&rft.isbn=&rft.btitle=&rft.title=Nucleic+acids+research&rft.issn=03051048&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-05-21 N1 - Date created - 1991-05-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Anal Biochem. 1971 Dec;44(2):486-95 [4943341] J Biol Chem. 1989 Jun 15;264(17):9720-3 [2524495] Cell. 1981 Aug;25(2):497-506 [6912798] Proc Natl Acad Sci U S A. 1982 Oct;79(20):6215-9 [6815648] FEBS Lett. 1984 Apr 24;169(2):319-22 [6325247] J Biol Chem. 1985 Feb 25;260(4):2501-8 [3156131] J Clin Invest. 1986 Apr;77(4):1402-4 [3457020] EMBO J. 1986 Jun;5(6):1221-7 [3015592] Anal Biochem. 1987 Apr;162(1):156-9 [2440339] J Biol Chem. 1989 Jun 15;264(17):9724-7 [2498338] Blood. 1989 Nov 15;74(7):2535-41 [2804377] Virology. 1989 Dec;173(2):736-42 [2556852] Proc Natl Acad Sci U S A. 1990 Jan;87(2):543-7 [2405383] Mol Cell Biol. 1990 May;10(5):1940-9 [2139169] Nucleic Acids Res. 1990 Nov 25;18(22):6727 [2251154] Nucleic Acids Res. 1988 Jun 24;16(12):5557-68 [2838821] Protein Eng. 1988 Sep;2(3):239-46 [2976939] Biochim Biophys Acta. 1979 Oct 25;564(3):414-23 [259017] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Lymphocyte activation and phospholipid pathways. 31P magnetic resonance studies. AN - 80448147; 1995623 AB - 31P NMR spectra of perfused lymphocytes, embedded in alginate capsules and activated by interleukin-2, were remarkably different from those of control lymphocytes. The main differences were the appearance and gradual increase in phosphodiester signals, glycerophosphocholine and glycerophosphoethanolamine. These metabolic changes also occurred following perfusion with phorbol ester and after incubation with phytohemagglutinin (PHA) and were not dependent on a special growth medium. Nifedipine, a calcium channel blocking drug, inhibited the effects of phytohemagglutinin, but not of interleukin-2. There were no NMR spectral differences between peripheral lymphocytes, stimulated for 3 weeks, and tumor-infiltrating lymphocytes. Thus, sustained accelerated turnover of phosphatidylcholine and phosphatidylethanolamine is an inherent feature of the activation process. 31P NMR spectra of lymphocytes are characterized by a low signal of phosphocholine. Perfusion studies with high concentrations of choline and the use of dapsone, an inhibitor of cytidylyltransferase, indicated that choline kinase plays a key role in regulating phosphaditylcholine synthesis in human lymphocytes. JF - The Journal of biological chemistry AU - Kaplan, O AU - Cohen, J S AD - Medicine Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/02/25/ PY - 1991 DA - 1991 Feb 25 SP - 3688 EP - 3694 VL - 266 IS - 6 SN - 0021-9258, 0021-9258 KW - Interleukin-2 KW - 0 KW - Phospholipids KW - Phosphorus Isotopes KW - Dapsone KW - 8W5C518302 KW - Choline KW - N91BDP6H0X KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Choline -- pharmacology KW - Interleukin-2 -- pharmacology KW - Humans KW - Dapsone -- pharmacology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Lymphocytes -- drug effects KW - Magnetic Resonance Spectroscopy KW - Lymphocyte Activation KW - Phospholipids -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80448147?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Lymphocyte+activation+and+phospholipid+pathways.+31P+magnetic+resonance+studies.&rft.au=Kaplan%2C+O%3BCohen%2C+J+S&rft.aulast=Kaplan&rft.aufirst=O&rft.date=1991-02-25&rft.volume=266&rft.issue=6&rft.spage=3688&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 - 1991-03-27 N1 - Date created - 1991-03-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alteration of high and low spin equilibrium by a single mutation of amino acid 209 in mouse cytochromes P450. AN - 80446808; 1995602 AB - The identities of the amino acid at position 209 are most critical in determining specific coumarin 7- and steroid 15 alpha-hydroxylase activity in P450coh and P450(15)alpha, respectively. This system, therefore, provides us with an excellent model to study the structural basis for P450 specificity as a monooxygenase. We expressed in Saccharomyces cerevisiae a series of the mutated P450s in which residue 209 was substituted with the various amino acids and characterized the spectral property and hydroxylase activity of these mutated P450s. The positioning of a hydrophobic residue including Phe, Leu, and Val at position 209 resulted in shifting the P450 to the high-spin state, while a charged amino acid such as Lys or Asp produced the low-spin form. Moreover, a P450 with Asn or Gly in this position exhibited spectra indicating a mixture of the high- and low-spin forms. This spin alteration, depending upon the hydrophobicity and size of residue at position 209, indicates that this position is likely to reside close to the sixth axial ligand on the distal surface of the heme in these P450s. This proximity of residue 209 to the ligand may explain the critical role of this residue in determining the hydroxylase specificity and activity of these P450s. JF - The Journal of biological chemistry AU - Iwasaki, M AU - Juvonen, R AU - Lindberg, R AU - Negishi, M AD - Pharmacogenetics Section, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709. Y1 - 1991/02/25/ PY - 1991 DA - 1991 Feb 25 SP - 3380 EP - 3382 VL - 266 IS - 6 SN - 0021-9258, 0021-9258 KW - Amino Acids KW - 0 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Mixed Function Oxygenases KW - EC 1.- KW - Steroid Hydroxylases KW - EC 1.14.- KW - Aryl Hydrocarbon Hydroxylases KW - EC 1.14.14.1 KW - Cytochrome P-450 CYP2A6 KW - steroid 15-alpha-hydroxylase KW - Index Medicus KW - Saccharomyces cerevisiae -- genetics KW - Mutagenesis, Site-Directed KW - Gene Expression Regulation, Fungal KW - Animals KW - Genes, Fungal KW - Spectrophotometry, Ultraviolet KW - Mice KW - Mutation KW - Catalysis KW - Cytochrome P-450 Enzyme System -- genetics KW - Amino Acids -- genetics KW - Steroid Hydroxylases -- genetics KW - Mixed Function Oxygenases -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80446808?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Alteration+of+high+and+low+spin+equilibrium+by+a+single+mutation+of+amino+acid+209+in+mouse+cytochromes+P450.&rft.au=Iwasaki%2C+M%3BJuvonen%2C+R%3BLindberg%2C+R%3BNegishi%2C+M&rft.aulast=Iwasaki&rft.aufirst=M&rft.date=1991-02-25&rft.volume=266&rft.issue=6&rft.spage=3380&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 - 1991-03-27 N1 - Date created - 1991-03-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Genetic factors influence changes in sensitivity to the convulsant properties of cocaine following chronic treatment. AN - 80629355; 2054648 AB - Repeated administration of doses of cocaine below the threshold for seizure induction results in the development of an increased susceptibility to cocaine-induced seizures (cocaine-kindling). Genetic differences in susceptibility to cocaine-kindled seizures were evaluated in 4 inbred mouse strains and compared with susceptibility to seizures induced by acute administration of cocaine. The acute administration of cocaine produced convulsant activity in mice from all 4 genotypes, however, there were significant differences in the dose of cocaine required to induce seizures. C57 mice were highly susceptible and SJL mice highly resistant to convulsions induced by acute administration of cocaine, while BALB and DBA mice showed an intermediate degree of seizure susceptibility. The repeated administration of subconvulsant doses of cocaine resulted in rapid sensitization to cocaine-induced seizures. The 4 strains differed in the rate at which sensitization to cocaine-induced seizures developed, with the SJL strain being most sensitive and the C57 strain the least sensitive to the cocaine-kindling process. The susceptibility of the 4 strains to cocaine kindling was virtually opposite to their susceptibility to seizures induced by the acute administration of cocaine, suggesting that different mechanisms may be involved in the control of acute and kindled seizures did not persist upon further exposure to cocaine. Following a period of increased sensitivity to cocaine-induced seizures, tolerance to the convulsant properties of cocaine developed among C57, BALB and DBA mice. Only among the SJL mice did the development of a kindled state persist upon repeated exposure to cocaine. These differences emphasize the potential importance of inheritance in determining the effects of cocaine and suggest novel approaches to understanding the the mechanisms underlying the effects of cocaine. JF - Brain research AU - Marley, R J AU - Witkin, J M AU - Goldberg, S R AD - National Institute on Drug Abuse-Addiction Research Center, Baltimore, MD 21224. Y1 - 1991/02/22/ PY - 1991 DA - 1991 Feb 22 SP - 1 EP - 7 VL - 542 IS - 1 SN - 0006-8993, 0006-8993 KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Animals KW - Kindling, Neurologic KW - Drug Resistance KW - Mice KW - Genetic Predisposition to Disease KW - Mice, Inbred Strains -- genetics KW - Time Factors KW - Male KW - Seizures -- chemically induced KW - Seizures -- genetics KW - Cocaine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80629355?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=unknown&rft.jtitle=The+Washington+Post+%281974-Current+file%29&rft.atitle=Real+Estate+Transaction+10+--+No+Title&rft.au=&rft.aulast=&rft.aufirst=&rft.date=2000-04-13&rft.volume=&rft.issue=&rft.spage=29&rft.isbn=&rft.btitle=&rft.title=The+Washington+Post+%281974-Current+file%29&rft.issn=01908286&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-01 N1 - Date created - 1991-08-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Synergistic inhibition of phorbol ester-induced transformation of JB6 cells by transforming growth factor-beta and retinoic acid. AN - 80456253; 1847657 AB - Transforming growth factor-beta (TGF-beta) plays a complex role as a regulator of proliferation and differentiation of many cell types, including cells of epithelial origin. In this study, we examined whether TGF-beta, alone or in combination with retinoic acid, was able to inhibit the transformation of the murine epidermal cell line JB6. When treated with phorbol myristate acetate (PMA) and other tumor promoters, the nontumorigenic and anchorage-dependent JB6 cells acquired a tumor phenotype, as shown by the acquisition of tumorigenicity and anchorage independence. We found that TGB-beta inhibited the PMA-induced transformation of a subclone of JB6 cells. The effect of TGF-beta was due to an anti-transformation promoting activity, rather than to generalized growth inhibition, since TGF-beta neither inhibited the growth of monolayer cultures of JB6 cells, nor affected the colony-forming efficiency in agar of the JB6-derived permanently transformed RT101 cell line. TGF-beta was synergistic with retinoic acid, a known anti-tumor promoter, in inhibiting the PMA-induced transformation of JB6 cells. Examination of TGF-beta receptor expression on JB6 cells, by both binding and affinity labeling, showed that treatment with PMA significantly decreased TGF-beta receptor expression while retinoic acid counteracted this effect of PMA, thus suggesting that the synergy between retinoic acid and TGF-beta may be due, at least in part, to modulation of TGF-beta receptor expression. TGF-beta, therefore, appears to function as an incomplete antipromoter whose action can be permitted and/or complemented by retinoic acid. Our data demonstrating that TGF-beta has anti-transformation promoting activity suggest that TGF-beta plays a role in maintaining homeostasis of epithelial cells, not only by regulating cell proliferation and differentiation, but also by counteracting events that lead to malignant transformation. JF - Cancer research AU - De Benedetti, F AU - Falk, L AU - Ruscetti, F W AU - Colburn, N H AU - Faltynek, C R AU - Oppenheim, J J AD - Laboratory of Molecular Immunoregulation, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1991/02/15/ PY - 1991 DA - 1991 Feb 15 SP - 1158 EP - 1164 VL - 51 IS - 4 SN - 0008-5472, 0008-5472 KW - Receptors, Cell Surface KW - 0 KW - Receptors, Transforming Growth Factor beta KW - Transforming Growth Factor beta KW - Tretinoin KW - 5688UTC01R KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Dose-Response Relationship, Drug KW - Cell Division -- drug effects KW - Mice KW - Mice, Inbred BALB C KW - Drug Synergism KW - Colony-Forming Units Assay KW - Receptors, Cell Surface -- biosynthesis KW - Cell Line KW - Receptors, Cell Surface -- drug effects KW - Tretinoin -- pharmacology KW - Transforming Growth Factor beta -- pharmacology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Cell Transformation, Neoplastic -- drug effects KW - Transforming Growth Factor beta -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80456253?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Synergistic+inhibition+of+phorbol+ester-induced+transformation+of+JB6+cells+by+transforming+growth+factor-beta+and+retinoic+acid.&rft.au=De+Benedetti%2C+F%3BFalk%2C+L%3BRuscetti%2C+F+W%3BColburn%2C+N+H%3BFaltynek%2C+C+R%3BOppenheim%2C+J+J&rft.aulast=De+Benedetti&rft.aufirst=F&rft.date=1991-02-15&rft.volume=51&rft.issue=4&rft.spage=1158&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 - 1991-04-02 N1 - Date created - 1991-04-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Activation of protooncogenes in spontaneously occurring non-liver tumors from C57BL/6 x C3H F1 mice. AN - 80456208; 1997158 AB - The C57BL/6 x C3H F1 (hereafter called B6C3F1) mouse is an important animal model for long-term carcinogenesis studies. Maintained under normal laboratory conditions, these mice develop various types of spontaneous tumors during their lifetime. Activated Ha-ras genes have been detected in 66% of spontaneous hepatocellular tumors in the B6C3F1 mouse [Reynolds et al., Science (Washington DC), 237:1309, 1988]. In this study 49 spontaneous non-liver tumors were investigated for oncogene activation by DNA transfection techniques. Of the 49 tumor DNAs analyzed, only 5 yielded multiple foci in the NIH 3T3 focus assay: 2 of 10 pulmonary adenocarcinomas; 0 of 25 lymphomas; 2 of 2 Harderian gland adenomas; 0 of 1 adenocarcinoma of the small intestine; 1 of 6 malignant skin tumors; 0 of 4 hemangiosarcomas; and 0 of 1 lung metastasis of a hepatocellular carcinoma. DNA from six lymphomas which were negative in the NIH 3T3 focus assay were further analyzed for transforming genes by the nude mouse tumorigenicity assay. One of the five lymphomas tested positive with this assay. Southern blot analysis identified five activated ras genes: H-ras in two Harderian gland adenomas; K-ras in one pulmonary adenocarcinoma and in one s.c. adenocarcinoma; and N-ras in one lymphoma. The mutations involved were CG to AT and AT to TA in codon 61 of the Ha-ras genes, GC to AT or TA in codon 12 of the K-ras genes, and a GC to AT mutation in codon 12 of the N-ras gene. Transformant DNA from a pulmonary adenocarcinoma which yielded multiple foci in the transfection assay did not hybridize to DNA probes specific for the K-, H-, and N-ras, raf, neu, and met genes. Thirteen additional tumor DNAs yielded a single focus in the NIH 3T3 transfection assay. The transformant DNAs retransmitted in a second cycle transfection assay. Rearranged and/or amplified raf genes were detected in six of the transformant DNAs. At present we do not know whether these activated raf genes were present in the original tumor DNA. The other seven transformant DNAs did not hybridize with any of the above mentioned specific DNA probes utilized in Southern blot analysis. Unlike liver tumors, the activation of ras protooncogenes is not a frequent event in the development of spontaneous non-liver tumors of the B6C3F1 mouse. The results from this study should aid in understanding the neoplastic development associated with exposure to chemical carcinogens in the B6C3F1 mouse. JF - Cancer research AU - Candrian, U AU - You, M AU - Goodrow, T AU - Maronpot, R R AU - Reynolds, S H AU - Anderson, M W AD - Laboratory of Molecular Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/02/15/ PY - 1991 DA - 1991 Feb 15 SP - 1148 EP - 1153 VL - 51 IS - 4 SN - 0008-5472, 0008-5472 KW - H-ras KW - K-ras KW - N-ras KW - met KW - neu KW - raf KW - Index Medicus KW - Animals KW - Adenocarcinoma -- genetics KW - Mice KW - Nucleic Acid Hybridization KW - Skin Neoplasms -- genetics KW - Polymerase Chain Reaction KW - Base Sequence KW - Transfection KW - Blotting, Southern KW - Lymphoma -- genetics KW - Hemangiosarcoma -- genetics KW - Molecular Sequence Data KW - Lung Neoplasms -- genetics KW - Intestinal Neoplasms -- genetics KW - Tumor Stem Cell Assay KW - Mutation KW - Cell Transformation, Neoplastic KW - Liver Neoplasms -- genetics KW - Gene Expression Regulation, Neoplastic KW - Neoplasms, Experimental -- genetics KW - Proto-Oncogenes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80456208?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Activation+of+protooncogenes+in+spontaneously+occurring+non-liver+tumors+from+C57BL%2F6+x+C3H+F1+mice.&rft.au=Candrian%2C+U%3BYou%2C+M%3BGoodrow%2C+T%3BMaronpot%2C+R+R%3BReynolds%2C+S+H%3BAnderson%2C+M+W&rft.aulast=Candrian&rft.aufirst=U&rft.date=1991-02-15&rft.volume=51&rft.issue=4&rft.spage=1148&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 - 1991-04-02 N1 - Date created - 1991-04-02 N1 - Date revised - 2017-01-13 N1 - Gene symbol - H-ras; K-ras; N-ras; met; neu; raf N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inducer-dependent conditional-lethal mutant animal viruses. AN - 80454410; 1899929 AB - Regulatory elements of the Escherichia coli lac operon were used to construct an inducer-dependent conditional-lethal mutant animal virus. The gene encoding the repressor protein of the lac operon was integrated into the vaccinia virus genome so that it was expressed constitutively, and the lac operator was inserted next to the promoter of a gene that encodes an 11-kDa virion-associated protein of unknown function. The addition of inducer to the cell culture medium provided permissive conditions for isolation of a conditional-lethal mutant virus. Under nonpermissive conditions, the isolated virus did not form plaques, and the yield was decreased by at least 1000-fold under one-step growth conditions. Transcription of the operator-controlled gene was inducer-dependent and necessary for synthesis of the 11-kDa protein. Application of this mutagenesis strategy to other viruses is discussed. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Zhang, Y F AU - Moss, B AD - Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/02/15/ PY - 1991 DA - 1991 Feb 15 SP - 1511 EP - 1515 VL - 88 IS - 4 SN - 0027-8424, 0027-8424 KW - Oligonucleotide Probes KW - 0 KW - Isopropyl Thiogalactoside KW - 367-93-1 KW - Index Medicus KW - Virus Replication KW - Animals KW - Viral Plaque Assay KW - Open Reading Frames KW - Escherichia coli -- genetics KW - Transcription, Genetic KW - Plasmids KW - Polymerase Chain Reaction KW - Base Sequence KW - Genetic Vectors KW - Restriction Mapping KW - Recombination, Genetic KW - Molecular Sequence Data KW - Lac Operon KW - Cell Line KW - Vaccinia virus -- genetics KW - Vaccinia virus -- physiology KW - Viruses -- genetics KW - Vaccinia virus -- drug effects KW - Isopropyl Thiogalactoside -- pharmacology KW - Mutation KW - Genes, Lethal UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80454410?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Inducer-dependent+conditional-lethal+mutant+animal+viruses.&rft.au=Zhang%2C+Y+F%3BMoss%2C+B&rft.aulast=Zhang&rft.aufirst=Y&rft.date=1991-02-15&rft.volume=88&rft.issue=4&rft.spage=1511&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 - 1991-03-27 N1 - Date created - 1991-03-27 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Mol Cell Biol. 1990 Jul;10(7):3343-56 [2162473] J Virol. 1990 Jun;64(6):3108-11 [2159565] J Virol. 1984 Mar;49(3):857-64 [6321770] Proc Natl Acad Sci U S A. 1983 Nov;80(22):6785-9 [6316325] J Virol. 1984 Feb;49(2):371-8 [6319738] Cell. 1982 Nov;31(1):137-46 [6760983] Proc Natl Acad Sci U S A. 1981 Apr;78(4):2072-6 [7017722] J Virol. 1982 Nov;44(2):647-57 [6890583] Proc Natl Acad Sci U S A. 1979 Aug;76(8):3665-9 [291030] Proc Natl Acad Sci U S A. 1970 Sep;67(1):394-9 [4318787] Proc Natl Acad Sci U S A. 1962 Jul 15;48:1114-21 [13867417] Nucleic Acids Res. 1990 Sep 25;18(18):5347-51 [2216706] Proc Natl Acad Sci U S A. 1989 Jul;86(14):5400-4 [2664783] Cell. 1987 Jun 5;49(5):603-12 [3034429] Cell. 1988 Mar 11;52(5):713-22 [2830990] Anal Biochem. 1986 May 15;155(1):83-8 [3454661] J Gen Virol. 1987 Dec;68 ( Pt 12):3033-44 [2826648] Cell. 1987 Feb 27;48(4):555-66 [3028641] Cell. 1987 Jul 31;50(3):379-89 [3038332] J Virol. 1985 Nov;56(2):558-70 [2997476] J Virol. 1988 Jun;62(6):1849-54 [3130492] Proc Natl Acad Sci U S A. 1989 Apr;86(8):2549-53 [2649884] Virology. 1990 Jul;177(1):239-50 [2191497] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Developmental changes in the expression of high mobility group chromosomal proteins. AN - 80441013; 1993650 AB - The high mobility group (HMG) chromosomal proteins may modulate the structure of distinct regions in chromatin, thereby affecting processes such as development and differentiation. Here we report that the levels of the HMG chromosomal proteins and their mRNAs change significantly during erythropoiesis. Erythroid cells from 5-day chicken embryos contain 2.5-10 times more HMG mRNAs than cells from 14-day embryos, whereas circulating cells from adult animals are devoid of HMG and most other mRNAs. Nuclear run-off experiments and Northern analysis of RNA from various developmental stages and from Percoll-fractionated cells indicate that the genes are transcribed in early cells of either the primitive or definitive erythroid lineage. The rate of synthesis of the various HMGs changes during erythropoiesis; in erythroid cells from 7-day embryos the ratio of HMG-14b or HMG-17 to HMG-14a is, respectively, 8 and 10 times lower than in 9-day erythroids. HMG-14a, the major chicken HMG-14 species, is synthesized mainly in primitive cells, while HMG-14b is preferentially synthesized in definitive cells. Thus, the change from primitive to definitive erythroid lineage during embryogenesis is accompanied by a change in the expression of HMG chromosomal proteins. Conceivably, these changes may affect the structure of certain regions in chromatin; however, it is not presently clear whether the switch in HMG protein gene expression is a consequence or a prerequisite for proper differentiation. JF - The Journal of biological chemistry AU - Crippa, M P AU - Nickol, J M AU - Bustin, M AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/02/15/ PY - 1991 DA - 1991 Feb 15 SP - 2712 EP - 2714 VL - 266 IS - 5 SN - 0021-9258, 0021-9258 KW - High Mobility Group Proteins KW - 0 KW - RNA, Messenger KW - Index Medicus KW - Animals KW - Chickens KW - Erythropoiesis KW - Blotting, Northern KW - Chick Embryo KW - RNA, Messenger -- genetics KW - Erythroid Precursor Cells -- metabolism KW - High Mobility Group Proteins -- biosynthesis KW - Erythrocytes -- metabolism KW - High Mobility Group Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80441013?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Developmental+changes+in+the+expression+of+high+mobility+group+chromosomal+proteins.&rft.au=Crippa%2C+M+P%3BNickol%2C+J+M%3BBustin%2C+M&rft.aulast=Crippa&rft.aufirst=M&rft.date=1991-02-15&rft.volume=266&rft.issue=5&rft.spage=2712&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 - 1991-03-20 N1 - Date created - 1991-03-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Retinoylation of proteins in leukemia, embryonal carcinoma, and normal kidney cell lines: differences associated with differential responses to retinoic acid. AN - 80432794; 1990968 AB - In HL60 cells a nuclear protein of Mr 55,000 is retinoylated, with the formation of a thioester bond. To gain further knowledge on the role of retinoylation we studied it in cell lines with varied responses to retinoic acid (RA). Compared to HL60 the extent of retinoylation (mol/cell) was about fivefold higher in HL60/MRI, a mutant which is more sensitive to RA than HL60. Retinoylation occurred to the same extent and at similar rates in HL60 and in HL60/RA-res, a mutant resistant to differentiation by RA. One-dimensional polyacrylamide gel electrophoresis patterns for the three HL60 cell lines were similar. However, two-dimensional polyacrylamide gel electrophoresis patterns of the three HL60 cell lines were distinct. While we saw the same major retinoylated protein of Mr 55,000 in the three cell lines, the HL60/RA-res cells also contained a high level of a protein with the same Mr and a lower pI. The extent of retinoylation was greater in the RA-sensitive embryonal carcinoma cell line, PCC4.aza1R, than in a RA-resistant cell line, PCC4.(RA)-2. One-dimensional polyacrylamide gel electrophoresis patterns of retinoylated proteins of the embryonal carcinoma cell lines were different from HL60 and from each other. The retinoylation pattern of the normal canine kidney cell line (MDCK) was different from either HL60 or the embryonal carcinoma cells. These results showed the retinoylation was widespread and that the response to RA of different cell types may depend on the retinoylation of specific proteins. JF - Archives of biochemistry and biophysics AU - Takahashi, N AU - Breitman, T R AD - Division of Cancer Treatment, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/02/15/ PY - 1991 DA - 1991 Feb 15 SP - 105 EP - 110 VL - 285 IS - 1 SN - 0003-9861, 0003-9861 KW - Neoplasm Proteins KW - 0 KW - Nuclear Proteins KW - Tretinoin KW - 5688UTC01R KW - Index Medicus KW - Drug Resistance -- genetics KW - Tumor Cells, Cultured KW - Humans KW - Electrophoresis, Gel, Two-Dimensional KW - Mutation KW - Molecular Weight KW - Cell Transformation, Neoplastic KW - Cell Line KW - Tretinoin -- pharmacology KW - Teratoma -- metabolism KW - Leukemia -- drug therapy KW - Kidney -- metabolism KW - Nuclear Proteins -- genetics KW - Teratoma -- drug therapy KW - Leukemia -- metabolism KW - Neoplasm Proteins -- genetics KW - Tretinoin -- metabolism KW - Kidney -- drug effects KW - Nuclear Proteins -- metabolism KW - Neoplasm Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80432794?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Retinoylation+of+proteins+in+leukemia%2C+embryonal+carcinoma%2C+and+normal+kidney+cell+lines%3A+differences+associated+with+differential+responses+to+retinoic+acid.&rft.au=Takahashi%2C+N%3BBreitman%2C+T+R&rft.aulast=Takahashi&rft.aufirst=N&rft.date=1991-02-15&rft.volume=285&rft.issue=1&rft.spage=105&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 - 1991-03-06 N1 - Date created - 1991-03-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - From the National Institutes of Health. AN - 80429319; 1990184 JF - JAMA AU - Raub, W AD - National Institutes of Health. Y1 - 1991/02/13/ PY - 1991 DA - 1991 Feb 13 SP - 706 VL - 265 IS - 6 SN - 0098-7484, 0098-7484 KW - Bacterial Vaccines KW - 0 KW - Haemophilus Vaccines KW - Haemophilus influenzae type b polysaccharide vaccine KW - Polysaccharides, Bacterial KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - United States KW - Infant KW - Risk Factors KW - Humans KW - National Institutes of Health (U.S.) KW - Bacterial Capsules KW - Adult KW - Aged KW - Middle Aged KW - Female KW - Salivary Glands -- physiopathology KW - Haemophilus influenzae KW - HIV Infections -- transmission KW - Meningitis, Haemophilus -- prevention & control KW - Occupational Diseases KW - HIV-1 KW - Menopause UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80429319?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=JAMA&rft.atitle=From+the+National+Institutes+of+Health.&rft.au=Raub%2C+W&rft.aulast=Raub&rft.aufirst=W&rft.date=1991-02-13&rft.volume=265&rft.issue=6&rft.spage=706&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-03-01 N1 - Date created - 1991-03-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Spontaneous lymphocyte proliferation in HTLV-II infection. AN - 80432245; 1671234 AB - We measured lymphocyte proliferation in the absence of antigenic stimulation in 45 HTLV-II infected, 9 HTLV-I infected, and 19 HTLV-I seronegative intravenous drug users (IVDU). Lymphocyte proliferation was higher in IVDUs infected with HTLV-II than in seronegative IVDUs but lower than among those infected with HTLV-I. Higher rates of proliferation were also associated with needle sharing, CD4+ and IL2R+ lymphocyte counts, and HTLV-I antibody titres. JF - Lancet (London, England) AU - Wiktor, S Z AU - Jacobson, S AU - Weiss, S H AU - Shaw, G M AU - Reuben, J S AU - Shorty, V J AU - McFarlin, D E AU - Blattner, W A AD - Viral Epidemiology Section, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 1991/02/09/ PY - 1991 DA - 1991 Feb 09 SP - 327 EP - 328 VL - 337 IS - 8737 SN - 0140-6736, 0140-6736 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Polymerase Chain Reaction KW - Diagnosis, Differential KW - Humans KW - Adult KW - HTLV-I Infections -- diagnosis KW - HTLV-I Infections -- blood KW - African Continental Ancestry Group KW - Male KW - Female KW - HTLV-II Infections -- diagnosis KW - Substance Abuse, Intravenous -- blood KW - Substance Abuse, Intravenous -- complications KW - Lymphocyte Activation -- physiology KW - HTLV-II Infections -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80432245?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Spontaneous+lymphocyte+proliferation+in+HTLV-II+infection.&rft.au=Wiktor%2C+S+Z%3BJacobson%2C+S%3BWeiss%2C+S+H%3BShaw%2C+G+M%3BReuben%2C+J+S%3BShorty%2C+V+J%3BMcFarlin%2C+D+E%3BBlattner%2C+W+A&rft.aulast=Wiktor&rft.aufirst=S&rft.date=1991-02-09&rft.volume=337&rft.issue=8737&rft.spage=327&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 - 1991-03-06 N1 - Date created - 1991-03-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Apparent unilateral visual neglect in MPTP-hemiparkinsonian monkeys is due to delayed initiation of motion. AN - 80564905; 2029630 AB - Monkeys made hemiparkinsonian by infusion of a solution of MPTP into one carotid artery appeared to ignore food presented from the contralateral side. Initial observations suggested neglect of visual stimuli presented as fruit treats by automated delivery system in the half-field contralateral to MPTP treatment. Further studies in which fruit treats were left in the 'neglected' visual field indicated that this apparent neglect, unlike neglect attending cortical lesions, was rather a marked delay in initiating movements (unilateral hypokinesia). These observations may explain apparent subcortical neglect and are consistent with the known role of nigrostriatal dopaminergic neurones in movement regulation. This is a useful animal model in which difficulties in initiation of movement (hypokinesia). a cardinal symptom of Parkinson's disease, can be studied separately from other deficits in motor performance. JF - Brain research AU - Bankiewicz, K S AU - Oldfield, E H AU - Plunkett, R J AU - Schuette, W H AU - Cogan, D G AU - Hogan, N AU - Zuddas, A AU - Kopin, I J AD - Surgical Neurology Branch, NINDS, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/02/08/ PY - 1991 DA - 1991 Feb 08 SP - 98 EP - 102 VL - 541 IS - 1 SN - 0006-8993, 0006-8993 KW - Levodopa KW - 46627O600J KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Index Medicus KW - Space life sciences KW - Levodopa -- pharmacology KW - Animals KW - Macaca fascicularis KW - Behavior, Animal -- physiology KW - Macaca mulatta KW - Female KW - Reaction Time KW - Visual Perception -- physiology KW - Parkinson Disease, Secondary -- physiopathology KW - Parkinson Disease, Secondary -- psychology KW - Parkinson Disease, Secondary -- chemically induced KW - Motor Activity -- physiology KW - Attention UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80564905?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Apparent+unilateral+visual+neglect+in+MPTP-hemiparkinsonian+monkeys+is+due+to+delayed+initiation+of+motion.&rft.au=Bankiewicz%2C+K+S%3BOldfield%2C+E+H%3BPlunkett%2C+R+J%3BSchuette%2C+W+H%3BCogan%2C+D+G%3BHogan%2C+N%3BZuddas%2C+A%3BKopin%2C+I+J&rft.aulast=Bankiewicz&rft.aufirst=K&rft.date=1991-02-08&rft.volume=541&rft.issue=1&rft.spage=98&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 - 1991-06-19 N1 - Date created - 1991-06-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Is NAN-190 an effective antagonist of the hypothermia and hyperglycemia induced by the 5-HT1A receptor agonist, 8-OH-DPAT? AN - 80618224; 1828770 AB - The putative 5-HT1A receptor antagonist properties of 1-(2-methoxyphenyl)-4-[4-(2-phtalimmido)butyl] piperazine (NAN-190) were studied in mice. The responses studied were hypothermia- and hyperglycemia-induced by the 5-HT1A agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT). NAN-190 (0.3-3 mg/kg) did not antagonize either response, but rather appeared to be additive with the effect produced by 8-OH-DPAT (0.25 mg/kg) alone, at least with respect to temperature. NAN-190, given alone in similar doses, caused hypothermia and hyperglycemia. These results suggest that NAN-190 has similar properties to 8-OH-DPAT with regard to temperature and glucose effects. Therefore, it does not appear to be a effective antagonist for all 5-HT1A-mediated responses. JF - European journal of pharmacology AU - Wozniak, K M AU - Durcan, M J AU - Linnoila, M AD - Laboratory of Clinical Studies, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892. Y1 - 1991/02/07/ PY - 1991 DA - 1991 Feb 07 SP - 253 EP - 256 VL - 193 IS - 2 SN - 0014-2999, 0014-2999 KW - Piperazines KW - 0 KW - Serotonin Antagonists KW - Tetrahydronaphthalenes KW - 1-(2-methoxyphenyl)-4-(4-(2-phthalimido)butyl)piperazine KW - 115338-32-4 KW - 8-Hydroxy-2-(di-n-propylamino)tetralin KW - 78950-78-4 KW - Index Medicus KW - Animals KW - Premedication KW - Mice KW - Male KW - Tetrahydronaphthalenes -- pharmacology KW - Serotonin Antagonists -- pharmacology KW - Hyperglycemia -- prevention & control KW - Hyperglycemia -- chemically induced KW - Piperazines -- pharmacology KW - Piperazines -- administration & dosage KW - Hypothermia, Induced KW - Tetrahydronaphthalenes -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80618224?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Is+NAN-190+an+effective+antagonist+of+the+hypothermia+and+hyperglycemia+induced+by+the+5-HT1A+receptor+agonist%2C+8-OH-DPAT%3F&rft.au=Wozniak%2C+K+M%3BDurcan%2C+M+J%3BLinnoila%2C+M&rft.aulast=Wozniak&rft.aufirst=K&rft.date=1991-02-07&rft.volume=193&rft.issue=2&rft.spage=253&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 - 1991-07-25 N1 - Date created - 1991-07-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Contingent tolerance to carbamazepine: a peripheral-type benzodiazepine mechanism. AN - 80614613; 1646732 AB - Rats were tested for anticonvulsant responsivity to agents active at central and peripheral-type benzodiazepine receptors before and after they were made tolerant to the anticonvulsant effects of carbamazepine on amygdala-kindled seizures. Tolerance to carbamazepine in this paradigm is a contingent process; it occurs when the drug is administered prior to, but not following the kindled seizure. In animals tolerant to carbamazepine, cross-tolerance was observed to the anticonvulsant effects of PK11195, which is active at peripheral-type benzodiazepine receptors, but not to diazepam, which affects central-type benzodiazepine receptors. In animals treated with carbamazepine after the kindled seizure (not tolerant), no alteration in the anticonvulsant effect of PK11195 was observed. These data extend previous biochemical and pharmacological findings suggesting the importance of peripheral-type benzodiazepine receptor mechanisms in the anticonvulsant effects of carbamazepine and suggest a role for this site in the process of contingent tolerance development. JF - European journal of pharmacology AU - Weiss, S R AU - Post, R M AD - Biological Psychiatry Branch, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1991/02/07/ PY - 1991 DA - 1991 Feb 07 SP - 159 EP - 163 VL - 193 IS - 2 SN - 0014-2999, 0014-2999 KW - Anticonvulsants KW - 0 KW - Isoquinolines KW - Receptors, GABA-A KW - Carbamazepine KW - 33CM23913M KW - PK 11195 KW - YNF83VN1RL KW - Index Medicus KW - Seizures -- chemically induced KW - Rats, Inbred Strains KW - Rats KW - Drug Tolerance KW - Anticonvulsants -- pharmacology KW - Animals KW - Kindling, Neurologic -- drug effects KW - Premedication KW - Amygdala -- drug effects KW - Time Factors KW - Male KW - Isoquinolines -- pharmacology KW - Carbamazepine -- pharmacology KW - Carbamazepine -- administration & dosage KW - Receptors, GABA-A -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80614613?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Contingent+tolerance+to+carbamazepine%3A+a+peripheral-type+benzodiazepine+mechanism.&rft.au=Weiss%2C+S+R%3BPost%2C+R+M&rft.aulast=Weiss&rft.aufirst=S&rft.date=1991-02-07&rft.volume=193&rft.issue=2&rft.spage=159&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 - 1991-07-25 N1 - Date created - 1991-07-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Survival of scrapie virus after 3 years' interment. AN - 80421153; 1671114 AB - Supernatant fluid from a scrapie-infected hamster brain homogenate was mixed with soil, packed into perforated petri dishes that were then embedded within soil-containing pots, and buried in a garden for 3 years. Between 2 and 3 log units of the input infectivity of nearly 5 log units survived this exposure, with little leaching of virus into deeper soil layers. These results have implications for environmental contamination by scrapie and by similar agents, including those of bovine spongiform encephalopathy and Creutzfeldt-Jakob disease. JF - Lancet (London, England) AU - Brown, P AU - Gajdusek, D C AD - Laboratory of CNS Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/02/02/ PY - 1991 DA - 1991 Feb 02 SP - 269 EP - 270 VL - 337 IS - 8736 SN - 0140-6736, 0140-6736 KW - Prions KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Evaluation Studies as Topic KW - Animals KW - Brain Chemistry KW - Environmental Exposure KW - Virus Activation KW - Virology -- methods KW - Time Factors KW - Female KW - Cricetinae KW - Soil Microbiology KW - Prions -- growth & development KW - Prions -- pathogenicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80421153?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Survival+of+scrapie+virus+after+3+years%27+interment.&rft.au=Brown%2C+P%3BGajdusek%2C+D+C&rft.aulast=Brown&rft.aufirst=P&rft.date=1991-02-02&rft.volume=337&rft.issue=8736&rft.spage=269&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 - 1991-02-22 N1 - Date created - 1991-02-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A human epidermal differentiation-specific keratin gene is regulated by calcium but not negative modulators of differentiation in transgenic mouse keratinocytes. AN - 80680059; 1712625 AB - Keratins K1 and K10 represent the major differentiation products of the maturing epidermal keratinocytes. Primary epidermal cell cultures from newborn K1 transgenic mice containing a 12-kilobase human K1 genomic fragment were established in order to examine the expression of both human and mouse K1 in the presence of known modulators of epidermal differentiation. Elevated levels of Ca2+ in the culture medium induced both mouse K1 and human K1. Supplementing the medium with retinoic acid or 12-O-tetradecanoylphorbol-13-acetate or introducing a Harvey viral ras oncogene (v-rasHa) into the cells completely suppressed mouse K1 but not human K1. Our results suggest that: (a) the human 12-kilobase insert contains all the necessary cis-acting elements to respond to the Ca2+ signal, and (b) other cis-acting elements, not present within this insert, may function independently to regulate the response of K1 to retinoids, 12-O-tetradecanoylphorbol-13-acetate, and v-rasHa transformation. This transgenic model provides an approach to identify elements required for the regulation of an epidermal differentiation-specific gene. JF - Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research AU - Rosenthal, D S AU - Steinert, P M AU - Chung, S AU - Huff, C A AU - Johnson, J AU - Yuspa, S H AU - Roop, D R AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 107 EP - 113 VL - 2 IS - 2 SN - 1044-9523, 1044-9523 KW - K1 KW - v-Ha-ras KW - v-rasHa KW - Tretinoin KW - 5688UTC01R KW - Keratins KW - 68238-35-7 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Tretinoin -- pharmacology KW - Animals KW - Humans KW - Keratinocytes -- drug effects KW - Moloney murine leukemia virus -- physiology KW - Mice KW - Mice, Transgenic KW - Genes, ras KW - Cells, Cultured KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Gene Expression Regulation -- drug effects KW - Keratinocytes -- metabolism KW - Moloney murine leukemia virus -- genetics KW - Cell Differentiation -- drug effects KW - Keratins -- genetics KW - Calcium -- pharmacology KW - Keratins -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80680059?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cell+growth+%26+differentiation+%3A+the+molecular+biology+journal+of+the+American+Association+for+Cancer+Research&rft.atitle=A+human+epidermal+differentiation-specific+keratin+gene+is+regulated+by+calcium+but+not+negative+modulators+of+differentiation+in+transgenic+mouse+keratinocytes.&rft.au=Rosenthal%2C+D+S%3BSteinert%2C+P+M%3BChung%2C+S%3BHuff%2C+C+A%3BJohnson%2C+J%3BYuspa%2C+S+H%3BRoop%2C+D+R&rft.aulast=Rosenthal&rft.aufirst=D&rft.date=1991-02-01&rft.volume=2&rft.issue=2&rft.spage=107&rft.isbn=&rft.btitle=&rft.title=Cell+growth+%26+differentiation+%3A+the+molecular+biology+journal+of+the+American+Association+for+Cancer+Research&rft.issn=10449523&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-22 N1 - Date created - 1991-08-22 N1 - Date revised - 2017-01-13 N1 - Gene symbol - K1; v-Ha-ras; v-rasHa N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Selective autoregulation of endothelins in primary astrocyte cultures: endothelin receptor-mediated potentiation of endothelin-1 secretion. AN - 80660898; 1648383 AB - Observations that primary rat astrocytes express high-affinity binding sites for endothelins and, in addition, are capable of producing not only endothelin-3 but also endothelin-1 prompted the investigation of a possible relation between endothelin peptides and receptors in these cells. Sarafotoxin S6b, an endothelin receptor agonist, was used as a tool to study endothelin receptor-mediated changes in the secretion of endothelin-1 and -3. The effects of sarafotoxin S6b and endothelin-1 in stimulating inositolphospholipid turnover as well as in inducing AP1 in primary astrocyte cultures were found to be similar. A low cross-reactivity of sarafotoxin S6b with endothelin-1 and -3 in the endothelin radioimmunoassays used here, along with a distinctly different elution position in high-performance liquid chromatography, allowed a clear discrimination between sarafotoxin and endothelins in the culture media. Stimulation of primary rat astrocytes with 10(-7) M sarafotoxin S6b for 1 hour resulted in a substantial increase in endothelin-1 immunoreactivity in the medium. This immunoreactivity reached a peak at 3 hours and showed no further increase after 8 and 24 hours. Treatment of our cultures with phorbol myristate acetate, lipopolysaccharide, tumor necrosis factor alpha, and norepinephrine for 24 hours led to only a moderate elevation of endothelin-1 immunoreactivity. Immunoreactive endothelin-3 was not affected by any of the treatments tested. Thus, our data suggest that endothelins in primary rat astrocytes are subject to selective autoregulation, as demonstrated by the potentiation of endothelin-1 secretion after activation of glial endothelin receptors. JF - The New biologist AU - Ehrenreich, H AU - Anderson, R W AU - Ogino, Y AU - Rieckmann, P AU - Costa, T AU - Wood, G P AU - Coligan, J E AU - Kehrl, J H AU - Fauci, A S AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 135 EP - 141 VL - 3 IS - 2 SN - 1043-4674, 1043-4674 KW - Endothelins KW - 0 KW - Lipopolysaccharides KW - Phosphatidylinositols KW - Proto-Oncogene Proteins c-jun KW - Receptors, Cell Surface KW - Receptors, Endothelin KW - Tumor Necrosis Factor-alpha KW - Vasoconstrictor Agents KW - Viper Venoms KW - sarafotoxins s6 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Animals KW - Phosphatidylinositols -- metabolism KW - Vasoconstrictor Agents -- pharmacology KW - Norepinephrine -- pharmacology KW - Lipopolysaccharides -- pharmacology KW - Tumor Necrosis Factor-alpha -- pharmacology KW - Proto-Oncogene Proteins c-jun -- biosynthesis KW - Homeostasis -- drug effects KW - Radioimmunoassay KW - Chromatography, High Pressure Liquid KW - Rats KW - Viper Venoms -- pharmacology KW - Cells, Cultured KW - In Vitro Techniques KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Endothelins -- biosynthesis KW - Astrocytes -- drug effects KW - Endothelins -- secretion KW - Receptors, Cell Surface -- physiology KW - Astrocytes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80660898?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+biologist&rft.atitle=Selective+autoregulation+of+endothelins+in+primary+astrocyte+cultures%3A+endothelin+receptor-mediated+potentiation+of+endothelin-1+secretion.&rft.au=Ehrenreich%2C+H%3BAnderson%2C+R+W%3BOgino%2C+Y%3BRieckmann%2C+P%3BCosta%2C+T%3BWood%2C+G+P%3BColigan%2C+J+E%3BKehrl%2C+J+H%3BFauci%2C+A+S&rft.aulast=Ehrenreich&rft.aufirst=H&rft.date=1991-02-01&rft.volume=3&rft.issue=2&rft.spage=135&rft.isbn=&rft.btitle=&rft.title=The+New+biologist&rft.issn=10434674&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-14 N1 - Date created - 1991-08-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A randomized pilot study of high-dose epirubicin as neoadjuvant chemotherapy in the treatment of cancer of the bilharzial bladder. AN - 80632369; 2054316 AB - Seventy-one patients with T2 and T3 bladder cancer were randomized to receive either two courses of epirubicin 120 mg/m2 i.v. push every 21 days pre-operatively, and four additional courses post-operatively (group I = 34 patients), or radical surgery (group II = 37 patients). At a median follow-up of 24 months (range 22 months to 38 months) 25 patients from group I and 14 patients from group II are still alive and disease-free. The estimated two-year disease-free survival percentages were 73.5 and 37.9%, respectively (P = 0.05). After initial chemotherapy, resected specimens were subjected to histopathological study of chemotherapeutic effects. Necrosis was detected in 95% of cases with squamous cell carcinoma and in 57.3% of cases with transitional cell carcinoma. We conclude that the benefit which was obtained by pre-operative and post-operative chemotherapy with epirubicin is promising and may represent a significant improvement in the treatment of patients with carcinoma of the bilharzial bladder. JF - Annals of oncology : official journal of the European Society for Medical Oncology AU - Gad el Mawla, N AU - Mansour, M A AU - Eissa, S AU - Ali, N M AU - Elattar, I AU - Hamza, M R AU - Khaled, H AU - Habboubi, N AU - Magrath, I AU - Elsebai, I AD - National Cancer Institute (NCI), Cairo, Egypt. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 137 EP - 140 VL - 2 IS - 2 SN - 0923-7534, 0923-7534 KW - Epirubicin KW - 3Z8479ZZ5X KW - Index Medicus KW - Carcinoma, Squamous Cell -- etiology KW - Combined Modality Therapy KW - Humans KW - Pilot Projects KW - Carcinoma, Transitional Cell -- etiology KW - Survival Rate KW - Postoperative Complications KW - Adult KW - Follow-Up Studies KW - Middle Aged KW - Neoplasm Recurrence, Local KW - Carcinoma, Squamous Cell -- drug therapy KW - Carcinoma, Transitional Cell -- drug therapy KW - Female KW - Male KW - Carcinoma -- secondary KW - Urinary Bladder Neoplasms -- etiology KW - Carcinoma -- etiology KW - Epirubicin -- therapeutic use KW - Carcinoma -- drug therapy KW - Urinary Bladder Neoplasms -- drug therapy KW - Schistosomiasis -- complications KW - Urinary Bladder Neoplasms -- mortality KW - Epirubicin -- adverse effects KW - Carcinoma -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80632369?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+randomized+pilot+study+of+high-dose+epirubicin+as+neoadjuvant+chemotherapy+in+the+treatment+of+cancer+of+the+bilharzial+bladder.&rft.au=Gad+el+Mawla%2C+N%3BMansour%2C+M+A%3BEissa%2C+S%3BAli%2C+N+M%3BElattar%2C+I%3BHamza%2C+M+R%3BKhaled%2C+H%3BHabboubi%2C+N%3BMagrath%2C+I%3BElsebai%2C+I&rft.aulast=Gad+el+Mawla&rft.aufirst=N&rft.date=1991-02-01&rft.volume=2&rft.issue=2&rft.spage=137&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 - 1991-08-01 N1 - Date created - 1991-08-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The occurrence of opportunistic non-Hodgkin's lymphomas in the setting of infection with the human immunodeficiency virus. AN - 80612182; 1646622 AB - The incidence of non-Hodgkin's lymphoma (NHL) has increased by over 50% in the United States since 1973. There is epidemiologic evidence that some of this increase is the result of AIDS-related lymphoma and that this component is increasing. Prolonged survival in the setting of a variety of immunodeficiency states is associated with an increased incidence of NHL. The development of antiretroviral therapy and improved therapy for the complications of AIDS has resulted in prolonged survival of patients with AIDS. As these patients survive longer with profound immunodeficiency, they have an increased cumulative risk of developing NHL. This may result in even more AIDS-related NHL in the future than predicted from current epidemiological studies. An increased understanding of the pathogenesis of AIDS-related NHL may lead to means of preventing their occurrence. Also, therapies that may prevent immunodeficiency from developing in HIV-infected patients may reduce the likelihood of NHL developing. Current efforts at treating these lymphomas are aimed at preventing the myelosuppression and immunosuppression associated with current regimens, lymphoma relapses within the central nervous system, and the opportunistic infections associated with treatment of these tumors. Ultimately, the best means of preventing the development of these lymphomas is by preventing infection with HIV. JF - Annals of oncology : official journal of the European Society for Medical Oncology AU - Pluda, J M AU - Yarchoan, R AU - Broder, S AD - Clinical Oncology Program, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 191 EP - 200 VL - 2 Suppl 2 SN - 0923-7534, 0923-7534 KW - Index Medicus KW - AIDS/HIV KW - Survival Rate KW - Humans KW - Incidence KW - Occupational Diseases -- epidemiology KW - United States -- epidemiology KW - Retroviridae Infections -- complications KW - Occupational Diseases -- chemically induced KW - Lymphoma, Non-Hodgkin -- epidemiology KW - Acquired Immunodeficiency Syndrome -- complications KW - Lymphoma, Non-Hodgkin -- mortality KW - Lymphoma, Non-Hodgkin -- etiology KW - Acquired Immunodeficiency Syndrome -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80612182?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+occurrence+of+opportunistic+non-Hodgkin%27s+lymphomas+in+the+setting+of+infection+with+the+human+immunodeficiency+virus.&rft.au=Pluda%2C+J+M%3BYarchoan%2C+R%3BBroder%2C+S&rft.aulast=Pluda&rft.aufirst=J&rft.date=1991-02-01&rft.volume=2+Suppl+2&rft.issue=&rft.spage=191&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 - 1991-07-25 N1 - Date created - 1991-07-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Wegener's granulomatosis. AN - 80598150; 2043454 AB - Wegner's granulomatosis is a clinicopathologic syndrome of unknown etiology characterized by granulomatous vasculitis of the upper and lower respiratory tracts and glomerulonephritis. During the period covered by this review several articles were published describing the clinical and pathologic features of Wegner's granulomatosis. Specifically, two large series are discussed reviewing the pulmonary manifestations of the disease and the histopathology of the head and neck disease associated with Wegner's granulomatosis. The majority of publications related to Wegner's granulomatosis concern anti-neutrophil cytoplasmic antibodies and their role in the diagnosis, management, and pathogenesis of Wegner's granulomatosis. In the period covered by this article, no new reports on the therapy of Wegner's granulomatosis were reviewed. However, two articles that address the efficacy of cyclophosphamide pulse therapy in Wegner's granulomatosis have recently been published with conflicting conclusions. The data from these articles are mentioned but will be reviewed in more detail in a subsequent article. JF - Current opinion in rheumatology AU - Leavitt, R Y AU - Fauci, A S AD - National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 8 EP - 14 VL - 3 IS - 1 SN - 1040-8711, 1040-8711 KW - Cyclophosphamide KW - 8N3DW7272P KW - Index Medicus KW - Cyclophosphamide -- therapeutic use KW - Humans KW - Granulomatosis with Polyangiitis -- immunology KW - Granulomatosis with Polyangiitis -- pathology KW - Granulomatosis with Polyangiitis -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80598150?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+rheumatology&rft.atitle=Wegener%27s+granulomatosis.&rft.au=Leavitt%2C+R+Y%3BFauci%2C+A+S&rft.aulast=Leavitt&rft.aufirst=R&rft.date=1991-02-01&rft.volume=3&rft.issue=1&rft.spage=8&rft.isbn=&rft.btitle=&rft.title=Current+opinion+in+rheumatology&rft.issn=10408711&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-12 N1 - Date created - 1991-07-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Molecular cloning and regional distribution of rat brain cyclophilin. AN - 80558776; 1851525 AB - Cyclosporine A (CsA) is a potent immunosuppressive drug that has widespread clinical uses in organ transplantation and the treatment of autoimmune disorders. However, the drug's clinical applications are on an empiric basis with a poor understanding of the basic mechanism(s) of action. CsA may exert some of its effects by binding to a cellular receptor protein--the cyclosporine receptor (also called cyclophilin). Cyclophilin (CyP) is an ubiquitous, soluble, cytoplasmic 17 kDa protein which has recently been shown to be a peptide-prolyl isomerase. CsA specifically binds to this protein and inhibits its isomerase activity. A rat cyclophilin cDNA clone was isolated from a rat brain lambda gt11 cDNA library. Northern blot analysis shows a single 1 kb messenger RNA in rat brain. In order to determine the regional distribution of the Cyp mRNA in situ hybridization was performed. The Cyp mRNA appeared to be expressed throughout the brain but there were particularly high levels in the cerebral cortex and hippocampus compared to the relatively low levels in white matter areas and tracts. At the cellular level, the Cyp mRNA is expressed at much higher levels in neurons than in glia. The high levels of Cyp in cortical (neuronal) areas may, in part, explain the global encephalopathic symptoms clinically observed in CsA neurotoxicity. JF - Brain research. Molecular brain research AU - Lad, R P AU - Smith, M A AU - Hilt, D C AD - Laboratory of Biochemical Genetics, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 239 EP - 244 VL - 9 IS - 3 SN - 0169-328X, 0169-328X KW - Carrier Proteins KW - 0 KW - Cyclosporins KW - Nerve Tissue Proteins KW - RNA, Messenger KW - Amino Acid Isomerases KW - EC 5.1.1.- KW - Peptidylprolyl Isomerase KW - EC 5.2.1.8 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Base Sequence KW - Blotting, Northern KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Nucleic Acid Hybridization KW - RNA, Messenger -- genetics KW - Cloning, Molecular KW - Nerve Tissue Proteins -- analysis KW - Amino Acid Isomerases -- genetics KW - Carrier Proteins -- genetics KW - Brain Chemistry KW - Carrier Proteins -- analysis KW - Nerve Tissue Proteins -- genetics KW - Amino Acid Isomerases -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80558776?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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.+Molecular+brain+research&rft.atitle=Molecular+cloning+and+regional+distribution+of+rat+brain+cyclophilin.&rft.au=Lad%2C+R+P%3BSmith%2C+M+A%3BHilt%2C+D+C&rft.aulast=Lad&rft.aufirst=R&rft.date=1991-02-01&rft.volume=9&rft.issue=3&rft.spage=239&rft.isbn=&rft.btitle=&rft.title=Brain+research.+Molecular+brain+research&rft.issn=0169328X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-06-19 N1 - Date created - 1991-06-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Morphine decreases cerebral glucose utilization in limbic and forebrain regions while pain has no effect. AN - 80555984; 2030820 AB - Morphine alters affective states in humans and produces reinforcement in humans and animal subjects. Therefore, the present study was designed to determine whether morphine affected the functional activity in brain structures involved in emotion and motivation. Since opioid-induced analgesia largely reflects an influence on the emotional component of pain, the effect of pain on activity in these structures was also studied. Local rates of glucose utilization were measured by the 2-deoxy-D[1-14C]glucose method in the brains of rats, that received morphine or saline, with or without a painful stimulus. Many rostral, and particularly diencephalic, nuclei showed decreased glucose utilization in morphine-treated rats, although caudal regions were mostly unaffected. There were dose-dependent decreases in glucose utilization with doses between 1 and 10 mg/kg morphine. However, nociceptive stimulation, with either formalin or tail-immersion, produced no significant effect on cerebral glucose utilization. The 2-deoxy-D-[1-14C]-glucose technique, as used here, may lack adequate sensitivity to delineate areas of the brain mediating nociception in rats. JF - Neuropharmacology AU - Cohen, S R AU - Kimes, A S AU - London, E D AD - Neuroscience Branch, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 125 EP - 134 VL - 30 IS - 2 SN - 0028-3908, 0028-3908 KW - Formaldehyde KW - 1HG84L3525 KW - Morphine KW - 76I7G6D29C KW - Deoxyglucose KW - 9G2MP84A8W KW - Glucose KW - IY9XDZ35W2 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Dose-Response Relationship, Drug KW - Blood Gas Analysis KW - Deoxyglucose -- pharmacology KW - Blood Pressure -- drug effects KW - Autoradiography KW - Male KW - Limbic System -- drug effects KW - Limbic System -- metabolism KW - Pain -- chemically induced KW - Glucose -- metabolism KW - Brain Chemistry -- drug effects KW - Pain -- metabolism KW - Morphine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80555984?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuropharmacology&rft.atitle=Morphine+decreases+cerebral+glucose+utilization+in+limbic+and+forebrain+regions+while+pain+has+no+effect.&rft.au=Cohen%2C+S+R%3BKimes%2C+A+S%3BLondon%2C+E+D&rft.aulast=Cohen&rft.aufirst=S&rft.date=1991-02-01&rft.volume=30&rft.issue=2&rft.spage=125&rft.isbn=&rft.btitle=&rft.title=Neuropharmacology&rft.issn=00283908&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-06-20 N1 - Date created - 1991-06-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Methylphenidate and dextroamphetamine treatments of hyperactivity: are there true nonresponders? AN - 80522247; 2017529 AB - The response to stimulant drugs of 48 boys with attention deficit/hyperactivity disorder was measured following dextroamphetamine, methylphenidate, and placebo in a double-blind crossover study. To distinguish lack of behavioral improvement from adverse drug effects, a day hospital setting and a wide dose range were used. Both drugs were highly and equally efficacious for the group as a whole, and frequently one drug or the other was superior for an individual child, or adverse effects occurred only on one of the stimulants. Only one of the 48 boys (2%) was discharged without the recommendation for continued stimulant drug treatment. "Nonresponse" appears to be extremely rare when both stimulants and a wide range of doses are given. JF - Psychiatry research AU - Elia, J AU - Borcherding, B G AU - Rapoport, J L AU - Keysor, C S AD - Child Psychiatry Branch, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 141 EP - 155 VL - 36 IS - 2 SN - 0165-1781, 0165-1781 KW - Placebos KW - 0 KW - Methylphenidate KW - 207ZZ9QZ49 KW - Dextroamphetamine KW - TZ47U051FI KW - Index Medicus KW - Analysis of Variance KW - Double-Blind Method KW - Humans KW - Child KW - Research Design KW - Day Care, Medical KW - Male KW - Dextroamphetamine -- therapeutic use KW - Attention Deficit Disorder with Hyperactivity -- psychology KW - Methylphenidate -- adverse effects KW - Methylphenidate -- therapeutic use KW - Dextroamphetamine -- adverse effects KW - Attention Deficit Disorder with Hyperactivity -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80522247?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Methylphenidate+and+dextroamphetamine+treatments+of+hyperactivity%3A+are+there+true+nonresponders%3F&rft.au=Elia%2C+J%3BBorcherding%2C+B+G%3BRapoport%2C+J+L%3BKeysor%2C+C+S&rft.aulast=Elia&rft.aufirst=J&rft.date=1991-02-01&rft.volume=36&rft.issue=2&rft.spage=141&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 - 1991-05-17 N1 - Date created - 1991-05-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - TCDD exposure of human embryonic palatal shelves in organ culture alters the differentiation of medial epithelial cells. AN - 80509093; 2014478 AB - The highly toxic, polychlorinated aromatic compound 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) occurs as a contaminant throughout the environment. Epidemiology studies of populations accidentally exposed to TCDD have failed to identify TCDD as a human teratogen, but these studies are limited by the small numbers of exposed pregnancies and imprecise estimates of exposure. TCDD is highly teratogenic in mice, inducing cleft palate and hydronephrosis. TCDD exposure in vivo of embryonic mice alters the differentiation and expression of growth factors in the medial epithelial palatal cells. These alterations also occur in rat and mouse palates exposed to TCDD in organ culture. In the present study, human embryonic palatal shelves were cultured in the rodent organ culture system. In order to achieve in vitro the developmental stage at which fusion would normally occur, GD 52 shelves were cultured for 4 days, GD 53 shelves were cultured for 3 days, and GD 54 shelves were cultured for 3 days. Three of four palatal shelves exposed to 5 x 10(-11) M TCDD were identical to their homologous controls (right shelf cultured with control medium; left shelf cultured with TCDD-containing medium). TCDD at 1 x 10(-7) M produced cytotoxicity detected by transmission electron microscopy (TEM). Exposure to 1 x 10(-8) M TCDD resulted in continued incorporation of thymidine ([3H]-TdR detected autoradiographically) by palatal medial cells, failure of the medial peridermal cells to degenerate as observed by scanning electron microscopy (SEM), and differentiation into a stratified, squamous epithelium. These alterations are identical to those induced by TCDD in vitro in rat and mouse palatal cells. The main difference between these species is the level of TCDD required to elicit the responses. Cultured mouse palates respond to 5 x 10(-11) M TCDD with altered medial cell differentiation, and 1 x 10(-10) M TCDD is cytotoxic. The rat shelves respond with altered differentiation at 1 x 10(-8) M and cytotoxicity at 1 x 10(-7) M. All the human shelves respond at 1 x 10(-8) M TCDD with altered differentiation, 1 out of 4 responded at 5 x 10(-11) M, and cytotoxicity occurred at 1 x 10(-7) M. The present data suggest human embryonic palates are less sensitive than those of the C57BL/6N mouse, and that exposure to high levels of TCDD would be required to elicit altered differentiation in the palatal shelf. JF - Teratology AU - Abbott, B D AU - Birnbaum, L S AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 119 EP - 132 VL - 43 IS - 2 SN - 0040-3709, 0040-3709 KW - Polychlorinated Dibenzodioxins KW - 0 KW - Transforming Growth Factor alpha KW - Transforming Growth Factor beta KW - Epidermal Growth Factor KW - 62229-50-9 KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Index Medicus KW - Transforming Growth Factor beta -- biosynthesis KW - Analysis of Variance KW - Epidermal Growth Factor -- biosynthesis KW - Dose-Response Relationship, Drug KW - Humans KW - Cell Division -- drug effects KW - Epithelium -- drug effects KW - Receptor, Epidermal Growth Factor -- drug effects KW - Cell Survival -- drug effects KW - Transforming Growth Factor alpha -- biosynthesis KW - Microscopy, Electron KW - Cell Differentiation -- drug effects KW - Immunohistochemistry KW - Organ Culture Techniques KW - Palate -- drug effects KW - Polychlorinated Dibenzodioxins -- toxicity KW - Congenital Abnormalities -- diagnosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80509093?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Teratology&rft.atitle=TCDD+exposure+of+human+embryonic+palatal+shelves+in+organ+culture+alters+the+differentiation+of+medial+epithelial+cells.&rft.au=Abbott%2C+B+D%3BBirnbaum%2C+L+S&rft.aulast=Abbott&rft.aufirst=B&rft.date=1991-02-01&rft.volume=43&rft.issue=2&rft.spage=119&rft.isbn=&rft.btitle=&rft.title=Teratology&rft.issn=00403709&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-05-16 N1 - Date created - 1991-05-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Quinolinic acid in cerebrospinal fluid and serum in HIV-1 infection: relationship to clinical and neurological status. AN - 80499707; 1826418 AB - Quinolinic acid is an "excitotoxic" metabolite and an agonist of N-methyl-D-aspartate receptors. Of patients infected with human immunodeficiency virus type 1 (HIV-1) who were neurologically normal or exhibited only equivocal and subclinical signs of the acquired immunodeficiency syndrome (AIDS) dementia complex, concentrations of quinolinic acid in cerebrospinal fluid (CSF) were increased twofold in patients in the early stages of disease (Walter Reed stages 1 and 2) and averaged 3.8 times above normal in later-stage patients (Walter Reed stages 4 through 6). However, in patients with either clinically overt AIDS dementia complex, aseptic meningitis, opportunistic infections, or neoplasms, CSF levels were elevated over 20-fold and generally paralleled the severity of cognitive and motor dysfunction. CSF concentrations of quinolinic acid were significantly correlated to the severity of the neuropsychological deficits. After treatment of AIDS dementia complex with zidovudine and treatment of the opportunistic infections with specific antimicrobial therapies, CSF levels of quinolinic acid decreased in parallel with clinical neurological improvement. By analysis of the relationship between levels of quinolinic acid in the CSF and serum and integrity of the blood-brain barrier, as measured by the CSF:serum albumin ratio, it appears that CSF levels of quinolinic acid may be derived predominantly from intracerebral sources and perhaps from the serum. While quinolinic acid may be another "marker" of host- and virus-mediated events in the brain, the established excitotoxic effects of quinolinic acid and the magnitude of the increases in CSF levels of the acid raise the possibility that quinolinic acid plays a direct role in the pathogenesis of brain dysfunction associated with HIV-1 infection. JF - Annals of neurology AU - Heyes, M P AU - Brew, B J AU - Martin, A AU - Price, R W AU - Salazar, A M AU - Sidtis, J J AU - Yergey, J A AU - Mouradian, M M AU - Sadler, A E AU - Keilp, J AD - Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 202 EP - 209 VL - 29 IS - 2 SN - 0364-5134, 0364-5134 KW - Convulsants KW - 0 KW - Neurotoxins KW - Quinolinic Acids KW - Zidovudine KW - 4B9XT59T7S KW - Quinolinic Acid KW - F6F0HK1URN KW - Index Medicus KW - AIDS/HIV KW - Zidovudine -- therapeutic use KW - Regression Analysis KW - Neurotoxins -- metabolism KW - Convulsants -- metabolism KW - Humans KW - Quinolinic Acids -- blood KW - AIDS Dementia Complex -- cerebrospinal fluid KW - AIDS Dementia Complex -- complications KW - Quinolinic Acids -- metabolism KW - HIV-1 KW - AIDS Dementia Complex -- drug therapy KW - AIDS Dementia Complex -- metabolism KW - HIV Infections -- blood KW - HIV Infections -- complications KW - AIDS Dementia Complex -- blood KW - HIV Infections -- metabolism KW - Quinolinic Acids -- cerebrospinal fluid KW - HIV Infections -- cerebrospinal fluid UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80499707?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Quinolinic+acid+in+cerebrospinal+fluid+and+serum+in+HIV-1+infection%3A+relationship+to+clinical+and+neurological+status.&rft.au=Heyes%2C+M+P%3BBrew%2C+B+J%3BMartin%2C+A%3BPrice%2C+R+W%3BSalazar%2C+A+M%3BSidtis%2C+J+J%3BYergey%2C+J+A%3BMouradian%2C+M+M%3BSadler%2C+A+E%3BKeilp%2C+J&rft.aulast=Heyes&rft.aufirst=M&rft.date=1991-02-01&rft.volume=29&rft.issue=2&rft.spage=202&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 - 1991-05-09 N1 - Date created - 1991-05-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Carcinogenicity of p-chloroaniline in rats and mice. AN - 80490997; 2010141 AB - p-Chloroaniline (PCA), a dye intermediate, was evaluated for potential long-term toxicity and carcinogenicity. Groups of 50 F344/N rats of each sex were given by gavage PCA hydrochloride in deionized water at doses of 0, 2, 6 or 18 mg/kg body weight, 5 days/wk for 103 wk. Groups of 50 male and female B6C3F1 mice of each sex were given 0, 3, 10 or 30 mg/kg on the same schedule. In general, body weights and survival were unaffected by PCA administration. In rats the group given 18 mg/kg had mild haemolytic anaemia and slight increases in methaemoglobin at various times during the study. Fibrosis of the spleen was significantly increased in all PCA-treated groups of male rats and in the 18-mg/kg group of female rats. Sarcomas of the spleen occurred in male rats, their incidence being 0/49, 1/50, 3/50 and 38/50 in control low-, mid- and high-dose groups, respectively. There was a slightly increased incidence of pheochromocytomas of the adrenal gland in both male and female rats. Dosed groups of male mice had increased incidences of hepatocellular adenomas or carcinomas (11/50, 21/49, 20/50 and 21/50 in controls, low- mid- and high-dose groups, respectively). Haemangiosarcomas of the liver or spleen were also increased in the high-dose group (incidences of 4/50, 4/49, 1/50 and 10/50 in controls, low-, mid- and high-dose groups, respectively). In conclusion, PCA was carcinogenic in male rats and male mice. JF - Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association AU - Chhabra, R S AU - Huff, J E AU - Haseman, J K AU - Elwell, M R AU - Peters, A C AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 119 EP - 124 VL - 29 IS - 2 SN - 0278-6915, 0278-6915 KW - Aniline Compounds KW - 0 KW - 4-chloroaniline KW - Z553SGH315 KW - Index Medicus KW - Animals KW - Splenic Neoplasms -- chemically induced KW - Sarcoma, Experimental -- chemically induced KW - Pheochromocytoma -- chemically induced KW - Fibrosis KW - Spleen -- pathology KW - Liver Neoplasms, Experimental -- chemically induced KW - Mice KW - Rats KW - Rats, Inbred F344 KW - Adenoma -- chemically induced KW - Adrenal Gland Neoplasms -- chemically induced KW - Female KW - Male KW - Carcinoma -- chemically induced KW - Neoplasms, Experimental -- chemically induced KW - Aniline Compounds -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80490997?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Carcinogenicity+of+p-chloroaniline+in+rats+and+mice.&rft.au=Chhabra%2C+R+S%3BHuff%2C+J+E%3BHaseman%2C+J+K%3BElwell%2C+M+R%3BPeters%2C+A+C&rft.aulast=Chhabra&rft.aufirst=R&rft.date=1991-02-01&rft.volume=29&rft.issue=2&rft.spage=119&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 - 1991-05-06 N1 - Date created - 1991-05-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Carcinogenesis studies of dichlorvos in Fischer rats and B6C3F1 mice. AN - 80482667; 1900819 AB - Dichlorvos (dichlorovinyl dimethyl phosphoric acid ester) is a cholinesterase inhibitor used widely as a contact and stomach insecticide for control of internal and external parasites. Carcinogenesis studies were conducted by administering dichlorvos in corn oil by gavage 5 times a week for 103 weeks to groups of 50 male and 50 female Fischer rats at 0, 4, or 8 mg/kg body weight, to groups of 50 male B6C3F1 mice at 0, 10, or 20 mg/kg, and to groups of 50 female B6C3F1 mice at 0, 20, or 40 mg/kg. During the course of the studies, body weights and survival rates of the male and female rats and mice were not different from those of their respective controls; females of both species appeared to gain more weight than controls. Neoplasms induced by dichlorvos included adenomas of the exocrine pancreas (male rats), mononuclear cell leukemia (male rats), and squamous cell papilloma of the forestomach (male and female mice; two other female mice had squamous cell carcinomas). Lesions observed in female rats that may have been due to dichlorvos administration included adenomas of the exocrine pancreas and fibroadenomas of the mammary gland. The results demonstrated that dichlorvos is carcinogenic for Fischer rats and B6C3F1 mice. JF - Japanese journal of cancer research : Gann AU - Chan, P C AU - Huff, J AU - Haseman, J K AU - Alison, R AU - Prejean, J D AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 157 EP - 164 VL - 82 IS - 2 SN - 0910-5050, 0910-5050 KW - Dichlorvos KW - 7U370BPS14 KW - Index Medicus KW - Rats KW - Mammary Neoplasms, Experimental -- chemically induced KW - Animals KW - Rats, Inbred F344 KW - Stomach Neoplasms -- chemically induced KW - Dose-Response Relationship, Drug KW - Body Weight -- drug effects KW - Adenoma -- chemically induced KW - Carcinoma, Squamous Cell -- chemically induced KW - Mice KW - Leukemia, Experimental -- chemically induced KW - Papilloma -- chemically induced KW - Male KW - Female KW - Pancreatic Neoplasms -- etiology KW - Neoplasms -- mortality KW - Dichlorvos -- adverse effects KW - Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80482667?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Carcinogenesis+studies+of+dichlorvos+in+Fischer+rats+and+B6C3F1+mice.&rft.au=Chan%2C+P+C%3BHuff%2C+J%3BHaseman%2C+J+K%3BAlison%2C+R%3BPrejean%2C+J+D&rft.aulast=Chan&rft.aufirst=P&rft.date=1991-02-01&rft.volume=82&rft.issue=2&rft.spage=157&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 - 1991-04-19 N1 - Date created - 1991-04-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of sulfhydryl modulation on ethyl acrylate-induced forestomach toxicity. AN - 80457367; 1998209 AB - Acute administration of a single dose of ethyl acrylate (EA) to F344 rats by gavage caused time- and dose-dependent forestomach edema. Evidence from our laboratory and others suggested that EA is hydrolyzed to acrylic acid (AA) and ethanol both in vivo and in vitro. The major metabolites detected in teh urine of rats treated with EA were derivatives of the glutathione conjugates of EA and AA. The current work was undertaken to investigate the effects of sulfhydryl-depleting agents (diethylmaleate and fasting) and sulfhydryl-containing agents (cysteine and cysteamine) on EA-induced forestomach edema. Results presented in this report revealed that pretreatment of rats with sulfhydryl-containing chemicals such as cysteine or cysteamine has potentiated EA-induced forestomach edema. In contrast, depletion of indigenous sulfhydryls by fasting of rats or pretreatment with diethylmaleate (DEM) protected against EA-induced forestomach edema. Furthermore, repetitive daily administration of EA by gavage induced mucosal forestomach hyperplasia. Co-administration of cysteamine and EA resulted in a significant enhancement of the severity of EA-induced forestomach mucosal hyperplasia. In conclusion, current data suggest that modulation of indigenous sulfhydryls play a role in EA-induced forestomach toxicity; however, the exact mechanism underlying this role remains to be characterized. JF - Toxicology letters AU - Ghanayem, B I AU - Maronpot, R R AU - Matthews, H B AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 215 EP - 221 VL - 55 IS - 2 SN - 0378-4274, 0378-4274 KW - Acrylates KW - 0 KW - Maleates KW - Mutagens KW - Cysteamine KW - 5UX2SD1KE2 KW - ethyl acrylate KW - 71E6178C9T KW - diethyl maleate KW - AK5N1DQX7U KW - Cysteine KW - K848JZ4886 KW - Index Medicus KW - Rats KW - Administration, Oral KW - Maleates -- pharmacology KW - Animals KW - Rats, Inbred F344 KW - Dose-Response Relationship, Drug KW - Fasting KW - Male KW - Stomach Diseases -- chemically induced KW - Edema -- chemically induced KW - Cysteine -- pharmacology KW - Mutagens -- metabolism KW - Acrylates -- metabolism KW - Mutagens -- toxicity KW - Stomach Diseases -- prevention & control KW - Cysteamine -- pharmacology KW - Acrylates -- toxicity KW - Mutagens -- antagonists & inhibitors KW - Acrylates -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80457367?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+letters&rft.atitle=Effects+of+sulfhydryl+modulation+on+ethyl+acrylate-induced+forestomach+toxicity.&rft.au=Ghanayem%2C+B+I%3BMaronpot%2C+R+R%3BMatthews%2C+H+B&rft.aulast=Ghanayem&rft.aufirst=B&rft.date=1991-02-01&rft.volume=55&rft.issue=2&rft.spage=215&rft.isbn=&rft.btitle=&rft.title=Toxicology+letters&rft.issn=03784274&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-01 N1 - Date created - 1991-04-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Frequent chest X-ray fluoroscopy and breast cancer incidence among tuberculosis patients in Massachusetts. AN - 80455422; 1996380 AB - The incidence of breast cancer was determined in 4940 women treated for tuberculosis between 1925 and 1954 in Massachusetts. Among 2573 women examined by X-ray fluoroscopy an average of 88 times during lung collapse therapy and followed for an average of 30 years, 147 breast cancers occurred in contrast to 113.6 expected [observed/expected (O/E) = 1.29; 95% confidence interval (CI) = 1.1-1.5]. No excess of breast cancer was seen among 2367 women treated by other means: 87 observed versus 100.9 expected. Increased rates for breast cancer were not apparent until about 10 to 15 years after the initial fluoroscopy examination. Excess risk then remained high throughout all intervals of follow-up, up to 50 years after first exposure. Age at exposure strongly influenced the risk of radiation-induced breast cancer with young women being at highest risk and those over age 40 being at lowest risk [relative risk (RR) = 1.06]. Mean radiation dose to the breast was estimated to be 79 cGy, and there was strong evidence for a linear relationship between dose and breast cancer risk. Allowing for a 10-year minimum latent period, the relative risk at 1 Gy was estimated as 1.61 and the absolute excess as 10.7 per 10(4) woman-years per gray. When compared to other studies, our data suggest that the breast is one of the most sensitive tissues to the carcinogenic force of radiation, that fractionated exposures are similar to single exposures of the same total dose in their ability to induce breast cancer, that risk remains high for many years after exposure, and that young women are especially vulnerable to radiation injury. JF - Radiation research AU - Boice, J D AU - Preston, D AU - Davis, F G AU - Monson, R R AD - Radiation Epidemiology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 214 EP - 222 VL - 125 IS - 2 SN - 0033-7587, 0033-7587 KW - Index Medicus KW - Space life sciences KW - Pneumoperitoneum, Artificial KW - Humans KW - Cohort Studies KW - Follow-Up Studies KW - Massachusetts -- epidemiology KW - Dose-Response Relationship, Radiation KW - Pneumothorax, Artificial KW - Fluoroscopy -- adverse effects KW - Female KW - Radiography, Thoracic -- adverse effects KW - Neoplasms, Radiation-Induced -- etiology KW - Neoplasms, Radiation-Induced -- epidemiology KW - Breast Neoplasms -- etiology KW - Breast Neoplasms -- epidemiology KW - Tuberculosis, Pulmonary -- diagnostic imaging KW - Tuberculosis, Pulmonary -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80455422?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Frequent+chest+X-ray+fluoroscopy+and+breast+cancer+incidence+among+tuberculosis+patients+in+Massachusetts.&rft.au=Boice%2C+J+D%3BPreston%2C+D%3BDavis%2C+F+G%3BMonson%2C+R+R&rft.aulast=Boice&rft.aufirst=J&rft.date=1991-02-01&rft.volume=125&rft.issue=2&rft.spage=214&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 - 1991-03-25 N1 - Date created - 1991-03-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Frequency of nonparenteral occupational exposures to blood and body fluids before and after universal precautions training. AN - 80449148; 1996583 AB - During annual periods before and after Universal Precautions training, we compared the frequency of health care workers' self-reported cutaneous exposures to blood and various body substances from any patient and from patients presumed infected with human immunodeficiency virus type 1 (HIV-1). Self-reported cutaneous exposures to blood, sputum, urine, feces, and other body substances were evaluated separately in 559 workers during the first survey and 269 workers during the second. Mean annual blood exposures decreased from 35.8 to 18.1, and mean annual exposures to all substances decreased from 77.8 to 40.0 (p less than 0.001 for both determinations). Two matched analyses of a subset of 200 participants who completed both surveys had similar results. Reported exposures to blood, presumably infectious blood, sputum, presumably infectious sputum, and urine were significantly decreased. Participants were tested for antibodies to HIV-1; no participant reporting cutaneous exposures acquired HIV-1 infection. The upper bound for the 95% confidence interval for the risk of HIV-1 infection associated with a single cutaneous exposure was 0.04% for blood presumed to contain HIV-1 and 0.02% for any body substance presumed to contain HIV-1. These data suggest that Universal Precautions training significantly decreased but did not eliminate cutaneous exposures to blood and body substances. The results further suggest that the risk for HIV-1 infection associated with cutaneous exposures is substantially lower than the risk associated with parenteral exposures. JF - The American journal of medicine AU - Fahey, B J AU - Koziol, D E AU - Banks, S M AU - Henderson, D K AD - Hospital Epidemiology Service, Warren G. Magnuson Clinical Center, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 145 EP - 153 VL - 90 IS - 2 SN - 0002-9343, 0002-9343 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Occupational Exposure KW - Feces -- microbiology KW - Prospective Studies KW - Skin Absorption KW - Humans KW - Surveys and Questionnaires KW - Incidence KW - HIV-1 -- analysis KW - Personnel, Hospital KW - Inservice Training KW - HIV Infections -- transmission KW - HIV Infections -- prevention & control KW - HIV Infections -- metabolism KW - Body Fluids -- microbiology KW - HIV Infections -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80449148?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+medicine&rft.atitle=Frequency+of+nonparenteral+occupational+exposures+to+blood+and+body+fluids+before+and+after+universal+precautions+training.&rft.au=Fahey%2C+B+J%3BKoziol%2C+D+E%3BBanks%2C+S+M%3BHenderson%2C+D+K&rft.aulast=Fahey&rft.aufirst=B&rft.date=1991-02-01&rft.volume=90&rft.issue=2&rft.spage=145&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+medicine&rft.issn=00029343&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-03-27 N1 - Date created - 1991-03-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Stimulation of prostaglandin H synthase mRNA levels and prostaglandin biosynthesis by phorbol ester: mediation by protein kinase C. AN - 80449135; 1899904 AB - We have investigated the mechanisms by which the tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) stimulates prostaglandin E2 (PGE2) formation in the rat tracheal epithelial cell line EGV-6aigT, which can be grown in serum-free medium. The addition of TPA to cells that were prelabeled with [3H]arachidonic acid did not enhance the release of [3H]arachidonic acid and/or [3H]PGE2, indicating that TPA does not stimulate phospholipase activity. The addition of exogenous arachidonic acid to cells pretreated with TPA resulted in increased PGE2 formation, compared with basal levels, indicating an elevation in prostaglandin H synthase (PHS) activity. PHS activity was maximal at 4 hr and was dependent upon the concentration of TPA. Actinomycin D and cycloheximide blocked the TPA response. The recovery of PHS activity of cells in which the existing PHS was inhibited by aspirin was enhanced by TPA treatment. TPA treatment enhanced the expression of PHS mRNA, as measured by Northern analysis. The addition of actinomycin D and cycloheximide reduced the TPA enhancement of PHS mRNA, indicating that the increase in PHS activity required de novo RNA and protein synthesis. Furthermore, pretreatment of the cells with protein kinase C inhibitors reduced the TPA-dependent stimulation of PHS activity and the expression of PHS mRNA. The data suggest that TPA-stimulated de novo synthesis of PHS is mediated by protein kinase C. JF - Molecular pharmacology AU - Duniec, Z M AU - Nettesheim, P AU - Eling, T E AD - Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 164 EP - 170 VL - 39 IS - 2 SN - 0026-895X, 0026-895X KW - Arachidonic Acids KW - 0 KW - Prostaglandins KW - RNA, Messenger KW - Arachidonic Acid KW - 27YG812J1I KW - Prostaglandin-Endoperoxide Synthases KW - EC 1.14.99.1 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Dinoprostone KW - K7Q1JQR04M KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Dinoprostone -- biosynthesis KW - Enzyme Activation KW - Epithelium -- enzymology KW - Trachea -- cytology KW - Arachidonic Acids -- metabolism KW - Arachidonic Acids -- pharmacology KW - Protein Kinase C -- metabolism KW - Rats KW - Stimulation, Chemical KW - Epithelial Cells KW - Cells, Cultured KW - Trachea -- enzymology KW - RNA, Messenger -- metabolism KW - Prostaglandins -- biosynthesis KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Prostaglandin-Endoperoxide Synthases -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80449135?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Stimulation+of+prostaglandin+H+synthase+mRNA+levels+and+prostaglandin+biosynthesis+by+phorbol+ester%3A+mediation+by+protein+kinase+C.&rft.au=Duniec%2C+Z+M%3BNettesheim%2C+P%3BEling%2C+T+E&rft.aulast=Duniec&rft.aufirst=Z&rft.date=1991-02-01&rft.volume=39&rft.issue=2&rft.spage=164&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 - 1991-03-22 N1 - Date created - 1991-03-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Retinoic acid inhibits sodium butyrate-induced monocytic differentiation of HL60 cells while synergistically inducing granulocytoid differentiation. AN - 80448827; 1995327 AB - The human myeloid leukemia cell line HL60 is an in vitro model to study myeloid differentiation. HL60 cells differentiate along different cell type lineages in response to a variety of compounds. The direction of differentiation is usually inducer-specific. However, the response of HL60 cells to sodium n-butyrate (NaB) is pleiotropic. NaB induces HL60 along the monocytic, neutrophilic, eosinophilic, and basophilic pathways. In this study we saw that physiologic concentrations of all-trans-retinoic acid (RA) switched the direction of NaB-induced differentiation from monocytic to granulocytic. We showed previously (Breitman & He, Cancer Res 1990: 50: 6268-6273) that combinations of RA and NaB synergistically induce HL60 to cells that reduce nitroblue tetrazolium. The present study shows that this synergy was even greater if the parameter measured was mature granulocytes. Our results raise the possibility that the endogenous RA in the serum used to grow cells in culture may affect the direction of differentiation of HL60 cells induced by NaB. Furthermore, our results may provide additional rationale for the use of combinations of RA and NaB in the treatment of some leukemias. JF - European journal of haematology AU - He, R Y AU - Breitman, T R AD - Laboratory of Biological Chemistry, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 93 EP - 100 VL - 46 IS - 2 SN - 0902-4441, 0902-4441 KW - Butyrates KW - 0 KW - Butyric Acid KW - 107-92-6 KW - Tretinoin KW - 5688UTC01R KW - Index Medicus KW - Tumor Cells, Cultured KW - Humans KW - Drug Synergism KW - Cell Differentiation -- drug effects KW - Tretinoin -- pharmacology KW - Butyrates -- metabolism KW - Butyrates -- pharmacology KW - Tretinoin -- blood KW - Monocytes -- pathology KW - Leukemia, Myeloid -- metabolism KW - Granulocytes -- pathology KW - Leukemia, Myeloid -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80448827?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+haematology&rft.atitle=Retinoic+acid+inhibits+sodium+butyrate-induced+monocytic+differentiation+of+HL60+cells+while+synergistically+inducing+granulocytoid+differentiation.&rft.au=He%2C+R+Y%3BBreitman%2C+T+R&rft.aulast=He&rft.aufirst=R&rft.date=1991-02-01&rft.volume=46&rft.issue=2&rft.spage=93&rft.isbn=&rft.btitle=&rft.title=European+journal+of+haematology&rft.issn=09024441&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-03-28 N1 - Date created - 1991-03-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Breast cancer and pregnancy. AN - 80446795; 1995352 JF - European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology AU - van der Vange, N AU - van Dongen, J A AD - Department of Surgery, National Cancer Institute, Amsterdam, The Netherlands. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 1 EP - 8 VL - 17 IS - 1 SN - 0748-7983, 0748-7983 KW - Antineoplastic Agents KW - 0 KW - Index Medicus KW - Combined Modality Therapy KW - Humans KW - Abortion, Therapeutic KW - Prognosis KW - Abnormalities, Radiation-Induced -- etiology KW - Biopsy, Needle KW - Radiotherapy -- adverse effects KW - Antineoplastic Agents -- adverse effects KW - Pregnancy KW - Mastectomy, Radical KW - Incidence KW - Abnormalities, Drug-Induced -- etiology KW - Female KW - Breast Neoplasms -- diagnosis KW - Pregnancy Complications, Neoplastic -- therapy KW - Breast Neoplasms -- therapy KW - Breast Neoplasms -- epidemiology KW - Pregnancy Complications, Neoplastic -- epidemiology KW - Pregnancy Complications, Neoplastic -- diagnosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80446795?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+surgical+oncology+%3A+the+journal+of+the+European+Society+of+Surgical+Oncology+and+the+British+Association+of+Surgical+Oncology&rft.atitle=Breast+cancer+and+pregnancy.&rft.au=van+der+Vange%2C+N%3Bvan+Dongen%2C+J+A&rft.aulast=van+der+Vange&rft.aufirst=N&rft.date=1991-02-01&rft.volume=17&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=European+journal+of+surgical+oncology+%3A+the+journal+of+the+European+Society+of+Surgical+Oncology+and+the+British+Association+of+Surgical+Oncology&rft.issn=07487983&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-03-22 N1 - Date created - 1991-03-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of ras protooncogene activation in the formation of spontaneous and nitrosamine-induced lung tumors in the resistant C3H mouse. AN - 80445799; 1995195 AB - The role of ras activation in the formation of spontaneous and chemically induced tumors was evaluated in the C3H mouse, a strain that has a low incidence of spontaneous lung tumors. Lung tumors were induced in C3H mice by treatment with 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK), 50 mg/kg, or nitrosodimethylamine (NDMA), 3 mg/kg for 7 weeks (3 times/week, i.p.). Eleven tumors from each treatment group were evaluated for activated ras genes by direct sequencing and oligonucleotide hybridization to slot blots of amplified DNA from these tumors. An activated K-ras gene was detected in 100% of NDMA- and NNK-induced lung tumors, and the activating mutation detected in all samples was a GC to AT transition (GGT to GAT) in codon 12. In contrast, only 40% of the seven spontaneous lung tumors analyzed contained an activated K-ras gene and the mutations identified were not localized to either a specific base or codon. Both NNK and NDMA can be activated via alpha-hydroxylation to methylating agents. The GC to AT mutation observed in codon 12 in the nitrosamine-induced tumors is consistent with the formation of an O6-methylguanine (O6MG) adduct. Similar concentrations (13-15 pmoles/mumol deoxyguanosine) of this promutagenic adduct were detected in lungs during treatment with either NNK or NDMA. Thus, both these nitrosamines appear to activate the K-ras gene in lung through a direct genotoxic mechanism involving the formation of the O6MG adduct. The frequency of K-ras activation was similar in chemically induced lung tumors from the sensitive A/J strain and the C3H mouse, indicating that susceptibility for neoplasia in these stains is not related to the ability to activate this gene. Although tumors were induced in lung from 100% of C3H mice following chronic carcinogen exposure, both the size and the multiplicity was significantly less, while latency was longer than that observed in the A/J mouse. These differences could not be attributed to an altered propensity for DNA damage, but rather suggest that genetic loci which regulate clonal expansion and growth of initiated cells play a major role in the susceptibility of pulmonary neoplasia. JF - Carcinogenesis AU - Devereux, T R AU - Anderson, M W AU - Belinsky, S A AD - Laboratory of Molecular Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 299 EP - 303 VL - 12 IS - 2 SN - 0143-3334, 0143-3334 KW - K-ras KW - ras KW - Codon KW - 0 KW - Nitrosamines KW - O-4-methylthymine KW - 25902-89-0 KW - 4-(methylnitrosoamino)-4-(3-pyridyl)-1-butanol KW - 59578-66-4 KW - Guanine KW - 5Z93L87A1R KW - DNA KW - 9007-49-2 KW - O-(6)-methylguanine KW - 9B710FV2AE KW - Dimethylnitrosamine KW - M43H21IO8R KW - Thymine KW - QR26YLT7LT KW - Index Medicus KW - Animals KW - Thymine -- analogs & derivatives KW - Codon -- genetics KW - Thymine -- metabolism KW - Dimethylnitrosamine -- toxicity KW - DNA -- metabolism KW - Drug Resistance KW - Mice KW - Guanine -- metabolism KW - Base Sequence KW - Molecular Sequence Data KW - Mice, Inbred C3H KW - Incidence KW - Guanine -- analogs & derivatives KW - Time Factors KW - Mutation KW - Dimethylnitrosamine -- administration & dosage KW - Male KW - Nitrosamines -- administration & dosage KW - Nitrosamines -- toxicity KW - Genes, ras -- genetics KW - Proto-Oncogenes -- genetics KW - Gene Expression Regulation, Neoplastic -- physiology KW - Lung Neoplasms -- genetics KW - Lung Neoplasms -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80445799?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+ras+protooncogene+activation+in+the+formation+of+spontaneous+and+nitrosamine-induced+lung+tumors+in+the+resistant+C3H+mouse.&rft.au=Devereux%2C+T+R%3BAnderson%2C+M+W%3BBelinsky%2C+S+A&rft.aulast=Devereux&rft.aufirst=T&rft.date=1991-02-01&rft.volume=12&rft.issue=2&rft.spage=299&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-03-25 N1 - Date created - 1991-03-25 N1 - Date revised - 2017-01-13 N1 - Gene symbol - K-ras; ras N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - MPTP-induced ATP depletion and cell death in neuroblastoma X glioma hybrid NG 108-15 cells: protection by glucose and sensitization by tetraphenylborate. AN - 80445094; 1994518 AB - The toxic effect of the Parkinsonism-producing neurotoxin MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) was investigated using a neuronal cell culture system, namely, neuroblastoma X glioma hybrid NG 108-15. The cells were able to metabolize MPTP into its active metabolite MPP+ (1-methyl-4-phenylpyridinium ion) and to convert its derivative, 2'-methyl MPTP, to the corresponding pyridinium ion. Degenerative changes were observed in NG 108-15 cells when they were examined with a phase-contrast microscope following exposure to MPTP, MPP+, or 2'-methyl MPTP. These compounds also caused an increased leakage of LDH from the treated cells. An enhanced release of [14C]adenine nucleotides was observed from treated cells which were prelabeled with [14C]adenine. The cell death as indicated by the leakage of LDH and the release of adenine nucleotides was markedly reduced in the presence of a high concentration (25 mM) of glucose in the medium. MPTP and MPP+ induced a drastic depletion in cell ATP content prior to cell death. The ATP depletion was also reduced by the presence of a high concentration of glucose. In contrast, tetraphenylborate, a lipophilic anion, highly potentiated the ATP depletion and the subsequent cell death induced by MPTP. Thus, ATP depletion could be a major factor in MPTP-induced neuronal cell death. JF - Toxicology and applied pharmacology AU - Kutty, R K AU - Santostasi, G AU - Horng, J AU - Krishna, G AD - Section on Drug-Tissue Interaction, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 377 EP - 388 VL - 107 IS - 2 SN - 0041-008X, 0041-008X KW - Adenine Nucleotides KW - 0 KW - 1-methyl-4-(2'-methylphenyl)-1,2,3,6-tetrahydropyridine KW - 102417-86-7 KW - Tetraphenylborate KW - 4358-26-3 KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - L-Lactate Dehydrogenase KW - EC 1.1.1.27 KW - Glucose KW - IY9XDZ35W2 KW - 1-Methyl-4-phenylpyridinium KW - R865A5OY8J KW - Index Medicus KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- analogs & derivatives KW - Tumor Cells, Cultured KW - Cell Survival -- drug effects KW - 1-Methyl-4-phenylpyridinium -- toxicity KW - Dose-Response Relationship, Drug KW - Adenine Nucleotides -- metabolism KW - Neurons -- drug effects KW - Humans KW - Neurons -- cytology KW - L-Lactate Dehydrogenase -- metabolism KW - Neuroblastoma -- pathology KW - Glioma -- pathology KW - Glioma -- drug therapy KW - Neuroblastoma -- drug therapy KW - Glucose -- pharmacology KW - MPTP Poisoning KW - Adenosine Triphosphate -- metabolism KW - Adenosine Triphosphate -- deficiency KW - Tetraphenylborate -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80445094?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=MPTP-induced+ATP+depletion+and+cell+death+in+neuroblastoma+X+glioma+hybrid+NG+108-15+cells%3A+protection+by+glucose+and+sensitization+by+tetraphenylborate.&rft.au=Kutty%2C+R+K%3BSantostasi%2C+G%3BHorng%2C+J%3BKrishna%2C+G&rft.aulast=Kutty&rft.aufirst=R&rft.date=1991-02-01&rft.volume=107&rft.issue=2&rft.spage=377&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 - 1991-03-20 N1 - Date created - 1991-03-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Development of testicular lesions in F344 rats after treatment with boric acid. AN - 80443134; 1994514 AB - Boric acid is an inorganic acid that impairs fertility in male rodents. A reproductive assessment by continuous breeding study found that male rats treated with boric acid had decreased fertility and sperm motility. In order to determine the cell type that is first affected by boric acid, we have examined the development of the boric acid-induced testicular lesion by light and electron microscopy. Adult F344 male rats were fed 9000 ppm boric acid in NIH-07 rat chow for up to 4 weeks. The first testicular lesion noted was an inhibition of spermiation, which appeared by Day 7. Widespread exfoliation of apparently viable germ cells, and pachytene cell death in stages VII and XIV, appeared as exposure continued. After 28 days of dosing, extreme epithelial disorganization and germ cell loss were evident. To determine if there was a hormonal component to the boric acid-induced testicular lesion, serum levels of basal, hCG-, and LHRH-stimulated testosterone levels were measured. After 4 days of dosing, basal testosterone levels were lower than controls and remained low during dosing. However, serum testosterone levels were similar in both boric acid-treated and control animals after either hCG or LHRH challenge. To determine if boron was preferentially accumulated by the testis, boron levels in testis, epididymis, liver, kidney, and blood were measured. Boron levels had effectively reached steady-state levels by Day 4 and were not differentially concentrated in the tissues examined. Thus, these studies characterize the testicular lesion produced by boric acid exposure and identify a decrease in basal serum testosterone levels in the absence of selective accumulation of boron in the testis. JF - Toxicology and applied pharmacology AU - Treinen, K A AU - Chapin, R E AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 325 EP - 335 VL - 107 IS - 2 SN - 0041-008X, 0041-008X KW - Androgen-Binding Protein KW - 0 KW - Boric Acids KW - Testosterone KW - 3XMK78S47O KW - Boron KW - N9E3X5056Q KW - boric acid KW - R57ZHV85D4 KW - Index Medicus KW - Animals KW - Sertoli Cells -- metabolism KW - Tissue Distribution KW - Boron -- pharmacokinetics KW - Leydig Cells -- drug effects KW - Boron -- analysis KW - Rats KW - Sertoli Cells -- drug effects KW - Leydig Cells -- metabolism KW - Rats, Inbred F344 KW - Testis -- drug effects KW - Testosterone -- blood KW - Body Weight -- drug effects KW - Androgen-Binding Protein -- blood KW - Microscopy, Electron KW - Male KW - Testis -- cytology KW - Boric Acids -- toxicity KW - Testicular Neoplasms -- pathology KW - Testicular Neoplasms -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80443134?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Development+of+testicular+lesions+in+F344+rats+after+treatment+with+boric+acid.&rft.au=Treinen%2C+K+A%3BChapin%2C+R+E&rft.aulast=Treinen&rft.aufirst=K&rft.date=1991-02-01&rft.volume=107&rft.issue=2&rft.spage=325&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 - 1991-03-20 N1 - Date created - 1991-03-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Current treatment approaches in colorectal cancer. AN - 80439963; 1992527 AB - Fluorouracil (5-FU) is still the mainstay of adjuvant treatment for colorectal cancer. Two trials have shown a disease-free and overall survival benefit for 5-FU combined with levamisole in patients with node-positive colon cancer. This regimen is fairly well tolerated and devoid of long-term sequelae, and is now considered standard treatment for node-positive colon cancer. One trial showed a modest improvement in disease-free survival for the semustine/vincristine/5-FU combination; the leukemogenicity and renal toxicity caused by semustine have prevented this regimen from being adopted. Although administering 5-FU directly into the portal vein may improve disease-free survival, most trials have failed to demonstrate a reduction in the incidence of hepatic metastases. This technique, therefore, remains investigational. Several trials in rectal cancer show an advantage for 5-FU combined with semustine and radiation therapy in terms of disease-free survival, overall survival, or both; the contribution of semustine has been questioned and is currently being investigated. In patients with metastatic disease, hepatic arterial infusion of floxuridine produces a higher objective response rate than intravenous administration, but has not resulted in a survival benefit; hepatobiliary toxicity limits the duration of therapy. Biochemical modulation of 5-FU with leucovorin increases the response rate produced by 5-FU alone; a survival benefit has also been observed. N-(phosphonacetyl)-L-aspartate has shown initial promise in combination with high-dose 5-FU infusions. Among the many new drugs tested, only tauromustine seems worthy of further study. JF - Seminars in oncology AU - Grem, J L AD - National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 17 EP - 26 VL - 18 IS - 1 Suppl 1 SN - 0093-7754, 0093-7754 KW - Fluorouracil KW - U3P01618RT KW - Index Medicus KW - Survival Rate KW - Humans KW - Fluorouracil -- administration & dosage KW - Rectal Neoplasms -- drug therapy KW - Colonic Neoplasms -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80439963?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Seminars+in+oncology&rft.atitle=Current+treatment+approaches+in+colorectal+cancer.&rft.au=Grem%2C+J+L&rft.aulast=Grem&rft.aufirst=J&rft.date=1991-02-01&rft.volume=18&rft.issue=1+Suppl+1&rft.spage=17&rft.isbn=&rft.btitle=&rft.title=Seminars+in+oncology&rft.issn=00937754&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-03-08 N1 - Date created - 1991-03-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Suppression of human immunodeficiency virus expression in chronically infected monocytic cells by glutathione, glutathione ester, and N-acetylcysteine. AN - 80439834; 1704137 AB - The effects of glutathione (GSH), glutathione ester (GSE), and N-acetyl-L-cysteine (NAC) on the induction of human immunodeficiency virus (HIV) expression were investigated in the chronically infected monocytic U1 cell line, a previously described cellular model for HIV latency. U1 cells constitutively express low levels of virus, which can be increased by phorbol 12-myristate 13-acetate (PMA), tumor necrosis factor alpha (TNF-alpha), interleukin 6 (IL-6), and other inducers. GSH, GSE, and NAC suppressed in a dose-dependent fashion the induction of HIV expression mediated by PMA, TNF-alpha, and IL-6, in the absence of cytotoxic or cytostatic effects. Reverse transcriptase activity, inducible by PMA, TNF-alpha, or IL-6, was decreased by 80-90% after pretreatment with GSH, GSE, or NAC. The induction of total HIV protein synthesis was also decreased appreciably after pretreatment with GSH, GSE, or NAC. The accumulation of HIV mRNA was substantially suppressed after pretreatment with NAC but to a lesser extent after pretreatment with GSH or GSE. Although PMA induces the expression of TNF-alpha in U1 cells, the suppressive effect of GSH, GSE, and NAC on PMA-induced HIV expression in U1 cells was not associated with the inhibition of TNF-alpha expression. The present findings, which elucidate relationships between cellular GSH and HIV expression, suggest that therapy with thiols may be of value in the treatment of HIV infection. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Kalebic, T AU - Kinter, A AU - Poli, G AU - Anderson, M E AU - Meister, A AU - Fauci, A S AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/02/01/ PY - 1991 DA - 1991 Feb 01 SP - 986 EP - 990 VL - 88 IS - 3 SN - 0027-8424, 0027-8424 KW - Antiviral Agents KW - 0 KW - Interleukin-6 KW - RNA, Messenger KW - Reverse Transcriptase Inhibitors KW - Tumor Necrosis Factor-alpha KW - Glutathione KW - GAN16C9B8O KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Acetylcysteine KW - WYQ7N0BPYC KW - Index Medicus KW - AIDS/HIV KW - Kinetics KW - Humans KW - Tumor Necrosis Factor-alpha -- pharmacology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Interleukin-6 -- pharmacology KW - RNA, Messenger -- genetics KW - Cell Line KW - HIV -- drug effects KW - HIV -- physiology KW - Acetylcysteine -- pharmacology KW - HIV -- genetics KW - Glutathione -- pharmacology KW - Glutathione -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80439834?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Suppression+of+human+immunodeficiency+virus+expression+in+chronically+infected+monocytic+cells+by+glutathione%2C+glutathione+ester%2C+and+N-acetylcysteine.&rft.au=Kalebic%2C+T%3BKinter%2C+A%3BPoli%2C+G%3BAnderson%2C+M+E%3BMeister%2C+A%3BFauci%2C+A+S&rft.aulast=Kalebic&rft.aufirst=T&rft.date=1991-02-01&rft.volume=88&rft.issue=3&rft.spage=986&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 - 1991-03-08 N1 - Date created - 1991-03-08 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Immunol. 1986 Jun 1;136(11):4220-5 [3009619] Annu Rev Biochem. 1983;52:711-60 [6137189] J Immunol. 1988 Feb 15;140(4):1117-22 [2449497] Lancet. 1989 Dec 2;2(8675):1294-8 [2574255] Immunol Lett. 1989 May;21(2):177-84 [2548955] J Immunol. 1989 Jul 15;143(2):470-5 [2544645] Proc Natl Acad Sci U S A. 1989 Apr;86(7):2336-40 [2494664] Clin Immunol Immunopathol. 1989 Mar;50(3):374-84 [2492910] Mol Cell Biol. 1989 Mar;9(3):1041-8 [2498643] Science. 1989 Jul 21;245(4915):305-8 [2665081] J Neuroimmunol. 1989 Jul;23(2):109-16 [2656753] Anal Biochem. 1989 Nov 15;183(1):16-20 [2619041] J Immunol. 1989 Jan 15;142(2):531-6 [2783441] J Virol. 1989 Oct;63(10):4404-8 [2789293] J Exp Med. 1991 Jan 1;173(1):1-5 [1985116] Proc Natl Acad Sci U S A. 1990 Dec;87(24):9943-7 [2263644] Am J Med. 1988 Sep;85(3):289-91 [3414726] FEBS Lett. 1988 Aug 29;236(2):282-6 [3410042] Biol Chem Hoppe Seyler. 1989 Feb;370(2):101-8 [2784973] Eur J Clin Pharmacol. 1989;36(2):127-31 [2721538] Science. 1989 May 5;244(4904):575-7 [2470148] N Engl J Med. 1988 Dec 15;319(24):1557-62 [3059186] J Acquir Immune Defic Syndr. 1988;1(5):436-40 [3146635] Nature. 1989 May 4;339(6219):70-3 [2654643] AIDS Res Hum Retroviruses. 1989 Apr;5(2):131-8 [2713164] Blood. 1976 Apr;47(4):545-54 [1260119] N Engl J Med. 1989 Dec 14;321(24):1673-5 [2586569] J Immunol. 1985 Oct;135(4):2740-7 [4031498] J Virol. 1986 Aug;59(2):284-91 [3016298] Proc Natl Acad Sci U S A. 1989 Aug;86(15):5974-8 [2762307] J Immunol. 1989 Feb 15;142(4):1405-9 [2915120] Science. 1988 Feb 5;239(4840):617-22 [3277274] J Virol. 1988 Jan;62(1):139-47 [3257102] Immunobiology. 1986 Aug;172(1-2):151-6 [3490430] Am J Med. 1987 Sep;83(3):608 [3661606] Arch Biochem Biophys. 1985 Jun;239(2):538-48 [4004275] Proc Natl Acad Sci U S A. 1990 May;87(9):3343-7 [1970635] Proc Natl Acad Sci U S A. 1990 Sep;87(18):7245-9 [1698293] Proc Natl Acad Sci U S A. 1990 Jun;87(12):4884-8 [2112750] AIDS Res Hum Retroviruses. 1990 Jul;6(7):919-27 [2202353] J Exp Med. 1990 Jul 1;172(1):151-8 [2193094] Proc Natl Acad Sci U S A. 1990 Jan;87(2):782-5 [2300561] J Immunol. 1990 Jan 15;144(2):480-4 [2295799] Nature. 1987 Apr 16-22;326(6114):711-3 [3031512] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Use of suramin in treatment of prostatic carcinoma refractory to conventional hormonal manipulation. AN - 80439687; 1992566 AB - Suramin and related compounds, in view of their growth factor and enzyme binding properties, represent in many respects a novel approach to the treatment of cancer. Although in this preliminary analysis of suramin use in the treatment of metastatic prostate cancer, the objective response rate does not appear impressive, much work still needs to be done to optimize suramin's administration to patients and to elucidate its various postulated mechanisms of action. The development of related compounds with more specific enzyme and growth factor antagonist properties is under way. JF - The Urologic clinics of North America AU - LaRocca, R V AU - Cooper, M R AU - Uhrich, M AU - Danesi, R AU - Walther, M M AU - Linehan, W M AU - Myers, C E AD - Medicine Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 123 EP - 129 VL - 18 IS - 1 SN - 0094-0143, 0094-0143 KW - Enzymes KW - 0 KW - Growth Substances KW - Suramin KW - 6032D45BEM KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Tumor Cells, Cultured -- drug effects KW - Humans KW - Enzymes -- metabolism KW - Growth Substances -- metabolism KW - Male KW - Adrenal Cortex -- drug effects KW - Suramin -- metabolism KW - Suramin -- adverse effects KW - Prostatic Neoplasms -- drug therapy KW - Suramin -- pharmacology KW - Suramin -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80439687?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Urologic+clinics+of+North+America&rft.atitle=Use+of+suramin+in+treatment+of+prostatic+carcinoma+refractory+to+conventional+hormonal+manipulation.&rft.au=LaRocca%2C+R+V%3BCooper%2C+M+R%3BUhrich%2C+M%3BDanesi%2C+R%3BWalther%2C+M+M%3BLinehan%2C+W+M%3BMyers%2C+C+E&rft.aulast=LaRocca&rft.aufirst=R&rft.date=1991-02-01&rft.volume=18&rft.issue=1&rft.spage=123&rft.isbn=&rft.btitle=&rft.title=The+Urologic+clinics+of+North+America&rft.issn=00940143&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-03-13 N1 - Date created - 1991-03-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Point mutation causing a single amino acid substitution in the hormone binding domain of the glucocorticoid receptor in familial glucocorticoid resistance. AN - 80439151; 1704018 AB - Familial glucocorticoid resistance is a hypertensive, hyperandrogenic disorder characterized by increased serum cortisol concentrations in the absence of stigmata of Cushing's syndrome. Our previous studies of the first reported kindred showed a two- to threefold reduction in glucocorticoid receptor-ligand binding affinity in the propositus, and a lesser reduction in affinity in his mildly affected son and nephew. Glucocorticoid receptor cDNA from these three patients was amplified by polymerase chain reaction and sequenced. The cDNA nucleotide sequence was normal, except for nucleotide 2054, which substituted valine for aspartic acid at amino acid residue 641. The propositus was homozygous while the other relatives were heterozygous for the mutation. COS-7 monkey kidney cells were cotransfected with expression vectors for either wild type or Val 641-mutant receptors, together with the reporter plasmid pMMTV-CAT. Dexamethasone increased chloramphenicol acetyltransferase activity in cells expressing wild type receptor, but had no effect in cells expressing Val 641-mutant receptors, despite similar receptor concentrations, as indicated by Western blotting. The binding affinity for dexamethasone of the Val 641-mutant receptor was threefold lower than that of the wild type receptor. These results suggest that glucocorticoid resistance in this family is due to a point mutation in the steroid-binding domain of the glucocorticoid receptor. JF - The Journal of clinical investigation AU - Hurley, D M AU - Accili, D AU - Stratakis, C A AU - Karl, M AU - Vamvakopoulos, N AU - Rorer, E AU - Constantine, K AU - Taylor, S I AU - Chrousos, G P AD - Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 680 EP - 686 VL - 87 IS - 2 SN - 0021-9738, 0021-9738 KW - Amino Acids KW - 0 KW - Glucocorticoids KW - Receptors, Glucocorticoid KW - RNA KW - 63231-63-0 KW - DNA KW - 9007-49-2 KW - Abridged Index Medicus KW - Index Medicus KW - Pedigree KW - Polymerase Chain Reaction KW - Blotting, Western KW - Base Sequence KW - Humans KW - DNA -- genetics KW - RNA -- isolation & purification KW - Molecular Sequence Data KW - Nucleic Acid Hybridization KW - Plasmids KW - Autoradiography KW - Male KW - Mutagenesis, Site-Directed KW - Amino Acids -- genetics KW - Receptors, Glucocorticoid -- genetics KW - Glucocorticoids -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80439151?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Point+mutation+causing+a+single+amino+acid+substitution+in+the+hormone+binding+domain+of+the+glucocorticoid+receptor+in+familial+glucocorticoid+resistance.&rft.au=Hurley%2C+D+M%3BAccili%2C+D%3BStratakis%2C+C+A%3BKarl%2C+M%3BVamvakopoulos%2C+N%3BRorer%2C+E%3BConstantine%2C+K%3BTaylor%2C+S+I%3BChrousos%2C+G+P&rft.aulast=Hurley&rft.aufirst=D&rft.date=1991-02-01&rft.volume=87&rft.issue=2&rft.spage=680&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 - 1991-03-11 N1 - Date created - 1991-03-11 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Recent Prog Horm Res. 1985;41:199-247 [2996089] Science. 1987 Jul 17;237(4812):268-75 [3037703] N Engl J Med. 1980 Jan 24;302(4):198-209 [6985704] J Clin Endocrinol Metab. 1976 Nov;43(5):1128-33 [186477] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] J Mol Biol. 1975 Nov 5;98(3):503-17 [1195397] Science. 1988 May 13;240(4854):889-95 [3283939] J Steroid Biochem. 1989 Feb;32(2):243-9 [2537912] Proc Natl Acad Sci U S A. 1989 Nov;86(22):8977-81 [2510172] Cell. 1989 Feb 10;56(3):335-44 [2644044] Genomics. 1989 May;4(4):610-2 [2744768] J Steroid Biochem. 1988 Jul;31(1):1-7 [2899655] J Clin Endocrinol Metab. 1987 Aug;65(2):219-26 [3597702] J Clin Invest. 1986 Nov;78(5):1270-8 [3771797] Cell. 1986 Aug 1;46(3):389-99 [3755378] Cell. 1986 Aug 29;46(5):645-52 [3742595] J Clin Endocrinol Metab. 1985 May;60(5):967-71 [3980675] Proc Natl Acad Sci U S A. 1990 Jan;87(2):658-62 [2300553] J Clin Invest. 1990 Jan;85(1):93-100 [2153155] J Clin Endocrinol Metab. 1990 Feb;70(2):503-7 [2105334] J Clin Invest. 1990 May;85(5):1522-8 [2332504] Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] J Clin Invest. 1982 Jun;69(6):1261-9 [6282933] J Biol Chem. 1988 Oct 15;263(29):15217-25 [3170579] Proc Natl Acad Sci U S A. 1987 Nov;84(21):7413-7 [2823261] Science. 1988 Jan 29;239(4839):487-91 [2448875] EMBO J. 1989 Sep;8(9):2509-17 [2573522] J Biol Chem. 1987 Jul 15;262(20):9676-80 [3597435] J Clin Endocrinol Metab. 1986 Dec;63(6):1328-33 [3782421] Gene. 1989 Apr 15;77(1):51-9 [2744487] Anal Biochem. 1987 Apr;162(1):156-9 [2440339] EMBO J. 1986 Oct;5(10):2513-22 [3780669] Nature. 1985 Dec 19-1986 Jan 1;318(6047):635-41 [2867473] Science. 1988 Dec 23;242(4886):1702-5 [2849209] J Clin Endocrinol Metab. 1986 Jun;62(6):1145-54 [3009520] J Clin Endocrinol Metab. 1983 Jun;56(6):1243-5 [6841559] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Drug-induced pemphigus: autoantibodies directed against the pemphigus antigen complexes are present in penicillamine and captopril-induced pemphigus. AN - 80435812; 1991988 AB - Pemphigus is an autoimmune blistering disease characterized by circulating autoantibodies directed against the keratinocyte cell surface. The two variants, pemphigus foliaceus and pemphigus vulgaris, can be distinguished at the molecular level by immunochemical studies. The large majority of patients with pemphigus develop the disease spontaneously; however, there is a small group of patients who develop pemphigus after treatment with certain medications, of which penicillamine and captopril are the best documented. Most patients with drug-induced pemphigus have circulating and/or tissue bound epidermal cell surface autoantibodies; however, the molecular specificity of these autoantibodies has not been studied. We performed immunoprecipitation studies utilizing extracts of 125I-labeled suction blister epidermis and the sera of three patients with drug-induced pemphigus foliaceus (two due to penicillamine and one due to captopril) and one patient with captopril-induced pemphigus vulgaris. We found that the three patients with drug-induced pemphigus foliaceus had circulating autoantibodies that are directed against the pemphigus foliaceus antigen complex and that the one patient with drug-induced pemphigus vulgaris had circulating autoantibodies that are directed against the pemphigus vulgaris antigen complex. This study demonstrates that autoantibodies from drug-induced pemphigus patients have the same antigenic specificity, on a molecular level, as do autoantibodies from other pemphigus patients. JF - The Journal of investigative dermatology AU - Korman, N J AU - Eyre, R W AU - Zone, J AU - Stanley, J R AD - Dermatology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 273 EP - 276 VL - 96 IS - 2 SN - 0022-202X, 0022-202X KW - Antigen-Antibody Complex KW - 0 KW - Autoantibodies KW - HLA-DR Antigens KW - Captopril KW - 9G64RSX1XD KW - Penicillamine KW - GNN1DV99GX KW - Index Medicus KW - Humans KW - Aged KW - Middle Aged KW - Antigen-Antibody Complex -- isolation & purification KW - Molecular Weight KW - Male KW - Female KW - Penicillamine -- adverse effects KW - Captopril -- adverse effects KW - HLA-DR Antigens -- immunology KW - Autoantibodies -- analysis KW - Pemphigus -- immunology KW - Pemphigus -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80435812?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Drug-induced+pemphigus%3A+autoantibodies+directed+against+the+pemphigus+antigen+complexes+are+present+in+penicillamine+and+captopril-induced+pemphigus.&rft.au=Korman%2C+N+J%3BEyre%2C+R+W%3BZone%2C+J%3BStanley%2C+J+R&rft.aulast=Korman&rft.aufirst=N&rft.date=1991-02-01&rft.volume=96&rft.issue=2&rft.spage=273&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 - 1991-03-12 N1 - Date created - 1991-03-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of cytochrome P450 IA2 in acetanilide 4-hydroxylation as determined with cDNA expression and monoclonal antibodies. AN - 80434939; 1989524 AB - The role of P450 IA2 in the hydroxylation of acetanilide was examined using an inhibitory monoclonal antibody (MAb) 1-7-1 and vaccinia cDNA expression producing murine P450 IA1 (mIA1), murine P450 IA2 (mIA2), or human P450 IA2 (hIA2). Acetanilide hydroxylase (AcOH) activity was measured using an HPLC method with more than 500-fold greater sensitivity than previously described procedures. This method, which does not require the use of radioactive acetanilide, was achieved by optimizing both the gradient system and the amount of enzyme needed to achieve detection by uv light. MAb 1-7-1 inhibits up to 80% of the AcOH activity in both rat liver microsomes and cDNA expressed mouse and human P450 IA2. MAb 1-7-1, which recognizes both P450 IA1 and P450 IA2, completely inhibits the aryl hydrocarbon hydroxylase (AHH) activity of cDNA expressed in IA1. The inhibition of only 80% of the AHH activity present in MC liver microsomes by MAb 1-7-1 suggests that additional P450 forms are contributing to the overall AHH activity present in methylcholanthrene (MC)-liver microsomes as MAb 1-7-1 almost completely inhibits the AHH activity of expressed mIA1. Maximal inhibition of IA2 by 1-7-1 results in an 80% decrease in acetanilide hydroxylase activity in both liver microsomes and expressed mouse and human IA2. The capacity of MAb 1-7-1 to produce identical levels of inhibition of acetanilide hydroxylase activity in rat MC microsomes (80%) and in expressed mouse (81%) and human P450 IA2 (80%) strongly suggests that P450 IA2 is the major and perhaps the only enzyme responsible for the metabolism of acetanilide. These results demonstrate the complementary utility of monoclonal antibodies and cDNA expression for defining the contribution of specific P450 enzymes to the metabolism of a given substrate. This complementary approach allows for a more precise determination of the inhibitory capacity of MAb with respect to the metabolic capacity of the target P450. JF - Archives of biochemistry and biophysics AU - Liu, G AU - Gelboin, H V AU - Myers, M J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/02/01/ PY - 1991 DA - 1991 Feb 01 SP - 400 EP - 406 VL - 284 IS - 2 SN - 0003-9861, 0003-9861 KW - Antibodies, Monoclonal KW - 0 KW - DNA, Viral KW - Acetaminophen KW - 362O9ITL9D KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Oxidoreductases KW - EC 1.- KW - Aryl Hydrocarbon Hydroxylases KW - EC 1.14.14.1 KW - Cytochrome P-450 CYP1A2 KW - acetanilide hydroxylase KW - Index Medicus KW - Sensitivity and Specificity KW - Vaccinia virus -- genetics KW - Animals KW - Humans KW - Mice KW - Mice, Inbred BALB C KW - Chromatography, High Pressure Liquid KW - Antibodies, Monoclonal -- immunology KW - Hydroxylation KW - Rats KW - Rats, Inbred Strains KW - Substrate Specificity KW - Male KW - DNA, Viral -- biosynthesis KW - Aryl Hydrocarbon Hydroxylases -- metabolism KW - Oxidoreductases -- immunology KW - Oxidoreductases -- genetics KW - Cytochrome P-450 Enzyme System -- genetics KW - Microsomes, Liver -- enzymology KW - Cytochrome P-450 Enzyme System -- immunology KW - Acetaminophen -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80434939?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Role+of+cytochrome+P450+IA2+in+acetanilide+4-hydroxylation+as+determined+with+cDNA+expression+and+monoclonal+antibodies.&rft.au=Liu%2C+G%3BGelboin%2C+H+V%3BMyers%2C+M+J&rft.aulast=Liu&rft.aufirst=G&rft.date=1991-02-01&rft.volume=284&rft.issue=2&rft.spage=400&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 - 1991-02-28 N1 - Date created - 1991-02-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Increased efficiency of retroviral-mediated gene transfer and expression in primate bone marrow progenitors after 5-fluorouracil-induced hematopoietic suppression and recovery. AN - 80433495; 1846760 AB - To define conditions for improved efficiency of retroviral-mediated gene transfer and expression in primate progenitor cells, four rhesus monkeys were treated with a 200 mg/kg intravenous bolus of 5-fluorouracil (5-FU). The kinetics of hematopoietic suppression and recovery were assessed in peripheral blood, bone marrow mononuclear cells, and bone marrow cells fractionated in an albumin density gradient. Bone marrow mononuclear cells were transduced with N2, a retroviral vector carrying the bacterial neomycin phosphotransferase gene (NPT), which confers resistance to the otherwise toxic neomycin analogue, G418. Circulating colony-forming units-granulocyte-macrophage (CFU-GM) disappeared at 2 days. CFU-GM, transducible CFU-GM, CD34+ cells, and the percent of cells in cycle decreased at 3 days in unfractionated bone marrow cells and in a light density population known to be enriched for these progenitors and for stem cells. NPT activity in the light-density fraction, marginally detectable before treatment, disappeared at 3 days as well. At day 7 the CFU-GM plating efficiency, the CD34+ cell content, and the percentage of cells in cell cycle began to increase in the light-density fraction. The NPT assay became faintly positive again but the CFU-GM were not yet transducible, implying that it was an earlier progenitor population that was dividing and differentiating. By day 15, there was a marked rebound in all of the progenitors measured, and transduction efficiency assessed by G418R CFU-GM and NPT assay rebounded to several times pretreatment levels. The data suggest that CFU-GM are optimally transduced at 15 days but that earlier progenitors are more likely cycling and transducible before 5 days, a time when a gene transfer experiment would probably have the best chance to succeed. JF - Blood AU - Wieder, R AU - Cornetta, K AU - Kessler, S W AU - Anderson, W F AD - Molecular Hematology Branch, NHLBI, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/02/01/ PY - 1991 DA - 1991 Feb 01 SP - 448 EP - 455 VL - 77 IS - 3 SN - 0006-4971, 0006-4971 KW - Phosphotransferases KW - EC 2.7.- KW - Kanamycin Kinase KW - EC 2.7.1.95 KW - Fluorouracil KW - U3P01618RT KW - Abridged Index Medicus KW - Index Medicus KW - Phosphotransferases -- genetics KW - Animals KW - Injections, Intravenous KW - Bone Marrow -- physiology KW - Cell Cycle -- physiology KW - Suppression, Genetic -- physiology KW - Phosphotransferases -- metabolism KW - Genetic Vectors -- physiology KW - Genetic Vectors -- genetics KW - Suppression, Genetic -- drug effects KW - Bone Marrow -- drug effects KW - Cell Cycle -- drug effects KW - Female KW - Transfection -- physiology KW - Hematopoiesis -- physiology KW - Stem Cells -- drug effects KW - Gene Expression Regulation, Bacterial -- physiology KW - Retroviridae -- physiology KW - Stem Cells -- physiology KW - Bone Marrow Cells KW - Fluorouracil -- administration & dosage KW - Transfection -- drug effects KW - Stem Cells -- cytology KW - Hematopoiesis -- drug effects KW - Transfection -- genetics KW - Gene Expression Regulation, Bacterial -- drug effects KW - Fluorouracil -- pharmacology KW - Retroviridae -- genetics KW - Macaca mulatta -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80433495?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Increased+efficiency+of+retroviral-mediated+gene+transfer+and+expression+in+primate+bone+marrow+progenitors+after+5-fluorouracil-induced+hematopoietic+suppression+and+recovery.&rft.au=Wieder%2C+R%3BCornetta%2C+K%3BKessler%2C+S+W%3BAnderson%2C+W+F&rft.aulast=Wieder&rft.aufirst=R&rft.date=1991-02-01&rft.volume=77&rft.issue=3&rft.spage=448&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=00064971&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-03-08 N1 - Date created - 1991-03-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Induction by ionizing radiation of the gadd45 gene in cultured human cells: lack of mediation by protein kinase C. AN - 80431413; 1990262 AB - The effect of ionizing radiation on the expression of two DNA-damage-inducible genes, designated gadd45 and gadd153, was examined in cultured human cells. These genes have previously been shown to be strongly and coordinately induced by UV radiation and alkylating agents in human and hamster cells. We found that the gadd45 but not the gadd153 gene is strongly induced by X rays in human cells. The level of gadd45 mRNA increased rapidly after X rays at doses as low as 2 Gy. After 20 Gy of X rays, gadd45 induction, as measured by increased amounts of mRNA, was similar to that produced by the most effective dose of the alkylating agent methyl methanesulfonate. No induction was seen after treatment of either human or hamster cells with 12-O-tetradecanoylphorbol-13-acetate, a known activator of protein kinase C (PKC). Therefore, gadd45 represents the only known mammalian X-ray-responsive gene whose induction is not mediated by PKC. However, induction was blocked by the protein kinase inhibitor H7, indicating that induction is mediated by some other kinase(s). Sequence analysis of human and hamster cDNA clones demonstrated that this gene has been highly conserved and encodes a novel 165-amino-acid polypeptide which is 96% identical in the two species. This gene was localized to the short arm of human chromosome 1 between p12 and p34. When induction in lymphoblast lines from four normal individuals was compared with that in lines from four patients with ataxia telangiectasia, induction by X rays of gadd45 mRNA was less in the cell lines from this cancer-prone radiosensitive disorder. Our results provide evidence for the existence of an X-ray stress response in human cells which is independent of PKC and which is abnormal in taxia telangiectasia. JF - Molecular and cellular biology AU - Papathanasiou, M A AU - Kerr, N C AU - Robbins, J H AU - McBride, O W AU - Alamo, I AU - Barrett, S F AU - Hickson, I D AU - Fornace, A J AD - Laboratory of Molecular Pharmacology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 1009 EP - 1016 VL - 11 IS - 2 SN - 0270-7306, 0270-7306 KW - gadd45 KW - RNA, Messenger KW - 0 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Humans KW - Hybrid Cells -- cytology KW - Amino Acid Sequence KW - Dose-Response Relationship, Radiation KW - RNA, Messenger -- genetics KW - Cloning, Molecular KW - X-Rays KW - Base Sequence KW - Kinetics KW - Molecular Sequence Data KW - Cell Line KW - Cricetinae KW - Chromosomes, Human, Pair 1 KW - DNA -- isolation & purification KW - Ultraviolet Rays KW - Transcription, Genetic -- drug effects KW - DNA Damage KW - DNA -- genetics KW - DNA -- radiation effects KW - Genes -- radiation effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80431413?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+cellular+biology&rft.atitle=Induction+by+ionizing+radiation+of+the+gadd45+gene+in+cultured+human+cells%3A+lack+of+mediation+by+protein+kinase+C.&rft.au=Papathanasiou%2C+M+A%3BKerr%2C+N+C%3BRobbins%2C+J+H%3BMcBride%2C+O+W%3BAlamo%2C+I%3BBarrett%2C+S+F%3BHickson%2C+I+D%3BFornace%2C+A+J&rft.aulast=Papathanasiou&rft.aufirst=M&rft.date=1991-02-01&rft.volume=11&rft.issue=2&rft.spage=1009&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 - 1991-03-04 N1 - Date created - 1991-03-04 N1 - Date revised - 2017-01-13 N1 - Gene symbol - gadd45 N1 - Genetic sequence - M73693; GENBANK; M60973; M60974; M94891; M35700; M35699; M35698; M73695; M35697; M73694 N1 - SuppNotes - Cited By: J Neurol Neurosurg Psychiatry. 1985 Sep;48(9):916-23 [3876409] Cancer Res. 1989 Apr 1;49(7):1687-92 [2466559] Int J Radiat Oncol Biol Phys. 1987 May;13(5):733-9 [3570896] Mutat Res. 1987 Oct;180(2):215-21 [3657821] Nucleic Acids Res. 1987 Oct 26;15(20):8125-48 [3313277] Chem Biol Interact. 1971 Feb;3(1):29-47 [5156325] Proc Natl Acad Sci U S A. 1980 Dec;77(12):7315-7 [6938978] In Vitro. 1981 Apr;17(4):299-307 [6263790] J Exp Med. 1982 May 1;155(5):1480-90 [6802926] Mutat Res. 1982 Jun;94(2):263-76 [7110177] Nucleic Acids Res. 1982 Dec 20;10(24):8155-70 [6819544] Mol Cell Biol. 1983 Feb;3(2):280-9 [6300662] Nucleic Acids Res. 1984 Jan 25;12(2):857-72 [6694911] Science. 1984 Feb 10;223(4636):594-7 [6695170] Nucleic Acids Res. 1983 Dec 10;11(23):8221-36 [6672765] Microbiol Rev. 1984 Mar;48(1):60-93 [6371470] J Neurol Sci. 1985 May-Jun;69(1-2):103-12 [3159854] Annu Rev Immunol. 1989;7:625-55 [2540776] Exp Cell Res. 1989 May;182(1):61-74 [2541007] Cancer Res. 1989 Jun 1;49(11):2871-8 [2720648] J Exp Med. 1989 Jul 1;170(1):321-6 [2746161] J Exp Med. 1989 Oct 1;170(4):1463-8 [2677211] Mol Cell Biol. 1989 Oct;9(10):4196-203 [2573827] Oncogene. 1989 Dec;4(12):1497-502 [2687769] Proc Natl Acad Sci U S A. 1989 Dec;86(24):10104-7 [2602359] Proc Natl Acad Sci U S A. 1990 Jan;87(1):36-40 [2153296] Am J Hum Genet. 1990 Feb;46(2):340-9 [1967901] Exp Cell Res. 1990 Jul;189(1):33-40 [2161347] Mol Cell Biol. 1990 Jul;10(7):3750-60 [2355921] Proc Natl Acad Sci U S A. 1990 Aug;87(15):5663-6 [2116003] J Biol Chem. 1990 Sep 25;265(27):16521-6 [2398062] Biotechniques. 1990 Aug;9(2):174-9 [2205249] Proc Natl Acad Sci U S A. 1988 Apr;85(8):2444-8 [3162770] J Clin Invest. 1988 May;81(5):1506-10 [3366904] Radiat Res. 1988 Sep;115(3):413-20 [3174927] Proc Natl Acad Sci U S A. 1988 Dec;85(23):8800-4 [3194391] Biochem Biophys Res Commun. 1986 Apr 14;136(1):341-7 [2423078] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Keynote address: multidrug resistance: a pleiotropic response to cytotoxic drugs. AN - 80431394; 1671383 AB - Tumor cells exposed in tissue culture to one of several different classes of antineoplastic agents, including anthracyclines, vinca alkaloids, epipodophyllotoxins, and certain antitumor antibiotics, can develop resistance to the selecting agent and cross resistance to the other classes of agents. This phenomena of multidrug resistance is generally associated with decreased drug accumulation and overexpression of a membrane glycoprotein. This membrane protein, referred to as P-glycoprotein, apparently acts as an energy-dependent drug efflux pump. Multidrug resistance in human MCF-7 breast cancer cells selected for resistance to adriamycin (AdrR MCF-7) is associated with amplification and overexpression of the mdr1 gene which encodes P-glycoprotein. A number of other changes are also seen in this resistant cell line including alterations in Phase I and Phase II drug metabolizing enzymes. Similar biochemical changes occur in a rat model for hepatocellular carcinogenesis and are associated in that system with broad spectrum resistance to hepatotoxins. The similar changes in these two models of resistance suggests that these changes might be part of a battery of genes whose expression can be altered in response to cytotoxic stress, thus rendering the cell resistant to a wide variety of cytotoxic agents. JF - International journal of radiation oncology, biology, physics AU - Fairchild, C R AU - Cowan, K H AD - Medicine Branch, Division of Cancer Treatment, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 361 EP - 367 VL - 20 IS - 2 SN - 0360-3016, 0360-3016 KW - Membrane Glycoproteins KW - 0 KW - P-Glycoprotein KW - Glutathione Transferase KW - EC 2.5.1.18 KW - Index Medicus KW - Animals KW - Tumor Cells, Cultured -- physiology KW - Tumor Cells, Cultured -- drug effects KW - Humans KW - Glutathione Transferase -- metabolism KW - Drug Resistance KW - Gene Expression Regulation, Neoplastic -- drug effects KW - Membrane Glycoproteins -- genetics KW - Neoplasms -- drug therapy KW - Neoplasms -- enzymology KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80431394?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+radiation+oncology%2C+biology%2C+physics&rft.atitle=Keynote+address%3A+multidrug+resistance%3A+a+pleiotropic+response+to+cytotoxic+drugs.&rft.au=Fairchild%2C+C+R%3BCowan%2C+K+H&rft.aulast=Fairchild&rft.aufirst=C&rft.date=1991-02-01&rft.volume=20&rft.issue=2&rft.spage=361&rft.isbn=&rft.btitle=&rft.title=International+journal+of+radiation+oncology%2C+biology%2C+physics&rft.issn=03603016&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-03-13 N1 - Date created - 1991-03-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Basement membrane increases G-protein levels and follicle-stimulating hormone responsiveness of Sertoli cell adenylyl cyclase activity. AN - 80430195; 1846579 AB - On a basement membrane substrate, Sertoli cells in culture have been shown to assume a phenotype similar to that of the in vivo differentiated cells. Sertoli cells from 10-day-old rats were cultured on plastic and on different extracellular matrix substrates [laminin, a reconstituted basement membrane (Matrigel), and a synthetic laminin peptide containing the arginine-glycine-aspartic acid (RGD) tripeptide sequence] to investigate the effects of the extracellular matrix on FSH responsiveness. Both laminin and Matrigel markedly enhanced the cAMP response to FSH and cholera toxin, indicating modifications at the level of guanine nucleotide-binding regulatory (G) proteins. Furthermore, Sertoli cell grown on either of these two substrates responded to physiological levels of FSH (25-50 ng/ml), whereas pharmacological levels of FSH (500 ng/ml) were required for cells grown on either plastic or on the RGD-containing laminin peptide. Immunoblotting of Sertoli cell plasma membranes with antibodies directed against the alpha-subunit of the stimulatory G-protein (Gs alpha) of adenylyl cyclase indicated that Sertoli cell culture on either laminin or Matrigel increased the amounts of Gs alpha. These results were further confirmed by immunoprecipitating the Gs alpha protein from the particulate fraction of [35S]methionine metabolically labeled Sertoli cells. However, Northern blot analysis using a cDNA probe for Gs alpha did not demonstrate changes in gene expression when Sertoli cells were grown on the various substrates. Immunofluorescent studies revealed that the Gs complex of adenylyl cyclase was preferentially located at the base of the Sertoli cells at the site of contact with the extracellular matrix. These data suggest that culture of epithelial Sertoli cells on basement membrane substrates enhances the Gs complex of adenylyl cyclase and the cAMP response to FSH, consistent with the more differentiated morphology and function of the cells. JF - Endocrinology AU - Dym, M AU - Lamsam-Casalotti, S AU - Jia, M C AU - Kleinman, H K AU - Papadopoulos, V AD - Laboratory of Developmental Biology and Anomalies, National Institute of Dental Research, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 1167 EP - 1176 VL - 128 IS - 2 SN - 0013-7227, 0013-7227 KW - RNA, Messenger KW - 0 KW - Colforsin KW - 1F7A44V6OU KW - Follicle Stimulating Hormone KW - 9002-68-0 KW - Cholera Toxin KW - 9012-63-9 KW - Cyclic AMP KW - E0399OZS9N KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Adenylyl Cyclases KW - EC 4.6.1.1 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Colforsin -- pharmacology KW - RNA, Messenger -- metabolism KW - Cyclic AMP -- metabolism KW - Cholera Toxin -- pharmacology KW - Radioimmunoassay KW - Male KW - Sertoli Cells -- enzymology KW - Basement Membrane -- metabolism KW - GTP-Binding Proteins -- metabolism KW - Adenylyl Cyclases -- metabolism KW - Follicle Stimulating Hormone -- pharmacology KW - GTP-Binding Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80430195?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Basement+membrane+increases+G-protein+levels+and+follicle-stimulating+hormone+responsiveness+of+Sertoli+cell+adenylyl+cyclase+activity.&rft.au=Dym%2C+M%3BLamsam-Casalotti%2C+S%3BJia%2C+M+C%3BKleinman%2C+H+K%3BPapadopoulos%2C+V&rft.aulast=Dym&rft.aufirst=M&rft.date=1991-02-01&rft.volume=128&rft.issue=2&rft.spage=1167&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=00137227&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-03-04 N1 - Date created - 1991-03-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Epidermal growth factor (EGF) stimulates association and kinase activity of Raf-1 with the EGF receptor. AN - 80429220; 1990291 AB - Raf-1 serine- and threonine-specific protein kinase is transiently activated in cells expressing the epidermal growth factor (EGF) receptor upon treatment with EGF. The stimulated EGF receptor coimmunoprecipitates with Raf-1 kinase and mediates protein kinase C-independent phosphorylation of Raf-1 on serine residues. Hyperphosphorylated Raf-1 has lower mobility on sodium dodecyl sulfate gels and has sixfold-increased activity in immunocomplex kinase assay with histone H1 or Raf-1 sequence-derived peptide as a substrate. Raf-1 activation requires kinase-active EGF receptor; a point mutant lacking tyrosine kinase activity in inactive in Raf-1 coupling and association. It is noteworthy that tyrosine phosphorylation of c-Raf-1 induced by EGF was not detected in these cells. These observations suggest that Raf-1 kinase may act as an important downstream effector of EGF signal transduction. JF - Molecular and cellular biology AU - App, H AU - Hazan, R AU - Zilberstein, A AU - Ullrich, A AU - Schlessinger, J AU - Rapp, U AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick, Maryland 21702. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 913 EP - 919 VL - 11 IS - 2 SN - 0270-7306, 0270-7306 KW - Amino Acids KW - 0 KW - Antigen-Antibody Complex KW - Immune Sera KW - Proto-Oncogene Proteins KW - Epidermal Growth Factor KW - 62229-50-9 KW - Protein Kinases KW - EC 2.7.- KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Proto-Oncogene Proteins c-raf KW - EC 2.7.11.1 KW - Index Medicus KW - Animals KW - Phosphorylation KW - Transfection KW - Kinetics KW - Amino Acids -- analysis KW - Molecular Sequence Data KW - Mice KW - Amino Acid Sequence KW - Antigen-Antibody Complex -- analysis KW - Cell Line KW - Protein Kinases -- metabolism KW - Receptor, Epidermal Growth Factor -- metabolism KW - Receptor, Epidermal Growth Factor -- genetics KW - Proto-Oncogene Proteins -- metabolism KW - Epidermal Growth Factor -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80429220?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Epidermal+growth+factor+%28EGF%29+stimulates+association+and+kinase+activity+of+Raf-1+with+the+EGF+receptor.&rft.au=App%2C+H%3BHazan%2C+R%3BZilberstein%2C+A%3BUllrich%2C+A%3BSchlessinger%2C+J%3BRapp%2C+U&rft.aulast=App&rft.aufirst=H&rft.date=1991-02-01&rft.volume=11&rft.issue=2&rft.spage=913&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 - 1991-03-04 N1 - Date created - 1991-03-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Mol Cell Biol. 1990 Jul;10(7):3828-33 [2192265] Cell. 1990 May 18;61(4):623-34 [2344614] J Biol Chem. 1990 Jul 25;265(21):12131-4 [2197271] EMBO J. 1990 Nov;9(11):3649-57 [1698619] J Biol Chem. 1990 Oct 25;265(30):18472-80 [2170413] J Biol Chem. 1990 Nov 15;265(32):19812-7 [1700980] Anal Biochem. 1976 May 7;72:248-54 [942051] Nature. 1979 Jun 21;279(5715):679-85 [221835] Proc Natl Acad Sci U S A. 1980 Mar;77(3):1311-5 [6246487] Methods Enzymol. 1983;99:387-402 [6196603] Proc Natl Acad Sci U S A. 1985 Jul;82(13):4369-73 [3892533] J Biol Chem. 1986 Jan 5;261(1):350-5 [3941081] Nucleic Acids Res. 1986 Jan 24;14(2):1009-15 [3003687] Proc Natl Acad Sci U S A. 1986 Mar;83(6):1733-7 [3081899] Nature. 1986 Apr 10-16;320(6062):540-3 [2938016] Science. 1986 Jul 18;233(4761):305-12 [3014651] J Biol Chem. 1986 Sep 25;261(27):12490-7 [3017977] Annu Rev Cell Biol. 1985;1:1-39 [2881559] Cell. 1987 Oct 23;51(2):199-209 [3499230] EMBO J. 1987 Sep;6(9):2669-76 [2824188] Proc Natl Acad Sci U S A. 1988 Jan;85(2):406-10 [3257566] Biochim Biophys Acta. 1988 Feb 28;949(2):233-9 [3277669] Mol Cell Biol. 1987 Dec;7(12):4568-71 [3501826] Mol Cell Biol. 1988 Jun;8(6):2651-4 [3043188] J Biol Chem. 1988 Sep 5;263(25):12721-7 [2842341] Proc Natl Acad Sci U S A. 1988 Dec;85(23):8855-9 [3057494] J Biol Chem. 1989 Jan 15;264(2):1293-7 [2910854] Proc Natl Acad Sci U S A. 1989 Mar;86(5):1568-72 [2466293] Cell. 1989 Jun 30;57(7):1101-7 [2472218] Cell. 1989 Jun 30;57(7):1109-22 [2472219] Mol Cell Biol. 1989 May;9(5):2247-50 [2501665] Cold Spring Harb Symp Quant Biol. 1988;53 Pt 1:173-84 [2978288] Cell. 1989 Aug 25;58(4):649-57 [2475255] Proc Natl Acad Sci U S A. 1989 Sep;86(18):6940-3 [2550926] J Biol Chem. 1989 Dec 15;264(35):20855-8 [2556385] Mol Cell Biol. 1990 Feb;10(2):435-41 [2153914] Oncogene. 1990 Mar;5(3):345-51 [1690378] Nature. 1990 Mar 29;344(6265):463-6 [2157161] Cell. 1990 Apr 20;61(2):203-12 [2158859] Mol Cell Biol. 1990 Jun;10(6):2503-12 [2188091] J Biol Chem. 1990 Jul 25;265(21):12115-8 [2197270] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Treatment of advanced-stage massive mediastinal Hodgkin's disease: the case for combined modality treatment. AN - 80428516; 1988570 AB - In the initial series of 198 patients treated at the National Cancer Institute (NCI) with mechlorethamine, vincristine, procarbazine, and prednisone (MOPP) chemotherapy for Hodgkin's disease, a review of presenting chest radiographs available on 192 of these patients showed 49 patients with mediastinal masses greater than one third the greatest posteroanterior chest diameter. Five patients had stage IIB disease, and 44 had stage III or IV disease. Thirty-five (71%) patients achieved a complete remission with MOPP chemotherapy. Fourteen (40%) of the complete responders relapsed, but four of these achieved durable remissions in response to subsequent therapy. Thirty (61%) patients have died (14 induction failures, nine relapsed patients, seven complete responders in remission). Thus, with a median follow-up of 20 years (range, 15 to 23), the overall survival for the group is 39%, and the disease-free survival for the complete responders is 60%. A subset of 10 patients received mantle radiation therapy after maximal response to MOPP. One of these patients failed to achieve complete remission, but among the nine complete responders only one has relapsed. In contrast, 13 of 26 (50%) patients achieving a complete response to MOPP alone have relapsed (P2 = .0536). Although MOPP alone was not prospectively compared with MOPP plus radiation therapy in the treatment of advanced-stage massive mediastinal Hodgkin's disease in this series, the retrospective analysis shows a nearly significant difference in disease-free survival favoring combined modality treatment. The difference in tumor mortality between MOPP-treated (44%) and combined modality-treated patients (80%) was also nearly significant (P2 = .055). However, overall survival differences between patients treated with MOPP alone and those treated with combined modality therapy were not significantly different (P2 = 0.23) because of the mortality related to late complications of combined modality treatment. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Longo, D L AU - Russo, A AU - Duffey, P L AU - Hubbard, S M AU - Glatstein, E AU - Hill, J B AU - Jaffe, E S AU - Young, R C AU - DeVita, V T AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, MD. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 227 EP - 235 VL - 9 IS - 2 SN - 0732-183X, 0732-183X KW - Procarbazine KW - 35S93Y190K KW - Mechlorethamine KW - 50D9XSG0VR KW - Vincristine KW - 5J49Q6B70F KW - Prednisone KW - VB0R961HZT KW - Index Medicus KW - Mechlorethamine -- administration & dosage KW - Neoplasm Staging KW - Combined Modality Therapy KW - Humans KW - Vincristine -- administration & dosage KW - Child KW - Recurrence KW - Procarbazine -- administration & dosage KW - Survival Rate KW - Adult KW - Follow-Up Studies KW - Middle Aged KW - Adolescent KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Prednisone -- administration & dosage KW - Female KW - Male KW - Remission Induction KW - Hodgkin Disease -- pathology KW - Hodgkin Disease -- therapy KW - Hodgkin Disease -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80428516?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Treatment+of+advanced-stage+massive+mediastinal+Hodgkin%27s+disease%3A+the+case+for+combined+modality+treatment.&rft.au=Longo%2C+D+L%3BRusso%2C+A%3BDuffey%2C+P+L%3BHubbard%2C+S+M%3BGlatstein%2C+E%3BHill%2C+J+B%3BJaffe%2C+E+S%3BYoung%2C+R+C%3BDeVita%2C+V+T&rft.aulast=Longo&rft.aufirst=D&rft.date=1991-02-01&rft.volume=9&rft.issue=2&rft.spage=227&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 - 1991-02-28 N1 - Date created - 1991-02-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A role for the interleukin 1 receptor in the synergistic antitumor effects of human interleukin 1 alpha and etoposide against human melanoma cells. AN - 80425159; 1824825 AB - To investigate the possibility that anticancer drugs combined with cytokines may show increased activity, human tumor cells were treated with combinations of human recombinant interleukin 1 alpha (rIL-1 alpha) and etoposide (VP-16). The cytotoxicity of these combinations was evaluated by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide assay using rIL-1 alpha-sensitive A375-C6 melanoma cells and A375-C5 cells, a clonal variant line that is resistant to IL-1 alpha. Data were analyzed for synergism by the median effect principle of T-C. Chou and P. Talalay (J. Biol. Chem., 252: 6438-6442, 1977). At a dose ratio of VP-16 to rIL-1 alpha of 12 nM:1 unit/ml in either simultaneous or sequential exposure (VP-16 first), the calculated combination index values indicated synergistic cytotoxicity toward both A375-C6 cells and A375-C5 cells. IL-1 alpha treatment 24 h prior to VP-16 exposure had no advantage over simultaneous treatment. Surface IL-1 alpha receptors on both A375-C6 and A375-C5 cells were measured using 125I-radiolabeled rIL-1 alpha binding; A375-C6 cells had 701 +/- 128 (SD) receptor molecules/cell and A375-C5 cells only had 58 +/- 33 receptor molecules/cell. The dissociation constants for IL-1 alpha were similar in both cell types (19 +/- 6 pM for A375-C6 and 17 +/- 2 pM for A375-C5). The specific binding of rIL-1 alpha to the surface IL-1 alpha receptors of both sensitive and resistant cells was significantly increased in a dose-dependent fashion by the prior treatment with VP-16 (1.75-fold on A375-C6 cells and 3.5-fold on A375-C5 cells). VP-16 also enhanced the internalization of receptor-bound rIL-1 alpha, suggesting that a possible mechanism of the synergistic cytotoxicity of rIL-1 alpha and VP-16 might be related to the modulation of rIL-1 alpha receptors by VP-16, resulting in increased internalization of rIL-1 alpha. JF - Cancer research AU - Usui, N AU - Mimnaugh, E G AU - Sinha, B K AD - Clinical Pharmacology Branch, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1991/02/01/ PY - 1991 DA - 1991 Feb 01 SP - 769 EP - 774 VL - 51 IS - 3 SN - 0008-5472, 0008-5472 KW - Interleukin-1 KW - 0 KW - Receptors, Immunologic KW - Receptors, Interleukin-1 KW - Recombinant Proteins KW - Etoposide KW - 6PLQ3CP4P3 KW - Index Medicus KW - Drug Administration Schedule KW - Recombinant Proteins -- pharmacology KW - Tumor Cells, Cultured -- metabolism KW - Recombinant Proteins -- metabolism KW - Humans KW - Drug Synergism KW - Melanoma -- metabolism KW - Recombinant Proteins -- administration & dosage KW - Etoposide -- pharmacology KW - Receptors, Immunologic -- drug effects KW - Interleukin-1 -- pharmacology KW - Interleukin-1 -- metabolism KW - Interleukin-1 -- administration & dosage KW - Etoposide -- administration & dosage KW - Receptors, Immunologic -- metabolism KW - Etoposide -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80425159?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=A+role+for+the+interleukin+1+receptor+in+the+synergistic+antitumor+effects+of+human+interleukin+1+alpha+and+etoposide+against+human+melanoma+cells.&rft.au=Usui%2C+N%3BMimnaugh%2C+E+G%3BSinha%2C+B+K&rft.aulast=Usui&rft.aufirst=N&rft.date=1991-02-01&rft.volume=51&rft.issue=3&rft.spage=769&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 - 1991-02-28 N1 - Date created - 1991-02-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dose response of hepatic and renal DNA synthetic rates to continuous exposure of bromodeoxyuridine (BrdU) via slow-release pellets or osmotic minipumps in male B6C3F1 mice. AN - 80422841; 1987261 AB - We studied the use of acute and chronic 5-bromo-2'-deoxyuridine (BrdU) administration for detection of DNA-synthesizing cells in the liver and kidney of B6C3F1 male mice. Six-week-old mice were exposed to BrdU either acutely with a single-pulse (IP) injection 1 hr before sacrifice or chronically with the use of slow-release pellets or osmotic minipumps at one of four BrdU dose rates. Pellets (2.5, 10, 25, and 50 mg) and minipumps (2.5 and 10 mg equivalents) were implanted subcutaneously on the backs of the animals 4 or 7 days before sacrifice). BrdU incorporation into DNA was determined by immunohistochemistry using an anti-BrdU antibody. Mice chronically exposed to BrdU demonstrated increased levels of nuclear labeling compared with those receiving a single-pulse injection. No time-related increases in nuclear labeling were detected in hepatocytes or renal tubule cells of mice exposed to BrdU pellets and in the kidneys of mice receiving BrdU minipumps at the 7-day compared with the 4-day time point. In some cases, the labeling indices at 7 days were significantly decreased compared with those at 4 days. In contrast, a time-related increase in nuclear labeling was seen in hepatocytes and Kupffer cells of mice exposed to BrdU minipumps. Therefore, the method used to administer BrdU chronically to the animal appears to play an important role in presenting the true proliferative scenario in cell kinetic studies. Our findings also provide evidence for an effect of BrdU on normal proliferation rates in these tissues. JF - The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society AU - Weghorst, C M AU - Henneman, J R AU - Ward, J M AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland 21701. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 177 EP - 184 VL - 39 IS - 2 SN - 0022-1554, 0022-1554 KW - DNA KW - 9007-49-2 KW - Bromodeoxyuridine KW - G34N38R2N1 KW - Index Medicus KW - Body Weight KW - Animals KW - Dose-Response Relationship, Drug KW - Mice KW - Organ Size KW - Immunohistochemistry KW - Male KW - Osmosis KW - Kidney -- metabolism KW - Liver -- drug effects KW - Kidney -- drug effects KW - Liver -- metabolism KW - Bromodeoxyuridine -- toxicity KW - DNA -- biosynthesis KW - Bromodeoxyuridine -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80422841?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+histochemistry+and+cytochemistry+%3A+official+journal+of+the+Histochemistry+Society&rft.atitle=Dose+response+of+hepatic+and+renal+DNA+synthetic+rates+to+continuous+exposure+of+bromodeoxyuridine+%28BrdU%29+via+slow-release+pellets+or+osmotic+minipumps+in+male+B6C3F1+mice.&rft.au=Weghorst%2C+C+M%3BHenneman%2C+J+R%3BWard%2C+J+M&rft.aulast=Weghorst&rft.aufirst=C&rft.date=1991-02-01&rft.volume=39&rft.issue=2&rft.spage=177&rft.isbn=&rft.btitle=&rft.title=The+journal+of+histochemistry+and+cytochemistry+%3A+official+journal+of+the+Histochemistry+Society&rft.issn=00221554&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-02-21 N1 - Date created - 1991-02-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of the cis elements involved in basal and E2-transactivated expression of the bovine papillomavirus P2443 promoter. AN - 80419332; 1846195 AB - Transcriptional transactivation and repression by the viral E2 proteins are important regulatory mechanisms for the papillomaviruses. In the bovine papillomavirus type 1 (BPV-1), several viral promoters can be transactivated by E2 through E2-dependent enhancer elements located in the viral long control region (LCR), including promoters involved in E2 expression itself. This report demonstrates that the BPV-1 P2443 promoter is transactivated by E2-responsive elements in the LCR and that this promoter is responsible for a major part of the expression of the E2 and E5 gene products. Characterization of the cis elements involved in P2443 regulation indicated that the single E2-binding site directly upstream of P2443 is not required for either the E2 transactivation or for any E2 repression of the basal or transactivated activity of this promoter. Therefore, cooperative interactions between E2 bound at the LCR and E2 bound near P2443 do not have any role in the regulation of this promoter. Further definition of the cis regulatory elements of this promoter indicated that a binding site for the transcriptional factor Sp1 exists directly upstream of the P2443 TATA box and is critical for the basal level of transcription from this promoter. Disruption of this Sp1 site eliminated P2443 promoter activity in transient expression assays for E2 and E5 and resulted in a loss of transforming activity when introduced into the full viral genome. JF - Journal of virology AU - Spalholz, B A AU - Vande Pol, S B AU - Howley, P M AD - Laboratory of Tumor Virus Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 743 EP - 753 VL - 65 IS - 2 SN - 0022-538X, 0022-538X KW - DNA, Viral KW - 0 KW - DNA-Binding Proteins KW - E2 protein, Bovine papillomavirus KW - Oligonucleotide Probes KW - Viral Proteins KW - Index Medicus KW - Mutagenesis, Site-Directed KW - HeLa Cells -- metabolism KW - Animals KW - Base Sequence KW - Cell Nucleus -- metabolism KW - Humans KW - Molecular Sequence Data KW - Plasmids KW - DNA, Viral -- genetics KW - Cell Line KW - DNA, Viral -- metabolism KW - Promoter Regions, Genetic KW - Viral Proteins -- metabolism KW - Transcription, Genetic KW - Transcriptional Activation KW - DNA-Binding Proteins -- metabolism KW - Bovine papillomavirus 1 -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80419332?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Characterization+of+the+cis+elements+involved+in+basal+and+E2-transactivated+expression+of+the+bovine+papillomavirus+P2443+promoter.&rft.au=Spalholz%2C+B+A%3BVande+Pol%2C+S+B%3BHowley%2C+P+M&rft.aulast=Spalholz&rft.aufirst=B&rft.date=1991-02-01&rft.volume=65&rft.issue=2&rft.spage=743&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 - 1991-02-19 N1 - Date created - 1991-02-19 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Genes Dev. 1989 Apr;3(4):510-26 [2542129] EMBO J. 1987 Jan;6(1):145-52 [3034572] Nature. 1985 May 2-8;315(6014):73-5 [2986013] Cell. 1989 Dec 1;59(5):827-36 [2512012] J Virol. 1989 Oct;63(10):4317-24 [2476572] EMBO J. 1988 Sep;7(9):2823-9 [2846285] EMBO J. 1988 Sep;7(9):2815-22 [2846284] J Virol. 1988 Oct;62(10):3608-13 [2843663] J Virol. 1988 Nov;62(11):4009-15 [2845119] Cell. 1985 Aug;42(1):183-91 [2990724] Nature. 1985 Dec 12-18;318(6046):575-7 [2999614] EMBO J. 1988 Dec 20;7(13):4245-53 [2854060] J Virol. 1987 Jul;61(7):2240-4 [2884331] Nucleic Acids Res. 1987 Dec 23;15(24):10267-84 [2827118] J Virol. 1988 Jun;62(6):1925-31 [2835497] J Virol. 1988 Aug;62(8):2994-3002 [2839716] EMBO J. 1988 Feb;7(2):533-9 [2835232] EMBO J. 1988 Feb;7(2):525-31 [2835231] J Virol. 1989 Apr;63(4):1775-82 [2538656] J Virol. 1989 Apr;63(4):1743-55 [2538655] J Virol. 1989 Jul;63(7):3151-4 [2542621] Genes Dev. 1989 Jan;3(1):38-48 [2540059] Proc Natl Acad Sci U S A. 1989 Jan;86(2):510-4 [2536165] Cell. 1988 Feb 12;52(3):303-5 [2894251] Science. 1988 Dec 9;242(4884):1418-20 [3201230] Proc Natl Acad Sci U S A. 1984 Dec;81(24):7880-4 [6096867] J Virol. 1984 Nov;52(2):377-88 [6092667] Cell. 1987 Dec 24;51(6):1079-90 [3319186] Nature. 1987 Jun 4-10;327(6121):369-70 [3587357] Mol Cell Biol. 1990 Aug;10(8):4431-7 [2164642] J Virol. 1990 Aug;64(8):3927-37 [2164604] J Virol. 1990 Jun;64(6):2849-59 [2159546] Genes Dev. 1990 Jan;4(1):123-36 [2155158] Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] Nucleic Acids Res. 1983 Mar 11;11(5):1475-89 [6828386] Proc Natl Acad Sci U S A. 1982 Nov;79(21):6453-7 [6292901] Cell. 1983 Nov;35(1):79-87 [6313230] Virology. 1982 May;119(1):22-34 [6280384] Proc Natl Acad Sci U S A. 1982 Dec;79(23):7147-51 [6296820] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Proc Natl Acad Sci U S A. 1988 Aug;85(16):5864-8 [2842752] EMBO J. 1988 Dec 1;7(12):3807-16 [2850174] Biochemistry. 1979 Nov 27;18(24):5294-9 [518835] Proc Natl Acad Sci U S A. 1987 Mar;84(5):1215-8 [3029771] J Virol. 1986 Nov;60(2):626-34 [3021996] Nature. 1987 Jan 1-7;325(6099):70-3 [3025749] Proc Natl Acad Sci U S A. 1986 Mar;83(6):1797-801 [3006073] J Virol. 1986 Feb;57(2):475-80 [3003380] Virology. 1986 Apr 15;150(1):221-30 [3006336] EMBO J. 1987 Apr;6(4):1027-35 [3036488] J Virol. 1987 Jul;61(7):2128-37 [3035214] Cell. 1987 Jul 3;50(1):69-78 [3036366] Proc Natl Acad Sci U S A. 1985 Feb;82(4):1030-4 [2983327] J Mol Biol. 1985 Apr 20;182(4):541-54 [2989533] Nature. 1988 Oct 20;335(6192):683-9 [3050531] Genes Dev. 1988 Mar;2(3):267-81 [3288540] Nucleic Acids Res. 1989 Apr 25;17(8):2959-72 [2542891] J Virol. 1990 Nov;64(11):5420-9 [2170679] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effect of suramin on human prostate cancer cells in vitro. AN - 80418235; 1824865 AB - Suramin, a polyanionic compound with known antiparasitic activity, has been shown to be adrenocorticolytic in primates and to have clinical efficacy in the treatment of patients with metastatic prostate cancer refractory to conventional hormonal manipulation. To better characterize the activity of suramin on prostate cancer biology, we studied the effect of the drug on plasma adrenal androgens of patients and on the human prostate adenocarcinoma cell lines PC-3, DU 145 and LNCaP-FGC. Five cancer patients treated with suramin had an approximate 40% decline in circulating androstenedione, dehydroepiandrosterone and dehydroepiandrosterone sulfate levels. The drug inhibited the colony formation in two of the three cell lines at concentrations clinically achievable in humans without excessive drug-related toxicity. The presence of suramin 300 micrograms./ml. partially inhibited the growth stimulatory effect of testosterone and basic fibroblast growth factor, but not that of epidermal growth factor. The cellular concentration of suramin following exposure to a single dose increases linearly over time in each of the cell lines with LNCaP-FGC accumulating the highest levels of the drug; cellular levels of suramin, not androgen or growth factor sensitivity, correlated with the sensitivity to the drug. The concentrations of prostatic acid phosphatase and prostatic specific antigen released by LNCaP-FGC cells in cell culture medium declined in the presence of increasing levels of suramin in a manner which exceeded the decrease in cell number. We conclude that suramin, aside from decreasing circulating androgens through its adrenocorticolytic effect, is also capable exerting a direct inhibitory effect on cell proliferation of prostate cancer cells, and interfere at a cellular level with the growth stimulatory effects of exogenous testosterone and basic fibroblast growth factor. JF - The Journal of urology AU - La Rocca, R V AU - Danesi, R AU - Cooper, M R AU - Jamis-Dow, C A AU - Ewing, M W AU - Linehan, W M AU - Myers, C E AD - Medicine Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 393 EP - 398 VL - 145 IS - 2 SN - 0022-5347, 0022-5347 KW - Antineoplastic Agents KW - 0 KW - Androstenedione KW - 409J2J96VR KW - Dehydroepiandrosterone KW - 459AG36T1B KW - Dehydroepiandrosterone Sulfate KW - 57B09Q7FJR KW - Suramin KW - 6032D45BEM KW - Abridged Index Medicus KW - Index Medicus KW - Tumor Cells, Cultured -- drug effects KW - Humans KW - In Vitro Techniques KW - Dehydroepiandrosterone -- blood KW - Dehydroepiandrosterone -- analogs & derivatives KW - Male KW - Cell Line KW - Androstenedione -- blood KW - Prostatic Neoplasms -- pathology KW - Prostatic Neoplasms -- drug therapy KW - Suramin -- pharmacology KW - Adenocarcinoma -- drug therapy KW - Suramin -- therapeutic use KW - Adenocarcinoma -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80418235?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+urology&rft.atitle=Effect+of+suramin+on+human+prostate+cancer+cells+in+vitro.&rft.au=La+Rocca%2C+R+V%3BDanesi%2C+R%3BCooper%2C+M+R%3BJamis-Dow%2C+C+A%3BEwing%2C+M+W%3BLinehan%2C+W+M%3BMyers%2C+C+E&rft.aulast=La+Rocca&rft.aufirst=R&rft.date=1991-02-01&rft.volume=145&rft.issue=2&rft.spage=393&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+urology&rft.issn=00225347&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-02-27 N1 - Date created - 1991-02-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Retinoids enhance lectin binding to gp130, a glycoprotein of NIH-3T3 cells: correlation with cell growth and adhesion. AN - 80417116; 1988285 AB - Our previous work has shown that retinoic acid (RA) enhances fibroblast cell attachment to plastic and to laminin. The treatment of NIH-3T3 cells with RA for 2 days also caused a reproducible increase in the binding of the lectin Phaseolus vulgaris leukoagglutinin (PHA-L) to a glycoprotein of molecular weight 130,000 (gp130) as judged by SDS-PAGE analysis. This finding is consistent with an increased number of beta-1,6-linked N-acetylglucosaminyl residues on gp130. Of the 11 additional lectins tested Ricinus communis agglutinin I (RCA), Phaseolus vulgaris erythroagglutinin (PHA-E), soybean agglutinin (SBA), and succinylated wheat germ agglutinin (sWGA) showed a significant increase in binding specifically to gp130. Similar to RA, 13-cis-RA and 3,5-di-tert-butyl-4-chalcone carboxylic acid, a synthetic retinoid, also increased PHA-L binding to gp130; they also enhanced cell adhesiveness and inhibited cell growth. N-(4-Hydroxyphenyl)-all-trans-retinamide and thyroxine failed to influence adhesion and did not increase PHA-L binding to gp130. Moreover these compounds also failed to inhibit cell growth and to alter the morphology of the cultured cells. Since trypsin is utilized to remove cells from the culture dishes before they are used in the attachment assay to laminin, we studied the effect of this trypsinization step on PHA-L binding to gp130. Trypsin reduced PHA-L binding thus suggesting cell surface localization of gp130. After trypsin treatment RA-treated cells still showed enhanced PHA-L binding compared to dimethyl sulfoxide (DMSO) control. In conclusion RA-induced cell adhesiveness and growth inhibition are accompanied by an increase in the PHA-L, PHA-E, SBA, RCA, and sWGA binding to gp130. The sensitivity of gp130 to trypsin suggests that it is a cell surface glycoprotein. JF - Experimental cell research AU - Cai, D AU - Webber, M M AU - De Luca, L M AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 366 EP - 372 VL - 192 IS - 2 SN - 0014-4827, 0014-4827 KW - Membrane Glycoproteins KW - 0 KW - Receptors, Mitogen KW - Tretinoin KW - 5688UTC01R KW - Thyroxine KW - Q51BO43MG4 KW - Index Medicus KW - Animals KW - Thyroxine -- pharmacology KW - Cell Adhesion -- physiology KW - Cell Division -- physiology KW - Molecular Weight KW - Cell Line KW - Tretinoin -- pharmacology KW - Membrane Glycoproteins -- drug effects KW - Receptors, Mitogen -- drug effects KW - Membrane Glycoproteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80417116?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Retinoids+enhance+lectin+binding+to+gp130%2C+a+glycoprotein+of+NIH-3T3+cells%3A+correlation+with+cell+growth+and+adhesion.&rft.au=Cai%2C+D%3BWebber%2C+M+M%3BDe+Luca%2C+L+M&rft.aulast=Cai&rft.aufirst=D&rft.date=1991-02-01&rft.volume=192&rft.issue=2&rft.spage=366&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 - 1991-02-25 N1 - Date created - 1991-02-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Primary treatment of large and massive adult sarcomas with iododeoxyuridine and aggressive hyperfractionated irradiation. AN - 80361520; 1985751 AB - For a decade, the authors have experimented with treatment for unresectable adult soft tissue and bony sarcomas. Over the last 6 years, they have combined hyperfractionated radiation therapy and intravenous iododeoxyuridine as a radiosensitizer, in regimens designed to minimize toxicity and permit delivery of aggressive radiation therapy. Patients with solitary lesions and those with metastasis (38%) were treated in the hope of both potential cure in some and durable palliation in others. The most formidable of these cancers have been those that are large or massive, often requiring five or more fields and extensive treatment planning. The authors report results from 36 patients with large unresectable sarcomas (tumors ranging from 5 to 35 cm; average 14 cm) treated with hyperfractionated radiation therapy, with a minimum follow-up of 1 year, follow-up of 4 or more years (in 50%), or follow-up until death. Overall local control has been 60%, with control of 66% of lesions from 5 to 9 cm, 63% of those from 10 to 14 cm, 63% of those from 15 to 19 cm, and 57% of those greater than 20 to 40 cm. Morbidity has been modest. This experience compares favorably with the authors' earlier trials with misonidazole, and toxicity has been reduced considerably. JF - Cancer AU - Goffman, T AU - Tochner, Z AU - Glatstein, E AD - National Institutes of Health, National Cancer Institute, Radiation Oncology Branch, Room Bethesda, MD 20892. Y1 - 1991/02/01/ PY - 1991 DA - 1991 Feb 01 SP - 572 EP - 576 VL - 67 IS - 3 SN - 0008-543X, 0008-543X KW - Idoxuridine KW - LGP81V5245 KW - Abridged Index Medicus KW - Index Medicus KW - Survival Rate KW - Combined Modality Therapy KW - Radiotherapy Dosage KW - Humans KW - Adult KW - Platelet Count -- drug effects KW - Aged KW - Pilot Projects KW - Middle Aged KW - Follow-Up Studies KW - Male KW - Female KW - Sarcoma -- radiotherapy KW - Soft Tissue Neoplasms -- radiotherapy KW - Soft Tissue Neoplasms -- mortality KW - Soft Tissue Neoplasms -- pathology KW - Sarcoma -- mortality KW - Bone Neoplasms -- mortality KW - Bone Neoplasms -- radiotherapy KW - Bone Neoplasms -- pathology KW - Idoxuridine -- therapeutic use KW - Idoxuridine -- adverse effects KW - Sarcoma -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80361520?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Primary+treatment+of+large+and+massive+adult+sarcomas+with+iododeoxyuridine+and+aggressive+hyperfractionated+irradiation.&rft.au=Goffman%2C+T%3BTochner%2C+Z%3BGlatstein%2C+E&rft.aulast=Goffman&rft.aufirst=T&rft.date=1991-02-01&rft.volume=67&rft.issue=3&rft.spage=572&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-02-14 N1 - Date created - 1991-02-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Redirecting Pseudomonas exotoxin. AN - 72494136; 1954341 AB - Pseudomonas exotoxin (PE) is a three-domain bacterial toxin that kills mammalian cells by gaining entry to the cytosol and inactivating protein synthesis. The pathway of toxin entry includes binding to a surface receptor, internalization via coated pits and endosomes, proteolytic processing, reduction of disulfide bonds and finally the translocation of an enzymatically active C-terminal fragment to the cytosol. Once in the cytosol this fragment inhibits protein synthesis by ADP ribosylating elongation factor 2. Because of its potency PE and its derivatives have been directed to kill various target cells. It is hoped this strategy will lead to the development of a novel kind of therapeutic agent for the treatment of various human diseases including cancer, AIDS and various immunological disorders. JF - Seminars in cell biology AU - FitzGerald, D AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 31 EP - 37 VL - 2 IS - 1 SN - 1043-4682, 1043-4682 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - Immunotoxins KW - Protein Synthesis Inhibitors 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 - Endocytosis KW - Cytosol -- metabolism KW - Structure-Activity Relationship KW - Bacterial Toxins -- genetics KW - Exotoxins -- genetics KW - Pseudomonas aeruginosa -- genetics KW - Bacterial Toxins -- metabolism KW - Exotoxins -- metabolism KW - Bacterial Toxins -- chemistry KW - Exotoxins -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72494136?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+cell+biology&rft.atitle=Redirecting+Pseudomonas+exotoxin.&rft.au=FitzGerald%2C+D%3BPastan%2C+I&rft.aulast=FitzGerald&rft.aufirst=D&rft.date=1991-02-01&rft.volume=2&rft.issue=1&rft.spage=31&rft.isbn=&rft.btitle=&rft.title=Seminars+in+cell+biology&rft.issn=10434682&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-02 N1 - Date created - 1992-01-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutations in diphtheria toxin to improve immunotoxin selectivity and understand toxin entry into cells. AN - 72492369; 1954342 AB - Diphtheria toxin can be used to selectively kill target cells by coupling it to cell-type-specific binding moieties such as monoclonal antibodies. These reagents have important potential in treating diseases, selectively ablating cell populations in experimental systems and for understanding how proteins cross membranes. Point mutations and deletions in the diphtheria toxin gene have been used to identify and localize regions of diphtheria toxin involved in cell killing. Mutations have been identified that prevent binding of the toxin to a cell surface receptor yet these mutations do not inhibit the cell entry activity or the intracellular cytotoxicity of the toxin. Coupling of these mutant toxins to new, cell-type-specific binding moieties yields potent reagents with up to 200,000-fold selectivity between target and nontarget cells. Mutations and deletions in the membrane transport regions are beginning to explain how the toxin enters cells and may also help in the design of more effective therapeutic reagents. JF - Seminars in cell biology AU - Youle, R J AD - Biochemistry Section, NINDS, NIH Bethesda, MD 20892. Y1 - 1991/02// PY - 1991 DA - February 1991 SP - 39 EP - 45 VL - 2 IS - 1 SN - 1043-4682, 1043-4682 KW - Diphtheria Toxin KW - 0 KW - Immunotoxins KW - Index Medicus KW - Animals KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Diphtheria Toxin -- metabolism KW - Immunotoxins -- metabolism KW - Diphtheria Toxin -- genetics KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72492369?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+cell+biology&rft.atitle=Mutations+in+diphtheria+toxin+to+improve+immunotoxin+selectivity+and+understand+toxin+entry+into+cells.&rft.au=Youle%2C+R+J&rft.aulast=Youle&rft.aufirst=R&rft.date=1991-02-01&rft.volume=2&rft.issue=1&rft.spage=39&rft.isbn=&rft.btitle=&rft.title=Seminars+in+cell+biology&rft.issn=10434682&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-02 N1 - Date created - 1992-01-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The Toxicity, Bioaccumulation, Metabolism and Elimination of Dioctyl Sodium Sulfosuccinate DSS in Rainbow Trout (Oncorhynchus mykiss) AN - 19119285; 9108045 AB - The acute toxicity (LC50) of the anionic surfactant dioctyl sodium sulfosuccinate (DSS) was determined to be 28 mg/L in rainbow trout. A static non-replacement exposure of rainbow trout to C14-labeled DSS was used to measure the bioaccumulation and elimination of DSS within four separate body compartments: blood, bile, viscera, and carcass. The trout were exposed for 72 h followed by 72 h for depuration. Tissue samples were analyzed at 2, 4, 12, 24, 48, and 72 h during both the exposure and depuration phases of the experiment. Using scintillation counting, DSS concentrations were measured in tissues and used to calculate uptake rate constants, bioconcentration factors, elimination rate constants, half-lives of DSS elimination for each body compartment. The greatest rate of appearance of DSS was in the bile of the trout, while the slowest uptake occurred within the carcass. Elimination of DSS from the carcass and viscera of the trout was found to follow second order kinetics, while elimination from the blood and bile followed first order kinetics. The evaluation of (C14)DSS metabolism was conducted using the HPLC analysis of biliary metabolites following an intraperitoneal injection. Two major peaks were found containing C14 that were not associated with the parent DSS peak. (Author's abstract) JF - Water Research WATRAG, Vol. 25, No. 2, p 119-124, February 1991. 4 fig, 4 tab, 16 ref. NIH Grants ES01080 and ES04184. AU - Goodrich AU - Melancon, MJ AU - Davis, R A AU - Lech, J J AD - NIEHS Aquatic Biomedical Center, Great Lakes Research Facility, Milwaukee, WI 53204 Y1 - 1991/02// PY - 1991 DA - Feb 1991 KW - Water Resources Abstracts KW - Bioaccumulation KW - Fish physiology KW - Metabolism KW - Surfactants KW - Toxicity KW - Toxicology KW - Trout KW - Biological magnification KW - Blood KW - Carbon radioisotopes KW - Excretion KW - Fish KW - Kinetics KW - Tissue analysis KW - SW 3020:Sources and fate of pollution KW - SW 3030:Effects of pollution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/19119285?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Awaterresources&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=&rft.atitle=The+Toxicity%2C+Bioaccumulation%2C+Metabolism+and+Elimination+of+Dioctyl+Sodium+Sulfosuccinate+DSS+in+Rainbow+Trout+%28Oncorhynchus+mykiss%29&rft.au=Goodrich%3BMelancon%2C+MJ%3BDavis%2C+R+A%3BLech%2C+J+J&rft.aulast=Goodrich&rft.aufirst=&rft.date=1991-02-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-14 ER - TY - JOUR T1 - Monoclonal antibodies to glutathione S-transferase pi-immunohistochemical analysis of human tissues and cancers. AN - 80418082; 1703126 AB - Mouse monoclonal antibodies (MAb) have been generated against the anionic isozyme of human glutathione S-transferase (GST pi). MAb AGST I can inhibit 50-70% of GST pi enzymatic activity and reacts with a 3-dimensional epitope which includes a putative glutathione binding site on GST pi. A sandwich enzyme-immunoassay established using MAb AGST I and a polyclonal antibody displayed a sensitivity of 0.5 ng/ml. Immunohistochemical analysis of human tissues demonstrated marked increases in GST pi levels in cancers of the brain, cervix, endometrium, colon, rectum and testis and in fibro- and chondrosarcomas. JF - International journal of cancer AU - Kantor, R R AU - Giardina, S L AU - Bartolazzi, A AU - Townsend, A J AU - Myers, C E AU - Cowan, K H AU - Longo, D L AU - Natali, P G AD - Biological Carcinogenesis Development Program, Program Resources, Inc./DynCorp, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21701. Y1 - 1991/01/21/ PY - 1991 DA - 1991 Jan 21 SP - 193 EP - 201 VL - 47 IS - 2 SN - 0020-7136, 0020-7136 KW - Antibodies, Monoclonal KW - 0 KW - Epitopes KW - Isoenzymes KW - Glutathione Transferase KW - EC 2.5.1.18 KW - Glutathione KW - GAN16C9B8O KW - Index Medicus KW - Uterine Cervical Neoplasms -- enzymology KW - Testicular Neoplasms -- enzymology KW - Rectal Neoplasms -- enzymology KW - Glutathione -- metabolism KW - Humans KW - Uterine Neoplasms -- enzymology KW - Hybridomas -- immunology KW - Binding Sites KW - Colonic Neoplasms -- enzymology KW - Brain Neoplasms -- enzymology KW - Enzyme-Linked Immunosorbent Assay KW - Fibrosarcoma -- enzymology KW - Chondrosarcoma -- enzymology KW - Epitopes -- immunology KW - Female KW - Male KW - Isoenzymes -- analysis KW - Neoplasms -- enzymology KW - Glutathione Transferase -- immunology KW - Glutathione Transferase -- analysis KW - Immunohistochemistry KW - Antibodies, Monoclonal -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80418082?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Monoclonal+antibodies+to+glutathione+S-transferase+pi-immunohistochemical+analysis+of+human+tissues+and+cancers.&rft.au=Kantor%2C+R+R%3BGiardina%2C+S+L%3BBartolazzi%2C+A%3BTownsend%2C+A+J%3BMyers%2C+C+E%3BCowan%2C+K+H%3BLongo%2C+D+L%3BNatali%2C+P+G&rft.aulast=Kantor&rft.aufirst=R&rft.date=1991-01-21&rft.volume=47&rft.issue=2&rft.spage=193&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 - 1991-02-25 N1 - Date created - 1991-02-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Current status of HIV therapy: I. Antiretroviral agents. AN - 80424299; 1702791 AB - Zidovudine has proved to be an important palliative agent in all stages of HIV infection. It delays progression of disease in patients with asymptomatic or mildly symptomatic infection and decreases the frequency and severity of opportunistic disease in those with AIDS. The search for other, more effective antiretroviral agents goes on, with some promising possibilities. JF - Hospital practice (Office ed.) AU - Hoth, D F AU - Myers, M W AD - National Institute of Allergy and Infectious Diseases, Bethesda. Y1 - 1991/01/15/ PY - 1991 DA - 1991 Jan 15 SP - 174 EP - 9, 183-4, 189 passim VL - 26 IS - 1 SN - 8750-2836, 8750-2836 KW - Antiviral Agents KW - 0 KW - Zidovudine KW - 4B9XT59T7S KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Zidovudine -- therapeutic use KW - Drug Therapy, Combination KW - Zidovudine -- adverse effects KW - Virus Replication -- drug effects KW - Humans KW - Zidovudine -- pharmacology KW - Adult KW - Palliative Care KW - Child KW - Immunity -- drug effects KW - Antiviral Agents -- therapeutic use KW - HIV Infections -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80424299?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hospital+practice+%28Office+ed.%29&rft.atitle=Current+status+of+HIV+therapy%3A+I.+Antiretroviral+agents.&rft.au=Hoth%2C+D+F%3BMyers%2C+M+W&rft.aulast=Hoth&rft.aufirst=D&rft.date=1991-01-15&rft.volume=26&rft.issue=1&rft.spage=174&rft.isbn=&rft.btitle=&rft.title=Hospital+practice+%28Office+ed.%29&rft.issn=87502836&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-02-21 N1 - Date created - 1991-02-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Sudden death during empiric amiodarone therapy in symptomatic hypertrophic cardiomyopathy. AN - 80417013; 1987718 AB - Amiodarone is reported to improve symptoms and to prevent sudden death in patients with hypertrophic cardiomyopathy (HC). Amiodarone treatment (loading dose 30 g given over 6 weeks; maintenance dose 400 mg/day) was prospectively evaluated in 50 patients with HC in whom the drug was initiated because of symptoms refractory to conventional drug therapy (calcium antagonists and beta blockers). Twenty-one (42%) patients had ventricular tachycardia (VT) during Holter monitoring. Amiodarone significantly and often markedly improved the patients' New York Heart Association functional class status (from 3.3 to 2.7 at 2 months, p less than 0.001) and treadmill exercise duration (p less than 0.001). Eight patients, however, died (7 suddenly) during a mean follow-up period of 2.2 +/- 1.8 years. Of the 7 sudden deaths, 6 occurred within 5 months of initiation of treatment. The 6-month and 1- and 2-year survival rates were 87, 85 and 80%, respectively. The survival rate of patients with VT was significantly worse than that of patients without VT (61 vs 97% at 2 years; p less than 0.01). Sudden death occurred despite abolition of VT on Holter monitoring. Amiodarone increased left ventricular peak filling rate by radionuclide angiography in 20 of 33 patients (61%) (p less than 0.01). Decrease in peak left ventricular filling rate within 10 days of amiodarone therapy (8 of 33 patients) was associated with subsequent sudden death (p less than 0.04).(ABSTRACT TRUNCATED AT 250 WORDS) JF - The American journal of cardiology AU - Fananapazir, L AU - Leon, M B AU - Bonow, R O AU - Tracy, C M AU - Cannon, R O AU - Epstein, S E AD - Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/01/15/ PY - 1991 DA - 1991 Jan 15 SP - 169 EP - 174 VL - 67 IS - 2 SN - 0002-9149, 0002-9149 KW - Amiodarone KW - N3RQ532IUT KW - Abridged Index Medicus KW - Index Medicus KW - Electrocardiography, Ambulatory KW - Tachycardia -- drug therapy KW - Risk Factors KW - Humans KW - Adult KW - Follow-Up Studies KW - Tachycardia -- etiology KW - Time Factors KW - Male KW - Female KW - Cardiomyopathy, Hypertrophic -- drug therapy KW - Cardiomyopathy, Hypertrophic -- mortality KW - Death, Sudden -- etiology KW - Amiodarone -- therapeutic use KW - Cardiomyopathy, Hypertrophic -- complications KW - Amiodarone -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80417013?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+cardiology&rft.atitle=Sudden+death+during+empiric+amiodarone+therapy+in+symptomatic+hypertrophic+cardiomyopathy.&rft.au=Fananapazir%2C+L%3BLeon%2C+M+B%3BBonow%2C+R+O%3BTracy%2C+C+M%3BCannon%2C+R+O%3BEpstein%2C+S+E&rft.aulast=Fananapazir&rft.aufirst=L&rft.date=1991-01-15&rft.volume=67&rft.issue=2&rft.spage=169&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+cardiology&rft.issn=00029149&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-02-15 N1 - Date created - 1991-02-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Value of electrophysiologic studies in hypertrophic cardiomyopathy treated with amiodarone. AN - 80416683; 1987719 AB - The relation of electrophysiologic effects of amiodarone to long-term outcome was studied in 35 patients with hypertrophic cardiomyopathy (HC). Indications for electrophysiologic studies were: cardiac arrest (n = 3), syncope/presyncope (n = 27) and asymptomatic ventricular tachycardia (VT) (n = 5). Twenty-eight patients (80%) had VT, 3 (9%) atrial tachycardia and 3 (9%) paroxysmal atrial fibrillation during 24-hour Holter monitoring. The studies were repeated after a total amiodarone dose of 58 +/- 122 g and during a maintenance median daily dose of 400 mg. Amiodarone abolished paroxysmal atrial arrhythmias in all 6 patients. However, it caused marked atrioventricular nodal conduction abnormality in 3 patients and heart block or marked HV interval prolongation (to greater than or equal to 100 ms) in 4 patients. Sustained VT was induced in 26 patients (74%) at baseline study and in 23 patients (66%) taking amiodarone therapy. With amiodarone, VT was no longer inducible or was more difficult to induce in 11 patients (31%), and the drug abolished VT during Holter monitoring in all patients. However, VT was easier to induce with amiodarone or was induced only with amiodarone in 18 (51%) patients. Amiodarone significantly slowed the rate of induced VT (from 248 +/- 29 to 214 +/- 37 beats/min, p less than 0.001). This was associated with a change in its morphology from polymorphic to monomorphic VT in 7 patients. During a follow up of 18 +/- 14 months (range 2 to 56), amiodarone was discontinued because of adverse effects in 8 patients (23%).(ABSTRACT TRUNCATED AT 250 WORDS) JF - The American journal of cardiology AU - Fananapazir, L AU - Epstein, S E AD - Clinical Electrophysiology Laboratory, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/01/15/ PY - 1991 DA - 1991 Jan 15 SP - 175 EP - 182 VL - 67 IS - 2 SN - 0002-9149, 0002-9149 KW - Amiodarone KW - N3RQ532IUT KW - Abridged Index Medicus KW - Index Medicus KW - Electrocardiography, Ambulatory KW - Death, Sudden -- etiology KW - Risk Factors KW - Humans KW - Middle Aged KW - Male KW - Female KW - Cardiomyopathy, Hypertrophic -- drug therapy KW - Tachycardia -- diagnosis KW - Cardiomyopathy, Hypertrophic -- mortality KW - Cardiac Pacing, Artificial KW - Arrhythmias, Cardiac -- etiology KW - Heart Conduction System -- drug effects KW - Tachycardia -- drug therapy KW - Amiodarone -- therapeutic use KW - Heart Conduction System -- physiopathology KW - Amiodarone -- adverse effects KW - Cardiomyopathy, Hypertrophic -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80416683?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+cardiology&rft.atitle=Value+of+electrophysiologic+studies+in+hypertrophic+cardiomyopathy+treated+with+amiodarone.&rft.au=Fananapazir%2C+L%3BEpstein%2C+S+E&rft.aulast=Fananapazir&rft.aufirst=L&rft.date=1991-01-15&rft.volume=67&rft.issue=2&rft.spage=175&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+cardiology&rft.issn=00029149&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-02-15 N1 - Date created - 1991-02-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interactions among cytochromes P-450 in the endoplasmic reticulum. Detection of chemically cross-linked complexes with monoclonal antibodies. AN - 80361883; 1985961 AB - The quaternary structure of rat liver cytochrome P-450 within microsomal membranes from 3-methyl-cholanthrene-treated rats was examined by a novel chemical cross-linking-monoclonal antibody approach. Complex formation among the different forms of P-450 was probed by cross-linking of membrane proteins followed by immunopurification with a monoclonal antibody (mAb) to P-450c, the major 3-methylcholanthrene-inducible form. Subsequent immunoblot analysis of the immunopurified proteins with this mAb indicated that P-450c formed complexes with other microsomal proteins. Immunoblots with mAbs to different P-450s were carried out to identify the P-450s that were cross-linked to P-450c. This approach detected specific cross-linking of P-450c to P-450 2a. Immunoinhibition experiments suggest that P-450 2a further metabolizes the primary phenols produced by P-450c-catalyzed hydroxylation of benzo[a]pyrene. Complex formation among membrane-bound enzymes has implications for their catalytic efficiency and an approach combining cross-linking and monoclonal antibody-based characterization of cross-linked proteins will be useful for elucidating such membrane protein macrostructures. JF - The Journal of biological chemistry AU - Alston, K AU - Robinson, R C AU - Park, S S AU - Gelboin, H V AU - Friedman, F K AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/01/15/ PY - 1991 DA - 1991 Jan 15 SP - 735 EP - 739 VL - 266 IS - 2 SN - 0021-9258, 0021-9258 KW - Antibodies, Monoclonal KW - 0 KW - Cross-Linking Reagents 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 - Electrophoresis, Polyacrylamide Gel KW - Microsomes, Liver -- enzymology KW - Enzyme Induction KW - Male KW - Hydroxylation KW - Antibodies, Monoclonal -- immunology KW - Endoplasmic Reticulum -- enzymology KW - Cytochrome P-450 Enzyme System -- immunology KW - Cytochrome P-450 Enzyme System -- metabolism KW - Cytochrome P-450 Enzyme System -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80361883?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Interactions+among+cytochromes+P-450+in+the+endoplasmic+reticulum.+Detection+of+chemically+cross-linked+complexes+with+monoclonal+antibodies.&rft.au=Alston%2C+K%3BRobinson%2C+R+C%3BPark%2C+S+S%3BGelboin%2C+H+V%3BFriedman%2C+F+K&rft.aulast=Alston&rft.aufirst=K&rft.date=1991-01-15&rft.volume=266&rft.issue=2&rft.spage=735&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 - 1991-02-12 N1 - Date created - 1991-02-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Prolonged venous infusion of cisplatin and concurrent radiation therapy for lung carcinoma. A feasibility study. AN - 80361426; 1985730 AB - Fifty patients with non resectable and/or inoperable bronchogenic carcinoma were entered into a feasibility study of cisplatin (CDDP) given in continuous infusion with concurrent radiation therapy. The radiation therapy regimen consisted of 2 Gy given 5 days a week in the first 3 and last 2 weeks of a 7-week split course (50 Gy of total dose). The CDDP (daily dose of 4 to 6 mg/m2) was administered to cover the days of radiation treatment by means of a central venous catheter and a portable pump. Less than 1% of predicted duration of infusion was lost due to complications related to venous access and pump. Toxicity was moderate. The overall probability of a locoregional major response (complete + partial) within 1 month after treatment completion was 86%. Twenty-three patients underwent resection. The 1-year actuarial probability of survival was 64%. The high response and survival rates warrant further studies on concurrent CDDP continuous infusion and radiation therapy in inoperable lung carcinoma. JF - Cancer AU - Bedini, A V AU - Tavecchio, L AU - Milani, F AU - Gramaglia, A AU - Spreafico, C AU - Marchianò, A AU - Ravasi, G AD - Department of Thoracic Surgical Oncology, National Cancer Institute, Milan, Italy. Y1 - 1991/01/15/ PY - 1991 DA - 1991 Jan 15 SP - 357 EP - 362 VL - 67 IS - 2 SN - 0008-543X, 0008-543X KW - Cisplatin KW - Q20Q21Q62J KW - Abridged Index Medicus KW - Index Medicus KW - Infusions, Intravenous KW - Neoplasm Staging KW - Combined Modality Therapy KW - Humans KW - Aged KW - Cisplatin -- administration & dosage KW - Feasibility Studies KW - Survival Rate KW - Radiotherapy Dosage KW - Adult KW - Middle Aged KW - Female KW - Male KW - Carcinoma, Bronchogenic -- therapy KW - Carcinoma, Bronchogenic -- secondary KW - Carcinoma, Bronchogenic -- pathology KW - Lung Neoplasms -- therapy KW - Lung Neoplasms -- mortality KW - Carcinoma, Bronchogenic -- mortality KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80361426?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Prolonged+venous+infusion+of+cisplatin+and+concurrent+radiation+therapy+for+lung+carcinoma.+A+feasibility+study.&rft.au=Bedini%2C+A+V%3BTavecchio%2C+L%3BMilani%2C+F%3BGramaglia%2C+A%3BSpreafico%2C+C%3BMarchian%C3%B2%2C+A%3BRavasi%2C+G&rft.aulast=Bedini&rft.aufirst=A&rft.date=1991-01-15&rft.volume=67&rft.issue=2&rft.spage=357&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-02-12 N1 - Date created - 1991-02-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differentiation-dependent alteration in the chromatin structure of chromosomal protein HMG-17 gene during erythropoiesis. AN - 80420430; 1988681 AB - The expression of the gene coding for chromosomal protein HMG-17 is down regulated during chicken erythrocyte maturation. The transcriptional down regulation is associated with major alterations in the chromatin structure of this gene. The 5' region of the gene contains both constitutive and developmental stage-specific deoxyribonuclease I (DNase I) hypersensitive sites. The constitutive sites bracket the "CpG island" present in the gene, which remains hypomethylated throughout the various developmental stages. During erythropoiesis, the gene acquires a distinct structure that, upon digestion with micrococcal nuclease (MNase) yields an unusual repeat. Two nucleosomes, with a 200 base-pair repeat, are positioned immediately downstream from the start of transcription. Immediately downstream and upstream from these nucleosomes, the boundaries between MNase sites change to a 75 base-pair repeat, which indicates an unusual chromatin structure. The differentiation related changes in the DNase I and MNase digestion pattern in the 5' region of the gene suggest that sequences present in the first intron may be involved in gene regulation. The results may be relevant to the regulation of the entire HMG-14/-17 gene family. JF - Journal of molecular biology AU - Crippa, M P AU - Nickol, J M AU - Bustin, M AD - Laboratory of Molecular Carcinogenesis, N.C.I., National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/01/05/ PY - 1991 DA - 1991 Jan 05 SP - 75 EP - 84 VL - 217 IS - 1 SN - 0022-2836, 0022-2836 KW - HMG-17 KW - Chromatin KW - 0 KW - High Mobility Group Proteins KW - RNA, Messenger KW - Deoxyribonuclease I KW - EC 3.1.21.1 KW - Index Medicus KW - Animals KW - Chickens KW - Blotting, Northern KW - Base Composition KW - RNA, Messenger -- metabolism KW - Down-Regulation KW - Deoxyribonuclease I -- metabolism KW - Blotting, Southern KW - Chick Embryo KW - Restriction Mapping KW - Cell Differentiation -- genetics KW - Transcription, Genetic KW - Methylation KW - Chromatin -- metabolism KW - High Mobility Group Proteins -- genetics KW - Erythropoiesis -- genetics KW - Chromatin -- chemistry KW - Gene Expression Regulation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80420430?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+molecular+biology&rft.atitle=Differentiation-dependent+alteration+in+the+chromatin+structure+of+chromosomal+protein+HMG-17+gene+during+erythropoiesis.&rft.au=Crippa%2C+M+P%3BNickol%2C+J+M%3BBustin%2C+M&rft.aulast=Crippa&rft.aufirst=M&rft.date=1991-01-05&rft.volume=217&rft.issue=1&rft.spage=75&rft.isbn=&rft.btitle=&rft.title=Journal+of+molecular+biology&rft.issn=00222836&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-02-27 N1 - Date created - 1991-02-27 N1 - Date revised - 2017-01-13 N1 - Gene symbol - HMG-17 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of protein kinase C in the regulation of glucose transport in the rat adipose cell. Translocation of glucose transporters without stimulation of glucose transport activity. AN - 80370149; 1985898 AB - The possible role of protein kinase C in the regulation of glucose transport in the rat adipose cell has been examined. Both insulin and phorbol 12-myristate 13-acetate (PMA) stimulate 3-O-methylglucose transport in the intact cell ein association with the subcellular redistribution of glucose transporters from the low density microsomes to the plasma membranes, as assessed by cytochalasin B binding. In addition, the actions of insulin and PMA on glucose transport activity and glucose transporter redistribution are additive. Furthermore, PMA accelerates insulin's stimulation of glucose transport activity, reducing the t1/2 from 3.2 +/- 0.4 to 2.1 +/- 0.2 min (mean +/- S.E.). However, the effect of PMA on glucose transport activity is approximately 10% of that for insulin whereas its effect on glucose transporter redistribution is approximately 50% of the insulin response. Immunoblots of the GLUT1 and GLUT4 glucose transporter isoforms in subcellular membrane fractions also demonstrate that the translocations of GLUT1 in response to PMA and insulin are of similar magnitude whereas the translocation of GLUT4 in response to insulin is markedly greater than that in response to PMA. Thus, glucose transport activity in the intact cell with PMA and insulin correlates more closely with the appearance of GLUT4 in the plasma membrane than cytochalasin B-assayable glucose transporters. Although these data do not clarify the potential role of protein kinase C in the mechanism of insulin action, they do suggest that the mechanisms through which insulin and PMA stimulate glucose transport are distinct but interactive. JF - The Journal of biological chemistry AU - Saltis, J AU - Habberfield, A D AU - Egan, J J AU - Londos, C AU - Simpson, I A AU - Cushman, S W AD - Experimental Diabetes, Metabolism and Nutrition Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/01/05/ PY - 1991 DA - 1991 Jan 05 SP - 261 EP - 267 VL - 266 IS - 1 SN - 0021-9258, 0021-9258 KW - Insulin KW - 0 KW - Methylglucosides KW - 3-O-Methylglucose KW - 146-72-5 KW - Protein Kinase C KW - EC 2.7.11.13 KW - Glucose KW - IY9XDZ35W2 KW - Potassium Cyanide KW - MQD255M2ZO KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Methylglucosides -- metabolism KW - Kinetics KW - In Vitro Techniques KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Insulin -- pharmacology KW - Homeostasis KW - Cell Membrane -- metabolism KW - Potassium Cyanide -- pharmacology KW - Male KW - Protein Kinase C -- metabolism KW - Adipose Tissue -- metabolism KW - Glucose -- metabolism KW - Adipose Tissue -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80370149?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+protein+kinase+C+in+the+regulation+of+glucose+transport+in+the+rat+adipose+cell.+Translocation+of+glucose+transporters+without+stimulation+of+glucose+transport+activity.&rft.au=Saltis%2C+J%3BHabberfield%2C+A+D%3BEgan%2C+J+J%3BLondos%2C+C%3BSimpson%2C+I+A%3BCushman%2C+S+W&rft.aulast=Saltis&rft.aufirst=J&rft.date=1991-01-05&rft.volume=266&rft.issue=1&rft.spage=261&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 - 1991-02-14 N1 - Date created - 1991-02-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - TTX-sensitive action potentials and excitability of adult rat sensory neurons cultured in serum- and exogenous nerve growth factor-free medium. AN - 80525094; 2020393 AB - The excitability of adult rat dorsal root ganglion (DRG) neurons cultured in the absence of serum and exogenously added nerve growth factor (NGF) was studied. Current-clamp recordings revealed the presence of tetrodotoxin (TTX)-sensitive action potentials. Voltage-clamp recordings demonstrated the presence of both inward and outward currents. The inward Na+ current had a maximal amplitude near -10 mV and was completely blocked by TTX. A sustained Ca2+ inward current and a slowly activating outward K+ current were also observed. TTX-sensitive and TTX-resistant action potentials have been observed in previous studies in DRG neurons cultured in the presence of serum. By contrast, in the study reported here, only TTX-sensitive action potentials and Na+ currents were found in the neurons cultured in the absence of serum and nerve growth factor. JF - Neuroscience letters AU - Aguayo, L G AU - Weight, F F AU - White, G AD - Section of Electrophysiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20852. Y1 - 1991/01/02/ PY - 1991 DA - 1991 Jan 02 SP - 88 EP - 92 VL - 121 IS - 1-2 SN - 0304-3940, 0304-3940 KW - Culture Media KW - 0 KW - Nerve Growth Factors KW - Tetrodotoxin KW - 4368-28-9 KW - Potassium KW - RWP5GA015D KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Ganglia, Spinal -- cytology KW - Calcium -- metabolism KW - Animals KW - Cells, Cultured KW - Electrophysiology KW - Potassium -- metabolism KW - Male KW - Neurons, Afferent -- drug effects KW - Nerve Growth Factors -- physiology KW - Action Potentials -- drug effects KW - Tetrodotoxin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80525094?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=TTX-sensitive+action+potentials+and+excitability+of+adult+rat+sensory+neurons+cultured+in+serum-+and+exogenous+nerve+growth+factor-free+medium.&rft.au=Aguayo%2C+L+G%3BWeight%2C+F+F%3BWhite%2C+G&rft.aulast=Aguayo&rft.aufirst=L&rft.date=1991-01-02&rft.volume=121&rft.issue=1-2&rft.spage=88&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 - 1991-05-29 N1 - Date created - 1991-05-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alveolar Proteinosis and Phospholipidoses of the Lungs* super(1) AN - 856755877; 13645451 AB - Three pulmonary disease conditions result from the accumulation of phospholipids in the lung. These conditions are the human lung disease known as pulmonary alveolar proteinosis, the lipoproteinosis that arises in the lungs of rats during acute silicosis, and the phospholipidoses induced by numerous cationic amphiphilic therapeutic agents. In this paper, the status of phospholipid metabolism in the lungs during the process of each of these lung conditions has been reviewed and possible mechanisms for their establishment are discussed. Pulmonary alveolar proteinosis is characterized by the accumulation of tubular myelin-like multilamellated structures in the alveoli and distal airways of patients. These structures appear to be formed by a process of spontaneous assembly involving surfactant protein A and surfactant phospholipids. Structures similar to tubular myelin-like multilamellated structures can be seen in the alveoli of rats during acute silicosis and, as with the human condition, both surfactant protein A and surfactant phospholipids accumulate in the alveoli. Excessive accumulation of surfactant protein A and surfactant phospholipids in the alveoli could arise from their overproduction and hypersecretion by a subpopulation of Type II cells that are activated by silica, and possibly other agents. Phospholipidoses caused by cationic amphiphilic therapeutic agents arise as a result of their inhibition of phospholipid catabolism. Inhibition of phospholipases results in the accumulation of phospholipids in the cytoplasm of alveolar macrophages and other cells. While inhibition of phospholipases by these agents undoubtedly occurs, there are many anomalous features, such as the accumulation of extracellular phospholipids and surfactant protein A, that cannot be accounted for by this simplistic hypothesis. JF - Toxicologic Pathology AU - Hook, Gary ER AD - Biochemical Pathology Group, Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, P.O. Box 12233, Research Triangle Park, North Carolina 27709 Y1 - 1991 PY - 1991 DA - 1991 SP - 482 EP - 513 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU UK VL - 19 IS - 4-1 SN - 0192-6233, 0192-6233 KW - Toxicology Abstracts KW - Macrophages KW - Lung diseases KW - phospholipase KW - Alveoli KW - Lipid metabolism KW - Silica KW - surfactant protein A KW - Silicosis KW - Cytoplasm KW - Surfactants KW - Phospholipids KW - Respiratory tract KW - X 24350:Industrial Chemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/856755877?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+Pathology&rft.atitle=Alveolar+Proteinosis+and+Phospholipidoses+of+the+Lungs*+super%281%29&rft.au=Hook%2C+Gary+ER&rft.aulast=Hook&rft.aufirst=Gary&rft.date=1991-01-01&rft.volume=19&rft.issue=4-1&rft.spage=482&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F019262339101900416 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2010-10-01 N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - Macrophages; Silica; surfactant protein A; Cytoplasm; Silicosis; Lung diseases; phospholipase; Surfactants; Alveoli; Lipid metabolism; Respiratory tract; Phospholipids DO - http://dx.doi.org/10.1177/019262339101900416 ER - TY - JOUR T1 - Review Article: Linguistic Considerations of Idiomatization AN - 85547420; 9106881 AB - A review of Xiao-jun Heng's & Xue-zhi Zhang's A Chinese-English Dictionary of Idioms and Proverbs (Tubingen: Max Niemeyer Verlag, 1988 [see listing in IRPL, this issue]). Two issues are discussed in reference to the development of this dictionary: (1) how idioms are formed, & (2) how a referential scale can be developed to evaluate idiomaticity. Diachronically formed (fossilized) idioms are contrasted with synchronically formed idioms. Three scales of idiomatization are derived: syntagmatic, paradigmatic, & pragmatic. The pragmatic scale is argued to be the most important in idiomatization. 4 References. B. Annesser Murray JF - Semiotica AU - Zhao, Shikai AD - Instit Linguistics Chinese Academy Social Sciences, 5 Jianguomen Nei Da Jie 5 Hao Beijing People's Republic China Y1 - 1991///0, PY - 1991 DA - 0, 1991 SP - 113 EP - 119 VL - 84 IS - 1-2 SN - 0037-1998, 0037-1998 KW - idiomatization scales, diachromic vs synchronic idiom formation, H. Heng's/X. Zhang's Chinese-English Dictionary of Idioms and Proverbs reviewed KW - Chinese (ch2) KW - English (en2) KW - Idiomatic Speech (id2) KW - Pragmatics (pq1) KW - Dictionary (di4) KW - article KW - 5210: lexicography/lexicology; lexicography UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85547420?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Allba&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Semiotica&rft.atitle=Review+Article%3A+Linguistic+Considerations+of+Idiomatization&rft.au=Zhao%2C+Shikai&rft.aulast=Zhao&rft.aufirst=Shikai&rft.date=1991-01-01&rft.volume=84&rft.issue=1-2&rft.spage=113&rft.isbn=&rft.btitle=&rft.title=Semiotica&rft.issn=00371998&rft_id=info:doi/ LA - English DB - Linguistics and Language Behavior Abstracts (LLBA) N1 - Date revised - 2003-10-01 N1 - Last updated - 2016-09-27 N1 - CODEN - SMOTA3 N1 - SubjectsTermNotLitGenreText - Pragmatics (pq1); Dictionary (di4); Chinese (ch2); English (en2); Idiomatic Speech (id2) ER - TY - JOUR T1 - Visuospatial cognition in Huntington's disease. AN - 85275539; pmid-1829137 AB - The notion of specificity of visuospatial dysfunction in Huntington's disease (HD) was evaluated in a sample of afflicted patients as a function of symptom duration, age at onset, and overall dementia severity. Factor analytic procedures indicated that overall visuospatial processing capacity (factor 1) as well as the ability for spatial manipulation (factor 3) was markedly affected in HD patients. In contrast, consistency of spatial judgment (factor 2) appeared to remain relatively intact in these patients. Age at onset seemed to have no relationship with any of these variables, whereas dementia severity demonstrated a significant relationship with overall visuospatial processing capacity. Most importantly, duration of symptoms was significantly associated with the declining ability to mentally perform spatial manipulations. The observation of circumscribed visuospatial impairment in HD patients may have important consequences for the further understanding of the neurobehavioral consequences of this disorder. JF - Movement Disorders AU - Mohr, E AU - Brouwers, P AU - Claus, J J AU - Mann, U M AU - Fedio, P AU - Chase, T N AD - Medical Neurology Branch, NINDS, National Institutes of Health, Bethesda, Maryland. PY - 1991 SP - 127 EP - 132 VL - 6 IS - 2 SN - 0885-3185, 0885-3185 KW - Orientation KW - Human KW - Caudate Nucleus KW - Aged KW - Mental Recall KW - Wechsler Scales KW - Imagination KW - Pattern Recognition, Visual KW - Adult KW - Middle Age KW - Psychomotor Performance KW - Atrophy KW - Neuropsychological Tests KW - Dementia KW - Male KW - Huntington Disease KW - Female UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85275539?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Movement+Disorders&rft.atitle=Visuospatial+cognition+in+Huntington%27s+disease.&rft.au=Mohr%2C+E%3BBrouwers%2C+P%3BClaus%2C+J+J%3BMann%2C+U+M%3BFedio%2C+P%3BChase%2C+T+N&rft.aulast=Mohr&rft.aufirst=E&rft.date=1991-01-01&rft.volume=6&rft.issue=2&rft.spage=127&rft.isbn=&rft.btitle=&rft.title=Movement+Disorders&rft.issn=08853185&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Analysis of one-dimensional gels and two-dimensional Serwer-type gels on the basis of the extended Ogston model using personal computers. AN - 85261591; pmid-2050096 AB - This report presents the stand-alone computer application ELPHOFIT, a software package for the analysis of gel electrophoretic data based on Ferguson plots. Either conventional one-dimensional gels or two-dimensional agarose gels (Serwer-type) can be evaluated. Special emphasis is on the latter gel type, which has been applied previously for the separation of DNA, intact viruses and polydisperse meningitis vaccines. ELPHOFIT is designed for Macintosh PCs and for the IBM XT, AT, PS/2 and compatibles. The program operates interactively with the user, who determines the course of evaluation. Data input is in the format of files providing values of gel electrophoretic migration distances or particle mobility (absolute or relative). Data processing involves a simultaneous least-square curve fitting algorithm (Newton-Gauss, Marquardt-Levenberg) which uses equations derived from the extended Ogston model. Functions are fit to the database by adjusting their variables, representing physical parameters of the gel and the electrophoresed particle. The program output consists of tables and graphics accompanied by an explanatory text providing the following information: (i) radius and free mobility of the electrophoresed particle, (ii) fiber radius, length and volume, mean or median pore radius of the gel, (iii) linear Ferguson plots, (iv) iso-free-mobility/iso-size nomogram for two-dimensional gels, (v) confidence ellipses, (vi) required parameters for image processing program GELFIT and (vii) goodness-of-fit and other statistical parameters, such as standard errors, dependency values, root-mean-square (RMS) error and determination coefficient. Other features of the program are (i) simulation of Serwer-type two-dimensional electrophoresis, (ii) standardization according to size, or size and free mobility, (iii) the conversion of particle radii to molecular (or particle) weight and vice versa, (iv) interconversion of DNA size specifications, i.e. the number of base pairs and the geometric mean radii, (v) computation of gel concentration for optimal resolution of two components, (vi) option to obtain a session record, (viii) option to establish a data output file containing the information of generated graphics (IBM only) and (ix) a text editing facility, e.g., for creating data files. Graphics (Macintosh version, PICT format) and text output files (both IBM and Macintosh versions, standard ASCII format) generated by ELPHOFIT are compatible with commercially available software. JF - Electrophoresis AU - Tietz, D AD - Laboratory of Theoretical and Physical Biology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. PY - 1991 SP - 28 EP - 39 VL - 12 IS - 1 SN - 0173-0835, 0173-0835 KW - Software KW - Reproducibility of Results KW - DNA KW - Models, Statistical KW - Molecular Weight KW - Electrophoresis KW - Computers KW - Electrophoresis, Gel, Two-Dimensional UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85261591?accountid=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=Electrophoresis&rft.atitle=Analysis+of+one-dimensional+gels+and+two-dimensional+Serwer-type+gels+on+the+basis+of+the+extended+Ogston+model+using+personal+computers.&rft.au=Tietz%2C+D&rft.aulast=Tietz&rft.aufirst=D&rft.date=1991-01-01&rft.volume=12&rft.issue=1&rft.spage=28&rft.isbn=&rft.btitle=&rft.title=Electrophoresis&rft.issn=01730835&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Neuropsychological testing of patients with borderline personality disorder. AN - 85245787; pmid-1984693 AB - OBJECTIVE AND METHOD: This study examined whether a battery of neuropsychological tests could detect cognitive deficits--particularly in the areas of perception, learning, and memory--in patients with borderline personality disorder. The test battery was completed by 16 research outpatients with borderline personality disorder, typified by behavioral dyscontrol and diagnosed according to DSM-III-R criteria and the Diagnostic Interview for Borderline Patients. A comparison group of 16 normal volunteers also completed the test battery. RESULTS: The performance of the borderline patients was significantly impaired in comparison with that of the normal group on memory tests requiring uncued recall of complex, recently learned material. Cues given on an auditory memory task partially corrected that deficit. The patients' performance was also significantly impaired on several visual perceptual tests. These deficits do not appear to have been attributable to attentional problems, psychomotor impairment, current major depression, or history of alcohol abuse. CONCLUSIONS: The observed difficulties in separating essential from extraneous visual information and in recalling complex material may be relevant in understanding some of the clinical features of borderline personality disorder. The observed memory improvement resulting from cueing suggests specific strategies that may be used to aid patients' recall of complex material. JF - The American Journal of Psychiatry AU - O'Leary, K M AU - Brouwers, P AU - Gardner, D L AU - Cowdry, R W AD - Division of Intramural Research Programs, NIMH, Neuroscience Center at St. Elizabeths, Washington, DC 20032. PY - 1991 SP - 106 EP - 111 VL - 148 IS - 1 SN - 0002-953X, 0002-953X KW - Wechsler Scales KW - Memory KW - Human KW - Adult KW - Psychomotor Performance KW - Borderline Personality Disorder KW - Cognition Disorders KW - Female KW - Male KW - Visual Perception KW - Ambulatory Care KW - Neuropsychological Tests UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85245787?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acomdisdome&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+Journal+of+Psychiatry&rft.atitle=Neuropsychological+testing+of+patients+with+borderline+personality+disorder.&rft.au=O%27Leary%2C+K+M%3BBrouwers%2C+P%3BGardner%2C+D+L%3BCowdry%2C+R+W&rft.aulast=O%27Leary&rft.aufirst=K&rft.date=1991-01-01&rft.volume=148&rft.issue=1&rft.spage=106&rft.isbn=&rft.btitle=&rft.title=The+American+Journal+of+Psychiatry&rft.issn=0002953X&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - Functionally complex muscles of the cat hindlimb. III. Differential activation within biceps femoris during postural perturbations. AN - 85238883; pmid-1893980 AB - The biceps femoris (BF) muscle is divided into three neuromuscular compartments defined by the innervation patterns of the main nerve branches (English and Weeks 1987). The goals of this study were i) to determine how different regions of the biceps femoris muscle are activated in the intact cat during a broad range of limb movements evoked by perturbations of stance posture, and ii) to determine the relationship between the anatomical compartments of biceps femoris and the functional units as defined in this task. Cats were trained to stand on a moveable platform with each paw on a triaxial force plate. The animal's stance was perturbed by linear translation of the platform in each of sixteen different directions in the horizontal plane. EMG activity was recorded from eight sites across the width of the left biceps femoris muscle. During quiet stance only the anterior compartment was tonically active, presumably contributing to hip extensor torque in the maintenance of stance. During platform translation, evoked EMG activity was recorded from each electrode pair for a wide range of directions of perturbation; as direction changed progressively, the amplitude of evoked activity from any electrode pair increased to a maximum and then decreased. When the EMG amplitude was plotted in polar coordinates as a function of translation direction, the region of response formed a petal shaped area in the horizontal plane, termed the EMG tuning curve. The compartments of the BF muscle were not activated homogeneously. The tuning curve of the anterior BF compartment was similar to that of other hip extensors, and coincided with the region of postero-lateral force production by the hindlimb against the support. The tuning curve of the middle BF compartment was shifted in a counterclockwise direction from that of the anterior compartment, but overlapped extensively with it; the middle BF tuning curve was similar to that of anterior gracilis. The tuning curve of the posterior biceps compartment was rotated further counterclockwise and overlapped very little with that of the middle BF compartment. The posterior BF was activated in a pattern similar to that of other knee flexors. The functional units of BF activation were not identical with the neuromuscular compartments defined by the main nerve branches. As direction of the perturbation changed, the region of BF that was activated moved progressively across the muscle. This progression of the active region was continuous across BFa and BFm, whereas there was a jump, or discontinuity at the border between BFm and BFp.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Experimental Brain Research AU - Chanaud, C M AU - Macpherson, J M AD - Laboratory of Neural Control, National Institute of Neurological and Communicative Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. PY - 1991 SP - 271 EP - 280 VL - 85 IS - 2 SN - 0014-4819, 0014-4819 KW - Hindlimb KW - Cats KW - Animal KW - Electromyography KW - Muscles KW - Support, Non-U.S. Gov't KW - Electric Stimulation KW - Biomechanics KW - Female KW - Posture UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/85238883?accountid=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=Experimental+Brain+Research&rft.atitle=Functionally+complex+muscles+of+the+cat+hindlimb.+III.+Differential+activation+within+biceps+femoris+during+postural+perturbations.&rft.au=Chanaud%2C+C+M%3BMacpherson%2C+J+M&rft.aulast=Chanaud&rft.aufirst=C&rft.date=1991-01-01&rft.volume=85&rft.issue=2&rft.spage=271&rft.isbn=&rft.btitle=&rft.title=Experimental+Brain+Research&rft.issn=00144819&rft_id=info:doi/ LA - eng DB - ComDisDome N1 - Last updated - 2010-05-07 ER - TY - JOUR T1 - [The use of 1,1,1-trichloroethane (methylchloroform) in industrial operations: the neurotoxicity risk]. TT - Utilizzo di 1,1,1-tricloroetano (metilcloroformio) in lavorazioni industriali: il rischio neurotossicità. AN - 80725663; 1865846 AB - 1,1,1-Trichloroethane (1,1,1-TE) is a widely used organic solvent which is thought to be relatively safe. The present review is mainly focused on the neurotoxic effects of 1,1,1-TE. Concentrations above 350 ppm are considered capable of negatively conditioning the performance of the exposed person, in particular reaction time and manual abilities. Peripheral neuropathies have also been described. More recently the potential neurotoxicity of 1,1,1-TE has been underscored by animal studies investigating the effects of this substance in neurobehavioral tests and on neurochemical parameters. 1,1,1-TE alters the motor activity in small laboratory rodents. In fixed interval responding in mice, the effects of 1,1,1-TE are qualitatively similar to those of other volatile (ethanol) and non volatile (benzodiazepines and barbiturates) CNS depressants. In addition, in drug discrimination procedures 1,1,1-TE shares discriminative stimulus properties with barbiturates, toluene, halotane, and oxazepam indicating that this solvent has behavioral effects in common with central nervous system depressant drugs. From a neurochemical point of view long-term exposure to 1,1,1-TE induces astrogliosis in the cerebral cortex of gerbils as indicated by an increased concentration of glial fibrillary acidic protein. In addition low dose inhalation of 1,1,1-TE for 3 months decreases DNA concentrations in several brain regions of the gerbil. 1,1,1-TE affects also brain concentrations of cAMP and cGMP as well as calcium ion control, possibly through an action on voltage-dependent calcium channels. It has been also suggested that intermediate metabolites of 1,1,1-TE may give origin to condensation products with dopamine, ultimately impairing dopaminergic transmission. Some of the neurochemical effects of 1,1,1-TE are shared by other chlorinated organic solvents as well as by CNS depressants. The literature analyzed indicates that 1,1,1-TE may exert significant neurotoxic effects suggesting that more caution in its use is needed and that attention should be paid to the possibility of an additive effect of 1,1,1-TE and CNS depressants (ethanol, barbiturates, benzodiazepines and other volatile solvents) giving origin to severe neurotoxicity. JF - La Medicina del lavoro AU - Fernicola, C AU - Govoni, S AU - Coniglio, L AU - Daniele, E AU - Trabucchi, M AD - Unità Operativa Tutela della Salute nei Luoghi di Lavoro, USL 41, Brescia. PY - 1991 SP - 38 EP - 49 VL - 82 IS - 1 SN - 0025-7818, 0025-7818 KW - Solvents KW - 0 KW - Trichloroethanes KW - 1,1,1-trichloroethane KW - 113C650IR1 KW - Index Medicus KW - Animals KW - Maximum Allowable Concentration KW - Liver -- drug effects KW - Humans KW - Heart -- drug effects KW - Solvents -- toxicity KW - Trichloroethanes -- toxicity KW - Nervous System -- drug effects KW - Solvents -- adverse effects KW - Occupational Exposure -- adverse effects KW - Nervous System -- metabolism KW - Trichloroethanes -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80725663?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=La+Medicina+del+lavoro&rft.atitle=%5BThe+use+of+1%2C1%2C1-trichloroethane+%28methylchloroform%29+in+industrial+operations%3A+the+neurotoxicity+risk%5D.&rft.au=Fernicola%2C+C%3BGovoni%2C+S%3BConiglio%2C+L%3BDaniele%2C+E%3BTrabucchi%2C+M&rft.aulast=Fernicola&rft.aufirst=C&rft.date=1991-01-01&rft.volume=82&rft.issue=1&rft.spage=38&rft.isbn=&rft.btitle=&rft.title=La+Medicina+del+lavoro&rft.issn=00257818&rft_id=info:doi/ LA - Italian DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-11 N1 - Date created - 1991-09-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Safety issues related to retroviral-mediated gene transfer in humans. AN - 80717835; 1863639 AB - The first three approved human clinical trials utilizing retroviral-mediated gene transfer are now underway. While this technology holds great promise for the study and treatment of human disease, it also poses a number of safety concerns. In evaluating clinical protocols, potential complications and the likelihood of their occurrence are estimated by review committees so that a risk/benefit assessment can be made. Current knowledge, reviewed in this article, suggests that no acute complications secondary to retroviral-mediated gene transfer are likely, but the possibility of long-term or unforeseen sequelae in patients suggests the need for post-treatment monitoring. JF - Human gene therapy AU - Cornetta, K AU - Morgan, R A AU - Anderson, W F AD - Molecular Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 5 EP - 14 VL - 2 IS - 1 SN - 1043-0342, 1043-0342 KW - env KW - gag KW - myc KW - pim-1 KW - pol KW - ras KW - Bioethics KW - Index Medicus KW - Biomedical and Behavioral Research KW - Genetics and Reproduction KW - Virus Replication KW - Animals KW - Defective Viruses -- genetics KW - Oncogenes KW - Transformation, Genetic KW - Risk Factors KW - Humans KW - Recombination, Genetic KW - Primates KW - Mutagenesis, Insertional KW - Cell Transformation, Neoplastic -- genetics KW - Genetic Therapy -- adverse effects KW - Transfection KW - Genetic Vectors KW - Retroviridae -- genetics KW - Risk Assessment UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80717835?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Human+gene+therapy&rft.atitle=Safety+issues+related+to+retroviral-mediated+gene+transfer+in+humans.&rft.au=Cornetta%2C+K%3BMorgan%2C+R+A%3BAnderson%2C+W+F&rft.aulast=Cornetta&rft.aufirst=K&rft.date=1991-01-01&rft.volume=2&rft.issue=1&rft.spage=5&rft.isbn=&rft.btitle=&rft.title=Human+gene+therapy&rft.issn=10430342&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-09 N1 - Date created - 1991-09-09 N1 - Date revised - 2017-01-13 N1 - Gene symbol - env; gag; myc; pim-1; pol; ras N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of naphthalene metabolites on cultured cells from eye lens. AN - 80703798; 1906827 AB - Naphthalene is toxic to the eye and results in opacification of the lens. To investigate the metabolic events that may be occurring in the lens epithelial cells, a cell line of lens from a transgenic mouse was incubated with various metabolites of naphthalene. Naphthoquinone at 50 microM was toxic to most cells with a depletion of glutathione levels noted within 6 h of incubation. At 10 microM, naphthoquinone caused an increase in specific activity of the enzyme DT-diaphorase. This enzyme is thought to be a defense against quinones since semiquinone formation is thought to be lessened. Naphthalene-1,2-dihydrodiol at 50 microM also caused an increase in the specific activity of the DT-diaphorase, while at 10 microM no apparent change occurred in the cells. Although there was evidence of metabolic alterations in the cells with the metabolites of naphthalene, the protein profile by two-dimensional gel electrophoresis did not change and there was no indication of an increase in carbonyl formation in the soluble proteins of the cells. These experiments indicate that the metabolites of naphthalene can cause alteration in the metabolism of the lens cells but may not cause apparent changes in the major proteins within the lens epithelium. JF - Free radical biology & medicine AU - Russell, P AU - Yamada, T AU - Xu, G T AU - Garland, D AU - Zigler, J S AD - National Eye Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 255 EP - 261 VL - 10 IS - 5 SN - 0891-5849, 0891-5849 KW - Free Radicals KW - 0 KW - Naphthalenes KW - NAD(P)H Dehydrogenase (Quinone) KW - EC 1.6.5.2 KW - Quinone Reductases KW - EC 1.6.99.- KW - Glutathione Reductase KW - EC 1.8.1.7 KW - Glutathione KW - GAN16C9B8O KW - Index Medicus KW - Rats KW - Animals KW - Liver -- enzymology KW - Glutathione Reductase -- metabolism KW - Glutathione -- metabolism KW - Mice KW - Models, Biological KW - Cell Line KW - Quinone Reductases -- metabolism KW - Lens, Crystalline -- metabolism KW - Lens, Crystalline -- drug effects KW - Lens, Crystalline -- enzymology KW - Naphthalenes -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80703798?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Free+radical+biology+%26+medicine&rft.atitle=Effects+of+naphthalene+metabolites+on+cultured+cells+from+eye+lens.&rft.au=Russell%2C+P%3BYamada%2C+T%3BXu%2C+G+T%3BGarland%2C+D%3BZigler%2C+J+S&rft.aulast=Russell&rft.aufirst=P&rft.date=1991-01-01&rft.volume=10&rft.issue=5&rft.spage=255&rft.isbn=&rft.btitle=&rft.title=Free+radical+biology+%26+medicine&rft.issn=08915849&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-28 N1 - Date created - 1991-08-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alkylation of DNA related to organ-specific carcinogenesis by N-nitroso compounds. AN - 80703515; 1855869 AB - Alkylation of DNA by a number of methylating and ethylating carcinogens, mainly N-nitroso compounds, has been examined in target and non-target organs of rats and Syrian hamsters. Six hours after administration by gavage of small doses identical to those given twice weekly for several months to elicit tumours, animals were killed and dissected. DNA was isolated from several organs and hydrolysed, and the content of methyl- and ethylguanines was measured using high-performance liquid chromatography for separation. In most experiments, radiolabelled carcinogen was used, but in some cases measurement of alkylguanines was by fluorescence. Methylation, O6- and N7-, by methylating compounds was much more extensive than ethylation by the corresponding ethyl compounds, irrespective of their relative potencies in inducing tumours. Similar patterns of alkylation were found in target organs and in non-target organs of the carcinogens. Only marginal differences in methylation were seen with N-nitro-sobis(2-oxopropyl)amine between male and female rat livers, although liver tumours are induced only in females, in feminized males and in old males. Deuterium labelling of the methylene of N-nitrosoethylmethylamine had little effect on methylation or ethylation of DNA in rat liver, although the deuterated compound was a much more potent liver carcinogen. The conclusion is that reactions of the carcinogen other than alkylation of DNA are important in giving rise to tumours. JF - IARC scientific publications AU - Lijinsky, W AD - National Cancer Institute, Frederick Cancer Research Facility, Bionetics Research Inc., MD. Y1 - 1991 PY - 1991 DA - 1991 SP - 305 EP - 310 IS - 105 SN - 0300-5038, 0300-5038 KW - Nitroso Compounds KW - 0 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Rats KW - Animals KW - Mesocricetus KW - Organ Specificity KW - Cricetinae KW - Alkylation KW - Neoplasms, Experimental -- chemically induced KW - DNA -- metabolism KW - Nitroso Compounds -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80703515?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=IARC+scientific+publications&rft.atitle=Alkylation+of+DNA+related+to+organ-specific+carcinogenesis+by+N-nitroso+compounds.&rft.au=Lijinsky%2C+W&rft.aulast=Lijinsky&rft.aufirst=W&rft.date=1991-01-01&rft.volume=&rft.issue=105&rft.spage=305&rft.isbn=&rft.btitle=&rft.title=IARC+scientific+publications&rft.issn=03005038&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-29 N1 - Date created - 1991-08-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of oncogenes and tumour suppressor genes in human lung carcinogenesis. AN - 80703332; 1855868 AB - Six families of activated protooncogenes, ras, raf, fur, neu, jun and myc have so far been associated with human lung cancer. Human bronchial epithelial cells in vitro are being used to investigate the functional role of these specific oncogenes and growth regulatory genes in carcinogenesis and tumour progression. When transferred into normal human bronchial epithelial cells by the highly efficient protoplast fusion method, the v-Ha-ras oncogene initiates a cascade of events leading to decreased responsiveness of these cells to inducers of squamous differentiation, aneuploidy and, less frequently, 'immortality' and tumorigenicity with metastasis in athymic nude mice. Transfection of the SV40 T antigen gene results in nontumorigenic cell lines that have a nearly normal pathway of terminal squamous differentiation and can be transformed into malignant cells by transfected Ha-ras, N-ras or Ki-ras. The combination of transfected c-myc and c-raf-1 also transforms human bronchial epithelial cells into neoplastic cells that exhibit some phenotypic traits found in small-cell carcinomas. These and other results indicate that proto-oncogenes dysregulate the pathways of growth and differentiation of human bronchial epithelial cells and play an important role in human carcinogenesis. Analyses of allelic deletion and somatic cell hybrids are being used to identify the chromosomal localization of tumour suppressor genes. We have examined 54 non-small-cell bronchogenic carcinomas with 13 polymorphic markers. Loss of heterozygosity was more frequent than among 23 squamous-cell carcinomas than among 23 adenocarcinomas or eight large-cell carcinomas. Loss of heterozygosity for chromosome 17p was found in 89% of cases of squamous-cell carcinoma and 18% of adenocarcinomas. Analysis of chromosome 11 for allelic deletions revealed two commonly deleted regions (11p13 and 11p15.5). Somatic cell hybrids between normal human bronchial epithelial cells and Hut292DM, a lung carcinoma cell line, had a finite lifespan in vitro and were nontumorigenic in athymic nude mice. Tumour suppressive effects of individual or combinations of specific human chromosomes on Hut292DM are being examined by formation of microcell-cell hybrids. Chromosome 11 has tumour suppressor activity in these hybrids. Both of these studies suggest that tumour suppressor genes play a dominant role in lung carcinogenesis and provide in-vitro model systems for isolating these genes by subtraction library and insertional mutagenesis techniques. JF - IARC scientific publications AU - Harris, C C AU - Reddel, R AU - Pfeifer, A AU - Iman, D AU - McMenamin, M AU - Trump, B F AU - Weston, A AD - Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD. Y1 - 1991 PY - 1991 DA - 1991 SP - 294 EP - 304 IS - 105 SN - 0300-5038, 0300-5038 KW - Index Medicus KW - Humans KW - Bronchi -- pathology KW - Cell Transformation, Neoplastic KW - Chromosomes, Human, Pair 11 KW - Oncogenes KW - Genes, Tumor Suppressor KW - Lung Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80703332?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=IARC+scientific+publications&rft.atitle=Role+of+oncogenes+and+tumour+suppressor+genes+in+human+lung+carcinogenesis.&rft.au=Harris%2C+C+C%3BReddel%2C+R%3BPfeifer%2C+A%3BIman%2C+D%3BMcMenamin%2C+M%3BTrump%2C+B+F%3BWeston%2C+A&rft.aulast=Harris&rft.aufirst=C&rft.date=1991-01-01&rft.volume=&rft.issue=105&rft.spage=294&rft.isbn=&rft.btitle=&rft.title=IARC+scientific+publications&rft.issn=03005038&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-29 N1 - Date created - 1991-08-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - On radical production by PMA-stimulated neutrophils as monitored by luminol-amplified chemiluminescence. AN - 80703279; 1649785 AB - The means by which neutrophils within the body ward off infectious and neoplastic processes by the activation of molecular oxygen, as well as how such mechanisms dysfunction, is the subject of extensive ongoing research. Most previous studies of neutrophil activation indicate that there is a transient production of reactive oxygen species. Luminol-amplified chemiluminescence surveillance of O2-. and H2O2 supported these general findings. Yet, recent studies showed that production of reactive oxygen species by PMA-stimulated neutrophils is not transient but persistent; however, luminol-dependent methods do not corroborate such findings. The kinetics of O2-. production by human neutrophils were studied using luminol-amplified chemiluminescence (CL), spin trapping combined with electron spin resonance detection, and ferricytochrome c reduction. The effects of pH and O2 level on luminol-amplified CL were determined using hypoxanthine/xanthine oxidase to produce O2-. and H2O2 in cell-free systems. As we have found by electron spin resonance and ferricytochrome c reduction, stimulated neutrophils continued to generate O2-. for several hours, yet when luminol-amplified CL was used to continuously follow radical production, CL was shortly lost. Similar loss of CL was observed with continuous enzymatic formation of O2-. and H2O2. The failure of the CL assay to report O2-. and H2O2 formation results from some luminol reaction product which interferes with the light reaction. Our results show that the cells are operative for long periods indicating that cell exposure to prolonged O2-. fluxes does not terminate radical production, and even when pH, [O2], and reagents are optimized, the use of luminol-amplified CL is not a valid assay for continuous monitoring of O2-. and H2O2 generated by either stimulated neutrophils or in cell-free systems. JF - Free radical biology & medicine AU - Samuni, A AU - Krishna, C M AU - Cook, J AU - Black, C D AU - Russo, A AD - Radiation Oncology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 305 EP - 313 VL - 10 IS - 5 SN - 0891-5849, 0891-5849 KW - Free Radicals KW - 0 KW - Luminol KW - 5EXP385Q4F KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Oxygen KW - S88TT14065 KW - Index Medicus KW - Cell-Free System -- metabolism KW - Oxygen -- blood KW - Kinetics KW - Hydrogen-Ion Concentration KW - Humans KW - Electron Spin Resonance Spectroscopy KW - Neutrophils -- metabolism KW - Neutrophils -- drug effects KW - Luminescent Measurements KW - Tetradecanoylphorbol Acetate -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80703279?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Free+radical+biology+%26+medicine&rft.atitle=On+radical+production+by+PMA-stimulated+neutrophils+as+monitored+by+luminol-amplified+chemiluminescence.&rft.au=Samuni%2C+A%3BKrishna%2C+C+M%3BCook%2C+J%3BBlack%2C+C+D%3BRusso%2C+A&rft.aulast=Samuni&rft.aufirst=A&rft.date=1991-01-01&rft.volume=10&rft.issue=5&rft.spage=305&rft.isbn=&rft.btitle=&rft.title=Free+radical+biology+%26+medicine&rft.issn=08915849&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-28 N1 - Date created - 1991-08-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mechanism of DNA binding by the oesophageal carcinogen N-nitroso-N-methylaniline. AN - 80701860; 1855878 AB - N-Nitroso-N-methylaniline (NMA) is a strong oesophageal carcinogen in rats but exhibits few overt genotoxic effects. Previous work from our laboratory established that NMA is readily metabolized by cytochrome P450-catalysed N-demethylation to produce the benzenediazonium ion (BDI), a relatively stable but reactive electrophilic agent. We have also shown that BDI reacts with DNA to form an acid-labile adduct. We have now shown that BDI, generated chemically or by the metabolism of NMA in vitro, reacts with DNA to form a triazene coupling product at the N6-position of adenine residues. This adduct has also been shown to be produced in the liver DNA of rats treated with NMA. Procedures for the isolation of DNA and for analysis of the adduct are presented. JF - IARC scientific publications AU - Koepke, S R AU - Kroeger-Koepke, M B AU - Michejda, C J AD - Laboratory of Chemical and Physical Carcinogenesis, National Cancer Institute-Frederick Cancer Research and Development Center, MD. Y1 - 1991 PY - 1991 DA - 1991 SP - 346 EP - 350 IS - 105 SN - 0300-5038, 0300-5038 KW - Carcinogens KW - 0 KW - Nitrosamines KW - DNA KW - 9007-49-2 KW - N-methyl-N-nitrosoaniline KW - 9SM68I29WQ KW - Index Medicus KW - Rats KW - Animals KW - Esophageal Neoplasms -- chemically induced KW - Nitrosamines -- toxicity KW - Carcinogens -- metabolism KW - DNA -- metabolism KW - Nitrosamines -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80701860?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=IARC+scientific+publications&rft.atitle=Mechanism+of+DNA+binding+by+the+oesophageal+carcinogen+N-nitroso-N-methylaniline.&rft.au=Koepke%2C+S+R%3BKroeger-Koepke%2C+M+B%3BMichejda%2C+C+J&rft.aulast=Koepke&rft.aufirst=S&rft.date=1991-01-01&rft.volume=&rft.issue=105&rft.spage=346&rft.isbn=&rft.btitle=&rft.title=IARC+scientific+publications&rft.issn=03005038&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-29 N1 - Date created - 1991-08-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Potential occupational exposure associated with parenteral administration of N-nitrosodiethylamine to Macaca mulatta: evidence of post-injection release to the atmosphere. AN - 80701449; 1855856 AB - In order to assess the exposure of workers administering N-nitrosodiethylamine (NDEA) parenterally to Macaca mulatta, air samples were drawn through Thermosorb/N cartridges. Samples were analysed by gas chromatography-thermal energy analysis; the limit of detection was 0.02 micrograms/m3. Significant amounts of NDEA were found in those samples taken in the animal holding room. The NDEA recovered may be accounted for by its expiration by the animals (the contribution from excreta and leakage from the injection site is probably minor). On the basis of the total amount of NDEA administered (840 mg during the first experiment and 250 mg in the second) and the rate at which the animal holding room was ventilated, and assuming that the samples were representative, we estimate that 0.9% of the NDEA administered was released to the atmosphere in 5 h in the first experiment and that 2.7% and 0.8% were released in the first and second 24-h periods, respectively, in the second experiment. It should be noted that this potential source of exposure may be significant not only for workers but also for control or other experimental animals housed in the same room. JF - IARC scientific publications AU - Sansone, E B AU - Keimig, S D AD - Environmental Control and Research Program, NCI-Frederick Cancer Research Facility, MD. Y1 - 1991 PY - 1991 DA - 1991 SP - 226 EP - 229 IS - 105 SN - 0300-5038, 0300-5038 KW - Air Pollutants, Occupational KW - 0 KW - Diethylnitrosamine KW - 3IQ78TTX1A KW - Index Medicus KW - Animals KW - Humans KW - Macaca mulatta KW - Injections KW - Female KW - Pregnancy KW - Occupational Exposure KW - Diethylnitrosamine -- analysis KW - Air Pollutants, Occupational -- analysis KW - Diethylnitrosamine -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80701449?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=IARC+scientific+publications&rft.atitle=Potential+occupational+exposure+associated+with+parenteral+administration+of+N-nitrosodiethylamine+to+Macaca+mulatta%3A+evidence+of+post-injection+release+to+the+atmosphere.&rft.au=Sansone%2C+E+B%3BKeimig%2C+S+D&rft.aulast=Sansone&rft.aufirst=E&rft.date=1991-01-01&rft.volume=&rft.issue=105&rft.spage=226&rft.isbn=&rft.btitle=&rft.title=IARC+scientific+publications&rft.issn=03005038&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-29 N1 - Date created - 1991-08-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Endogenous nitrosamines and liver fluke as risk factors for cholangiocarcinoma in Thailand. AN - 80701043; 1649794 AB - Cholangiocarcinoma (CCA) is one of the most prevalent cancers in north-east Thailand and has been associated with infestation by the liver fluke Opisthorchis viverrini (OV). Two samples of 12-h overnight urine (after dosing with 500 mg proline and 200 mg ascorbic acid or 500 mg proline alone) were collected from about 100 inhabitants in five contrasting incidence areas for CCA and hepatocellular carcinoma. The incidences of CCA and hepatocellular carcinoma were not correlated with either the amount of NPRO or other nitrosamino acids, endogenous nitrosation potential (difference in NPRO levels between proline dose and proline and ascorbic acid dose), or nitrate level. However, when urinary levels of nitrosamino acids were compared in subjects living in high-risk areas, subjects who were positive for OV antibody excreted significantly more (p less than 0.01) NPRO (12.3 +/- 18.7 micrograms/12 h) after proline ingestion than those who were negative 3.5 +/- 3.2 micrograms/12 h). After ingestion of ascorbic acid, the NPRO levels in the positive subjects were significantly reduced (p less than 0.01) to 2.4 +/- 2.0 micrograms/12 h, suggesting that endogenous nitrosation of proline was inhibited. Thus, endogenous nitrosation potential estimated from the difference of NPRO and sum of nitrosamino acids excreted in the two urine samples was significantly higher in subjects positive for the OV antibody. In addition, of the representative food samples and beverages consumed frequently in high-risk areas for CCA, fermented fish and pork contained N-nitrosodimethylamine (0-26 micrograms/kg), N-nitrosopyrrolidine (0-117 micrograms/kg) and N-nitrosopiperidine (0-23 micrograms/kg).(ABSTRACT TRUNCATED AT 250 WORDS) JF - IARC scientific publications AU - Srivatanakul, P AU - Ohshima, H AU - Khlat, M AU - Parkin, M AU - Sukarayodhin, S AU - Brouet, I AU - Bartsch, H AD - National Cancer Institute of Thailand, Bangkok. Y1 - 1991 PY - 1991 DA - 1991 SP - 88 EP - 95 IS - 105 SN - 0300-5038, 0300-5038 KW - Nitrosamines KW - 0 KW - Index Medicus KW - Carcinoma, Hepatocellular -- etiology KW - Thailand KW - Risk Factors KW - Humans KW - Food Analysis KW - Male KW - Female KW - Carcinoma, Hepatocellular -- urine KW - Nitrosamines -- toxicity KW - Adenoma, Bile Duct -- urine KW - Opisthorchiasis -- complications KW - Nitrosamines -- urine KW - Opisthorchiasis -- urine KW - Adenoma, Bile Duct -- etiology KW - Nitrosamines -- analysis KW - Liver Neoplasms -- etiology KW - Liver Neoplasms -- urine UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80701043?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=IARC+scientific+publications&rft.atitle=Endogenous+nitrosamines+and+liver+fluke+as+risk+factors+for+cholangiocarcinoma+in+Thailand.&rft.au=Srivatanakul%2C+P%3BOhshima%2C+H%3BKhlat%2C+M%3BParkin%2C+M%3BSukarayodhin%2C+S%3BBrouet%2C+I%3BBartsch%2C+H&rft.aulast=Srivatanakul&rft.aufirst=P&rft.date=1991-01-01&rft.volume=&rft.issue=105&rft.spage=88&rft.isbn=&rft.btitle=&rft.title=IARC+scientific+publications&rft.issn=03005038&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-29 N1 - Date created - 1991-08-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vivo distribution and cytokine gene expression by enriched mouse LAK effector cells. AN - 80699327; 1906724 AB - Lymphokine activated killer (LAK) cells administered in combination with interleukin 2 (IL2) can mediate antitumor activity in tumor-bearing mice and advanced cancer patients. Relatively little is known about the mechanism by which adoptively transferred LAK cells plus IL2 mediate these antitumor effects in vivo, and it remains unclear to what extent the actual LAK effector cells can accumulate in tumors. In the present study, enriched cytolytic LAK effector cells were obtained by fractionation of bulk LAK cell cultures on Percoll density gradients. About 95% of the total lytic activity was recovered from the 55% of cells isolated in fraction 2 (Fr2). The cells recovered in Fr2 are mostly large, proliferating lymphoblasts that express either the NK-associated surface markers NK1.1 (38%) or LGL-1 (31%), or the cytotoxic T cell phenotype, Lyt2 (39%). The cytolytic lymphoblasts obtained from Fr2 were radiolabelled with either 111Indium-Oxine (111InOx) which labels all cells in the population, or with 125Iododeoxyuridine (125IUdR) which labels only proliferating cells, and injected iv into mice bearing murine renal cancer (Renca). 111InOx-labeled Fr2 cells migrated mostly to spleen (28%) and liver (35%), with approximately 5% of the injected label detectable in the Renca-bearing kidney by 24 hrs. In contrast, Fr2 cells labeled with 125IUdR, which labels only the proliferating blasts thought to include the actual effector cells, exhibited a very different localization pattern. 125IUdR-Fr2 cells were retained in the lungs at higher levels than were 111InOx-Fr2 cells and very little label was detectable in liver (6%), spleen (3%), or tumor bearing kidney (2%) at 24 hrs. These results suggest that most of the large, proliferating lymphoblasts are cleared from the body by 24 hrs and very few localize into even large tumors. Subsequently, Northern blot analyses performed on bulk LAK cells revealed a potent induction of mRNA for TNF alpha by 6 hrs and for IFN gamma by 48 hrs. The intensity of gene expression for both cytokines was increased in Fr2 as compared to the unfractionated bulk LAK cells or to non-cytolytic cells obtained from Fr3. Overall, these results suggest that at least some of the antitumor effects mediated by LAK cells occur by the release of cytokines that synergize with exogenous IL2 for the activation of host effector cells. JF - Biotherapy (Dordrecht, Netherlands) AU - Futami, H AU - Pilaro, A M AU - Gruys, M E AU - Back, T C AU - Young, H A AU - Wiltrout, R H AD - Laboratory of Experimental Immunology, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21702-6013. Y1 - 1991 PY - 1991 DA - 1991 SP - 219 EP - 232 VL - 3 IS - 3 SN - 0921-299X, 0921-299X KW - Cytokines KW - 0 KW - Indium Radioisotopes KW - RNA, Messenger KW - Tumor Necrosis Factor-alpha KW - Interferon-gamma KW - 82115-62-6 KW - Idoxuridine KW - LGP81V5245 KW - Index Medicus KW - Animals KW - Interferon-gamma -- genetics KW - Blotting, Northern KW - Interferon-gamma -- biosynthesis KW - Tumor Necrosis Factor-alpha -- biosynthesis KW - Mice KW - Mice, Inbred BALB C KW - Tumor Necrosis Factor-alpha -- genetics KW - Phenotype KW - RNA, Messenger -- metabolism KW - Idoxuridine -- metabolism KW - Mice, Inbred C57BL KW - Cytotoxicity Tests, Immunologic KW - Male KW - Cytokines -- genetics KW - Tumor Cells, Cultured -- metabolism KW - Tumor Cells, Cultured -- immunology KW - Cytokines -- biosynthesis KW - Killer Cells, Lymphokine-Activated -- immunology KW - Gene Expression KW - Killer Cells, Lymphokine-Activated -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80699327?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biotherapy+%28Dordrecht%2C+Netherlands%29&rft.atitle=In+vivo+distribution+and+cytokine+gene+expression+by+enriched+mouse+LAK+effector+cells.&rft.au=Futami%2C+H%3BPilaro%2C+A+M%3BGruys%2C+M+E%3BBack%2C+T+C%3BYoung%2C+H+A%3BWiltrout%2C+R+H&rft.aulast=Futami&rft.aufirst=H&rft.date=1991-01-01&rft.volume=3&rft.issue=3&rft.spage=219&rft.isbn=&rft.btitle=&rft.title=Biotherapy+%28Dordrecht%2C+Netherlands%29&rft.issn=0921299X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-28 N1 - Date created - 1991-08-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Oncogenes and tumor suppressor genes in human lung carcinogenesis. AN - 80698446; 1649643 JF - Critical reviews in oncogenesis AU - Iman, D S AU - Harris, C C AD - Laboratory of Human Carcinogenesis, NCI, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 161 EP - 171 VL - 2 IS - 2 SN - 0893-9675, 0893-9675 KW - Ha-ras KW - Ki-ras KW - L-myc KW - N-myc KW - N-ras KW - c-fms KW - c-jun KW - c-myb KW - c-myc KW - c-raf-1 KW - fur KW - neu(erbB-2) KW - Index Medicus KW - Chromosomes, Human, Pair 17 KW - Chromosomes, Human, Pair 3 KW - Humans KW - Carcinoma, Non-Small-Cell Lung -- genetics KW - Carcinoma, Squamous Cell -- genetics KW - Oncogenes -- physiology KW - Adenocarcinoma -- genetics KW - Carcinoma, Small Cell -- genetics KW - Chromosomes, Human, Pair 11 KW - Lung Neoplasms -- genetics KW - Genes, Tumor Suppressor -- physiology KW - Cell Transformation, Neoplastic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80698446?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Critical+reviews+in+oncogenesis&rft.atitle=Oncogenes+and+tumor+suppressor+genes+in+human+lung+carcinogenesis.&rft.au=Iman%2C+D+S%3BHarris%2C+C+C&rft.aulast=Iman&rft.aufirst=D&rft.date=1991-01-01&rft.volume=2&rft.issue=2&rft.spage=161&rft.isbn=&rft.btitle=&rft.title=Critical+reviews+in+oncogenesis&rft.issn=08939675&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-29 N1 - Date created - 1991-08-29 N1 - Date revised - 2017-01-13 N1 - Gene symbol - Ha-ras; Ki-ras; L-myc; N-myc; N-ras; c-fms; c-jun; c-myb; c-myc; c-raf-1; fur; neu(erbB-2) N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Toxicokinetic studies of N-nitrosamine carcinogenesis. AN - 80698282; 1855881 JF - IARC scientific publications AU - Streeter, A J AU - Nims, R W AU - Keefer, L K AD - Chemistry Section, National Cancer Institute, Frederick Cancer ResearchFacility, MD. Y1 - 1991 PY - 1991 DA - 1991 SP - 362 EP - 365 IS - 105 SN - 0300-5038, 0300-5038 KW - Carcinogens KW - 0 KW - Nitrosamines KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Sex Factors KW - Male KW - Female KW - Nitrosamines -- toxicity KW - Carcinogens -- pharmacokinetics KW - Nitrosamines -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80698282?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=IARC+scientific+publications&rft.atitle=Toxicokinetic+studies+of+N-nitrosamine+carcinogenesis.&rft.au=Streeter%2C+A+J%3BNims%2C+R+W%3BKeefer%2C+L+K&rft.aulast=Streeter&rft.aufirst=A&rft.date=1991-01-01&rft.volume=&rft.issue=105&rft.spage=362&rft.isbn=&rft.btitle=&rft.title=IARC+scientific+publications&rft.issn=03005038&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-29 N1 - Date created - 1991-08-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Experimental models of aluminum-induced motor neuron degeneration. AN - 80695837; 1853766 JF - Advances in neurology AU - Garruto, R M AU - Strong, M J AU - Yanagihara, R AD - Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland. Y1 - 1991 PY - 1991 DA - 1991 SP - 327 EP - 340 VL - 56 SN - 0091-3952, 0091-3952 KW - Aluminum KW - CPD4NFA903 KW - Index Medicus KW - Pacific Islands KW - Animals KW - Cells, Cultured KW - Humans KW - Disease Models, Animal KW - Amyotrophic Lateral Sclerosis -- chemically induced KW - Nerve Degeneration KW - Aluminum -- pharmacology KW - Motor Neurons -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80695837?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advances+in+neurology&rft.atitle=Experimental+models+of+aluminum-induced+motor+neuron+degeneration.&rft.au=Garruto%2C+R+M%3BStrong%2C+M+J%3BYanagihara%2C+R&rft.aulast=Garruto&rft.aufirst=R&rft.date=1991-01-01&rft.volume=56&rft.issue=&rft.spage=327&rft.isbn=&rft.btitle=&rft.title=Advances+in+neurology&rft.issn=00913952&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-16 N1 - Date created - 1991-08-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of the cycad neurotoxin BMAA in the amyotrophic lateral sclerosis-parkinsonism dementia complex of the western Pacific. AN - 80695066; 1853765 JF - Advances in neurology AU - Duncan, M W AD - Clinical Neurosciences Branch, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, Maryland 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 301 EP - 310 VL - 56 SN - 0091-3952, 0091-3952 KW - Amino Acids, Diamino KW - 0 KW - Neurotoxins KW - beta-N-methylamino-L-alanine KW - 108SA6URTV KW - Index Medicus KW - Seeds -- analysis KW - Pacific Islands KW - Mass Spectrometry KW - Flour -- analysis KW - Chromatography, Gas KW - Cells, Cultured KW - Syndrome KW - Neurons -- drug effects KW - Humans KW - Biological Transport KW - Blood-Brain Barrier KW - Plants, Toxic KW - Parkinson Disease, Secondary -- chemically induced KW - Dementia -- chemically induced KW - Amyotrophic Lateral Sclerosis -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80695066?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advances+in+neurology&rft.atitle=Role+of+the+cycad+neurotoxin+BMAA+in+the+amyotrophic+lateral+sclerosis-parkinsonism+dementia+complex+of+the+western+Pacific.&rft.au=Duncan%2C+M+W&rft.aulast=Duncan&rft.aufirst=M&rft.date=1991-01-01&rft.volume=56&rft.issue=&rft.spage=301&rft.isbn=&rft.btitle=&rft.title=Advances+in+neurology&rft.issn=00913952&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-16 N1 - Date created - 1991-08-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Principles and practice of DNA filter elution. AN - 80687116; 1852788 AB - DNA filter elution assays have proved useful in studies of DNA strand breaks and crosslinks produced in mammalian cells or tissues by a wide variety of carcinogenic and cancer chemotherapeutic agents. The basic types of DNA lesions that can be measured include single and double-strand breaks, interstrand crosslinks and DNA-protein crosslinks. DNA filter elution has also been adapted to the assay of other lesions such as alkali-labile sites and the protein-associated strand breaks of topoisomerase DNA cleavage complexes. The essential concepts and theory of the technique are discussed and the applications of the technique to various types of studies are critically reviewed. JF - Pharmacology & therapeutics AU - Kohn, K W AD - Laboratory of Molecular Pharmacology, National Cancer Institute, Bethesda, MD 20814. Y1 - 1991 PY - 1991 DA - 1991 SP - 55 EP - 77 VL - 49 IS - 1-2 SN - 0163-7258, 0163-7258 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Filtration KW - Humans KW - DNA -- isolation & purification KW - DNA Damage KW - DNA -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80687116?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacology+%26+therapeutics&rft.atitle=Principles+and+practice+of+DNA+filter+elution.&rft.au=Kohn%2C+K+W&rft.aulast=Kohn&rft.aufirst=K&rft.date=1991-01-01&rft.volume=49&rft.issue=1-2&rft.spage=55&rft.isbn=&rft.btitle=&rft.title=Pharmacology+%26+therapeutics&rft.issn=01637258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-16 N1 - Date created - 1991-08-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vivo and in vitro effects of TGF-beta 1 on normal and neoplastic haemopoiesis. AN - 80685567; 1649034 AB - TGF-beta 1 and TGF-beta 2 are equipotent selective inhibitors of murine and human haemopoiesis in vitro. Primitive haemopoietic cells such as the high proliferative potential progenitor cell and the colony-forming unit (CFU)-GEMM are directly inhibited by TGF-beta whereas the more differentiated CFU-G, CFU-M and CFU-E are not. Recombinant TGF-beta 1 administered intraperitoneally or intravenously to mice selectively inhibits haemopoietic colony formation in a time- and dose-dependent manner to the same extent as seen in vitro. The progenitors are reversibly prevented from entering the cell cycle. This inhibitory action of TGF-beta functions on at least two levels: (1) down-modulation of the cell surface expression of receptors for growth stimulatory molecules and (2) interference with the intracellular signalling pathways of these molecules. In addition, expression of TGF-beta receptors is regulated during cytokine stimulation of haemopoiesis. Neoplastic B lymphocytes can proliferate by escaping from a TGF-beta-mediated autocrine inhibitory loop. Activation signals (e.g. phorbol esters) inhibit tumour cell growth by stimulating active TGF-beta production and inducing cell surface expression of TGF-beta receptors. These results indicate that TGF-beta may be useful as a bone marrow protective and/or an antitumour agent. JF - Ciba Foundation symposium AU - Ruscetti, F W AU - Dubois, C AU - Falk, L A AU - Jacobsen, S E AU - Sing, G AU - Longo, D L AU - Wiltrout, R H AU - Keller, J R AD - Biological Response Modifiers Program, National Cancer Institute-Frederick Cancer Research and Development Center, MD 21701-1201. Y1 - 1991 PY - 1991 DA - 1991 SP - 212 EP - 27; discussion 227-31 VL - 157 SN - 0300-5208, 0300-5208 KW - Rb KW - v-Ki-ras KW - Antineoplastic Agents KW - 0 KW - Cytokines KW - Immunologic Factors KW - Receptors, Cell Surface KW - Receptors, Transforming Growth Factor beta KW - Recombinant Proteins KW - Transforming Growth Factor beta KW - Granulocyte-Macrophage Colony-Stimulating Factor KW - 83869-56-1 KW - Index Medicus KW - Animals KW - Recombinant Proteins -- pharmacology KW - Cytokines -- pharmacology KW - Tumor Cells, Cultured -- drug effects KW - Humans KW - Mice KW - Leukemia, Promyelocytic, Acute -- pathology KW - Granulocyte-Macrophage Colony-Stimulating Factor -- pharmacology KW - Receptors, Cell Surface -- biosynthesis KW - B-Lymphocytes -- drug effects KW - Down-Regulation KW - Cells, Cultured KW - Lymphoma, B-Cell -- pathology KW - Immunologic Factors -- pharmacology KW - Drug Synergism KW - Antineoplastic Agents -- pharmacology KW - Cell Cycle -- drug effects KW - Transforming Growth Factor beta -- pharmacology KW - Hematopoiesis -- drug effects KW - Neoplastic Stem Cells -- drug effects KW - Hematopoietic Stem Cells -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80685567?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Ciba+Foundation+symposium&rft.atitle=In+vivo+and+in+vitro+effects+of+TGF-beta+1+on+normal+and+neoplastic+haemopoiesis.&rft.au=Ruscetti%2C+F+W%3BDubois%2C+C%3BFalk%2C+L+A%3BJacobsen%2C+S+E%3BSing%2C+G%3BLongo%2C+D+L%3BWiltrout%2C+R+H%3BKeller%2C+J+R&rft.aulast=Ruscetti&rft.aufirst=F&rft.date=1991-01-01&rft.volume=157&rft.issue=&rft.spage=212&rft.isbn=&rft.btitle=&rft.title=Ciba+Foundation+symposium&rft.issn=03005208&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-20 N1 - Date created - 1991-08-20 N1 - Date revised - 2017-01-13 N1 - Gene symbol - Rb; v-Ki-ras N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Administration of IL-2-PE40 via osmotic pumps prevents adjuvant induced arthritis in rats. Improved therapeutic index of IL-2-PE40 administered by continuous infusion. AN - 80682122; 2071302 AB - IL-2-PE40 is a chimeric cytotoxin composed of interleukin 2 (IL-2) fused to a truncated form of Pseudomonas exotoxin (PE) that lacks its binding domain. IL-2-PE40 has been shown to exhibit therapeutic potency in several models in vivo when administered i.p. twice a day. Here we show that the continuous administration of IL-2-PE40 by an osmotic pump specifically prevents the development of adjuvant induced arthritis in rats with an improved therapeutic efficacy as compared to daily repeated i.p. injections. Stabilization of IL-2-PE40 at 37 degrees C for the continuous administration by pumps was achieved by adding NAD, the substrate for the enzyme portion of the chimeric toxin. JF - International journal of immunopharmacology AU - Lorberboum-Galski, H AU - Lafyatis, R AU - Case, J P AU - FitzGerald, D AU - Wilder, R L AU - Pastan, I AD - Division of Cancer Biology and Diagnosis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 305 EP - 315 VL - 13 IS - 2-3 SN - 0192-0561, 0192-0561 KW - Exotoxins KW - 0 KW - IL-2-PE40 chimeric protein, recombinant KW - Immunosuppressive Agents KW - Immunotoxins KW - Interleukin-2 KW - Recombinant Proteins KW - NAD KW - 0U46U6E8UK KW - Index Medicus KW - Rats KW - Drug Stability KW - Animals KW - Rats, Inbred Lew KW - Infusion Pumps, Implantable KW - Temperature KW - NAD -- administration & dosage KW - Female KW - Immunosuppressive Agents -- administration & dosage KW - Arthritis, Experimental -- etiology KW - Interleukin-2 -- blood KW - Interleukin-2 -- administration & dosage KW - Exotoxins -- administration & dosage KW - Exotoxins -- blood KW - Immunotoxins -- administration & dosage KW - Immunotoxins -- blood KW - Arthritis, Experimental -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80682122?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+immunopharmacology&rft.atitle=Administration+of+IL-2-PE40+via+osmotic+pumps+prevents+adjuvant+induced+arthritis+in+rats.+Improved+therapeutic+index+of+IL-2-PE40+administered+by+continuous+infusion.&rft.au=Lorberboum-Galski%2C+H%3BLafyatis%2C+R%3BCase%2C+J+P%3BFitzGerald%2C+D%3BWilder%2C+R+L%3BPastan%2C+I&rft.aulast=Lorberboum-Galski&rft.aufirst=H&rft.date=1991-01-01&rft.volume=13&rft.issue=2-3&rft.spage=305&rft.isbn=&rft.btitle=&rft.title=International+journal+of+immunopharmacology&rft.issn=01920561&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-22 N1 - Date created - 1991-08-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Superoxide production by stimulated neutrophils: temperature effect. AN - 80678828; 1649095 AB - Activation of neutrophils results in a one-electron reduction of oxygen to produce the superoxide anion and other oxygen-derived, microbicidal species. Evidence from many kinetic studies of oxygen-derived radicals generated by stimulated neutrophils in vitro shows that radical production is optimal at 37 degrees C but only lasts several minutes and then rapidly subsides. These findings support the widely held perception that the neutrophil's "oxidative burst" is a transitory event that peaks within minutes of stimulation and ends shortly thereafter. However, while some studies have shown that under controlled conditions stimulated neutrophils can generate superoxide continuously for several hours, others have observed that the superoxide formation by neutrophils stimulated in buffer at 37 degrees C does not persist. To reconcile the conflicting findings and to better understand neutrophil function, we have reinvestigated the effect of temperature on the kinetics of radical generation by PMA-stimulated cells. Electron paramagnetic resonance spectroscopy coupled with spin-trapping and SOD-inhibitable ferricytochrome c reduction were used to monitor superoxide production by neutrophils stimulated at either 25 degrees C or 37 degrees C in RPMI 1640 medium or in Hank's balanced salt solution. When oxygen was supplied continuously, neutrophils stimulated at 25 degrees C in buffer or in medium generated superoxide for several hours but at 37 degrees C, particularly in HBSS, O2- formation strikingly and rapidly decreased. This cessation of superoxide generation was reversible by lowering the temperature back to 25 degrees C. These data imply that in vivo neutrophils may be capable of generating oxy-radicals for prolonged periods. In part, our results may also explain the often observed termination of neutrophil-derived radical formation in vitro and help to dispel the perception that neutrophil-derived oxy-radical production is an ephemeral phenomenon. JF - Free radical research communications AU - Black, C D AU - Cook, J A AU - Russo, A AU - Samuni, A AD - Radiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 27 EP - 37 VL - 12-13 Pt 1 SN - 8755-0199, 8755-0199 KW - Cyclic N-Oxides KW - 0 KW - Cytochrome c Group KW - Free Radicals KW - Spin Labels KW - Superoxides KW - 11062-77-4 KW - 5,5-dimethyl-1-pyrroline-1-oxide KW - 7170JZ1QF3 KW - 5,5-dimethyl-5-hydroperoxy-1-pyrrolidinyloxy KW - 85963-89-9 KW - Peroxidase KW - EC 1.11.1.7 KW - Superoxide Dismutase KW - EC 1.15.1.1 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Oxygen KW - S88TT14065 KW - Index Medicus KW - Oxidation-Reduction KW - Cyclic N-Oxides -- analysis KW - Oxygen -- metabolism KW - Humans KW - Electron Spin Resonance Spectroscopy KW - Peroxidase -- metabolism KW - Temperature KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Superoxide Dismutase -- metabolism KW - Cytochrome c Group -- metabolism KW - Time Factors KW - Neutrophils -- metabolism KW - Neutrophils -- drug effects KW - Superoxides -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80678828?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Free+radical+research+communications&rft.atitle=Superoxide+production+by+stimulated+neutrophils%3A+temperature+effect.&rft.au=Black%2C+C+D%3BCook%2C+J+A%3BRusso%2C+A%3BSamuni%2C+A&rft.aulast=Black&rft.aufirst=C&rft.date=1991-01-01&rft.volume=12-13+Pt+1&rft.issue=&rft.spage=27&rft.isbn=&rft.btitle=&rft.title=Free+radical+research+communications&rft.issn=87550199&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-22 N1 - Date created - 1991-08-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Proto-oncogene activation in rodent and human tumors. AN - 80675293; 2068988 AB - The transformation of a normal cell into a tumorigenic cell involves both the activation and concerted expression of proto-oncogenes and inactivation of suppressor genes. The activation of ras proto-oncogenes represents one step in the multistep process of carcinogenesis for a variety of rodent and human tumors. This activation is probably an early event in tumorigenesis in many cases and may be the 'initiation' event in some cases. Thus, a chemical that induces rodent tumors by activation of ras proto-oncogenes can potentially invoke one step of the neoplastic process in humans exposed to the chemical. Moreover, dominant transforming oncogenes other than ras have been detected in human tumors as well as rodent tumors. The involvement of these putative proto-oncogenes in the development of neoplasia is unclear at present. JF - Advances in experimental medicine and biology AU - Anderson, M W AU - You, M AU - Reynolds, S H AD - Department of Health and Human Services, National Institutes of Health, Research Triangle Park, NC 27709. Y1 - 1991 PY - 1991 DA - 1991 SP - 235 EP - 243 VL - 283 SN - 0065-2598, 0065-2598 KW - Index Medicus KW - Animals KW - Humans KW - Lung Neoplasms -- genetics KW - Mice KW - Gene Expression Regulation KW - Mutation KW - Proto-Oncogenes KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80675293?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advances+in+experimental+medicine+and+biology&rft.atitle=Proto-oncogene+activation+in+rodent+and+human+tumors.&rft.au=Anderson%2C+M+W%3BYou%2C+M%3BReynolds%2C+S+H&rft.aulast=Anderson&rft.aufirst=M&rft.date=1991-01-01&rft.volume=283&rft.issue=&rft.spage=235&rft.isbn=&rft.btitle=&rft.title=Advances+in+experimental+medicine+and+biology&rft.issn=00652598&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-14 N1 - Date created - 1991-08-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Hapten carrier conjugates associated with halothane hepatitis. AN - 80675068; 2068977 JF - Advances in experimental medicine and biology AU - Pohl, L R AU - Thomassen, D AU - Pumford, N R AU - Butler, L E AU - Satoh, H AU - Ferrans, V J AU - Perrone, A AU - Martin, B M AU - Martin, J L AD - Laboratory of Chemical Pharmacology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 111 EP - 120 VL - 283 SN - 0065-2598, 0065-2598 KW - Carrier Proteins KW - 0 KW - Haptens KW - Trifluoroacetic Acid KW - E5R8Z4G708 KW - Halothane KW - UQT9G45D1P KW - Index Medicus KW - Rats KW - Animals KW - Trifluoroacetic Acid -- immunology KW - Drug Hypersensitivity -- etiology KW - Carrier Proteins -- immunology KW - Humans KW - Haptens -- immunology KW - Microsomes, Liver -- immunology KW - Chemical and Drug Induced Liver Injury -- etiology KW - Halothane -- immunology KW - Halothane -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80675068?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advances+in+experimental+medicine+and+biology&rft.atitle=Hapten+carrier+conjugates+associated+with+halothane+hepatitis.&rft.au=Pohl%2C+L+R%3BThomassen%2C+D%3BPumford%2C+N+R%3BButler%2C+L+E%3BSatoh%2C+H%3BFerrans%2C+V+J%3BPerrone%2C+A%3BMartin%2C+B+M%3BMartin%2C+J+L&rft.aulast=Pohl&rft.aufirst=L&rft.date=1991-01-01&rft.volume=283&rft.issue=&rft.spage=111&rft.isbn=&rft.btitle=&rft.title=Advances+in+experimental+medicine+and+biology&rft.issn=00652598&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-14 N1 - Date created - 1991-08-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Covalent bonding of bay-region diol epoxides to nucleic acids. AN - 80673426; 2069024 AB - Although the solution chemistry of diol epoxides is now fairly well understood, a great deal remains to be elucidated regarding their reaction in the presence of DNA. Not only DNA but also small molecules are capable of sequestering diol epoxides in aqueous solutions with equilibrium constants on the order of 10(2)-10(4) M-1. In the case of DNA, at least two major families of complexes are presently recognized, possibly the result of groove binding vs. intercalation. As is the case for diol epoxides free in solution, the complexed diol epoxides undergo solvolysis to tetraols and in some cases possibly to keto diols as well. Fractionation between covalent bonding and solvolysis from within the complex(s) is determined more by the nature of the parent hydrocarbon from which the diol epoxide is derived than any other factor. Studies of a wide variety of alkylating and arylating agents have show that practically every potentially nucleophilic site on DNA can serve as a target for modification. In the case of the diol epoxides, practically all of the modification occurs at the exocyclic amino groups of the purine bases. In contrast to the diol epoxides, other epoxides such as those derived from aflatoxin B1, vinyl chloride, propylene, 9-vinylanthracene, and styrene preferentially bind to the aromatic ring nitrogens N-7 in guanine and N-3 in adenine (cf. Chadha et al., 1989). Molecular modeling as well as the spectroscopic evidence suggests that the hydrocarbon portion of the diol epoxides lies in the minor groove of DNA when bound to the exocyclic 2-amino group of guanine and in the major groove when bound to the exocyclic 6-amino group of adenine. Detailed conformational analysis of adducted DNA should prove to be extremely valuable in developing mechanistic models for the enzymatic processing of chemically altered DNA. At present, the critical lesion or lesions responsible for induction of neoplasia remains obscured by the large number of apparently noncritical adducts which form when polycyclic hydrocarbon diol epoxides bond to DNA. JF - Advances in experimental medicine and biology AU - Jerina, D M AU - Chadha, A AU - Cheh, A M AU - Schurdak, M E AU - Wood, A W AU - Sayer, J M AD - Laboratory of Bioorganic Chemistry, National Institutes of Health NIDDK, Bethesda 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 533 EP - 553 VL - 283 SN - 0065-2598, 0065-2598 KW - Epoxy Compounds KW - 0 KW - Mutagens KW - Polycyclic Compounds KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Molecular Structure KW - Animals KW - Base Sequence KW - Kinetics KW - Polycyclic Compounds -- pharmacology KW - Polycyclic Compounds -- metabolism KW - Polycyclic Compounds -- chemistry KW - Binding Sites KW - Epoxy Compounds -- pharmacology KW - DNA -- metabolism KW - Epoxy Compounds -- metabolism KW - Epoxy Compounds -- chemistry KW - DNA -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80673426?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advances+in+experimental+medicine+and+biology&rft.atitle=Covalent+bonding+of+bay-region+diol+epoxides+to+nucleic+acids.&rft.au=Jerina%2C+D+M%3BChadha%2C+A%3BCheh%2C+A+M%3BSchurdak%2C+M+E%3BWood%2C+A+W%3BSayer%2C+J+M&rft.aulast=Jerina&rft.aufirst=D&rft.date=1991-01-01&rft.volume=283&rft.issue=&rft.spage=533&rft.isbn=&rft.btitle=&rft.title=Advances+in+experimental+medicine+and+biology&rft.issn=00652598&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-14 N1 - Date created - 1991-08-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Tumorigenicity, metastasis and suppression of MHC class-I expression in murine fibroblasts transformed by mutant v-ras deficient in GTP binding. AN - 80667440; 2066184 AB - We have introduced point mutations in v-rasH to study their effects on biochemical and biological properties of the ras-encoded protein p21. Several of these mutant proteins do not bind GTP and thus lack GTPase activity, while others were shown to have their GTP binding reduced. We have introduced these ras mutants into NIH 3T3 fibroblastoid cells to study major parameters of clinical importance which are associated with neoplastic transformation, particularly MHC expression in cells, metastasis and tumorigenesis in both nude mice and immune competent mice. Our data show that certain mutations in v-ras differentially affect the expression of the transformed phenotype. Mutant ras molecules deficient in GTP binding fail to generate rapidly progressing tumors in immune competent mice, and not all morphologically transformed cells were capable of experimental metastasis. Cells transformed by certain v-ras mutants form tumors in immunocompetent mice and show reduced expression of MHC class-I antigens. Other cells are morphologically transformed and tumorigenic in athymic nude mice, but fail to form tumors in normal mice and show levels of MHC class-I antigen expression similar to non-transformed 3T3 cells. The inverse relationship between MHC class-I-antigen expression and the degree of transformation in fibroblastoid cells suggests that the ras gene product could be involved in regulating MHC expression. JF - International journal of cancer. Supplement = Journal international du cancer. Supplement AU - Lu, Y Y AU - Blair, D G AU - Segal, S AU - Shih, T Y AU - Clanton, D J AD - Laboratory of Molecular Oncology, National Cancer Institute, Frederick, MD 21702-1201. Y1 - 1991 PY - 1991 DA - 1991 SP - 45 EP - 53 VL - 6 SN - 0898-6924, 0898-6924 KW - DNA, Neoplasm KW - 0 KW - Guanosine Triphosphate KW - 86-01-1 KW - GTP Phosphohydrolases KW - EC 3.6.1.- KW - Proto-Oncogene Proteins p21(ras) KW - EC 3.6.5.2 KW - Index Medicus KW - Clone Cells KW - Animals KW - Neoplasms, Experimental -- genetics KW - Mice KW - Mice, Nude KW - Neoplasms, Experimental -- pathology KW - DNA, Neoplasm -- isolation & purification KW - Mice, Inbred BALB C KW - Fibroblasts KW - Mutagenesis KW - Transfection KW - Blotting, Southern KW - Neoplasm Metastasis KW - DNA, Neoplasm -- genetics KW - Cell Line KW - Genes, ras KW - Gene Expression Regulation, Neoplastic KW - GTP Phosphohydrolases -- genetics KW - GTP Phosphohydrolases -- metabolism KW - Major Histocompatibility Complex KW - Cell Transformation, Neoplastic KW - Proto-Oncogene Proteins p21(ras) -- genetics KW - Guanosine Triphosphate -- metabolism KW - Genes, MHC Class I UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80667440?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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.+Supplement+%3D+Journal+international+du+cancer.+Supplement&rft.atitle=Tumorigenicity%2C+metastasis+and+suppression+of+MHC+class-I+expression+in+murine+fibroblasts+transformed+by+mutant+v-ras+deficient+in+GTP+binding.&rft.au=Lu%2C+Y+Y%3BBlair%2C+D+G%3BSegal%2C+S%3BShih%2C+T+Y%3BClanton%2C+D+J&rft.aulast=Lu&rft.aufirst=Y&rft.date=1991-01-01&rft.volume=6&rft.issue=&rft.spage=45&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer.+Supplement+%3D+Journal+international+du+cancer.+Supplement&rft.issn=08986924&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-09 N1 - Date created - 1991-08-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Unique human neutrophil populations are defined by monoclonal antibody ED12F8C10. AN - 80663574; 1829650 AB - A mouse IgG1 monoclonal antibody ED12F8C10 (C10) binds a constant percentage of peripheral blood neutrophils in the same individual when studied over time, defining a distinct subset of neutrophils in all normal individuals studied to date. Bone marrow studies confirm that the heterogeneity is present to the same degree at all stages of neutrophil development from the myelocyte to the mature neutrophil. Neither in vivo nor in vitro activation of neutrophils explains or significantly alters the relative percentages of C10-positive and -negative neutrophils in the same individual. With both activation and exudation, however, expression of the C10-defined epitope increases in intensity in the C10 binding subpopulation. Studies of NBT reduction, phagocytosis, adherence, light scattering characteristics, and monoclonal antibody surface binding have failed to demonstrate physical or functional differences between the C10-defined populations. We examined C10 binding in patients with different defects of phagocyte function. In two patients with neutrophil-specific granule deficiency, less than 1% of the neutrophils were found to be C10 positive, while neutrophils from a patient with idiopathic leukemoid reaction and recurrent infections demonstrated greater than 99% C10 binding. Although the present study does not delineate the physiologic significance of C10 binding heterogeneity, it firmly supports the concept of neutrophil heterogeneity at the level of surface antigen expression. JF - Cellular immunology AU - Brown, C C AU - Malech, H L AU - Jacobson, R J AU - Shrimpton, C F AU - Beverly, P C AU - Segal, A W AU - Gallin, J I AD - Bacterial Diseases Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 102 EP - 114 VL - 132 IS - 1 SN - 0008-8749, 0008-8749 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Differentiation KW - Endotoxins KW - Macrophage-1 Antigen KW - Receptors, Fc KW - Receptors, IgG KW - Lactoferrin KW - EC 3.4.21.- KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Hydrocortisone KW - WI4X0X7BPJ KW - Epinephrine KW - YKH834O4BH KW - Index Medicus KW - Hydrocortisone -- pharmacology KW - Macrophage-1 Antigen -- metabolism KW - Humans KW - Epinephrine -- pharmacology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Flow Cytometry KW - Lactoferrin -- metabolism KW - Cell Separation KW - Receptors, Fc -- metabolism KW - Endotoxins -- pharmacology KW - Neutrophils -- immunology KW - Antigens, Differentiation -- metabolism KW - Antigens, Differentiation -- immunology KW - Antibodies, Monoclonal -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80663574?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Unique+human+neutrophil+populations+are+defined+by+monoclonal+antibody+ED12F8C10.&rft.au=Brown%2C+C+C%3BMalech%2C+H+L%3BJacobson%2C+R+J%3BShrimpton%2C+C+F%3BBeverly%2C+P+C%3BSegal%2C+A+W%3BGallin%2C+J+I&rft.aulast=Brown&rft.aufirst=C&rft.date=1991-01-01&rft.volume=132&rft.issue=1&rft.spage=102&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 - 1991-08-13 N1 - Date created - 1991-08-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Genetic influences in human substance abuse. AN - 80663348; 2065117 AB - The importance of clinical studies to genetic research on substance abuse is discussed. This paper compares the advantages and limitations of methods employed in clinical studies to those employed in animal studies. It stresses the complementary nature of human and animal studies for improving our understanding of genetic influences in substance abuse. Finally, it reviews findings from adoption and twin studies of substance abuse. Whereas much is known about genetic influences in human alcoholism, relatively little is known about genetic influences in other types of drug abuse. This disparity is directly related to the amount of research that has been conducted in the two areas over the past several years. JF - Journal of addictive diseases AU - Pickens, R W AU - Svikis, D S AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1991 PY - 1991 DA - 1991 SP - 205 EP - 213 VL - 10 IS - 1-2 SN - 1055-0887, 1055-0887 KW - Index Medicus KW - Animals KW - Humans KW - Disease Models, Animal KW - Diseases in Twins -- psychology KW - Adoption KW - Alcoholism -- genetics KW - Selection, Genetic KW - Diseases in Twins -- genetics KW - Alcoholism -- psychology KW - Social Environment KW - Substance-Related Disorders -- psychology KW - Substance-Related Disorders -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80663348?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+addictive+diseases&rft.atitle=Genetic+influences+in+human+substance+abuse.&rft.au=Pickens%2C+R+W%3BSvikis%2C+D+S&rft.aulast=Pickens&rft.aufirst=R&rft.date=1991-01-01&rft.volume=10&rft.issue=1-2&rft.spage=205&rft.isbn=&rft.btitle=&rft.title=Journal+of+addictive+diseases&rft.issn=10550887&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-15 N1 - Date created - 1991-08-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Biochemical genetic differences in vulnerability to drug effects: is statistically significant always physiologically important and vice versa? AN - 80661100; 1648408 AB - The goal of biochemical genetic experiments, which are designed to better understand vulnerability to drug effects, is to determine variation in biochemical traits which can account for variation in behavioral and physiological effects of drugs. Biochemical genetic experiments commonly span several distinct scientific disciplines and many different methodologies, both behavioral and biochemical. In most cases, biochemical genetic experiments involve at least three different levels of analysis, including sophisticated mathematical models of genetic inheritance, many behavioral paradigms used to assess various drug-related phenotypes, and a variety of biochemical methodologies used to determine biochemical correlates. Both the multidisciplinary nature of this scientific endeavor and the traditional uses of the scientific methods which are now being applied to pharmacogenetic experiments necessitate careful consideration of many often conflicting theoretical perspectives in the process of interpretation of experimental results. Several scientific considerations are discussed which emphasize the presentation of the results of pharmacogenetic studies within the context of expectations concerning genetic variance as well as traditional uses and assumptions related to methodology. JF - Journal of addictive diseases AU - Ritz, M C AD - Behavioral Pharmacology and Genetics Laboratory, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1991 PY - 1991 DA - 1991 SP - 189 EP - 203 VL - 10 IS - 1-2 SN - 1055-0887, 1055-0887 KW - Psychotropic Drugs KW - 0 KW - Receptors, Neurotransmitter KW - Index Medicus KW - Animals KW - Models, Genetic KW - Humans KW - Psychotropic Drugs -- pharmacology KW - Brain -- drug effects KW - Receptors, Neurotransmitter -- genetics KW - Receptors, Neurotransmitter -- drug effects KW - Substance-Related Disorders -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80661100?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+addictive+diseases&rft.atitle=Biochemical+genetic+differences+in+vulnerability+to+drug+effects%3A+is+statistically+significant+always+physiologically+important+and+vice+versa%3F&rft.au=Ritz%2C+M+C&rft.aulast=Ritz&rft.aufirst=M&rft.date=1991-01-01&rft.volume=10&rft.issue=1-2&rft.spage=189&rft.isbn=&rft.btitle=&rft.title=Journal+of+addictive+diseases&rft.issn=10550887&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-15 N1 - Date created - 1991-08-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Preferential mutagenesis at G.C base pairs by the anti 3,4-dihydrodiol 1,2-epoxide of 7-methylbenz[a]anthracene. AN - 80659608; 2064722 AB - The racemic anti-dihydrodiol epoxide of 7-methylbenz[a]anthracene preferentially induced mutations at G.C base pairs in the pS189 shuttle vector. Mutations were not randomly distributed throughout the supF target gene, but were concentrated at five hotspots. The hotspots for this agent did not correspond exactly to those produced by any other dihydrodiol epoxide examined to date, indicating that dihydrodiol epoxide structure and reactivity play a major role in determining mutagenic hotspots. JF - Molecular carcinogenesis AU - Bigger, C A AU - Flickinger, D J AU - St John, J AU - Harvey, R G AU - Dipple, A AD - Chemistry of Carcinogenesis Laboratory, ABL-Basic Research Program, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland 21701. Y1 - 1991 PY - 1991 DA - 1991 SP - 176 EP - 179 VL - 4 IS - 3 SN - 0899-1987, 0899-1987 KW - Benz(a)Anthracenes KW - 0 KW - Carcinogens KW - 7-methylbenz(a)anthracene 3,4-dihydrodiol 1,2-epoxide KW - 133645-02-0 KW - DNA KW - 9007-49-2 KW - 7-methylbenzanthracene KW - F0662CQU1Q KW - Index Medicus KW - Base Composition -- drug effects KW - Base Sequence -- drug effects KW - Stereoisomerism KW - Tumor Cells, Cultured KW - Humans KW - Molecular Sequence Data KW - Suppression, Genetic KW - Benz(a)Anthracenes -- administration & dosage KW - Benz(a)Anthracenes -- toxicity KW - Mutagenesis KW - DNA -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80659608?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+carcinogenesis&rft.atitle=Preferential+mutagenesis+at+G.C+base+pairs+by+the+anti+3%2C4-dihydrodiol+1%2C2-epoxide+of+7-methylbenz%5Ba%5Danthracene.&rft.au=Bigger%2C+C+A%3BFlickinger%2C+D+J%3BSt+John%2C+J%3BHarvey%2C+R+G%3BDipple%2C+A&rft.aulast=Bigger&rft.aufirst=C&rft.date=1991-01-01&rft.volume=4&rft.issue=3&rft.spage=176&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-12 N1 - Date created - 1991-08-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Altered regulation of TGF-beta 1 and TGF-alpha in primary keratinocytes and papillomas expressing v-Ha-ras. AN - 80659536; 2064727 AB - The influence of an oncogenic v-Ha-ras gene on the expression of TGF-beta and TGF-alpha by mouse keratinocytes and derived tumors has been investigated. Normal mouse keratinocytes cultured as basal cells in 0.05 mM Ca2+ secreted low levels of TGF-beta 2 peptide, and this increased markedly following culture in 1.4 mM Ca2+, retinoic acid, or phorbol esters. In contrast, introduction of a v-Ha-ras gene into normal keratinocytes increased basal expression and secretion of TGF-beta 1 (rather than TGF-beta 2) in response to all three agents. The selective secretion of TGF-beta 1 in v-Ha-ras keratinocytes in response to 1.4 mM Ca2+ occurred even though the four TGF-beta 2 transcripts were induced and the TGF-beta 1 transcript decreased, suggesting that the activated v-Ha-ras gene product regulates expression of the TGF-beta isoforms at the posttranscriptional level. Immunohistochemical analysis of papillomas formed following skin grafting of v-Ha-ras keratinocytes onto nude mice indicated that TGF-beta 1 was abundant in the basal and spinous layers, while there was no expression of TGF-beta 1 in normal skin. In contrast, both normal and neoplastic tissues expressed TGF-beta 2 and TGF-beta 3 in the granular layers. Furthermore, TGF-alpha mRNA expression was also elevated fivefold in cultured v-Ha-ras keratinocytes, and TGF-alpha protein was overexpressed in the grafted papillomas, but there was no detectable expression in normal skin. Elevated expression of both TGF-beta 1 and TGF-alpha in the basal and spinous layers of benign tumors may be important for the high proliferation rate in these tumors as well as for increased proliferation in the suprabasal layer. JF - Molecular carcinogenesis AU - Glick, A B AU - Sporn, M B AU - Yuspa, S H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 210 EP - 219 VL - 4 IS - 3 SN - 0899-1987, 0899-1987 KW - Transforming Growth Factor alpha KW - 0 KW - Transforming Growth Factor beta KW - Index Medicus KW - Animals KW - Tumor Cells, Cultured KW - Mice, Nude KW - Mice KW - Mice, Inbred BALB C KW - Down-Regulation -- drug effects KW - Cell Differentiation -- drug effects KW - Keratinocytes -- secretion KW - Transforming Growth Factor alpha -- genetics KW - Papilloma -- pathology KW - Genes, ras -- drug effects KW - Keratinocytes -- drug effects KW - Keratinocytes -- metabolism KW - Transforming Growth Factor beta -- genetics KW - Papilloma -- genetics KW - Gene Expression Regulation, Neoplastic -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80659536?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+carcinogenesis&rft.atitle=Altered+regulation+of+TGF-beta+1+and+TGF-alpha+in+primary+keratinocytes+and+papillomas+expressing+v-Ha-ras.&rft.au=Glick%2C+A+B%3BSporn%2C+M+B%3BYuspa%2C+S+H&rft.aulast=Glick&rft.aufirst=A&rft.date=1991-01-01&rft.volume=4&rft.issue=3&rft.spage=210&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-12 N1 - Date created - 1991-08-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - DNA methylation and oncogene expression in methapyrilene-induced rat liver tumors and in treated hepatocytes in culture. AN - 80658766; 2064726 AB - Continued exposure of rats to carcinogenic doses of methapyrilene (MP) leads to elevated levels of 5-methyl-deoxycytidine (5MC) in liver DNA. Since gene expression often correlates with DNA methylation, we investigated these parameters in the MP-induced hepatocellular carcinomas of Fischer 344 rats. DNA was hypermethylated in liver tissue surrounding the tumors relative to liver tissue of untreated controls of the same age, while tumor DNA was not; DNA methylation declined to normal levels when MP treatment ceased. Gene expression analysis showed measurable levels of mRNA for c-Ki-ras, erb-B, erb-B2, hck, src, lyn, vav, trk, raf-1, l-myc, c-jun, c-yes, c-myc, c-abl, and p53. No significant differences in expression for these and other oncogenes were seen between tumors and surrounding livers, although erb-B2 and vav showed visible decreases compared with normal liver. Hypermethylation of DNA and expression of these oncogenes in MP-treated tissues were not correlated. Levels of mRNA for the same genes in MP-treated hepatocytes in culture were similar to in vivo levels; analysis of DNA synthesis levels showed that this gene expression pattern occurred in the absence of proliferation bursts or toxicity in these cells, thus suggesting that treatment in vivo may produce the same results. JF - Molecular carcinogenesis AU - Hernandez, L AU - Petropoulos, C J AU - Hughes, S H AU - Lijinsky, W AD - ABL-Basic Research Program, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland 21702. Y1 - 1991 PY - 1991 DA - 1991 SP - 203 EP - 209 VL - 4 IS - 3 SN - 0899-1987, 0899-1987 KW - 1-myc KW - C-Ki-ras KW - c-abl KW - c-jun KW - c-myc KW - c-yes KW - erb-B KW - erb-B2hcK KW - lyn KW - raf-1 KW - src KW - trk KW - vav(onc-f) KW - Deoxycytidine KW - 0W860991D6 KW - DNA KW - 9007-49-2 KW - Methapyrilene KW - A01LX40298 KW - 5-methyldeoxycytidine KW - B200GV71QM KW - Index Medicus KW - Rats KW - Gene Expression -- drug effects KW - Animals KW - Rats, Inbred F344 KW - Deoxycytidine -- metabolism KW - Tumor Cells, Cultured KW - Deoxycytidine -- analogs & derivatives KW - Methylation KW - Male KW - Liver Neoplasms, Experimental -- genetics KW - Oncogenes -- drug effects KW - Liver Neoplasms, Experimental -- metabolism KW - Liver -- drug effects KW - DNA -- metabolism KW - Methapyrilene -- toxicity KW - Liver Neoplasms, Experimental -- chemically induced KW - Liver -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80658766?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+carcinogenesis&rft.atitle=DNA+methylation+and+oncogene+expression+in+methapyrilene-induced+rat+liver+tumors+and+in+treated+hepatocytes+in+culture.&rft.au=Hernandez%2C+L%3BPetropoulos%2C+C+J%3BHughes%2C+S+H%3BLijinsky%2C+W&rft.aulast=Hernandez&rft.aufirst=L&rft.date=1991-01-01&rft.volume=4&rft.issue=3&rft.spage=203&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-12 N1 - Date created - 1991-08-12 N1 - Date revised - 2017-01-13 N1 - Gene symbol - 1-myc; C-Ki-ras; c-abl; c-jun; c-myc; c-yes; erb-B; erb-B2hcK; lyn; raf-1; src; trk; vav(onc-f) N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Scientific concepts, value, and significance of chemical carcinogenesis studies. AN - 80658364; 2064387 JF - Annual review of pharmacology and toxicology AU - Huff, J AU - Haseman, J AU - Rall, D AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991 PY - 1991 DA - 1991 SP - 621 EP - 652 VL - 31 SN - 0362-1642, 0362-1642 KW - Carcinogens KW - 0 KW - Index Medicus KW - Animals KW - Humans KW - Neoplasms -- chemically induced KW - Carcinogenicity Tests UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80658364?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annual+review+of+pharmacology+and+toxicology&rft.atitle=Scientific+concepts%2C+value%2C+and+significance+of+chemical+carcinogenesis+studies.&rft.au=Huff%2C+J%3BHaseman%2C+J%3BRall%2C+D&rft.aulast=Huff&rft.aufirst=J&rft.date=1991-01-01&rft.volume=31&rft.issue=&rft.spage=621&rft.isbn=&rft.btitle=&rft.title=Annual+review+of+pharmacology+and+toxicology&rft.issn=03621642&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-02 N1 - Date created - 1991-08-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Intravenous buprenorphine reduces pupil size and the light reflex in humans. AN - 80651283; 2062170 AB - The pupillary effects of intravenous buprenorphine were studied in eight nondependent male subjects who reported previous opiate use. Buprenorphine (0.3, 0.6, and 1.2 mg) decreased pupil size, the amplitude of the light reflex, and the velocities of constriction and dilation. Significant pupillary effects occurred within 15 min of the injection and persisted for 24 hr. At 48 hr most measures returned to baseline levels. Generally the magnitude of the effect was not dose related although recovery occurred sooner after the lower dose. The time course of the pupillary effects of buprenorphine exceeds duration of its analgesic and subjective effects. Previous studies have reported that pupillary measures are especially sensitive to the acute effects of full opiate agonists. The results of the present study indicate that buprenorphine, a partial opiate agonist, causes profound and persistent effects on pupillary size and dynamic measures. JF - Life sciences AU - Pickworth, W B AU - Bunker, E AU - Welch, P AU - Cone, E AD - National Institute on Drug Abuse, Addiction Research Center, Baltimore, Maryland. Y1 - 1991 PY - 1991 DA - 1991 SP - 129 EP - 138 VL - 49 IS - 2 SN - 0024-3205, 0024-3205 KW - Buprenorphine KW - 40D3SCR4GZ KW - Index Medicus KW - Injections, Intravenous KW - Kinetics KW - Humans KW - Adult KW - Male KW - Reflex, Pupillary -- drug effects KW - Pupil -- drug effects KW - Buprenorphine -- pharmacology KW - Buprenorphine -- administration & dosage KW - Miosis -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80651283?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Life+sciences&rft.atitle=Intravenous+buprenorphine+reduces+pupil+size+and+the+light+reflex+in+humans.&rft.au=Pickworth%2C+W+B%3BBunker%2C+E%3BWelch%2C+P%3BCone%2C+E&rft.aulast=Pickworth&rft.aufirst=W&rft.date=1991-01-01&rft.volume=49&rft.issue=2&rft.spage=129&rft.isbn=&rft.btitle=&rft.title=Life+sciences&rft.issn=00243205&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-02 N1 - Date created - 1991-08-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - New mutants of Drosophila that are resistant to the anesthetic effects of halothane. AN - 80646008; 1905503 JF - Annals of the New York Academy of Sciences AU - Nash, H A AU - Campbell, D B AU - Krishnan, K S AD - Laboratory of Molecular Biology, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 540 EP - 544 VL - 625 SN - 0077-8923, 0077-8923 KW - Ethyl Methanesulfonate KW - 9H154DI0UP KW - Halothane KW - UQT9G45D1P KW - Index Medicus KW - Animals KW - Alleles KW - Mutagenesis KW - X Chromosome KW - Halothane -- pharmacology KW - Drosophila melanogaster -- genetics KW - Anesthesia, General KW - Drosophila melanogaster -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80646008?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=New+mutants+of+Drosophila+that+are+resistant+to+the+anesthetic+effects+of+halothane.&rft.au=Nash%2C+H+A%3BCampbell%2C+D+B%3BKrishnan%2C+K+S&rft.aulast=Nash&rft.aufirst=H&rft.date=1991-01-01&rft.volume=625&rft.issue=&rft.spage=540&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 - 1991-08-01 N1 - Date created - 1991-08-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - N-butyl benzenesulfonamide: a neurotoxic plasticizer inducing a spastic myelopathy in rabbits. AN - 80643637; 2058361 AB - N-Butyl benzenesulfonamide (NBBS), a plasticizer used commercially in the polymerization of polyamide compounds, is neurotoxic. Young adult New Zealand white rabbits, inoculated repeatedly with NBBS by the intracisternal or intraperitoneal routes, developed a dose-dependent motor dysfunction characterized by limb splaying, hyperreflexia, hypertonia, gait impairment, and abnormal righting reflexes. Histopathological changes consisted of intramedullary thickening of the ventral horn axons, random neuroaxonal spheroids confined to brain stem nuclei and spinal motor neurons, and swollen dendritic processes of spinal motor neurons. Immunoreactivity to a monoclonal antibody against microtubule-associated protein-2 (MAP-2) was markedly increased in the dendrites of spinal motor neurons following thrice weekly intraperitoneal inoculations of NBBS for 4 months, whereas after 12 monthly intracisternal inoculations, MAP-2 immunoreactivity was absent or strikingly reduced in the same neuronal populations. Ultrastructurally, postsynaptic zones contained vacuoles and multilamellar bodies. These findings raise questions about the safety of NBBS to humans. JF - Acta neuropathologica AU - Strong, M J AU - Garruto, R M AU - Wolff, A V AU - Chou, S M AU - Fox, S D AU - Yanagihara, R AD - Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 235 EP - 241 VL - 81 IS - 3 SN - 0001-6322, 0001-6322 KW - Microtubule-Associated Proteins KW - 0 KW - Plasticizers KW - Sulfonamides KW - N-butylbenzenesulfonamide KW - 3622-84-2 KW - Index Medicus KW - Injections, Intraperitoneal KW - Animals KW - Blood Chemical Analysis KW - Microtubule-Associated Proteins -- metabolism KW - Rabbits KW - Microtubule-Associated Proteins -- immunology KW - Nervous System Diseases -- chemically induced KW - Nervous System Diseases -- pathology KW - Injections, Subcutaneous KW - Microscopy, Electron KW - Nervous System Diseases -- physiopathology KW - Immunohistochemistry KW - Female KW - Muscle Spasticity -- chemically induced KW - Muscle Spasticity -- pathology KW - Sulfonamides -- toxicity KW - Muscle Spasticity -- physiopathology KW - Sulfonamides -- administration & dosage KW - Plasticizers -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80643637?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Acta+neuropathologica&rft.atitle=N-butyl+benzenesulfonamide%3A+a+neurotoxic+plasticizer+inducing+a+spastic+myelopathy+in+rabbits.&rft.au=Strong%2C+M+J%3BGarruto%2C+R+M%3BWolff%2C+A+V%3BChou%2C+S+M%3BFox%2C+S+D%3BYanagihara%2C+R&rft.aulast=Strong&rft.aufirst=M&rft.date=1991-01-01&rft.volume=81&rft.issue=3&rft.spage=235&rft.isbn=&rft.btitle=&rft.title=Acta+neuropathologica&rft.issn=00016322&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-26 N1 - Date created - 1991-07-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Long-term carcinogenesis studies on 2,3,7,8-tetrachlorodibenzo-p-dioxin and hexachlorodibenzo-p-dioxins. AN - 80630423; 2054688 AB - 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and 1,2,3,6,7,8- and 1,2,3,7,8,9-hexachlorodibenzo-p-dioxins (HCDDs) are among the most toxic and carcinogenic of "man-made" chemicals. These "dioxins," as well as many of the other polychlorinated dibenzodioxins (PCDDs) and dibenzofuran (PCDFs) derivatives, are chlorinated aromatic compounds which are chemically stable, insoluble in water, and highly soluble in fats and oils. TCDD acts as a complete carcinogen in several species, causing both common and uncommon tumors at multiple sites. It is a highly potent chemical carcinogen in chronic animal studies, producing carcinogenic effects in laboratory animals with doses as low as 0.001 micrograms/kg/day. In rats, TCDD induces neoplasms in the lung, oral/nasal cavities, thyroid and adrenal glands, and liver. In mice, TCDD induces neoplasms in the liver and subcutaneous tissue, thyroid gland, and thymic lymphomas. In hamsters, it induces squamous cell carcinomas of the facial skin. Tumors of the integumentary system are reported after oral (mice and rats), intraperitoneal (hamsters), and dermal (mice) administration. A mixture of HCDDS (defined as the mixture of the 1,2,3,6,7,8- and 1,2,3,7,8,9 isomers used in the NTP experiments) are potent liver carcinogens in mice and rats. Pharmacokinetic studies in laboratory animals indicate that 50-90% of dietary TCDD is absorbed. It concentrates in adipose tissue and the liver. In mammals, the TCDD present in the liver is slowly redistributed and stored in fatty tissue. Elimination of TCDD occurs via excretion of metabolites in the bile and urine and passively through the gut wall. Metabolism is slow: the biological half-life of TCDD varies from weeks (rodents) to years (humans), and is strongly dependent upon the rate of TCDD metabolism. Many of the toxic effects of TCDD, including teratogenicity, may arise by receptor-mediated mechanisms. The induction of cytochrome P-448 and related enzymes by TCDD occurs by such a mechanism, and is related to the binding of TCDD to the Ah receptor. The specific mechanism(s) by which TCDD exerts its carcinogenic effects is unclear: receptor-binding may be part of the story. The role of the Ah receptor has been indicated in a skin promotion assay. The evidence for mutagenicity is inconclusive. TCDD did not induce lethal mutations, chromosomal aberrations, micronuclei or sister chromatid exchanges in rodents treated in vivo, nor was it mutagenic to bacteria, but it did enhance transformation of mouse C3H 10T1/2 cells by N-methyl-N'-nitro-N-nitrosoguanidine and was mutagenic to mouse lymphoma cells.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Cell biology and toxicology AU - Huff, J E AU - Salmon, A G AU - Hooper, N K AU - Zeise, L AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 67 EP - 94 VL - 7 IS - 1 SN - 0742-2091, 0742-2091 KW - Polychlorinated Dibenzodioxins KW - 0 KW - Index Medicus KW - Animals KW - Humans KW - Mutation KW - Male KW - Female KW - Cell Line KW - Polychlorinated Dibenzodioxins -- analogs & derivatives KW - Polychlorinated Dibenzodioxins -- pharmacokinetics KW - Polychlorinated Dibenzodioxins -- adverse effects KW - Neoplasms -- chemically induced KW - Polychlorinated Dibenzodioxins -- toxicity KW - Neoplasms -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80630423?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+biology+and+toxicology&rft.atitle=Long-term+carcinogenesis+studies+on+2%2C3%2C7%2C8-tetrachlorodibenzo-p-dioxin+and+hexachlorodibenzo-p-dioxins.&rft.au=Huff%2C+J+E%3BSalmon%2C+A+G%3BHooper%2C+N+K%3BZeise%2C+L&rft.aulast=Huff&rft.aufirst=J&rft.date=1991-01-01&rft.volume=7&rft.issue=1&rft.spage=67&rft.isbn=&rft.btitle=&rft.title=Cell+biology+and+toxicology&rft.issn=07422091&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-31 N1 - Date created - 1991-07-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Carcinogenicity of chrysotile asbestos: a case control study of textile workers. AN - 80628708; 1647260 AB - Chrysotile is the predominant type of asbestos used in the United States and thus represents the most important source of exposure to asbestos already in place. While the steepest exposure-response observed for lung cancer has been in workers exposed to chrysotile in textile operations, some argue that chrysotile is less carcinogenic than amphibole asbestos types. Mineral oil exposures have been hypothesized to be responsible for the highly elevated lung cancer risk seen in textile workers. A lung cancer case-control analysis among a cohort of South Carolina chrysotile asbestos textile workers was conducted. Only a modest reduction in the slope of the lung cancer exposure-response relationship was observed after controlling for mineral oil exposures. These data do not support mineral oil exposure as a plausible explanation for the elevated lung cancer risk seen in chrysotile asbestos textile workers. The possible role of longer, thinner, more carcinogenic fibers in textiles is one plausible hypothesis needing further investigation. JF - Cell biology and toxicology AU - Dement, J M AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 17709. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 59 EP - 65 VL - 7 IS - 1 SN - 0742-2091, 0742-2091 KW - Asbestos, Serpentine KW - 0 KW - Asbestos KW - 1332-21-4 KW - Mineral Oil KW - 8020-83-5 KW - Index Medicus KW - South Carolina KW - Humans KW - Cohort Studies KW - Mineral Oil -- adverse effects KW - Case-Control Studies KW - Male KW - Lung Neoplasms -- etiology KW - Lung Neoplasms -- epidemiology KW - Occupational Diseases -- etiology KW - Asbestos -- adverse effects KW - Lung Neoplasms -- mortality KW - Textile Industry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80628708?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+biology+and+toxicology&rft.atitle=Carcinogenicity+of+chrysotile+asbestos%3A+a+case+control+study+of+textile+workers.&rft.au=Dement%2C+J+M&rft.aulast=Dement&rft.aufirst=J&rft.date=1991-01-01&rft.volume=7&rft.issue=1&rft.spage=59&rft.isbn=&rft.btitle=&rft.title=Cell+biology+and+toxicology&rft.issn=07422091&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-31 N1 - Date created - 1991-07-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Structural basis for catalysis by tryptophan synthase. AN - 80628354; 2053470 JF - Advances in enzymology and related areas of molecular biology AU - Miles, E W AD - Laboratory of Biochemistry and Pharmacology, National Institutes of Health, Bethesda, Maryland. Y1 - 1991 PY - 1991 DA - 1991 SP - 93 EP - 172 VL - 64 SN - 0065-258X, 0065-258X KW - Macromolecular Substances KW - 0 KW - Tryptophan Synthase KW - EC 4.2.1.20 KW - Index Medicus KW - Mutagenesis, Site-Directed KW - X-Ray Diffraction KW - Models, Molecular KW - Kinetics KW - Escherichia coli -- genetics KW - Escherichia coli -- enzymology KW - Amino Acid Sequence KW - Salmonella typhimurium -- genetics KW - Salmonella typhimurium -- enzymology KW - Protein Conformation KW - Catalysis KW - Tryptophan Synthase -- metabolism KW - Tryptophan Synthase -- chemistry KW - Tryptophan Synthase -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80628354?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advances+in+enzymology+and+related+areas+of+molecular+biology&rft.atitle=Structural+basis+for+catalysis+by+tryptophan+synthase.&rft.au=Miles%2C+E+W&rft.aulast=Miles&rft.aufirst=E&rft.date=1991-01-01&rft.volume=64&rft.issue=&rft.spage=93&rft.isbn=&rft.btitle=&rft.title=Advances+in+enzymology+and+related+areas+of+molecular+biology&rft.issn=0065258X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-24 N1 - Date created - 1991-07-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Upregulation of the opioid receptor complex by the chronic administration of morphine: a biochemical marker related to the development of tolerance and dependence. AN - 80624591; 1646998 AB - Studies conducted after the development of the rapid filtration assay for opiate receptors, and before the recognition of multiple opioid receptors, failed to detect changes in opioid receptors induced by chronic morphine. Recent experiments conducted in our laboratories were designed to examine the hypothesis that only one of several opioid receptor types might be altered by chronic morphine. Using binding surface analysis and irreversible ligands to increase the "resolving power" of the ligand binding assay, the results indicated that chronic morphine increased both the Bmax and Kd of the opioid receptor complex, labeled with either [3H][D-Ala2,D-Leu5]enkephalin, [3H][D-Ala2-MePhe4,Gly-ol5]enkephalin or [3H]6-desoxy-6 beta-fluoronaltreone. In the present study rats were pretreated with drugs known to attenuate the development of tolerance and dependence [the irreversible mu-receptor antagonist, beta-funaltrexamine (beta-FNA), and the inhibitor of tryptophan hydroxylase, para-chlorophenylalanine], prior to subcutaneous implantation of morphine pellets. The results demonstrated that 1) unlike chronic naltrexone, beta-FNA failed to upregulate opioid receptors and 2) both beta-funaltrexamine and PCPA pretreatment attenuated the chronic morphine-induced increase in the Bmax, but not the Kd, of the opioid receptor complex. These results provide evidence that naltrex-one-induced upregulation of the opioid receptor complex might occur indirectly as a consequence of interactions at beta-funaltrexamine-insensitive opioid receptors and that morphine-induced upregulation (increased Bmax) of the opioid receptor complex is a relevant in vitro marker related to the development of tolerance and dependence. These data collectively support the hypothesis that endogenous antiopiate peptides play an important role in the development of tolerance and dependence to morphine. JF - Peptides AU - Rothman, R B AU - Long, J B AU - Bykov, V AU - Xu, H AU - Jacobson, A E AU - Rice, K C AU - Holaday, J W AD - Unit on Receptor Studies, NIMH, Bethesda, MD 20892. PY - 1991 SP - 151 EP - 160 VL - 12 IS - 1 SN - 0196-9781, 0196-9781 KW - Biomarkers KW - 0 KW - Narcotic Antagonists KW - Receptors, Opioid KW - Receptors, Opioid, delta KW - Receptors, Opioid, mu KW - Naltrexone KW - 5S6W795CQM KW - beta-funaltrexamine KW - 72782-05-9 KW - Morphine KW - 76I7G6D29C KW - Index Medicus KW - Animals KW - Naltrexone -- analogs & derivatives KW - Amino Acid Sequence KW - Radioligand Assay KW - Rats KW - Rats, Inbred Strains KW - Biomarkers -- chemistry KW - Drug Tolerance -- physiology KW - Up-Regulation -- drug effects KW - Molecular Sequence Data KW - Naltrexone -- pharmacology KW - Time Factors KW - Narcotic Antagonists -- pharmacology KW - Male KW - Morphine Dependence -- metabolism KW - Receptors, Opioid -- drug effects KW - Morphine Dependence -- prevention & control KW - Morphine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80624591?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Peptides&rft.atitle=Upregulation+of+the+opioid+receptor+complex+by+the+chronic+administration+of+morphine%3A+a+biochemical+marker+related+to+the+development+of+tolerance+and+dependence.&rft.au=Rothman%2C+R+B%3BLong%2C+J+B%3BBykov%2C+V%3BXu%2C+H%3BJacobson%2C+A+E%3BRice%2C+K+C%3BHoladay%2C+J+W&rft.aulast=Rothman&rft.aufirst=R&rft.date=1991-01-01&rft.volume=12&rft.issue=1&rft.spage=151&rft.isbn=&rft.btitle=&rft.title=Peptides&rft.issn=01969781&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-22 N1 - Date created - 1991-07-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Peptides 1991 May-Jun;12(3):671 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Selective retention of MPP+ within the monoaminergic systems of the primate brain following MPTP administration: an in vivo autoradiographic study. AN - 80624355; 2052148 AB - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) selectively destroys dopaminergic neurons of the substantia nigra pars compacta in humans and other primates, producing a parkinsonian condition. MPTP is metabolized to the toxin 1-methyl-4-phenylpyridine (MPP+) which is taken up by dopamine terminals. The subsequent events culminating in cell death in the substantia nigra pars compacta are not understood. To examine these events we first produced a chronic hemiparkinsonian condition in monkeys by administering a toxic dose of MPTP via the right carotid artery. One year later, these monkeys were given a trace dose of [14C]MPTP intravenously and allowed to survive 1, 3, or 10 days. In two acute conditions, monkeys were either given the radiolabeled trace dose intravenously immediately following the toxic intracarotid dose, or were given a single toxic intracarotid radiolabeled dose, and allowed to survive 1, 3, or 10 days. We show by histology and autoradiography that the chronic hemiparkinsonian condition is characterized by selective unilateral loss of nigrostriatal dopamine neurons and absence of MPP+ retention in the caudate-putamen. In the acute conditions, MPP+ is accumulated and selectively retained in high concentrations in the caudate-putamen bilaterally and throughout the nigrostriatal pathway only on the side receiving the toxic dose. In the substantia nigra pars compacta. MPP+ is accumulated in very low concentrations in the dopamine cell bodies and is not selectively retained there. At 10 days survival, the caudate-putamen on the side receiving the toxic dose loses its ability to retain MPP+. The apparent degeneration of the dopamine axon terminals in the caudate-putamen and the development of Parkinson-like behavioral signs seen at 10 days survival were observed to precede the loss of cell bodies in the substantia nigra, which appeared normal by the criteria of Nissl staining and neuromelanin content at all time points in the acute conditions. Other areas of dense MPP+ retention in all cases include noradrenergic and serotonergic cell groups and noradrenergic pathways. MPP+ in the locus coeruleus and other caudal catecholaminergic cell groups is apparently retrogradely transported there after uptake in terminal regions, and although it is retained in high concentrations, no cell loss occurs. These findings suggest that experimentally induced Parkinsonism results from molecular events initiated in the neostriatum and selectively elaborated in the nigrostriatal pathway, ultimately resulting in the death of substantia nigra pars compacta dopamine neurons. They do not support a significant role for neuromelanin binding in the toxicity of MPP+. JF - Neuroscience AU - Herkenham, M AU - Little, M D AU - Bankiewicz, K AU - Yang, S C AU - Markey, S P AU - Johannessen, J N AD - Section on Functional Neuroanatomy, NIMH, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 133 EP - 158 VL - 40 IS - 1 SN - 0306-4522, 0306-4522 KW - Biogenic Amines KW - 0 KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - 1-Methyl-4-phenylpyridinium KW - R865A5OY8J KW - Index Medicus KW - Substantia Nigra -- metabolism KW - Animals KW - Macaca fascicularis KW - Corpus Striatum -- metabolism KW - Autoradiography KW - Densitometry KW - Biogenic Amines -- metabolism KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- pharmacology KW - 1-Methyl-4-phenylpyridinium -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80624355?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroscience&rft.atitle=Selective+retention+of+MPP%2B+within+the+monoaminergic+systems+of+the+primate+brain+following+MPTP+administration%3A+an+in+vivo+autoradiographic+study.&rft.au=Herkenham%2C+M%3BLittle%2C+M+D%3BBankiewicz%2C+K%3BYang%2C+S+C%3BMarkey%2C+S+P%3BJohannessen%2C+J+N&rft.aulast=Herkenham&rft.aufirst=M&rft.date=1991-01-01&rft.volume=40&rft.issue=1&rft.spage=133&rft.isbn=&rft.btitle=&rft.title=Neuroscience&rft.issn=03064522&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-22 N1 - Date created - 1991-07-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Multidrug resistance gene family and chemical carcinogens. AN - 80622197; 1675806 AB - The data discussed in this review indicate that the coordinated induction of both the mdr gene family and a subfamily of the cytochrome P-450 supergene family provide a unified response of the organism to prevent lethal accumulation of xenobiotics. Consequently, a distinct physiological role for the mdr multigene family now exists. Furthermore, recent evidence suggests the existence of multiple receptors with overlapping substrate specificity that are involved in the induction of both mdr and P-4501A gene families. The increased expression of mdr gene(s) in the early stages of liver carcinogenesis and presumably in other tissues is associated with the development of xenobiotic resistance that is observed in the preneoplastic cell populations. These observations may have important clinical implications and may provide an explanation for resistance to chemotherapy of tumors in organs such as liver and colon that are frequently exposed to both environmental and dietary xenobiotics. JF - Pharmacology & therapeutics AU - Thorgeirsson, S S AU - Silverman, J A AU - Gant, T W AU - Marino, P A AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD. Y1 - 1991 PY - 1991 DA - 1991 SP - 283 EP - 292 VL - 49 IS - 3 SN - 0163-7258, 0163-7258 KW - mdr KW - Carcinogens KW - 0 KW - Membrane Glycoproteins KW - P-Glycoprotein KW - Xenobiotics KW - Index Medicus KW - Animals KW - Membrane Glycoproteins -- isolation & purification KW - Carcinogens -- pharmacology KW - Gene Expression Regulation -- physiology KW - Drug Tolerance -- genetics KW - Xenobiotics -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80622197?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacology+%26+therapeutics&rft.atitle=Multidrug+resistance+gene+family+and+chemical+carcinogens.&rft.au=Thorgeirsson%2C+S+S%3BSilverman%2C+J+A%3BGant%2C+T+W%3BMarino%2C+P+A&rft.aulast=Thorgeirsson&rft.aufirst=S&rft.date=1991-01-01&rft.volume=49&rft.issue=3&rft.spage=283&rft.isbn=&rft.btitle=&rft.title=Pharmacology+%26+therapeutics&rft.issn=01637258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-22 N1 - Date created - 1991-07-22 N1 - Date revised - 2017-01-13 N1 - Gene symbol - mdr N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Carcinogenesis studies in rodents for evaluating risks associated with chemical carcinogens in aquatic food animals. AN - 80617708; 2050050 AB - Fish and shellfish caught in polluted waters contain potentially dangerous amounts of toxic and carcinogenic chemicals. Public concern was heightened when a large percentage of winter flounder taken from Boston Harbor was found to have visible cancer of the liver; winter flounder outside the estuary area had no liver lesions. Long-term chemical carcinogenesis studies could be easily and feasibly designed using laboratory rodents offered diets containing fish caught in polluted waters. Induced cancers in rodents would corroborate field observations in fish; positive results from these studies would provide further evidence about potential human health hazards from eating substantial amounts of chemically contaminated fish. Nonetheless, fish and aquatic organisms should be viewed as environmental biological monitors of pollution or of potential human health hazards, and authorities responsible for assuring clean and safe rivers, bodies of water, and biota should give more attention to these valid biological indicators or sentinels of environmental pollution. Consequently, fish and other sea creatures alone should serve as alarms regarding whether water areas constitute public health hazards. JF - Environmental health perspectives AU - Huff, J AU - Bucher, J AU - Yang, R AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 127 EP - 132 VL - 90 SN - 0091-6765, 0091-6765 KW - Carcinogens, Environmental KW - 0 KW - Water Pollutants, Chemical KW - Index Medicus KW - Risk KW - Animals KW - Confounding Factors (Epidemiology) KW - Liver Neoplasms -- chemically induced KW - Carcinogenicity Tests -- methods KW - Mice KW - Research Design KW - Carcinogens, Environmental -- adverse effects KW - Water Pollutants, Chemical -- adverse effects KW - Fishes KW - Food Contamination -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80617708?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Carcinogenesis+studies+in+rodents+for+evaluating+risks+associated+with+chemical+carcinogens+in+aquatic+food+animals.&rft.au=Huff%2C+J%3BBucher%2C+J%3BYang%2C+R&rft.aulast=Huff&rft.aufirst=J&rft.date=1991-01-01&rft.volume=90&rft.issue=&rft.spage=127&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 - 1991-07-25 N1 - Date created - 1991-07-25 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Sci Total Environ. 1990 May 1;94(1-2):155-67 [2163106] Environ Health Perspect. 1991 Jan;90:7-15 [2050084] Environ Health Perspect. 1991 Jan;90:111-6 [2050048] Environ Health Perspect. 1991 Jan;90:141-6 [2050052] Fed Proc. 1967 Jul-Aug;26(4):1047-55 [5339255] Ann N Y Acad Sci. 1978 Sep 29;298:1 [280175] J Toxicol Environ Health. 1981 Jul-Aug;8(1-2):251-80 [7328708] Bull Environ Contam Toxicol. 1981 Dec;27(6):829-35 [6802204] Gan. 1983 Oct;74(5):633-9 [6642137] Science. 1984 Mar 9;223(4640):1077-9 [6695194] Transplant Proc. 1984 Apr;16(2):406-11 [6719546] Natl Cancer Inst Monogr. 1984 May;65:223-35 [6749256] Natl Cancer Inst Monogr. 1984 May;65:35-43 [6462195] J Natl Cancer Inst. 1985 Feb;74(2):487-94 [3856055] Proc Natl Acad Sci U S A. 1986 Jan;83(1):33-7 [3510430] Science. 1986 Apr 25;232(4749):497-9 [3961492] Fundam Appl Toxicol. 1986 Feb;6(2):364-71 [3084326] Proc Natl Acad Sci U S A. 1986 Aug;83(16):5825-9 [3016723] J Natl Cancer Inst. 1987 Feb;78(2):333-63 [3543454] Comp Biochem Physiol C. 1987;86(2):233-45 [2882912] Arch Toxicol Suppl. 1987;10:10-26 [3555413] Environ Health Perspect. 1987 Apr;71:129-37 [3297655] Environ Health Perspect. 1987 Apr;71:155-70 [3297658] Environ Health Perspect. 1987 Apr;71:5-16 [3297664] J Natl Cancer Inst. 1987 Aug;79(2):297-321 [3474464] Annu Rev Biochem. 1987;56:779-827 [3304147] Science. 1987 Sep 11;237(4820):1309-16 [3629242] Cancer Lett. 1987 Oct 30;37(2):125-32 [3677049] Toxicology. 1987 Dec 1;47(1-2):15-34 [3686528] Environ Health Perspect. 1987 Oct;74:229-35 [3691430] Environ Health Perspect. 1987 Nov;75:153-8 [3691436] Symp Fundam Cancer Res. 1986;39:45-56 [3321309] FASEB J. 1988 Apr;2(7):2241-51 [3280378] Jpn J Cancer Res. 1988 May;79(5):545-55 [3136106] Environ Health Perspect. 1988 Jun;78:175-7 [3203636] Am J Public Health. 1989 Mar;79(3):322-5 [2916719] Cancer Res. 1989 Jul 15;49(14):3713-21 [2660980] Cancer Metastasis Rev. 1989 Jun;8(1):1-22 [2667783] Jpn J Cancer Res. 1989 Sep;80(9):795-807 [2513295] Toxicol Lett. 1989 Dec;49(2-3):183-97 [2690403] Fundam Appl Toxicol. 1989 Oct;13(3):366-76 [2612771] Proc Natl Acad Sci U S A. 1990 Jan;87(2):841-5 [2405390] Pharmacol Ther. 1990;46(3):469-86 [2188272] Environ Health Perspect. 1991 Jan;90:17-26 [1646709] Environ Health Perspect. 1991 Jan;90:27-33 [2050071] Environ Health Perspect. 1991 Jan;90:69-73 [1904811] Environ Health Perspect. 1991 Jan;90:101-9 [2050047] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Genotoxicity of multifunctional acrylates in the Salmonella/mammalian-microsome assay and mouse lymphoma TK+/-assay. AN - 80617120; 2050134 AB - Multifunctional acrylates are being used increasingly as replacements for solvents, and occupational and general population exposure to this structural class is expanding. Four multifunctional acrylates and acrylic acid were tested for mutagenicity in the Salmonella typhimurium and mouse lymphoma L5178Y TK+/-assays. In the Salmonella assay, two of the compounds (trimethylolpropane triacrylate and trimethylolpropane trimethacrylate) showed weakly positive results with a single tester strain (TA1535) in the presence of hamster liver S9; the other three compounds were negative. All five compounds were negative in the Salmonella assay without S9 activation. In the mouse lymphoma assay, two of the compounds (acrylic acid and ethylene glycol diacrylate) were positive in both the presence and the absence of S9, one compound was positive only in the presence of S9 (ethylene glycol dimethacrylate), and one compound was positive only in the absence of S9 (trimethylolpropane triacrylate). JF - Environmental and molecular mutagenesis AU - Cameron, T P AU - Rogers-Back, A M AU - Lawlor, T E AU - Harbell, J W AU - Seifried, H E AU - Dunkel, V C AD - National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 264 EP - 271 VL - 17 IS - 4 SN - 0893-6692, 0893-6692 KW - Acrylates KW - 0 KW - acrylic acid KW - J94PBK7X8S KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Tumor Cells, Cultured -- drug effects KW - Mesocricetus KW - Mice KW - Male KW - Cricetinae KW - Mutagenicity Tests KW - Microsomes, Liver -- drug effects KW - Salmonella typhimurium -- drug effects KW - Leukemia L5178 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80617120?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+and+molecular+mutagenesis&rft.atitle=Genotoxicity+of+multifunctional+acrylates+in+the+Salmonella%2Fmammalian-microsome+assay+and+mouse+lymphoma+TK%2B%2F-assay.&rft.au=Cameron%2C+T+P%3BRogers-Back%2C+A+M%3BLawlor%2C+T+E%3BHarbell%2C+J+W%3BSeifried%2C+H+E%3BDunkel%2C+V+C&rft.aulast=Cameron&rft.aufirst=T&rft.date=1991-01-01&rft.volume=17&rft.issue=4&rft.spage=264&rft.isbn=&rft.btitle=&rft.title=Environmental+and+molecular+mutagenesis&rft.issn=08936692&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-22 N1 - Date created - 1991-07-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Relative roles of metabolism and renal excretory mechanisms in xenobiotic elimination by fish. AN - 80616450; 2050085 AB - Renal clearance techniques were used to examine the relative contributions of metabolism and renal tubular transport in determining the rates of excretion of benzo(a)pyrene (BaP) and several of its phase I metabolites by southern flounder, Paralichthys lethostigma. Each compound (3H-labeled) was injected at a dose of 2.5 mumole/kg, producing plasma concentrations of 1 to 5 microM. Despite extensive plasma binding (greater than 95%), the uncorrected renal clearance of BaP-7,8-dihydrodiol exceeded the glomerular filtration rate (GFR) by more than 20-fold. Phenolic BaP metabolites also showed net secretion (1.5- to 3-fold). At times prior to 3 hr, BaP itself showed an average clearance of only 0.2 times the GFR. After 3 hr, BaP clearance increased to three times the GFR. Decreasing the dose of BaP injected also dramatically increased its clearance. Clearances of all four compounds studied were reduced by probenecid and other organic anion, including the herbicide 2,4-dichlorophenoxyacetic acid. HPLC analysis demonstrated that the bulk of the material excreted in the urine was not the parent compound, but sulfate or glucuronide conjugates of its phenolic or dihydrodiol metabolites. Excretion of sulfate conjugates predominated over the first 24 hr, whereas the glucuronide conjugates were the primary excretory products in succeeding days. In vitro, isolated renal tubules transported both glucuronide and sulfate conjugates, but sulfates were the preferred substrates. Isolated tubules were shown to be capable of catalyzing conjugation reactions, producing predominantly glucuronide conjugates. Liver slices produced both types of conjugates. Thus, the rapid excretion of BaP-7,8-dihydrodiol reflected a combination of two processes.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Environmental health perspectives AU - Pritchard, J B AU - Bend, J R AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 85 EP - 92 VL - 90 SN - 0091-6765, 0091-6765 KW - Water Pollutants, Chemical KW - 0 KW - Benzo(a)pyrene KW - 3417WMA06D KW - Hymecromone KW - 3T5NG4Q468 KW - Probenecid KW - PO572Z7917 KW - Index Medicus KW - Animals KW - Hymecromone -- pharmacology KW - Liver -- drug effects KW - Metabolic Clearance Rate -- physiology KW - In Vitro Techniques KW - Metabolic Clearance Rate -- drug effects KW - Liver -- metabolism KW - Probenecid -- pharmacology KW - Male KW - Female KW - Chromatography, High Pressure Liquid KW - Kidney Tubules -- drug effects KW - Water Pollutants, Chemical -- pharmacokinetics KW - Kidney Tubules -- metabolism KW - Benzo(a)pyrene -- pharmacokinetics KW - Flounder -- metabolism KW - Benzo(a)pyrene -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80616450?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Relative+roles+of+metabolism+and+renal+excretory+mechanisms+in+xenobiotic+elimination+by+fish.&rft.au=Pritchard%2C+J+B%3BBend%2C+J+R&rft.aulast=Pritchard&rft.aufirst=J&rft.date=1991-01-01&rft.volume=90&rft.issue=&rft.spage=85&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 - 1991-07-25 N1 - Date created - 1991-07-25 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Am J Physiol. 1977 Aug;233(2):F126-32 [888953] J Pharmacol Exp Ther. 1979 Feb;208(2):280-6 [762661] Chem Biol Interact. 1979 May;25(2-3):321-44 [466737] Toxicol Appl Pharmacol. 1980 Jun 15;54(1):117-33 [7394780] Am J Physiol. 1976 Aug;231(2):603-7 [961913] Drug Metab Dispos. 1984 Jul-Aug;12(4):389-95 [6148203] J Environ Pathol Toxicol Oncol. 1984 Jul;5(4-5):309-20 [6520733] Science. 1948 Jul 16;108(2794):65-7 [17777516] Science. 1976 Aug 20;193(4254):680-1 [948743] Fed Proc. 1980 Dec;39(14):3207-12 [7002623] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transplacental induction of mouse lung tumors: stage of fetal organogenesis in relation to frequency, morphology, size, and neoplastic progression of N-nitrosoethylurea-induced tumors. AN - 80612539; 2047706 AB - Pregnant C3H/HeNCr MTV- mice were given a single intraperitoneal injection of 0.5 mmol N-nitrosoethylurea/kg on days 14, 16, or 18 of gestation. Six of the male offspring were sacrificed for study at the ages of 2, 4, 8, 16, 32, and 52 weeks. Grossly visible lung tumors were counted and all lungs were sectioned completely, saving every tenth section for histologic evaluation. All N-nitrosoethylurea-induced mouse lung tumors have previously been shown to originate from alveolar type II cells. Lung tumors were diagnosed as solid, papillary, or mixed solid/papillary types, and at the largest area of each tumor, the perimeter was measured and compared with the number of sections per tumor. The fraction of tumors detected grossly depended on size and, on average, only 51% of neoplasms present were detected macroscopically. A significant correlation was seen between the mean number of histological sections and perimeter length per tumor, in particular for small and medium sized papillary neoplasms. The growth of solid tumors was limited to a maximum size, after which they progressed towards papillary types. The numbers of transplacentally induced mouse lung tumors were distributed in direct proportion to the weight of the individual lung lobes, unrelated to day of treatment of type or tumor. Tumor biology depended on the day of treatment reflecting numbers of degree of differentiation of fetal alveolar type II cells, i.e., the target cell: most tumors developed in offspring treated on day 16, tumor size was greater and progression from solid to papillary neoplasms faster at earlier treatments, increase in tumor multiplicity postnatally was only seen in mice treated late in gestation, and mice treated on day 14 or day 16 showed a consistent ratio of solid to papillary tumors. JF - Toxicologic pathology AU - Rehm, S AU - Ward, J M AU - Anderson, L M AU - Riggs, C W AU - Rice, J M AD - Tumor Pathology and Pathogenesis Section, National Cancer Institute, Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1991 PY - 1991 DA - 1991 SP - 35 EP - 46 VL - 19 IS - 1 SN - 0192-6233, 0192-6233 KW - Ethylnitrosourea KW - P8M1T4190R KW - Index Medicus KW - Animals KW - Gestational Age KW - Mice, Inbred C3H KW - Mice KW - Male KW - Female KW - Pregnancy KW - Maternal-Fetal Exchange KW - Fetal Diseases -- chemically induced KW - Fetal Diseases -- pathology KW - Lung Neoplasms -- chemically induced KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80612539?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+pathology&rft.atitle=Transplacental+induction+of+mouse+lung+tumors%3A+stage+of+fetal+organogenesis+in+relation+to+frequency%2C+morphology%2C+size%2C+and+neoplastic+progression+of+N-nitrosoethylurea-induced+tumors.&rft.au=Rehm%2C+S%3BWard%2C+J+M%3BAnderson%2C+L+M%3BRiggs%2C+C+W%3BRice%2C+J+M&rft.aulast=Rehm&rft.aufirst=S&rft.date=1991-01-01&rft.volume=19&rft.issue=1&rft.spage=35&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=01926233&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-17 N1 - Date created - 1991-07-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Detection and cellular localization of lead by electron probe analysis in the diagnosis of suspected lead poisoning in rhesus monkeys. AN - 80612503; 1646479 AB - Lead poisoning of unknown source was diagnosed histologically in 2 rhesus monkeys (Macaca mulatta) by finding acid-fast intranuclear inclusion bodies in the epithelial cells of renal cortical tubules. The presence of lead in the inclusions was determined by scanning electron microscopy/energy dispersive x-ray analysis using sections from paraffin embedded tissues. This observation indicates the usefulness of this technique for the detection and cellular localization of lead in tissues, even from archival material. JF - Toxicologic pathology AU - Sass, B AU - Banfield, W G AU - Saffiotti, U AD - Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 30 EP - 34 VL - 19 IS - 1 SN - 0192-6233, 0192-6233 KW - Lead KW - 2P299V784P KW - Index Medicus KW - Electron Probe Microanalysis KW - Animals KW - Macaca mulatta KW - Inclusion Bodies -- chemistry KW - Female KW - Microscopy, Electron, Scanning KW - Lead Poisoning -- diagnosis KW - Lead -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80612503?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+pathology&rft.atitle=Detection+and+cellular+localization+of+lead+by+electron+probe+analysis+in+the+diagnosis+of+suspected+lead+poisoning+in+rhesus+monkeys.&rft.au=Sass%2C+B%3BBanfield%2C+W+G%3BSaffiotti%2C+U&rft.aulast=Sass&rft.aufirst=B&rft.date=1991-01-01&rft.volume=19&rft.issue=1&rft.spage=30&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=01926233&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-17 N1 - Date created - 1991-07-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Charybdotoxin-sensitive K(Ca) channel is not involved in glucose-induced electrical activity in pancreatic beta-cells. AN - 80609224; 1710672 AB - The effects of charybdotoxin (CTX) on single [Ca2+]-activated potassium channel (K(Ca)) activity and whole-cell K+ currents were examined in rat and mouse pancreatic beta-cells in culture using the patch-clamp method. The effects of CTX on glucose-induced electrical activity from both cultured beta-cells and beta-cells in intact islets were compared. K(Ca) activity was very infrequent at negative patch potentials (-70 less than Vm less than 0 mV), channel activity appearing at highly depolarized Vm. K(Ca) open probability at these depolarized Vm values was insensitive to glucose (10 and 20 mM) and the metabolic uncoupler 2,4 dinitrophenol (DNP). However, DNP blocked glucose-evoked action potential firing and reversed glucose-induced inhibition of the activity of K+ channels of smaller conductance. The venom from Leiurus quinquestriatus hebreus (LQV) and highly purified CTX inhibited K(Ca) channel activity when applied to the outer aspect of the excised membrane patch. CTX (5.8 and 18 nM) inhibited channel activity by 50 and 100%, respectively. Whole-cell outward K+ currents exhibited an early transient component which was blocked by CTX, and a delayed component which was insensitive to the toxin. The individual spikes evoked by glucose, recorded in the perforated-patch modality, were not affected by CTX (20 nM). Moreover, the frequency of slow oscillations in membrane potential, the frequency of action potentials and the rate of repolarization of the action potentials recorded from pancreatic islet beta-cells in the presence of glucose were not affected by CTX. We conclude that the K(Ca) does not participate in the steady-state glucose-induced electrical activity in rodent pancreatic islets. JF - The Journal of membrane biology AU - Kukuljan, M AU - Goncalves, A A AU - Atwater, I AD - Laboratory of Cell Biology and Genetics, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 187 EP - 195 VL - 119 IS - 2 SN - 0022-2631, 0022-2631 KW - Dinitrophenols KW - 0 KW - Potassium Channels KW - Scorpion Venoms KW - Charybdotoxin KW - 115422-61-2 KW - Glucose KW - IY9XDZ35W2 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Cells, Cultured KW - Membrane Potentials KW - Dinitrophenols -- pharmacology KW - Mice KW - Male KW - Potassium Channels -- metabolism KW - Scorpion Venoms -- pharmacology KW - Glucose -- physiology KW - Islets of Langerhans -- cytology KW - Islets of Langerhans -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80609224?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+membrane+biology&rft.atitle=Charybdotoxin-sensitive+K%28Ca%29+channel+is+not+involved+in+glucose-induced+electrical+activity+in+pancreatic+beta-cells.&rft.au=Kukuljan%2C+M%3BGoncalves%2C+A+A%3BAtwater%2C+I&rft.aulast=Kukuljan&rft.aufirst=M&rft.date=1991-01-01&rft.volume=119&rft.issue=2&rft.spage=187&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+membrane+biology&rft.issn=00222631&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-16 N1 - Date created - 1991-07-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Long-term follow-up of ProMACE-CytaBOM in non-Hodgkin's lymphomas. AN - 80601468; 1710487 AB - Initial results from studies with third-generation combination chemotherapy regimens for the treatment of aggressive non-Hodgkin's lymphomas (NHL) demonstrated complete remission (CR) rates higher than those reported with first-generation regimens. Long-term follow-up of these studies is required to know if the increased number of CRs translates into an increased number of long-term disease-free survivors. In this report, results obtained with one of the third-generation regimens, ProMACE (prednisone/methotrexate/doxorubicin/cyclophosphamide/etoposide)-Cyta BOM (cytarabine/bleomycin/vincristine/methotrexate) are described. From 1981 to 1988, 193 patients with stage II, III, or IV aggressive NHL treated at the National Cancer Institute were randomly assigned to receive either ProMACE (day 1)-CytaBOM (day 8) or ProMACE (day 1)-MOPP (mechlorethamine/vincristine/procarbazine/prednisone) (day 8). With a median follow-up of 5 years, the CR rate was 86% for ProMACE-CytaBOM v 74% for ProMACE-MOPP (P = 0.048). A plateau in the disease-free survival curve is seen at 69% for ProMACE-CytaBOM v 54% for ProMACE-MOPP (P = 0.082). A plateau is also seen in the overall survival curves at 69% for ProMACE-CytaBOM v 53% for ProMACE-MOPP (P = 0.046). The Southwest Oncology Group also conducted a phase II study of ProMACE-CytaBOM in 78 patients with stages II to IV intermediate- or high-grade NHL to determine the CR rate and long-term disease-free survival of this regimen in a national cooperative group setting. The CR rate was 65%. With a median follow-up of 38 months, disease-free survival is 50% at 3 years and overall survival is 57% at the same time point.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Annals of oncology : official journal of the European Society for Medical Oncology AU - Fisher, R I AU - Longo, D L AU - DeVita, V T AU - Hubbard, S M AU - Miller, T P AU - Young, R C AD - National Cancer Institute, Bethesda, Maryland. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 33 EP - 35 VL - 2 Suppl 1 SN - 0923-7534, 0923-7534 KW - Cytarabine KW - 04079A1RDZ KW - Bleomycin KW - 11056-06-7 KW - Procarbazine KW - 35S93Y190K KW - Mechlorethamine KW - 50D9XSG0VR KW - Vincristine KW - 5J49Q6B70F KW - Etoposide KW - 6PLQ3CP4P3 KW - Doxorubicin KW - 80168379AG KW - Cyclophosphamide KW - 8N3DW7272P KW - Prednisone KW - VB0R961HZT KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - Cyclophosphamide -- administration & dosage KW - Mechlorethamine -- administration & dosage KW - Bleomycin -- administration & dosage KW - Humans KW - Vincristine -- administration & dosage KW - Aged KW - Doxorubicin -- administration & dosage KW - Cytarabine -- administration & dosage KW - Drug Evaluation KW - Procarbazine -- administration & dosage KW - Survival Rate KW - Etoposide -- administration & dosage KW - Follow-Up Studies KW - Middle Aged KW - Methotrexate -- administration & dosage KW - Prednisone -- administration & dosage KW - Remission Induction KW - Lymphoma, Non-Hodgkin -- drug therapy KW - Lymphoma, Non-Hodgkin -- mortality KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80601468?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Long-term+follow-up+of+ProMACE-CytaBOM+in+non-Hodgkin%27s+lymphomas.&rft.au=Fisher%2C+R+I%3BLongo%2C+D+L%3BDeVita%2C+V+T%3BHubbard%2C+S+M%3BMiller%2C+T+P%3BYoung%2C+R+C&rft.aulast=Fisher&rft.aufirst=R&rft.date=1991-01-01&rft.volume=2+Suppl+1&rft.issue=&rft.spage=33&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 - 1991-07-17 N1 - Date created - 1991-07-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Calcium-dependent regulation of the enkephalin phenotype by neuronal activity during early ontogeny. AN - 80592040; 1645773 AB - Genetic components of the neuronal phenotype are regulated by epigenetic factors--trophic molecules and neuronal activity--during neurodifferentiation. Developing neurons in dissociated cultures of embryonic mouse spinal cord show spontaneous electrical activity after one week in culture. We now report that the blockade of this spontaneous electrical activity for two days with tetrodotoxin (TTX) causes virtually complete down-regulation of preproenkephalin A gene transcripts in embryonic spinal cord cultures. This TTX-induced down-regulation is fully reversed upon reinitiation of neuronal activity (removal of TTX from cultures). This reversible, tetrodotoxin-induced down-regulation of enkephalin mRNA is confined to a restricted period of early neurodevelopment (days 7 to 21 in culture). Since depolarization triggers calcium entry through voltage-activated calcium channels, we have investigated the involvement of calcium in the mechanism of this activity- and age-dependent regulation of preproenkephalin A expression. The selective activation of the L-type of voltage-sensitive calcium channels by a dihydropyridine derivative [(+) 202-791] prevented this TTX-induced down-regulation without reducing methionine enkephalin secretion. This effect was observed only when the drug was applied to electrically active cultures, prior to the addition of TTX. Simultaneous application of (+) 202-791 and TTX, or pretreatment with TTX, failed to prevent TTX-induced down-regulation. Thus, activity-dependent phenotypic plasticity of met-enkephalinergic neurons in spinal cord is: 1) maximum at an early age of neuronal development (less than 10 days in culture) and becomes less apparent in old cultures (greater than 30 days); 2) reversible throughout; and 3) mediated by calcium entry through L-type channels. JF - Journal of neuroscience research AU - Agoston, D V AU - Eiden, L E AU - Brenneman, D E AD - Laboratory of Cell Biology, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 140 EP - 148 VL - 28 IS - 1 SN - 0360-4012, 0360-4012 KW - Calcium Channel Blockers KW - 0 KW - Enkephalins KW - Nicotinic Acids KW - Oxadiazoles KW - Protein Precursors KW - RNA, Messenger KW - Sodium Channels KW - PN 202-791 KW - 101342-80-7 KW - Tetrodotoxin KW - 4368-28-9 KW - Enkephalin, Methionine KW - 58569-55-4 KW - preproenkephalin KW - 93443-35-7 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Phenotype KW - Animals KW - Nicotinic Acids -- pharmacology KW - Calcium Channel Blockers -- pharmacology KW - RNA, Messenger -- analysis KW - Mice, Inbred C57BL KW - Membrane Potentials KW - Mice KW - Tetrodotoxin -- pharmacology KW - Sodium Channels -- drug effects KW - Signal Transduction KW - Ion Channel Gating -- drug effects KW - Enkephalins -- genetics KW - Neurons -- drug effects KW - Enkephalin, Methionine -- genetics KW - Protein Precursors -- genetics KW - Neuronal Plasticity -- physiology KW - Calcium -- pharmacology KW - Spinal Cord -- embryology KW - Ganglia, Spinal -- embryology KW - Enkephalin, Methionine -- biosynthesis KW - Ganglia, Spinal -- cytology KW - Enkephalins -- biosynthesis KW - Protein Precursors -- biosynthesis KW - Calcium -- physiology KW - Neurons -- physiology KW - Gene Expression Regulation -- drug effects KW - Synaptic Transmission KW - Spinal Cord -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80592040?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Calcium-dependent+regulation+of+the+enkephalin+phenotype+by+neuronal+activity+during+early+ontogeny.&rft.au=Agoston%2C+D+V%3BEiden%2C+L+E%3BBrenneman%2C+D+E&rft.aulast=Agoston&rft.aufirst=D&rft.date=1991-01-01&rft.volume=28&rft.issue=1&rft.spage=140&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 - 1991-07-11 N1 - Date created - 1991-07-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Regulation of transferrin receptor expression and control of cell growth. AN - 80590543; 1645975 AB - Transferrin receptor expression is vital for the continuous growth of most cells. Although iron plays a key role in modulating transferrin receptor expression, other physiological factors are also capable of affecting receptor expression. In hematopoietic cells, these include interleukin-2, interleukin-6, calcium channels, cyclic nucleotides, phorbol esters and viruses. In this review, we will describe how these agents can alter transferrin receptor expression at the levels of transcription, translation and receptor re-cycling. JF - Pathobiology : journal of immunopathology, molecular and cellular biology AU - Neckers, L M AD - Medicine Branch, NCI, NIH, Bethesda, Md. Y1 - 1991 PY - 1991 DA - 1991 SP - 11 EP - 18 VL - 59 IS - 1 SN - 1015-2008, 1015-2008 KW - Calcium Channels KW - 0 KW - Interleukin-6 KW - Phorbol Esters KW - Receptors, Interleukin-2 KW - Receptors, Transferrin KW - Transferrin KW - Bucladesine KW - 63X7MBT2LQ KW - Cyclic AMP KW - E0399OZS9N KW - Diltiazem KW - EE92BBP03H KW - Index Medicus KW - AIDS/HIV KW - Human T-lymphotropic virus 1 -- physiology KW - Calcium Channels -- physiology KW - Humans KW - Receptors, Interleukin-2 -- biosynthesis KW - Lymphocytes -- metabolism KW - Interphase -- drug effects KW - Interleukin-6 -- pharmacology KW - Bucladesine -- pharmacology KW - HTLV-I Infections -- genetics KW - Lymphocyte Activation KW - Phorbol Esters -- pharmacology KW - Diltiazem -- pharmacology KW - Tumor Cells, Cultured KW - Calcium Channels -- drug effects KW - Cyclic AMP -- pharmacology KW - Gene Expression Regulation -- drug effects KW - Receptors, Transferrin -- physiology KW - Receptors, Transferrin -- biosynthesis KW - Transferrin -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80590543?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pathobiology+%3A+journal+of+immunopathology%2C+molecular+and+cellular+biology&rft.atitle=Regulation+of+transferrin+receptor+expression+and+control+of+cell+growth.&rft.au=Neckers%2C+L+M&rft.aulast=Neckers&rft.aufirst=L&rft.date=1991-01-01&rft.volume=59&rft.issue=1&rft.spage=11&rft.isbn=&rft.btitle=&rft.title=Pathobiology+%3A+journal+of+immunopathology%2C+molecular+and+cellular+biology&rft.issn=10152008&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-17 N1 - Date created - 1991-07-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modulation of cytosine arabinoside toxicity by 3-deazauridine in a murine leukemia model. AN - 80565325; 2030604 AB - 3-Deazauridine (DAUrd), a competitive inhibitor of CTP synthetase, inhibits both RNA and DNA synthesis. Murine leukemia cells resistant to cytosine arabinoside (ara-C) due to a deletion of deoxycytidine kinase are collaterally sensitive to DAUrd, which inhibits the de novo production of CTP and hence results in dCTP depletion. We evaluated DAUrd in combination with the palmitate derivative of ara-C (palmO-ara-C) in mice bearing L1210 leukemia cells with a subpopulation resistant to ara-C. Both simultaneous administration and a sequential schedule of palmO-ara-C at its maximally tolerated dose (MTD), followed by DAUrd treatment, failed to produce a therapeutic gain. We also studied whether non-toxic doses of DAUrd (15-250 mg/kg i.p. at h 0 and 6 on days 4 and 8) could modulate the antileukemic activity of palmO-ara-C (7.5-120 mg/kg i.p. at h 3 on days 4 and 8). The addition of DAUrd produced a modest (but statistically significant) prolongation of life span and a further 2-log10 reduction in tumor burden compared to the same dose of palmO-ara-C alone, and resulted in long-term survivors in five of 30 treated animals. Two-dimensional dose-response analysis of the survival data indicated a positive drug interaction (p less than or equal to 0.01) when the dosage of DAUrd was modeled to reflect an apparent threshold effect. Cyclopentenyl cytosine (CPE-C; 0.625-2.5 mg/kg i.p. at h 0 and 6 on days 4 and 8), a more potent inhibitor of CTP synthetase, was also given with palmO-ara-C. This combination resulted in an additional 2-6 log10 units of cell kill and occasional long-term survivors at palmO-ara-C dosages that alone resulted in no more than 2 log10 units of cell kill and no long-term survivors. However, DAUrd and CPE-C given with palmO-ara-C increased host toxicity, compromising the tolerable dose of palmO-ara-C. Single-agent palmO-ara-C given at its MTD produced a similar reduction in tumor burden and increase in life span compared to the highest palmO-ara-C dose that could be given in combination with either modulator. JF - Leukemia research AU - Grem, J L AU - Plowman, J AU - Rubinstein, L AU - Hawkins, M J AU - Harrison, S D AD - Medicine Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 229 EP - 236 VL - 15 IS - 4 SN - 0145-2126, 0145-2126 KW - Cytarabine KW - 04079A1RDZ KW - 3-Deazauridine KW - 263CU738ZY KW - Cytidine KW - 5CSZ8459RP KW - cyclopentenyl cytosine KW - 69MO0NDN8K KW - 5'-palmitoyl cytarabine KW - O57A51JE0D KW - Index Medicus KW - Mice, Inbred Strains KW - Animals KW - Survival Rate KW - Cytidine -- administration & dosage KW - Drug Resistance KW - Mice KW - Cytarabine -- analogs & derivatives KW - Cytarabine -- administration & dosage KW - Drug Synergism KW - Cytidine -- analogs & derivatives KW - Male KW - Female KW - 3-Deazauridine -- administration & dosage KW - Remission Induction KW - Leukemia L1210 -- mortality KW - Leukemia L1210 -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80565325?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Leukemia+research&rft.atitle=Modulation+of+cytosine+arabinoside+toxicity+by+3-deazauridine+in+a+murine+leukemia+model.&rft.au=Grem%2C+J+L%3BPlowman%2C+J%3BRubinstein%2C+L%3BHawkins%2C+M+J%3BHarrison%2C+S+D&rft.aulast=Grem&rft.aufirst=J&rft.date=1991-01-01&rft.volume=15&rft.issue=4&rft.spage=229&rft.isbn=&rft.btitle=&rft.title=Leukemia+research&rft.issn=01452126&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-06-18 N1 - Date created - 1991-06-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Lack of neurochemical evidence for neurotoxic effects of repeated cocaine administration in rats on brain monoamine neurons. AN - 80561843; 1709403 AB - Rats were injected with cocaine (20 mg/kg, s.c. or i.p. twice daily for 8 days) or saline and killed at 1, 8, 15 or 48 days after the last injection. The concentrations of norepinephrine (NE), dopamine (DA), serotonin (5-HT) and their metabolites, assayed by HPLC-EC, in frontal cortex, hippocampus, striatum, hypothalamus, midbrain, pons-medulla and spinal cord were not significantly different from those in the saline-injected controls at any of the time points examined. These data suggest that the repeated cocaine administration in rats does not produce any long-term depletion in brain catecholamine and 5-HT content suggesting no neurotoxic effects of the drug. JF - Drug and alcohol dependence AU - Yeh, S Y AU - De Souza, E B AD - National Institute On Drug Abuse, Addiction Research Center, Baltimore, Maryland 21224. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 51 EP - 61 VL - 27 IS - 1 SN - 0376-8716, 0376-8716 KW - Receptors, Adrenergic KW - 0 KW - Receptors, Dopamine KW - Receptors, Serotonin KW - 3,4-Dihydroxyphenylacetic Acid KW - 102-32-9 KW - Serotonin KW - 333DO1RDJY KW - Hydroxyindoleacetic Acid KW - 54-16-0 KW - Cocaine KW - I5Y540LHVR KW - Dopamine KW - VTD58H1Z2X KW - Norepinephrine KW - X4W3ENH1CV KW - Homovanillic Acid KW - X77S6GMS36 KW - Index Medicus KW - Receptors, Serotonin -- drug effects KW - Receptors, Dopamine -- drug effects KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Brain Mapping KW - 3,4-Dihydroxyphenylacetic Acid -- metabolism KW - Neurons -- drug effects KW - Hydroxyindoleacetic Acid -- metabolism KW - Spinal Cord -- drug effects KW - Homovanillic Acid -- metabolism KW - Male KW - Receptors, Adrenergic -- drug effects KW - Norepinephrine -- metabolism KW - Brain -- drug effects KW - Dopamine -- metabolism KW - Cocaine -- toxicity KW - Serotonin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80561843?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Drug+and+alcohol+dependence&rft.atitle=Lack+of+neurochemical+evidence+for+neurotoxic+effects+of+repeated+cocaine+administration+in+rats+on+brain+monoamine+neurons.&rft.au=Yeh%2C+S+Y%3BDe+Souza%2C+E+B&rft.aulast=Yeh&rft.aufirst=S&rft.date=1991-01-01&rft.volume=27&rft.issue=1&rft.spage=51&rft.isbn=&rft.btitle=&rft.title=Drug+and+alcohol+dependence&rft.issn=03768716&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-06-14 N1 - Date created - 1991-06-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Modulation of cervical carcinogenesis by tamoxifen in a mouse model system. AN - 80541129; 2023707 AB - Insertion of cotton thread impregnated with beeswax and 20-methylcholanthrene (carcinogen) inside the canal of the uterine cervix in intact and oophorectomized mice results in the expression of dysplasia and carcinoma of the cervical epithelium. Based upon the experimental cervical carcinogenesis observed in this mouse model system, the present study shows distinctly the modulatory effect of tamoxifen on the incidence of cervical carcinoma. Besides this, tamoxifen significantly lengthens the latent period for both dysplasia and carcinoma in the cervical epithelium. This manifestation was found more marked in oophorectomized animals. JF - Oncology AU - Sengupta, A AU - Dutta, S AU - Mallick, R AD - Department of Experimental Carcinology, Chittaranjan National Cancer Institute, Calcutta, India. Y1 - 1991 PY - 1991 DA - 1991 SP - 258 EP - 261 VL - 48 IS - 3 SN - 0030-2414, 0030-2414 KW - Tamoxifen KW - 094ZI81Y45 KW - Methylcholanthrene KW - 56-49-5 KW - Index Medicus KW - Mice, Inbred Strains KW - Animals KW - Uterine Cervical Dysplasia -- prevention & control KW - Mice KW - Uterine Cervical Dysplasia -- chemically induced KW - Female KW - Uterine Cervical Neoplasms -- prevention & control KW - Tamoxifen -- pharmacology KW - Carcinoma -- prevention & control KW - Uterine Cervical Neoplasms -- chemically induced KW - Carcinoma -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80541129?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncology&rft.atitle=Modulation+of+cervical+carcinogenesis+by+tamoxifen+in+a+mouse+model+system.&rft.au=Sengupta%2C+A%3BDutta%2C+S%3BMallick%2C+R&rft.aulast=Sengupta&rft.aufirst=A&rft.date=1991-01-01&rft.volume=48&rft.issue=3&rft.spage=258&rft.isbn=&rft.btitle=&rft.title=Oncology&rft.issn=00302414&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-05-31 N1 - Date created - 1991-05-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - HTLV-I/II seroprevalence and HIV/HTLV coinfection among U.S. intravenous drug users. AN - 80519033; 2016683 AB - Data from a continuing multiyear seroprevalence survey of human T-lymphotropic virus types I or II (HTLV-I/II) among intravenous drug users in seven U.S. locations were analyzed to detect demographic patterns of seropositivity and coinfection with human immunodeficiency virus type 1 (HIV-1). Seropositivity for HTLV-I/II and HIV-1 was detected by whole-virus enzyme immunoassay, with Western blot confirmation. Of 1,800 subjects recruited from methadone maintenance and detoxification clinics, 207 (11.5%) were infected with HTLV-I/II. Seropositivity for HTLV-I/II varied by racial group, age, sex, and geographic location. Blacks had a higher (age- and location-adjusted) infection rate (17.1%) than Hispanics (8.7%) or whites (5.6%), and seropositivity showed a strong gradient with increasing age. Females had a slightly higher rate (14.0%) than males (10.0%), after adjustment for age and location. Among the seven locations, the rate varied from approximately 1% (Miami and Baltimore) to 20% (Los Angeles), although the former rates were based on relatively few subjects (47 and 65, respectively). Overall, the occurrence of coinfection by HIV-1 and HTLV-I/II did not occur more frequently than expected by chance. JF - Journal of acquired immune deficiency syndromes AU - Cantor, K P AU - Weiss, S H AU - Goedert, J J AU - Battjes, R J AD - Environmental Epidemiology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 460 EP - 467 VL - 4 IS - 5 SN - 0894-9255, 0894-9255 KW - Index Medicus KW - AIDS/HIV KW - Age Factors KW - Hispanic Americans KW - HIV Seroprevalence KW - Humans KW - European Continental Ancestry Group KW - Adult KW - Incidence KW - African Americans KW - Middle Aged KW - United States -- epidemiology KW - Male KW - Female KW - Acquired Immunodeficiency Syndrome -- complications KW - HTLV-I Infections -- epidemiology KW - Acquired Immunodeficiency Syndrome -- epidemiology KW - HTLV-II Infections -- epidemiology KW - HTLV-II Infections -- complications KW - Substance Abuse, Intravenous -- complications KW - HTLV-I Infections -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80519033?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+acquired+immune+deficiency+syndromes&rft.atitle=HTLV-I%2FII+seroprevalence+and+HIV%2FHTLV+coinfection+among+U.S.+intravenous+drug+users.&rft.au=Cantor%2C+K+P%3BWeiss%2C+S+H%3BGoedert%2C+J+J%3BBattjes%2C+R+J&rft.aulast=Cantor&rft.aufirst=K&rft.date=1991-01-01&rft.volume=4&rft.issue=5&rft.spage=460&rft.isbn=&rft.btitle=&rft.title=Journal+of+acquired+immune+deficiency+syndromes&rft.issn=08949255&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-05-20 N1 - Date created - 1991-05-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: J Acquir Immune Defic Syndr. 1992;5(5):535-6 [1560356] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Aluminum-induced chronic myelopathy in rabbits. AN - 80505453; 1901636 AB - Young adult New Zealand white rabbits, inoculated intracisternally once monthly with 100 micrograms AlCl3, developed progressive hyperreflexia, hypertonia, gait impairment, weight loss, muscle wasting and abnormal righting reflexes over the course of 8 months. No overt encephalopathic features were present. In spinal motor neuron perikarya, dendrites and axonal processes, argentophilic globular inclusions were extensive. Additionally, neurofibrillary tangle-like argentophilic inclusions were consistently present in the gigantocellularis, reticularis, raphe and trapezoid nuclei, but rarely present in the dorsal and ventral subiculum, parasubiculum and anterior thalamus, and never found in the cerebral cortex, substantia nigra, locus ceruleus, or cerebellum. All neuronal inclusions were immunoreactive with monoclonal antibodies recognizing phosphorylated and nonphosphorylated high and intermediate weight neurofilament proteins (SMI 31, SMI 32). Also, some spinal motor neuron inclusions were immunoreactive with a monoclonal antibody recognizing an 'age-related' phosphorylation state of neurofilament (SMI 34). Ultrastructurally, the inclusions consisted of straight or interwoven skeins of 10 nm filaments. This study demonstrates unique variability in the phosphorylation state of aluminum-induced neurofilamentous inclusions in a predominantly motor system degeneration induced by chronic low dose AlCl3. JF - Neurotoxicology AU - Strong, M J AU - Wolff, A V AU - Wakayama, I AU - Garruto, R M AD - Laboratory of Central Nervous System Studies, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 9 EP - 21 VL - 12 IS - 1 SN - 0161-813X, 0161-813X KW - Intermediate Filament Proteins KW - 0 KW - Neurofilament Proteins KW - Aluminum KW - CPD4NFA903 KW - Index Medicus KW - Animals KW - Rabbits KW - Microscopy, Electron KW - Motor Neurons -- ultrastructure KW - Intermediate Filament Proteins -- metabolism KW - Immunohistochemistry KW - Female KW - Phosphorylation -- drug effects KW - Spinal Cord Diseases -- metabolism KW - Spinal Cord Diseases -- chemically induced KW - Aluminum -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80505453?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurotoxicology&rft.atitle=Aluminum-induced+chronic+myelopathy+in+rabbits.&rft.au=Strong%2C+M+J%3BWolff%2C+A+V%3BWakayama%2C+I%3BGarruto%2C+R+M&rft.aulast=Strong&rft.aufirst=M&rft.date=1991-01-01&rft.volume=12&rft.issue=1&rft.spage=9&rft.isbn=&rft.btitle=&rft.title=Neurotoxicology&rft.issn=0161813X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-05-10 N1 - Date created - 1991-05-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Long-term behavioral and neurochemical effects of intradentate administration of colchicine in rats. AN - 80504801; 1849622 AB - Previous work in our laboratory has shown that the intradentate administration of colchicine produces time-dependent behavioral and neurochemical changes. Deficits in learning and memory and alterations in the signal transduction process for the cholinergic muscarinic receptor have been observed up to 12 weeks after colchicine treatment. To study the long-term effects of colchicine administration on cognitive function and the cholinergic system, 6 month-old male, Fischer-344 rats were injected with 2.5 micrograms of colchicine bilaterally in the dorsal and ventral hippocampus. Twelve months later the animals were tested for the acquisition of a spatial reference memory task in the Morris water maze for 8 days, with 4 trials of 60 seconds each day. At the completion of the behavioral testing, one set of rats from each treatment group was used for histochemical studies. The remaining animals were sacrificed, the hippocampi removed and used for the estimation of receptor-stimulated turnover of phosphoinositides (Pl). [3H]-inositol was incorporated into the hippocampal slices, and various receptor agonists (carbachol, norepinephrine, serotonin) used to stimulate Pl turnover in the presence of lithium. A significant deficit in acquisition in the water maze was observed in animals 1 year after colchicine administration. Neurochemical studies showed an increase in carbachol-induced Pl metabolism in the rat hippocampus 1 year post-lesion with colchicine. However, in contrast to results obtained 12 weeks after lesioning, no significant changes were observed in norepinephrine or serotonin-induced Pl metabolism 1 year after lesioning. Pirenzepine, a M1 receptor antagonist, produced a greater degree of inhibition (62%) in lesioned animals as compared to the age-matched controls (20%). Increased staining for acetylcholinesterase was found in the hippocampus of treated rats. This effect is similar to that observed 12 weeks after lesioning. These data suggest that the effects of colchicine on the cholinergic system are long-lasting and can be observed a year after treatment. JF - Neurotoxicology AU - Tandon, P AU - Barone, S AU - Drust, E G AU - Tilson, H A AD - Laboratory of Molecular and Integrative Neuroscience, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991 PY - 1991 DA - 1991 SP - 67 EP - 77 VL - 12 IS - 1 SN - 0161-813X, 0161-813X KW - Phosphatidylinositols KW - 0 KW - Choline O-Acetyltransferase KW - EC 2.3.1.6 KW - Acetylcholine KW - N9YNS0M02X KW - Colchicine KW - SML2Y3J35T KW - Index Medicus KW - Rats KW - Phosphatidylinositols -- metabolism KW - Animals KW - Acetylcholine -- metabolism KW - Rats, Inbred F344 KW - Space Perception -- drug effects KW - Memory -- drug effects KW - Learning -- drug effects KW - Histocytochemistry KW - Time Factors KW - Choline O-Acetyltransferase -- metabolism KW - Male KW - Colchicine -- toxicity KW - Behavior, Animal -- drug effects KW - Hippocampus -- metabolism KW - Hippocampus -- drug effects KW - Colchicine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80504801?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurotoxicology&rft.atitle=Long-term+behavioral+and+neurochemical+effects+of+intradentate+administration+of+colchicine+in+rats.&rft.au=Tandon%2C+P%3BBarone%2C+S%3BDrust%2C+E+G%3BTilson%2C+H+A&rft.aulast=Tandon&rft.aufirst=P&rft.date=1991-01-01&rft.volume=12&rft.issue=1&rft.spage=67&rft.isbn=&rft.btitle=&rft.title=Neurotoxicology&rft.issn=0161813X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-05-10 N1 - Date created - 1991-05-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Lung cancer risk associated with cancer in relatives. AN - 80492226; 2010787 AB - Family history data from an incident case-control study of lung cancer conducted in the Texas Gulf Coast region between 1976 and 1980 were analyzed to evaluate the contribution of cancer in first-degree relatives to lung cancer risk. Odds ratios (OR) increased slightly as the number of relatives with any cancer increased (reaching 1.5 with 4 or more relatives with cancer). Risks were higher for tobacco-related cancers (OR = 1.5 for 2 or more relatives with these tumors) and greatest for first-degree relatives with lung cancer (OR = 2.8 for lung cancer in 2 or more relatives). For cases of squamous cell carcinoma and adenocarcinoma of the lung, risks with 3 or more relatives with any cancer were increased 2-fold (OR = 1.8 and 1.9 respectively), and a significantly elevated risk was found for having a first-degree relative with lung cancer for each histologic type (ORs from 1.7-2.1). Having a spouse with lung cancer increased lung cancer risk (OR = 2.5), and cases with lung cancer reported in a first-degree relative were diagnosed at an earlier age, as were case siblings with lung cancer. JF - Journal of clinical epidemiology AU - Shaw, G L AU - Falk, R T AU - Pickle, L W AU - Mason, T J AU - Buffler, P A AD - Environmental Epidemiology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 429 EP - 437 VL - 44 IS - 4-5 SN - 0895-4356, 0895-4356 KW - Index Medicus KW - Educational Status KW - Risk Factors KW - Humans KW - Environmental Exposure KW - Case-Control Studies KW - Smoking -- adverse effects KW - Family KW - Aged KW - Texas KW - Middle Aged KW - Male KW - Female KW - Adenocarcinoma -- epidemiology KW - Lung Neoplasms -- etiology KW - Carcinoma, Squamous Cell -- etiology KW - Lung Neoplasms -- epidemiology KW - Carcinoma, Squamous Cell -- epidemiology KW - Adenocarcinoma -- etiology KW - Carcinoma, Squamous Cell -- genetics KW - Lung Neoplasms -- genetics KW - Adenocarcinoma -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80492226?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+epidemiology&rft.atitle=Lung+cancer+risk+associated+with+cancer+in+relatives.&rft.au=Shaw%2C+G+L%3BFalk%2C+R+T%3BPickle%2C+L+W%3BMason%2C+T+J%3BBuffler%2C+P+A&rft.aulast=Shaw&rft.aufirst=G&rft.date=1991-01-01&rft.volume=44&rft.issue=4-5&rft.spage=429&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+epidemiology&rft.issn=08954356&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-05-08 N1 - Date created - 1991-05-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Loss of a tumor suppressor gene function is correlated with downregulation of chondrocyte-specific collagen expression in Syrian hamster embryo cells. AN - 80492208; 2009131 AB - We previously described the isolation of closely related, preneoplastic Syrian hamster cell lines that have retained (supB+) or lost (supB-) the ability to suppress the anchorage-independent growth and tumorigenicity of a sarcoma cell line (BP6T) in cell hybrids. In this report, we have used differential cDNA screening to clone several genes that are expressed in supB+ cells and downregulated in supB- cells. The nontumorigenic supB+ and supB- variants are advantageous for differential cDNA cloning because multiple independent cell lines differing in their tumor suppressor activity have been isolated. Differentially expressed cDNAs were isolated and placed into one of four groups based on DNA cross-hybridization. Representative cDNAs from Groups I and II, which were expressed at relatively high levels in two independently derived supB+ cell lines (DES4 and 10W) and downregulated in the supB- and tumor cell lines, were sequenced. The DNA and predicted amino acid sequences of these genes were found to be highly homologous to the chondrocyte-specific collagens type II and type IX. In contrast to the chondrocyte-specific collagens, another collagen isoform, collagen type I, was expressed at similar levels in both supB+ and supB- cells. These results suggest that carcinogen-induced immortalization selected for chondrocyte-like cell lines from the mixed embryo cell population. As these cells progressed toward tumorigenicity, the ability to express the chondrocyte differentiation markers was lost concomitantly with the ability to suppress the tumorigenicity of the BP6T sarcoma cell line. These results are consistent with the hypothesis that the supB+ tumor suppressor gene is involved in the regulation of differentiation. The identification of genes regulated by this suppressor gene may aid in its isolation. JF - Molecular carcinogenesis AU - Cizdziel, P E AU - Hosoi, J AU - Montgomery, J C AU - Wiseman, R W AU - Barrett, J C AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991 PY - 1991 DA - 1991 SP - 14 EP - 24 VL - 4 IS - 1 SN - 0899-1987, 0899-1987 KW - DNA, Neoplasm KW - 0 KW - RNA, Messenger KW - Collagen KW - 9007-34-5 KW - Index Medicus KW - Animals KW - Base Sequence KW - Tumor Cells, Cultured KW - Molecular Sequence Data KW - Mesocricetus KW - Species Specificity KW - Gene Library KW - Cricetinae KW - DNA, Neoplasm -- chemistry KW - Collagen -- genetics KW - Down-Regulation KW - Cartilage -- cytology KW - RNA, Messenger -- genetics KW - Fibrosarcoma -- genetics KW - Genes, Suppressor -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80492208?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+carcinogenesis&rft.atitle=Loss+of+a+tumor+suppressor+gene+function+is+correlated+with+downregulation+of+chondrocyte-specific+collagen+expression+in+Syrian+hamster+embryo+cells.&rft.au=Cizdziel%2C+P+E%3BHosoi%2C+J%3BMontgomery%2C+J+C%3BWiseman%2C+R+W%3BBarrett%2C+J+C&rft.aulast=Cizdziel&rft.aufirst=P&rft.date=1991-01-01&rft.volume=4&rft.issue=1&rft.spage=14&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-05-07 N1 - Date created - 1991-05-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Foscarnet sodium. AN - 80491210; 1848959 AB - Cytomegalovirus (CMV), a major opportunistic viral pathogen frequently causing disease in immunocompromised patients such as organ transplant recipients and people with AIDS, may present as pneumonitis, gastrointestinal disease, or encephalitis. Its most common manifestation in patients with AIDS is retinitis which, if left untreated, invariably progresses to extensive retinal necrosis and ultimately to blindness. Ganciclovir sodium, currently the only licensed antiviral agent for the treatment of CMV retinitis, effectively controls this infection in a majority of AIDS patients, but significant granulocytopenia or thrombocytopenia related to ganciclovir therapy often limit its clinical application. Myelosuppression may be further exacerbated in AIDS patients by such other agents as zidovudine or trimethoprim/sulfamethoxazole, often necessitating dosage reductions or discontinuation of these agents in patients receiving ganciclovir. Foscarnet sodium, a pyrophosphate analog active against both cytomegalovirus and the human immunodeficiency virus type 1 (HIV), may be an effective alternative to ganciclovir in the management of CMV retinitis. Trials with intravenous foscarnet in CMV retinitis have reported favorable results using initial daily doses of 180-230 mg/kg/d given as intermittent infusions every eight hours, followed by maintenance regimens of 60-90 mg/kg/d given as single daily one- or two-hour infusions. Foscarnet therapy may result in renal impairment, and indefinite intravenous maintenance therapy may be required to prevent recurrence of CMV infection. Despite these drawbacks, foscarnet's lack of major myelosuppressive toxicity, and its activity in suppressing HIV replication, make this a potentially safe and effective alternative agent for the management of CMV infection, especially in AIDS patients. JF - DICP : the annals of pharmacotherapy AU - Minor, J R AU - Baltz, J K AD - Pharmacy Department, Warren G. Magnuson Clinical Center, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 41 EP - 47 VL - 25 IS - 1 SN - 1042-9611, 1042-9611 KW - Antiviral Agents KW - 0 KW - Foscarnet KW - 364P9RVW4X KW - Phosphonoacetic Acid KW - N919E46723 KW - Index Medicus KW - AIDS/HIV KW - Cytomegalovirus Infections -- drug therapy KW - Humans KW - Herpes Simplex -- drug therapy KW - Antiviral Agents -- therapeutic use KW - Retinitis -- drug therapy KW - Acquired Immunodeficiency Syndrome -- complications KW - Antiviral Agents -- administration & dosage KW - Eye Infections, Viral -- complications KW - Phosphonoacetic Acid -- adverse effects KW - Phosphonoacetic Acid -- analogs & derivatives KW - Acquired Immunodeficiency Syndrome -- drug therapy KW - Retinitis -- complications KW - Phosphonoacetic Acid -- pharmacokinetics KW - Eye Infections, Viral -- drug therapy KW - Antiviral Agents -- pharmacokinetics KW - Phosphonoacetic Acid -- administration & dosage KW - Phosphonoacetic Acid -- therapeutic use KW - Antiviral Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80491210?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=DICP+%3A+the+annals+of+pharmacotherapy&rft.atitle=Foscarnet+sodium.&rft.au=Minor%2C+J+R%3BBaltz%2C+J+K&rft.aulast=Minor&rft.aufirst=J&rft.date=1991-01-01&rft.volume=25&rft.issue=1&rft.spage=41&rft.isbn=&rft.btitle=&rft.title=DICP+%3A+the+annals+of+pharmacotherapy&rft.issn=10429611&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-26 N1 - Date created - 1991-04-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - National AIDS incidence trends and the extent of zidovudine therapy in selected demographic and transmission groups. AN - 80488006; 2007974 AB - After mid-1987 fewer than the expected number of cases of AIDS were reported in the United States in some demographic and transmission groups but not in others. Gay men (regardless of intravenous drug use), adults with hemophilia, and transfusion recipients exhibited fewer cases than expected based on previously reliable models. These favorable trends could not be explained by assuming earlier cessation of human immunodeficiency virus (HIV) infection. Favorable AIDS incidence trends were not found in heterosexual intravenous drug users or in persons infected through heterosexual contact. White gay men from New York City, Los Angeles, and San Francisco experienced markedly favorable trends, whereas little changes was observed for nonwhite gay men from nonurban areas. AIDS incidence trends were quantitatively consistent with the fraction of AIDS-free persons with severe immunodeficiency who received zidovudine in three cohorts. Gay men in San Francisco used zidovudine more frequently than did adults with hemophilia, while little was used by intravenous drug users in New York City. Data describing the initial national distribution of zidovudine (March 31-September 18, 1987) indicated relatively high use by patients with severe immunodeficiency in those groups, such as urban white gay men, that subsequently experienced fewer cases of AIDS than expected. Available data suggest that zidovudine, perhaps in combination with other therapies, has been one factor contributing to favorable AIDS incidence trends in some groups. Broader application of therapy might further retard the incidence of AIDS, especially in intravenous drug users, persons infected through heterosexual contact, minorities, women, and persons diagnosed outside major metropolitan areas. JF - Journal of acquired immune deficiency syndromes AU - Rosenberg, P S AU - Gail, M H AU - Schrager, L K AU - Vermund, S H AU - Creagh-Kirk, T AU - Andrews, E B AU - Winkelstein, W AU - Marmor, M AU - Des Jarlais, D C AU - Biggar, R J AD - Epidemiologic Methods Section, National Cancer Institute, Rockville, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 392 EP - 401 VL - 4 IS - 4 SN - 0894-9255, 0894-9255 KW - Zidovudine KW - 4B9XT59T7S KW - Index Medicus KW - AIDS/HIV KW - Los Angeles -- epidemiology KW - Humans KW - African Americans KW - Hemophilia A -- complications KW - Homosexuality KW - New York -- epidemiology KW - Sexual Behavior KW - Hispanic Americans KW - European Continental Ancestry Group KW - Cohort Studies KW - Blood Transfusion KW - Incidence KW - San Francisco -- epidemiology KW - Substance Abuse, Intravenous -- complications KW - Urban Population KW - United States -- epidemiology KW - Female KW - Male KW - Zidovudine -- therapeutic use KW - Acquired Immunodeficiency Syndrome -- ethnology KW - Acquired Immunodeficiency Syndrome -- complications KW - Acquired Immunodeficiency Syndrome -- epidemiology KW - Acquired Immunodeficiency Syndrome -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80488006?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+acquired+immune+deficiency+syndromes&rft.atitle=National+AIDS+incidence+trends+and+the+extent+of+zidovudine+therapy+in+selected+demographic+and+transmission+groups.&rft.au=Rosenberg%2C+P+S%3BGail%2C+M+H%3BSchrager%2C+L+K%3BVermund%2C+S+H%3BCreagh-Kirk%2C+T%3BAndrews%2C+E+B%3BWinkelstein%2C+W%3BMarmor%2C+M%3BDes+Jarlais%2C+D+C%3BBiggar%2C+R+J&rft.aulast=Rosenberg&rft.aufirst=P&rft.date=1991-01-01&rft.volume=4&rft.issue=4&rft.spage=392&rft.isbn=&rft.btitle=&rft.title=Journal+of+acquired+immune+deficiency+syndromes&rft.issn=08949255&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-05-02 N1 - Date created - 1991-05-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Retrovirus-mediated gene transfer into CD4+ and CD8+ human T cell subsets derived from tumor-infiltrating lymphocytes and peripheral blood mononuclear cells. AN - 80482308; 2007247 AB - Studies were undertaken to test the susceptibility of individual T cell subpopulations to retroviral-mediated gene transduction. Gene transfer into human tumor-infiltrating lymphocytes (TIL) or peripheral blood mononuclear cells (PBMC) was carried out by transduction with an amphotropic murine retroviral vector (LNL6 or N2) containing the bacterial neoR gene. The presence of the neoR gene in the TIL population was demonstrated by Southern blot analysis, detection of the enzymatic activity of the gene product and by the ability of transduced TIL to proliferate in high concentrations of G418, a neomycin analog that is toxic to eukaryotic cells. The presence of the neoR gene in TIL did not alter their proliferation or interleukin-2 dependence compared to nontransduced TIL. The differential susceptibility of CD4+ and CD8+ lymphoid cells to the retro-virus-mediated gene transfer was then tested. Transduction of heterogeneous TIL cultures containing both CD4+ and CD8+ cells resulted in gene insertion into both T cell subsets with no preferential transduction frequency into either CD4+ or CD8+ cells. In other experiments highly purified CD4+ and CD8+ T cell subpopulations from either TIL or PBMC could be successfully transduced with the neoR gene as demonstrated by Southern blot analysis and detection of the gene product neophosphotransferase activity. No such activity of vector DNA could be detected in controls of nontransduced cells. In these highly purified cell subsets the distinctive T cell phenotypic markers were continually expressed after transduction, G418 selection and long-term growth. Clinical trials have begun in patients with advanced cancer using heterogeneous populations of CD4+ and CD8+ gene-modified TIL. JF - Cancer immunology, immunotherapy : CII AU - Morecki, S AU - Karson, E AU - Cornetta, K AU - Kasid, A AU - Aebersold, P AU - Blaese, R M AU - Anderson, W F AU - Rosenberg, S A AD - Surgery Branches, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 342 EP - 352 VL - 32 IS - 6 SN - 0340-7004, 0340-7004 KW - neoR KW - Genetic Markers KW - 0 KW - Gentamicins KW - Interleukin-2 KW - DNA KW - 9007-49-2 KW - antibiotic G 418 KW - A08F5XTI6G KW - Index Medicus KW - Phenotype KW - Interleukin-2 -- pharmacology KW - Genes, Bacterial KW - Cell Survival -- drug effects KW - Cells, Cultured KW - Blotting, Southern KW - Humans KW - DNA -- analysis KW - Cell Division -- drug effects KW - Gentamicins -- pharmacology KW - Lymphocytes, Tumor-Infiltrating -- ultrastructure KW - Lymphocytes, Tumor-Infiltrating -- immunology KW - Transduction, Genetic KW - Leukocytes, Mononuclear -- ultrastructure KW - Leukocytes, Mononuclear -- immunology KW - Retroviridae -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80482308?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+immunology%2C+immunotherapy+%3A+CII&rft.atitle=Retrovirus-mediated+gene+transfer+into+CD4%2B+and+CD8%2B+human+T+cell+subsets+derived+from+tumor-infiltrating+lymphocytes+and+peripheral+blood+mononuclear+cells.&rft.au=Morecki%2C+S%3BKarson%2C+E%3BCornetta%2C+K%3BKasid%2C+A%3BAebersold%2C+P%3BBlaese%2C+R+M%3BAnderson%2C+W+F%3BRosenberg%2C+S+A&rft.aulast=Morecki&rft.aufirst=S&rft.date=1991-01-01&rft.volume=32&rft.issue=6&rft.spage=342&rft.isbn=&rft.btitle=&rft.title=Cancer+immunology%2C+immunotherapy+%3A+CII&rft.issn=03407004&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-26 N1 - Date created - 1991-04-26 N1 - Date revised - 2017-01-13 N1 - Gene symbol - neoR N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Downstream sequences mediate induction of the mouse cathepsin L promoter by phorbol esters. AN - 80481585; 1848774 AB - The major excreted protein (MEP) of mouse fibroblasts is the precursor to a lysosomal acid protease (cathepsin L) whose synthesis is induced by malignant transformation, growth factors, tumor promoters, and cyclic AMP. We have previously cloned a functional gene for MEP from NIH 3T3 cells. When subcloned into chloramphenicol acetyl transferase (CAT) expression vectors, both 4-kilobase and 300 base pair fragments in the 5'-flanking region of the MEP gene confer CAT activity that is stimulated by cyclic AMP treatment but is not stimulated by phorbol ester treatment of NIH 3T3 cells. These fragments confer constitutive promoter activity that is comparable to that of the SV40 promoter. Primer extension, using RNA from cells transiently transfected with MEP-CAT fusion plasmids, demonstrates that phorbol ester treatment increases the amount of transcript from constructs containing both the promoter and sequences downstream of the transcription initiation site, including the first three introns, but not from constructs containing only the 5'-flanking region of the MEP gene. Nuclear run-off experiments confirm that the increase in endogenous MEP mRNA is mediated by increased transcription and not via relief of transcriptional attenuation. Since both the MEP promoter, which contains three potential binding sites for the AP-2 transcription factor, and the SV40 promoter, which contains both AP-1 and AP-2 binding sites, fail to respond to 12-O-tetradecanoylphorbol-13-acetate in NIH 3T3 cells, these upstream motifs are not sufficient to confer phorbol ester responsiveness in NIH 3T3 cells. These results suggest that the MEP gene is regulated in a complex manner by sequences both upstream and downstream of the transcription initiation site. JF - Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research AU - Troen, B R AU - Chauhan, S S AU - Ray, D AU - Gottesman, M M AD - Laboratory of Cell Biology, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 23 EP - 31 VL - 2 IS - 1 SN - 1044-9523, 1044-9523 KW - MEP KW - Enzyme Precursors KW - 0 KW - RNA, Messenger KW - Cyclic AMP KW - E0399OZS9N KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Cathepsins KW - EC 3.4.- KW - Endopeptidases KW - Cysteine Endopeptidases KW - EC 3.4.22.- KW - Cathepsin L KW - EC 3.4.22.15 KW - Ctsl protein, mouse KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Animals KW - Base Sequence KW - Plasmids -- genetics KW - Transfection -- genetics KW - Cyclic AMP -- pharmacology KW - Molecular Sequence Data KW - Mice KW - RNA, Messenger -- biosynthesis KW - Regulatory Sequences, Nucleic Acid KW - Cathepsins -- genetics KW - Gene Expression Regulation, Enzymologic -- drug effects KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Promoter Regions, Genetic -- genetics KW - Enzyme Precursors -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80481585?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cell+growth+%26+differentiation+%3A+the+molecular+biology+journal+of+the+American+Association+for+Cancer+Research&rft.atitle=Downstream+sequences+mediate+induction+of+the+mouse+cathepsin+L+promoter+by+phorbol+esters.&rft.au=Troen%2C+B+R%3BChauhan%2C+S+S%3BRay%2C+D%3BGottesman%2C+M+M&rft.aulast=Troen&rft.aufirst=B&rft.date=1991-01-01&rft.volume=2&rft.issue=1&rft.spage=23&rft.isbn=&rft.btitle=&rft.title=Cell+growth+%26+differentiation+%3A+the+molecular+biology+journal+of+the+American+Association+for+Cancer+Research&rft.issn=10449523&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-05-01 N1 - Date created - 1991-05-01 N1 - Date revised - 2017-01-13 N1 - Gene symbol - MEP N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Molecular biology of adrenergic receptors: model systems for the study of G-protein-mediated signal transduction. AN - 80470208; 1848129 AB - Elucidation of the gene structure of several receptors known to mediate the signal of hormone or transmitter binding to intracellular effector systems through guanine-nucleotide-binding proteins (G proteins) has revealed that these receptors comprise a super-family of related proteins. The hallmark of all G-protein-linked receptors is a presumed topography of 7 membrane-spanning loops, analogous to the structure of bacteriorhodopsin. Members of this gene superfamily contain regions, particularly with the hydrophobic domains, of homologous sequence. The expression of G-protein-linked receptors in heterologous cell systems has allowed for the study of the pharmacological and biochemical properties of individual receptor subtypes in a manner not previously possible with intact tissues containing multiple receptors. Site-directed mutagenesis experiments have identified many conserved amino acids which are involved in ligand binding, receptor activation by agonists and receptor-G protein coupling, and suggest that the conservation of receptor structure throughout this gene family may reflect a conservation of important functional domains within these proteins. JF - Blood vessels AU - Fraser, C M AD - Section on Molecular Neurobiology, National Institute on Alcohol Abuse and Alcoholism, Rockville, Md. Y1 - 1991 PY - 1991 DA - 1991 SP - 93 EP - 103 VL - 28 IS - 1-3 SN - 0303-6847, 0303-6847 KW - Receptors, Adrenergic, alpha KW - 0 KW - Receptors, Adrenergic, beta KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Animals KW - Humans KW - Molecular Sequence Data KW - Gene Expression KW - Amino Acid Sequence KW - Signal Transduction -- physiology KW - Receptors, Adrenergic, beta -- genetics KW - Receptors, Adrenergic, alpha -- genetics KW - Receptors, Adrenergic, beta -- physiology KW - GTP-Binding Proteins -- physiology KW - Receptors, Adrenergic, beta -- chemistry KW - Receptors, Adrenergic, alpha -- physiology KW - Receptors, Adrenergic, alpha -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80470208?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+vessels&rft.atitle=Molecular+biology+of+adrenergic+receptors%3A+model+systems+for+the+study+of+G-protein-mediated+signal+transduction.&rft.au=Fraser%2C+C+M&rft.aulast=Fraser&rft.aufirst=C&rft.date=1991-01-01&rft.volume=28&rft.issue=1-3&rft.spage=93&rft.isbn=&rft.btitle=&rft.title=Blood+vessels&rft.issn=03036847&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-12 N1 - Date created - 1991-04-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Multiple estrogen binding sites in the uterus: stereochemistry of receptor and non-receptor binding of diethylstilbestrol and its metabolites. AN - 80455524; 1997122 AB - Indenestrol A (IA), an oxidative metabolite of the synthetic estrogen diethylstilbestrol (DES), has high binding affinity for estrogen receptor in mouse uterine cytosol but possesses weak biological activity. Racemic mixture of optically active [3H]indenestrol A (IA-Rac) was separated and purified into individual enantiomers on a semi-preparative scale by HPLC with a Chiralpak OP(+) column. The structure-activity relationship was investigated among the [3H]IA enantiomers (IA-R and IA-S) and [3H]DES through direct saturation binding assays using mouse uterine cytosol. Specific binding curves and Scatchard plots were obtained for each [3H]ligand; DES, IA-Rac, IA-R and IA-S. IA-S enantiomer (Kd = 0.67) binds to the estrogen receptor with the same affinity as DES (Kd = 0.71) and four times higher affinity than IA-R (Kd = 2.56). The number of binding sites for IA-S is approximately the same as estradiol, DES and IA-Rac while IA-R binds far fewer sites than the other ligands. Saturation binding assays indicated that [3H]DES and [3H]IA enantiomers exhibited a higher level of non-specific binding to the cytosol receptor compared to estradiol which has a low level of non-specific binding. These binding studies led to the detection of an additional binding component for the stilbestrol compounds in estrogen target tissue cytosol preparations. Sucrose density gradient separation assays under low salt conditions showed that both [3H]DES and [3H]IA compounds bound to the 8S form of the receptor, the same as E2. But, in addition both DES and IA bound to another binding component in 4S region. The binding to the 4S component were partially displaced by the addition of excess unlabeled E2 and DES. Further characterization of the 4S component is described. JF - The Journal of steroid biochemistry and molecular biology AU - Chae, K AU - Johnston, S H AU - Korach, K S AD - Receptor Biology Section, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 35 EP - 42 VL - 38 IS - 1 SN - 0960-0760, 0960-0760 KW - Indenes KW - 0 KW - Receptors, Estrogen KW - indenestrol KW - 4A464K3BSI KW - Estradiol KW - 4TI98Z838E KW - Diethylstilbestrol KW - 731DCA35BT KW - Index Medicus KW - Centrifugation, Density Gradient KW - Cytosol -- metabolism KW - Animals KW - Stereoisomerism KW - In Vitro Techniques KW - Mice KW - Female KW - Structure-Activity Relationship KW - Uterus -- metabolism KW - Diethylstilbestrol -- metabolism KW - Diethylstilbestrol -- analogs & derivatives KW - Receptors, Estrogen -- metabolism KW - Indenes -- metabolism KW - Estradiol -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80455524?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+steroid+biochemistry+and+molecular+biology&rft.atitle=Multiple+estrogen+binding+sites+in+the+uterus%3A+stereochemistry+of+receptor+and+non-receptor+binding+of+diethylstilbestrol+and+its+metabolites.&rft.au=Chae%2C+K%3BJohnston%2C+S+H%3BKorach%2C+K+S&rft.aulast=Chae&rft.aufirst=K&rft.date=1991-01-01&rft.volume=38&rft.issue=1&rft.spage=35&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+steroid+biochemistry+and+molecular+biology&rft.issn=09600760&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-01 N1 - Date created - 1991-04-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Identification of an amino acid sequence in the laminin A chain mediating mast cell attachment and spreading. AN - 80453354; 1997398 AB - PT18 mast cells and mouse bone marrow-derived mast cells have been shown to adhere and spread when in contact with a laminin substratum. Mouse bone marrow cells, however, first require activation with phorbol myristate acetate (PMA), ionophore, or antigen-specific IgE with antigen in order to exhibit these phenomena. Here, we have studied the interaction of these cells with three active synthetic peptides derived from different domains of laminin. PT18 cells and mouse bone marrow mast cells attached and spread on the 19 amino acid synthetic laminin A chain-derived peptide PA22-2, containing the active five amino acid sequence IKVAV, and this attachment did not require prior activation of the mouse bone marrow mast cells with PMA or IgE plus antigen. These cells did not adhere to the B1 chain peptide YIGSR-NH2 or the RGD-containing peptide from the A chain. PT18 cell adherence to laminin was inhibited by soluble peptide PA22-2, but not by either YIGSR-NH2, the RGD-containing, or control peptides. Antisera to the PA22-2 peptide completely abolished adherence to PA22-2, but only partially inhibited mast cell adherence to laminin. Antibody to the 67,000-32,000 MW laminin-binding protein receptor blocked cell adhesion to laminin and to the active A chain peptide. Thus, mast cell adhesion and spreading on laminin may be mediated by an interaction with the IKVAV sequence on the laminin A chain. JF - Immunology AU - Thompson, H L AU - Burbelo, P D AU - Yamada, Y AU - Kleinman, H K AU - Metcalfe, D D AD - Mast Cell Physiology Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 144 EP - 149 VL - 72 IS - 1 SN - 0019-2805, 0019-2805 KW - Immune Sera KW - 0 KW - Laminin KW - Peptide Fragments KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Peptide Fragments -- metabolism KW - Bone Marrow Cells KW - Animals KW - Cell Adhesion -- physiology KW - Cells, Cultured KW - Binding, Competitive KW - Molecular Sequence Data KW - Immune Sera -- immunology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Mice KW - Amino Acid Sequence KW - Laminin -- chemistry KW - Mast Cells -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80453354?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Immunology&rft.atitle=Identification+of+an+amino+acid+sequence+in+the+laminin+A+chain+mediating+mast+cell+attachment+and+spreading.&rft.au=Thompson%2C+H+L%3BBurbelo%2C+P+D%3BYamada%2C+Y%3BKleinman%2C+H+K%3BMetcalfe%2C+D+D&rft.aulast=Thompson&rft.aufirst=H&rft.date=1991-01-01&rft.volume=72&rft.issue=1&rft.spage=144&rft.isbn=&rft.btitle=&rft.title=Immunology&rft.issn=00192805&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-04 N1 - Date created - 1991-04-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Cell Biochem. 1985;27(4):317-25 [3889019] EMBO J. 1984 Oct;3(10):2355-62 [6209134] J Cell Biol. 1985 Dec;101(6):2134-44 [2933413] Biochim Biophys Acta. 1985 Dec 17;823(2):147-60 [2934094] Biochemistry. 1985 Dec 17;24(26):7753-60 [4092036] Cell. 1987 Feb 27;48(4):549-54 [3028640] Cell. 1987 Mar 27;48(6):989-96 [2951015] J Cell Biol. 1987 Jul;105(1):589-98 [3038930] J Biol Chem. 1987 Aug 25;262(24):11532-8 [3114248] Science. 1987 Nov 20;238(4830):1132-4 [2961059] Proc Natl Acad Sci U S A. 1988 Feb;85(4):1282-6 [2963341] J Cell Physiol. 1988 Feb;134(2):287-91 [3346340] J Cell Physiol. 1988 Apr;135(1):71-8 [3259238] Cancer Res. 1988 Jun 15;48(12):3307-12 [2836052] Proc Natl Acad Sci U S A. 1988 Sep;85(17):6394-8 [2970639] Science. 1988 Sep 2;241(4870):1228-9 [2970671] Exp Cell Res. 1988 Nov;179(1):31-41 [3169149] J Biol Chem. 1988 Nov 15;263(32):16536-44 [3182802] J Cell Biol. 1988 Nov;107(5):1873-80 [2972733] Anal Biochem. 1989 Mar;177(2):373-7 [2729557] J Biol Chem. 1989 Sep 25;264(27):16174-82 [2777785] J Immunol. 1989 Oct 1;143(7):2323-7 [2528592] J Cell Biol. 1990 Jan;110(1):185-92 [2136861] Proc Natl Acad Sci U S A. 1990 Mar;87(6):2279-83 [2156266] J Immunol. 1990 Nov 15;145(10):3425-31 [2146320] J Biol Chem. 1979 Oct 10;254(19):9933-7 [114518] J Immunol. 1981 Sep;127(3):1256-8 [6790617] J Immunol. 1981 Nov;127(5):1941-7 [6795264] J Mol Biol. 1981 Jul 25;150(1):97-120 [6795355] J Biol Chem. 1983 Jul 25;258(14):8922-7 [6408095] J Immunol. 1983 Jul;131(1):282-7 [6190911] J Immunol. 1984 Mar;132(3):1479-86 [6198393] J Cell Biol. 1984 Jul;99(1 Pt 1):29-36 [6736130] EMBO J. 1985 Feb;4(2):309-16 [3848400] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The impact of breakthrough clinical trials on survival in population based tumor registries. AN - 80453194; 1704907 AB - Three statistical models are developed to study the impact that two breakthrough clinical trials (MOPP for Hodgkin's disease and PVB for disseminated testicular cancer) had on survival in the Connecticut tumor registry and the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) registry program. A segmented regression model is used in conjunction with the Cox semi-parametric proportional hazards model, as well as the parametric Weibull and exponential cure models. These models allow us to determine approximately when survival first began to improve dramatically, indicating that improved treatments had become available, and how long it took for survival to level off again indicating that the full population survival impact had been realized. In addition, the degree to which the parametric models fit allows us to determine if the survival improvements occur within a parametric family. Results of the modelling indicate that dissemination took approximately 11 years in Hodgkin's disease while only 3 years in disseminated testicular cancer. In both disease sites survival first broke with prior trends between the time that the breakthrough trial started and its publication, indicating that earlier moderately successful 'precursor' trials with combination chemotherapy may have initiated the improved population survival trends. Reasons for the difference in dissemination time in the two cancer sites are examined in order to understand what factors may be responsible for the speed of dissemination and effective utilization of new therapies. JF - Journal of clinical epidemiology AU - Feuer, E J AU - Kessler, L G AU - Baker, S G AU - Triolo, H E AU - Green, D T AD - Division of Cancer Prevention and Control, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 141 EP - 153 VL - 44 IS - 2 SN - 0895-4356, 0895-4356 KW - Bleomycin KW - 11056-06-7 KW - Procarbazine KW - 35S93Y190K KW - Mechlorethamine KW - 50D9XSG0VR KW - Vincristine KW - 5J49Q6B70F KW - Vinblastine KW - 5V9KLZ54CY KW - Cisplatin KW - Q20Q21Q62J KW - Prednisone KW - VB0R961HZT KW - Index Medicus KW - Vinblastine -- therapeutic use KW - Regression Analysis KW - Procarbazine -- therapeutic use KW - Cisplatin -- therapeutic use KW - Mechlorethamine -- therapeutic use KW - Vincristine -- therapeutic use KW - Prednisone -- therapeutic use KW - Humans KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Bleomycin -- therapeutic use KW - Male KW - Survival Analysis KW - Proportional Hazards Models KW - Testicular Neoplasms -- mortality KW - Registries KW - Testicular Neoplasms -- drug therapy KW - Hodgkin Disease -- drug therapy KW - Clinical Trials as Topic KW - Models, Statistical KW - Hodgkin Disease -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80453194?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+epidemiology&rft.atitle=The+impact+of+breakthrough+clinical+trials+on+survival+in+population+based+tumor+registries.&rft.au=Feuer%2C+E+J%3BKessler%2C+L+G%3BBaker%2C+S+G%3BTriolo%2C+H+E%3BGreen%2C+D+T&rft.aulast=Feuer&rft.aufirst=E&rft.date=1991-01-01&rft.volume=44&rft.issue=2&rft.spage=141&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+epidemiology&rft.issn=08954356&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-03-27 N1 - Date created - 1991-03-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Studies on focal alveolar bone healing with technetium (Tc)-99m labeled methylene diphosphonate and gold-collimated cadmium telluride probe. AN - 80442549; 1994312 AB - The benefit of using a collimator for a miniaturized cadmium telluride probe was evaluated by monitoring the bone-healing processes for 13 weeks after the induction of small iatrogenic alveolar bone lesions in one side of the mandible in beagles. Technetium (Tc)-99m labeled methylene diphosphonate (200 to 300 MBq, 5.1 to 8.1 mCi, in a solution of 0.5 to 1 ml, intravenously) was used as a bone-seeking radiopharmaceutical. The radioactivity over the bone lesion (L) and the contralateral normal site (C) in the mandible were measured between 1.5 and 2 hours after injection of the tracer, and the activity ratio L/C served as an index of relative bone uptake. A study of six dogs revealed that the healing response to a hemispheric bone defect of 2 mm diameter in the cortical bone could not be detected by an uncollimated probe, and in a repeated study in two dogs the use of a gold collimator (5 mm in diameter, 5 mm in length) did not increase the L/C ratio significantly. A second study in six dogs with 5 mm lesions showed that although systematic trends in the time courses of the L/C ratio obtained both with and without the collimator could be demonstrated, the L/C ratio of collimated versus uncollimated measurements was significantly (p less than 0.005) increased. In three of the latter six dogs, abscesses developed after 9 weeks, leading to a second increase (p less than 0.05) of the L/C ratio with collimation compared with the noninflammation group; without collimation no significant (p greater than 0.15) difference between the two groups could be demonstrated.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Oral surgery, oral medicine, and oral pathology AU - Tsuchimochi, M AU - Hosain, F AU - Engelke, W AU - Zeichner, S J AU - Ruttimann, U E AU - Webber, R L AD - Diagnostic Systems Branch, National Institute of Dental Research, National Institutes of Health, Bethesda. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 110 EP - 115 VL - 71 IS - 1 SN - 0030-4220, 0030-4220 KW - Cadmium Compounds KW - 0 KW - Cadmium KW - 00BH33GNGH KW - Gold KW - 7440-57-5 KW - Tellurium KW - NQA0O090ZJ KW - cadmium telluride KW - STG188WO13 KW - Technetium Tc 99m Medronate KW - X89XV46R07 KW - Dentistry KW - Index Medicus KW - Evaluation Studies as Topic KW - Animals KW - Dogs KW - Radiation Monitoring -- instrumentation KW - Female KW - Radionuclide Imaging KW - Alveolar Process -- diagnostic imaging KW - Bone Regeneration UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80442549?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oral+surgery%2C+oral+medicine%2C+and+oral+pathology&rft.atitle=Studies+on+focal+alveolar+bone+healing+with+technetium+%28Tc%29-99m+labeled+methylene+diphosphonate+and+gold-collimated+cadmium+telluride+probe.&rft.au=Tsuchimochi%2C+M%3BHosain%2C+F%3BEngelke%2C+W%3BZeichner%2C+S+J%3BRuttimann%2C+U+E%3BWebber%2C+R+L&rft.aulast=Tsuchimochi&rft.aufirst=M&rft.date=1991-01-01&rft.volume=71&rft.issue=1&rft.spage=110&rft.isbn=&rft.btitle=&rft.title=Oral+surgery%2C+oral+medicine%2C+and+oral+pathology&rft.issn=00304220&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-03-19 N1 - Date created - 1991-03-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Synthesis of two cyclopentenyl-3-deazapyrimidine carbocyclic nucleosides related to cytidine and uridine. AN - 80435860; 1992119 AB - The cytosine analogue of neplanocin A, cyclopentenylcytosine (CPE-C, 3), has significant antitumor and antiviral activity commensurate with the drug's ability to produce a significant depletion of cytidine triphosphate (CTP) levels that result from the potent inhibition of cytidine triphosphate synthetase. Another important antitumor agent, previously identified as a potent inhibitor of the same enzyme, is 3-deazauridine (2). The synthesis of the cyclopentenyl nucleosides 3-deaza-CPE-C (5) and 3-deaza-CPE-U (6) was undertaken in order to investigate the effects of a modified 3-deaza pyrimidine aglycon moiety on the biological activity of the parent CPE-C. These compounds were synthesized via an SN2 displacement reaction on cyclopenten-1-ol methanesulfonate (10) by the sodium salt of the corresponding aglycon. In each case, separation and characterization of the corresponding N- and O-alkylated products was necessary before final removal of the blocking groups. The target compounds were devoid of in vitro antiviral activity against the HSV-1 and human influenza viruses. Although 3-deaza-CPE-C was nontoxic to L1210 cells in culture, 3-deaza-CPE-U displayed significant cytotoxicity against murine L1210 leukemia in vitro. JF - Journal of medicinal chemistry AU - Copp, R R AU - Marquez, V E AD - Laboratory of Medicinal Chemistry, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 208 EP - 212 VL - 34 IS - 1 SN - 0022-2623, 0022-2623 KW - Antimetabolites, Antineoplastic KW - 0 KW - Antiviral Agents KW - Indicators and Reagents KW - cyclopentenyl-3-deazacytidine KW - 130378-88-0 KW - 3-deazacyclopentenylcytosine KW - 130378-89-1 KW - 3-Deazauridine KW - 263CU738ZY KW - Cytidine KW - 5CSZ8459RP KW - Uridine KW - WHI7HQ7H85 KW - Index Medicus KW - Molecular Structure KW - Drug Screening Assays, Antitumor KW - Animals KW - Mice KW - Structure-Activity Relationship KW - Leukemia L1210 KW - 3-Deazauridine -- chemistry KW - Uridine -- chemical synthesis KW - Uridine -- chemistry KW - 3-Deazauridine -- chemical synthesis KW - 3-Deazauridine -- pharmacology KW - 3-Deazauridine -- analogs & derivatives KW - Antimetabolites, Antineoplastic -- chemical synthesis KW - Cytidine -- analogs & derivatives KW - Antiviral Agents -- chemical synthesis KW - Cytidine -- chemistry KW - Cytidine -- chemical synthesis KW - Cytidine -- pharmacology KW - Uridine -- pharmacology KW - Uridine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80435860?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+medicinal+chemistry&rft.atitle=Synthesis+of+two+cyclopentenyl-3-deazapyrimidine+carbocyclic+nucleosides+related+to+cytidine+and+uridine.&rft.au=Copp%2C+R+R%3BMarquez%2C+V+E&rft.aulast=Copp&rft.aufirst=R&rft.date=1991-01-01&rft.volume=34&rft.issue=1&rft.spage=208&rft.isbn=&rft.btitle=&rft.title=Journal+of+medicinal+chemistry&rft.issn=00222623&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-03-12 N1 - Date created - 1991-03-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Aerial oxidation of hydrazines to nitrosamines. AN - 80434656; 1991461 AB - When 1,1-dimethylhydrazine and N-aminopiperidine were deliberately exposed to air substantial amounts of the corresponding carcinogenic nitrosamines were formed. Unoxidized samples of 1,1-dimethylhydrazine were not mutagenic while oxidized samples (which contained much higher levels of nitrosamines) were mutagenic. Both unoxidized and oxidized samples of N-aminopiperidine were mutagenic. JF - Environmental and molecular mutagenesis AU - Lunn, G AU - Sansone, E B AU - Andrews, A W AD - Environmental Control and Research Program, NCI-Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1991 PY - 1991 DA - 1991 SP - 59 EP - 62 VL - 17 IS - 1 SN - 0893-6692, 0893-6692 KW - Dimethylhydrazines KW - 0 KW - Hydrazines KW - Mutagens KW - Nitrosamines KW - Piperidines KW - N-aminopiperidine KW - 2213-43-6 KW - 1,2-Dimethylhydrazine KW - IX068S9745 KW - Index Medicus KW - Animals KW - Chromatography, Gas KW - Microsomes, Liver -- metabolism KW - Salmonella typhimurium -- drug effects KW - Oxidation-Reduction KW - Rats KW - Rats, Inbred Strains KW - Mutagenicity Tests KW - Biotransformation KW - Mesocricetus KW - Male KW - Cricetinae KW - Piperidines -- pharmacology KW - Dimethylhydrazines -- pharmacology KW - Piperidines -- chemistry KW - Hydrazines -- chemistry KW - Mutagens -- chemistry KW - Dimethylhydrazines -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80434656?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+and+molecular+mutagenesis&rft.atitle=Aerial+oxidation+of+hydrazines+to+nitrosamines.&rft.au=Lunn%2C+G%3BSansone%2C+E+B%3BAndrews%2C+A+W&rft.aulast=Lunn&rft.aufirst=G&rft.date=1991-01-01&rft.volume=17&rft.issue=1&rft.spage=59&rft.isbn=&rft.btitle=&rft.title=Environmental+and+molecular+mutagenesis&rft.issn=08936692&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-03-12 N1 - Date created - 1991-03-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dosimetric estimates for clinical positron emission tomographic scanning after injection of [18F]-6-fluorodopamine. AN - 80429291; 1988612 AB - Positron emission tomographic (PET) scanning after systemic i.v. injection of fluorine-18-6-fluorodopamine ([18F]-6F-DA) is a method for visualizing and measuring regional sympathetic nervous system innervation and function. Based on results of preclinical studies of rats and dogs and on previous literature about the fate of injected tracer-labeled catecholamines, dosimetric estimates for clinical studies are presented here. After injection of 1 mCi of [18F]-F-DA, the radiation dose would be highest to the wall of the urinary bladder (1.40 rem/mCi), due to accumulation of radioactive metabolites of [18F]-F-DA in urine. Radioactivity also would accumulate in bile. Organs receiving the next highest dose would be the kidneys (0.9 rem/mCi) and small intestine (0.2 rem/mCi). The parenchymal radiation dose would be lowest in the brain, since there is an effective blood-brain barrier for circulating catecholamines. Radiation doses to all organs after administration of 1 mCi of [18F]-F-DA to humans would be less than 3 rem and, therefore, within current FDA guidelines. JF - Journal of nuclear medicine : official publication, Society of Nuclear Medicine AU - Goldstein, D S AU - Chang, P C AU - Smith, C B AU - Herscovitch, P AU - Austin, S M AU - Eisenhofer, G AU - Kopin, I J AD - Hypertension-Endocrine Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 102 EP - 110 VL - 32 IS - 1 SN - 0161-5505, 0161-5505 KW - Fluorine Radioisotopes KW - 0 KW - 6-fluorodopamine KW - 59043-70-8 KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Radiation Dosage KW - Animals KW - Dogs KW - Tissue Distribution KW - Male KW - Dopamine -- analogs & derivatives KW - Tomography, Emission-Computed KW - Sympathetic Nervous System -- diagnostic imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80429291?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Dosimetric+estimates+for+clinical+positron+emission+tomographic+scanning+after+injection+of+%5B18F%5D-6-fluorodopamine.&rft.au=Goldstein%2C+D+S%3BChang%2C+P+C%3BSmith%2C+C+B%3BHerscovitch%2C+P%3BAustin%2C+S+M%3BEisenhofer%2C+G%3BKopin%2C+I+J&rft.aulast=Goldstein&rft.aufirst=D&rft.date=1991-01-01&rft.volume=32&rft.issue=1&rft.spage=102&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 - 1991-02-25 N1 - Date created - 1991-02-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The early promoters of bacteriophage HK022: contrasts and similarities to other lambdoid phages. AN - 80425518; 1824767 AB - The pL, pR and pM promoters of lambdoid phages direct the transcription of early phage genes and the prophage repressor gene. We have determined the start points of transcription for these three promoters in the lambdoid phage HK022 and have shown that the HK022 repressor represses the early promoters, pL and pR, and activates the repressor promoter, pM. HK022 resembles other phages of the lambda family in these respects, as it does in the functional organization of most of its early genes and sites. One exception is nun, the first gene of the HK022 pL operon, which is expressed in the presence of prophage repressor and thus differs from its lambda counterpart, gene N. We show that transcription of nun in a lysogen does not initiate at pL but instead starts upstream at the pM promoter. This difference in transcription fits the different roles of Nun and N proteins in the physiology of the two phages: Nun protects HK022 lysogens against superinfection with certain other lambdoid phages, while N promotes the transcription of early lambda genes. JF - Journal of bacteriology AU - Cam, K M AU - Oberto, J AU - Weisberg, R A AD - Laboratory of Molecular Genetics, National Institute of Child Health and Human Development, Bethesda, Maryland 20892. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 734 EP - 740 VL - 173 IS - 2 SN - 0021-9193, 0021-9193 KW - DNA, Bacterial KW - 0 KW - DNA, Viral KW - Oligonucleotide Probes KW - RNA, Viral KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Base Sequence KW - DNA, Bacterial -- genetics KW - Molecular Sequence Data KW - Transcription, Genetic KW - RNA, Viral -- isolation & purification KW - RNA, Viral -- genetics KW - Plasmids KW - Nucleic Acid Conformation KW - DNA, Viral -- genetics KW - Promoter Regions, Genetic KW - Bacteriophage lambda -- genetics KW - Escherichia coli -- genetics KW - Coliphages -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80425518?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+bacteriology&rft.atitle=The+early+promoters+of+bacteriophage+HK022%3A+contrasts+and+similarities+to+other+lambdoid+phages.&rft.au=Cam%2C+K+M%3BOberto%2C+J%3BWeisberg%2C+R+A&rft.aulast=Cam&rft.aufirst=K&rft.date=1991-01-01&rft.volume=173&rft.issue=2&rft.spage=734&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 - 1991-02-20 N1 - Date created - 1991-02-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Mol Biol. 1988 Aug 5;202(3):551-63 [3172226] J Bacteriol. 1989 Jun;171(6):3440-8 [2524470] J Biomol Struct Dyn. 1986 Feb;3(4):705-23 [3078109] Cell. 1987 Nov 6;51(3):483-92 [2822258] Cell. 1987 Nov 20;51(4):631-41 [2445491] Cell. 1987 Sep 11;50(6):885-99 [3040263] Nucleic Acids Res. 1986 Mar 25;14(6):2763-77 [2421252] Nature. 1976 Aug 19;262(5570):665-9 [958438] J Mol Biol. 1989 Jun 20;207(4):675-93 [2760929] J Mol Appl Genet. 1984;2(6):507-17 [6099398] Virology. 1987 Oct;160(2):456-64 [3660589] J Mol Biol. 1990 Apr 20;212(4):635-43 [2139472] J Bacteriol. 1990 Jun;172(6):3146-51 [2188952] Nucleic Acids Res. 1981 Jan 10;9(1):133-48 [6163133] Cell. 1983 Apr;32(4):1337-46 [6188537] Proc Natl Acad Sci U S A. 1983 Jun;80(11):3401-5 [6304708] Gene. 1982 Nov;20(1):11-24 [6219041] Virology. 1981 Feb;109(1):198-200 [6451073] Jpn J Microbiol. 1976 Oct;20(5):385-96 [994348] Science. 1976 Oct 8;194(4261):156-61 [959843] Jpn J Microbiol. 1972 Jul;16(4):297-306 [4569213] J Mol Biol. 1989 Jun 20;207(4):695-717 [2547971] Proc Natl Acad Sci U S A. 1975 Dec;72(12):4785-89 [1061069] Nucleic Acids Res. 1975 Sep;2(9):1441-58 [1178525] J Mol Biol. 1970 Apr 28;49(2):393-404 [5447824] Cell. 1986 Jan 17;44(1):125-36 [2416472] Virology. 1976 Jul 1;72(1):147-53 [779239] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Nephrocalcinosis in homozygous familial hypercholesterolemia: ultrasound and CT findings. AN - 80424411; 1987176 AB - An association between homozygous familial hypercholesterolemia (FH) and nephrocalcinosis has not, to our knowledge, been previously reported. Evaluation in 10 cases of homozygous FH revealed evidence of nephrocalcinosis in 7 cases. Fine, uniform calcifications in the renal papillae were demonstrated by renal ultrasound or CT. Renal papillary necrosis was demonstrated by intravenous pyelogram in one case. No renal function impairment was noted in these seven patients. There was no evidence of hypercalcemia. These findings may have implications for the use of a potentially nephrotoxic drug for the treatment of this disease--in particular, when an immunosuppressive agent is required following liver transplantation. JF - Journal of computer assisted tomography AU - Hill, S C AU - Hoeg, J M AU - Avila, N A AD - Diagnostic Radiology Department, Warren G. Magnuson Clinical Center, National Institutes of Health, Bethesda, MD 20892. PY - 1991 SP - 101 EP - 103 VL - 15 IS - 1 SN - 0363-8715, 0363-8715 KW - Index Medicus KW - Prospective Studies KW - Humans KW - Adult KW - Retrospective Studies KW - Child KW - Adolescent KW - Ultrasonography KW - Male KW - Female KW - Child, Preschool KW - Hyperlipoproteinemia Type II -- complications KW - Hyperlipoproteinemia Type II -- diagnostic imaging KW - Calcinosis -- etiology KW - Calcinosis -- diagnostic imaging KW - Tomography, X-Ray Computed KW - Kidney Diseases -- etiology KW - Kidney Diseases -- diagnostic imaging KW - Hyperlipoproteinemia Type II -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80424411?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+computer+assisted+tomography&rft.atitle=Nephrocalcinosis+in+homozygous+familial+hypercholesterolemia%3A+ultrasound+and+CT+findings.&rft.au=Hill%2C+S+C%3BHoeg%2C+J+M%3BAvila%2C+N+A&rft.aulast=Hill&rft.aufirst=S&rft.date=1991-01-01&rft.volume=15&rft.issue=1&rft.spage=101&rft.isbn=&rft.btitle=&rft.title=Journal+of+computer+assisted+tomography&rft.issn=03638715&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-02-15 N1 - Date created - 1991-02-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cytotoxic activity of a recombinant fusion protein between insulin-like growth factor I and Pseudomonas exotoxin. AN - 80423572; 1846308 AB - A chimeric toxin in which the cell binding domain of Pseudomonas exotoxin was replaced with mature human insulin-like growth factor I (IGF-I) was produced in Escherichia coli. This protein, IGF-I-PE40, was cytotoxic to human cell lines derived from a variety of tumor types, with a breast carcinoma line (MCF-7) and two hepatoma lines (HEP3B and HEPG2) showing the highest sensitivity to the toxin. The specificity of IGF-I-PE40 cytotoxicity was confirmed through competition with excess IGF-I and through blockage of toxin binding using an antibody specific to the type I IGF receptor. A potential interaction between the toxin and soluble IGF-binding proteins was also demonstrated. IGF-I-PE40 may be useful in the selective elimination of cells bearing the type I IGF receptor. JF - Cancer research AU - Prior, T I AU - Helman, L J AU - FitzGerald, D J AU - Pastan, I AD - Laboratory of Molecular Biology, DCBDC, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1991/01/01/ PY - 1991 DA - 1991 Jan 01 SP - 174 EP - 180 VL - 51 IS - 1 SN - 0008-5472, 0008-5472 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - Neoplasm Proteins KW - Oligonucleotides KW - Receptors, Cell Surface KW - Receptors, Somatomedin KW - Recombinant Fusion Proteins KW - Virulence Factors KW - Insulin-Like Growth Factor I KW - 67763-96-6 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 Proteins -- biosynthesis KW - Animals KW - Base Sequence KW - Tumor Cells, Cultured KW - Oligonucleotides -- chemistry KW - Humans KW - In Vitro Techniques KW - Recombinant Fusion Proteins -- isolation & purification KW - Molecular Sequence Data KW - Cloning, Molecular -- methods KW - Mice KW - Recombinant Fusion Proteins -- toxicity KW - Receptors, Cell Surface -- metabolism KW - Exotoxins -- administration & dosage KW - Insulin-Like Growth Factor I -- metabolism KW - Insulin-Like Growth Factor I -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80423572?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cytotoxic+activity+of+a+recombinant+fusion+protein+between+insulin-like+growth+factor+I+and+Pseudomonas+exotoxin.&rft.au=Prior%2C+T+I%3BHelman%2C+L+J%3BFitzGerald%2C+D+J%3BPastan%2C+I&rft.aulast=Prior&rft.aufirst=T&rft.date=1991-01-01&rft.volume=51&rft.issue=1&rft.spage=174&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 - 1991-02-27 N1 - Date created - 1991-02-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Numbers of cortical vitreous cells and onset of cataracts in Royal College of surgeons rats. AN - 80423463; 1987101 AB - Royal College of Surgeons (RCS) rats have hereditary retinal degeneration with associated posterior subcapsular opacities. A link between light, retinal degeneration, and cataracts may consist in peroxidation of polyunsaturated fatty acids of rod outer segment lipids to yield water-soluble toxic aldehydes that can traverse the vitreous and react with bow cells and posterior lens fibers. In an immune reaction to the retinal degeneration, macrophages multiply in the retina and in the cortex of the vitreous. In dystrophics, the cortical vitreous separates readily from attachments to retina, ciliary body and lens, and from the vitreous gel. This web-like structure was stained and spread on a counting chamber. Cells were counted at 15-130 postnatal days in pink- and black-eyed RCS dystrophics and in congenic controls to correlate numbers of cells, temporal and geographic patterns of retinal degeneration, and onset of opacities. Rats were reared in cyclic light (10-40 lux inside the cage) and fed a natural ingredient diet (NIH-07). Cortical vitreous cells increased markedly in pink- and black-eyed dystrophics at 50-53 days when slit-lamp detectable opacities occurred in both. The increase was 4.6-fold in pink- and 2.3-fold in black-eyed rats compared with controls. At 50-53 days, the dystrophy affected all quadrants of the retina severely in pink-eyed RCS but only the inferior periphery in black-eyed RCS. Consequently, severe degeneration in one quadrant may suffice to initiate an opacity.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Investigative ophthalmology & visual science AU - Hess, H H AU - O'Keefe, T L AU - Kuwabara, T AU - Westney, I V AD - Office of the Scientific Director, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 200 EP - 207 VL - 32 IS - 1 SN - 0146-0404, 0146-0404 KW - Index Medicus KW - Rats KW - Macrophages KW - Animals KW - Circadian Rhythm KW - Cell Count KW - Rats, Mutant Strains KW - Aging KW - Light KW - Eye Color KW - Retinal Degeneration -- complications KW - Vitreous Body -- pathology KW - Retinal Degeneration -- pathology KW - Cataract -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80423463?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Numbers+of+cortical+vitreous+cells+and+onset+of+cataracts+in+Royal+College+of+surgeons+rats.&rft.au=Hess%2C+H+H%3BO%27Keefe%2C+T+L%3BKuwabara%2C+T%3BWestney%2C+I+V&rft.aulast=Hess&rft.aufirst=H&rft.date=1991-01-01&rft.volume=32&rft.issue=1&rft.spage=200&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 - 1991-02-15 N1 - Date created - 1991-02-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Promotion of hepatocellular foci in female rats by chenodeoxycholic acid. AN - 80418531; 1988183 AB - Chenodeoxycholic acid (CDC), a dihydroxylated primary bile acid, was evaluated for promotional activity in the liver of rats using a two-stage initiation-promotion model. CDC is a primary bile acid that can attain high concentrations in serum and liver during induced or naturally occurring hepatocellular disorders. Female Sprague-Dawley rats were injected once (i.p.) with diethylnitrosamine (DEN, 150 mg/kg) or sterile physiologic saline (SAL, 0.85% NaCl). Two weeks later, rats in each group were placed into one of two subgroups and fed either NIH-31 mash (Control) or NIH-31 mash containing 0.5% CDC for a 10 week period. At the end of the feeding period, blood and liver samples were collected for determination of bile acid profiles and quantitation of hepatocellular foci respectively. Serum samples were analyzed for concentrations of individual bile acids using a HPLC method that utilizes a post-column enzymatic reaction and fluorescence detection. Liver slices from the left hepatic lobe were stained for foci positive for placental glutathione S-transferase. In serum, significant increases occurred in concentrations of all forms of CDC and were accompanied by mild, insignificant increases in lithocholic acid. Decreased serum concentrations occurred in all forms of cholic and deoxycholic acids. Analysis of liver sections revealed that rats treated with DEN-CDC had significant increases in numbers and volume of foci compared to those treated with DEN-Control. For rats in groups DEN-CDC and DEN-Control, the numbers of foci per square centimeter were 32 and 12; per cubic centimeter, 2221 and 937; and the per cent volume of foci, 1.487 and 0.385 respectively. In this study, CDC was a promoter of hepatocellular foci. Because concentrations of CDC in liver and serum increase in a variety of hepatobiliary disorders, the possibility that increases in endogenous concentrations can enhance the formation of hepatocellular foci is being explored. JF - Carcinogenesis AU - Blair, P C AU - Popp, J A AU - Bryant-Varela, B J AU - Thompson, M B AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 59 EP - 63 VL - 12 IS - 1 SN - 0143-3334, 0143-3334 KW - Bile Acids and Salts KW - 0 KW - Chenodeoxycholic Acid KW - 0GEI24LG0J KW - Diethylnitrosamine KW - 3IQ78TTX1A KW - Lithocholic Acid KW - 5QU0I8393U KW - Glutathione Transferase KW - EC 2.5.1.18 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Liver -- enzymology KW - Lithocholic Acid -- toxicity KW - Glutathione Transferase -- analysis KW - Bile Acids and Salts -- analysis KW - Female KW - Chenodeoxycholic Acid -- toxicity KW - Precancerous Conditions -- chemically induced KW - Liver Neoplasms, Experimental -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80418531?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Promotion+of+hepatocellular+foci+in+female+rats+by+chenodeoxycholic+acid.&rft.au=Blair%2C+P+C%3BPopp%2C+J+A%3BBryant-Varela%2C+B+J%3BThompson%2C+M+B&rft.aulast=Blair&rft.aufirst=P&rft.date=1991-01-01&rft.volume=12&rft.issue=1&rft.spage=59&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-02-25 N1 - Date created - 1991-02-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Teratogenic effects of 2,3,7,8-tetrabromodibenzo-p-dioxin and three polybrominated dibenzofurans in C57BL/6N mice. AN - 80413851; 1987653 AB - Brominated flame retardants involved in many industrial uses contain polybrominated dibenzo-p-dioxins (PBDDs) and dibenzofurans (PBDFs) as contaminants. The levels of these contaminants can be dramatically increased by combustion. These chemicals are closely related in structure to the polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs), of which 2,3,7,8-tetrachloridibenzo-p-dioxin (TCDD) is the most toxic isomer. TCDD and related PCDFs are potent mouse teratogens inducing cleft palate and hydronephrosis at doses below those at which overt maternal and embryo/fetal toxicity occurs. This study examines the teratogenic effects of 2,3,7,8-tetrabromodibenzo-p-dioxin (TBDD), 2,3,7,8-tetrabromodibenzofuran (TBDF), 1,2,3,7,8-pentabromodibenzofuran (1PeBDF), and 2,3,4,7,8-pentabromodibenzofuran (4PeBDF) in C57BL/6N mice treated on gestation day (gd) 10 and examined on gd 18. Pregnant dams were treated with 0-4000 micrograms of each congener per kilogram body weight in 10 ml corn oil/kg. Dose selection was based on the relative toxicity of the chlorinated isomers. Maternal toxicity and developmental toxicity were assessed, and the hard palate and kidney, the target organs for the teratogenic effects of TCDD and related compounds, were examined for structural abnormalities. While the maternal liver weight increased at all dose levels examined for all four compounds, there was no evidence of any maternal toxicity. Embryo/fetal mortality was increased only at greater than or equal to 500 microgram TBDF/kg, while fetal weight increased in a dose-related manner following exposure to TBDD and TBDF. All compounds produced hydronephrosis (HN) at doses below that at which cleft palate (CP) occurred. The incidence of HN was significantly increased above background levels at the following doses (micrograms/kg): TBDD, 3; TBDF, 25; 1PeBDF, 500; 4PeBDF, 400. The LOELs (micrograms/kg) for CP were: TBDD, 48; TBDF, 200; 1PeBDF, 4000; 4PeBDF, 2400. The cleft palate incidence for all four brominated compounds and TCDD could be fit to a common slope, compatible with the concept that these chemicals all exert their teratogenic effects through a common mechanism. The potency of these chemicals, relative to TCDD as 1 for the induction of cleft palate, is TBDD, 0.24; TBDF, 0.10; 1PeBDF, 0.004; and 4PeBDF, 0.005. Previous studies from our laboratory had determined that the chlorinated dibenzofuran isomers had relative potencies of 0.05 (TCDF), 0.03 (1PeCDF), and 0.09 (4PeCDF). Thus, bromination decreases the teratogenic activity of TBDD relative to TCDD and of both 1- and 4PeBDF relative to the chlorinated isomers. However, substitution of bromines for chlorines increases the potency of TBDF relative to TCDF.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Toxicology and applied pharmacology AU - Birnbaum, L S AU - Morrissey, R E AU - Harris, M W AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 141 EP - 152 VL - 107 IS - 1 SN - 0041-008X, 0041-008X KW - Benzofurans KW - 0 KW - Dioxins KW - Flame Retardants KW - Polychlorinated Dibenzodioxins KW - 2,3,7,8-tetrabromodibenzo-4-dioxin KW - 04PL7F455E KW - Index Medicus KW - Animals KW - Analysis of Variance KW - Dose-Response Relationship, Drug KW - Polychlorinated Dibenzodioxins -- toxicity KW - Mice, Inbred C57BL KW - Mice KW - Female KW - Pregnancy KW - Embryonic and Fetal Development -- drug effects KW - Cleft Palate -- chemically induced KW - Abnormalities, Drug-Induced -- etiology KW - Dioxins -- toxicity KW - Benzofurans -- toxicity KW - Hydronephrosis -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80413851?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Teratogenic+effects+of+2%2C3%2C7%2C8-tetrabromodibenzo-p-dioxin+and+three+polybrominated+dibenzofurans+in+C57BL%2F6N+mice.&rft.au=Birnbaum%2C+L+S%3BMorrissey%2C+R+E%3BHarris%2C+M+W&rft.aulast=Birnbaum&rft.aufirst=L&rft.date=1991-01-01&rft.volume=107&rft.issue=1&rft.spage=141&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 - 1991-02-20 N1 - Date created - 1991-02-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A consensus approach to electrolytes and blood pressure. Could we all be right? AN - 80370016; 1986999 AB - This commentary sets forth the hypothesis that the putative beneficial or detrimental effects of specific electrolytes on blood pressure regulation in fact reflect highly integrated responses to interactions among these cationic and anionic species. In this paradigm, the impact of any given intake of an electrolyte on arterial pressure will be influenced by the concurrent consumption of other electrolytes. Thus, the heterogeneous blood pressure response in humans to isolated manipulations of nutrients such as sodium, calcium, and potassium may be determined, in part, by the adequacy of the dietary intake of other mineral elements. If this hypothesis is validated by continued research in this area, we would have new strategies available to improve blood pressure control in humans. For example, treatment of "NaCl sensitivity" in some humans might be more effectively approached by correcting dietary deficiencies of either potassium or calcium than by restricting dietary NaCl. JF - Hypertension (Dallas, Tex. : 1979) AU - McCarron, D A AD - Division of Nephrology and Hypertension, National Institute of Diabetes, Digestive and Kidney Disease (NIDDK) Clinical Nutrition Research Unit, Oregon Health Sciences University, Portland 97201. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - I170 EP - I172 VL - 17 IS - 1 Suppl SN - 0194-911X, 0194-911X KW - Electrolytes KW - 0 KW - Sodium Chloride KW - 451W47IQ8X KW - Potassium KW - RWP5GA015D KW - Index Medicus KW - Models, Cardiovascular KW - Hypertension -- chemically induced KW - Humans KW - Sodium Chloride -- metabolism KW - Homeostasis KW - Potassium -- metabolism KW - Blood Pressure -- drug effects KW - Electrolytes -- metabolism KW - Electrolytes -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80370016?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hypertension+%28Dallas%2C+Tex.+%3A+1979%29&rft.atitle=A+consensus+approach+to+electrolytes+and+blood+pressure.+Could+we+all+be+right%3F&rft.au=McCarron%2C+D+A&rft.aulast=McCarron&rft.aufirst=D&rft.date=1991-01-01&rft.volume=17&rft.issue=1+Suppl&rft.spage=I170&rft.isbn=&rft.btitle=&rft.title=Hypertension+%28Dallas%2C+Tex.+%3A+1979%29&rft.issn=0194911X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-02-19 N1 - Date created - 1991-02-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Calcium, network activity, and the role of NMDA channels in synaptic plasticity in vitro. AN - 80369898; 1702460 AB - Functionally effective neuronal circuits are constructed through a competitive process that requires patterned neuronal activity elicited by structured input from the environment. To explore the mechanisms of this activity-dependent synaptic restructuring, we have developed an in vitro preparation of mouse spinal cord neurons maintained in a 3-chambered cell-culture system. Sensory afferents that received chronic electrical stimulation for 3-5 d developed stronger synaptic connections than unstimulated afferents converging onto the same postsynaptic spinal cord neuron. Exposure to 100 microM DL-2-amino-5-phosphonovaleric acid (APV), an antagonist of the NMDA channel, during the stimulation period prevented the competitive advantage associated with electric stimulation. However, when APV was applied with a higher concentration of calcium (3 mM), activity-dependent synaptic plasticity was no longer inhibited by the NMDA receptor antagonist. This reversal of APV block of the plasticity was not impaired by reducing transmitter release with 3 mM magnesium (in addition to 3 mM calcium and APV). A suppressant effect of APV on spontaneous activity was observed, which was attributed to loss of the NMDA component of the EPSP. Activity-dependent plasticity was also blocked if spontaneous activity was suppressed with dilute tetrodotoxin (TTX; 5-10 nM), a dosage that reduces excitability of neurons but is insufficient to block sodium-dependent action potentials. These experiments bring into question how NMDA channel activation is involved in the processes of synaptic remodeling during development. The data suggest that postsynaptic activity is required for synaptic remodeling, but this activity need not involve NMDA receptor activation specifically for activity-evoked synaptic plasticity. Instead, the mechanism for plasticity appears to operate through calcium-dependent processes in general. JF - The Journal of neuroscience : the official journal of the Society for Neuroscience AU - Fields, R D AU - Yu, C AU - Nelson, P G AD - National Institutes of Health, NICHD, Laboratory of Developmental Neurobiology, Bethesda, Maryland 20892. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 134 EP - 146 VL - 11 IS - 1 SN - 0270-6474, 0270-6474 KW - Ion Channels KW - 0 KW - Receptors, N-Methyl-D-Aspartate KW - Tetrodotoxin KW - 4368-28-9 KW - N-Methylaspartate KW - 6384-92-5 KW - 2-Amino-5-phosphonovalerate KW - 76726-92-6 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Fetus KW - Evoked Potentials -- drug effects KW - Animals KW - 2-Amino-5-phosphonovalerate -- pharmacology KW - N-Methylaspartate -- pharmacology KW - Cells, Cultured KW - Mice KW - Spinal Cord -- physiology KW - Tetrodotoxin -- pharmacology KW - Electric Stimulation KW - Receptors, N-Methyl-D-Aspartate -- physiology KW - Neurons -- drug effects KW - Neurons -- physiology KW - Calcium -- pharmacology KW - Neuronal Plasticity KW - Ion Channels -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80369898?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+neuroscience+%3A+the+official+journal+of+the+Society+for+Neuroscience&rft.atitle=Calcium%2C+network+activity%2C+and+the+role+of+NMDA+channels+in+synaptic+plasticity+in+vitro.&rft.au=Fields%2C+R+D%3BYu%2C+C%3BNelson%2C+P+G&rft.aulast=Fields&rft.aufirst=R&rft.date=1991-01-01&rft.volume=11&rft.issue=1&rft.spage=134&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+neuroscience+%3A+the+official+journal+of+the+Society+for+Neuroscience&rft.issn=02706474&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-02-14 N1 - Date created - 1991-02-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Norepinephrine stimulates potassium efflux from pinealocytes: evidence for involvement of biochemical "AND" gate operated by calcium and adenosine 3',5'-monophosphate. AN - 80368447; 1846112 AB - Biochemical studies of K+ efflux from rat pinealocytes revealed for the first time that norepinephrine (NE) increases 86Rb+ and 42K+ efflux. The effects of NE depend upon concurrent activation of both alpha 1- and beta-adrenoceptors. This effect is mediated by cAMP and Ca2+, which appear to act in conjunction to control K+ efflux; studies with charybdotoxin and tetraethylammonium indicate that a Ca2(+)-sensitive K+ channel (K(Ca] appears to be involved. Patch clamp studies identified a large conductance (approximately 100 psec) K+ channel. This study also revealed for the first time that NE treatment increases the fraction of time that this channel was open. Studies of inside-out pineal membrane patches indicated that increasing Ca2+ at the cytoplasmic surface of the membrane increased the frequency of channel opening, as is typical of K(Ca) channels in this type of preparation. Outward K+ currents were almost completely blocked by tetraethylammonium (10 mM) and scorpion venom (L. quinquestriatum; 100 ng/ml). Cell-attached studies confirm that the effects of NE are mediated by intracellular second messengers. These investigations suggest that NE elevates K+ flux, probably through a large conductance K(Ca) channel, that NE acts through alpha 1- and beta-adrenergic receptors, and that Ca2+ and cAMP act together through a biochemical "AND" gate to mediate the effects of receptor activation. Activation of this K(Ca) channel would have a hyperpolarizing influence and might contribute to the adrenergic hyperpolarization of pinealocytes. JF - Endocrinology AU - Ceña, V AU - Halperin, J I AU - Yeandle, S AU - Klein, D C AD - Section on Neuroendocrinology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 559 EP - 569 VL - 128 IS - 1 SN - 0013-7227, 0013-7227 KW - Potassium Channels KW - 0 KW - Receptors, Adrenergic, alpha KW - Receptors, Adrenergic, beta KW - Calcimycin KW - 37H9VM9WZL KW - Sodium KW - 9NEZ333N27 KW - Propranolol KW - 9Y8NXQ24VQ KW - Cyclic AMP KW - E0399OZS9N KW - Rubidium KW - MLT4718TJW KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Potassium KW - RWP5GA015D KW - Calcium KW - SY7Q814VUP KW - Norepinephrine KW - X4W3ENH1CV KW - Prazosin KW - XM03YJ541D KW - Abridged Index Medicus KW - Index Medicus KW - Rubidium -- metabolism KW - Animals KW - Propranolol -- pharmacology KW - Calcimycin -- pharmacology KW - Models, Biological KW - Sodium -- pharmacology KW - Rats KW - Rats, Inbred Strains KW - Cells, Cultured KW - Kinetics KW - Prazosin -- pharmacology KW - Ovariectomy KW - Female KW - Male KW - Norepinephrine -- pharmacology KW - Receptors, Adrenergic, alpha -- drug effects KW - Pineal Gland -- drug effects KW - Potassium Channels -- physiology KW - Cyclic AMP -- physiology KW - Potassium Channels -- drug effects KW - Potassium -- metabolism KW - Norepinephrine -- physiology KW - Calcium -- physiology KW - Receptors, Adrenergic, beta -- physiology KW - Receptors, Adrenergic, beta -- drug effects KW - Pineal Gland -- physiology KW - Receptors, Adrenergic, alpha -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80368447?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Norepinephrine+stimulates+potassium+efflux+from+pinealocytes%3A+evidence+for+involvement+of+biochemical+%22AND%22+gate+operated+by+calcium+and+adenosine+3%27%2C5%27-monophosphate.&rft.au=Ce%C3%B1a%2C+V%3BHalperin%2C+J+I%3BYeandle%2C+S%3BKlein%2C+D+C&rft.aulast=Ce%C3%B1a&rft.aufirst=V&rft.date=1991-01-01&rft.volume=128&rft.issue=1&rft.spage=559&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=00137227&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-02-21 N1 - Date created - 1991-02-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ultraviolet mutational spectrum in a shuttle vector propagated in xeroderma pigmentosum lymphoblastoid cells and fibroblasts. AN - 80365824; 1986277 AB - In order to examine possible cell-type specificity in mutagenic events, a shuttle-vector plasmid, pZ189, carrying a bacterial suppressor tRNA marker gene, was treated with ultraviolet radiation and propagated in Epstein-Barr virus transformed lymphoblastoid cell lines from a patient, XP12BE, with xeroderma pigmentosum (XP), group A, and a normal control. XP is a skin-cancer-prone disorder with UV hypersensitivity and defective DNA repair. Plasmid survival and mutations inactivating the marker gene were scored by transforming an indicator strain of E. coli. An earlier report on this data [Seetharam et al., (1990) J. Mol. Biol., 212, 433] indicated lower survival and higher mutation frequency with the UV-treated plasmid passed through the XP12Be(EBV) line. In the present report, sequence analysis of 198 mutant plasmids revealed a predominance of G:C----A:T transitions with both lymphoblastoid cell lines. This finding is consistent with the bias of polymerases toward insertion of an adenine opposite non-coding photoproducts (dinucleotides or other lesions). Transversion mutagenesis, non-adjacent double mutations, and triple-base mutations may involve other mechanisms. These results were compared to similar data from a fibroblast line from the same patient [Bredberg et al., (1986) Proc. Natl. Acad. Sci. (U.S.A.), 83, 8273]. The frequency of G:C----A:T transitions was higher, and there were fewer plasmids with multiple-base substitutions and with transversion mutations with both XP lymphoblasts and fibroblasts than with the normal lymphoblasts and fibroblasts. There were no significant differences in classes or types of mutations in the UV-treated plasmid replicated in the XP lymphoblasts and the XP fibroblasts. This suggests that the major features of UV mutagenesis in different cell types from the same individual are similar. JF - Mutation research AU - Seetharam, S AU - Kraemer, K H AU - Waters, H L AU - Seidman, M M AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 97 EP - 105 VL - 254 IS - 1 SN - 0027-5107, 0027-5107 KW - Index Medicus KW - Base Sequence KW - DNA Repair KW - Humans KW - DNA Mutational Analysis KW - Molecular Sequence Data KW - Escherichia coli -- genetics KW - Lymphocytes KW - Genes, Suppressor KW - Cell Line KW - Fibroblasts KW - Ultraviolet Rays KW - Genetic Vectors KW - Xeroderma Pigmentosum -- genetics KW - Plasmids KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80365824?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Ultraviolet+mutational+spectrum+in+a+shuttle+vector+propagated+in+xeroderma+pigmentosum+lymphoblastoid+cells+and+fibroblasts.&rft.au=Seetharam%2C+S%3BKraemer%2C+K+H%3BWaters%2C+H+L%3BSeidman%2C+M+M&rft.aulast=Seetharam&rft.aufirst=S&rft.date=1991-01-01&rft.volume=254&rft.issue=1&rft.spage=97&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 - 1991-02-14 N1 - Date created - 1991-02-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Binding of the transcription factor EBP-80 mediates the methylation response of an intracisternal A-particle long terminal repeat promoter. AN - 80365410; 1898760 AB - Intracisternal A-particle (IAP) expression in mouse cells has been correlated with hypomethylation of HhaI and HpaII sites in proviral long terminal repeats (LTRs). In a previous study, in vitro methylation of three HhaI sites in the U3 region of the LTR from the cloned genomic IAP element, MIA14, was shown to inhibit promoter activity in vivo. In this study, we found by site-directed mutagenesis that the two more downstream HhaI sites within this LTR were responsible for the methylation effects on promoter activity in vivo; methylation of the other (5') HhaI site, which lies within a putative SP1 binding domain, did not affect promoter activity. Methylation of the HhaI sites also inhibited promoter activity of the LTR in a cell-free transcription system. Exonuclease III footprinting demonstrated methylation-induced changes in protein binding over the region encompassing the downstream HhaI site, designated the Enh2 domain. The protein that interacts specifically with this domain, EBP-80, was characterized in a previous study (M. Falzon and E. L. Kuff, J. Biol. Chem. 264:21915-21922, 1989). We show here that the presence of methylcytosine in the HhaI site within the Enh2 domain inhibited binding of EBP-80 in vitro. The methylated MIA14 LTR construct was much less responsive to added EBP-80 in an in vitro transcription system than was the unmethylated construct. These data suggest that CpG methylation within the Enh2 domain may exert its effect on transcription in vivo by altering the interaction between EBP-80 and its cognate DNA sequence. JF - Molecular and cellular biology AU - Falzon, M AU - Kuff, E L AD - Laboratory of Biochemistry, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 117 EP - 125 VL - 11 IS - 1 SN - 0270-7306, 0270-7306 KW - DNA-Binding Proteins KW - 0 KW - Transcription Factors KW - Index Medicus KW - Regulatory Sequences, Nucleic Acid KW - Base Sequence KW - Humans KW - Restriction Mapping KW - In Vitro Techniques KW - Molecular Sequence Data KW - Transcription, Genetic KW - Protein Binding KW - Methylation KW - Cell Line KW - Binding Sites KW - Promoter Regions, Genetic KW - Transcription Factors -- metabolism KW - Genes, Intracisternal A-Particle KW - Repetitive Sequences, Nucleic Acid KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80365410?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Binding+of+the+transcription+factor+EBP-80+mediates+the+methylation+response+of+an+intracisternal+A-particle+long+terminal+repeat+promoter.&rft.au=Falzon%2C+M%3BKuff%2C+E+L&rft.aulast=Falzon&rft.aufirst=M&rft.date=1991-01-01&rft.volume=11&rft.issue=1&rft.spage=117&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 - 1991-02-14 N1 - Date created - 1991-02-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] Genes Dev. 1988 Sep;2(9):1127-35 [3056778] Proc Natl Acad Sci U S A. 1983 Dec;80(24):7586-90 [6324179] Proc Natl Acad Sci U S A. 1981 Mar;78(3):1619-23 [6262820] Methods Enzymol. 1980;65(1):499-560 [6246368] Virology. 1983 Jul 30;128(2):485-9 [6193633] Nature. 1983 Jun 23-29;303(5919):674-9 [6304535] Science. 1983 Feb 11;219(4585):626-31 [6297005] EMBO J. 1987 Aug;6(8):2329-35 [3665878] Mol Cell Biol. 1988 Mar;8(3):1093-102 [2452971] Prog Clin Biol Res. 1985;198:157-76 [2415989] Genes Dev. 1989 May;3(5):612-9 [2545524] J Mol Biol. 1989 Nov 20;210(2):411-5 [2532258] J Biol Chem. 1989 Dec 25;264(36):21915-22 [2513327] Science. 1989 Oct 20;246(4928):358-63 [2678475] Proc Natl Acad Sci U S A. 1988 Apr;85(7):2066-70 [3281160] Genes Dev. 1988 Sep;2(9):1136-43 [3192075] Mol Cell Biol. 1984 Oct;4(10):2128-35 [6095042] Cancer Res. 1984 Nov;44(11):5234-41 [6091872] Science. 1986 Oct 3;234(4772):47-52 [3529394] Proc Natl Acad Sci U S A. 1986 Aug;83(16):5889-93 [3461465] Mol Cell Biol. 1987 Mar;7(3):1101-10 [3561410] Biochem J. 1986 Feb 15;234(1):213-6 [3707542] Proc Natl Acad Sci U S A. 1985 May;82(9):2560-4 [3857599] J Biol Chem. 1990 Aug 5;265(22):13084-90 [2165492] EMBO J. 1990 Apr;9(4):1157-64 [2323336] Cell. 1983 Aug;34(1):197-206 [6883509] Nucleic Acids Res. 1986 May 27;14(10):4343-52 [2423967] Gene. 1988 May 30;65(2):219-27 [2842233] Proc Natl Acad Sci U S A. 1988 May;85(10):3396-400 [2835770] Proc Natl Acad Sci U S A. 1987 Mar;84(5):1177-81 [3029768] Nucleic Acids Res. 1985 Dec 20;13(24):8765-85 [3001650] Nucleic Acids Res. 1985 Dec 20;13(24):8749-64 [3001649] Cell. 1986 Apr 11;45(1):35-44 [3006925] Nature. 1985 Sep 5-11;317(6032):84-7 [2993917] Mol Cell Biol. 1983 Aug;3(8):1371-80 [6621530] Cell. 1984 Feb;36(2):357-69 [6537904] Nucleic Acids Res. 1985 Aug 12;13(15):5503-13 [2994001] J Virol. 1983 Apr;46(1):307-10 [6827653] Proc Natl Acad Sci U S A. 1981 Dec;78(12):7609-13 [6950402] Cancer Res. 1979 May;39(5):1455-61 [427789] J Gen Virol. 1977 Jul;36(1):59-74 [886304] J Mol Biol. 1970 Feb 28;48(1):67-83 [4915295] Proc Natl Acad Sci U S A. 1987 Apr;84(8):2180-4 [2951737] J Virol. 1988 Nov;62(11):4070-7 [3139894] Annu Rev Biochem. 1983;52:93-124 [6311083] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A -1 ribosomal frameshift in a double-stranded RNA virus of yeast forms a gag-pol fusion protein. AN - 80365223; 1986362 AB - The L-A double-stranded RNA (dsRNA) virus of Saccharomyces cerevisiae has two open reading frames (ORFs). ORF1 encodes the 80-kDa major coat protein (gag). ORF2, which is expressed only as a 180-kDa fusion protein with ORF1, encodes a single-stranded RNA-binding domain and has the consensus sequence for RNA-dependent RNA polymerases of (+)-strand and double-stranded RNA viruses (pol). We show that the 180-kDa protein is formed by -1 ribosomal frame-shifting by a mechanism indistinguishable from that of retro-viruses. Analysis of the "slippery site" suggests that a low probability of unpairing of the aminoacyl-tRNA from the 0-frame codon at the ribosomal A site reduces the efficiency of frameshifting more than the reluctance of a given tRNA to have its wobble base mispaired. Frameshifting of L-A requires a pseudoknot structure just downstream of the shift site. The efficiency of the L-A frameshift site is 1.8%, similar to the observed molar ratio in viral particles of the 180-kDa fusion protein to the major coat protein. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Dinman, J D AU - Icho, T AU - Wickner, R B AD - Section on the Genetics of Simple Eukaryotes, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991/01/01/ PY - 1991 DA - 1991 Jan 01 SP - 174 EP - 178 VL - 88 IS - 1 SN - 0027-8424, 0027-8424 KW - Fusion Proteins, gag-pol KW - 0 KW - Oligonucleotide Probes KW - RNA, Double-Stranded KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Protein Biosynthesis KW - Base Sequence KW - Genetic Vectors KW - Molecular Sequence Data KW - Transcription, Genetic KW - Amino Acid Sequence KW - Plasmids KW - Saccharomyces cerevisiae -- genetics KW - Frameshift Mutation KW - Ribosomes -- metabolism KW - RNA, Double-Stranded -- genetics KW - Open Reading Frames KW - Fusion Proteins, gag-pol -- genetics KW - RNA Viruses -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80365223?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=A+-1+ribosomal+frameshift+in+a+double-stranded+RNA+virus+of+yeast+forms+a+gag-pol+fusion+protein.&rft.au=Dinman%2C+J+D%3BIcho%2C+T%3BWickner%2C+R+B&rft.aulast=Dinman&rft.aufirst=J&rft.date=1991-01-01&rft.volume=88&rft.issue=1&rft.spage=174&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 - 1991-02-14 N1 - Date created - 1991-02-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Methods Enzymol. 1983;100:293-308 [6312261] Nature. 1985 Jan 17-23;313(5999):243-6 [2982101] Proc Natl Acad Sci U S A. 1985 Jan;82(2):488-92 [3881765] Proc Natl Acad Sci U S A. 1985 Mar;82(6):1618-22 [3885215] Proc Natl Acad Sci U S A. 1985 May;82(9):2829-33 [2581255] Nucleic Acids Res. 1985 Feb 25;13(4):1103-18 [3858795] Nucleic Acids Res. 1985 Mar 11;13(5):1717-31 [4000943] Proc Natl Acad Sci U S A. 1985 Jun;82(11):3616-20 [3889910] Science. 1985 Dec 13;230(4731):1237-42 [2416054] Gene. 1986;49(3):383-8 [3552889] J Mol Biol. 1986 Dec 20;192(4):725-35 [3295253] Proc Natl Acad Sci U S A. 1987 Jul;84(14):4767-71 [3474623] Genetics. 1979 Jul;92(3):803-21 [395022] Nature. 1981 Oct 15-21;293(5833):543-8 [6169994] J Mol Biol. 1982 Jul 15;158(4):573-97 [6750137] J Bacteriol. 1983 Jan;153(1):163-8 [6336730] Science. 1983 Feb 11;219(4585):620-5 [6186023] Cell. 1982 Dec;31(2 Pt 1):429-41 [6819084] Cell. 1983 Mar;32(3):853-69 [6299578] J Mol Biol. 1983 Jun 5;166(4):477-535 [6864790] Methods Enzymol. 1983;101:181-91 [6310321] Proc Natl Acad Sci U S A. 1987 Oct;84(20):7041-5 [2823251] Nature. 1988 Jan 21;331(6153):280-3 [2447506] Nature. 1988 Jan 21;331(6153):283-6 [3336440] EMBO J. 1987 Dec 1;6(12):3779-85 [3428275] Cold Spring Harb Symp Quant Biol. 1987;52:687-93 [3135981] EMBO J. 1988 May;7(5):1503-7 [2457498] Proc Natl Acad Sci U S A. 1988 Sep;85(18):6816-20 [2842793] Cell. 1988 Nov 4;55(3):447-58 [2846182] Cell. 1988 Nov 18;55(4):663-71 [2460245] J Biol Chem. 1989 Apr 25;264(12):6716-23 [2651431] Nucleic Acids Res. 1989;17 Suppl:r1-172 [2470031] Cell. 1989 May 19;57(4):537-47 [2720781] Science. 1989 May 26;244(4907):986-9 [2471265] FASEB J. 1989 Sep;3(11):2257-65 [2550303] Virology. 1989 Dec;173(2):736-42 [2556852] Proc Natl Acad Sci U S A. 1990 Apr;87(7):2516-20 [2181440] Nucleic Acids Res. 1990 Apr 11;18(7):1725-9 [2186364] Nucleic Acids Res. 1990 Apr 11;18(7):1825-32 [2159623] Proc Natl Acad Sci U S A. 1990 May;87(10):3713-7 [2187190] Trends Biochem Sci. 1990 May;15(5):186-90 [2193436] Cell. 1990 Jul 27;62(2):339-52 [2164889] Cell. 1990 Aug 24;62(4):819-28 [2117501] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Heterogeneity in the inheritance of alcoholism. A study of male and female twins. AN - 80364191; 1984758 AB - Genetic influence on risk for alcoholism was examined in a US treatment sample of 50 monozygotic (MZ) and 64 dizygotic (DZ) male and 31 MZ and 24 DZ female same-sex twin pairs. For the DSM-III composite diagnosis of Alcohol Abuse and/or Dependence, statistically significant MZ/DZ differences in concordance were found with male, but not female, twins. For specific diagnoses, MZ/DZ differences were found in male subjects for both Alcohol Abuse and Alcohol Dependence, while MZ/DZ differences in female subjects were found only for Alcohol Dependence. The male MZ/DZ concordance difference for composite diagnosis but not for Alcohol Dependence could be accounted for statistically by differences in age of onset between MZ and DZ probands. As with alcohol, differences in MZ/DZ concordance were found for DSM-III composite diagnoses of Other Substance Abuse and/or Dependence with male, but not female, twins. Using Epidemiological Catchment Area data to estimate the population base rates of both alcohol and other substance use disorders allowed for heritability analyses that showed genetic factors to have only a modest influence on overall risk in both sexes (heritability estimates of approximately 0.35 for male subjects and 0.24 for female subjects). However, evidence for heterogeneity in the pattern of inheritance was also found, suggesting forms of alcoholism that may be moderately to highly heritable. JF - Archives of general psychiatry AU - Pickens, R W AU - Svikis, D S AU - McGue, M AU - Lykken, D T AU - Heston, L L AU - Clayton, P J AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 19 EP - 28 VL - 48 IS - 1 SN - 0003-990X, 0003-990X KW - Genetic Markers KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Phenotype KW - Substance-Related Disorders -- diagnosis KW - Age Factors KW - Sex Factors KW - Twins, Monozygotic KW - Risk Factors KW - Humans KW - Twins, Dizygotic KW - Substance-Related Disorders -- genetics KW - Male KW - Female KW - Substance-Related Disorders -- epidemiology KW - Alcoholism -- epidemiology KW - Alcoholism -- diagnosis KW - Diseases in Twins KW - Alcoholism -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80364191?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Heterogeneity+in+the+inheritance+of+alcoholism.+A+study+of+male+and+female+twins.&rft.au=Pickens%2C+R+W%3BSvikis%2C+D+S%3BMcGue%2C+M%3BLykken%2C+D+T%3BHeston%2C+L+L%3BClayton%2C+P+J&rft.aulast=Pickens&rft.aufirst=R&rft.date=1991-01-01&rft.volume=48&rft.issue=1&rft.spage=19&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 - 1991-01-30 N1 - Date created - 1991-01-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Antibody to human retroviruses among drug users in three east coast American cities, 1972-1976. AN - 80363574; 1670608 AB - Between 1972 and 1976, 585 persons attending methadone maintenance clinics at East Coast veterans hospitals were enrolled in a survey of hepatitis antibody prevalence. Sera were tested for human immunodeficiency virus (HIV) and human T lymphotropic virus (HTLV) using both HTLV-I and HTLV-II immunoblots. Clinical and death records were also reviewed. None of the sera had HIV antibodies (upper 95% confidence limit, 0.5%); however, 103 (18%) had reactivity to HTLV. The profile of reactivity suggested that these subjects had been exposed to HTLV-II rather than to HTLV-I. Prevalence was as high in the early 1970s as today and correlated with duration of drug use rather than age. Neither cancers, specific neurologic diseases, nor excess deaths from any cause (overall 14%) could be ascribed to seropositivity. Therefore, HTLV (probably HTLV-II) has been a common infection of drug users for many years but adverse outcomes following infection were not demonstrated. JF - The Journal of infectious diseases AU - Biggar, R J AU - Buskell-Bales, Z AU - Yakshe, P N AU - Caussy, D AU - Gridley, G AU - Seeff, L AD - Viral Epidemiology Section, National Cancer Institute, Bethesda, Maryland 20852. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 57 EP - 63 VL - 163 IS - 1 SN - 0022-1899, 0022-1899 KW - Deltaretrovirus Antibodies KW - 0 KW - HTLV-I Antibodies KW - HTLV-II Antibodies KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Regression Analysis KW - Immunoblotting KW - Humans KW - Retrospective Studies KW - Florida -- epidemiology KW - HTLV-I Antibodies -- blood KW - New Jersey -- epidemiology KW - Adult KW - District of Columbia -- epidemiology KW - HTLV-II Antibodies -- blood KW - Follow-Up Studies KW - Heroin Dependence -- complications KW - Female KW - Male KW - Prevalence KW - Deltaretrovirus Infections -- epidemiology KW - Substance-Related Disorders -- complications KW - Deltaretrovirus Antibodies -- blood KW - Deltaretrovirus Infections -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80363574?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+infectious+diseases&rft.atitle=Antibody+to+human+retroviruses+among+drug+users+in+three+east+coast+American+cities%2C+1972-1976.&rft.au=Biggar%2C+R+J%3BBuskell-Bales%2C+Z%3BYakshe%2C+P+N%3BCaussy%2C+D%3BGridley%2C+G%3BSeeff%2C+L&rft.aulast=Biggar&rft.aufirst=R&rft.date=1991-01-01&rft.volume=163&rft.issue=1&rft.spage=57&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+infectious+diseases&rft.issn=00221899&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-01-25 N1 - Date created - 1991-01-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Fludarabine phosphate: a synthetic purine antimetabolite with significant activity against lymphoid malignancies. AN - 80363297; 1702143 AB - Fludarabine phosphate is the 2-fluoro, 5'-monophosphate derivative of vidarabine (ara-A) with the advantages of resistance to deamination by adenosine deaminase (ADA) and improved solubility. The mechanism of cytotoxic action of the compound appears to involve metabolic conversion to the active triphosphate. Fludarabine phosphate has substantial activity against lymphoid malignancies, particularly chronic lymphocytic leukemia (CLL) and low-grade non-Hodgkin's lymphoma (NHL). Its single-agent activity in CLL appears at least comparable to those of other conventional combination regimens. Its activity in Hodgkin's disease, mycosis fungoides, and macroglobulinemia, although suggestive, needs to be further defined and clinical trials are warranted in hairy cell leukemia, prolymphocytic leukemia, and previously untreated myeloma. The compound does not appear active against most common solid tumors. Early clinical trials indicated significant myelosuppression and the potential for severe neurotoxicity. Toxicity on the currently used low-dose schedules includes transient and reversible myelosuppression, nausea and vomiting, diarrhea, somnolence/fatigue, and elevations of liver enzymes and/or serum creatinine. Possible pulmonary toxicity has been suggested in several patients. The currently used low-doses of fludarabine phosphate, even with repeated administration, are well tolerated and appear safe with a negligible risk for severe neurotoxicity. Based on its single-agent activity and tolerability, the Food and Drug Administration recently granted group C designation of the drug for the treatment of patients with refractory CLL outside the clinical trials setting. The use of fludarabine phosphate in combination regimens and its impact on the natural history of the lymphoid malignancies is yet to be determined. Fludarabine phosphate may well occupy a pivotal role in the management of CLL and low-grade NHL. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Chun, H G AU - Leyland-Jones, B AU - Cheson, B D AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, MD. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 175 EP - 188 VL - 9 IS - 1 SN - 0732-183X, 0732-183X KW - Antimetabolites, Antineoplastic KW - 0 KW - Vidarabine Phosphate KW - 106XV160TZ KW - fludarabine phosphate KW - 1X9VK9O1SC KW - Index Medicus KW - Humans KW - Neoplasms -- drug therapy KW - Leukemia -- drug therapy KW - Vidarabine Phosphate -- therapeutic use KW - Vidarabine Phosphate -- adverse effects KW - Antimetabolites, Antineoplastic -- adverse effects KW - Antimetabolites, Antineoplastic -- pharmacokinetics KW - Antimetabolites, Antineoplastic -- therapeutic use KW - Vidarabine Phosphate -- pharmacokinetics KW - Vidarabine Phosphate -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80363297?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Fludarabine+phosphate%3A+a+synthetic+purine+antimetabolite+with+significant+activity+against+lymphoid+malignancies.&rft.au=Chun%2C+H+G%3BLeyland-Jones%2C+B%3BCheson%2C+B+D&rft.aulast=Chun&rft.aufirst=H&rft.date=1991-01-01&rft.volume=9&rft.issue=1&rft.spage=175&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 - 1991-02-07 N1 - Date created - 1991-02-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Superiority of ProMACE-CytaBOM over ProMACE-MOPP in the treatment of advanced diffuse aggressive lymphoma: results of a prospective randomized trial. AN - 80363169; 1702144 AB - One hundred ninety-three patients with stage II, III, or IV follicular large-cell, diffuse large-cell, diffuse mixed, immunoblastic, or diffuse small noncleaved-cell (non-Burkitt's) lymphoma were randomized to receive either cyclophosphamide 650 mg/m2 intravenously (IV), doxorubicin 25 mg/m2 IV, etoposide 120 mg/m2 IV on day 1, mechlorethamine 6 mg/m2 IV, vincristine 1.4 mg/m2 (no cap at 2 mg total dose) IV on day 8, prednisone 60 mg/m2 orally daily days 1 through 14, procarbazine 100 mg/m2 orally daily days 8 through 14, and methotrexate 500 mg/m2 IV on day 15 with leucovorin 50 mg/m2 orally every 6 hours for four doses beginning 24 hours after methotrexate with cycles repeated every 28 days (ProMACE-MOPP) or same day-1 treatment as ProMACE-MOPP plus cytarabine 300 mg/m2 IV, bleomycin 5 U/m2 IV, vincristine 1.4 mg/m2 (no cap at 2 mg total dose) IV, and methotrexate 120 mg/m2 IV on day 8, leucovorin 25 mg/m2 orally every 6 hours for four doses beginning 24 hours after methotrexate, and prednisone 60 mg/m2 orally daily days 1 through 14 with cycles repeated every 21 days (ProMACE-CytaBOM). Co-trimoxazole two double-strength tablets orally twice daily throughout the period of treatment was added to the ProMACE-CytaBOM regimen when an increased risk of Pneumocystis carinii pneumonia was found in the first 35 patients receiving this combination. Median follow-up is 5 years. Among the 99 patients treated with ProMACE-MOPP, 73 achieved a complete remission (CR) (74%), 30 complete responders have relapsed (41%), and 45 patients have died (45%), including two (2%) of treatment-related causes. Among the 94 patients treated with ProMACE-CytaBOM, 81 achieved a CR (86%), 22 complete responders have relapsed (27%), and 31 patients have died (33%). The complete response rate (P2 = .048) and survival (P2 = .046) were significantly higher for patients treated with ProMACE-CytaBOM. The mortality of ProMACE-CytaBOM treatment overall was six of 94 patients (6.4%). There was no treatment-related mortality among patients treated with prophylactic co-trimoxazole (n = 59). ProMACE-CytaBOM combination chemotherapy with co-trimoxazole prophylaxis is a safe and effective treatment for patients with aggressive histology malignant lymphoma and is superior to ProMACE-MOPP. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Longo, D L AU - DeVita, V T AU - Duffey, P L AU - Wesley, M N AU - Ihde, D C AU - Hubbard, S M AU - Gilliom, M AU - Jaffe, E S AU - Cossman, J AU - Fisher, R I AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, MD. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 25 EP - 38 VL - 9 IS - 1 SN - 0732-183X, 0732-183X KW - Cytarabine KW - 04079A1RDZ KW - Bleomycin KW - 11056-06-7 KW - Procarbazine KW - 35S93Y190K KW - Mechlorethamine KW - 50D9XSG0VR KW - Vincristine KW - 5J49Q6B70F KW - Etoposide KW - 6PLQ3CP4P3 KW - Doxorubicin KW - 80168379AG KW - Cyclophosphamide KW - 8N3DW7272P KW - Prednisone KW - VB0R961HZT KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - Cyclophosphamide -- administration & dosage KW - Mechlorethamine -- administration & dosage KW - Neoplasm Staging KW - Bleomycin -- administration & dosage KW - Humans KW - Vincristine -- administration & dosage KW - Aged KW - Doxorubicin -- administration & dosage KW - Cytarabine -- administration & dosage KW - Procarbazine -- administration & dosage KW - Prospective Studies KW - Survival Rate KW - Etoposide -- administration & dosage KW - Middle Aged KW - Methotrexate -- administration & dosage KW - Prednisone -- administration & dosage KW - Female KW - Male KW - Remission Induction KW - Lymphoma, Non-Hodgkin -- drug therapy KW - Lymphoma, Non-Hodgkin -- mortality KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Lymphoma, Non-Hodgkin -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80363169?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Superiority+of+ProMACE-CytaBOM+over+ProMACE-MOPP+in+the+treatment+of+advanced+diffuse+aggressive+lymphoma%3A+results+of+a+prospective+randomized+trial.&rft.au=Longo%2C+D+L%3BDeVita%2C+V+T%3BDuffey%2C+P+L%3BWesley%2C+M+N%3BIhde%2C+D+C%3BHubbard%2C+S+M%3BGilliom%2C+M%3BJaffe%2C+E+S%3BCossman%2C+J%3BFisher%2C+R+I&rft.aulast=Longo&rft.aufirst=D&rft.date=1991-01-01&rft.volume=9&rft.issue=1&rft.spage=25&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 - 1991-02-07 N1 - Date created - 1991-02-07 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: J Clin Oncol 1991 Apr;9(4):710 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression of yeast L-A double-stranded RNA virus proteins produces derepressed replication: a ski- phenocopy. AN - 80362777; 1985195 AB - The plus strand of the L-A double-stranded RNA virus of Saccharomyces cerevisiae has two large open reading frames, ORF1, which encodes the major coat protein, and ORF2, which encodes a single-stranded RNA-binding protein having a sequence diagnostic of viral RNA-dependent RNA polymerases. ORF2 is expressed only as a Gag-Pol-type fusion protein with ORF1. We have constructed a plasmid which expresses these proteins from the yeast PGK1 promoter. We show that this plasmid can support the replication of the killer toxin-encoding M1 satellite virus in the absence of an L-A double-stranded RNA helper virus itself. This requires ORF2 expression, providing a potential in vivo assay for the RNA polymerase and single-stranded RNA-binding activities of the fusion protein determined by ORF2. ORF1 expression, like a host ski- mutation, can suppress the usual requirement of M1 for the MAK11, MAK18, and MAK27 genes and allow a defective L-A (L-A-E) to support M1 replication. These results suggest that expression of ORF1 from the vector makes the cell a ski- phenocopy. Indeed, expression of ORF1 in a wild-type killer makes it a superkiller, suggesting that a target of the SKI antiviral system may be the major coat protein. JF - Journal of virology AU - Wickner, R B AU - Icho, T AU - Fujimura, T AU - Widner, W R AD - Section on the Genetics of Simple Eukaryotes, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 155 EP - 161 VL - 65 IS - 1 SN - 0022-538X, 0022-538X KW - ski KW - RNA, Double-Stranded KW - 0 KW - DNA-Directed RNA Polymerases KW - EC 2.7.7.6 KW - Index Medicus KW - Genotype KW - Genetic Vectors KW - Capsid -- genetics KW - Restriction Mapping KW - Suppression, Genetic KW - Escherichia coli -- genetics KW - Genes, Viral KW - Plasmids KW - Mutagenesis KW - DNA-Directed RNA Polymerases -- genetics KW - Saccharomyces cerevisiae -- genetics KW - RNA Viruses -- enzymology KW - RNA, Double-Stranded -- genetics KW - Open Reading Frames KW - RNA Viruses -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80362777?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Expression+of+yeast+L-A+double-stranded+RNA+virus+proteins+produces+derepressed+replication%3A+a+ski-+phenocopy.&rft.au=Wickner%2C+R+B%3BIcho%2C+T%3BFujimura%2C+T%3BWidner%2C+W+R&rft.aulast=Wickner&rft.aufirst=R&rft.date=1991-01-01&rft.volume=65&rft.issue=1&rft.spage=155&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 - 1991-02-07 N1 - Date created - 1991-02-07 N1 - Date revised - 2017-01-13 N1 - Gene symbol - ski N1 - SuppNotes - Cited By: Mol Cell Biol. 1987 Jan;7(1):420-6 [3550421] Proc Natl Acad Sci U S A. 1987 Oct;84(20):7041-5 [2823251] Genetics. 1987 Nov;117(3):399-408 [3319767] J Biol Chem. 1988 Jan 5;263(1):454-60 [3275647] J Virol. 1988 Apr;62(4):1278-85 [3279233] Mol Cell Biol. 1988 Feb;8(2):938-44 [3280972] Cell. 1988 Nov 4;55(3):447-58 [2846182] Cell. 1988 Nov 18;55(4):663-71 [2460245] Yeast. 1988 Mar;4(1):17-26 [3059710] Yeast. 1985 Sep;1(1):57-65 [3916860] Yeast. 1985 Dec;1(2):159-71 [3916862] J Biol Chem. 1989 Apr 25;264(12):6716-23 [2651431] Mol Cell Biol. 1989 Mar;9(3):1100-8 [2657386] J Biol Chem. 1989 Jun 25;264(18):10872-7 [2659596] Yeast. 1989 May-Jun;5(3):149-58 [2660461] FASEB J. 1989 Sep;3(11):2257-65 [2550303] Proc Natl Acad Sci U S A. 1990 Oct;87(19):7628-32 [1699230] Proc Natl Acad Sci U S A. 1976 Oct;73(10):3651-5 [790391] J Biol Chem. 1977 Dec 25;252(24):9010-7 [336627] Genetics. 1978 Mar;88(3):419-25 [346439] Proc Natl Acad Sci U S A. 1978 Sep;75(9):4224-8 [360211] J Bacteriol. 1978 Dec;136(3):1002-7 [363683] J Bacteriol. 1979 Oct;140(1):154-60 [387719] Genetics. 1979 Jul;92(3):803-21 [395022] Proc Natl Acad Sci U S A. 1980 Jan;77(1):527-30 [6987655] Cell. 1980 Aug;21(1):217-26 [6996833] Genetics. 1982 Feb;100(2):159-74 [7049830] Science. 1983 Feb 11;219(4585):620-5 [6186023] Cell. 1982 Dec;31(2 Pt 1):429-41 [6819084] Mol Cell Biol. 1983 Apr;3(4):654-61 [6343841] Mol Cell Biol. 1984 Apr;4(4):761-70 [6371496] Nucleic Acids Res. 1985 Feb 25;13(4):1103-18 [3858795] Science. 1985 Dec 13;230(4731):1237-42 [2416054] Mol Cell Biol. 1986 Feb;6(2):404-10 [3537688] Mol Cell Biol. 1986 May;6(5):1552-61 [3537705] Virology. 1987 Mar;157(1):252-6 [3029964] J Mol Biol. 1976 Aug 15;105(3):427-43 [787537] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effect of felbamate on plasma levels of carbamazepine and its metabolites. AN - 80362273; 1985822 AB - Felbamate (FBM) is a novel antiepileptic drug (AED) currently undergoing clinical evaluation in the United States. During a controlled clinical trial conducted at the National Institutes of Health Clinical Center, FBM was added to constant carbamazepine (CBZ) monotherapy. CBZ total concentrations were reduced during active FBM treatment (mean reduction 25%, range 10-42%, p less than 0.001). The effect was evident after the first week of treatment and reached a plateau in 2-4 weeks. To clarify the interaction mechanism, free and total concentrations of CBZ and its plasma metabolites were determined by high-performance liquid chromatography (HPLC) and ultrafiltration in four patients. In these patients, FBM treatment reduced CBZ concentrations and increased CBZ-epoxide (CBZ-E) concentrations (p less than 0.01). Free fractions of all compounds were unmodified. FBM appears to be capable of inducing CBZ metabolism. CBZ-FBM interaction may be clinically relevant. JF - Epilepsia AU - Albani, F AU - Theodore, W H AU - Washington, P AU - Devinsky, O AU - Bromfield, E AU - Porter, R J AU - Nice, F J AD - Preclinical Pharmacology Section, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland. PY - 1991 SP - 130 EP - 132 VL - 32 IS - 1 SN - 0013-9580, 0013-9580 KW - Anticonvulsants KW - 0 KW - Phenylcarbamates KW - Placebos KW - Propylene Glycols KW - Carbamazepine KW - 33CM23913M KW - 10,11-dihydro-10,11-dihydroxy-5H-dibenzazepine-5-carboxamide KW - 35079-97-1 KW - carbamazepine epoxide KW - QC9505F279 KW - felbamate KW - X72RBB02N8 KW - Index Medicus KW - Ultrafiltration KW - Epilepsy -- blood KW - Drug Therapy, Combination KW - Drug Interactions KW - Double-Blind Method KW - Humans KW - Epilepsy -- drug therapy KW - Chromatography, High Pressure Liquid KW - Propylene Glycols -- pharmacology KW - Anticonvulsants -- pharmacology KW - Propylene Glycols -- therapeutic use KW - Carbamazepine -- blood KW - Carbamazepine -- analogs & derivatives KW - Carbamazepine -- pharmacology KW - Carbamazepine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80362273?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Epilepsia&rft.atitle=Effect+of+felbamate+on+plasma+levels+of+carbamazepine+and+its+metabolites.&rft.au=Albani%2C+F%3BTheodore%2C+W+H%3BWashington%2C+P%3BDevinsky%2C+O%3BBromfield%2C+E%3BPorter%2C+R+J%3BNice%2C+F+J&rft.aulast=Albani&rft.aufirst=F&rft.date=1991-01-01&rft.volume=32&rft.issue=1&rft.spage=130&rft.isbn=&rft.btitle=&rft.title=Epilepsia&rft.issn=00139580&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-02-11 N1 - Date created - 1991-02-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Biological and immunological properties of human immunodeficiency virus type 1 envelope glycoprotein: analysis of proteins with truncations and deletions expressed by recombinant vaccinia viruses. AN - 80362204; 1985202 AB - The effects of C-terminal and internal deletions on the synthesis, transport, biological properties, and antigenicity of the human immunodeficiency virus type 1 envelope protein were determined. A family of recombinant vaccinia viruses that express N-terminal overlapping env proteins of 204, 287, 393, 502 (full-length gp120), 635, 747, and 851 (full-length gp160) amino acids was constructed. All of the proteins were detected in intra- and extracellular forms which differed in the extent of glycosylation. The 747- and 851-amino-acid proteins were cleaved, were expressed on the surface of infected cells, and bound CD4. The 635-amino-acid env protein was cleaved inefficiently, and both the precursor and product were secreted, indicating absence of the transmembrane sequence. The 635- as well as the 502-amino-acid protein, which was also largely secreted, could still bind CD4. Unexpectedly, the 393-amino-acid protein was anchored in the plasma membrane, but neither it nor smaller proteins bound to soluble CD4. When amino acids at the gp120-gp41 junction were deleted, proteolytic cleavage of gp160 did not occur. Nevertheless, gp160 was inserted into the plasma membrane and bound soluble CD4. The predominant conserved B-cell epitopes were mapped to gp41 and the C terminus of gp120, whereas cytotoxic T-cell epitopes were distributed throughout the length of the glycoproteins. JF - Journal of virology AU - Earl, P L AU - Koenig, S AU - Moss, B AD - Laboratories of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 31 EP - 41 VL - 65 IS - 1 SN - 0022-538X, 0022-538X KW - env KW - Antigens, CD4 KW - 0 KW - Viral Envelope Proteins KW - Index Medicus KW - AIDS/HIV KW - Mutagenesis, Site-Directed KW - Animals KW - Chromosome Deletion KW - HIV Seropositivity KW - Humans KW - T-Lymphocytes, Cytotoxic -- immunology KW - Genes, Viral KW - Fluorescent Antibody Technique KW - Cell Line KW - Antigens, CD4 -- immunology KW - Cloning, Molecular KW - Vaccinia virus -- genetics KW - HIV-1 -- genetics KW - HIV-1 -- immunology KW - Viral Envelope Proteins -- analysis KW - Recombination, Genetic KW - HIV-1 -- analysis KW - Viral Envelope Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80362204?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Biological+and+immunological+properties+of+human+immunodeficiency+virus+type+1+envelope+glycoprotein%3A+analysis+of+proteins+with+truncations+and+deletions+expressed+by+recombinant+vaccinia+viruses.&rft.au=Earl%2C+P+L%3BKoenig%2C+S%3BMoss%2C+B&rft.aulast=Earl&rft.aufirst=P&rft.date=1991-01-01&rft.volume=65&rft.issue=1&rft.spage=31&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 - 1991-02-07 N1 - Date created - 1991-02-07 N1 - Date revised - 2017-01-13 N1 - Gene symbol - env N1 - SuppNotes - Cited By: J Virol. 1988 Nov;62(11):4195-200 [2845130] Nature. 1989 Aug 17;340(6234):571-4 [2475780] J Virol. 1988 Dec;62(12):4703-11 [2460639] Proc Natl Acad Sci U S A. 1988 Nov;85(22):8638-42 [2460873] Proc Natl Acad Sci U S A. 1988 Dec;85(23):9273-7 [2461565] J Virol. 1989 Feb;63(2):584-90 [2536094] Protein Eng. 1988 Sep;2(3):219-25 [3237686] J Virol. 1989 Jun;63(6):2674-9 [2786089] AIDS Res Hum Retroviruses. 1989 Aug;5(4):431-40 [2788443] J Virol. 1987 Jun;61(6):2024-8 [2437327] Proc Natl Acad Sci U S A. 1987 Jun;84(12):4249-53 [2438696] J Virol. 1987 Aug;61(8):2639-41 [2439707] Nature. 1987 Jul 23-29;328(6128):345-8 [3496541] Nature. 1987 Jul 23-29;328(6128):348-51 [3496542] Proc Natl Acad Sci U S A. 1987 Jul;84(13):4601-5 [3037522] Cell. 1987 Sep 11;50(6):975-85 [2441877] Science. 1987 Sep 11;237(4820):1351-5 [3629244] J Virol. 1988 Jan;62(1):139-47 [3257102] Science. 1988 Feb 26;239(4843):1021-3 [2830667] Proc Natl Acad Sci U S A. 1988 Mar;85(6):1932-6 [2450351] Cell. 1988 Apr 8;53(1):55-67 [2450679] AIDS. 1988 Feb;2(1):25-9 [2451922] AIDS Res Hum Retroviruses. 1987;3(4):409-22 [2833917] Proc Natl Acad Sci U S A. 1988 May;85(9):3105-9 [2452443] J Virol. 1988 Sep;62(9):3135-42 [2841466] J Virol. 1988 Oct;62(10):3695-702 [2458487] J Virol. 1988 Oct;62(10):3779-88 [3047430] J Virol. 1984 Mar;49(3):857-64 [6321770] Nature. 1985 Jan 24-30;313(6000):277-84 [2578615] Science. 1985 May 31;228(4703):1091-4 [2986290] Science. 1985 Sep 27;229(4720):1402-5 [2994223] Virology. 1985 Jul 15;144(1):283-9 [2414918] Nature. 1986 Apr 10-16;320(6062):535-7 [3008001] Virology. 1989 Sep;172(1):367-9 [2672564] J Virol. 1989 Oct;63(10):4464-8 [2550679] Proc Natl Acad Sci U S A. 1989 Dec;86(23):9514-8 [2480604] Proc Natl Acad Sci U S A. 1990 Jan;87(2):648-52 [2300552] J Cell Biol. 1988 Nov;107(5):1677-87 [3053734] Cell. 1986 Jun 6;45(5):637-48 [2423250] Proc Natl Acad Sci U S A. 1986 Jul;83(14):5038-42 [3014529] Science. 1986 Jul 11;233(4760):209-12 [3014647] Mol Cell Biol. 1985 Dec;5(12):3403-9 [3939316] Nature. 1986 Oct 23-29;323(6090):725-8 [3095663] EMBO J. 1986 Nov;5(11):3051-6 [3491755] Proc Natl Acad Sci U S A. 1987 Apr;84(8):2479-83 [2436231] J Virol. 1990 May;64(5):2448-51 [2182912] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Fetal nondopaminergic neural implants in parkinsonian primates. Histochemical and behavioral studies. AN - 80361480; 1670609 AB - Implantation of fetal dopamine-containing tissue into preformed cavities in the caudate nucleus of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonian monkeys leads to behavioral recovery. Recovery may be related to two sources of dopamine: the grafted cells and/or the sprouted fibers from host dopaminergic neurons. The authors undertook this study to determine whether behavioral recovery requires release of dopamine by the implanted tissue, and to establish if nondopaminergic fetal central nervous system implants can induce sprouting of dopamine fibers in the primate brain and cause behavioral recovery. Rhesus monkeys with MPTP-induced hemiparkinsonism or full parkinsonism and a stable neurological deficit were used for this study. Cavities were created in the caudate nuclei anterior to the foramen of Monro via an open microsurgical approach. Fetal cerebellum or spinal cord was implanted into the preformed cavities of three monkeys. Control parkinsonian monkeys showed no recovery. However, implant-induced improvement was stable for up to 6 months after implantation. Sprouted dopaminergic fibers oriented from the ventral striatum and nucleus accumbens were found in the area of the tissue implant in the animals that received fetal grafts but were not present in the control monkeys. It is concluded that brain implants do not need to contain dopamine to induce functional recovery in MPTP-induced parkinsonian primates. Implant-induced and trophic factor-mediated dopaminergic sprouting by the host brain plays a role in the behavioral recovery and may well be responsible for the clinical improvement seen in parkinsonian patients after brain implants. JF - Journal of neurosurgery AU - Bankiewicz, K S AU - Plunkett, R J AU - Jacobowitz, D M AU - Kopin, I J AU - Oldfield, E H AD - Laboratory of Central Nervous System Implantation, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 97 EP - 104 VL - 74 IS - 1 SN - 0022-3085, 0022-3085 KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - Tyrosine 3-Monooxygenase KW - EC 1.14.16.2 KW - Dopamine KW - VTD58H1Z2X KW - Abridged Index Medicus KW - Index Medicus KW - Behavior, Animal -- drug effects KW - Animals KW - Behavior, Animal -- physiology KW - Macaca mulatta KW - Immunohistochemistry KW - Parkinson Disease, Secondary -- physiopathology KW - Parkinson Disease, Secondary -- chemically induced KW - Dopamine -- pharmacology KW - Caudate Nucleus -- surgery KW - Caudate Nucleus -- metabolism KW - Spinal Cord -- metabolism KW - Parkinson Disease, Secondary -- surgery KW - Cerebellum -- transplantation KW - Spinal Cord -- transplantation KW - Brain Tissue Transplantation KW - Fetal Tissue Transplantation KW - Cerebellum -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80361480?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+neurosurgery&rft.atitle=Fetal+nondopaminergic+neural+implants+in+parkinsonian+primates.+Histochemical+and+behavioral+studies.&rft.au=Bankiewicz%2C+K+S%3BPlunkett%2C+R+J%3BJacobowitz%2C+D+M%3BKopin%2C+I+J%3BOldfield%2C+E+H&rft.aulast=Bankiewicz&rft.aufirst=K&rft.date=1991-01-01&rft.volume=74&rft.issue=1&rft.spage=97&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurosurgery&rft.issn=00223085&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-01-28 N1 - Date created - 1991-01-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Histomorphologic Features of Spontaneous and Chemically-Induced Pulmonary Neoplasms in B6C3F1 Mice and Fischer 344 Rats* super(1) AN - 755137322; 13645454 AB - The histomorphologic features of spontaneous and chemically-induced lung neoplasms in male and female B6C3F1 mice and Fischer 344 rats are described. Primary pulmonary neoplasms in mice and rats were classified as alveolar/bronchiolar (A/B) adenoma or carcinoma (including variants with squamous and mucinous cell differentiation), bronchial adenoma or carcinoma, squamous cell carcinoma or mesenchymal tumors. A/B adenomas and carcinomas were the most common spontaneous pulmonary neoplasms observed in both mice and rats, but were observed less frequently in rats. In the National Toxicology Program (NTP) historical control database the incidence of spontaneous A/B adenomas in male (n = 2,084) and female (n = 2,079) mice is 13.8% and 4.9%, respectively; for A/B carcinomas, it is 5.3% and 2.4%, respectively. In male (n = 3,877) and female (n = 3,919) rats, spontaneous pulmonary neoplasms are rare with historical control rates less than 3% for A/B adenomas or carcinomas in either sex. The spontaneous A/B adenomas and carcinomas observed in mice and rats typically had papillary, solid or mixed (papillary and solid) histologic growth patterns. Pulmonary neoplasms from mice and rats treated with chemical carcinogens reviewed from 2-year studies consisted primarily of A/B adenomas and carcinomas. These tumors had papillary, glandular/tubular, solid or mixed (combination of 2 or more) histologic growth patterns. A few of the A/B neoplasms had areas of squamous or mucinous cell differentiation. Other less frequently occurring spontaneous and chemically-induced neoplasms included squamous cell carcinomas, bronchial adenomas and carcinomas, and sarcomas. JF - Toxicologic Pathology AU - Dixon, Darlene AU - Maronpot, Robert R AD - National Institute of Environmental Health Sciences, National Toxicology Program, P.O. Box 12233, Research Triangle Park, North Carolina 27709 Y1 - 1991 PY - 1991 DA - 1991 SP - 540 EP - 555 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU UK VL - 19 IS - 4-1 SN - 0192-6233, 0192-6233 KW - Toxicology Abstracts UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/755137322?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+Pathology&rft.atitle=Histomorphologic+Features+of+Spontaneous+and+Chemically-Induced+Pulmonary+Neoplasms+in+B6C3F1+Mice+and+Fischer+344+Rats*+super%281%29&rft.au=Dixon%2C+Darlene%3BMaronpot%2C+Robert+R&rft.aulast=Dixon&rft.aufirst=Darlene&rft.date=1991-01-01&rft.volume=19&rft.issue=4-1&rft.spage=540&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F019262339101900419 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2010-09-01 N1 - Last updated - 2011-12-14 DO - http://dx.doi.org/10.1177/019262339101900419 ER - TY - JOUR T1 - Destruction of patulin in animal litter using ammoniation. AN - 72795421; 8778044 JF - IARC scientific publications AU - Lunn, G AU - Sansone, E B AD - NCI-Frederick Cancer Research and Development Center, MD 21702, USA. Y1 - 1991 PY - 1991 DA - 1991 SP - 31 EP - 33 IS - 113 SN - 0300-5038, 0300-5038 KW - Carcinogens KW - 0 KW - Quaternary Ammonium Compounds KW - Patulin KW - 95X2BV4W8R KW - Index Medicus KW - Decontamination -- methods KW - Patulin -- chemistry KW - Carcinogens -- chemistry KW - Quaternary Ammonium Compounds -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72795421?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=IARC+scientific+publications&rft.atitle=Destruction+of+patulin+in+animal+litter+using+ammoniation.&rft.au=Lunn%2C+G%3BSansone%2C+E+B&rft.aulast=Lunn&rft.aufirst=G&rft.date=1991-01-01&rft.volume=&rft.issue=113&rft.spage=31&rft.isbn=&rft.btitle=&rft.title=IARC+scientific+publications&rft.issn=03005038&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1996-09-17 N1 - Date created - 1996-09-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Folate transport and the modulation of antifolate sensitivity in a methotrexate-resistant human breast cancer cell line. AN - 72787551; 16296001 AB - The mechanism of acquired methotrexate-resistance in an estrogen-receptor positive human breast cancer cell line (MTX(R)ZR-75-1) was studied. MTX(R) ZR-75-1 cells are 250-fold resistant to methotrexate when grown in the presence of 1 microM folinic acid and 2,400-fold resistant in the presence of 1 microM folic acid. This drug resistant cell line also showed collateral sensitivity (10-fold) to trimetrexate (TMQ), when grown in the presence of folinic acid. Using fluoresceinated methotrexate (F-MTX), FACS analysis indicated that there is no intracellular accumulation of methotrexate into MTX(R) ZR-75-1 cells, as determined by competition of F-MTX and methotrexate binding to dihydrofolate reductase. These characteristics strongly indicate that the mechanism of resistance involved down regulation of the reduced-folate transporter. To investigate this further, the transport kinetics of parental and MTX(R) ZR-75-1 cells were examined. Although the V(max) for methotrexate transport in wild-type (WT) ZR-75-1 breast cancer cells was 1-2 orders of magnitude lower than that in the well characterized leukemia cell lines, such as L1210 and CCRF-CEM cells, kinetic analysis indicated that transport of methotrexate into WT ZR-75-1 cells involved a mechanism that was similar if not identical to the reduced folate transporter. In contrast, no specific uptake of methotrexate was detected in MTX(R) ZR-75-1cells. Furthermore, neither cell line expressed detectable levels of folate binding protein, a binding protein with high affinity for folic acid as well as for reduced folates and antifolates. These results indicate that the level of expression of the reduced-folate carrier may be an important factor in determining the sensitivity of breast cancer cells as well as leukemia cells to antifolate compounds. JF - Cancer communications AU - Dixon, K H AU - Trepel, J B AU - Eng, S C AU - Cowan, K H AD - Building 10, Room 12N226, Medicine Branch and Clinical Pharmacology Branch, National Cancer Institute, Bethesda, Maryland 20892, USA. Y1 - 1991 PY - 1991 DA - 1991 SP - 357 EP - 365 VL - 3 IS - 12 SN - 0955-3541, 0955-3541 KW - Antimetabolites, Antineoplastic KW - 0 KW - Carrier Proteins KW - Folate Receptors, GPI-Anchored KW - Folic Acid Antagonists KW - Receptors, Cell Surface KW - Receptors, Estrogen KW - fluoresceinated methotrexate KW - Vitamin B Complex KW - 12001-76-2 KW - Folic Acid KW - 935E97BOY8 KW - Tetrahydrofolate Dehydrogenase KW - EC 1.5.1.3 KW - Leucovorin KW - Q573I9DVLP KW - Trimetrexate KW - UPN4ITI8T4 KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - Animals KW - Trimetrexate -- pharmacology KW - Humans KW - Biological Transport KW - Mice KW - Receptors, Estrogen -- metabolism KW - Antimetabolites, Antineoplastic -- pharmacology KW - Leukemia -- drug therapy KW - Vitamin B Complex -- pharmacology KW - Tumor Cells, Cultured KW - Leukemia -- metabolism KW - Flow Cytometry KW - Leucovorin -- pharmacology KW - Tetrahydrofolate Dehydrogenase -- metabolism KW - Receptors, Cell Surface -- metabolism KW - Breast Neoplasms -- drug therapy KW - Methotrexate -- pharmacology KW - Methotrexate -- analogs & derivatives KW - Folic Acid -- metabolism KW - Carrier Proteins -- metabolism KW - Folic Acid Antagonists -- toxicity KW - Breast Neoplasms -- metabolism KW - Drug Resistance, Neoplasm UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72787551?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+communications&rft.atitle=Folate+transport+and+the+modulation+of+antifolate+sensitivity+in+a+methotrexate-resistant+human+breast+cancer+cell+line.&rft.au=Dixon%2C+K+H%3BTrepel%2C+J+B%3BEng%2C+S+C%3BCowan%2C+K+H&rft.aulast=Dixon&rft.aufirst=K&rft.date=1991-01-01&rft.volume=3&rft.issue=12&rft.spage=357&rft.isbn=&rft.btitle=&rft.title=Cancer+communications&rft.issn=09553541&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2005-12-06 N1 - Date created - 2005-11-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Destruction of some polycyclic heterocyclic compounds using concentrated sulfuric acid. AN - 72778547; 8690470 JF - IARC scientific publications AU - Lunn, G AU - Sansone, E B AD - NCI-Frederick Cancer Research and Development Center, MD, USA. Y1 - 1991 PY - 1991 DA - 1991 SP - 31 EP - 36 IS - 114 SN - 0300-5038, 0300-5038 KW - Carcinogens KW - 0 KW - Heterocyclic Compounds KW - Polycyclic Compounds KW - Sulfuric Acids KW - Index Medicus KW - Decontamination -- methods KW - Mutagenicity Tests KW - Heterocyclic Compounds -- chemistry KW - Carcinogens -- chemistry KW - Sulfuric Acids -- chemistry KW - Polycyclic Compounds -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72778547?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=IARC+scientific+publications&rft.atitle=Destruction+of+some+polycyclic+heterocyclic+compounds+using+concentrated+sulfuric+acid.&rft.au=Lunn%2C+G%3BSansone%2C+E+B&rft.aulast=Lunn&rft.aufirst=G&rft.date=1991-01-01&rft.volume=&rft.issue=114&rft.spage=31&rft.isbn=&rft.btitle=&rft.title=IARC+scientific+publications&rft.issn=03005038&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1996-08-27 N1 - Date created - 1996-08-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Assessment of treatment outcome. AN - 72777548; 1845591 AB - Treatment outcome research consists of two types: controlled clinical trials and in-house program evaluations. Controlled clinical trials are experimental studies designed to test whether or not a treatment is efficacious. In-house program evaluations provide information about the results (outcome) of an individual treatment program. The key components of clinical trials include control groups; randomization procedures; enumeration of those who were screened for inclusion in, those accepted into, and those excluded from the study; a description of the relevant patient characteristics of the sample studied; "double-blinding" for pharmacological studies; raters of treatment effects who are not the therapists for verbal therapies; objective measures of treatment response; follow-up of at least 70% of the original sample; and appropriate statistical analysis of the data collected. In-house program evaluations rarely have control groups or employ randomization. However, a description of the type of patients treated by the program, independent raters, and adequate follow-up of those entering treatment are essential for program evaluation; and the credibility of program evaluation would be enhanced by the use of objective measures of treatment response. JF - Alcohol and alcoholism (Oxford, Oxfordshire). Supplement AU - Fuller, R K AD - Division of Clinical and Prevention Research, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20857. Y1 - 1991 PY - 1991 DA - 1991 SP - 519 EP - 522 VL - 1 SN - 1358-6173, 1358-6173 KW - Index Medicus KW - Life Tables KW - Patient Compliance KW - Humans KW - Treatment Outcome KW - Follow-Up Studies KW - Randomized Controlled Trials as Topic -- methods KW - Clinical Trials as Topic -- methods KW - Alcoholism -- rehabilitation KW - Alcoholism -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72777548?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcohol+and+alcoholism+%28Oxford%2C+Oxfordshire%29.+Supplement&rft.atitle=Assessment+of+treatment+outcome.&rft.au=Fuller%2C+R+K&rft.aulast=Fuller&rft.aufirst=R&rft.date=1991-01-01&rft.volume=1&rft.issue=&rft.spage=519&rft.isbn=&rft.btitle=&rft.title=Alcohol+and+alcoholism+%28Oxford%2C+Oxfordshire%29.+Supplement&rft.issn=13586173&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-07 N1 - Date created - 1993-10-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Experimental studies of the hematologic and immune system toxicity of nucleoside derivatives used against HIV infection. AN - 72776908; 1668555 AB - Adverse effects stemming from the therapeutic use of dideoxynucleoside derivatives continue to occur in patients with AIDS or AIDS-related complex. For example, the continued use of 3'-azido-3'-deoxythymidine (AZT) and 2',3'-didoxycytidine (ddC), both of which confer clinical benefits in AIDS patients, may be complicated by anemia, neutropenia and thrombocytopenia and ddC also causes peripheral neuropathy. Subsequently, the National Toxicology Program (NTP) has undertaken efforts to define and characterize the toxicities associated with currently employed and potential AIDS therapeutics in experimental animals, with particular emphasis on the hematopoietic and immune systems. In addition to AZT and ddC, 2',3'-dideoxyadenosine (ddA), 2',3'-dideoxyinosine (ddI) and 2',3'-didehydrodideoxythymidine (d4T) have been examined. The present studies describe: (1) the development of a poorly regenerative macrocytic anemia in mice exposed to AZT or ddC. This anemia demonstrates a rapid and progressive time course of toxicity and reversibility after cessation of treatment; (2) the selective suppression of erythroid progenitor cells in mice exposed to d4T without concomitant effects on myeloid stem cells. Myelotoxicity appears to show metabolism-dependent strain-specificity and is more evident following in vitro exposure than in vivo exposure; and (3) the immunosuppressive effects following subchronic (30-day) exposure. Of the nucleoside derivatives studied, only ddA and ddI altered immune function and these changes were confined to suppression of antibody responses. It can be concluded that the overall similarities in the hematopoietic and immune system effects between rodents and humans indicate that such animal toxicology studies provide important information relevant to the toxicity of these drugs. JF - International journal of immunopharmacology AU - Luster, M I AU - Rosenthal, G J AU - Cao, W AU - Thompson, M B AU - Munson, A E AU - Prejean, J D AU - Shopp, G AU - Fuchs, B A AU - Germolec, D R AU - Tomaszewski, J E AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991 PY - 1991 DA - 1991 SP - 99 EP - 107 VL - 13 Suppl 1 SN - 0192-0561, 0192-0561 KW - Immunoglobulin M KW - 0 KW - Zidovudine KW - 4B9XT59T7S KW - Dideoxyadenosine KW - 4Q86AH641A KW - Zalcitabine KW - 6L3XT8CB3I KW - Didanosine KW - K3GDH6OH08 KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Mice, Inbred C57BL KW - Mice KW - Immunoglobulin M -- biosynthesis KW - Female KW - Mice, Inbred DBA KW - Didanosine -- toxicity KW - Immune System -- drug effects KW - Zidovudine -- toxicity KW - HIV Infections -- drug therapy KW - Zalcitabine -- toxicity KW - Dideoxyadenosine -- toxicity KW - Bone Marrow -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72776908?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+immunopharmacology&rft.atitle=Experimental+studies+of+the+hematologic+and+immune+system+toxicity+of+nucleoside+derivatives+used+against+HIV+infection.&rft.au=Luster%2C+M+I%3BRosenthal%2C+G+J%3BCao%2C+W%3BThompson%2C+M+B%3BMunson%2C+A+E%3BPrejean%2C+J+D%3BShopp%2C+G%3BFuchs%2C+B+A%3BGermolec%2C+D+R%3BTomaszewski%2C+J+E&rft.aulast=Luster&rft.aufirst=M&rft.date=1991-01-01&rft.volume=13+Suppl+1&rft.issue=&rft.spage=99&rft.isbn=&rft.btitle=&rft.title=International+journal+of+immunopharmacology&rft.issn=01920561&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 - Science and social policy problems: resolution of some, creation of others. AN - 72775251; 1845596 AB - The scientist has two jobs: to do good science, and to be a spokesperson for science in the creation of rational social policy. Three categories of interaction between science and policy are described and examples given. The first is where science has provided data that were decisive in causing policy to be enacted. The second is where science is capable of resolving equity issues that have arisen from problems that science itself created. The third is where the issues are ultimately resolved by extra-scientific considerations. Two major issues where it is hoped that science can make a significant contribution include outcomes analysis, a new approach to dealing with health care costs and variations in clinical practice; and the disease concept of alcoholism, with questions it raises of volition, personal responsibility, and punishment. However, science alone is never the dominant force in the shaping of policy, which is determined by the interaction of many social forces, such as morals, values, politics, and economics. JF - Alcohol and alcoholism (Oxford, Oxfordshire). Supplement AU - Gordis, E AD - National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20857. Y1 - 1991 PY - 1991 DA - 1991 SP - 65 EP - 76 VL - 1 SN - 1358-6173, 1358-6173 KW - Index Medicus KW - United States KW - Cystic Fibrosis -- prevention & control KW - Humans KW - Adult KW - Employment KW - Liver Transplantation KW - Huntington Disease -- genetics KW - Cystic Fibrosis -- diagnosis KW - Automobile Driving KW - Alcoholism KW - Alcoholic Intoxication KW - Social Problems KW - Public Policy KW - Alcohol Drinking KW - Science UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72775251?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcohol+and+alcoholism+%28Oxford%2C+Oxfordshire%29.+Supplement&rft.atitle=Science+and+social+policy+problems%3A+resolution+of+some%2C+creation+of+others.&rft.au=Gordis%2C+E&rft.aulast=Gordis&rft.aufirst=E&rft.date=1991-01-01&rft.volume=1&rft.issue=&rft.spage=65&rft.isbn=&rft.btitle=&rft.title=Alcohol+and+alcoholism+%28Oxford%2C+Oxfordshire%29.+Supplement&rft.issn=13586173&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-07 N1 - Date created - 1993-10-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cellular targets of the oncoproteins encoded by the cancer associated human papillomaviruses. AN - 72774738; 1668886 AB - Insight into the mechanisms by which DNA tumor viruses transform cells has come from the recognition that the virus-encoded oncoproteins interact specifically with important cell regulatory proteins. The "high risk" human papillomaviruses such as HPV-16 and HPV-18 which are associated with human anogenital carcinomas encode two transforming genes (E6 and E7) which are expressed in HPV positive cancers and derived cell lines. E7 shares functional and structural features with the adenovirus E1A proteins. Like Ad E1A and the large T proteins of the polyomaviruses, E7 can complex pRB. The E7 proteins of the "high risk" HPVs associate with pRB with approximately a 10-fold higher affinity than do the E7 proteins of the "low risk" HPVs, and important biological differences between the E7 proteins of these two groups of HPVs are determined by amino-terminal sequences which include the pRB binding domain. Like SV40 large T and Ad 5 E1B, the E6 oncoprotein encoded by the "high risk" HPVs can form a complex with p53. In vitro, E6 promotes the degradation of p53 and this degradation involves the ubiquitin-dependent protease system. The selective degradation of cellular proteins such as p53 with negative regulatory functions provides a novel mechanism of action for dominant acting oncoproteins. The relevance of the inactivation of the normal functions of pRB and p53 in human cervical carcinogenesis has recently been demonstrated by the analysis of these two genes and their products in a series of HPV-positive and HPV-negative cell lines. Each of five HPV-positive cervical cancer cell lines expressed normal pRB and low levels of wild type p53 proteins, which are presumed to be altered in function as a consequence of association with the HPV oncoproteins. In contrast, mutations were identified in the p53 and RB genes expressed in the HPV-negative cervical carcinoma cell lines, C33-A and HT-3. These results support the hypothesis that the inactivation of the normal functions of the tumor suppressor proteins pRB and p53 are important steps in human cervical carcinogenesis, either by mutation or through complex formation with HPV E6 and E7 oncoproteins. JF - Princess Takamatsu symposia AU - Howley, P M AU - Münger, K AU - Romanczuk, H AU - Scheffner, M AU - Huibregtse, J M AD - Laboratory of Tumor Virus Biology, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 239 EP - 248 VL - 22 KW - Oncogene Proteins, Viral KW - 0 KW - Index Medicus KW - Genes, p53 KW - Genes, Retinoblastoma KW - Humans KW - Female KW - Cell Line KW - Uterine Cervical Neoplasms -- etiology KW - Oncogene Proteins, Viral -- genetics KW - Papillomaviridae -- genetics KW - Oncogene Proteins, Viral -- physiology KW - Cell Transformation, Viral KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72774738?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Princess+Takamatsu+symposia&rft.atitle=Cellular+targets+of+the+oncoproteins+encoded+by+the+cancer+associated+human+papillomaviruses.&rft.au=Howley%2C+P+M%3BM%C3%BCnger%2C+K%3BRomanczuk%2C+H%3BScheffner%2C+M%3BHuibregtse%2C+J+M&rft.aulast=Howley&rft.aufirst=P&rft.date=1991-01-01&rft.volume=22&rft.issue=&rft.spage=239&rft.isbn=&rft.btitle=&rft.title=Princess+Takamatsu+symposia&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-21 N1 - Date created - 1993-04-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Common mechanisms of reinforcement from alcohol and other drugs. AN - 72774478; 1845572 AB - Vulnerability to substance abuse is an important social and scientific issue. A critical aspect of this phenomenon is the degree to which individuals who abuse one substance are likely to abuse other substances. The extent to which several pharmacologically distinct drugs will come to serve as positive reinforcers within genetically defined subjects defines their community with respect to abuse liability. Questions in this area are directed at determining whether reinforcement from and abuse of alcohol and other drugs define variations within a single behavioral phenomenon, or whether reinforcement and abuse must be individually defined for each substance involved. Previous studies have shown that ethanol can be readily established as a positive reinforcer in LEWIS rats and C57BL/6J mice. In low ethanol preferring F344 rats, ethanol maintains significant but low levels of responding. Ethanol does not maintain behavior in BALB/cJ or DBA/2J mice. These genotypic patterns of reinforcement from ethanol appear to correlate highly with patterns of reinforcement from cocaine and opiates. Other studies suggest that some aspects of drug self-administration may be mediated in part by common dopaminergic and serotonergic mechanisms, and animals which differ in ethanol drinking behavior show substantial differences in parameters of serotonergic function. Thus, there may exist important genetic determinants of drug reinforced behavior. JF - Alcohol and alcoholism (Oxford, Oxfordshire). Supplement AU - George, F R AU - Ritz, M C AD - Preclinical Pharmacology Branch, National Institute on Drug Abuse, Addiction Research Center, Baltimore, MD 21224. Y1 - 1991 PY - 1991 DA - 1991 SP - 427 EP - 431 VL - 1 SN - 1358-6173, 1358-6173 KW - Serotonin KW - 333DO1RDJY KW - Index Medicus KW - Animals KW - Alcohol Drinking -- metabolism KW - Self Administration KW - Humans KW - Serotonin -- metabolism KW - Reinforcement (Psychology) KW - Alcoholism -- metabolism KW - Substance-Related Disorders -- psychology KW - Alcoholism -- genetics KW - Alcoholism -- psychology KW - Substance-Related Disorders -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72774478?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcohol+and+alcoholism+%28Oxford%2C+Oxfordshire%29.+Supplement&rft.atitle=Common+mechanisms+of+reinforcement+from+alcohol+and+other+drugs.&rft.au=George%2C+F+R%3BRitz%2C+M+C&rft.aulast=George&rft.aufirst=F&rft.date=1991-01-01&rft.volume=1&rft.issue=&rft.spage=427&rft.isbn=&rft.btitle=&rft.title=Alcohol+and+alcoholism+%28Oxford%2C+Oxfordshire%29.+Supplement&rft.issn=13586173&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-07 N1 - Date created - 1993-10-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ethanol potentiates ion current mediated by 5-HT3 receptors on neuroblastoma cells and isolated neurons. AN - 72774372; 1845535 AB - Effects of ethanol on receptor/channel complexes appear to play an important role in acute intoxication. One such receptor that has not previously been investigated for ethanol sensitivity is the 5-HT3 receptor for the neurotransmitter serotonin. Ethanol potentiates ion current mediated by 5-HT3 receptors in NCB-20 neuroblastoma cells and isolated Nodose ganglion neurons examined with whole-cell patch-clamp recording. Potentiation increases in a concentration-dependent manner over a range of concentrations (25-100 mM) achieved during acute intoxication. Potentiation appears to be due to a direct effect on the 5-HT3 receptor. Ethanol's effect on 5-HT3 receptor-mediated current decreases with increasing agonist concentration, providing an initial clue as to the mechanism of ethanol's action. These data are discussed in light of recent behavioral data suggesting a role for 5-HT3 receptors in the discriminative stimulus and reinforcing properties of ethanol. JF - Alcohol and alcoholism (Oxford, Oxfordshire). Supplement AU - Lovinger, D M AD - Unit of Synaptic Pharmacology, LPPS, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20852. Y1 - 1991 PY - 1991 DA - 1991 SP - 181 EP - 185 VL - 1 SN - 1358-6173, 1358-6173 KW - Receptors, Serotonin KW - 0 KW - Serotonin KW - 333DO1RDJY KW - Ethanol KW - 3K9958V90M KW - Curare KW - 8063-06-7 KW - Index Medicus KW - Animals KW - Tumor Cells, Cultured KW - Curare -- toxicity KW - Brain -- drug effects KW - In Vitro Techniques KW - Membrane Potentials -- drug effects KW - Drug Synergism KW - Brain -- physiology KW - Neuroblastoma KW - Receptors, Serotonin -- physiology KW - Receptors, Serotonin -- drug effects KW - Serotonin -- pharmacology KW - Ethanol -- pharmacology KW - Neurons -- drug effects KW - Nodose Ganglion -- physiology KW - Neurons -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72774372?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcohol+and+alcoholism+%28Oxford%2C+Oxfordshire%29.+Supplement&rft.atitle=Ethanol+potentiates+ion+current+mediated+by+5-HT3+receptors+on+neuroblastoma+cells+and+isolated+neurons.&rft.au=Lovinger%2C+D+M&rft.aulast=Lovinger&rft.aufirst=D&rft.date=1991-01-01&rft.volume=1&rft.issue=&rft.spage=181&rft.isbn=&rft.btitle=&rft.title=Alcohol+and+alcoholism+%28Oxford%2C+Oxfordshire%29.+Supplement&rft.issn=13586173&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-07 N1 - Date created - 1993-10-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - In vitro autoradiographic evidence for adenosine modulation of ethanol-induced motor disturbances in rats. AN - 72774189; 1845538 AB - It was previously shown that adenosine agonists and antagonists potentiate and decrease ethanol-induced motor disturbances, respectively. This interaction of adenosine and ethanol was functionally correlated with a significant increase in Bmax of cerebellar cortical high affinity adenosine A1 receptors after a single ethanol injection. Quantitative autoradiographic analysis of adenosine A1 and A2 binding sites in rat brain was carried out in animals treated acutely with saline or ethanol. Adenosine agonist binding at A1 receptors was increased in the molecular layer of cerebellum 15 min after ethanol injection. This increase returned to control values by 60 min. Adenosine antagonist binding at A1 receptors was not altered by ethanol treatment. Inclusion of a poorly hydrolyzable analogue of GTP in the incubation medium decreased binding throughout the brain for adenosine agonists but had less effect on agonist binding in the cerebellum and hippocampus of ethanol-treated rats 15 min after injection. The inhibitory effect of the GTP analogue was equal in saline- and ethanol-treated rats after 60 min. These findings suggest that acute ethanol treatment elicits a transitory increase in adenosine A1 receptor binding that is limited to the cerebellum and hippocampus and that this increased binding reflects an increased (or stabilized) coupling of the receptors to GTP-binding proteins. Acute ethanol treatment did not alter agonist binding at the high affinity A2a subtype of adenosine receptors in striatum. JF - Alcohol and alcoholism (Oxford, Oxfordshire). Supplement AU - Clark, M AU - Dar, M S AD - Biological Psychiatry Branch, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 203 EP - 206 VL - 1 SN - 1358-6173, 1358-6173 KW - Phenethylamines KW - 0 KW - Receptors, Purinergic KW - Tritium KW - 10028-17-8 KW - 2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine KW - 120225-54-9 KW - Phenylisopropyladenosine KW - 29193-86-0 KW - Guanylyl Imidodiphosphate KW - 34273-04-6 KW - Ethanol KW - 3K9958V90M KW - Adenosine KW - K72T3FS567 KW - Index Medicus KW - Rats KW - Animals KW - Guanylyl Imidodiphosphate -- pharmacology KW - Autoradiography -- methods KW - Adenosine -- analogs & derivatives KW - Brain -- drug effects KW - Ethanol -- antagonists & inhibitors KW - Brain -- metabolism KW - Receptors, Purinergic -- drug effects KW - Brain -- physiology KW - Phenylisopropyladenosine -- metabolism KW - Phenethylamines -- metabolism KW - Receptors, Purinergic -- metabolism KW - Adenosine -- pharmacology KW - Receptors, Purinergic -- physiology KW - Ethanol -- toxicity KW - Adenosine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72774189?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcohol+and+alcoholism+%28Oxford%2C+Oxfordshire%29.+Supplement&rft.atitle=In+vitro+autoradiographic+evidence+for+adenosine+modulation+of+ethanol-induced+motor+disturbances+in+rats.&rft.au=Clark%2C+M%3BDar%2C+M+S&rft.aulast=Clark&rft.aufirst=M&rft.date=1991-01-01&rft.volume=1&rft.issue=&rft.spage=203&rft.isbn=&rft.btitle=&rft.title=Alcohol+and+alcoholism+%28Oxford%2C+Oxfordshire%29.+Supplement&rft.issn=13586173&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-07 N1 - Date created - 1993-10-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Selecting combinations of chemotherapeutic drugs to maximize dose intensity. AN - 72773163; 1844700 AB - A mathematical model is described for selecting combinations of chemotherapeutic drugs in order to maximize antitumor dose intensity subject to constraints on toxicity to normal organ systems. Determination of which drugs to combine and in what proportions to combine them offers combinatorially huge numbers of possibilities. The method described here offers one approach to identifying combinations worthy of evaluation in prospective comparative clinical trials. JF - Journal of biopharmaceutical statistics AU - Simon, R AU - Korn, E L AD - Biometric Research Branch, National Cancer Institute, Bethesda, Maryland. Y1 - 1991 PY - 1991 DA - 1991 SP - 247 EP - 259 VL - 1 IS - 2 SN - 1054-3406, 1054-3406 KW - Index Medicus KW - Drug Administration Schedule KW - Prospective Studies KW - Humans KW - Models, Statistical KW - Clinical Trials as Topic -- methods KW - Clinical Trials as Topic -- statistics & numerical data KW - Dose-Response Relationship, Drug KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72773163?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+biopharmaceutical+statistics&rft.atitle=Selecting+combinations+of+chemotherapeutic+drugs+to+maximize+dose+intensity.&rft.au=Simon%2C+R%3BKorn%2C+E+L&rft.aulast=Simon&rft.aufirst=R&rft.date=1991-01-01&rft.volume=1&rft.issue=2&rft.spage=247&rft.isbn=&rft.btitle=&rft.title=Journal+of+biopharmaceutical+statistics&rft.issn=10543406&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-05-27 N1 - Date created - 1993-05-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Immune-associated toxicities induced by in vivo and in vitro exposure to interferon-alpha alone or in combination with nucleoside analogs. AN - 72767023; 1668554 AB - The present studies examine whether immune-associated toxicities develop in rodents exposed to recombinant human interferon-alpha A/D (rHuIFN-alpha) alone or in combination with anti-retroviral nucleoside analogs. Four findings have emerged from these studies: (1) lymphocyte cell number and functional activity are suppressed after subchronic (1, 8 or 10 day) in vivo exposure to therapeutic doses of rHuIFN-alpha; (2) lymphocyte-associated toxicities lessen as in vivo exposure time to rHuIFN-alpha is extended; (3) T-cell-dependent antibody production is decreased after in vitro exposure of both antigen-specific T- and B-cells to rHuIFN-alpha; and (4) in vivo-induced leukocyte toxicities associated with either rHuIFN-alpha or the nucleoside analogs alone do not synergize when the therapies are combined. These data suggest that certain key immune parameters should be monitored carefully in the early stages of IFN-alpha therapy. JF - International journal of immunopharmacology AU - Sanders, V M AU - Powell-Oliver, F E AU - Rosenthal, G J AU - Germolec, D R AU - Luster, M I AD - National Institute of Environmental Health Sciences, NIH, Systems Toxicity Branch, Research Triangle Park, NC 27709. Y1 - 1991 PY - 1991 DA - 1991 SP - 109 EP - 115 VL - 13 Suppl 1 SN - 0192-0561, 0192-0561 KW - Interferon Type I KW - 0 KW - Recombinant Proteins KW - Zidovudine KW - 4B9XT59T7S KW - Zalcitabine KW - 6L3XT8CB3I KW - Index Medicus KW - AIDS/HIV KW - Lymphocyte Activation -- drug effects KW - Mice, Inbred Strains KW - Animals KW - Zalcitabine -- administration & dosage KW - Zidovudine -- toxicity KW - Cells, Cultured KW - Zidovudine -- administration & dosage KW - Zalcitabine -- toxicity KW - Mice KW - Female KW - Interferon Type I -- administration & dosage KW - Immune System -- drug effects KW - Interferon Type I -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72767023?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+immunopharmacology&rft.atitle=Immune-associated+toxicities+induced+by+in+vivo+and+in+vitro+exposure+to+interferon-alpha+alone+or+in+combination+with+nucleoside+analogs.&rft.au=Sanders%2C+V+M%3BPowell-Oliver%2C+F+E%3BRosenthal%2C+G+J%3BGermolec%2C+D+R%3BLuster%2C+M+I&rft.aulast=Sanders&rft.aufirst=V&rft.date=1991-01-01&rft.volume=13+Suppl+1&rft.issue=&rft.spage=109&rft.isbn=&rft.btitle=&rft.title=International+journal+of+immunopharmacology&rft.issn=01920561&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 - The extracellular domain of the TSH receptor has an immunogenic epitope reactive with Graves' IgG but unrelated to receptor function as well as determinants having different roles for high affinity TSH binding and the activity of thyroid-stimulating autoantibodies. AN - 72766484; 1726785 AB - The possibility that thyroid-stimulating antibodies (TSAbs) might interact with receptor determinants different from those important for high affinity TSH binding has been evaluated. Deletion mutants of the extracellular domain of the rat TSH receptor as well as point mutations of potential N-linked glycosylation sites were created. TSH binding and the ability of TSH or a TSAb to increase cAMP levels after transfection in Cos-7 cells were then measured. Mutation of two glycosylation sites (residues 77 and 198) was shown to significantly decrease high affinity TSH binding but not the activity of a TSAb. A third glycosylation site mutant (residue 302) was identified that enhanced TSAb activity but had no effect on high affinity TSH binding, and a deletion mutant (residues 308-410) lost TSAb activity but preserved TSH binding. The last two mutations are within a region having low homology with gonadotropin receptors. This same region has, in addition, a determinant that is not important for receptor activity, yet is reactive with Graves' IgG. Thus, a deletion of residues 339-367 has no effect on TSH binding or TSH/TSAb activity, yet contains a peptide (residues 352-367) reactive in ELISA assays with IgG from greater than 80% of Graves' patients but not with IgG from normal individuals, patients with nonautoimmune thyroid disease, or patients with autoimmune disease not related to the thyroid. We, therefore, identify different receptor determinants for TSAb and high affinity TSH binding, consistent with predictions from TSH receptor monoclonal antibody studies. In addition, we identify a receptor peptide that is reactive with TSH receptor antibodies in Graves' patients, despite its having no determinants important for TSH or autoantibody activity in functional assays. JF - Thyroid : official journal of the American Thyroid Association AU - Kosugi, S AU - Akamizu, T AU - Takai, O AU - Prabhakar, B S AU - Kohn, L D AD - Cell Regulation Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland. Y1 - 1991 PY - 1991 DA - 1991 SP - 321 EP - 330 VL - 1 IS - 4 SN - 1050-7256, 1050-7256 KW - Autoantibodies KW - 0 KW - Epitopes KW - Immunoglobulin G KW - Immunoglobulins, Thyroid-Stimulating KW - Receptors, Thyrotropin KW - RNA KW - 63231-63-0 KW - Thyrotropin KW - 9002-71-5 KW - Index Medicus KW - Animals KW - Protein Biosynthesis KW - Blotting, Northern KW - Transcription, Genetic KW - Amino Acid Sequence KW - RNA -- analysis KW - Glycosylation KW - Mutagenesis, Site-Directed KW - Rats KW - Transfection KW - In Vitro Techniques KW - Molecular Sequence Data KW - RNA -- isolation & purification KW - Epitopes -- analysis KW - Receptors, Thyrotropin -- immunology KW - Autoantibodies -- immunology KW - Immunoglobulin G -- immunology KW - Thyrotropin -- metabolism KW - Graves Disease -- immunology KW - Receptors, Thyrotropin -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72766484?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Thyroid+%3A+official+journal+of+the+American+Thyroid+Association&rft.atitle=The+extracellular+domain+of+the+TSH+receptor+has+an+immunogenic+epitope+reactive+with+Graves%27+IgG+but+unrelated+to+receptor+function+as+well+as+determinants+having+different+roles+for+high+affinity+TSH+binding+and+the+activity+of+thyroid-stimulating+autoantibodies.&rft.au=Kosugi%2C+S%3BAkamizu%2C+T%3BTakai%2C+O%3BPrabhakar%2C+B+S%3BKohn%2C+L+D&rft.aulast=Kosugi&rft.aufirst=S&rft.date=1991-01-01&rft.volume=1&rft.issue=4&rft.spage=321&rft.isbn=&rft.btitle=&rft.title=Thyroid+%3A+official+journal+of+the+American+Thyroid+Association&rft.issn=10507256&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 - The contribution of voltage-gated and NMDA receptor-gated calcium channels to ethanol withdrawal seizures. AN - 72765483; 1669005 JF - Alcohol and alcoholism (Oxford, Oxfordshire). Supplement AU - Hoffman, P L AU - Tabakoff, B AD - Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 171 EP - 175 VL - 1 SN - 1358-6173, 1358-6173 KW - Calcium Channels KW - 0 KW - Receptors, N-Methyl-D-Aspartate KW - Ethanol KW - 3K9958V90M KW - Index Medicus KW - Animals KW - Drug Tolerance -- physiology KW - Ion Channel Gating -- drug effects KW - Brain -- physiopathology KW - Receptors, N-Methyl-D-Aspartate -- physiology KW - Calcium Channels -- physiology KW - Substance Withdrawal Syndrome -- physiopathology KW - Seizures -- physiopathology KW - Receptors, N-Methyl-D-Aspartate -- drug effects KW - Brain -- drug effects KW - Ethanol -- toxicity KW - Brain -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72765483?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcohol+and+alcoholism+%28Oxford%2C+Oxfordshire%29.+Supplement&rft.atitle=The+contribution+of+voltage-gated+and+NMDA+receptor-gated+calcium+channels+to+ethanol+withdrawal+seizures.&rft.au=Hoffman%2C+P+L%3BTabakoff%2C+B&rft.aulast=Hoffman&rft.aufirst=P&rft.date=1991-01-01&rft.volume=1&rft.issue=&rft.spage=171&rft.isbn=&rft.btitle=&rft.title=Alcohol+and+alcoholism+%28Oxford%2C+Oxfordshire%29.+Supplement&rft.issn=13586173&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-07 N1 - Date created - 1993-10-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Molecular basis of multistage carcinogenesis. AN - 72762418; 1844248 AB - Revealing the molecular basis of human disease including cancer will be viewed as one of the triumphs of biomedical research in the 20th Century. One successful strategy has been to analyze abnormalities in cancer-related genes occurring in preneoplastic and neoplastic lesions in humans and animal models. These gene abnormalities, e.g., mutations, can be specifically linked in some cases to environmental carcinogens in molecular epidemiological studies of human populations and in more controlled experimental conditions using animal or in vitro models of carcinogenesis. A second successful strategy has been to capitalize on advances from basic research such as defining signal transduction pathways in mammalian cells and the genetic control of the cell cycle in yeast. Mutations in yeast cell division control genes can lead to genomic instability and aneuploidy which are hallmarks of cancer. Therefore, the role of these genes in human carcinogenesis is being intensely investigated. The involvement of the p53 gene in the majority of human cancers has focused attention on the molecular and biochemical mechanisms of this tumor suppressor gene. The analysis of the p53 mutational spectrum in human cancers has provided evidence that both exogenous and endogenous causes of mutation contribute to human carcinogenesis. The increased understanding of the molecular basis of carcinogenesis has important implications in the prevention, diagnosis and treatment of human cancer. JF - Princess Takamatsu symposia AU - Harris, C C AD - Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 3 EP - 19 VL - 22 KW - Index Medicus KW - Animals KW - Genes, Tumor Suppressor KW - Humans KW - Proto-Oncogenes KW - Mutation KW - Cocarcinogenesis KW - Neoplasms -- genetics KW - Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72762418?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Princess+Takamatsu+symposia&rft.atitle=Molecular+basis+of+multistage+carcinogenesis.&rft.au=Harris%2C+C+C&rft.aulast=Harris&rft.aufirst=C&rft.date=1991-01-01&rft.volume=22&rft.issue=&rft.spage=3&rft.isbn=&rft.btitle=&rft.title=Princess+Takamatsu+symposia&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-04-21 N1 - Date created - 1993-04-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Molecular mechanisms of memory and drug dependence. AN - 72762371; 1845561 AB - Addiction has long been thought to include both metabolic and psychological dependence. Psychological dependence must involve long-term memory of behavioral patterns in response to specific experimental contexts. Mammalian memory, and more specifically, human memory, is largely associative. Animal models of associative memory have been provided by Pavlovian conditioning of the snail Hermissenda crassicornis and the rabbit. Striking parallels have been observed in the intrinsic molecular and biophysical transformations which accompany acquisition of the conditioned response in these different animals. In brief, associated stimuli cause elevation of Ca2+ and diacylglycerol, translocation of protein kinase C, phosphorylation of a membrane-associated G-protein, reduction of K+ currents, modification of axonal transport and structural alterations of neuronal branches. These changes can be understood and modelled as a plausible basis for memory acquisition during conditioning as well as more cognitively relevant learning such as spatial maze learning for which related neuronal alterations have recently been found. Identification of memory-specific molecular steps may help target pharmacologic agents for amelioration of learned aspects of psychiatric syndromes such as those of drug dependence. JF - Alcohol and alcoholism (Oxford, Oxfordshire). Supplement AU - Alkon, D L AU - Matzel, L D AU - Collin, C AD - National Institutes of Health, Laboratory of Molecular and Cellular Neurobiology, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 35 EP - 37 VL - 1 SN - 1358-6173, 1358-6173 KW - Index Medicus KW - Animals KW - Synapses -- physiology KW - Humans KW - Substance-Related Disorders -- physiopathology KW - Memory -- physiology KW - Snails -- physiology KW - Substance-Related Disorders -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72762371?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcohol+and+alcoholism+%28Oxford%2C+Oxfordshire%29.+Supplement&rft.atitle=Molecular+mechanisms+of+memory+and+drug+dependence.&rft.au=Alkon%2C+D+L%3BMatzel%2C+L+D%3BCollin%2C+C&rft.aulast=Alkon&rft.aufirst=D&rft.date=1991-01-01&rft.volume=1&rft.issue=&rft.spage=35&rft.isbn=&rft.btitle=&rft.title=Alcohol+and+alcoholism+%28Oxford%2C+Oxfordshire%29.+Supplement&rft.issn=13586173&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-07 N1 - Date created - 1993-10-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Microsomal ethanol oxidizing system: transcriptional and posttranscriptional regulation of cytochrome P450, CYP2E1. AN - 72762213; 1845601 AB - CYP2E1 is solely responsible for microsomal P450-mediated ethanol oxidation activity. This enzyme is also involved in a pathway leading to gluconeogenesis from ketone bodies and in metabolic activation of numerous foreign compounds to intermediates that can be toxic to cells. Metabolic activation of certain procarcinogens by CYP2E1 may also lead to cell transformation. Regulation of CYP2E1 is especially intriguing. The CYP2E1 gene is transcriptionally activated in rat liver from a dormant state within a few hours after birth. This activation is due in part to the participation of a transcription factor designated hepatocyte nuclear factor 1 or HNF-1. In adult animals, constitutive expression of the enzyme is controlled to some degree by growth hormone. CYP2E1 is also regulated by many of its substrates through a substrate-induced stabilization of the enzyme. Under extreme conditions of fasting and uncontrolled diabetes CYP2E1 mRNA is stabilized. JF - Alcohol and alcoholism (Oxford, Oxfordshire). Supplement AU - Gonzalez, F J AU - Ueno, T AU - Umeno, M AU - Song, B J AU - Veech, R L AU - Gelboin, H V AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 97 EP - 101 VL - 1 SN - 1358-6173, 1358-6173 KW - CYP2E1 KW - Transcription Factors KW - 0 KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Cytochrome P-450 CYP2E1 KW - EC 1.14.13.- KW - Oxidoreductases, N-Demethylating KW - EC 1.5.- KW - Index Medicus KW - Rats KW - Animals KW - Base Sequence KW - Transcription Factors -- metabolism KW - Sequence Homology, Nucleic Acid KW - Humans KW - DNA -- metabolism KW - DNA -- genetics KW - Molecular Sequence Data KW - Substrate Specificity KW - Gene Expression Regulation, Enzymologic KW - Microsomes, Liver -- enzymology KW - Cytochrome P-450 Enzyme System -- metabolism KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Transcription, Genetic KW - Microsomes -- enzymology KW - Oxidoreductases, N-Demethylating -- metabolism KW - Oxidoreductases, N-Demethylating -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72762213?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcohol+and+alcoholism+%28Oxford%2C+Oxfordshire%29.+Supplement&rft.atitle=Microsomal+ethanol+oxidizing+system%3A+transcriptional+and+posttranscriptional+regulation+of+cytochrome+P450%2C+CYP2E1.&rft.au=Gonzalez%2C+F+J%3BUeno%2C+T%3BUmeno%2C+M%3BSong%2C+B+J%3BVeech%2C+R+L%3BGelboin%2C+H+V&rft.aulast=Gonzalez&rft.aufirst=F&rft.date=1991-01-01&rft.volume=1&rft.issue=&rft.spage=97&rft.isbn=&rft.btitle=&rft.title=Alcohol+and+alcoholism+%28Oxford%2C+Oxfordshire%29.+Supplement&rft.issn=13586173&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-07 N1 - Date created - 1993-10-07 N1 - Date revised - 2017-01-13 N1 - Gene symbol - CYP2E1 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Demonstration that ethanol potentiates the GABAA-activated Cl- current in central mammalian neurons. AN - 72761235; 1726983 AB - Previous studies have suggested that ethanol potentiates GABA-mediated responses in the mammalian brain. In the present study, using patch-clamp techniques, we show that the GABAA-activated Cl- current was potentiated by ethanol in a subpopulation of mouse hippocampal cells. JF - Alcohol and alcoholism (Oxford, Oxfordshire). Supplement AU - Aguayo, L G AD - Section of Electrophysiology, NIAAA, Rockville, MD 20852. Y1 - 1991 PY - 1991 DA - 1991 SP - 187 EP - 190 VL - 1 SN - 1358-6173, 1358-6173 KW - Chloride Channels KW - 0 KW - Ion Channels KW - Membrane Proteins KW - Receptors, GABA-A KW - Ethanol KW - 3K9958V90M KW - gamma-Aminobutyric Acid KW - 56-12-2 KW - Index Medicus KW - Fetus KW - Animals KW - Cells, Cultured KW - Mice, Inbred C57BL KW - Mice KW - Drug Synergism KW - Receptors, GABA-A -- physiology KW - Hippocampus -- physiology KW - Ethanol -- pharmacology KW - gamma-Aminobutyric Acid -- pharmacology KW - Neurons -- drug effects KW - Ion Channels -- drug effects KW - Neurons -- physiology KW - Receptors, GABA-A -- drug effects KW - Membrane Proteins -- drug effects KW - Ion Channels -- physiology KW - Membrane Proteins -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72761235?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcohol+and+alcoholism+%28Oxford%2C+Oxfordshire%29.+Supplement&rft.atitle=Demonstration+that+ethanol+potentiates+the+GABAA-activated+Cl-+current+in+central+mammalian+neurons.&rft.au=Aguayo%2C+L+G&rft.aulast=Aguayo&rft.aufirst=L&rft.date=1991-01-01&rft.volume=1&rft.issue=&rft.spage=187&rft.isbn=&rft.btitle=&rft.title=Alcohol+and+alcoholism+%28Oxford%2C+Oxfordshire%29.+Supplement&rft.issn=13586173&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1993-10-07 N1 - Date created - 1993-10-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Study design and genetic susceptibility factors in the risk assessment of chemical carcinogens. AN - 72760398; 1820735 AB - Molecular epidemiology approaches are being employed to examine the validity and elucidate the basis for hypothesized associations of genetic susceptibility factors with common malignancies due to carcinogen exposure. This approach integrates traditional epidemiologic study designs with state-of-the-art laboratory assays. Advantages of this strategy include the possibility of gaining insight into mechanisms and better exposure assessment. Disadvantages include added complexity and cost. Three examples of pharmacogenetic risk factors are discussed: the first two are p450 enzymes whose activity has been associated with susceptibility to lung cancer (debrisoquine hydroxylase, aryl hydrocarbon hydroxylase), and the last, N-acetyltransferase, a non-p450 enzyme, has been associated with bladder cancer susceptibility. In this context, a case-control study which examined the hypothesis of an association between the debrisoquine metabolic phenotype and lung cancer is discussed. While various studies from the molecular to the population level provide evidence to support each of these associations, methodologic problems exist and a causal association remains to be decisively demonstrated. New epidemiologic studies, the application of improved DNA based tests for the genotype, and further basic investigations regarding the mechanisms of the proposed associations continue, and progress is anticipated in the resolution of these questions with important consequences for our understanding of chemical carcinogenesis in these common malignancies. While these associations remain controversial, the existence of wide interindividual variation in the population in the ability to metabolize certain chemical carcinogens is certain and this argues for a conservative approach in the regulation of chemical carcinogens. JF - Annali dell'Istituto superiore di sanita AU - Caporaso, N AD - Family Studies Section, NCI, Bethesda. Y1 - 1991 PY - 1991 DA - 1991 SP - 621 EP - 630 VL - 27 IS - 4 SN - 0021-2571, 0021-2571 KW - CYP2D6 KW - HA-ras-vtr KW - L-myc KW - Carcinogens, Environmental KW - 0 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Mixed Function Oxygenases KW - EC 1.- KW - Cytochrome P-450 CYP2D6 KW - EC 1.14.14.1 KW - Debrisoquin KW - X31CDK040E KW - Index Medicus KW - Lung Neoplasms -- enzymology KW - Debrisoquin -- metabolism KW - Epidemiologic Methods KW - Urinary Bladder Neoplasms -- epidemiology KW - Humans KW - Cytochrome P-450 Enzyme System -- metabolism KW - Research Design KW - Carcinogens, Environmental -- pharmacokinetics KW - Phenotype KW - Lung Neoplasms -- epidemiology KW - Oncogenes KW - Biotransformation KW - Heterozygote KW - Cytochrome P-450 Enzyme System -- physiology KW - Urinary Bladder Neoplasms -- enzymology KW - Genetic Predisposition to Disease KW - Lung Neoplasms -- chemically induced KW - Urinary Bladder Neoplasms -- chemically induced KW - Cytochrome P-450 Enzyme System -- genetics KW - Urinary Bladder Neoplasms -- genetics KW - Mixed Function Oxygenases -- metabolism KW - Risk Factors KW - Environmental Exposure KW - Case-Control Studies KW - Lung Neoplasms -- genetics KW - Mixed Function Oxygenases -- genetics KW - Neoplasms -- epidemiology KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72760398?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annali+dell%27Istituto+superiore+di+sanita&rft.atitle=Study+design+and+genetic+susceptibility+factors+in+the+risk+assessment+of+chemical+carcinogens.&rft.au=Caporaso%2C+N&rft.aulast=Caporaso&rft.aufirst=N&rft.date=1991-01-01&rft.volume=27&rft.issue=4&rft.spage=621&rft.isbn=&rft.btitle=&rft.title=Annali+dell%27Istituto+superiore+di+sanita&rft.issn=00212571&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 - Gene symbol - CYP2D6; HA-ras-vtr; L-myc N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Carcinogenicity of ochratoxin A in experimental animals. AN - 72760147; 1820337 AB - The carcinogenicity of ochratoxin A, a naturally occurring mycotoxin of the fungal genera Aspergillus and Penicillium, was evaluated in three strains of mice and in one strain of rats. The kidney, and in particular the tubular epithelial cells, was the major target organ for ochratoxin A-induced lesions. In male ddY and DDD mice, atypical hyperplasia, cystadenomas and carcinomas of the renal tubular cells were induced, as were neoplastic nodules and hepatocyte tumours of the liver. In B6C3F1 mice, tubular-cell adenomas and carcinomas of the kidneys were induced in male mice, and the incidences of hepatocellular adenomas and carcinomas were increased in male and female mice. In male and female F344 rats, ochratoxin A induced nonneoplastic (degeneration, karyomegaly, proliferation, cytoplasmic alteration, hyperplasia) and neoplastic effects (adenomas, and carcinomas with metastases) in the kidneys; the incidence of fibroadenomas of the mammary glands was also increased in female rats. Other studies on ochratoxin A were considered inadequate for evaluating the presence or absence of a carcinogenic effect; however, these are mentioned and referenced below. The collective experimental findings, together with accumulating evidence in humans, forecast further toxic and carcinogenic effects in humans exposed to ochratoxin A, mainly via foodstuffs. JF - IARC scientific publications AU - Huff, J E AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina. Y1 - 1991 PY - 1991 DA - 1991 SP - 229 EP - 244 IS - 115 SN - 0300-5038, 0300-5038 KW - Mycotoxins KW - 0 KW - Ochratoxins KW - ochratoxin A KW - 1779SX6LUY KW - Aflatoxin B1 KW - 9N2N2Y55MH KW - Index Medicus KW - Animals KW - Adenofibroma -- chemically induced KW - Chemical and Drug Induced Liver Injury KW - Humans KW - Romania -- epidemiology KW - Balkan Nephropathy -- chemically induced KW - Precancerous Conditions -- pathology KW - Comorbidity KW - Hepatectomy -- adverse effects KW - Adenofibroma -- pathology KW - Mammary Neoplasms, Experimental -- pathology KW - Rats KW - Yugoslavia -- epidemiology KW - Mammary Neoplasms, Experimental -- chemically induced KW - Urologic Neoplasms -- epidemiology KW - Rats, Inbred F344 KW - Adult KW - Male KW - Cocarcinogenesis KW - Kidney -- pathology KW - Bulgaria -- epidemiology KW - Mice KW - Balkan Nephropathy -- epidemiology KW - Mice, Inbred Strains KW - Mice, Mutant Strains KW - Hyperplasia KW - Precancerous Conditions -- chemically induced KW - Liver Diseases -- pathology KW - Carcinogenicity Tests KW - Incidence KW - Middle Aged KW - Aflatoxin B1 -- toxicity KW - Species Specificity KW - Mycotoxins -- toxicity KW - Female KW - Carcinoma, Transitional Cell -- epidemiology KW - Kidney Neoplasms -- pathology KW - Liver Neoplasms, Experimental -- pathology KW - Carcinoma -- pathology KW - Ochratoxins -- toxicity KW - Kidney Neoplasms -- chemically induced KW - Adenoma -- chemically induced KW - Liver Neoplasms, Experimental -- chemically induced KW - Ochratoxins -- adverse effects KW - Adenoma -- pathology KW - Carcinoma -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72760147?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=IARC+scientific+publications&rft.atitle=Carcinogenicity+of+ochratoxin+A+in+experimental+animals.&rft.au=Huff%2C+J+E&rft.aulast=Huff&rft.aufirst=J&rft.date=1991-01-01&rft.volume=&rft.issue=115&rft.spage=229&rft.isbn=&rft.btitle=&rft.title=IARC+scientific+publications&rft.issn=03005038&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-08-05 N1 - Date created - 1992-08-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Furan-induced hepatic cholangiocarcinomas in Fischer 344 rats. AN - 72748236; 1668599 AB - In a 2-yr carcinogenicity bioassay, 0, 2, 4, or 8 mg furan/kg body weight (BW) was administered to male and female Fischer (F344) rats and resulted in an 86-100% incidence of cholangiocarcinomas with occasional metastasis. In a separate but concurrent study, male F344 rats dosed with 30 mg furan/kg BW for 90 days developed marked cholangiofibrosis and cholangiohepatitis and, when subsequently maintained without further treatment for an additional 6, 12, or 18 months, the cholangiofibrosis progressed to yield a 100% incidence of cholangiocarcinomas. Transplantation of 21 primary cholangiocarcinomas into syngeneic recipients resulted in growth from 4 donors. The 4 transplanted lines were successfully transferred through 8 serial passages and resulted in metastases in the recipients. The progressive growth of these proliferative hepatocholangial lesions over time, their transplantability, and the development of metastases in some of the cases provide biological evidence of the malignant potential of the furan-induced liver changes. JF - Toxicologic pathology AU - Maronpot, R R AU - Giles, H D AU - Dykes, D J AU - Irwin, R D AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991 PY - 1991 DA - 1991 SP - 561 EP - 570 VL - 19 IS - 4 Pt 2 SN - 0192-6233, 0192-6233 KW - Furans KW - 0 KW - furan KW - UC0XV6A8N9 KW - Index Medicus KW - Rats KW - Neoplasm Transplantation KW - Animals KW - Rats, Inbred F344 KW - Time Factors KW - Male KW - Female KW - Adenoma, Bile Duct -- chemically induced KW - Liver Neoplasms, Experimental -- pathology KW - Adenoma, Bile Duct -- pathology KW - Furans -- toxicity KW - Liver Neoplasms, Experimental -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72748236?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+pathology&rft.atitle=Furan-induced+hepatic+cholangiocarcinomas+in+Fischer+344+rats.&rft.au=Maronpot%2C+R+R%3BGiles%2C+H+D%3BDykes%2C+D+J%3BIrwin%2C+R+D&rft.aulast=Maronpot&rft.aufirst=R&rft.date=1991-01-01&rft.volume=19&rft.issue=4+Pt+2&rft.spage=561&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=01926233&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-10-14 N1 - Date created - 1992-10-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Ontogeny of peroxidase activity in epithelium and eosinophils of the mouse uterus. AN - 72745168; 1687904 AB - Outbred CD-1 mice treated for 1 or 4 days with 1 mg/kg of diethylstilbestrol (DES) at various ages after birth were examined for histochemical localization of peroxidase in the uterine epithelium. Peroxidase activity in uterine extracts was also measured by a radiometric assay and the conversion of [3H]DES to [3H]Z,Z-diensestrol (Z,Z-DIES). While no peroxidase activity was detected by a histochemical method in uterine epithelium from untreated 5-day old mice, the enzyme was apparent in mice treated for 4 days with DES; uterine eosinophils were absent at this age. By day 9, DES-induced staining for peroxidase in uterine epithelial cells and the number of uterine eosinophils had increased significantly. In addition, at this age, the biochemical assays for uterine peroxidase were sensitive enough to show that DES is converted to Z,Z-DIES and that [3H]estradiol gives rise to 3H2O and water-soluble radioactive metabolites. The peroxidase response to DES, determined by both histochemical and biochemical methods, increased with the age of the immature mice. These data indicate that the neonatal uterus, although deficient in eosinophils, demonstrates a peroxidase response to estrogen and that this response is localized primarily in the luminal epithelium. The role of this DES-induced peroxidase activity in converting DES to activated metabolites that may cause cell damage is discussed. JF - Teratogenesis, carcinogenesis, and mutagenesis AU - Newbold, R R AU - Jellinck, P H AU - Metzler, M AU - McLachlan, J A AD - Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991 PY - 1991 DA - 1991 SP - 267 EP - 278 VL - 11 IS - 5 SN - 0270-3211, 0270-3211 KW - Estradiol KW - 4TI98Z838E KW - Diethylstilbestrol KW - 731DCA35BT KW - Peroxidases KW - EC 1.11.1.- KW - Index Medicus KW - Animals, Newborn KW - Animals KW - Age Factors KW - Enzyme Induction -- drug effects KW - Biotransformation KW - Estradiol -- pharmacology KW - Epithelium -- enzymology KW - Mice KW - Female KW - Epithelium -- drug effects KW - Uterus -- growth & development KW - Eosinophils -- enzymology KW - Diethylstilbestrol -- toxicity KW - Eosinophils -- drug effects KW - Diethylstilbestrol -- pharmacology KW - Diethylstilbestrol -- pharmacokinetics KW - Uterus -- pathology KW - Uterus -- enzymology KW - Uterus -- drug effects KW - Peroxidases -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72745168?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Teratogenesis%2C+carcinogenesis%2C+and+mutagenesis&rft.atitle=Ontogeny+of+peroxidase+activity+in+epithelium+and+eosinophils+of+the+mouse+uterus.&rft.au=Newbold%2C+R+R%3BJellinck%2C+P+H%3BMetzler%2C+M%3BMcLachlan%2C+J+A&rft.aulast=Newbold&rft.aufirst=R&rft.date=1991-01-01&rft.volume=11&rft.issue=5&rft.spage=267&rft.isbn=&rft.btitle=&rft.title=Teratogenesis%2C+carcinogenesis%2C+and+mutagenesis&rft.issn=02703211&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-07-30 N1 - Date created - 1992-07-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Differential diagnosis of choreiform tardive dyskinesia. AN - 72741438; 1821242 AB - Orofacial dyskinesias and choreiform movements of limbs occur with moderate frequency among psychiatric patients. Abnormal involuntary movements are symptoms of a wide variety of neurological and medical disorders. For both therapeutic and medicolegal reasons, psychiatric patients should be thoroughly evaluated before being given the diagnosis of tardive dyskinesia. This review presents the differential diagnosis of disorders associated with orofacial and appendicular choreiform involuntary movements. In addition, this paper provides a guide to the clinical and laboratory evaluation of patients with these symptoms. JF - The Journal of neuropsychiatry and clinical neurosciences AU - Hyde, T M AU - Hotson, J R AU - Kleinman, J E AD - Clinical Brain Disorders Branch, National Institute of Mental Health, Washington, D.C. Y1 - 1991 PY - 1991 DA - 1991 SP - 255 EP - 268 VL - 3 IS - 3 SN - 0895-0172, 0895-0172 KW - Psychotropic Drugs KW - 0 KW - Index Medicus KW - Athetosis -- etiology KW - Diagnosis, Differential KW - Humans KW - Neurologic Examination KW - Athetosis -- chemically induced KW - Psychotropic Drugs -- adverse effects KW - Psychotropic Drugs -- administration & dosage KW - Chorea -- chemically induced KW - Dyskinesia, Drug-Induced -- etiology KW - Chorea -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72741438?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+neuropsychiatry+and+clinical+neurosciences&rft.atitle=Differential+diagnosis+of+choreiform+tardive+dyskinesia.&rft.au=Hyde%2C+T+M%3BHotson%2C+J+R%3BKleinman%2C+J+E&rft.aulast=Hyde&rft.aufirst=T&rft.date=1991-01-01&rft.volume=3&rft.issue=3&rft.spage=255&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+neuropsychiatry+and+clinical+neurosciences&rft.issn=08950172&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 - Identification and characterization of differentially expressed genes in tumor metastasis: the nm23 gene. AN - 72730860; 1667573 JF - Basic life sciences AU - Steeg, P S AU - Bevilacqua, G AU - Sobel, M E AU - Liotta, L A AD - Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 355 EP - 60; discussion 360-1 VL - 57 SN - 0090-5542, 0090-5542 KW - NM23 KW - c-Ha-ras KW - nm23 KW - DNA, Neoplasm KW - 0 KW - Methylnitrosourea KW - 684-93-5 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Melanoma, Experimental -- secondary KW - Lymphatic Metastasis KW - Humans KW - Tumor Cells, Cultured -- transplantation KW - Mice, Inbred BALB C KW - Mammary Neoplasms, Experimental -- pathology KW - Rats KW - Mammary Neoplasms, Experimental -- chemically induced KW - Fibroblasts -- pathology KW - Breast Neoplasms -- pathology KW - Mice, Inbred C3H -- microbiology KW - Tumor Cells, Cultured -- pathology KW - Carcinoma, Intraductal, Noninfiltrating -- genetics KW - Cell Line, Transformed KW - Melanoma, Experimental -- genetics KW - Breast Neoplasms -- genetics KW - Mammary Neoplasms, Experimental -- microbiology KW - Mammary Tumor Virus, Mouse -- physiology KW - Methylnitrosourea -- toxicity KW - Mammary Neoplasms, Experimental -- genetics KW - Mice KW - Melanoma, Experimental -- pathology KW - Carcinoma, Intraductal, Noninfiltrating -- pathology KW - Transfection KW - DNA -- genetics KW - DNA, Neoplasm -- genetics KW - Cell Transformation, Viral KW - Gene Expression Regulation, Neoplastic KW - Neoplasm Metastasis -- genetics KW - Genes, Tumor Suppressor UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72730860?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Basic+life+sciences&rft.atitle=Identification+and+characterization+of+differentially+expressed+genes+in+tumor+metastasis%3A+the+nm23+gene.&rft.au=Steeg%2C+P+S%3BBevilacqua%2C+G%3BSobel%2C+M+E%3BLiotta%2C+L+A&rft.aulast=Steeg&rft.aufirst=P&rft.date=1991-01-01&rft.volume=57&rft.issue=&rft.spage=355&rft.isbn=&rft.btitle=&rft.title=Basic+life+sciences&rft.issn=00905542&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-12 N1 - Date created - 1992-06-12 N1 - Date revised - 2017-01-13 N1 - Gene symbol - NM23; c-Ha-ras; nm23 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alveolar proteinosis and phospholipidoses of the lungs. AN - 72723910; 1667556 AB - Three pulmonary disease conditions result from the accumulation of phospholipids in the lung. These conditions are the human lung disease known as pulmonary alveolar proteinosis, the lipoproteinosis that arises in the lungs of rats during acute silicosis, and the phospholipidoses induced by numerous cationic amphiphilic therapeutic agents. In this paper, the status of phospholipid metabolism in the lungs during the process of each of these lung conditions has been reviewed and possible mechanisms for their establishment are discussed. Pulmonary alveolar proteinosis is characterized by the accumulation of tubular myelin-like multilamellated structures in the alveoli and distal airways of patients. These structures appear to be formed by a process of spontaneous assembly involving surfactant protein A and surfactant phospholipids. Structures similar to tubular myelin-like multilamellated structures can be seen in the alveoli of rats during acute silicosis and, as with the human condition, both surfactant protein A and surfactant phospholipids accumulate in the alveoli. Excessive accumulation of surfactant protein A and surfactant phospholipids in the alveoli could arise from their overproduction and hypersecretion by a subpopulation of Type II cells that are activated by silica, and possibly other agents. Phospholipidoses caused by cationic amphiphilic therapeutic agents arise as a result of their inhibition of phospholipid catabolism. Inhibition of phospholipases results in the accumulation of phospholipids in the cytoplasm of alveolar macrophages and other cells. While inhibition of phospholipases by these agents undoubtedly occurs, there are many anomalous features, such as the accumulation of extracellular phospholipids and surfactant protein A, that cannot be accounted for by this simplistic hypothesis. JF - Toxicologic pathology AU - Hook, G E AD - Biochemical Pathology Group, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991 PY - 1991 DA - 1991 SP - 482 EP - 513 VL - 19 IS - 4 Pt 1 SN - 0192-6233, 0192-6233 KW - Lipoproteins KW - 0 KW - Phospholipids KW - Proteins KW - Pulmonary Surfactants KW - Silicon Dioxide KW - 7631-86-9 KW - Index Medicus KW - Pulmonary Surfactants -- metabolism KW - Animals KW - Lipoproteins -- metabolism KW - Humans KW - Silicon Dioxide -- toxicity KW - Lipidoses -- etiology KW - Lung Diseases -- chemically induced KW - Pulmonary Alveoli -- metabolism KW - Phospholipids -- metabolism KW - Pulmonary Alveoli -- drug effects KW - Lung Diseases -- metabolism KW - Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72723910?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+pathology&rft.atitle=Alveolar+proteinosis+and+phospholipidoses+of+the+lungs.&rft.au=Hook%2C+G+E&rft.aulast=Hook&rft.aufirst=G&rft.date=1991-01-01&rft.volume=19&rft.issue=4+Pt+1&rft.spage=482&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=01926233&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-17 N1 - Date created - 1992-06-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Histomorphologic features of spontaneous and chemically-induced pulmonary neoplasms in B6C3F1 mice and Fischer 344 rats. AN - 72722299; 1813992 AB - The histomorphologic features of spontaneous and chemically-induced lung neoplasms in male and female B6C3F1 mice and Fischer 344 rats are described. Primary pulmonary neoplasms in mice and rats were classified as alveolar/bronchiolar (A/B) adenoma or carcinoma (including variants with squamous and mucinous cell differentiation), bronchial adenoma or carcinoma, squamous cell carcinoma or mesenchymal tumors. A/B adenomas and carcinomas were the most common spontaneous pulmonary neoplasms observed in both mice and rats, but were observed less frequently in rats. In the National Toxicology Program (NTP) historical control database the incidence of spontaneous A/B adenomas in male (n = 2,084) and female (n = 2,079) mice is 13.8% and 4.9%, respectively; for A/B carcinomas, it is 5.3% and 2.4%, respectively. In male (n = 3,877) and female (n = 3,919) rats, spontaneous pulmonary neoplasms are rare with historical control rates less than 3% for A/B adenomas or carcinomas in either sex. The spontaneous A/B adenomas and carcinomas observed in mice and rats typically had papillary, solid or mixed (papillary and solid) histologic growth patterns. Pulmonary neoplasms from mice and rats treated with chemical carcinogens reviewed from 2-year studies consisted primarily of A/B adenomas and carcinomas. These tumors had papillary, glandular/tubular, solid or mixed (combination of 2 or more) histologic growth patterns. A few of the A/B neoplasms had areas of squamous or mucinous cell differentiation. Other less frequently occurring spontaneous and chemically-induced neoplasms included squamous cell carcinomas, bronchial adenomas and carcinomas, and sarcomas. JF - Toxicologic pathology AU - Dixon, D AU - Maronpot, R R AD - National Institute of Environmental Health Sciences, National Toxicology Program, Research Triangle Park, North Carolina 27709. Y1 - 1991 PY - 1991 DA - 1991 SP - 540 EP - 556 VL - 19 IS - 4 Pt 1 SN - 0192-6233, 0192-6233 KW - Index Medicus KW - Rats KW - Animals KW - Carcinoma -- pathology KW - Mice KW - Adenoma -- pathology KW - Species Specificity KW - Male KW - Female KW - Mice, Inbred Strains KW - Rodent Diseases -- chemically induced KW - Rats, Inbred F344 KW - Lung Neoplasms -- chemically induced KW - Rodent Diseases -- pathology KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72722299?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+pathology&rft.atitle=Histomorphologic+features+of+spontaneous+and+chemically-induced+pulmonary+neoplasms+in+B6C3F1+mice+and+Fischer+344+rats.&rft.au=Dixon%2C+D%3BMaronpot%2C+R+R&rft.aulast=Dixon&rft.aufirst=D&rft.date=1991-01-01&rft.volume=19&rft.issue=4+Pt+1&rft.spage=540&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=01926233&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-17 N1 - Date created - 1992-06-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interaction of ethanol and smoking on the pharmacokinetics and pharmacodynamics of psychotropic medications. AN - 72721243; 1813903 AB - Ethanol and smoking are known to affect the pharmacokinetics and pharmacodynamics of many medications. This review focuses on the interactions between ethanol and smoking and psychotropic medications, in particular, antidepressants, anxiolytics, and neuroleptics. A discussion of the various mechanisms by which ethanol and smoking may exert their effects precedes a summary of specific interactions. JF - Psychopharmacology bulletin AU - Shoaf, S E AU - Linnoila, M AD - Laboratory of Clinical Studies, DICBR, NIAAA, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 577 EP - 594 VL - 27 IS - 4 SN - 0048-5764, 0048-5764 KW - Psychotropic Drugs KW - 0 KW - Ethanol KW - 3K9958V90M KW - Index Medicus KW - Drug Interactions KW - Humans KW - Ethanol -- pharmacology KW - Psychotropic Drugs -- pharmacology KW - Smoking -- metabolism KW - Psychotropic Drugs -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72721243?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychopharmacology+bulletin&rft.atitle=Interaction+of+ethanol+and+smoking+on+the+pharmacokinetics+and+pharmacodynamics+of+psychotropic+medications.&rft.au=Shoaf%2C+S+E%3BLinnoila%2C+M&rft.aulast=Shoaf&rft.aufirst=S&rft.date=1991-01-01&rft.volume=27&rft.issue=4&rft.spage=577&rft.isbn=&rft.btitle=&rft.title=Psychopharmacology+bulletin&rft.issn=00485764&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-12 N1 - Date created - 1992-06-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of tumor suppressor genes in a multistep model of carcinogenesis. AN - 72719615; 1814282 JF - Basic life sciences AU - Boyd, J A AU - Barrett, J C AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991 PY - 1991 DA - 1991 SP - 183 EP - 94; discussion 194-6 VL - 57 SN - 0090-5542, 0090-5542 KW - Rb KW - SA KW - c-myc KW - ras KW - sup KW - tum KW - Index Medicus KW - Animals KW - Cricetulus KW - Humans KW - Neoplasms, Experimental -- genetics KW - Cell Differentiation KW - Mice KW - Neoplasms, Experimental -- pathology KW - Gene Expression Regulation, Neoplastic KW - Oncogenes KW - Neoplastic Syndromes, Hereditary -- genetics KW - Crosses, Genetic KW - Mesocricetus KW - Cell Line, Transformed KW - Cricetinae KW - Neoplasms -- pathology KW - Cocarcinogenesis KW - Cell Transformation, Neoplastic -- pathology KW - Genes, Tumor Suppressor KW - Cell Transformation, Neoplastic -- chemically induced KW - Neoplasms -- genetics KW - Cell Transformation, Neoplastic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72719615?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Basic+life+sciences&rft.atitle=Role+of+tumor+suppressor+genes+in+a+multistep+model+of+carcinogenesis.&rft.au=Boyd%2C+J+A%3BBarrett%2C+J+C&rft.aulast=Boyd&rft.aufirst=J&rft.date=1991-01-01&rft.volume=57&rft.issue=&rft.spage=183&rft.isbn=&rft.btitle=&rft.title=Basic+life+sciences&rft.issn=00905542&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-12 N1 - Date created - 1992-06-12 N1 - Date revised - 2017-01-13 N1 - Gene symbol - Rb; SA; c-myc; ras; sup; tum N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The human spongiform encephalopathies: kuru, Creutzfeldt-Jakob disease, and the Gerstmann-Sträussler-Scheinker syndrome. AN - 72715914; 1687378 JF - Current topics in microbiology and immunology AU - Brown, P AU - Gajdusek, D C AD - Laboratory of CNS Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 1 EP - 20 VL - 172 SN - 0070-217X, 0070-217X KW - Amyloid KW - 0 KW - Amyloid beta-Protein Precursor KW - Nerve Tissue Proteins KW - PrPC Proteins KW - Prions KW - Protein Precursors KW - Index Medicus KW - Animals KW - Iatrogenic Disease KW - Slow Virus Diseases -- veterinary KW - Humans KW - Cannibalism KW - Sheep -- microbiology KW - Amyloid -- genetics KW - Infant KW - Prions -- genetics KW - Genes, Dominant KW - Adult KW - Slow Virus Diseases -- microbiology KW - Adolescent KW - Slow Virus Diseases -- transmission KW - Male KW - Protein Conformation KW - Amyloid beta-Protein Precursor -- chemistry KW - Scrapie -- transmission KW - Amyloid -- chemistry KW - Protein Precursors -- genetics KW - Primates -- microbiology KW - Nerve Tissue Proteins -- genetics KW - Amyloid beta-Protein Precursor -- genetics KW - New Guinea -- epidemiology KW - Global Health KW - Prions -- chemistry KW - Protein Precursors -- chemistry KW - Food Contamination KW - Incidence KW - Middle Aged KW - Nerve Tissue Proteins -- chemistry KW - Mutation KW - Female KW - Prevalence KW - Gerstmann-Straussler-Scheinker Disease -- microbiology KW - Creutzfeldt-Jakob Syndrome -- pathology KW - Kuru -- transmission KW - Creutzfeldt-Jakob Syndrome -- microbiology KW - Gerstmann-Straussler-Scheinker Disease -- pathology KW - Creutzfeldt-Jakob Syndrome -- genetics KW - Gerstmann-Straussler-Scheinker Disease -- epidemiology KW - Creutzfeldt-Jakob Syndrome -- transmission KW - Kuru -- pathology KW - Gerstmann-Straussler-Scheinker Disease -- genetics KW - Kuru -- microbiology KW - Kuru -- epidemiology KW - Creutzfeldt-Jakob Syndrome -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72715914?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+topics+in+microbiology+and+immunology&rft.atitle=The+human+spongiform+encephalopathies%3A+kuru%2C+Creutzfeldt-Jakob+disease%2C+and+the+Gerstmann-Str%C3%A4ussler-Scheinker+syndrome.&rft.au=Brown%2C+P%3BGajdusek%2C+D+C&rft.aulast=Brown&rft.aufirst=P&rft.date=1991-01-01&rft.volume=172&rft.issue=&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Current+topics+in+microbiology+and+immunology&rft.issn=0070217X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-02 N1 - Date created - 1992-06-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutagenesis of the mouse germline using retroviruses. AN - 72707636; 1667628 JF - Current topics in microbiology and immunology AU - Lock, L F AU - Jenkins, N A AU - Copeland, N G AD - Mammalian Genetics Laboratory, NCI-Frederick Cancer Research and Development Center, MD 21702. Y1 - 1991 PY - 1991 DA - 1991 SP - 27 EP - 41 VL - 171 SN - 0070-217X, 0070-217X KW - Emv KW - Emv-1 KW - Emv-16 KW - Emv-17 KW - Fv-1 KW - Fv-1n KW - Mov-13 KW - Mov-34 KW - Srev KW - Srev-5 KW - dv KW - gag KW - hprt KW - hr KW - pol env KW - DNA Transposable Elements KW - 0 KW - Index Medicus KW - Animals KW - Hybridization, Genetic KW - Alleles KW - Chimera KW - Proviruses -- genetics KW - Mice, Inbred Strains -- genetics KW - Genes, Lethal KW - Mice -- embryology KW - Genetic Vectors KW - Mice -- genetics KW - Genetic Engineering -- methods KW - Retroviridae -- genetics KW - Mutagenesis, Insertional UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72707636?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+topics+in+microbiology+and+immunology&rft.atitle=Mutagenesis+of+the+mouse+germline+using+retroviruses.&rft.au=Lock%2C+L+F%3BJenkins%2C+N+A%3BCopeland%2C+N+G&rft.aulast=Lock&rft.aufirst=L&rft.date=1991-01-01&rft.volume=171&rft.issue=&rft.spage=27&rft.isbn=&rft.btitle=&rft.title=Current+topics+in+microbiology+and+immunology&rft.issn=0070217X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-23 N1 - Date created - 1992-06-23 N1 - Date revised - 2017-01-13 N1 - Gene symbol - Emv; Emv-1; Emv-16; Emv-17; Fv-1; Fv-1n; Mov-13; Mov-34; Srev; Srev-5; dv; gag; hprt; hr; pol env N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Malignant conversion, the first stage in progression, is distinct from phorbol ester promotion in mouse skin. AN - 72703780; 1814291 AB - Papillomas induced by DMBA initiation-TPA promotion protocols are necessary precursor lesions of squamous cell carcinomas. The papillomas are heterogeneous in their potential for progression to carcinomas, a property apparently induced at the time of initiation. The probability of conversion to malignancy is highest for the papillomas most easily promoted, by either the first few TPA treatments or by "weak" promoters such as mezerein or chrysarobin. The conversion frequency is lowest for TPA-dependent papillomas and those papillomas which appear late in a TPA promotion protocol. The spontaneous rate of malignant conversion is not altered by continued TPA treatment; TPA promotion may simply expand clones of initiated cells which are already programmed with a given probability of conversion. Treatment of papilloma-bearing mice with a genotoxic agent, such as 4-NQO, urethane or cisplatin, increases the rate of malignant conversion. The properties of active converting agents differ markedly from those of the phorbol ester promoting agents, suggesting differences in the mechanisms of action of these two classes of compounds. A genetic mechanism appears likely to explain conversion. The differences between the two stages are further emphasized by the finding that inhibitors of tumor promotion are not inhibitory when given during malignant conversion. The converting agent urethane also affects the subsequent discrete stage in tumor progression, tumor metastasis. Differences in metastatic potential have been found between carcinomas which progress spontaneously after TPA promotion and carcinomas induced in TPA-promoted papillomas by urethane. The multistage nature of experimental epidermal carcinogenesis is well established. The mouse skin model will continue to be valuable for mechanistic studies since similar stages have been described in other tissues as well as in man. JF - Basic life sciences AU - Hennings, H AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, National Institutes of Health, Bethesda, MD. Y1 - 1991 PY - 1991 DA - 1991 SP - 31 EP - 9; discussion 39-42 VL - 57 SN - 0090-5542, 0090-5542 KW - Phorbol Esters KW - 0 KW - Acetone KW - 1364PS73AF KW - Urethane KW - 3IN71E75Z5 KW - 4-Nitroquinoline-1-oxide KW - 56-57-5 KW - 9,10-Dimethyl-1,2-benzanthracene KW - 57-97-6 KW - Index Medicus KW - Animals KW - 4-Nitroquinoline-1-oxide -- toxicity KW - Hyperplasia KW - Neoplasms, Multiple Primary -- pathology KW - Skin -- pathology KW - Neoplasm Metastasis KW - Mice KW - Urethane -- toxicity KW - Neoplasms, Multiple Primary -- chemically induced KW - Female KW - Acetone -- toxicity KW - Cell Transformation, Neoplastic -- pathology KW - Cocarcinogenesis KW - Papilloma -- pathology KW - Skin Neoplasms -- pathology KW - Carcinoma, Squamous Cell -- chemically induced KW - Papilloma -- genetics KW - Phorbol Esters -- toxicity KW - Skin Neoplasms -- genetics KW - Carcinoma, Squamous Cell -- pathology KW - Skin Neoplasms -- chemically induced KW - Carcinoma, Squamous Cell -- genetics KW - Cell Transformation, Neoplastic -- chemically induced KW - Papilloma -- chemically induced KW - Cell Transformation, Neoplastic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72703780?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Basic+life+sciences&rft.atitle=Malignant+conversion%2C+the+first+stage+in+progression%2C+is+distinct+from+phorbol+ester+promotion+in+mouse+skin.&rft.au=Hennings%2C+H&rft.aulast=Hennings&rft.aufirst=H&rft.date=1991-01-01&rft.volume=57&rft.issue=&rft.spage=31&rft.isbn=&rft.btitle=&rft.title=Basic+life+sciences&rft.issn=00905542&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-12 N1 - Date created - 1992-06-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Androgen metabolism in control and neonatally estrogenized male mice. AN - 72702435; 1807546 AB - Reduction, oxidation, and aromatization of androgens were studied in the male genital tract of untreated control and neonatally estrogenized mice. This study shows regional differences in 5 alpha-reductase and 17 beta-hydroxysteroid oxidoreductase activities in untreated male genital tract; 3 alpha/3 beta-hydroxysteroid oxidoreductase (3 alpha/3 beta-HSOR) activity varied little between tissues. Neonatal treatment with diethylstilbestrol (DES, 2 micrograms/pup/day on days 1 through 5) caused an alteration in the androgen metabolism of the male genital tract, resulting in apparent decreased net accumulation of dihydrotestosterone (DHT). This developmentally-induced 5 alpha-reductase deficiency may play a role in the long-term inhibitory effects of early estrogenization by DES in the growth and function of male sex accessory glands. No aromatase activity could be demonstrated in the male genital tract of control or neonatally estrogenized mice. JF - Reproductive toxicology (Elmsford, N.Y.) AU - Santti, R AU - Newbold, R R AU - McLachlan, J A AD - Developmental Endocrinology and Pharmacology Section, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina. Y1 - 1991 PY - 1991 DA - 1991 SP - 149 EP - 155 VL - 5 IS - 2 SN - 0890-6238, 0890-6238 KW - Androgens KW - 0 KW - Diethylstilbestrol KW - 731DCA35BT KW - Index Medicus KW - Oxidation-Reduction KW - Animals KW - Mice KW - Male KW - Genitalia, Male -- metabolism KW - Diethylstilbestrol -- pharmacology KW - Genitalia, Male -- growth & development KW - Animals, Newborn -- growth & development KW - Androgens -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72702435?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Reproductive+toxicology+%28Elmsford%2C+N.Y.%29&rft.atitle=Androgen+metabolism+in+control+and+neonatally+estrogenized+male+mice.&rft.au=Santti%2C+R%3BNewbold%2C+R+R%3BMcLachlan%2C+J+A&rft.aulast=Santti&rft.aufirst=R&rft.date=1991-01-01&rft.volume=5&rft.issue=2&rft.spage=149&rft.isbn=&rft.btitle=&rft.title=Reproductive+toxicology+%28Elmsford%2C+N.Y.%29&rft.issn=08906238&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-21 N1 - Date created - 1992-05-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Analysis of class II gene regulation. AN - 72701383; 1811143 JF - Methods in cell biology AU - Sargent, T D AU - Mathers, P H AD - Laboratory of Molecular Genetics, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 347 EP - 365 VL - 36 SN - 0091-679X, 0091-679X KW - Phenanthrolines KW - 0 KW - Sulfuric Acid Esters KW - dimethyl sulfate KW - JW5CW40Z50 KW - 1,10-phenanthroline KW - W4X6ZO7939 KW - Index Medicus KW - Polymerase Chain Reaction KW - Animals KW - DNA Mutational Analysis KW - Microinjections KW - Immunohistochemistry KW - Regulatory Sequences, Nucleic Acid -- genetics KW - Xenopus -- embryology KW - Gene Expression Regulation KW - Genes, MHC Class II UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72701383?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Methods+in+cell+biology&rft.atitle=Analysis+of+class+II+gene+regulation.&rft.au=Sargent%2C+T+D%3BMathers%2C+P+H&rft.aulast=Sargent&rft.aufirst=T&rft.date=1991-01-01&rft.volume=36&rft.issue=&rft.spage=347&rft.isbn=&rft.btitle=&rft.title=Methods+in+cell+biology&rft.issn=0091679X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-02 N1 - Date created - 1992-06-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Research on matching alcoholic patients to treatments: findings, issues, and implications. AN - 72695005; 1811759 AB - No single treatment has emerged as effective for all persons diagnosed as alcoholics. "Patient-treatment matching" is a method of choosing between alternative treatment options based on particular patient characteristics that interact differentially with interventions to produce more beneficial results than if "matching" had not been done. This review distinguishes three models for interactions between patient characteristics and interventions in terms of their clinical implications. Supporting empirical evidence for matching is also summarized. Requirements for the future research agenda are discussed and the pros and cons of implementing patient treatment matching in the clinical setting are addressed. JF - Journal of addictive diseases AU - Mattson, M E AU - Allen, J P AD - Treatment Research Branch, National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20857. Y1 - 1991 PY - 1991 DA - 1991 SP - 33 EP - 49 VL - 11 IS - 2 SN - 1055-0887, 1055-0887 KW - Index Medicus KW - Humans KW - Male KW - Female KW - Alcoholism -- therapy KW - Patient Care Planning -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72695005?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+addictive+diseases&rft.atitle=Research+on+matching+alcoholic+patients+to+treatments%3A+findings%2C+issues%2C+and+implications.&rft.au=Mattson%2C+M+E%3BAllen%2C+J+P&rft.aulast=Mattson&rft.aufirst=M&rft.date=1991-01-01&rft.volume=11&rft.issue=2&rft.spage=33&rft.isbn=&rft.btitle=&rft.title=Journal+of+addictive+diseases&rft.issn=10550887&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-06-09 N1 - Date created - 1992-06-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Alterations in serotonin receptor subtypes in ethanol-dependent rats. AN - 72691316; 1839497 AB - Serotonin (5-HT) receptor subtypes were investigated during severe ethanol intoxication and withdrawal. Ethanol was administered intragastrically five times a day for 4 days (12 g/kg per day). 5-HT receptor subtypes were studied: (1) in severely intoxicated animals (mean blood ethanol concentration (BEC) = 4.7 g/l); (2) during the withdrawal reaction; and (3) in a control group. The maximal density of [3H] 8-hydroxy-2-(di-n- propylamino)tetralin [( 3H] 8-OH-DPAT) binding (Bmax) to 5-HT1a receptors was decreased by 25 and 17% in the hippocampus during chronic ethanol intoxication and withdrawal, respectively. [3H]Ketanserin binding to 5-HT2 receptors in the cortex, (-)[125I]-iodo-cyanopindolol [( 125I]CYP) binding to 5-HT1b receptors in the striatum and hypothalamus, and [3H] 8-OH-DPAT binding in the cortex were not affected by chronic ethanol administration. Previous in vitro experiments have shown that 5-HT1a receptors in the hippocampus are inhibitory. The down-regulation of these receptors may play a role in physical ethanol dependence, by inducing hyperexcitability of the hippocampus. JF - Alcohol and alcoholism (Oxford, Oxfordshire) AU - Ulrichsen, J AD - Laboratory of Clinical Psychopharmacology, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1991 PY - 1991 DA - 1991 SP - 567 EP - 573 VL - 26 IS - 5-6 SN - 0735-0414, 0735-0414 KW - Receptors, Serotonin KW - 0 KW - Serotonin Antagonists KW - Tetrahydronaphthalenes KW - Serotonin KW - 333DO1RDJY KW - Ethanol KW - 3K9958V90M KW - cyanopindolol KW - 4K0SD5SNFS KW - 8-Hydroxy-2-(di-n-propylamino)tetralin KW - 78950-78-4 KW - Ketanserin KW - 97F9DE4CT4 KW - Pindolol KW - BJ4HF6IU1D KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Pindolol -- pharmacokinetics KW - Ethanol -- pharmacokinetics KW - Ketanserin -- pharmacokinetics KW - Radioligand Assay KW - Pindolol -- analogs & derivatives KW - Tetrahydronaphthalenes -- pharmacokinetics KW - Receptors, Serotonin -- physiology KW - Brain -- physiopathology KW - Alcoholic Intoxication -- physiopathology KW - Alcohol Withdrawal Delirium -- physiopathology KW - Alcoholism -- physiopathology KW - Serotonin -- metabolism KW - Receptors, Serotonin -- classification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72691316?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcohol+and+alcoholism+%28Oxford%2C+Oxfordshire%29&rft.atitle=Alterations+in+serotonin+receptor+subtypes+in+ethanol-dependent+rats.&rft.au=Ulrichsen%2C+J&rft.aulast=Ulrichsen&rft.aufirst=J&rft.date=1991-01-01&rft.volume=26&rft.issue=5-6&rft.spage=567&rft.isbn=&rft.btitle=&rft.title=Alcohol+and+alcoholism+%28Oxford%2C+Oxfordshire%29&rft.issn=07350414&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-01 N1 - Date created - 1992-05-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Endothelin-induced activation of phosphoinositide turnover, calcium mobilization, and transmitter release in cultured neurons and neurally related cell types. AN - 72688148; 1725440 AB - Endothelin (ET)-related peptides robustly stimulated [3H]-inositol phosphate (IP) formation in cultured cerebellar granule cells, astrocytes, and C6 glioma cells. Their agonist selectivities were ET-1 = ET-2 greater than or equal to sarafotoxin S6b greater than ET-3 greater than big ET-1 for granule cells and ET-1 greater than or equal to ET-2 greater than or equal to S6b greater than big ET-1 greater than ET-3 for cerebellar astrocytes and C6 glioma cells. These effects were Ca(2+)-dependent but insensitive to antagonists of L-type Ca2+ channels and the Na+/Ca2+ antiporter. Pretreatment of cells with ET-1 or S6b induced homologous desensitization of phosphoinositide (PI) response mediated by ET receptors. Long-term pertussis toxin (PTX) treatment attenuated the phosphoinositide (PI) response in astrocytes and glioma but not in granule cells. ET-1 and its related peptides increased [Ca2+]i in C6 glioma by two distinct pathways: IP3-induced Ca2+ mobilization or receptor-operated Ca2+ influx. La3+, Mn2+, and Cd2+ inhibited the Ca2+ influx and sustained PI turnover, while Ca2+ mobilization was attenuated by phorbol ester and TMB-8. ET-induced Ca2+ influx was essential for the sustained [Ca2+]i increase and PI turnover. Homologous desensitization of [Ca2+]i increase was also noted. In cerebellar granule cells, ET evoked the release of [3H]D-aspartate from these neurons. This action appears to be dependent on PI hydrolysis and [Ca2+]i increase and modulated by protein kinase C. JF - Journal of cardiovascular pharmacology AU - Chuang, D M AU - Lin, W W AU - Lee, C Y AD - Biological Psychiatry Branch, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - S85 EP - S88 VL - 17 Suppl 7 SN - 0160-2446, 0160-2446 KW - Endothelins KW - 0 KW - Neurotransmitter Agents KW - Phosphatidylinositols KW - Receptors, Cell Surface KW - Receptors, Endothelin KW - Aspartic Acid KW - 30KYC7MIAI KW - Phorbol 12,13-Dibutyrate KW - 37558-16-0 KW - Inositol KW - 4L6452S749 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Aspartic Acid -- metabolism KW - Animals KW - Cells, Cultured KW - Inositol -- metabolism KW - Glioma -- metabolism KW - Receptors, Cell Surface -- physiology KW - Phorbol 12,13-Dibutyrate -- pharmacology KW - Cerebellum -- metabolism KW - Calcium -- metabolism KW - Phosphatidylinositols -- metabolism KW - Endothelins -- pharmacology KW - Neurotransmitter Agents -- metabolism KW - Neurons -- metabolism KW - Neurons -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72688148?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+cardiovascular+pharmacology&rft.atitle=Endothelin-induced+activation+of+phosphoinositide+turnover%2C+calcium+mobilization%2C+and+transmitter+release+in+cultured+neurons+and+neurally+related+cell+types.&rft.au=Chuang%2C+D+M%3BLin%2C+W+W%3BLee%2C+C+Y&rft.aulast=Chuang&rft.aufirst=D&rft.date=1991-01-01&rft.volume=17+Suppl+7&rft.issue=&rft.spage=S85&rft.isbn=&rft.btitle=&rft.title=Journal+of+cardiovascular+pharmacology&rft.issn=01602446&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-05-12 N1 - Date created - 1992-05-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Statistical methods for analyzing developmental toxicity data. AN - 72686106; 1686820 AB - A description and review of methods for performing per-litter analyses involving extrabinomial proportion response is provided. It is stressed that the litter should be regarded as the appropriate experimental unit for quantitative analysis in studies for teratogenic or heritable mutagenic effects. Attention is directed at statistical identification of possible treatment effects, such as a positive dose response to a chemical stimulus. The methods range from distribution-free, nonparametric analyses to models involving parametric distributions such as the beta-binomial density. It is seen that most current methods require computer implementation. When concern is raised over misspecification of assumptions critical to the statistical analysis, it is argued that relatively parameter-free methods are appropriate for use. These include statistical bootstrapping and rank-based analyses. JF - Teratogenesis, carcinogenesis, and mutagenesis AU - Piegorsch, W W AU - Haseman, J K AD - Statistics and Biomathematics Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991 PY - 1991 DA - 1991 SP - 115 EP - 133 VL - 11 IS - 3 SN - 0270-3211, 0270-3211 KW - Index Medicus KW - Models, Statistical KW - Statistics as Topic -- methods KW - Toxicology -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72686106?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Teratogenesis%2C+carcinogenesis%2C+and+mutagenesis&rft.atitle=Statistical+methods+for+analyzing+developmental+toxicity+data.&rft.au=Piegorsch%2C+W+W%3BHaseman%2C+J+K&rft.aulast=Piegorsch&rft.aufirst=W&rft.date=1991-01-01&rft.volume=11&rft.issue=3&rft.spage=115&rft.isbn=&rft.btitle=&rft.title=Teratogenesis%2C+carcinogenesis%2C+and+mutagenesis&rft.issn=02703211&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-13 N1 - Date created - 1992-04-13 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Teratog Carcinog Mutagen. 1993;13(4):191-7 [7903487] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Evidence that toxic injury is not always associated with induction of chemical carcinogenesis. AN - 72676431; 1793481 AB - Long-term rodent bioassays with chemicals administered at maximum tolerated doses identify noncarcinogens as well as carcinogens. Thirty-one chemicals recently evaluated for carcinogenic potential by the National Toxicology Program provide unique data on the relationships between mutagenicity, toxicity, and carcinogenicity. Twenty-two substances were classified as carcinogens, and nine showed no evidence of carcinogenicity. Although cellular proliferation does play an intrinsic role in neoplastic processes, the responses associated with chronic toxicity in these studies were not always sufficient to induce neoplasia. Regardless of their mutagenic potential, 19 carcinogens induced toxic effects at sites that did not show neoplastic changes; similar toxic lesions were also seen among the mutagenic and nonmutagenic noncarcinogens. Although many nonmutagens induced neoplasia at sites that showed toxic effects, some of the same chemicals also exhibited toxicity at other sites that showed no neoplastic effect. These results suggest that for some chemicals, properties other than mutagenicity or toxicity may be responsible for their carcinogenic potential. JF - Molecular carcinogenesis AU - Tennant, R W AU - Elwell, M R AU - Spalding, J W AU - Griesemer, R A AD - Division of Toxicology Research and Testing, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991 PY - 1991 DA - 1991 SP - 420 EP - 440 VL - 4 IS - 6 SN - 0899-1987, 0899-1987 KW - Carcinogens KW - 0 KW - Mutagens KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Biological Assay KW - Male KW - Female KW - Neoplasms, Experimental -- chemically induced KW - Carcinogens -- toxicity KW - Mutagens -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72676431?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+carcinogenesis&rft.atitle=Evidence+that+toxic+injury+is+not+always+associated+with+induction+of+chemical+carcinogenesis.&rft.au=Tennant%2C+R+W%3BElwell%2C+M+R%3BSpalding%2C+J+W%3BGriesemer%2C+R+A&rft.aulast=Tennant&rft.aufirst=R&rft.date=1991-01-01&rft.volume=4&rft.issue=6&rft.spage=420&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-06 N1 - Date created - 1992-04-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Mol Carcinog. 1992;5(4):247-9 [1497799] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Regulation of 2-acetylaminofluorene-and 3-methylcholanthrene--mediated induction of multidrug resistance and cytochrome P450IA gene family expression in primary hepatocyte cultures and rat liver. AN - 72673182; 1686552 AB - Previous studies by this laboratory have indicated that expression of the multidrug resistance (mdr) gene can be increased in vivo by exposure to a variety of xenobiotics. Because of the nature of these compounds, it was proposed that mdr gene expression might, at least in part, be regulated by the arylhydrocarbon (Ah) receptor. In the present study, we used a primary hepatocyte culture model to examine the relationship between induction of cytochrome P450IA and mdr expression in vitro. Both 3-methylcholanthrene (MC) and 2-acetylaminofluorene (AAF) were efficient inducers of mdr expression in this model. Induction of mdr gene expression by both MC and AAF obeyed a log10 concentration/response relationship. In contrast, 2,3,7,8-tetrachlorodibenzo-P-dioxin did not induce mdr expression at concentrations that yielded maximum induction of cytochrome P450IA expression. These data suggest that mdr induction was not mediated via the Ah receptor. Nuclear run-off analysis indicated that both AAF and MC induced mdr expression by increasing transcription. Primer extension analysis indicated that mdr gene transcription was initiated at one major site 151 bp upstream of the ATG site in both the uninduced and induced state in vivo and in vitro. The sequence of the primer and the site of initiation of gene transcription indicate that the main gene induced was the mdr 1b gene. JF - Molecular carcinogenesis AU - Gant, T W AU - Silverman, J A AU - Bisgaard, H C AU - Burt, R K AU - Marino, P A AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 499 EP - 509 VL - 4 IS - 6 SN - 0899-1987, 0899-1987 KW - Membrane Glycoproteins KW - 0 KW - P-Glycoprotein KW - RNA, Messenger KW - Methylcholanthrene KW - 56-49-5 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - 2-Acetylaminofluorene KW - 9M98QLJ2DL KW - Oxidoreductases KW - EC 1.- KW - Cytochrome P-450 CYP1A2 KW - EC 1.14.14.1 KW - Index Medicus KW - Animals KW - Transcription, Genetic -- drug effects KW - Blotting, Northern KW - Multigene Family KW - RNA, Messenger -- genetics KW - Rats KW - Rats, Inbred F344 KW - Enzyme Induction -- drug effects KW - Cells, Cultured KW - In Vitro Techniques KW - Gene Expression Regulation -- drug effects KW - Time Factors KW - Male KW - Oxidoreductases -- genetics KW - 2-Acetylaminofluorene -- pharmacology KW - Methylcholanthrene -- pharmacology KW - Cytochrome P-450 Enzyme System -- genetics KW - Drug Resistance KW - Liver -- physiology KW - Membrane Glycoproteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72673182?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+carcinogenesis&rft.atitle=Regulation+of+2-acetylaminofluorene-and+3-methylcholanthrene--mediated+induction+of+multidrug+resistance+and+cytochrome+P450IA+gene+family+expression+in+primary+hepatocyte+cultures+and+rat+liver.&rft.au=Gant%2C+T+W%3BSilverman%2C+J+A%3BBisgaard%2C+H+C%3BBurt%2C+R+K%3BMarino%2C+P+A%3BThorgeirsson%2C+S+S&rft.aulast=Gant&rft.aufirst=T&rft.date=1991-01-01&rft.volume=4&rft.issue=6&rft.spage=499&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-06 N1 - Date created - 1992-04-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Dissociation of the acute effects of alcohol on implicit and explicit memory processes. AN - 72660156; 1791932 AB - The effects of alcohol (0, 0.3 and 0.6 g/kg) on learning and memory were assessed in independent groups of male student volunteers. Subjects were shown a list of words and asked to form an image of a scene involving each word 1 hr after drinking an alcohol-containing beverage. Alcohol consumption impaired the ability of subjects to explicitly remember the words in a test of free recall. However, no impairment was observed if memory for the same material was assessed implicitly using a backwards-reading or word-completion task. That is, both alcohol-and placebo-treated subjects showed similar degrees of priming. The data indicate that alcohol's effects on memory are selective. JF - Neuropsychologia AU - Lister, R G AU - Gorenstein, C AU - Fisher-Flowers, D AU - Weingartner, H J AU - Eckardt, M J AD - Laboratory of Clinical Studies, NIAAA, DICBR, NIH, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 1205 EP - 1212 VL - 29 IS - 12 SN - 0028-3932, 0028-3932 KW - Ethanol KW - 3K9958V90M KW - Index Medicus KW - Imagination -- drug effects KW - Paired-Associate Learning -- drug effects KW - Ethanol -- pharmacokinetics KW - Reading KW - Dose-Response Relationship, Drug KW - Humans KW - Adult KW - Attention -- drug effects KW - Male KW - Alcoholic Intoxication -- psychology KW - Verbal Learning -- drug effects KW - Retention (Psychology) -- drug effects KW - Mental Recall -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72660156?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuropsychologia&rft.atitle=Dissociation+of+the+acute+effects+of+alcohol+on+implicit+and+explicit+memory+processes.&rft.au=Lister%2C+R+G%3BGorenstein%2C+C%3BFisher-Flowers%2C+D%3BWeingartner%2C+H+J%3BEckardt%2C+M+J&rft.aulast=Lister&rft.aufirst=R&rft.date=1991-01-01&rft.volume=29&rft.issue=12&rft.spage=1205&rft.isbn=&rft.btitle=&rft.title=Neuropsychologia&rft.issn=00283932&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-01 N1 - Date created - 1992-04-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - National substance abuse epidemiology initiatives in the United States: what works for what. AN - 72657159; 1790153 AB - Data concerning the epidemiology of drug abuse in the United States are presented in this paper. The paper includes an integrating approach from various data sources: national, state, and local level; surveillance systems; and outbreak investigations. An analysis of trends and patterns of drug abuse are discussed, both from the perspective of historical development and the current situation. Analyses focus on changes in levels of use for different drugs as well as changes in user characteristics and consequences of use. Current studies concerning the epidemiology of drug abuse in special populations and findings from recent field investigations are presented. Future research directions in the field of epidemiology from a national perspective are outlined. JF - Journal of addictive diseases AU - Tomas, J M AU - Kozel, N J AD - Division of Epidemiology and Prevention Research, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1991 PY - 1991 DA - 1991 SP - 5 EP - 21 VL - 11 IS - 1 SN - 1055-0887, 1055-0887 KW - Index Medicus KW - Health Planning KW - Risk Factors KW - Humans KW - Research KW - United States -- epidemiology KW - Male KW - Female KW - Population Surveillance KW - Substance-Related Disorders -- therapy KW - Epidemiologic Methods KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72657159?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+addictive+diseases&rft.atitle=National+substance+abuse+epidemiology+initiatives+in+the+United+States%3A+what+works+for+what.&rft.au=Tomas%2C+J+M%3BKozel%2C+N+J&rft.aulast=Tomas&rft.aufirst=J&rft.date=1991-01-01&rft.volume=11&rft.issue=1&rft.spage=5&rft.isbn=&rft.btitle=&rft.title=Journal+of+addictive+diseases&rft.issn=10550887&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-04-02 N1 - Date created - 1992-04-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Infectious diseases and drug abuse. Prevention and treatment in the drug abuse treatment system. AN - 72644717; 1787552 AB - Several communicable infectious diseases, including AIDS, hepatitis B infection, gonorrhea, syphilis, and tuberculosis, are increasing among drug abusers. Drug abuse treatment programs may be ideal sites to identify those infections and initiate and maintain appropriate medical management. This paper reviews the epidemiology of those infections among drug abusers in the USA, presents rudimentary aspects of medical management of selected infectious diseases, and discusses the need to integrate infectious diseases, drug abuse treatment, and public health approaches if we are to reverse, or at least stabilize, the trends of those diseases. JF - Journal of substance abuse treatment AU - Haverkos, H W AD - Division of Clinical Research, National Institute on Drug Abuse, United States Public Health Service, Rockville, Maryland 20857. Y1 - 1991 PY - 1991 DA - 1991 SP - 269 EP - 275 VL - 8 IS - 4 SN - 0740-5472, 0740-5472 KW - Index Medicus KW - AIDS/HIV KW - Gonorrhea -- transmission KW - Hepatitis B -- prevention & control KW - HIV Infections -- transmission KW - Risk Factors KW - Humans KW - HIV Infections -- prevention & control KW - Tuberculosis, Pulmonary -- transmission KW - Tuberculosis, Pulmonary -- prevention & control KW - Syphilis -- transmission KW - Syphilis -- prevention & control KW - Hepatitis B -- transmission KW - Gonorrhea -- prevention & control KW - Communicable Disease Control -- methods KW - Substance Abuse, Intravenous -- rehabilitation KW - Substance Abuse, Intravenous -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72644717?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+substance+abuse+treatment&rft.atitle=Infectious+diseases+and+drug+abuse.+Prevention+and+treatment+in+the+drug+abuse+treatment+system.&rft.au=Haverkos%2C+H+W&rft.aulast=Haverkos&rft.aufirst=H&rft.date=1991-01-01&rft.volume=8&rft.issue=4&rft.spage=269&rft.isbn=&rft.btitle=&rft.title=Journal+of+substance+abuse+treatment&rft.issn=07405472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-23 N1 - Date created - 1992-03-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Basal forebrain involvement in self-administration of drugs of abuse. AN - 72632208; 1776576 JF - Advances in experimental medicine and biology AU - Porrino, L J AU - Dworkin, S I AU - Smith, J E AD - Unit on Brain Imaging, NINDS, Bethesda, MD. Y1 - 1991 PY - 1991 DA - 1991 SP - 339 EP - 351 VL - 295 SN - 0065-2598, 0065-2598 KW - Neurotoxins KW - 0 KW - Heroin KW - 70D95007SX KW - Morphine KW - 76I7G6D29C KW - Amphetamine KW - CK833KGX7E KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Animals KW - Amphetamine -- administration & dosage KW - Morphine -- administration & dosage KW - Neurotoxins -- toxicity KW - Cocaine -- administration & dosage KW - Heroin -- administration & dosage KW - Substance-Related Disorders -- physiopathology KW - Self Administration KW - Prosencephalon -- drug effects KW - Prosencephalon -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72632208?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advances+in+experimental+medicine+and+biology&rft.atitle=Basal+forebrain+involvement+in+self-administration+of+drugs+of+abuse.&rft.au=Porrino%2C+L+J%3BDworkin%2C+S+I%3BSmith%2C+J+E&rft.aulast=Porrino&rft.aufirst=L&rft.date=1991-01-01&rft.volume=295&rft.issue=&rft.spage=339&rft.isbn=&rft.btitle=&rft.title=Advances+in+experimental+medicine+and+biology&rft.issn=00652598&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-02 N1 - Date created - 1992-03-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cellular and molecular mechanisms of chemically induced renal carcinogenesis. AN - 72632035; 1780490 JF - Renal failure AU - Barrett, J C AU - Huff, J AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991 PY - 1991 DA - 1991 SP - 211 EP - 225 VL - 13 IS - 4 SN - 0886-022X, 0886-022X KW - Index Medicus KW - Rats KW - Animals KW - Carcinogenicity Tests KW - Mice KW - Male KW - Female KW - Cricetinae KW - Kidney Neoplasms -- genetics KW - Oncogenes KW - Kidney Neoplasms -- chemically induced KW - Genes, Tumor Suppressor KW - Proto-Oncogenes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72632035?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Renal+failure&rft.atitle=Cellular+and+molecular+mechanisms+of+chemically+induced+renal+carcinogenesis.&rft.au=Barrett%2C+J+C%3BHuff%2C+J&rft.aulast=Barrett&rft.aufirst=J&rft.date=1991-01-01&rft.volume=13&rft.issue=4&rft.spage=211&rft.isbn=&rft.btitle=&rft.title=Renal+failure&rft.issn=0886022X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-12 N1 - Date created - 1992-03-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Sustainability of forestomach hyperplasia in rats treated with ethyl acrylate for 13 weeks and regression after cessation of dosing. AN - 72629332; 1723532 AB - In a chronic study conducted by the National Toxicology Program (NTP), gavage administration of 100 or 200 mg ethyl acrylate (EA)/kg/day, 5 days/week, to F344 rats and B6C3F1 mice resulted in a significant dose-dependent increase in the incidence of squamous cell papillomas and carcinomas of the forestomach of both sexes of rats and mice. No increase in the incidence of tumors was observed at any other site in these rats. Chemically-induced cell proliferation is currently thought to play a role in the development and progression of chemically-induced neoplasia. Therefore, a stop-study was initiated where 100 or 200 mg EA/kg (in corn oil) was administered daily, 5 days/week, for 13 weeks. Rats sacrificed at the end of the treatment regimen had severe epithelial hyperplasia of the forestomach. No lesions were observed in the glandular stomach or liver of EA-treated rats. Forestomach hyperplasia induced by EA included upward and downward cell proliferation. However, forestomachs of rats treated for 13 weeks and sacrificed 8 weeks after the last EA dose exhibited a significant decline in the incidence and severity of forestomach mucosal hyperplasia. Histopathologic evaluation of forestomachs of EA-treated rats (13 weeks) which were allowed a 19-month-recovery (with no exposure to EA) showed further decline in the incidence and severity of mucosal cell hyperplasia. These results indicate that gavage administration of EA to rats results in extensive and sustained forestomach mucosal hyperplasia. The sustainability of forestomach hyperplasia is apparently dependent on the continued exposure of rats to ethyl acrylate, and regressed after cessation of dosing. Furthermore, although enough post-treatment time was allowed for tumors to develop after cessation of EA administration, forestomachs exhibited a nearly complete recovery with no increased incidence of papillomas or carcinomas. It, therefore, remains to be determined what duration of exposure or other factors are critical for reversibility or progression of EA-induced forestomach mucosal hyperplasia to neoplasia. JF - Toxicologic pathology AU - Ghanayem, B I AU - Matthews, H B AU - Maronpot, R R AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991 PY - 1991 DA - 1991 SP - 273 EP - 279 VL - 19 IS - 3 SN - 0192-6233, 0192-6233 KW - Acrylates KW - 0 KW - ethyl acrylate KW - 71E6178C9T KW - Index Medicus KW - Rats KW - Neoplasm Regression, Spontaneous -- pathology KW - Animals KW - Rats, Inbred F344 KW - Hyperplasia -- chemically induced KW - Epithelial Cells KW - Liver -- drug effects KW - Cell Division -- drug effects KW - Time Factors KW - Staining and Labeling KW - Male KW - Epithelium -- drug effects KW - Stomach -- pathology KW - Stomach -- drug effects KW - Acrylates -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72629332?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+pathology&rft.atitle=Sustainability+of+forestomach+hyperplasia+in+rats+treated+with+ethyl+acrylate+for+13+weeks+and+regression+after+cessation+of+dosing.&rft.au=Ghanayem%2C+B+I%3BMatthews%2C+H+B%3BMaronpot%2C+R+R&rft.aulast=Ghanayem&rft.aufirst=B&rft.date=1991-01-01&rft.volume=19&rft.issue=3&rft.spage=273&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=01926233&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-11 N1 - Date created - 1992-03-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Critical periods of neuroendocrine development: effects of prenatal xenobiotics. AN - 72629135; 1781340 AB - Phenobarbital, when administered prenatally in a small dose to animals, produced profound, and permanent effects on reproductive function in the offspring. Preliminary analysis of a unique cohort of adolescents who were exposed to phenobarbital in utero, suggests that long-term effects are also evident in the human. The precise nature of these effects is currently being determined and will be reported separately. These effects may be qualitatively and quantitatively different from effects seen in animals because of species difference in the timing or neuroendocrine differentiation. Of greater importance, however, is the fact that biologic and pharmacologic effects can be seen in the human following exposure to xenobiotics perinatally. Implications for other pharmacologic agents await further investigation. The rat model appears to have validity for extrapolation to man. JF - Advances in experimental medicine and biology AU - Yaffe, S J AU - Dorn, L D AD - National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 81 EP - 89 VL - 296 SN - 0065-2598, 0065-2598 KW - Phenobarbital KW - YQE403BP4D KW - Index Medicus KW - Animals KW - Reference Values KW - Double-Blind Method KW - Humans KW - Infant, Newborn KW - Genitalia, Male -- abnormalities KW - Follow-Up Studies KW - Estrus -- drug effects KW - Male KW - Female KW - Pregnancy KW - Maternal-Fetal Exchange KW - Phenobarbital -- adverse effects KW - Jaundice, Neonatal -- prevention & control KW - Phenobarbital -- toxicity KW - Phenobarbital -- therapeutic use KW - Embryonic and Fetal Development -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72629135?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advances+in+experimental+medicine+and+biology&rft.atitle=Critical+periods+of+neuroendocrine+development%3A+effects+of+prenatal+xenobiotics.&rft.au=Yaffe%2C+S+J%3BDorn%2C+L+D&rft.aulast=Yaffe&rft.aufirst=S&rft.date=1991-01-01&rft.volume=296&rft.issue=&rft.spage=81&rft.isbn=&rft.btitle=&rft.title=Advances+in+experimental+medicine+and+biology&rft.issn=00652598&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-10 N1 - Date created - 1992-03-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Results of extended peptide T administration in AIDS and ARC patients. AN - 72627205; 1775594 AB - We report here the extended Phase I testing of d-ala-Peptide-T-amide (Peptide T) in open trial. The drug was given intravenously in doses ranging from 0.1 to 3.2 mg/kg/day to 14 acquired immunodeficiency syndrome (AIDS) and AIDS-related complex (ARC) patients for 12 weeks. Following a 4-week off-drug period, the first 6 patients finishing the intravenous testing were continued on intranasal drug, 25 mg/day, for 8 weeks. Control subjects were tested on the same neuropsychologic tests, but did not receive drug. Minimal evidence of toxicity was found. Performance increments in cognitive and neuromotor function were observed in patients with moderate neuropsychologic impairment compared with controls. Changes in constitutional symptoms included weight gain averaging 2 kg and reported improved sense of well-being. The latter findings were independent of variation in cognitive and neuromotor function. Measures of immunologic function and antiviral activity did not change significantly during the study. These data provide a scientific rationale for Phase II testing of Peptide T in human immunodeficiency virus-1 (HIV-1) patients focusing on neuropsychiatric outcome. JF - Psychopharmacology bulletin AU - Bridge, T P AU - Heseltine, P N AU - Parker, E S AU - Eaton, E M AU - Ingraham, L J AU - McGrail, M L AU - Goodwin, F K AD - Intramural Research Program, NIMH, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 237 EP - 245 VL - 27 IS - 3 SN - 0048-5764, 0048-5764 KW - Peptide T KW - 106362-33-8 KW - Index Medicus KW - AIDS/HIV KW - Drug Evaluation KW - Humans KW - Adult KW - Middle Aged KW - Male KW - Peptide T -- adverse effects KW - Peptide T -- therapeutic use KW - AIDS-Related Complex -- psychology KW - AIDS-Related Complex -- drug therapy KW - Acquired Immunodeficiency Syndrome -- psychology KW - Acquired Immunodeficiency Syndrome -- drug therapy KW - Peptide T -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72627205?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychopharmacology+bulletin&rft.atitle=Results+of+extended+peptide+T+administration+in+AIDS+and+ARC+patients.&rft.au=Bridge%2C+T+P%3BHeseltine%2C+P+N%3BParker%2C+E+S%3BEaton%2C+E+M%3BIngraham%2C+L+J%3BMcGrail%2C+M+L%3BGoodwin%2C+F+K&rft.aulast=Bridge&rft.aufirst=T&rft.date=1991-01-01&rft.volume=27&rft.issue=3&rft.spage=237&rft.isbn=&rft.btitle=&rft.title=Psychopharmacology+bulletin&rft.issn=00485764&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-02 N1 - Date created - 1992-03-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Addition of a C-terminal extension sequence to transforming growth factor-beta 1 interferes with biosynthetic processing and abolishes biological activity. AN - 72624593; 1663772 AB - Transforming growth factor-beta 1 (TGF-beta 1) is synthesized and secreted as a biologically latent complex. It has been proposed that one role of the latent complex is to prevent premature interaction of ligand and receptor intracellularly during biosynthesis (Wakefield et al., J. Cell Biol. (1987) 105, 965-975). To test this hypothesis, the endoplasmic reticulum retention sequence Lys-Asp-Glu-Leu (KDEL) was added to the C-terminus of the wildtype TGF-beta 1 coding sequence, and to a construct in which mutagenesis of two cysteine residues in the precursor pro region results in the synthesis and secretion of active, as opposed to latent, TGF-beta. Addition of either SEKDEL, or the control sequence SEKDVS to the TGF-beta 1 protein abolished biological activity. Western blot analysis indicated that the extended gene products are synthesized, but that the extension sequence partially interferes with the normal dimerization of the protein product, and totally inhibits the normal proteolytic processing and glycosylation of the precursor protein. The data suggest that correct folding of the highly conserved C terminus of TGF-beta 1 is critical for subsequent proteolytic cleavage and glycosylation at sites that are quite distant in the primary sequence. Thus molecular strategies for the generation of TGF-beta antagonists or superagonists should avoid extensive modification of this region of the molecule. Since synthesis of the endogenous TGF-beta 1 is unaffected by the presence of the mutated analog, the data further indicate that transfection with the KDEL-extended TGF-beta 1 sequence cannot be used as a dominant negative mutation to prevent secretion of the endogenous TGF-beta protein. JF - Growth factors (Chur, Switzerland) AU - Wakefield, L M AU - Kondaiah, P AU - Hollands, R S AU - Winokur, T S AU - Sporn, M B AD - Laboratory of Chemoprevention, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 243 EP - 253 VL - 5 IS - 3 SN - 0897-7194, 0897-7194 KW - Protein Precursors KW - 0 KW - Receptors, Cell Surface KW - Receptors, Transforming Growth Factor beta KW - Transforming Growth Factor beta KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Swine KW - Animals KW - Blotting, Northern KW - Amino Acid Sequence KW - Glycosylation KW - Plasmids KW - Cloning, Molecular KW - Receptors, Cell Surface -- metabolism KW - Mutagenesis, Site-Directed KW - Base Sequence KW - Blotting, Western KW - Transfection KW - Molecular Sequence Data KW - Protein Conformation KW - Protein Precursors -- metabolism KW - Protein Precursors -- chemistry KW - Protein Precursors -- genetics KW - Transforming Growth Factor beta -- chemistry KW - Transforming Growth Factor beta -- genetics KW - Transforming Growth Factor beta -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72624593?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Growth+factors+%28Chur%2C+Switzerland%29&rft.atitle=Addition+of+a+C-terminal+extension+sequence+to+transforming+growth+factor-beta+1+interferes+with+biosynthetic+processing+and+abolishes+biological+activity.&rft.au=Wakefield%2C+L+M%3BKondaiah%2C+P%3BHollands%2C+R+S%3BWinokur%2C+T+S%3BSporn%2C+M+B&rft.aulast=Wakefield&rft.aufirst=L&rft.date=1991-01-01&rft.volume=5&rft.issue=3&rft.spage=243&rft.isbn=&rft.btitle=&rft.title=Growth+factors+%28Chur%2C+Switzerland%29&rft.issn=08977194&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-12 N1 - Date created - 1992-03-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human cytochrome P450: possible roles of drug-metabolizing enzymes and polymorphic drug oxidation in addiction. AN - 72623883; 1775182 JF - NIDA research monograph AU - Gonzalez, F J AD - Nucleic Acid Section, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 202 EP - 213 VL - 111 SN - 1046-9516, 1046-9516 KW - Pharmaceutical Preparations KW - 0 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Oxidation-Reduction KW - Humans KW - Pharmaceutical Preparations -- metabolism KW - Polymorphism, Genetic KW - Cytochrome P-450 Enzyme System -- genetics KW - Cytochrome P-450 Enzyme System -- physiology KW - Substance-Related Disorders -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72623883?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Human+cytochrome+P450%3A+possible+roles+of+drug-metabolizing+enzymes+and+polymorphic+drug+oxidation+in+addiction.&rft.au=Gonzalez%2C+F+J&rft.aulast=Gonzalez&rft.aufirst=F&rft.date=1991-01-01&rft.volume=111&rft.issue=&rft.spage=202&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-03-02 N1 - Date created - 1992-03-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Light intensity-associated eye lesions of Fischer 344 rats in long-term studies. AN - 72616283; 1663269 AB - Albino rats and mice are sensitive to light and the recommended illumination of animal rooms (75-125 ft-candles) is known to cause retinal damage. When a room is illuminated by ceiling lights, animals in the cages of the top row and, to some extent, in the side columns of cage racks will be exposed to higher light intensity than those in the other cages of the rack. In 2-yr chemical carcinogenicity studies of the National Toxicology Program (previously the Carcinogenicity Bioassay Program of the National Cancer Institute), Fischer 344 rats were group-housed in hanging drawer-type clear polycarbonate cages. During the course of the chronic studies, a number of rats developed opacity of the eye. Ocular examination indicated chronic uveitis, deep interstitial keratitis, cataract formation leading to panophthalmitis, and in severe cases, phthisis bulbi. Histologic examination showed cataract and retinal degeneration. Incidences of these lesions were highest (greater than 55%) in the rats of the top rows and lowest in those of the bottom rows (less than 10%) of cages with no relation to chemical treatment, indicating an association with light intensity. The incidence of these eye lesions was markedly decreased (less than 15%) by decreasing the light intensity of the animal room to less than 50 ft-candles at 5 ft from the floor and rotating the cages in each column of a rack from top to bottom when cages or racks were changed. JF - Toxicologic pathology AU - Rao, G N AD - Division of Toxicology Research and Testing, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991 PY - 1991 DA - 1991 SP - 148 EP - 155 VL - 19 IS - 2 SN - 0192-6233, 0192-6233 KW - Index Medicus KW - Animals KW - Paramyxoviridae Infections -- prevention & control KW - Retrospective Studies KW - Uveitis -- etiology KW - Cataract -- etiology KW - Coronaviridae Infections -- etiology KW - Rats KW - Rats, Inbred F344 KW - Cataract -- prevention & control KW - Uveitis -- epidemiology KW - Keratitis -- prevention & control KW - Time Factors KW - Male KW - Uveitis -- prevention & control KW - Coronaviridae Infections -- epidemiology KW - Keratitis -- epidemiology KW - Cataract -- epidemiology KW - Eye Infections, Viral -- epidemiology KW - Eye Infections, Viral -- prevention & control KW - Keratitis -- etiology KW - Paramyxoviridae Infections -- etiology KW - Incidence KW - Coronaviridae Infections -- prevention & control KW - Paramyxoviridae Infections -- epidemiology KW - Female KW - Eye Infections, Viral -- etiology KW - Eye Diseases -- etiology KW - Eye Diseases -- epidemiology KW - Light KW - Eye Diseases -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72616283?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+pathology&rft.atitle=Light+intensity-associated+eye+lesions+of+Fischer+344+rats+in+long-term+studies.&rft.au=Rao%2C+G+N&rft.aulast=Rao&rft.aufirst=G&rft.date=1991-01-01&rft.volume=19&rft.issue=2&rft.spage=148&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=01926233&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-25 N1 - Date created - 1992-02-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Serotonergic modulation of the rat pup ultrasonic isolation call: studies with 5HT1 and 5HT2 subtype-selective agonists and antagonists. AN - 72613285; 1771219 AB - A modulatory role for serotonin has been described for the development and expression of the ultrasonic call of infant rat pups during brief maternal separations. In previous studies, serotonin reuptake inhibitors selectively reduced the rate of calling following acute administration to 9-11-day-old pups and a serotonin neurotoxin (MDMA) systematically disrupted the development of ultrasonic vocalizations but not other measures of motor development. In the current studies, we extended our investigations to include drugs with purported receptor subtype selectivities. Consistent with previous reports, acute administration of 5HT1A agonists buspirone and 8-OH-DPAT [+/-)-8-hydroxy-2-(di-N-propylamino)tetralin) reduced the rate of calling at doses which did not affect motor activity or core body temperature. The rate reducing effects of buspirone persisted up to 1 but not 2 h after injection. Administration of purported 5HT1B receptor agonists, CGS12066B (7-trifluoromethyl-4(4-methyl-1-piperazinyl)-pyrrolo[1,2-a] quinoxaline) and TFMPP (1-[3-fluoromethyl)phenyl]-piperazine) increased the rate of calling depending on the specificity of the drug for the 5HT1B receptor. d,l-Propranolol, a 5HT1 receptor antagonist, blocked the effects of both 8-OH-DPAT and TFMPP. m-CPP (1-(3-chlorophenyl)piperazine) and DOI [+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane), drugs with putative actions at 5HT1C and 5HT2 receptor sites both decreased calling but differed according to their effects on motor activity. Ritanserin, a 5HT2 and 5HT1C antagonist, produced a dose-related increase in call rate. A dose of ritanserin with no apparent intrinsic effects effectively antagonized DOI rate reducing effects but potentiated the rate reducing effects of m-CPP.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Psychopharmacology AU - Winslow, J T AU - Insel, T R AD - Laboratory of Clinical Science, National Institute of Mental Health, NIHAC, Poolesville, MD 20837. Y1 - 1991 PY - 1991 DA - 1991 SP - 513 EP - 520 VL - 105 IS - 4 SN - 0033-3158, 0033-3158 KW - Receptors, Serotonin KW - 0 KW - Serotonin Antagonists KW - Serotonin KW - 333DO1RDJY KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals, Newborn KW - Animals KW - Analysis of Variance KW - Anxiety, Separation -- physiopathology KW - Time Factors KW - Vocalization, Animal -- drug effects KW - Receptors, Serotonin -- drug effects KW - Serotonin -- pharmacology KW - Serotonin Antagonists -- pharmacology KW - Receptors, Serotonin -- classification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72613285?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychopharmacology&rft.atitle=Serotonergic+modulation+of+the+rat+pup+ultrasonic+isolation+call%3A+studies+with+5HT1+and+5HT2+subtype-selective+agonists+and+antagonists.&rft.au=Winslow%2C+J+T%3BInsel%2C+T+R&rft.aulast=Winslow&rft.aufirst=J&rft.date=1991-01-01&rft.volume=105&rft.issue=4&rft.spage=513&rft.isbn=&rft.btitle=&rft.title=Psychopharmacology&rft.issn=00333158&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-27 N1 - Date created - 1992-02-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of profound insulin-induced hypoglycemia on quinolinic acid in hippocampus and plasma. AN - 72607829; 1722957 JF - Advances in experimental medicine and biology AU - Heyes, M P AU - Papagapiou, M AU - Leonard, C AU - Markey, S P AU - Auer, R N AD - Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, Maryland 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 679 EP - 682 VL - 294 SN - 0065-2598, 0065-2598 KW - Insulin KW - 0 KW - Quinolinic Acids KW - Receptors, N-Methyl-D-Aspartate KW - Serotonin KW - 333DO1RDJY KW - Hydroxyindoleacetic Acid KW - 54-16-0 KW - Tryptophan KW - 8DUH1N11BX KW - Quinolinic Acid KW - F6F0HK1URN KW - Index Medicus KW - Animals KW - Dialysis KW - Serotonin -- analysis KW - Hydroxyindoleacetic Acid -- analysis KW - Extracellular Space -- chemistry KW - Brain Chemistry KW - Electroencephalography KW - Rats KW - Rats, Inbred Strains KW - Receptors, N-Methyl-D-Aspartate -- physiology KW - Tryptophan -- analysis KW - Insulin -- toxicity KW - Male KW - Hypoglycemia -- metabolism KW - Quinolinic Acids -- blood KW - Hippocampus -- metabolism KW - Quinolinic Acids -- metabolism KW - Brain Diseases, Metabolic -- metabolism KW - Brain Diseases, Metabolic -- chemically induced KW - Hypoglycemia -- chemically induced KW - Brain Diseases, Metabolic -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72607829?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advances+in+experimental+medicine+and+biology&rft.atitle=Effects+of+profound+insulin-induced+hypoglycemia+on+quinolinic+acid+in+hippocampus+and+plasma.&rft.au=Heyes%2C+M+P%3BPapagapiou%2C+M%3BLeonard%2C+C%3BMarkey%2C+S+P%3BAuer%2C+R+N&rft.aulast=Heyes&rft.aufirst=M&rft.date=1991-01-01&rft.volume=294&rft.issue=&rft.spage=679&rft.isbn=&rft.btitle=&rft.title=Advances+in+experimental+medicine+and+biology&rft.issn=00652598&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-25 N1 - Date created - 1992-02-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Targets of herpes simplex virus type 1 infection in a mouse corneal model. AN - 72606882; 1662854 AB - In animal models, spread of herpes simplex virus type 1 (HSV-1) from epithelial replication sites to the peripheral and central nervous system is known from analysis of individually dissected tissues. To examine virus spread in undissociated tissues, corneas of adult mice were inoculated with HSV-1. After 1 to 13 days groups of mice were perfused with formalin, and decalcified blocks of head and neck were embedded in paraffin. At intervals, serial sections were screened for HSV antigen. On days 1 and 2, viral antigen was restricted to cornea and conjunctiva but by days 3 and 4 was also seen in autonomic ganglia and the trigeminal system. On day 6, HSV antigen reached its maximum extent; infected sites included the trigeminal complex (ganglion, root, peripheral ophthalmic and maxillary branches and spinal nucleus and tract), ethmoid sinus and olfactory bulb, visual system, and autonomic ganglia (ciliary, pterygopalatine and superior cervical). Antigen progressively diminished on days 8 and 10, and was not detected on day 13. This method demonstrates a broader range of infected tissues and suggests a more complex pattern of HSV spread than has been previously recognized. Virus appears to reach the intracranial compartment by four different neural routes. When effects of higher and lower corneal inoculation doses were compared, a lower dose resulted in lower peak HSV titers in trigeminal ganglion and brain stem and later virus appearance in these tissues. Thus, dose may influence the kinetics of HSV spread from the peripheral inoculation site to the CNS. JF - Acta neuropathologica AU - Martin, J R AU - Jenkins, F J AU - Henken, D B AD - Laboratory of Experimental Neuropathology, NINDS, NIH, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 353 EP - 363 VL - 82 IS - 5 SN - 0001-6322, 0001-6322 KW - Antigens, Viral KW - 0 KW - Index Medicus KW - Brain Stem -- microbiology KW - Animals KW - Simplexvirus -- isolation & purification KW - Trigeminal Ganglion -- microbiology KW - Lethal Dose 50 KW - Simplexvirus -- physiology KW - Mice KW - Simplexvirus -- immunology KW - Mice, Inbred BALB C KW - Eye -- microbiology KW - Female KW - Antigens, Viral -- analysis KW - Herpes Simplex -- immunology KW - Herpes Simplex -- microbiology KW - Corneal Diseases -- microbiology KW - Corneal Diseases -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72606882?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Acta+neuropathologica&rft.atitle=Targets+of+herpes+simplex+virus+type+1+infection+in+a+mouse+corneal+model.&rft.au=Martin%2C+J+R%3BJenkins%2C+F+J%3BHenken%2C+D+B&rft.aulast=Martin&rft.aufirst=J&rft.date=1991-01-01&rft.volume=82&rft.issue=5&rft.spage=353&rft.isbn=&rft.btitle=&rft.title=Acta+neuropathologica&rft.issn=00016322&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-19 N1 - Date created - 1992-02-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparison of two non-cross-resistant combinations (ABVP/LOPP) with COPP plus bleomycin in the treatment of advanced Hodgkin's disease. AN - 72605047; 1722564 AB - Eighty patients with advanced Hodgkin's disease were randomized either to treatment with combination of doxorubicin, bleomycin, vinblastine, and prednisone (ABVP), alternating with lomustine, vincristine, procarbazine, and prednisone (LOPP)--Group A, or to combination of cyclophosphamide, vincristine, procarbazine, prednisone, and low dose of bleomycin (COPP-Bleo)--Group B. Thirty-nine out of 41 patients (95%) in Group A achieved complete remission (CR) as compared to 25 CR in 39 patients (64%) in Group B. Patients with systemic symptoms, bulky disease, and nodular sclerosis achieved significantly more CR after treatment with ABVP/LOPP regimen than with COPP-Bleo regimen. Ninety percent of patients are alive in Group A (median observation time 97+ months) as compared to 58% in Group B (median observation time 97+ months). Ninety-two percent of complete responders are in CR in Group A as compared to 53% of complete responders in Group B. These differences between both groups are significant. More serious (WHO grade III and IV) myelosuppression as well as stomatitis and alopecia were observed in Group A. Gastrointestinal toxicity and neurotoxicity was more frequent in Group A. No patient died due to toxicity in Group A as compared to one patient in Group B. Non-cross-resistant alternating regimen ABVP/LOPP was more effective in the treatment of advanced Hodgkin's disease than the COPP-Bleo regimen, especially for patients with advanced Stage IVB Hodgkin's disease. JF - Neoplasma AU - Koza, I AU - Bohunický, L AU - Mociková, K AU - Gyárfás, J AU - Svancárová, L AU - Mardiak, J AU - Spánik, S AU - Fuchsberger, P AU - Thalmeinerová, Z AU - Sufliarsky, J AD - National Cancer Institute, Bratislava, Czechoslovakia. Y1 - 1991 PY - 1991 DA - 1991 SP - 583 EP - 593 VL - 38 IS - 6 SN - 0028-2685, 0028-2685 KW - Bleomycin KW - 11056-06-7 KW - Procarbazine KW - 35S93Y190K KW - Vincristine KW - 5J49Q6B70F KW - Lomustine KW - 7BRF0Z81KG KW - Doxorubicin KW - 80168379AG KW - Cyclophosphamide KW - 8N3DW7272P KW - Prednisolone KW - 9PHQ9Y1OLM KW - Prednisone KW - VB0R961HZT KW - Index Medicus KW - Bleomycin -- administration & dosage KW - Prednisone -- therapeutic use KW - Humans KW - Lomustine -- therapeutic use KW - Aged KW - Drug Resistance KW - Cause of Death KW - Prednisolone -- therapeutic use KW - Procarbazine -- therapeutic use KW - Cyclophosphamide -- therapeutic use KW - Survival Rate KW - Vincristine -- therapeutic use KW - Adult KW - Middle Aged KW - Doxorubicin -- therapeutic use KW - Adolescent KW - Bleomycin -- therapeutic use KW - Male KW - Female KW - Hodgkin Disease -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Hodgkin Disease -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72605047?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neoplasma&rft.atitle=Comparison+of+two+non-cross-resistant+combinations+%28ABVP%2FLOPP%29+with+COPP+plus+bleomycin+in+the+treatment+of+advanced+Hodgkin%27s+disease.&rft.au=Koza%2C+I%3BBohunick%C3%BD%2C+L%3BMocikov%C3%A1%2C+K%3BGy%C3%A1rf%C3%A1s%2C+J%3BSvanc%C3%A1rov%C3%A1%2C+L%3BMardiak%2C+J%3BSp%C3%A1nik%2C+S%3BFuchsberger%2C+P%3BThalmeinerov%C3%A1%2C+Z%3BSufliarsky%2C+J&rft.aulast=Koza&rft.aufirst=I&rft.date=1991-01-01&rft.volume=38&rft.issue=6&rft.spage=583&rft.isbn=&rft.btitle=&rft.title=Neoplasma&rft.issn=00282685&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-20 N1 - Date created - 1992-02-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Vulnerability to cardiac disease. AN - 72579125; 1758986 AB - Chronic consumption of ethanol has deleterious effects on the cardiovascular system, as manifested by an attenuation in myocardial contractility, a reduction in cardiac output, and the induction of arrhythmia. The arrhythmogenic effect of ethanol is associated with the high incidence of sudden death in alcoholics. Further, alcohol was found to potentiate arrhythmias due to nonpenetrating chest trauma, a finding of profound clinical significance. In addition, chronic ethanol consumption is closely linked to hypertension. Whether modest alcohol consumption may protect against coronary artery disease is controversial and not clearly established. Cessation of alcohol consumption occasionally results in reversal of ethanol-induced myocardial injury. However, the transition from ethanol-induced reversible injury to permanent heart damage is not well understood. Finally, the combined effects on the myocardium of alcohol and other abused drugs, such as cocaine and amphetamines, and the interaction of ethanol with chemicals such as nicotine, digitalis, and other medicaments are not well understood and may be fatal. JF - Recent developments in alcoholism : an official publication of the American Medical Society on Alcoholism, the Research Society on Alcoholism, and the National Council on Alcoholism AU - Zakhari, S AD - Biomedical Research Branch, National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland 20857. Y1 - 1991 PY - 1991 DA - 1991 SP - 225 EP - 260 VL - 9 SN - 0738-422X, 0738-422X KW - Index Medicus KW - Hemodynamics -- drug effects KW - Animals KW - Death, Sudden -- etiology KW - Risk Factors KW - Humans KW - Electrocardiography -- drug effects KW - Cardiomyopathy, Alcoholic -- diagnosis KW - Alcoholic Beverages -- adverse effects KW - Cardiomyopathy, Alcoholic -- etiology KW - Alcoholism -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72579125?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Recent+developments+in+alcoholism+%3A+an+official+publication+of+the+American+Medical+Society+on+Alcoholism%2C+the+Research+Society+on+Alcoholism%2C+and+the+National+Council+on+Alcoholism&rft.atitle=Vulnerability+to+cardiac+disease.&rft.au=Zakhari%2C+S&rft.aulast=Zakhari&rft.aufirst=S&rft.date=1991-01-01&rft.volume=9&rft.issue=&rft.spage=225&rft.isbn=&rft.btitle=&rft.title=Recent+developments+in+alcoholism+%3A+an+official+publication+of+the+American+Medical+Society+on+Alcoholism%2C+the+Research+Society+on+Alcoholism%2C+and+the+National+Council+on+Alcoholism&rft.issn=0738422X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-06 N1 - Date created - 1992-02-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Transient impairment of recognition memory following ibotenic-acid lesions of the basal forebrain in macaques. AN - 72578833; 1756788 AB - To assess the contributions of the basal forebrain cholinergic nuclei to visual recognition memory in macaques, we compared the effects of lesions of (a) the nucleus basalis of Meynert, (b) the medial septal and diagonal band nuclei, and (c) all nuclei combined on performance of delayed nonmatching-to-sample with trial-unique stimuli. Whereas monkeys with the separate lesions did not differ from each other or from normal control animals, those with combined lesions showed a significant impairment. With time and extended practice, however, the performance of the animals with combined lesions recovered to normal levels. During the recovery period, these monkeys showed an initially increased sensitivity to scopolamine that later dissipated, at which time they also failed to show the improvement that follows physostigmine administration in normal animals. Postmortem assessment of cortical choline acetyltransferase activity revealed that only the group with combined lesions had significant depletion of this enzyme. The results suggest that (1) the basal forebrain cholinergic system participates in mnemonic processes in primates and that (2) extensive damage to this system is necessary before impairments in recognition memory, even transient ones, can be observed. JF - Experimental brain research AU - Aigner, T G AU - Mitchell, S J AU - Aggleton, J P AU - DeLong, M R AU - Struble, R G AU - Price, D L AU - Wenk, G L AU - Pettigrew, K D AU - Mishkin, M AD - Laboratory of Neuropsychology, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 18 EP - 26 VL - 86 IS - 1 SN - 0014-4819, 0014-4819 KW - Ibotenic Acid KW - 2552-55-8 KW - Scopolamine Hydrobromide KW - 451IFR0GXB KW - Physostigmine KW - 9U1VM840SP KW - Choline O-Acetyltransferase KW - EC 2.3.1.6 KW - Acetylcholinesterase KW - EC 3.1.1.7 KW - Index Medicus KW - Substantia Innominata -- metabolism KW - Animals KW - Scopolamine Hydrobromide -- pharmacology KW - Macaca fascicularis KW - Cerebral Cortex -- enzymology KW - Physostigmine -- pharmacology KW - Acetylcholinesterase -- metabolism KW - Substantia Innominata -- drug effects KW - Choline O-Acetyltransferase -- metabolism KW - Visual Perception KW - Parasympathetic Nervous System -- physiology KW - Cognition -- drug effects KW - Memory -- drug effects KW - Parasympathetic Nervous System -- drug effects KW - Prosencephalon -- enzymology KW - Prosencephalon -- drug effects KW - Ibotenic Acid -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72578833?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+brain+research&rft.atitle=Transient+impairment+of+recognition+memory+following+ibotenic-acid+lesions+of+the+basal+forebrain+in+macaques.&rft.au=Aigner%2C+T+G%3BMitchell%2C+S+J%3BAggleton%2C+J+P%3BDeLong%2C+M+R%3BStruble%2C+R+G%3BPrice%2C+D+L%3BWenk%2C+G+L%3BPettigrew%2C+K+D%3BMishkin%2C+M&rft.aulast=Aigner&rft.aufirst=T&rft.date=1991-01-01&rft.volume=86&rft.issue=1&rft.spage=18&rft.isbn=&rft.btitle=&rft.title=Experimental+brain+research&rft.issn=00144819&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-31 N1 - Date created - 1992-01-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Affinity of antineoplastic amino acid drugs for the large neutral amino acid transporter of the blood-brain barrier. AN - 72578618; 1760863 AB - The relative affinity of six anticancer amino acid drugs for the neutral amino acid carrier of the blood-brain barrier was examined in rats using an in situ brain perfusion technique. Affinity was evaluated from the concentration-dependent inhibition of L-[14C]-leucine uptake into rat brain during perfusion at tracer leucine concentrations and in the absence of competing amino acids. Of the six drugs tested, five, including melphalan, azaserine, acivicin, 6-diazo-5-oxo-L-norleucine, and buthionine sulfoximine, exhibited only low affinity for the carrier, displaying transport inhibition constants (Ki, concentrations producing 50% inhibition) ranging from 0.09 to 4.7 mM. However, one agent - D,L-2-amino-7-bis[(2-chloroethyl)amino]- 1,2,3,4-tetrahydro-2-naphthoic acid (D,L-NAM) - demonstrated remarkably high affinity for the carrier, showing a Ki value of approximately 0.2 microM. The relative affinity (1/Ki) of D,L-NAM was greater than 100-fold that of the other drugs and greater than 10-fold that of any compound previously tested. As the blood-brain barrier penetrability of most endogenous neutral amino acids is related to their carrier affinity, the results suggest that D,L-NAM may be a promising agent which may show enhanced uptake and distribution to brain tumors. JF - Cancer chemotherapy and pharmacology AU - Takada, Y AU - Greig, N H AU - Vistica, D T AU - Rapoport, S I AU - Smith, Q R AD - Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 89 EP - 94 VL - 29 IS - 2 SN - 0344-5704, 0344-5704 KW - Amino Acid Transport Systems KW - 0 KW - Carrier Proteins KW - Isoxazoles KW - Nitrogen Mustard Compounds KW - Diazooxonorleucine KW - 03J0H273KZ KW - 2-amino-7-(bis(2-chloroethyl)amino)-1,2,3,4-tetrahydro-2-naphthoic acid KW - 106094-83-1 KW - Methionine Sulfoximine KW - 1982-67-8 KW - Buthionine Sulfoximine KW - 5072-26-4 KW - Azaserine KW - 87299V3Q9W KW - 2-Naphthylamine KW - CKR7XL41N4 KW - acivicin KW - O0X60K76I6 KW - Melphalan KW - Q41OR9510P KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Male KW - Carrier Proteins -- pharmacokinetics KW - 2-Naphthylamine -- pharmacokinetics KW - Brain -- metabolism KW - Nitrogen Mustard Compounds -- pharmacokinetics KW - Isoxazoles -- pharmacokinetics KW - Methionine Sulfoximine -- analogs & derivatives KW - Azaserine -- pharmacokinetics KW - Melphalan -- pharmacokinetics KW - Diazooxonorleucine -- pharmacokinetics KW - 2-Naphthylamine -- analogs & derivatives KW - Methionine Sulfoximine -- pharmacokinetics KW - Blood-Brain Barrier UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72578618?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+chemotherapy+and+pharmacology&rft.atitle=Affinity+of+antineoplastic+amino+acid+drugs+for+the+large+neutral+amino+acid+transporter+of+the+blood-brain+barrier.&rft.au=Takada%2C+Y%3BGreig%2C+N+H%3BVistica%2C+D+T%3BRapoport%2C+S+I%3BSmith%2C+Q+R&rft.aulast=Takada&rft.aufirst=Y&rft.date=1991-01-01&rft.volume=29&rft.issue=2&rft.spage=89&rft.isbn=&rft.btitle=&rft.title=Cancer+chemotherapy+and+pharmacology&rft.issn=03445704&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-07 N1 - Date created - 1992-02-07 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Cancer Chemother Pharmacol 1992;30(2):164 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Health insurance coverage questions, public health surveys, and drug abuse. AN - 72578409; 1762640 JF - NIDA research monograph AU - Cartwright, W S AU - Woodward, A M AD - Financing and Services Research Branch, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1991 PY - 1991 DA - 1991 SP - 190 EP - 204 VL - 113 SN - 1046-9516, 1046-9516 KW - Index Medicus KW - United States KW - Health Expenditures KW - Humans KW - National Institutes of Health (U.S.) KW - Health Services Research KW - Adult KW - Child KW - Adolescent KW - Prevalence KW - Substance-Related Disorders -- therapy KW - Insurance, Health -- statistics & numerical data KW - Health Surveys KW - Substance-Related Disorders -- economics KW - Insurance, Health -- standards KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72578409?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Health+insurance+coverage+questions%2C+public+health+surveys%2C+and+drug+abuse.&rft.au=Cartwright%2C+W+S%3BWoodward%2C+A+M&rft.aulast=Cartwright&rft.aufirst=W&rft.date=1991-01-01&rft.volume=113&rft.issue=&rft.spage=190&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-11 N1 - Date created - 1992-02-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Coculture of neoplastic and normal keratinocytes as a model to study tumor promotion. AN - 72574353; 1764251 AB - In order to study skin tumor promotion, a cell culture model system analogous to initiated mouse epidermis was developed. Keratinocytes of the neoplastic cell line 308 display the initiated phenotype since papillomas are produced when the cells are grafted to the backs of athymic mice. Coculture of a small number of these initiated cells with confluent normal keratinocytes results in the suppression of growth of colonies of 308 cells. This inhibition, which is calcium dependent, epidermal cell specific, and requires cell contact, can be overcome by exposure to various tumor promoters. Promoters and antipromoters of diverse structure and mechanism of action are recognized in this keratinocyte coculture model. JF - Skin pharmacology : the official journal of the Skin Pharmacology Society AU - Hennings, H AU - Lowry, D T AU - Robinson, V A AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, National Institutes of Health, Bethesda, Md. Y1 - 1991 PY - 1991 DA - 1991 SP - 79 EP - 84 VL - 4 Suppl 1 SN - 1011-0283, 1011-0283 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Cells, Cultured KW - Calcium -- physiology KW - Cell Communication KW - Mice KW - Mice, Inbred BALB C KW - Models, Biological KW - Skin Neoplasms -- chemically induced KW - Keratinocytes -- cytology KW - Skin Neoplasms -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72574353?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Skin+pharmacology+%3A+the+official+journal+of+the+Skin+Pharmacology+Society&rft.atitle=Coculture+of+neoplastic+and+normal+keratinocytes+as+a+model+to+study+tumor+promotion.&rft.au=Hennings%2C+H%3BLowry%2C+D+T%3BRobinson%2C+V+A&rft.aulast=Hennings&rft.aufirst=H&rft.date=1991-01-01&rft.volume=4+Suppl+1&rft.issue=&rft.spage=79&rft.isbn=&rft.btitle=&rft.title=Skin+pharmacology+%3A+the+official+journal+of+the+Skin+Pharmacology+Society&rft.issn=10110283&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-20 N1 - Date created - 1992-02-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The effects of prenatal alcohol on the central nervous system. AN - 72573621; 1758981 AB - Prenatal alcohol exposure has a profound effect on the developing brain. In fetal alcohol syndrome (FAS), mental retardation and microcephaly are commonly observed. A partial syndrome, fetal alcohol effects (FAE) can result in neurobehavioral sequelae, which may present at birth or appear later in development. This chapter discusses the clinical evidence supporting the concept of FAE, the range of cognitive disturbances seen in FAS and FAE children, and studies on long-term outcome. We review studies that suggest that even in the absence of the stigmata of FAS, neonatal signs of central nervous system dysfunction may predict later developmental deviation. However, the clinical research on the cognitive and behavioral disorders in the FAE population is limited. Examination of electroencephalograms, evoked potentials, and sleep pattern provide additional evidence that the functional integrity of the brain has been altered. An abbreviated review of behavioral animal studies provides additional support for the clinical investigations presented. JF - Recent developments in alcoholism : an official publication of the American Medical Society on Alcoholism, the Research Society on Alcoholism, and the National Council on Alcoholism AU - Smith, K J AU - Eckardt, M J AD - Section of Clinical Brain Research, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 151 EP - 164 VL - 9 SN - 0738-422X, 0738-422X KW - Index Medicus KW - Fetal Growth Retardation -- etiology KW - Risk Factors KW - Humans KW - Neurologic Examination KW - Infant, Newborn KW - Fetal Growth Retardation -- prevention & control KW - Neuropsychological Tests KW - Fetal Growth Retardation -- diagnosis KW - Female KW - Pregnancy KW - Fetal Alcohol Spectrum Disorders -- prevention & control KW - Brain Damage, Chronic -- diagnosis KW - Alcohol Drinking -- adverse effects KW - Brain Damage, Chronic -- prevention & control KW - Brain Damage, Chronic -- etiology KW - Fetal Alcohol Spectrum Disorders -- etiology KW - Fetal Alcohol Spectrum Disorders -- diagnosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72573621?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Recent+developments+in+alcoholism+%3A+an+official+publication+of+the+American+Medical+Society+on+Alcoholism%2C+the+Research+Society+on+Alcoholism%2C+and+the+National+Council+on+Alcoholism&rft.atitle=The+effects+of+prenatal+alcohol+on+the+central+nervous+system.&rft.au=Smith%2C+K+J%3BEckardt%2C+M+J&rft.aulast=Smith&rft.aufirst=K&rft.date=1991-01-01&rft.volume=9&rft.issue=&rft.spage=151&rft.isbn=&rft.btitle=&rft.title=Recent+developments+in+alcoholism+%3A+an+official+publication+of+the+American+Medical+Society+on+Alcoholism%2C+the+Research+Society+on+Alcoholism%2C+and+the+National+Council+on+Alcoholism&rft.issn=0738422X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-06 N1 - Date created - 1992-02-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Potential biochemical markers for the predisposition toward alcoholism. AN - 72572579; 1758992 AB - For over two decades, evidence has been accumulating that supports a genetic predisposition to alcoholism and the presence of subgroups among alcoholics. With this knowledge, searches are underway for biological markers, including biochemical trait markers, for predisposition to alcoholism. Most promising results to date have been obtained in studies on various enzyme activities in lymphocytes, platelets, and fibroblasts. Measurement of monoamine oxidase activity in platelets and adenylate cyclase activity in platelets and lymphocytes should enable rapid investigation of relatively large groups of subjects at high risk to become alcoholics. Such studies could generate a valid biochemical marker for vulnerability in alcoholism, which is not available at the present time. JF - Recent developments in alcoholism : an official publication of the American Medical Society on Alcoholism, the Research Society on Alcoholism, and the National Council on Alcoholism AU - Eskay, R AU - Linnoila, M AD - Laboratory of Clinical Studies, DICBR, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 41 EP - 51 VL - 9 SN - 0738-422X, 0738-422X KW - Enzymes KW - 0 KW - Genetic Markers KW - Index Medicus KW - Risk Factors KW - Humans KW - Genetic Markers -- genetics KW - Enzymes -- blood KW - Alcoholism -- enzymology KW - Alcoholism -- genetics KW - Child of Impaired Parents KW - Enzymes -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72572579?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Recent+developments+in+alcoholism+%3A+an+official+publication+of+the+American+Medical+Society+on+Alcoholism%2C+the+Research+Society+on+Alcoholism%2C+and+the+National+Council+on+Alcoholism&rft.atitle=Potential+biochemical+markers+for+the+predisposition+toward+alcoholism.&rft.au=Eskay%2C+R%3BLinnoila%2C+M&rft.aulast=Eskay&rft.aufirst=R&rft.date=1991-01-01&rft.volume=9&rft.issue=&rft.spage=41&rft.isbn=&rft.btitle=&rft.title=Recent+developments+in+alcoholism+%3A+an+official+publication+of+the+American+Medical+Society+on+Alcoholism%2C+the+Research+Society+on+Alcoholism%2C+and+the+National+Council+on+Alcoholism&rft.issn=0738422X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-06 N1 - Date created - 1992-02-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Trends and patterns of methamphetamine smoking in Hawaii. AN - 72568135; 1758485 JF - NIDA research monograph AU - Miller, M A AD - Epidemiology Studies and Surveillance Branch, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1991 PY - 1991 DA - 1991 SP - 72 EP - 83 VL - 115 SN - 1046-9516, 1046-9516 KW - Amphetamine KW - CK833KGX7E KW - Index Medicus KW - Smoking -- trends KW - Humans KW - Hawaii -- epidemiology KW - Adult KW - Adolescent KW - Male KW - Female KW - Substance-Related Disorders -- ethnology KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72568135?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Trends+and+patterns+of+methamphetamine+smoking+in+Hawaii.&rft.au=Miller%2C+M+A&rft.aulast=Miller&rft.aufirst=M&rft.date=1991-01-01&rft.volume=115&rft.issue=&rft.spage=72&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-04 N1 - Date created - 1992-02-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Treating adults raised by alcoholic parents. AN - 72563878; 1758991 AB - The concept of adult children of alcoholics (ACOAs) is a recent one, yet ACOAs have had a formidable influence on the chemical dependence and mental health treatment field. Through their sponsorship of workshops and conferences, development of specialized inpatient and outpatient treatment programs, and generation of publications dedicated to understanding themselves with common interpersonal and intrapersonal problems, ACOAs have organized themselves into an influential social movement. Most ACOA treatment philosophies and programs are derived from the ACOA social movement using the concept of the "inner child" to guide the treatment. Unfortunately, few studies of treatment efficacy are available in the scientific literature. In this chapter, our discussion concentrates on the central treatment theme of the ACOA movement as it influences the treatment ideologies that currently guide ACOA treatment programs. We conclude by addressing the obvious need for research and the necessity for maintaining our ethical responsibility both in scientific inquiry and in the treatment of needy individuals. JF - Recent developments in alcoholism : an official publication of the American Medical Society on Alcoholism, the Research Society on Alcoholism, and the National Council on Alcoholism AU - Johnson, J L AU - Tiegel, S AD - Division of Applied Research, Community Research Branch, National Institute on Drug Abuse, Rockville, Maryland 20857. Y1 - 1991 PY - 1991 DA - 1991 SP - 347 EP - 359 VL - 9 SN - 0738-422X, 0738-422X KW - Index Medicus KW - Risk Factors KW - Humans KW - Adult KW - Alcoholism -- rehabilitation KW - Child of Impaired Parents -- psychology KW - Psychotherapy -- methods KW - Personality Development KW - Alcoholism -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72563878?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Recent+developments+in+alcoholism+%3A+an+official+publication+of+the+American+Medical+Society+on+Alcoholism%2C+the+Research+Society+on+Alcoholism%2C+and+the+National+Council+on+Alcoholism&rft.atitle=Treating+adults+raised+by+alcoholic+parents.&rft.au=Johnson%2C+J+L%3BTiegel%2C+S&rft.aulast=Johnson&rft.aufirst=J&rft.date=1991-01-01&rft.volume=9&rft.issue=&rft.spage=347&rft.isbn=&rft.btitle=&rft.title=Recent+developments+in+alcoholism+%3A+an+official+publication+of+the+American+Medical+Society+on+Alcoholism%2C+the+Research+Society+on+Alcoholism%2C+and+the+National+Council+on+Alcoholism&rft.issn=0738422X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-02-06 N1 - Date created - 1992-02-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Detection of DNA sequence polymorphisms in carcinogen metabolism genes by polymerase chain reaction. AN - 72562253; 1684153 AB - The glutathione transferase mu gene (GST1) and the debrisoquine hydroxylase gene (CYP2D6) are known to be polymorphic in the human population and have been associated with increased susceptibility to cancer. Smokers with low lymphocyte GST mu activity are at higher risk for lung cancer, while low debrisoquine hydroxylase activity has been correlated with lower risk for lung and bladder cancer. Phenotypic characterization of these polymorphisms by lymphocyte enzyme activity (GST) and urine metabolite ratios (debrisoquine) is cumbersome for population studies. Recent cloning and sequencing of the mutant alleles of these genes has allowed genotyping via the polymerase chain reaction (PCR). Advantages of PCR approaches are speed, technical simplicity, and minimal sample requirements. This article reviews the PCR-based methods for detection of genetic polymorphisms in human cancer susceptibility genes. JF - Environmental and molecular mutagenesis AU - Bell, D A AD - Laboratory of Biochemical Risk Analysis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1991 PY - 1991 DA - 1991 SP - 245 EP - 248 VL - 18 IS - 4 SN - 0893-6692, 0893-6692 KW - CYP2D6 KW - GST1 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Mixed Function Oxygenases KW - EC 1.- KW - Cytochrome P-450 CYP2D6 KW - EC 1.14.14.1 KW - Glutathione Transferase KW - EC 2.5.1.18 KW - Index Medicus KW - Chromosome Deletion KW - Polymorphism, Restriction Fragment Length KW - Humans KW - Polymorphism, Genetic KW - Cytochrome P-450 Enzyme System -- genetics KW - DNA Mutational Analysis KW - Polymerase Chain Reaction -- methods KW - Glutathione Transferase -- genetics KW - Mixed Function Oxygenases -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72562253?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+and+molecular+mutagenesis&rft.atitle=Detection+of+DNA+sequence+polymorphisms+in+carcinogen+metabolism+genes+by+polymerase+chain+reaction.&rft.au=Bell%2C+D+A&rft.aulast=Bell&rft.aufirst=D&rft.date=1991-01-01&rft.volume=18&rft.issue=4&rft.spage=245&rft.isbn=&rft.btitle=&rft.title=Environmental+and+molecular+mutagenesis&rft.issn=08936692&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-23 N1 - Date created - 1992-01-23 N1 - Date revised - 2017-01-13 N1 - Gene symbol - CYP2D6; GST1 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Kidney disease in systemic lupus erythematosus. AN - 72559598; 1754812 AB - Glomerulonephritis is a major determinant of outcome in patients with systemic lupus erythematosus. Persistently active lupus nephritis imposes serious threats of end-stage renal failure and cardiovascular morbidity. Sustained corticosteroid treatment has been characterized as having an uncertain net benefit on the control of lupus nephritis, mainly because these drugs have relatively weak efficacy and they have been shown to confer their own set of cardiovascular risk factors. Controlled trials of corticosteroids, azathioprine and cyclophosphamide have demonstrated that the best control of clinical activity of proliferative lupus nephritis is attained with cyclophosphamide. To date, intermittent pulse cyclophosphamide treatment has produced the most favorable balance of efficacy and toxicity in patients with lupus nephritis. JF - Rheumatology international AU - Balow, J E AD - National Institutes of Health, Clinical Center, Bethesda, Maryland 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 113 EP - 115 VL - 11 IS - 3 SN - 0172-8172, 0172-8172 KW - Adrenal Cortex Hormones KW - 0 KW - Antineoplastic Agents KW - Immunosuppressive Agents KW - Index Medicus KW - Adrenal Cortex Hormones -- therapeutic use KW - Kidney -- pathology KW - Humans KW - Clinical Trials as Topic KW - Biopsy KW - Antineoplastic Agents -- therapeutic use KW - Immunosuppressive Agents -- therapeutic use KW - Lupus Nephritis -- therapy KW - Lupus Nephritis -- diagnosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72559598?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Rheumatology+international&rft.atitle=Kidney+disease+in+systemic+lupus+erythematosus.&rft.au=Balow%2C+J+E&rft.aulast=Balow&rft.aufirst=J&rft.date=1991-01-01&rft.volume=11&rft.issue=3&rft.spage=113&rft.isbn=&rft.btitle=&rft.title=Rheumatology+international&rft.issn=01728172&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-30 N1 - Date created - 1992-01-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Emerging technologies and new directions in drug abuse research. An overview. AN - 72559337; 1753994 JF - NIDA research monograph AU - Snyder, M AD - Office of Policy and External Affairs, National Institute on Drug Abuse. Y1 - 1991 PY - 1991 DA - 1991 SP - 1 EP - 6 VL - 112 SN - 1046-9516, 1046-9516 KW - Index Medicus KW - Humans KW - Substance-Related Disorders UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72559337?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Emerging+technologies+and+new+directions+in+drug+abuse+research.+An+overview.&rft.au=Snyder%2C+M&rft.aulast=Snyder&rft.aufirst=M&rft.date=1991-01-01&rft.volume=112&rft.issue=&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-30 N1 - Date created - 1992-01-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - HIV infection and AIDS risk behaviors among intravenous drug users entering methadone treatment in selected U.S. cities. AN - 72558176; 1753342 AB - To assess trends in HIV infection and AIDS risk behaviors among intravenous drug users (IVDUs), a series of nonblinded point-prevalence surveys was conducted with admissions to methadone treatment in seven areas, including New York City; Trenton and Asbury Park, New Jersey; Baltimore; Chicago; San Antonio, Texas; and Los Angeles County between February and December 1987 (n = 713), January and June 1988 (n = 1,089), July and December 1988 (n = 932), and January and June 1989 (n = 1,110). Over the 2-year period, significant changes in HIV seropositivity levels were found in only one of the seven cities (Chicago, with levels increasing from 8.4 to 14.7%). High levels of AIDS risk behaviors (frequency of injection, needle sharing, needle cleaning, and use of shooting galleries) were found in all cities. Comparisons of trends in recent risk behaviors (past year) within cities suggest that relatively little reduction in AIDS risk behaviors had occurred during the study. JF - Journal of acquired immune deficiency syndromes AU - Battjes, R J AU - Pickens, R W AU - Amsel, Z AD - National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1991 PY - 1991 DA - 1991 SP - 1148 EP - 1154 VL - 4 IS - 11 SN - 0894-9255, 0894-9255 KW - Methadone KW - UC6VBE7V1Z KW - Index Medicus KW - AIDS/HIV KW - Humans KW - Cohort Studies KW - Adult KW - United States -- epidemiology KW - Male KW - Female KW - Acquired Immunodeficiency Syndrome -- complications KW - Methadone -- therapeutic use KW - Acquired Immunodeficiency Syndrome -- epidemiology KW - Risk-Taking KW - HIV Infections -- complications KW - Substance Abuse, Intravenous -- drug therapy KW - Acquired Immunodeficiency Syndrome -- psychology KW - Substance Abuse, Intravenous -- epidemiology KW - Substance Abuse, Intravenous -- complications KW - HIV Infections -- psychology KW - HIV Infections -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72558176?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+acquired+immune+deficiency+syndromes&rft.atitle=HIV+infection+and+AIDS+risk+behaviors+among+intravenous+drug+users+entering+methadone+treatment+in+selected+U.S.+cities.&rft.au=Battjes%2C+R+J%3BPickens%2C+R+W%3BAmsel%2C+Z&rft.aulast=Battjes&rft.aufirst=R&rft.date=1991-01-01&rft.volume=4&rft.issue=11&rft.spage=1148&rft.isbn=&rft.btitle=&rft.title=Journal+of+acquired+immune+deficiency+syndromes&rft.issn=08949255&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-24 N1 - Date created - 1992-01-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Rationale and methodologies for developing nonhuman primate models of prenatal drug exposure. AN - 72558031; 1754018 JF - NIDA research monograph AU - Suomi, S J AU - Higley, J D AD - Laboratory of Comparative Ethology, National Institute of Child Health and Human Development, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 291 EP - 302 VL - 114 SN - 1046-9516, 1046-9516 KW - Index Medicus KW - Animals KW - Pregnancy Complications KW - Substance-Related Disorders KW - Toxicology -- methods KW - Primates KW - Female KW - Pregnancy KW - Fetus -- drug effects KW - Disease Models, Animal UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72558031?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Rationale+and+methodologies+for+developing+nonhuman+primate+models+of+prenatal+drug+exposure.&rft.au=Suomi%2C+S+J%3BHigley%2C+J+D&rft.aulast=Suomi&rft.aufirst=S&rft.date=1991-01-01&rft.volume=114&rft.issue=&rft.spage=291&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-29 N1 - Date created - 1992-01-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Immunomodulatory effects of drugs of abuse and the importance of structure-immunomodulatory activity studies. AN - 72557936; 1661380 JF - NIDA research monograph AU - Rapaka, R S AU - Hoiberg, C P AD - Medications Development Division, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1991 PY - 1991 DA - 1991 SP - 300 EP - 312 VL - 112 SN - 1046-9516, 1046-9516 KW - Endorphins KW - 0 KW - Narcotics KW - Street Drugs KW - Dronabinol KW - 7J8897W37S KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Endorphins -- pharmacology KW - Animals KW - Humans KW - Dronabinol -- toxicity KW - Cocaine -- toxicity KW - Narcotics -- pharmacology KW - Structure-Activity Relationship KW - Immune System -- drug effects KW - Street Drugs -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72557936?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Immunomodulatory+effects+of+drugs+of+abuse+and+the+importance+of+structure-immunomodulatory+activity+studies.&rft.au=Rapaka%2C+R+S%3BHoiberg%2C+C+P&rft.aulast=Rapaka&rft.aufirst=R&rft.date=1991-01-01&rft.volume=112&rft.issue=&rft.spage=300&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-30 N1 - Date created - 1992-01-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effects of nifedipine pretreatment on subjective and cardiovascular responses to intravenous cocaine in humans. AN - 72557410; 1745709 AB - The effects of oral nifedipine pretreatment on subjective and cardiovascular responses to intravenous cocaine infusions were studied in cocaine-using volunteers. Nifedipine, 10 mg or placebo, was administered 20-25 min before placebo, 20 mg, or 40 mg cocaine, using a repeated measures randomized double-blind design. The variables measured were self-reported subjective effects, general behavior rated by two observers, blood pressure and heart rate. Cocaine produced the expected dose-related effects on subjective and cardiovascular measures. Nifedipine pretreatment attenuated some subjective effects of cocaine. Nifedipine directly reduced blood pressure but did not antagonize the effects of cocaine on blood pressure. These findings suggest that dihydropyridine calcium channel modulators may be useful compounds in the clinical management of cocaine users. JF - Psychopharmacology AU - Muntaner, C AU - Kumor, K M AU - Nagoshi, C AU - Jaffe, J H AD - National Institute on Drug Abuse Addiction Research Center, Baltimore, MD 21224. Y1 - 1991 PY - 1991 DA - 1991 SP - 37 EP - 41 VL - 105 IS - 1 SN - 0033-3158, 0033-3158 KW - Cocaine KW - I5Y540LHVR KW - Nifedipine KW - I9ZF7L6G2L KW - Index Medicus KW - Confusion -- psychology KW - Affect -- drug effects KW - Anxiety -- psychology KW - Injections, Intravenous KW - Double-Blind Method KW - Infusions, Intravenous KW - Random Allocation KW - Anxiety -- chemically induced KW - Humans KW - Heart Rate -- drug effects KW - Psychiatric Status Rating Scales KW - Electrocardiography KW - Adult KW - Blood Pressure -- drug effects KW - Confusion -- chemically induced KW - Male KW - Nifedipine -- pharmacology KW - Hemodynamics -- drug effects KW - Cocaine -- pharmacology KW - Cocaine -- administration & dosage KW - Cocaine -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72557410?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychopharmacology&rft.atitle=Effects+of+nifedipine+pretreatment+on+subjective+and+cardiovascular+responses+to+intravenous+cocaine+in+humans.&rft.au=Muntaner%2C+C%3BKumor%2C+K+M%3BNagoshi%2C+C%3BJaffe%2C+J+H&rft.aulast=Muntaner&rft.aufirst=C&rft.date=1991-01-01&rft.volume=105&rft.issue=1&rft.spage=37&rft.isbn=&rft.btitle=&rft.title=Psychopharmacology&rft.issn=00333158&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-13 N1 - Date created - 1992-01-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pacific paradigms of environmentally-induced neurological disorders: clinical, epidemiological and molecular perspectives. AN - 72556672; 1745428 AB - During the past quarter century biomedical scientists have begun to recognize the unique opportunities for studying disease etiology and mechanisms of pathogenesis in non-Western anthropological populations with focal, endemic diseases. Such natural experiments as they are called, are important paradigms for solving etiological and epidemiological problems of widespread medical significance, with an ultimate goal towards treatment and prevention. The systematic search for etiological factors and mechanisms of pathogenesis of neurodegenerative disorders is perhaps nowhere better exemplified than in the western Pacific. During the past three decades, the opportunistic and multidisciplinary study of hyperendemic foci of amyotrophic lateral sclerosis and parkinsonism-dementia which occur in different cultures, in different ecological zones and among genetically divergent populations have served as natural models that have had a major impact on our thinking and enhanced our understanding of these and other neurodegenerative disorders such as Alzheimer disease and the process of early neuronal aging. Our cross-disciplinary approach to these intriguing neurobiological problems and the accumulated epidemiological, genetic, cellular and molecular evidence strongly implicates environmental factors in their causation, specifically the role of aluminum and its interaction with calcium in neuronal degeneration. As a direct consequence of our studies in these Pacific populations, we have undertaken the long-term development of experimental models of neuronal degeneration, in an attempt to understand the cellular and molecular mechanisms by which these toxicants affect the central nervous system. Our experimental studies have resulted in the establishment of an aluminum-induced chronic myelopathy in rabbits and the development of neurofilamentous lesions after low-dose aluminum administration in cell culture. These studies clearly demonstrate the philosophy that chronic rather than acute experimental models of toxicity are necessary in order to enhance our understanding of human neurodegenerative disorders with long-latency and slow progression. Finally, the ultimate significance of these Pacific paradigms may well depend on our ability to comprehensively evaluate and synthesize the growing body of relevant scientific data from other human disorders and from widely divergent academic fields, as well as our ability to recognize emerging new models in nature. JF - Neurotoxicology AU - Garruto, R M AD - Laboratory of Central Nervous System Studies, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 347 EP - 377 VL - 12 IS - 3 SN - 0161-813X, 0161-813X KW - Aluminum KW - CPD4NFA903 KW - Index Medicus KW - Aluminum -- adverse effects KW - Parkinson Disease, Secondary -- chemically induced KW - Animals KW - Humans KW - Pacific Islands -- epidemiology KW - Alzheimer Disease -- chemically induced KW - Aluminum -- toxicity KW - Amyotrophic Lateral Sclerosis -- chemically induced KW - Nervous System Diseases -- epidemiology KW - Environmental Exposure KW - Nervous System Diseases -- chemically induced KW - Nervous System Diseases -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72556672?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurotoxicology&rft.atitle=Pacific+paradigms+of+environmentally-induced+neurological+disorders%3A+clinical%2C+epidemiological+and+molecular+perspectives.&rft.au=Garruto%2C+R+M&rft.aulast=Garruto&rft.aufirst=R&rft.date=1991-01-01&rft.volume=12&rft.issue=3&rft.spage=347&rft.isbn=&rft.btitle=&rft.title=Neurotoxicology&rft.issn=0161813X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-16 N1 - Date created - 1992-01-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The use of rat brain slices as an in vitro model for mechanistic evaluation of neurotoxicity-studies with acrylamide. AN - 72502988; 1956583 AB - Biochemical mechanisms underlying acrylamide induced neurotoxicity were examined using an in vitro model consisting of sagittal slices of rat brain. Incubation of brain slices under oxygen in artificial cerebrospinal fluid containing acrylamide produced a dose and time dependent inhibition of glyceraldehyde 3-phosphate dehydrogenase (GAPDH). Lysosomal enzymes, acid phosphatase, N-acetyl glucosaminidase and beta-glucuronidase decreased in a similar manner, while no changes were observed in the activity of Na+K+ATPase, cytochrome c oxidase and lactate dehydrogenase. Incubation of slices with two structurally related compounds, acetamide (a non-neurotoxic amide) and methylene bis-acrylamide (a weak neurotoxin), indicated that acrylamide selectively inhibited GAPDH, enolase and N-acetyl glucosaminidase at low concentration; similar doses of acetamide and methylene bis-acrylamide did not have the same effect on brain slices. Incubation with acrylamide depleted glutathione levels in slices, and the addition of glutathione to the incubation medium prevented acrylamide induced inhibition of GAPDH and lysosomal enzymes. Time dependent inhibition of lysosomal enzymes was also observed in vivo, in the brain and sciatic nerve of rats following a single dose of acrylamide. These results demonstrate that both in vitro and in vivo, lysosomal enzymes are also inhibited following acrylamide exposure. The rat brain slice model exhibits both selectivity and sensitivity towards neurotoxicants and hence, may prove to be an useful in vitro model for the mechanistic evaluation of neurotoxicity. JF - Neurotoxicology AU - Ravindranath, V AU - Pai, K S AD - Department of Neurochemistry, National Institute of Mental Health and Neuro Sciences, Bangalore, India. Y1 - 1991 PY - 1991 DA - 1991 SP - 225 EP - 234 VL - 12 IS - 2 SN - 0161-813X, 0161-813X KW - Acrylamides KW - 0 KW - Acrylamide KW - 20R035KLCI KW - Glyceraldehyde-3-Phosphate Dehydrogenases KW - EC 1.2.1.- KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - In Vitro Techniques KW - Disease Models, Animal KW - Lysosomes -- enzymology KW - Glyceraldehyde-3-Phosphate Dehydrogenases -- antagonists & inhibitors KW - Female KW - Brain -- enzymology KW - Brain -- drug effects KW - Acrylamides -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72502988?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurotoxicology&rft.atitle=The+use+of+rat+brain+slices+as+an+in+vitro+model+for+mechanistic+evaluation+of+neurotoxicity-studies+with+acrylamide.&rft.au=Ravindranath%2C+V%3BPai%2C+K+S&rft.aulast=Ravindranath&rft.aufirst=V&rft.date=1991-01-01&rft.volume=12&rft.issue=2&rft.spage=225&rft.isbn=&rft.btitle=&rft.title=Neurotoxicology&rft.issn=0161813X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-02 N1 - Date created - 1992-01-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Calcium channels in the presynaptic nerve terminal of the chick ciliary ganglion giant synapse. AN - 72498529; 1660254 JF - Annals of the New York Academy of Sciences AU - Stanley, E F AU - Cox, C AD - Laboratory of Biophysics, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 70 EP - 79 VL - 635 SN - 0077-8923, 0077-8923 KW - Calcium Channel Blockers KW - 0 KW - Calcium Channels KW - Peptides, Cyclic KW - omega-Conotoxins KW - Conus magus toxin KW - 107407-86-3 KW - Index Medicus KW - Animals KW - Chickens KW - Electric Conductivity KW - Calcium Channel Blockers -- pharmacology KW - Peptides, Cyclic -- pharmacology KW - Nerve Endings -- physiology KW - Synapses -- physiology KW - Calcium Channels -- physiology KW - Ganglia, Parasympathetic -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72498529?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Calcium+channels+in+the+presynaptic+nerve+terminal+of+the+chick+ciliary+ganglion+giant+synapse.&rft.au=Stanley%2C+E+F%3BCox%2C+C&rft.aulast=Stanley&rft.aufirst=E&rft.date=1991-01-01&rft.volume=635&rft.issue=&rft.spage=70&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 - 1992-01-09 N1 - Date created - 1992-01-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - MPP+ enhances potassium-evoked striatal dopamine release through a omega-conotoxin-insensitive, tetrodotoxin- and nimodipine-sensitive calcium-dependent mechanism. AN - 72498402; 1741592 JF - Annals of the New York Academy of Sciences AU - Chiueh, C C AU - Huang, S J AD - Laboratory of Cerebral Metabolism, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 393 EP - 396 VL - 635 SN - 0077-8923, 0077-8923 KW - Peptides, Cyclic KW - 0 KW - omega-Conotoxins KW - Conus magus toxin KW - 107407-86-3 KW - Tetrodotoxin KW - 4368-28-9 KW - Nimodipine KW - 57WA9QZ5WH KW - 1-Methyl-4-phenylpyridinium KW - R865A5OY8J KW - Potassium KW - RWP5GA015D KW - Calcium KW - SY7Q814VUP KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Rats KW - Animals KW - Nimodipine -- pharmacology KW - Tetrodotoxin -- pharmacology KW - Peptides, Cyclic -- pharmacology KW - Dopamine -- secretion KW - Corpus Striatum -- secretion KW - Potassium -- pharmacology KW - Corpus Striatum -- drug effects KW - Calcium -- pharmacology KW - 1-Methyl-4-phenylpyridinium -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72498402?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=MPP%2B+enhances+potassium-evoked+striatal+dopamine+release+through+a+omega-conotoxin-insensitive%2C+tetrodotoxin-+and+nimodipine-sensitive+calcium-dependent+mechanism.&rft.au=Chiueh%2C+C+C%3BHuang%2C+S+J&rft.aulast=Chiueh&rft.aufirst=C&rft.date=1991-01-01&rft.volume=635&rft.issue=&rft.spage=393&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 - 1992-01-09 N1 - Date created - 1992-01-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - DNA adduct determination in humans. AN - 72491219; 1956919 AB - Carcinogen-DNA adduct formation, presumed to constitute tumorigenic initiation, provides irrefutable evidence of exposure and some indication of biologically effective dose to target tissues. Carcinogen-DNA adducts, representing a broad spectrum of chemical and physical insult, have been measured in humans using a variety of recently-developed, highly sensitive techniques. Evaluation of the results of these assays relies on detailed understanding of the strengths and weaknesses of the assays themselves. This review is primarily focussed on the application of immunoassays and 32P-postlabeling for human DNA adduct monitoring. Purification of adducts by high performance liquid chromatography or immunoaffinity chromatography, and structural determination by chemically-specific procedures such as synchronous fluorescence spectrometry and gas chromatography/mass spectrometry are also described. In addition, studies in which human DNA adduct dosimetry has been achieved are presented and evaluated. JF - Progress in clinical and biological research AU - Poirier, M C AU - Weston, A AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 205 EP - 218 VL - 372 SN - 0361-7742, 0361-7742 KW - Carcinogens KW - 0 KW - Phosphorus Radioisotopes KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Immunoassay -- methods KW - Carcinogens -- administration & dosage KW - Humans KW - Carcinogens -- toxicity KW - DNA Damage KW - DNA -- analysis KW - DNA -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72491219?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Progress+in+clinical+and+biological+research&rft.atitle=DNA+adduct+determination+in+humans.&rft.au=Poirier%2C+M+C%3BWeston%2C+A&rft.aulast=Poirier&rft.aufirst=M&rft.date=1991-01-01&rft.volume=372&rft.issue=&rft.spage=205&rft.isbn=&rft.btitle=&rft.title=Progress+in+clinical+and+biological+research&rft.issn=03617742&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-02 N1 - Date created - 1992-01-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Identification of cystic fibrosis mutations. AN - 72487721; 1719771 JF - Advances in experimental medicine and biology AU - Dean, M AU - Gerrard, B AU - Stewart, C AU - Krueger, L AU - Holsclaw, D AU - Quittell, L AU - Baranov, V AU - Kapronov, N AU - Leppert, M AU - Amos, J AD - Biological Carcinogenesis and Development Program, NCI-FCRF, Frederick, MD. Y1 - 1991 PY - 1991 DA - 1991 SP - 45 EP - 51 VL - 290 SN - 0065-2598, 0065-2598 KW - CFTR KW - CFTR protein, human KW - 0 KW - Membrane Proteins KW - Cystic Fibrosis Transmembrane Conductance Regulator KW - 126880-72-6 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Phenotype KW - Pedigree KW - Genotype KW - Humans KW - DNA Mutational Analysis KW - DNA -- genetics KW - Membrane Proteins -- genetics KW - Mutation KW - Male KW - Female KW - Cystic Fibrosis -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72487721?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Advances+in+experimental+medicine+and+biology&rft.atitle=Identification+of+cystic+fibrosis+mutations.&rft.au=Dean%2C+M%3BGerrard%2C+B%3BStewart%2C+C%3BKrueger%2C+L%3BHolsclaw%2C+D%3BQuittell%2C+L%3BBaranov%2C+V%3BKapronov%2C+N%3BLeppert%2C+M%3BAmos%2C+J&rft.aulast=Dean&rft.aufirst=M&rft.date=1991-01-01&rft.volume=290&rft.issue=&rft.spage=45&rft.isbn=&rft.btitle=&rft.title=Advances+in+experimental+medicine+and+biology&rft.issn=00652598&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-09 N1 - Date created - 1991-12-09 N1 - Date revised - 2017-01-13 N1 - Gene symbol - CFTR N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Elevation of brain manganese in calcium-deficient rats. AN - 72487070; 1956585 AB - Rats, 3 weeks of age, consumed diets low or normal in calcium (Ca) with or without supplemental manganese (Mn) as Mn (II) acetate in drinking water. After 6 weeks, the animals were killed and [Mn] was determined in 8 brain regions, spinal cord, liver, serum, kidney, femur, and skeletal muscle. Serum [Mn] increased 1.5-, 4-, and 40-fold respectively, in normal Ca-supplemented Mn rats, low Ca rats, and low Ca-supplemented Mn rats. Elevation of tissue [Mn] occurred in all experimental groups with the greatest changes in the low Ca-extra Mn group: 6 - 12 fold in brain and spinal cord, and 2.5 - 140 fold in muscle, liver, kidney, and femur. Ratios of serum [Mn]/tissue [Mn] decreased as serum [Mn] increased suggesting saturable distribution. The findings suggest that Ca deficiency may cause Mn neurotoxicity by increasing dietary Mn absorption and brain [Mn]. JF - Neurotoxicology AU - Murphy, V A AU - Rosenberg, J M AU - Smith, Q R AU - Rapoport, S I AD - Laboratory of Neurosciences, National Institute of Aging, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 255 EP - 263 VL - 12 IS - 2 SN - 0161-813X, 0161-813X KW - Manganese KW - 42Z2K6ZL8P KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Spinal Cord -- metabolism KW - Manganese Poisoning KW - Spinal Cord -- drug effects KW - Body Weight -- drug effects KW - Tissue Distribution -- drug effects KW - Male KW - Manganese -- metabolism KW - Brain -- drug effects KW - Brain -- metabolism KW - Calcium -- deficiency UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72487070?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurochemical+research&rft.atitle=Effect+of+chronic+ethanol+ingestion+on+phosphate+content+of+neurofilament+proteins+and+neurofilament+associated+protein+phosphatase+in+rat+spinal+cord.&rft.au=Guru%2C+S+C%3BShetty%2C+K+T%3BShankar%2C+S+K&rft.aulast=Guru&rft.aufirst=S&rft.date=1991-11-01&rft.volume=16&rft.issue=11&rft.spage=1193&rft.isbn=&rft.btitle=&rft.title=Neurochemical+research&rft.issn=03643190&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-02 N1 - Date created - 1992-01-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Molecular epidemiology of human cancer in the 1990's. AN - 72485623; 1956947 JF - Progress in clinical and biological research AU - Harris, C C AD - Laboratory of Human Carcinogenesis, NCI, NIH, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 543 EP - 557 VL - 372 SN - 0361-7742, 0361-7742 KW - Carcinogens KW - 0 KW - Index Medicus KW - DNA Repair KW - Carcinogens -- metabolism KW - Molecular Biology KW - Risk Factors KW - Humans KW - Epidemiologic Factors KW - Carcinogens -- toxicity KW - Neoplasms -- epidemiology KW - Neoplasms -- genetics KW - Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72485623?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Progress+in+clinical+and+biological+research&rft.atitle=Molecular+epidemiology+of+human+cancer+in+the+1990%27s.&rft.au=Harris%2C+C+C&rft.aulast=Harris&rft.aufirst=C&rft.date=1991-01-01&rft.volume=372&rft.issue=&rft.spage=543&rft.isbn=&rft.btitle=&rft.title=Progress+in+clinical+and+biological+research&rft.issn=03617742&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-02 N1 - Date created - 1992-01-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human cytochromes P450: evolution, catalytic activities and interindividual variations in expression. AN - 72484161; 1956910 JF - Progress in clinical and biological research AU - Gonzalez, F J AU - Gelboin, H V AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 11 EP - 20 VL - 372 SN - 0361-7742, 0361-7742 KW - Carcinogens KW - 0 KW - Molecular Probes KW - Sparteine KW - 298897D62S KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Debrisoquin KW - X31CDK040E KW - Index Medicus KW - Sparteine -- metabolism KW - Debrisoquin -- metabolism KW - Carcinogens -- metabolism KW - Polymorphism, Genetic KW - Biological Evolution KW - Humans KW - Gene Expression KW - Cytochrome P-450 Enzyme System -- genetics KW - Cytochrome P-450 Enzyme System -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72484161?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Progress+in+clinical+and+biological+research&rft.atitle=Human+cytochromes+P450%3A+evolution%2C+catalytic+activities+and+interindividual+variations+in+expression.&rft.au=Gonzalez%2C+F+J%3BGelboin%2C+H+V&rft.aulast=Gonzalez&rft.aufirst=F&rft.date=1991-01-01&rft.volume=372&rft.issue=&rft.spage=11&rft.isbn=&rft.btitle=&rft.title=Progress+in+clinical+and+biological+research&rft.issn=03617742&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1992-01-02 N1 - Date created - 1992-01-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Testicular cancer in young men and parental occupational exposure. AN - 72476990; 1951369 AB - To investigate whether parental occupation, especially during the 12 month period before birth, could be responsible for elevated rates of testicular cancer in young men, we used data from a case-control study of 223 cases and 212 controls conducted in the Washington, DC area. For all histologic types of testicular cancer combined, no significant associations were found for specific occupations, nor for the broad occupational categories of professional, other white collar, or blue collar workers. However, for cases with seminomas, excess risks were seen for those with parents employed in the following occupations: mothers in health-related occupations, O.R. = 4.6 (1.1-19.1), and fathers working in automobile service stations, O.R. = 4.0 (0.6-24.5), manufacturing industries, O.R. = 2.2 (1.0-4.2), and aircraft production and maintenance, O.R. = 5.3 (0.7-24.1). Although these findings for seminoma are intriguing, they do not explain the increase of testicular cancer in young men. JF - American journal of industrial medicine AU - Kardaun, J W AU - Hayes, R B AU - Pottern, L M AU - Brown, L M AU - Hoover, R N AD - Environmental Epidemiology Branch, National Cancer Institute, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 219 EP - 227 VL - 20 IS - 2 SN - 0271-3586, 0271-3586 KW - Index Medicus KW - Humans KW - Adult KW - Surveys and Questionnaires KW - Case-Control Studies KW - Fathers KW - Adolescent KW - United States -- epidemiology KW - Male KW - Female KW - Pregnancy KW - Health Occupations KW - Dysgerminoma -- epidemiology KW - Testicular Neoplasms -- etiology KW - Occupational Exposure -- adverse effects KW - Dysgerminoma -- etiology KW - Testicular Neoplasms -- epidemiology KW - Prenatal Exposure Delayed Effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72476990?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+industrial+medicine&rft.atitle=Testicular+cancer+in+young+men+and+parental+occupational+exposure.&rft.au=Kardaun%2C+J+W%3BHayes%2C+R+B%3BPottern%2C+L+M%3BBrown%2C+L+M%3BHoover%2C+R+N&rft.aulast=Kardaun&rft.aufirst=J&rft.date=1991-01-01&rft.volume=20&rft.issue=2&rft.spage=219&rft.isbn=&rft.btitle=&rft.title=American+journal+of+industrial+medicine&rft.issn=02713586&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-29 N1 - Date created - 1991-11-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Trends in cocaine use in the general population. AN - 72465459; 1944507 JF - NIDA research monograph AU - Rouse, B A AD - National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1991 PY - 1991 DA - 1991 SP - 5 EP - 18 VL - 110 SN - 1046-9516, 1046-9516 KW - Crack Cocaine KW - 0 KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Humans KW - Adult KW - Adolescent KW - United States -- epidemiology KW - Male KW - Female KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72465459?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Trends+in+cocaine+use+in+the+general+population.&rft.au=Rouse%2C+B+A&rft.aulast=Rouse&rft.aufirst=B&rft.date=1991-01-01&rft.volume=110&rft.issue=&rft.spage=5&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-26 N1 - Date created - 1991-12-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Risk of cocaine abuse and dependence. AN - 72459383; 1944501 JF - NIDA research monograph AU - Adams, E H AU - Gfroerer, J AD - Division of Epidemiology and Prevention Research, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1991 PY - 1991 DA - 1991 SP - 253 EP - 262 VL - 110 SN - 1046-9516, 1046-9516 KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - Risk Factors KW - Humans KW - Adult KW - Male KW - Female KW - Substance-Related Disorders -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72459383?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Risk+of+cocaine+abuse+and+dependence.&rft.au=Adams%2C+E+H%3BGfroerer%2C+J&rft.aulast=Adams&rft.aufirst=E&rft.date=1991-01-01&rft.volume=110&rft.issue=&rft.spage=253&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-26 N1 - Date created - 1991-12-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Use of naloxone in the assessment of opiate dependence. AN - 72452250; 1943484 AB - All subjects participating in an outpatient study comparing treatments for opiate dependence were given a naloxone challenge to document their level of dependence. Subjects were assessed at 0, 10, 20, and 30 minutes following the administration of intramuscular naloxone (0.4 mg) using an opiate withdrawal assessment scale and measurements of pupillary diameter. Subjects' self reports of daily dollar amounts of opiate use and time since last use were also examined for possible correlation with withdrawal scale scores and pupillary measurements. A significant negative correlation was obtained between pupil diameter and time since last reported use of an opiate. Results indicated that the scale was a reliable indicator of opiate dependence. Ways in which it might be improved are discussed. JF - Life sciences AU - Fudala, P J AU - Berkow, L C AU - Fralich, J L AU - Johnson, R E AD - National Institute on Drug Abuse, Addiction Research Center, Baltimore, Md. 21224. Y1 - 1991 PY - 1991 DA - 1991 SP - 1809 EP - 1814 VL - 49 IS - 24 SN - 0024-3205, 0024-3205 KW - Naloxone KW - 36B82AMQ7N KW - Index Medicus KW - Substance Withdrawal Syndrome -- physiopathology KW - Substance Withdrawal Syndrome -- etiology KW - Humans KW - Adult KW - Middle Aged KW - Male KW - Female KW - Substance Abuse, Intravenous KW - Opioid-Related Disorders -- diagnosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72452250?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Life+sciences&rft.atitle=Use+of+naloxone+in+the+assessment+of+opiate+dependence.&rft.au=Fudala%2C+P+J%3BBerkow%2C+L+C%3BFralich%2C+J+L%3BJohnson%2C+R+E&rft.aulast=Fudala&rft.aufirst=P&rft.date=1991-01-01&rft.volume=49&rft.issue=24&rft.spage=1809&rft.isbn=&rft.btitle=&rft.title=Life+sciences&rft.issn=00243205&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-26 N1 - Date created - 1991-12-26 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - New rapid analysis method demonstrates differences in 6-[18F] fluoro-L-dopa plasma input curves with and without carbidopa and in hemi-MPTP lesioned monkeys. AN - 72445958; 1657833 AB - Kinetic modeling of the PET tracer 6-[18F]fluoro-L-dopa ([18F]Dopa), used to measure presynaptic dopamine function, requires the accurate determination of the plasma input curve. We have developed a new method that uses alumina extraction preceded by cation and anion exchange resins to determine the parent compound, [18F]Dopa and its critical metabolite 3-O-methyl-6-[18F]fluoro-L-dopa. Using this method we found that carbidopa increases the plasma input of [18F]Dopa while decreasing the rate of metabolite formation, and that previous drug treatment can significantly effect [18F]Dopa metabolism. JF - International journal of radiation applications and instrumentation. Part A, Applied radiation and isotopes AU - McLellan, C A AU - Doudet, D J AU - Brücke, T AU - Aigner, T G AU - Cohen, R M AD - Laboratory of Cell Biology, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 847 EP - 854 VL - 42 IS - 9 SN - 0883-2889, 0883-2889 KW - Fluorine Radioisotopes KW - 0 KW - fluorodopa F 18 KW - 2C598205QX KW - Dihydroxyphenylalanine KW - 63-84-3 KW - Carbidopa KW - MNX7R8C5VO KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Animals KW - Synapses -- physiology KW - Reference Values KW - Kinetics KW - Dopamine -- metabolism KW - Macaca mulatta KW - Time Factors KW - Functional Laterality KW - Fluorine Radioisotopes -- pharmacokinetics KW - Carbidopa -- pharmacology KW - MPTP Poisoning KW - Dihydroxyphenylalanine -- blood KW - Dihydroxyphenylalanine -- pharmacokinetics KW - Dihydroxyphenylalanine -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72445958?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+radiation+applications+and+instrumentation.+Part+A%2C+Applied+radiation+and+isotopes&rft.atitle=New+rapid+analysis+method+demonstrates+differences+in+6-%5B18F%5D+fluoro-L-dopa+plasma+input+curves+with+and+without+carbidopa+and+in+hemi-MPTP+lesioned+monkeys.&rft.au=McLellan%2C+C+A%3BDoudet%2C+D+J%3BBr%C3%BCcke%2C+T%3BAigner%2C+T+G%3BCohen%2C+R+M&rft.aulast=McLellan&rft.aufirst=C&rft.date=1991-01-01&rft.volume=42&rft.issue=9&rft.spage=847&rft.isbn=&rft.btitle=&rft.title=International+journal+of+radiation+applications+and+instrumentation.+Part+A%2C+Applied+radiation+and+isotopes&rft.issn=08832889&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-12-11 N1 - Date created - 1991-12-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Carcinogenic consequences of DNA alkylation. AN - 72445773; 1935129 JF - Contributions to gynecology and obstetrics AU - Michejda, C J AD - Laboratory of Chemical and Physical Carcinogenesis, NCI-Frederick Cancer Research Facility, Md. Y1 - 1991 PY - 1991 DA - 1991 SP - 71 EP - 78 VL - 18 SN - 0304-4246, 0304-4246 KW - Alkylating Agents KW - 0 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Oncogenes -- genetics KW - Humans KW - Models, Biological KW - Mutagenesis KW - Cell Transformation, Neoplastic -- chemistry KW - Alkylating Agents -- metabolism KW - DNA -- genetics KW - Cell Transformation, Neoplastic -- drug effects KW - Alkylating Agents -- adverse effects KW - Cell Transformation, Neoplastic -- genetics KW - DNA -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72445773?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Contributions+to+gynecology+and+obstetrics&rft.atitle=Carcinogenic+consequences+of+DNA+alkylation.&rft.au=Michejda%2C+C+J&rft.aulast=Michejda&rft.aufirst=C&rft.date=1991-01-01&rft.volume=18&rft.issue=&rft.spage=71&rft.isbn=&rft.btitle=&rft.title=Contributions+to+gynecology+and+obstetrics&rft.issn=03044246&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-29 N1 - Date created - 1991-11-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Two-dimensional gel electrophoretic comparison of cytoplasmic proteins in C3H10T1/2 cells, a chemically transformed 10T1/2 line, and a transformation resistant C3H mouse ventral prostate cell line. AN - 72442268; 1932209 AB - The cytoplasmic proteins from three cell lines derived from the C3H mouse were compared after treatment with benzo(a)pyrene by two-dimensional gel electrophoresis and computerized image analysis. The three C3H lines were the transformable 10T1/2, the transformation resistant CVP and the methylcholanthrene transformed 10T1/2Cl line. Specialized algorithms were used to analyze gel images to record and compare individual proteins in the three cytoplasmic preparations. Multiple replicate gels were used to construct a master image to insure all the proteins were represented in the analytical system. In studies designed to examine the efficacy of utilizing image analysis, benzo(a)pyrene treatment caused significant alteration in the expression of numerous proteins in all three cell lines. Comparative analysis between cell types also showed most of the induced and repressed proteins were unique to a given cell line and did not match the induced or repressed proteins in either of the other cell lines. These results suggest that the response to chemical carcinogen treatment may be somewhat cell-specific and result in a variable response to the cells ability to respond to the chemical insult. JF - Applied and theoretical electrophoresis : the official journal of the International Electrophoresis Society AU - Selkirk, J K AU - Mansfield, B K AU - Riese, D J AU - Nikbakht, A AU - Mann, R C AD - Division of Toxicology Research and Testing, National Institute of Environmental Health Sciences, Research Triange Park, North Carolina 27709. Y1 - 1991 PY - 1991 DA - 1991 SP - 43 EP - 51 VL - 2 IS - 1 SN - 0954-6642, 0954-6642 KW - Neoplasm Proteins KW - 0 KW - Benzo(a)pyrene KW - 3417WMA06D KW - Index Medicus KW - Prostatic Neoplasms -- chemistry KW - Animals KW - Electrophoresis, Gel, Two-Dimensional KW - Benzo(a)pyrene -- toxicity KW - Mice KW - Cell Line, Transformed KW - Image Processing, Computer-Assisted KW - Cytoplasm -- chemistry KW - Male KW - Tumor Cells, Cultured -- chemistry KW - Tumor Cells, Cultured -- drug effects KW - Neoplasm Proteins -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72442268?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Applied+and+theoretical+electrophoresis+%3A+the+official+journal+of+the+International+Electrophoresis+Society&rft.atitle=Two-dimensional+gel+electrophoretic+comparison+of+cytoplasmic+proteins+in+C3H10T1%2F2+cells%2C+a+chemically+transformed+10T1%2F2+line%2C+and+a+transformation+resistant+C3H+mouse+ventral+prostate+cell+line.&rft.au=Selkirk%2C+J+K%3BMansfield%2C+B+K%3BRiese%2C+D+J%3BNikbakht%2C+A%3BMann%2C+R+C&rft.aulast=Selkirk&rft.aufirst=J&rft.date=1991-01-01&rft.volume=2&rft.issue=1&rft.spage=43&rft.isbn=&rft.btitle=&rft.title=Applied+and+theoretical+electrophoresis+%3A+the+official+journal+of+the+International+Electrophoresis+Society&rft.issn=09546642&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-25 N1 - Date created - 1991-11-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A double-blind trial of isoniazid for essential tremor and other action tremors. AN - 72148504; 1681430 AB - We conducted a double-blind trial of isoniazid in 11 patients with essential tremor and four patients with other types of postural action tremor. The tremor had not been helped by beta-blockers or primidone. Isoniazid was given in doses up to 1,200 mg daily, together with 100 mg pyridoxine, for four weeks. Results were assessed with subjective and objective scales. Only two patients with essential tremor appeared to benefit enough to continue the drug after the trial, and only one has benefited from its long-term use. Isoniazid may be useful in rare cases of essential tremor, but must be monitored carefully because of its toxicity. JF - Movement disorders : official journal of the Movement Disorder Society AU - Hallett, M AU - Ravits, J AU - Dubinsky, R M AU - Gillespie, M M AU - Moinfar, A AD - Human Motor Control Section, NINDS, NIH, Bethesda, MD 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 253 EP - 256 VL - 6 IS - 3 SN - 0885-3185, 0885-3185 KW - Adrenergic beta-Antagonists KW - 0 KW - Placebos KW - Primidone KW - 13AFD7670Q KW - Isoniazid KW - V83O1VOZ8L KW - Index Medicus KW - Double-Blind Method KW - Humans KW - Adult KW - Parkinson Disease -- complications KW - Aged KW - Middle Aged KW - Primidone -- therapeutic use KW - Adrenergic beta-Antagonists -- therapeutic use KW - Parkinson Disease -- drug therapy KW - Male KW - Female KW - Tremor -- drug therapy KW - Isoniazid -- therapeutic use KW - Isoniazid -- toxicity KW - Tremor -- etiology KW - Isoniazid -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72148504?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Movement+disorders+%3A+official+journal+of+the+Movement+Disorder+Society&rft.atitle=A+double-blind+trial+of+isoniazid+for+essential+tremor+and+other+action+tremors.&rft.au=Hallett%2C+M%3BRavits%2C+J%3BDubinsky%2C+R+M%3BGillespie%2C+M+M%3BMoinfar%2C+A&rft.aulast=Hallett&rft.aufirst=M&rft.date=1991-01-01&rft.volume=6&rft.issue=3&rft.spage=253&rft.isbn=&rft.btitle=&rft.title=Movement+disorders+%3A+official+journal+of+the+Movement+Disorder+Society&rft.issn=08853185&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-07 N1 - Date created - 1991-11-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Establishing a methadone quality assurance system: rationale and objectives. AN - 72145276; 1922297 JF - NIDA research monograph AU - Cooper, J R AD - Medical and International Affairs, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1991 PY - 1991 DA - 1991 SP - 358 EP - 364 VL - 106 SN - 1046-9516, 1046-9516 KW - Methadone KW - UC6VBE7V1Z KW - Index Medicus KW - United States KW - United States Food and Drug Administration KW - Humans KW - National Institutes of Health (U.S.) KW - Legislation, Medical KW - Methadone -- therapeutic use KW - Heroin Dependence -- rehabilitation KW - Quality Assurance, Health Care UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72145276?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Pediatric+infectious+disease+journal&rft.atitle=Bacterial+infections+in+human+immunodeficiency+virus+type+1-infected+children%3A+the+impact+of+central+venous+catheters+and+antiretroviral+agents.&rft.au=Roilides%2C+E%3BMarshall%2C+D%3BVenzon%2C+D%3BButler%2C+K%3BHusson%2C+R%3BPizzo%2C+P+A&rft.aulast=Roilides&rft.aufirst=E&rft.date=1991-11-01&rft.volume=10&rft.issue=11&rft.spage=813&rft.isbn=&rft.btitle=&rft.title=The+Pediatric+infectious+disease+journal&rft.issn=08913668&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-14 N1 - Date created - 1991-11-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Treatment outcomes for drug abuse clients. AN - 72145263; 1922300 JF - NIDA research monograph AU - Tims, F M AU - Fletcher, B W AU - Hubbard, R L AD - Division of Clinical Research, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1991 PY - 1991 DA - 1991 SP - 93 EP - 113 VL - 106 SN - 1046-9516, 1046-9516 KW - Index Medicus KW - United States KW - Humans KW - Substance-Related Disorders -- therapy KW - Outcome Assessment (Health Care) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72145263?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Treatment+outcomes+for+drug+abuse+clients.&rft.au=Tims%2C+F+M%3BFletcher%2C+B+W%3BHubbard%2C+R+L&rft.aulast=Tims&rft.aufirst=F&rft.date=1991-01-01&rft.volume=106&rft.issue=&rft.spage=93&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-14 N1 - Date created - 1991-11-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Improving drug abuse treatment. Overview of treatment issues. AN - 72145040; 1922282 JF - NIDA research monograph AU - Pickens, R W AU - Fletcher, B W AD - Addiction Research Center, National Institute on Drug Abuse, Baltimore, MD 21224. Y1 - 1991 PY - 1991 DA - 1991 SP - 1 EP - 19 VL - 106 SN - 1046-9516, 1046-9516 KW - Index Medicus KW - United States KW - Humans KW - Substance-Related Disorders -- therapy KW - Substance-Related Disorders -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72145040?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Improving+drug+abuse+treatment.+Overview+of+treatment+issues.&rft.au=Pickens%2C+R+W%3BFletcher%2C+B+W&rft.aulast=Pickens&rft.aufirst=R&rft.date=1991-01-01&rft.volume=185&rft.issue=1&rft.spage=39&rft.isbn=&rft.btitle=&rft.title=Virology&rft.issn=00426822&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-14 N1 - Date created - 1991-11-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Using psychotherapy effectively in drug abuse treatment. AN - 72144503; 1922291 JF - NIDA research monograph AU - Onken, L S AD - Division of Clinical Research, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1991 PY - 1991 DA - 1991 SP - 267 EP - 278 VL - 106 SN - 1046-9516, 1046-9516 KW - Index Medicus KW - Humans KW - Patients KW - Substance-Related Disorders -- therapy KW - Psychotherapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72144503?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Using+psychotherapy+effectively+in+drug+abuse+treatment.&rft.au=Onken%2C+L+S&rft.aulast=Onken&rft.aufirst=L&rft.date=1991-01-01&rft.volume=106&rft.issue=&rft.spage=267&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-14 N1 - Date created - 1991-11-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A framework for drug abuse prevention research. AN - 72143457; 1922313 JF - NIDA research monograph AU - Bukoski, W J AD - Prevention Research Branch, National Institute on Drug Abuse, Rockville, MD 20857. Y1 - 1991 PY - 1991 DA - 1991 SP - 7 EP - 28 VL - 107 SN - 1046-9516, 1046-9516 KW - Index Medicus KW - Risk Factors KW - Humans KW - Research Design KW - Models, Theoretical KW - Substance-Related Disorders -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72143457?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=A+framework+for+drug+abuse+prevention+research.&rft.au=Bukoski%2C+W+J&rft.aulast=Bukoski&rft.aufirst=W&rft.date=1991-01-01&rft.volume=107&rft.issue=&rft.spage=7&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-08 N1 - Date created - 1991-11-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Methadone maintenance and patients in alcoholism treatment. AN - 72142508; 1922298 JF - NIDA research monograph AU - Gordis, E AD - National Institute on Alcohol Abuse and Alcoholism, Rockville, MD 20857. Y1 - 1991 PY - 1991 DA - 1991 SP - 365 EP - 372 VL - 106 SN - 1046-9516, 1046-9516 KW - Methadone KW - UC6VBE7V1Z KW - Index Medicus KW - Humans KW - Alcoholism -- rehabilitation KW - Methadone -- therapeutic use KW - Heroin Dependence -- rehabilitation KW - Heroin Dependence -- complications KW - Alcoholism -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72142508?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NIDA+research+monograph&rft.atitle=Methadone+maintenance+and+patients+in+alcoholism+treatment.&rft.au=Gordis%2C+E&rft.aulast=Gordis&rft.aufirst=E&rft.date=1991-01-01&rft.volume=106&rft.issue=&rft.spage=365&rft.isbn=&rft.btitle=&rft.title=NIDA+research+monograph&rft.issn=10469516&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-14 N1 - Date created - 1991-11-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interactions of the salivary and gastrointestinal systems. II. Effects of salivary gland dysfunction on the gastrointestinal tract. AN - 72125171; 1914220 AB - Salivary gland dysfunction is uniformly detrimental to the oral cavity. Its effects on the GI tract have begun to be explored. Dry mouth is a common complaint among older adults, probably due to systemic disease and its therapy rather than the aging process per se. Evaluation of complaints of dry mouth should include medical history, sialometry and physical examination. Numerous medications can elicit drug-induced xerostomia. Patients who have received radiation therapy to the head and neck region often have permanent radiation-induced xerostomia, which has been linked to esophagitis. SS is an autoimmune systemic exocrinopathy resulting in irreversible salivary gland dysfunction. SS has numerous GI manifestations, including dysphagia, temporal defects of deglutition, esophageal dysmotility, gastritis, pancreatitis and liver disease. Management of salivary hypofunction is directed toward preserving the dentition and improving patient comfort. Drug-induced xerostomia is often correctable by altering the therapeutic modality. JF - Digestive diseases (Basel, Switzerland) AU - Valdez, I H AU - Fox, P C AD - Clinical Investigations and Patient Care Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, Md. Y1 - 1991 PY - 1991 DA - 1991 SP - 210 EP - 218 VL - 9 IS - 4 SN - 0257-2753, 0257-2753 KW - Index Medicus KW - Aging -- physiology KW - Humans KW - Xerostomia -- etiology KW - Xerostomia -- complications KW - Salivary Glands -- physiopathology KW - Xerostomia -- chemically induced KW - Gastrointestinal Diseases -- etiology KW - Sjogren's Syndrome -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72125171?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Digestive+diseases+%28Basel%2C+Switzerland%29&rft.atitle=Interactions+of+the+salivary+and+gastrointestinal+systems.+II.+Effects+of+salivary+gland+dysfunction+on+the+gastrointestinal+tract.&rft.au=Valdez%2C+I+H%3BFox%2C+P+C&rft.aulast=Valdez&rft.aufirst=I&rft.date=1991-01-01&rft.volume=9&rft.issue=4&rft.spage=210&rft.isbn=&rft.btitle=&rft.title=Digestive+diseases+%28Basel%2C+Switzerland%29&rft.issn=02572753&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-07 N1 - Date created - 1991-11-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mechanisms of nickel carcinogenesis. Interaction of Ni(II) with 2'-deoxynucleosides and 2'-deoxynucleotides. AN - 72120312; 1913976 AB - Interactions of Ni(II) with the base moieties of 2'-deoxynucleosides and 2'-deoxynucleotides were studied by means of UV difference spectroscopy in order to elucidate the mechanisms of site-specific enhancement by Ni(II) of DNA base oxidation with active oxygen species, observed previously (Kasprzak et al., Cancer Res., 49 (1989) 5964; Carcinogenesis, 11 (1990) 647). The interactions were generally weak and could be quantitated only at pH 7.2-7.9. The resulting coordination binding of Ni(II) was stronger with the purine derivatives, especially these of guanine, than with pyrimidine derivatives. Also, Ni(II) interacted more strongly with the bases of 2'-deoxynucleotides than with the bases of 2'-deoxynucleosides. The apparent stability constants for the interactions calculated with the use of a non-linear regression method, equalled 102 +/- 14, 159 +/- 30 and 290 +/- 70 M-1 for Ni(II) coordinated by 5'dAMP, 5'dADP and 5'dATP, respectively, and 305 +/- 73, 191 +/- 54, and 270 +/- 28 M-1 for 5'dGMP, 5'dGDP and 5'dGTP, respectively. Stability constant for the dG Ni(II) interaction was 39 +/- 7 M-1. Interactions of Ni(II) with the bases of dA, dC, dT and the dC- and dT- mono-, di- and tri-phosphates were too weak for meaningful quantitation. The strongest relative Ni(II) interaction with dG may explain high sensitivity of the dG site at the DNA molecule to Ni(II)-mediated oxidation observed in vitro and in vivo. The present results contrast with Ni(II)-directed site specific cleavage of DNA with H2O2 that occurs preferentially at the pyrimidine bases (Kawanishi et al., Carcinogenesis, 10 (1989) 2231). JF - Chemico-biological interactions AU - Datta, A K AU - Riggs, C W AU - Fivash, M J AU - Kasprzak, K S AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute-FCRDC, MD 21702-1201. Y1 - 1991 PY - 1991 DA - 1991 SP - 323 EP - 334 VL - 79 IS - 3 SN - 0009-2797, 0009-2797 KW - Carcinogens KW - 0 KW - Deoxyribonucleosides KW - Deoxyribonucleotides KW - Nickel KW - 7OV03QG267 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Drug Interactions KW - Spectrophotometry, Ultraviolet KW - DNA -- drug effects KW - Carcinogens -- metabolism KW - Deoxyribonucleotides -- metabolism KW - Carcinogens -- toxicity KW - Nickel -- toxicity KW - Nickel -- metabolism KW - Deoxyribonucleosides -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72120312?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mechanisms+of+nickel+carcinogenesis.+Interaction+of+Ni%28II%29+with+2%27-deoxynucleosides+and+2%27-deoxynucleotides.&rft.au=Datta%2C+A+K%3BRiggs%2C+C+W%3BFivash%2C+M+J%3BKasprzak%2C+K+S&rft.aulast=Datta&rft.aufirst=A&rft.date=1991-01-01&rft.volume=79&rft.issue=3&rft.spage=323&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 - 1991-11-01 N1 - Date created - 1991-11-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Gene expression, ontogeny and transplacental induction of hepatic UDP-glucuronosyl transferase activity in mice. AN - 72118175; 1914788 AB - The ontogeny and transplacental inducibility of UDP-glucuronosyl transferase (UDPGT) activities potentially relevant to detoxification of polycyclic aromatic hydrocarbons were studied in (C57BL/6 x DBA/2) F1 or (DBA/2 x C57BL/6) F1 fetal mouse liver, with p-nitrophenol (PNP) and 3-hydroxybenzo[a]pyrene (3-OH-BP) as substrates. Both UDPGT activities developed during the late fetal period and reached almost 60% of the adult activity at term; PNP, but not 3-OH-BP UDPGT decreased significantly on postnatal day 1 before rising to adult levels. A single exposure to beta-naphthoflavone (beta NF; 150 mg/kg) on day 17 of gestation induced the PNP-UDPGT activity significantly (1.5-fold) by day 19 in the B6D2 F1s but not D2B6 F1s. A single dose of 3-methylcholanthrene (MC; 100 mg/kg) or 2,3,7,8,-tetrachlorodibenzo-p-dioxin (10 micrograms/kg) did not induce, but three injections of MC also resulted in significant induction in the fetuses of C57BL/6 mothers. 3-OH-BP-UDPGT was not significantly induced by any of the chemicals in either genetic cross. In a parallel study, a gene for an inducible mouse UDPGT, designated UDPGTm-1, was shown by Northern blotting to be expressed in fetal liver by day 18 of gestation at low levels relative to adults, but was not induced transplacentally by MC, beta NF or phenobarbital (PB). These results show that (1) at least two functionally defined UDPGT activities toward phenolic substrates are present in the late fetal mouse liver; (2) one of these is transplacentally inducible by beta NF and MC, but only in fetuses of C57BL/6 mothers, (3) induction where achieved was relatively small in magnitude, and (4) a gene of a PB-inducible UDPGT was expressed at low levels in the fetuses but was not induced transplacentally. JF - Developmental pharmacology and therapeutics AU - Chauhan, D P AU - Miller, M S AU - Owens, I S AU - Anderson, L M AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick Cancer Research Facility, Md. Y1 - 1991 PY - 1991 DA - 1991 SP - 139 EP - 149 VL - 16 IS - 3 SN - 0379-8305, 0379-8305 KW - Benzoflavones KW - 0 KW - Polychlorinated Dibenzodioxins KW - Methylcholanthrene KW - 56-49-5 KW - beta-Naphthoflavone KW - 6051-87-2 KW - Glucuronosyltransferase KW - EC 2.4.1.17 KW - Index Medicus KW - Mice, Inbred C57BL -- embryology KW - Animals KW - Methylcholanthrene -- pharmacology KW - Polychlorinated Dibenzodioxins -- pharmacology KW - Mice, Inbred DBA -- embryology KW - Gestational Age KW - Gene Expression KW - Enzyme Induction KW - Mice KW - Mice, Inbred Strains -- embryology KW - Benzoflavones -- pharmacology KW - Liver -- enzymology KW - Glucuronosyltransferase -- biosynthesis KW - Fetus -- enzymology KW - Liver -- embryology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72118175?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Developmental+pharmacology+and+therapeutics&rft.atitle=Gene+expression%2C+ontogeny+and+transplacental+induction+of+hepatic+UDP-glucuronosyl+transferase+activity+in+mice.&rft.au=Chauhan%2C+D+P%3BMiller%2C+M+S%3BOwens%2C+I+S%3BAnderson%2C+L+M&rft.aulast=Chauhan&rft.aufirst=D&rft.date=1991-01-01&rft.volume=16&rft.issue=3&rft.spage=139&rft.isbn=&rft.btitle=&rft.title=Developmental+pharmacology+and+therapeutics&rft.issn=03798305&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-01 N1 - Date created - 1991-11-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cytochrome P4501A2 constitutively expressed from transduced DNA mediates metabolic activation and DNA-adduct formation of aromatic amine carcinogens in NIH 3T3 cells. AN - 72117139; 1910484 AB - We transduced mouse cytochrome P4501A2 DNA into NIH 3T3 cells by retrovirus-mediated gene transfer. The capacity of the transduced cytochrome P4501A2 for metabolic activation and DNA-carcinogen adduct formation of aromatic amine carcinogens was investigated. Clones of NIH 3T3 cells that constitutively express cytochrome P4501A2 and controls were exposed to a prototype food-derived carcinogenic heterocyclic amine, 2-amino-3-methylimidazo[4,5-f]quinoline (IQ), and an aromatic amine, 2-acetylaminofluorene (AAF), and their genomic DNAs were analyzed for adducts by 32P-postlabeling assays. Kinetic analysis of DNA-carcinogen adducts indicated that adduct formation was dependent on the level of the enzyme, the dose of carcinogen, and the duration of exposure. Addition of 7,8-benzoflavone, an inhibitor of P4501A2, blocked both the enzyme activity and DNA-adduct formation, indicating the specific role of P4501A2 in metabolic activation and adduct formation. Three specific IQ-DNA adducts were detected in cells expressing P4501A2. Fingerprints of the in situ DNA adducts were similar to those of the in vivo adducts in rodent hepatic DNA after the administration of IQ. A single AAF-DNA adduct was observed in cells exposed to AAF, but other minor adducts were also detected in vivo. These results show that cells expressing constitutive levels of single cytochrome P450s provide an excellent in situ model system for analyzing the catalytic specificity, metabolic activation, and genotoxicity of putative toxic, mutagenic, and carcinogenic substances. JF - Molecular carcinogenesis AU - Battula, N AU - Schut, H A AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, Bethesda, Maryland. Y1 - 1991 PY - 1991 DA - 1991 SP - 407 EP - 414 VL - 4 IS - 5 SN - 0899-1987, 0899-1987 KW - Benzoflavones KW - 0 KW - Carcinogens KW - Quinolines KW - 2-amino-3-methylimidazo(4,5-f)quinoline KW - 30GL3D3T0G KW - alpha-naphthoflavone KW - 604-59-1 KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Oxidoreductases KW - EC 1.- KW - 7-Alkoxycoumarin O-Dealkylase KW - EC 1.14.13.- KW - Cytochrome P-450 CYP1A2 KW - EC 1.14.14.1 KW - Index Medicus KW - Rats KW - Animals KW - 3T3 Cells KW - Transfection KW - DNA -- metabolism KW - In Vitro Techniques KW - 7-Alkoxycoumarin O-Dealkylase -- metabolism KW - Mice KW - Cloning, Molecular KW - Benzoflavones -- pharmacology KW - Quinolines -- metabolism KW - Oxidoreductases -- genetics KW - Carcinogens -- metabolism KW - Oxidoreductases -- metabolism KW - DNA Damage KW - Cytochrome P-450 Enzyme System -- genetics KW - Cytochrome P-450 Enzyme System -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72117139?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+carcinogenesis&rft.atitle=Cytochrome+P4501A2+constitutively+expressed+from+transduced+DNA+mediates+metabolic+activation+and+DNA-adduct+formation+of+aromatic+amine+carcinogens+in+NIH+3T3+cells.&rft.au=Battula%2C+N%3BSchut%2C+H+A%3BThorgeirsson%2C+S+S&rft.aulast=Battula&rft.aufirst=N&rft.date=1991-01-01&rft.volume=4&rft.issue=5&rft.spage=407&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-14 N1 - Date created - 1991-11-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Complexities of the protein kinase C pathway. AN - 72113880; 1910477 JF - Molecular carcinogenesis AU - Blumberg, P M AD - Molecular Mechanisms of Tumor Promotion Section, National Cancer Institute, Bethesda, Maryland. Y1 - 1991 PY - 1991 DA - 1991 SP - 339 EP - 344 VL - 4 IS - 5 SN - 0899-1987, 0899-1987 KW - Carcinogens KW - 0 KW - Isoenzymes KW - Phorbol Esters KW - Protein Kinase C KW - EC 2.7.11.13 KW - Endopeptidases KW - EC 3.4.- KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Phorbol Esters -- pharmacology KW - Carcinogens -- pharmacology KW - Animals KW - Isoenzymes -- classification KW - Isoenzymes -- physiology KW - Humans KW - Endopeptidases -- metabolism KW - Enzyme Activation -- drug effects KW - Calcium -- physiology KW - Protein Binding KW - Structure-Activity Relationship KW - Protein Kinase C -- classification KW - Protein Kinase C -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72113880?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+carcinogenesis&rft.atitle=Complexities+of+the+protein+kinase+C+pathway.&rft.au=Blumberg%2C+P+M&rft.aulast=Blumberg&rft.aufirst=P&rft.date=1991-01-01&rft.volume=4&rft.issue=5&rft.spage=339&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-11-14 N1 - Date created - 1991-11-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Trends in epidemiology of colorectal cancer. AN - 72100112; 1892516 JF - Journal of surgical oncology. Supplement AU - Crespi, M AU - Caperle, M AD - Service of Environmental Carcinogenesis, Epidemiology and Prevention, Regina Elena National Cancer Institute, Rome, Italy. Y1 - 1991 PY - 1991 DA - 1991 SP - 1 EP - 3 VL - 2 SN - 1046-7416, 1046-7416 KW - Index Medicus KW - Epidemiologic Methods KW - Risk Factors KW - Humans KW - Incidence KW - Europe -- epidemiology KW - Diet KW - United States -- epidemiology KW - Male KW - Female KW - Colorectal Neoplasms -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72100112?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+surgical+oncology.+Supplement&rft.atitle=Trends+in+epidemiology+of+colorectal+cancer.&rft.au=Crespi%2C+M%3BCaperle%2C+M&rft.aulast=Crespi&rft.aufirst=M&rft.date=1991-01-01&rft.volume=2&rft.issue=&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Journal+of+surgical+oncology.+Supplement&rft.issn=10467416&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-10-24 N1 - Date created - 1991-10-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Toxicity and carcinogenicity studies of nalidixic acid in rodents. AN - 72091431; 1889378 AB - Toxicity and carcinogenicity studies of nalidixic acid, an antimicrobial agent used to treat bacterial infections of the urinary tract, were conducted in F344/N rats and B6C3F1 mice of each sex for 13 weeks or 2 years. In the 13-week studies, nalidixic acid was administered at dietary concentrations ranging from 1,000 to 16,000 ppm. Body weights of both rats and mice were reduced in the groups receiving diet containing 8,000 and 16,000 ppm, and feed consumption of rats in the highest treatment groups was approximately two-thirds that of controls. Degeneration of the germinal epithelium in the seminiferous tubules of the testis was observed in male rats that received 16,000 ppm; no other compound-related histopathologic effects were observed in either species. Two-year studies were conducted by feeding diets containing 0, 2,000, or 4,000 ppm nalidixic acid to groups of 50 rats and mice/sex/group. The average daily feed consumption was slightly reduced compared to control groups and resulted in approximate daily doses of 82 or 175 mg nalidixic acid/kg for low dose and high dose rats, and 220 or 475 mg/kg for low dose and high dose mice. Mean body weights of dosed rats and mice were lower than those of controls, except for groups of low dose female rats and male mice. The incidences of preputial gland neoplasms in dosed male rats and of clitoral gland neoplasms in dosed female rats were significantly increased compared to those in controls; responses in low dose groups were similar to those in high dose groups. There were decreased incidences of leukemia and mammary gland neoplasms in dosed female rats and of pituitary gland neoplasms in dosed male rats. Subcutaneous tissue fibrosarcomas were marginally increased in dosed male mice. There were no increased incidences of neoplasms in dosed female mice. Under the conditions of these studies, the dietary administration of nalidixic acid was carcinogenic for rats, causing preputial gland or clitoral gland neoplasms in males and females, respectively. The association of subcutaneous neoplasms with administration of nalidixic acid to male mice was equivocal. JF - Drug and chemical toxicology AU - Morrissey, R E AU - Eustis, S AU - Haseman, J K AU - Huff, J AU - Bucher, J R AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1991 PY - 1991 DA - 1991 SP - 45 EP - 66 VL - 14 IS - 1-2 SN - 0148-0545, 0148-0545 KW - Nalidixic Acid KW - 3B91HWA56M KW - Index Medicus KW - Rats KW - Eating -- drug effects KW - Mice, Inbred Strains KW - Animals KW - Rats, Inbred F344 KW - Liver -- pathology KW - Liver -- drug effects KW - Cataract -- chemically induced KW - Body Weight -- drug effects KW - Mice KW - Male KW - Female KW - Neoplasms, Experimental -- chemically induced KW - Nalidixic Acid -- toxicity KW - Neoplasms, Experimental -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72091431?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Drug+and+chemical+toxicology&rft.atitle=Toxicity+and+carcinogenicity+studies+of+nalidixic+acid+in+rodents.&rft.au=Morrissey%2C+R+E%3BEustis%2C+S%3BHaseman%2C+J+K%3BHuff%2C+J%3BBucher%2C+J+R&rft.aulast=Morrissey&rft.aufirst=R&rft.date=1991-01-01&rft.volume=14&rft.issue=1-2&rft.spage=45&rft.isbn=&rft.btitle=&rft.title=Drug+and+chemical+toxicology&rft.issn=01480545&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-10-15 N1 - Date created - 1991-10-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of acid suppressants in patients with Zollinger-Ellison syndrome. AN - 72088926; 1679671 AB - Virtually all symptoms in patients with Zollinger-Ellison syndrome are due to acid hypersecretion, thus the control of acid secretion is the first and most important step in the management of patients with this syndrome. Antisecretory medication is prescribed as soon as the diagnosis of Zollinger-Ellison syndrome is made, as patients may bleed or perforate with little warning. Acid output is reduced to less than 10 mmol/h to heal mucosal lesions, but in patients with a Billroth I or II gastrectomy and those with severe oesophagitis and stricture formation, acid output is reduced to less than 5 or less than 1 mmol/h. Acid output and not symptomatic response is a reliable guide of the adequacy of therapy. In sufficient doses, all H2-receptor antagonists are useful; however, side effects associated with cimetidine therapy limit its use. The ratio of potencies of cimetidine:ranitidine:famotidine is 1:4:32. Ranitidine given as a 50-mg intravenous bolus, followed by a continuous infusion of 0.5 mg.kg/h, controls acid hypersecretion acutely in patients with Zollinger-Ellison syndrome. Acid output is checked after 4 h, and the dose increased until acid output is less than 10 mmol/h. In 70% of patients with Zollinger-Ellison syndrome, 1 mg.kg/h reduces acid output to less than 10 mmol/h; however, doses up to 4 mg.kg/h have been used. When patients are switched to oral ranitidine, a useful dosage conversion is to administer 1.5 times the total daily intravenous dose in four equal doses every 6 h. Four doses of oral drug are given before the infusion is stopped. Six hours after the first/last oral dose, acid output is checked. In our patients, the mean dose of ranitidine was 2100 mg/day (range, 450-9200 mg/day). No serious toxicity was observed. Omeprazole, which has a long duration of action and is a potent inhibitor of gastric acid secretion, has simplified management. Once-daily dosing is sufficient in most patients, and a reasonable starting dose is 60 mg daily. The dose may be increased to 120 mg once daily; if this dosage fails to control acid secretion, 60 mg is administered every 12 h. In our studies, the median dose was 90 mg/day (range, 20-120 mg/day). Omeprazole was more effective than H2-receptor antagonists in providing symptom relief and mucosal healing and did not cause significant toxicity. In particular, no gastric carcinoid tumours developed during four years of use. Omeprazole is, therefore, the treatment of choice for control of acid secretion in patients with Zollinger-Ellison syndrome.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Alimentary pharmacology & therapeutics AU - Maton, P N AD - Digestive Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland. Y1 - 1991 PY - 1991 DA - 1991 SP - 25 EP - 35 VL - 5 Suppl 1 SN - 0269-2813, 0269-2813 KW - Histamine H2 Antagonists KW - 0 KW - Omeprazole KW - KG60484QX9 KW - Index Medicus KW - Humans KW - Omeprazole -- therapeutic use KW - Histamine H2 Antagonists -- therapeutic use KW - Zollinger-Ellison Syndrome -- therapy KW - Gastric Acid -- secretion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72088926?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alimentary+pharmacology+%26+therapeutics&rft.atitle=Role+of+acid+suppressants+in+patients+with+Zollinger-Ellison+syndrome.&rft.au=Maton%2C+P+N&rft.aulast=Maton&rft.aufirst=P&rft.date=1991-01-01&rft.volume=5+Suppl+1&rft.issue=&rft.spage=25&rft.isbn=&rft.btitle=&rft.title=Alimentary+pharmacology+%26+therapeutics&rft.issn=02692813&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-10-17 N1 - Date created - 1991-10-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The relative contributions of different organ sites to the total cancer mortality associated with low-dose radiation exposure. AN - 72081906; 1888094 JF - Annals of the ICRP AU - Land, C E AU - Sinclair, W K AD - Radiation Epidemiology Branch, National Cancer Institute, Bethesda, MD. Y1 - 1991 PY - 1991 DA - 1991 SP - 31 EP - 57 VL - 22 IS - 1 SN - 0146-6453, 0146-6453 KW - Index Medicus KW - Space life sciences KW - Humans KW - Aged KW - Child KW - Dose-Response Relationship, Radiation KW - Child, Preschool KW - Infant KW - Organ Specificity -- radiation effects KW - Aged, 80 and over KW - Adult KW - Life Expectancy KW - Middle Aged KW - Adolescent KW - Female KW - Male KW - Survival Analysis KW - Neoplasms, Radiation-Induced -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72081906?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+ICRP&rft.atitle=The+relative+contributions+of+different+organ+sites+to+the+total+cancer+mortality+associated+with+low-dose+radiation+exposure.&rft.au=Land%2C+C+E%3BSinclair%2C+W+K&rft.aulast=Land&rft.aufirst=C&rft.date=1991-01-01&rft.volume=22&rft.issue=1&rft.spage=31&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+ICRP&rft.issn=01466453&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-10-04 N1 - Date created - 1991-10-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Down-regulation of c-Ki-ras2 gene expression associated with morphologic differentiation in human embryonal carcinoma cells treated with berberine. AN - 72065023; 1679102 AB - A pluripotent human embryonal carcinoma (EC) clone, NT2/D1, which was derived from the Tera-2 cell line, was induced to differentiate into cells with neuronal-like cell morphology by treatment with berberine, an alkaloid derived from a Chinese herbal medicine (Huang Lien). As early as one day after 24-hour treatment of cells with berberine at a nontoxic dose of 0.1 mg/ml in culture medium, the cells started to show morphologic changes, developing into terminally differentiated neuronal-like cells with long, inter-connecting network cellular structures. This process was much faster as compared with that induced by treatment with retinoic acid (RA), which took at least several days to develop. Unlike RA, berberine could not induce murine EC cell line, F9, to differentiate into endodermal cells. It was also found that although the NT2/D1 cell clone exhibited amplification and enhanced mRNA expression of c-Ki-ras2 gene as did the parent cell line, a marked down-regulation of c-Ki-ras2 mRNA expression was observed. However, there was no change in actin mRNA expression even after differentiation had occurred. Thus, morphologic differentiation of EC cells into neuronal-like cells was found to be associated with down-regulation of a protooncogene which plays some definite role in oncogenesis. The mechanism by which berberine induces differentiation in these cells needs further investigation. JF - Journal of the Formosan Medical Association = Taiwan yi zhi AU - Chang, K S AD - Laboratory of Cellular Oncology, National Cancer Institute, NIH, Bethesda, MD. Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 10 EP - 14 VL - 90 IS - 1 SN - 0929-6646, 0929-6646 KW - Actins KW - 0 KW - Drugs, Chinese Herbal KW - RNA, Messenger KW - Berberine KW - 0I8Y3P32UF KW - Tretinoin KW - 5688UTC01R KW - Index Medicus KW - Tretinoin -- pharmacology KW - Humans KW - Neurons -- drug effects KW - Cell Division -- drug effects KW - Actins -- metabolism KW - Gene Expression Regulation, Neoplastic -- drug effects KW - Tumor Cells, Cultured KW - RNA, Messenger -- metabolism KW - Neurons -- cytology KW - Down-Regulation -- drug effects KW - Cell Line KW - Male KW - Genes, ras KW - Berberine -- pharmacology KW - Teratoma -- genetics KW - Teratoma -- pathology KW - Cell Differentiation -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72065023?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Formosan+Medical+Association+%3D+Taiwan+yi+zhi&rft.atitle=Down-regulation+of+c-Ki-ras2+gene+expression+associated+with+morphologic+differentiation+in+human+embryonal+carcinoma+cells+treated+with+berberine.&rft.au=Chang%2C+K+S&rft.aulast=Chang&rft.aufirst=K&rft.date=1991-01-01&rft.volume=90&rft.issue=1&rft.spage=10&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+Formosan+Medical+Association+%3D+Taiwan+yi+zhi&rft.issn=09296646&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-10-01 N1 - Date created - 1991-10-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Racial variation in the distribution of Ha-ras-1 alleles. AN - 72043655; 1714739 AB - Restriction fragment length polymorphism analyses of the Ha-ras-1 proto-oncogene were undertaken in white and black populations residing in the Baltimore-Washington metropolitan area to address whether specific rare alleles of the Ha-ras-1 proto-oncogene locus vary in their distribution among different racial groups. High-molecular-weight genomic DNA samples from the lungs of 80 lung cancer patients and 92 accident victims were digested with appropriate restriction enzymes and subjected to Southern analysis using the 6.6-kb BamHI human Ha-ras-1 recombinant fragment from the plasmid pEC. Thirty allelomorphs of different sizes were detected among the 172 study subjects. An association was observed between race and specific alleles. Rare alleles were more frequent in black cancer patients and trauma victims than in whites. Within each racial category, lung cancer patients had an excess of rare alleles. These data indicate the importance of controlling for racial variation when designing studies to determine human cancer risk factors. JF - Molecular carcinogenesis AU - Weston, A AU - Vineis, P AU - Caporaso, N E AU - Krontiris, T G AU - Lonergan, J A AU - Sugimura, H AD - Laboratory of Human Carcinogenesis, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1991 PY - 1991 DA - 1991 SP - 265 EP - 268 VL - 4 IS - 4 SN - 0899-1987, 0899-1987 KW - Ha-ras-1 KW - DNA, Neoplasm KW - 0 KW - DNA KW - 9007-49-2 KW - Deoxyribonuclease HpaII KW - EC 3.1.21.- KW - Deoxyribonucleases, Type II Site-Specific KW - EC 3.1.21.4 KW - Index Medicus KW - Autopsy KW - Reference Values KW - Humans KW - Lung -- pathology KW - DNA, Neoplasm -- isolation & purification KW - DNA -- isolation & purification KW - Alleles KW - Adult KW - DNA -- genetics KW - DNA, Neoplasm -- genetics KW - Middle Aged KW - Genes, ras KW - Genetic Variation KW - African Continental Ancestry Group -- genetics KW - Polymorphism, Restriction Fragment Length KW - Lung Neoplasms -- genetics KW - European Continental Ancestry Group -- genetics KW - Lung Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72043655?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+carcinogenesis&rft.atitle=Racial+variation+in+the+distribution+of+Ha-ras-1+alleles.&rft.au=Weston%2C+A%3BVineis%2C+P%3BCaporaso%2C+N+E%3BKrontiris%2C+T+G%3BLonergan%2C+J+A%3BSugimura%2C+H&rft.aulast=Weston&rft.aufirst=A&rft.date=1991-01-01&rft.volume=4&rft.issue=4&rft.spage=265&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-20 N1 - Date created - 1991-09-20 N1 - Date revised - 2017-01-13 N1 - Gene symbol - Ha-ras-1 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Isolation and partial characterization of a transformation-associated sequence from human nasopharyngeal carcinoma. AN - 72041699; 1714741 AB - A transforming activity associated with Chinese nasopharyngeal carcinoma (NPC) cell line CNE2 DNA has been identified by transfer into nontransformed promotion-sensitive mouse JB6(P+) C141 cells. To clone this transformation-associated sequence, we carried out three cycles of transfection, followed by cloning of anchorage-independent transformants in soft agar. A tertiary CNE/JB6 clonal transfectant cell line 625 whose DNA showed transforming activity, as indicated in both soft-agar assay and nude-mice implantation, was used to make a genomic library in the vector lambda dash. Using the human repeated sequence Blur 8 to screen the library, we obtained 10 human Alu-positive clones. A cloned Alu-positive insert of 16 kbp, CNE 323, was characterized in detail. CNE 323 transferred moderate transforming activity when introduced into JB6 P+ cells and showed no homology to Ha-, Ki-, or N-ras genes; human promotion sensitivity genes; src, myb, jun, myc, fos, raf, or int-2 oncogenes; or epidermal growth factor receptor. The isolated CNE 323 DNA sequence appeared to preserve the genomic structure of the original sequence found in CNE2 cells and in nude mouse tumors induced by CNE2 cells or by CNE/JB6 transfectant cells, indicating that the cloned NPC sequence was activated during NPC carcinogenesis and not during transfection or construction of the library, and that the cloned sequence or a larger sequence of which it was part played a role in tumor formation. Finally, we identified a 1.3-kb mRNA that hybridizes to a subclone of the 16-kb NPC sequence in CNE2 cell poly (A)+ RNA. JF - Molecular carcinogenesis AU - Cao, Y AU - Sun, Y AU - Poirier, S AU - Winterstein, D AU - Hegamyer, G AU - Seed, J AU - Malin, S AU - Colburn, N H AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick Cancer Research, Maryland 21702-1201. Y1 - 1991 PY - 1991 DA - 1991 SP - 297 EP - 307 VL - 4 IS - 4 SN - 0899-1987, 0899-1987 KW - DNA, Neoplasm KW - 0 KW - RNA, Messenger KW - Poly A KW - 24937-83-5 KW - RNA KW - 63231-63-0 KW - Index Medicus KW - Animals KW - Skin KW - Sequence Homology, Nucleic Acid KW - Humans KW - Mice KW - Nucleic Acid Hybridization KW - RNA, Messenger -- genetics KW - Genomic Library KW - Cloning, Molecular KW - Base Sequence KW - Oncogenes KW - Blotting, Southern KW - Restriction Mapping KW - Poly A -- genetics KW - Cell Line KW - RNA -- genetics KW - Transfection KW - DNA, Neoplasm -- genetics KW - Nasopharyngeal Neoplasms -- genetics KW - DNA, Neoplasm -- isolation & purification KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/72041699?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+carcinogenesis&rft.atitle=Isolation+and+partial+characterization+of+a+transformation-associated+sequence+from+human+nasopharyngeal+carcinoma.&rft.au=Cao%2C+Y%3BSun%2C+Y%3BPoirier%2C+S%3BWinterstein%2C+D%3BHegamyer%2C+G%3BSeed%2C+J%3BMalin%2C+S%3BColburn%2C+N+H&rft.aulast=Cao&rft.aufirst=Y&rft.date=1991-01-01&rft.volume=4&rft.issue=4&rft.spage=297&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=08991987&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-09-20 N1 - Date created - 1991-09-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Decipherment of Yue-Ren-Ge (Song of the Yue Boatman) AN - 58241336; 9209293 AB - Presented is the decipherment of a song in the Yue language, the "Song of the Yue Ferryman." The song was transcribed into Chinese characters & translated by a sixth-century Chinese scholar. Based on the hypothesis that the Yue language was a member of the Thai language group, a comparison is made of the words of the song with words of written Thai. It is noted that many of the words of this 2,500-year-old song would be easily understood by modern speakers of Thai. 9 References. B. Annesser Murray JF - Cahiers de Linguistique Asie Orientale AU - Zhengzhang, Shangfang AD - Chinese Academy of Social Sciences, 5 Jianguomen Nei Da Jie 5 Hao Beijing People's Republic China Y1 - 1991/01// PY - 1991 DA - January 1991 SP - 159 EP - 168 VL - 20 IS - 2 SN - 0153-3320, 0153-3320 KW - Yue boatman song, Chinese translation, Thai relationship KW - Singing (78950) KW - Diachronic Linguistics (18500) KW - Chinese (12100) KW - Language Classification (41900) KW - Written Language (98900) KW - Kam Tai Languages (40250) KW - article KW - 5111: descriptive linguistics; diachronic linguistics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/58241336?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Allba&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cahiers+de+Linguistique+Asie+Orientale&rft.atitle=Decipherment+of+Yue-Ren-Ge+%28Song+of+the+Yue+Boatman%29&rft.au=Zhengzhang%2C+Shangfang&rft.aulast=Zhengzhang&rft.aufirst=Shangfang&rft.date=1991-01-01&rft.volume=20&rft.issue=2&rft.spage=159&rft.isbn=&rft.btitle=&rft.title=Cahiers+de+Linguistique+Asie+Orientale&rft.issn=01533320&rft_id=info:doi/ LA - English DB - Linguistics and Language Behavior Abstracts (LLBA) N1 - Date revised - 2003-10-01 N1 - Last updated - 2016-09-27 N1 - CODEN - CLAOEB N1 - SubjectsTermNotLitGenreText - Language Classification (41900); Diachronic Linguistics (18500); Chinese (12100); Kam Tai Languages (40250); Written Language (98900); Singing (78950) ER - TY - JOUR T1 - In-vivo effects of solar-simulated ultraviolet irradiation on antioxidant enzymes and lipid peroxidation in human epidermis AN - 16797483; 3548763 AB - The effects of solar-simulated UV-irradiation on the activity of antioxidant enzymes and the amount of diene conjugation were studied in human epidermis in vivo. A single dose of UV-irradiation was found to result in a transient reduction in superoxide dismutase activity and this was followed by increased amounts of conjugated diene double bonds, an index for oxidative stress. This suggests that in-vivo exposure of human epidermis to solar-simulated UV-irradiation causes changes in the enzymic antioxidant defence system which, in turn, are accompanied by increased level of oxidative stress. JF - British Journal of Dermatology AU - Punnonen, K AU - Autio, P AU - Kiistala, U AU - Ahotupa, M AD - Lab. Cell. Carcinog. and Tumor Promotion, NCI, Build. 37 3B26, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 18 EP - 20 VL - 125 IS - 1 SN - 0007-0963, 0007-0963 KW - antioxidant enzymes KW - Toxicology Abstracts KW - antioxidants KW - U.V. radiation KW - epidermis KW - enzymes KW - lipid peroxidation KW - man KW - X 24210:Radiation & radioactive materials UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16797483?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+Journal+of+Dermatology&rft.atitle=In-vivo+effects+of+solar-simulated+ultraviolet+irradiation+on+antioxidant+enzymes+and+lipid+peroxidation+in+human+epidermis&rft.au=Punnonen%2C+K%3BAutio%2C+P%3BKiistala%2C+U%3BAhotupa%2C+M&rft.aulast=Punnonen&rft.aufirst=K&rft.date=1991-01-01&rft.volume=125&rft.issue=1&rft.spage=18&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Dermatology&rft.issn=00070963&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - U.V. radiation; lipid peroxidation; epidermis; man; antioxidants; enzymes ER - TY - JOUR T1 - Oxoaporphine alkaloids: Conversion of lysicamine into liriodendronine and its 2-O-methyl ether, and antifungal activity AN - 16771842; 3529789 AB - Pschorr reaction of diazonium salt 7 in aqueous methanolic sulfuric acid afforded, besides lysicamine 2, the orange colored sulfate of oxodibenzopyrrocoline (8). The structure is fully supported by an X-ray analysis of its picrate salt. Selective ether cleavage of lysicamine (2) with 48% HBr afforded a hydrobromide of 9, and free betaine 9 on treatment with pyridine-water. Both compounds methylated on treatment with etherial diazomethane on nitrogen to give the known 2-O,N-dimethylliriodendronine (11). Liriodendronine (10) was obtained from lysicamine (2) on heating with pyridine-HBr at 189 degree C, and treatment with pyridine-water, as a dark violet betaine. Betaine 12 was obtained by heating 11-HCl to 200 degree C. The quatemary salts of lysicamine, lysicamine methiodine (3) and lysicamine methosulfate (4) were comparable in anticandidal activity to liriodenine (1), but were not as active as liriodenine methiodide (13). JF - Archiv der Pharmazie AU - Pabuccuoglu, V AU - Rozwadowska, MD AU - Brossi, A AU - Clark, A AU - Hufford, C D AU - George, C AU - Flippen-Anderson, J L AD - Med. Chem. Sect., LAC, NIDDK, NIH, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 29 EP - 34 VL - 324 IS - 1 SN - 0365-6233, 0365-6233 KW - lysicamine KW - liriodendronine KW - Microbiology Abstracts A: Industrial & Applied Microbiology KW - conversion KW - antifungal agents KW - antifungal activity KW - A 01067:Antifungal & fungicidal UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16771842?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archiv+der+Pharmazie&rft.atitle=Oxoaporphine+alkaloids%3A+Conversion+of+lysicamine+into+liriodendronine+and+its+2-O-methyl+ether%2C+and+antifungal+activity&rft.au=Pabuccuoglu%2C+V%3BRozwadowska%2C+MD%3BBrossi%2C+A%3BClark%2C+A%3BHufford%2C+C+D%3BGeorge%2C+C%3BFlippen-Anderson%2C+J+L&rft.aulast=Pabuccuoglu&rft.aufirst=V&rft.date=1991-01-01&rft.volume=324&rft.issue=1&rft.spage=29&rft.isbn=&rft.btitle=&rft.title=Archiv+der+Pharmazie&rft.issn=03656233&rft_id=info:doi/ LA - German DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - conversion; antifungal activity; antifungal agents ER - TY - JOUR T1 - A method for the detection and management of adverse events in clinical trials AN - 16746357; 3520479 AB - This paper describes a systematic approach to the detection, classification, and documentation of adverse events in a multicenter clinical trial. The system is designed to minimize investigator prejudgment, capture infrequent or unexpected adverse effects, track concurrent adverse events, and allow for comparison of effects across clinical centers. The method employs a standard questionnaire, which records health status and symptomatology of the patient at study entry as well as at follow-up visits to allow comparison. A systems review, to detect emerging or changing symptoms, is also included. The association of the adverse events to the study drug is classified according to standard criteria. All adverse events, whether or not judged to be drug related, are recorded. Dose modifications are prescribed and documented at each follow-up visit until the adverse event is resolved. This system combines standard methodology with continuous monitoring to provide a comprehensive approach to managing adverse events in a clinical trial. JF - Drug Information Journal AU - Tangrea, JA AU - Adrianza, ME AU - McAdams, M AD - Cancer Prev. Stud. Branch, NCI/NIH, Executive Plaza N., Room 211, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 63 EP - 80 VL - 25 IS - 1 SN - 0092-8615, 0092-8615 KW - Toxicology Abstracts KW - side effects KW - detection KW - clinical trials KW - pharmaceuticals KW - methodology KW - X 24221:Toxicity testing KW - X 24113:Side effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16746357?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Drug+Information+Journal&rft.atitle=A+method+for+the+detection+and+management+of+adverse+events+in+clinical+trials&rft.au=Tangrea%2C+JA%3BAdrianza%2C+ME%3BMcAdams%2C+M&rft.aulast=Tangrea&rft.aufirst=JA&rft.date=1991-01-01&rft.volume=25&rft.issue=1&rft.spage=63&rft.isbn=&rft.btitle=&rft.title=Drug+Information+Journal&rft.issn=00928615&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - pharmaceuticals; side effects; clinical trials; detection; methodology ER - TY - JOUR T1 - Clavepictines A and B: Cytotoxic quinolizidines from the tunicate Clavelina picta AN - 16697662; 3504871 AB - In our investigations of the chemistry and biological significance of the secondary metabolites of Bermudian tunicates, we found cytotoxicity (KB: IC sub(50) = 12 mu g/mL) and antimicrobial activity in the organic soluble extracts of Clavelina picta. From substantial collections (1-2 kg) made in the summer of 1984 and the spring of 1987, we have found the first quinolizidines from a tunicate and have evaluated the cytotoxicity of these novel compounds. JF - Journal of the American Chemical Society AU - Raub, M F AU - Cardellina, JH II AU - Choudhary, MI AU - Ni, C-Z AU - Clardy, J AU - Alley, M C AD - NCI, Build. 1052, Rm. 121, Frederick, MD 21702-1201, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 3178 EP - 3180 VL - 113 IS - 8 SN - 0002-7863, 0002-7863 KW - antimicrobial KW - clavepictine KW - cytotoxic KW - cytotoxins KW - quinolizidines KW - Toxicology Abstracts; ASFA 1: Biological Sciences & Living Resources KW - biochemical analysis KW - metabolites KW - Marine KW - Clavelina picta KW - pharmacology KW - Q1 08326:Physiology, biochemistry, biophysics KW - X 24173:Animals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16697662?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+American+Chemical+Society&rft.atitle=Clavepictines+A+and+B%3A+Cytotoxic+quinolizidines+from+the+tunicate+Clavelina+picta&rft.au=Raub%2C+M+F%3BCardellina%2C+JH+II%3BChoudhary%2C+MI%3BNi%2C+C-Z%3BClardy%2C+J%3BAlley%2C+M+C&rft.aulast=Raub&rft.aufirst=M&rft.date=1991-01-01&rft.volume=113&rft.issue=8&rft.spage=3178&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+American+Chemical+Society&rft.issn=00027863&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2014-05-06 N1 - SubjectsTermNotLitGenreText - metabolites; biochemical analysis; pharmacology; cytotoxins; Clavelina picta; Marine ER - TY - JOUR T1 - Rising trend of reported primary genital syphilis and genital ulcer disease in Burkina Faso. AN - 16675344; 3039881 AB - Recent trends in reported primary genital syphilis and genital ulcer disease (GUD) were assessed in Burkina Faso using incidence data reported to the Ministry of Health. From 1978 to 1983 the yearly reports of genital syphilis and GUD rose by 42%. A single period moving average was calculated for each consecutive 13-week period from 1978 to 1983, documenting an average 7% rise per year. Severe limitations in the Ministry of Health of personnel and other resources for surveillance were noted and no improvements in surveillance methods were evident during this study. The rising trend suggests a growing problem of ulcerative sexually transmitted diseases, which may, in turn, facilitate infection with sexually acquired human immunodeficiency virus, coincident with the expansion of this epidemic in Africa. Syphilis complications are also almost certain to include adverse pregnancy outcome due to maternal syphilis. The rising trend in genital syphilis and GUD, and the probable increase in associated adverse sequellae, require that prevention and control of sexually transmitted diseases should be made a high priority. JF - International Journal of Epidemiology AU - Damiba, A E AU - Kelley, K F AU - Vermund, SH AD - Div. AIDS, NIAID/NIH, 6003 Executive Blvd, Rm. 240P, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 490 EP - 494 VL - 20 IS - 2 SN - 0300-5771, 0300-5771 KW - Microbiology Abstracts B: Bacteriology KW - ulcers KW - genitalia KW - surveillance KW - sexually-transmitted diseases KW - man KW - syphilis KW - J 02849:Sexually-transmitted diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16675344?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Epidemiology&rft.atitle=Rising+trend+of+reported+primary+genital+syphilis+and+genital+ulcer+disease+in+Burkina+Faso.&rft.au=Damiba%2C+A+E%3BKelley%2C+K+F%3BVermund%2C+SH&rft.aulast=Damiba&rft.aufirst=A&rft.date=1991-01-01&rft.volume=20&rft.issue=2&rft.spage=490&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Epidemiology&rft.issn=03005771&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - sexually-transmitted diseases; surveillance; syphilis; genitalia; ulcers; man ER - TY - JOUR T1 - Reconstituted viral envelopes - "Trojan Horses" for drug delivery and gene therapy?. AN - 16538097; 2965863 AB - Reconstituted viral envelopes (RVEs) are formed by solubilizing intact virus in detergent and reassembling the envelope on removal of detergent. RVEs can be formed in the presence of agents that become encapsulated and can then be utilized in vitro and in vivo for drug delivery, cell destruction, transfer of membrane components, and as vectors for genetic engineering. The problems with biotechnological applications of RVEs and possible strategies for overcoming them are discussed in this article. JF - Trends in Biotechnology AU - Blumenthal, R AU - Loyter, A AD - Sect. Membrane Struct. and Funct., LMMB, NCI/NIH, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 41 EP - 45 VL - 9 IS - 2 SN - 0167-9430, 0167-9430 KW - Biotechnology and Bioengineering Abstracts; Medical and Pharmaceutical Biotechnology Abstracts KW - gene therapy KW - envelopes KW - drugs KW - transport KW - viruses KW - W 30965:Miscellaneous, Reviews KW - W3 33180:Gene based (protocols, clinical trials, and animal models) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16538097?accountid=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=Trends+in+Biotechnology&rft.atitle=Reconstituted+viral+envelopes+-+%22Trojan+Horses%22+for+drug+delivery+and+gene+therapy%3F.&rft.au=Blumenthal%2C+R%3BLoyter%2C+A&rft.aulast=Blumenthal&rft.aufirst=R&rft.date=1991-01-01&rft.volume=9&rft.issue=2&rft.spage=41&rft.isbn=&rft.btitle=&rft.title=Trends+in+Biotechnology&rft.issn=01679430&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - gene therapy; envelopes; transport; drugs; viruses ER - TY - JOUR T1 - Glycine reductase protein C: Properties and characterization of its role in the reductive cleavage of Se-carboxymethyl-selenoprotein A. AN - 16422881; 2905106 AB - The clostridial glycine reductase complex catalyzes the reductive deamination of glycine in an energy-conserving process that results in the esterification of orthophosphate. The complex consists of three protein components: selenoprotein A; protein B, a carbonyl group protein; and protein C, a sulfhydryl protein. The protein C component also catalyzes the arsenate-dependent decomposition of acetyl phosphate. Reaction of protein C with iodoacetate inhibits its ability to decompose acetyl phosphate, but this inactivation of the enzyme by alkylation is prevented in the presence of the substrate indicating the formation of an unreactive enzyme-bound acetylthiol ester. The Se-carboxymethyl-selenocysteine residue of the selenoprotein A component of glycine reductase was generated by selective alkylation of the ionized selenol group at pH 6 with ( super(14)C)bromoacetate. Using this pure alkylated selenoprotein A as substrate, it was shown that protein C catalyzes the conversion of the ( super(14)C)carboxymethyl group, in selenoether linkage to protein A, to ( super(14)C) acetate in the presence of arsenate, dithiothreitol, and Mg super(2+). A procedure using hydrophobic chromatographic matrices was developed for the large scale isolation of protein C, and a number of the properties of the enzyme were determined. JF - Journal of Biological Chemistry AU - Stadtman, T C AU - Davis, J N AD - Lab. Biochem., NHLBI, NIH, Build. 3, Rm. 108, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 22147 EP - 22153 VL - 266 IS - 33 SN - 0021-9258, 0021-9258 KW - Clostridium KW - Se-carboxymethyl-selenoprotein A KW - characterization KW - cleavage KW - enzymatic activity KW - glycine reductase KW - hydrophobic chromatography KW - protein C KW - purification KW - subunits KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology KW - J 02728:Enzymes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16422881?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=Glycine+reductase+protein+C%3A+Properties+and+characterization+of+its+role+in+the+reductive+cleavage+of+Se-carboxymethyl-selenoprotein+A.&rft.au=Stadtman%2C+T+C%3BDavis%2C+J+N&rft.aulast=Stadtman&rft.aufirst=T&rft.date=1991-01-01&rft.volume=266&rft.issue=33&rft.spage=22147&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - characterization; enzymatic activity; purification; subunits; cleavage; hydrophobic chromatography ER - TY - JOUR T1 - Sequence of the VP7 gene of chicken rotavirus Ch2 strain of serotype 7 rotavirus. AN - 16389250; 2882396 AB - The gene that encodes the VP7 protein of the Ch2 strain of group A chicken rotavirus (serotype G7) was sequenced, and its deduced amino sequence analyzed. The gene is 1067 bp in length and contains a single long open reading frame of 987 nt, capable of encoding a protein of 329 amino acids. Amino acid homology of the chicken rotavirus VP7 to the corresponding protein of rotaviruses representing each of the other twelve G serotypes ranged from 58 to 63%. In addition, the VP7 protein of the Ch2 strain contains a unique amino acid sequence in variable regions VR5 (A), VR7 (B), or VR8 (C), which is consistent with previous studies indicating that these three regions are involved in G serotype specificity. The VP7 protein had amino acid homology of 19 or 33% with that of groups B (ADRV) or C (Cowden) rotavirus strains, respectively. Attempts to produce reassortants in vivo or in vitro between the Ch2 strain and strains belonging to group A or C rotavirus were unsuccessful. The low level of nucleotide identity in the 5' end noncoding region of the VP7 gene between the Ch2 and the group A or C rotaviruses may account for this failure. JF - Virology AU - Nishikawa, K AU - Hoshino, Y AU - Gorziglia, M AD - Epidemiol. Sect., Lab. Infect. Dis., NIAID/NIH, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 853 EP - 856 VL - 185 IS - 2 SN - 0042-6822, 0042-6822 KW - VP7 protein KW - amino acid sequence KW - genes KW - nucleotide sequence KW - prediction KW - rotavirus (chicken) KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Virology & AIDS Abstracts KW - V 22050:Viral genetics including virus reactivation KW - G 07313:Viruses KW - N 14540:Structure, sequence & physical properties UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16389250?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Virology&rft.atitle=Sequence+of+the+VP7+gene+of+chicken+rotavirus+Ch2+strain+of+serotype+7+rotavirus.&rft.au=Nishikawa%2C+K%3BHoshino%2C+Y%3BGorziglia%2C+M&rft.aulast=Nishikawa&rft.aufirst=K&rft.date=1991-01-01&rft.volume=185&rft.issue=2&rft.spage=853&rft.isbn=&rft.btitle=&rft.title=Virology&rft.issn=00426822&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - nucleotide sequence; amino acid sequence; genes; prediction ER - TY - JOUR T1 - Serine/threonine phosphatases in the nervous system. AN - 16387816; 2878227 AB - The cloning and sequence determination of cDNAs encoding different types of serine/threonine protein phosphatases has provided a molecular basis for the protein phosphatase classification proposed by Ingebritsen and Cohen. Each of the phosphatases, phosphatase-1, -2A, -2B and -2C, exists as multiple isozymes raising the possibility that isozymes selectively expressed in different tissues may perform specific functions. The recent discovery of potent toxin inhibitors specific for protein phosphatase-1 and -2A will undoubtedly play an important role in the elucidation of the role of these enzymes in neuronal function. JF - Current Opinion in Neurobiology AU - Stemmer, P AU - Klee, C B AD - Lab. Biochem., NCI/NIH, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 53 EP - 64 VL - 1 IS - 1 SN - 0959-4388, 0959-4388 KW - dephosphorylation KW - nervous system KW - reviews KW - serine/threonine phosphatase KW - Microbiology Abstracts B: Bacteriology; CSA Neurosciences Abstracts KW - N3 11070:Neurochemistry and cellular biology KW - J:20320 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16387816?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+Opinion+in+Neurobiology&rft.atitle=Serine%2Fthreonine+phosphatases+in+the+nervous+system.&rft.au=Stemmer%2C+P%3BKlee%2C+C+B&rft.aulast=Stemmer&rft.aufirst=P&rft.date=1991-01-01&rft.volume=1&rft.issue=1&rft.spage=53&rft.isbn=&rft.btitle=&rft.title=Current+Opinion+in+Neurobiology&rft.issn=09594388&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - reviews; dephosphorylation; nervous system ER - TY - JOUR T1 - Implications of climate change for human health. AN - 16362190; 2858359 AB - The implications for human health from global warming are discussed. Direct effects of global warming include changes in biodiversity, outbreaks of infectious diseases, increased exposure to UV radiation, and increases in health problems related to indoor and outdoor air pollution and exposure to heavy metals due to acid rain. Indirect effects include substitute chemicals for chlorofluorocarbons, alternate fuels for motor vehicles, and exposure to toxic elements used in the production of solar energy devices. Research needs on human health related to these effects of global warming are identified. JF - Environmental Professional AU - Piver, W T AU - Fouts, J R AU - Rall, D P AD - Office of the Senior Sci. Advisor, Natl. Inst. Environ. Health Sci. (NIEHS), P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 79 EP - 91 VL - 13 IS - 1 SN - 0191-5398, 0191-5398 KW - global warming KW - human diseases KW - temperature effects KW - ASFA 3: Aquatic Pollution & Environmental Quality; Health & Safety Science Abstracts; Pollution Abstracts KW - climatic changes KW - air pollution KW - acid rain KW - climate KW - public health KW - H SE3.20:AIR POLLUTION/AIR QUALITY KW - P 0000:AIR POLLUTION KW - Q5 08521:Mechanical and natural changes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16362190?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Professional&rft.atitle=Implications+of+climate+change+for+human+health.&rft.au=Piver%2C+W+T%3BFouts%2C+J+R%3BRall%2C+D+P&rft.aulast=Piver&rft.aufirst=W&rft.date=1991-01-01&rft.volume=13&rft.issue=1&rft.spage=79&rft.isbn=&rft.btitle=&rft.title=Environmental+Professional&rft.issn=01915398&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2014-05-06 N1 - SubjectsTermNotLitGenreText - human diseases; temperature effects; climate; acid rain; air pollution; public health; climatic changes; global warming ER - TY - CONF T1 - Mobile solidification and the transportation/disposal of solidified radioactive waste products. AN - 16339146; 2851419 AB - NEI International Research and Development Ltd (NEI IRD) have recently completed a major solidification project using their mobile solidification plant. The project involved the retrieval of waste ion exchange resins from on-site storage vessels, solidification in cement and transportation to BNFL Drigg. A number of criteria must be considered in solidifying waste materials and these were addressed as part of the project. Assessments were made to ensure that all doses would be as low as reasonably practicable and compliance with the transport regulations and disposal criteria could be achieved. Subsequent analysis of project results has confirmed the validity of these assessments. JF - International Journal of Radioactive Materials Transport AU - Saul, D AU - McGeary, R Y1 - 1991 PY - 1991 DA - 1991 SP - 155 EP - 159 VL - 2 IS - 1-3 KW - solidification KW - Pollution Abstracts; Health & Safety Science Abstracts KW - transportation KW - materials handling KW - ion exchange KW - solid wastes KW - radioactive wastes KW - waste disposal KW - H SI4.23:MATERIALS HANDLING KW - P 8000:RADIATION KW - H SI4.24:WASTE DISPOSAL UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16339146?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Apollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Radioactive+Materials+Transport&rft.atitle=Mobile+solidification+and+the+transportation%2Fdisposal+of+solidified+radioactive+waste+products.&rft.au=Saul%2C+D%3BMcGeary%2C+R&rft.aulast=Saul&rft.aufirst=D&rft.date=1991-01-01&rft.volume=2&rft.issue=1-3&rft.spage=155&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Radioactive+Materials+Transport&rft.issn=0957476X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 ER - TY - JOUR T1 - Recurrent abortions in a bulimic: Implications regarding pathogenesis. AN - 16338412; 2843317 AB - Despite agreement in psychodynamic formulations that bulimia nervosa results from relatively early developmental difficulties, the role of transitional objects in the syndrome has been debated. We describe the case of a severe bulimic in which repeated pregnancies and abortions fulfilled the same calming function as repeated binging and vomiting. We suggest that the cycle of incorporation and explusion is central to affect regulation and is most compatible with the view that bulimics use their own bodies as transitional objects. We suggest further that such symptoms represent overdetermination, and reflect not only primitive deficits in regulation of internal states but also consequent unresolved conflicts. Thus therapy must be flexible enough to deal with both primary and secondary issues. JF - International Journal of Eating Disorders AU - El-Mallakh, R S AU - Tasman, A AD - Neuropsychiatr. Branch, NIMH, Neuropsychiatr. Res. Hosp., 2700 Martin Luther King, Jr., Ave., S.E., Washington DC 20032, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 215 EP - 219 VL - 10 IS - 2 SN - 0276-3478, 0276-3478 KW - eating disorders KW - bulimia KW - Health & Safety Science Abstracts KW - abortion KW - H SM10.8.6:DIET UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16338412?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Eating+Disorders&rft.atitle=Recurrent+abortions+in+a+bulimic%3A+Implications+regarding+pathogenesis.&rft.au=El-Mallakh%2C+R+S%3BTasman%2C+A&rft.aulast=El-Mallakh&rft.aufirst=R&rft.date=1991-01-01&rft.volume=10&rft.issue=2&rft.spage=215&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Eating+Disorders&rft.issn=02763478&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - abortion ER - TY - JOUR T1 - The 120 kilodalton outer membrane protein (rOmp B) of Rickettsia rickettsii is encoded by an unusually long open reading frame: Evidence for protein processing from a large precursor. AN - 16300288; 2812788 AB - A Rickettsia rickettsii outer surface membrane protein (rOmp B), of an apparent molecular mass of 120 kilodaltons, is a major surface antigen of the Rickettsiae that displays genus, species, and sub-species specific antigenic determinants. Genetic analysis revealed an unusually large open reading frame with the capacity to encode a product much larger than the mature protein. A 32 kilodalton peptide from purified rickettsiae was isolated and the amino terminus was sequenced, which revealed that the peptide is encoded by the 3' portion of this large open reading frame. This suggests a role for posttranslational processing of rOmp B from a large precursor molecule. JF - Molecular Microbiology AU - Gilmore, RD Jr AU - Cieplak, W Jr AU - Policastro, P F AU - Hackstadt, T AD - Lab. Intracellular Parasites, Rocky Mountain Lab., NIAID, NIH, Hamilton, MT 59840, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 2361 EP - 2370 VL - 5 IS - 10 SN - 0950-382X, 0950-382X KW - DNA KW - Rickettsia rickettsii KW - amino acid sequence KW - antigenic determinants KW - genes KW - membrane proteins KW - nucleotide sequence KW - western blotting KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - N 14640:Structure & sequence KW - G 07320:Bacterial genetics KW - J 02740:Genetics and evolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16300288?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+Microbiology&rft.atitle=The+120+kilodalton+outer+membrane+protein+%28rOmp+B%29+of+Rickettsia+rickettsii+is+encoded+by+an+unusually+long+open+reading+frame%3A+Evidence+for+protein+processing+from+a+large+precursor.&rft.au=Gilmore%2C+RD+Jr%3BCieplak%2C+W+Jr%3BPolicastro%2C+P+F%3BHackstadt%2C+T&rft.aulast=Gilmore&rft.aufirst=RD&rft.date=1991-01-01&rft.volume=5&rft.issue=10&rft.spage=2361&rft.isbn=&rft.btitle=&rft.title=Molecular+Microbiology&rft.issn=0950382X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - nucleotide sequence; antigenic determinants; membrane proteins; amino acid sequence; genes; DNA; western blotting ER - TY - JOUR T1 - Ability of the c-mos product to associate with and phosphorylate tubulin. AN - 16273453; 2805162 AB - The mos proto-oncogene product, pp39 super(mos), is a protein kinase and has been equated with cytostatic factor (CSF), an activity in unfertilized eggs that is thought to be responsible for the arrest of meiosis at metaphase II. The biochemical properties and potential substrates of pp39 super(mos) were examined in unfertilized eggs and in transformed cells in order to study how the protein functions both as CSF and in transformation. JF - Science (Washington) AU - Zhou, Renping AU - Oskarsson, M AU - Paules, R S AU - Schulz, N AU - Cleveland, D AU - Vande Woude, GF AD - ABL-Basic Res. Program, NCI-Fredrick Cancer Res. and Dev. Cent., Frederick, MD 21702, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 671 EP - 675 VL - 251 IS - 4949 SN - 0036-8075, 0036-8075 KW - NIH 3T3 cells KW - Xenopus laevis KW - association KW - c-mos KW - c-mos gene KW - gene products KW - oncogenes KW - phosphorylation KW - tubulin KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Oncogenes & Growth Factors Abstracts KW - B 26140:Mos oncogene UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16273453?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science+%28Washington%29&rft.atitle=Ability+of+the+c-mos+product+to+associate+with+and+phosphorylate+tubulin.&rft.au=Zhou%2C+Renping%3BOskarsson%2C+M%3BPaules%2C+R+S%3BSchulz%2C+N%3BCleveland%2C+D%3BVande+Woude%2C+GF&rft.aulast=Zhou&rft.aufirst=Renping&rft.date=1991-01-01&rft.volume=251&rft.issue=4949&rft.spage=671&rft.isbn=&rft.btitle=&rft.title=Science+%28Washington%29&rft.issn=00368075&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - association; oncogenes; phosphorylation; gene products ER - TY - JOUR T1 - Cytotoxic activity of chimeric proteins composed of acidic fibroblast growth factor and Pseudomonas exotoxin on a variety of cell types. AN - 16267647; 2796562 AB - Chimeric proteins composed of acidic fibroblast growth factor (acidic FGF) and several forms of Pseudomonas exotoxin (PE) that cannot bind to the PE receptor have been produced in Escherichia coli by expressing chimeric genes in which DNA encoding acidic FGF is fused to various mutant forms of PE. These acidic FGF-PE fusion proteins were found to be cytotoxic to a variety of tumor cell lines including hepatocellular (PLC/PRF/5 and HEPG2), prostatic (LNCaP), colon (HT29), and breast (MCF-7) carcinomas at concentrations of 1-70 ng/ml. JF - FASEB Journal AU - Siegall, C B AU - Epstein, S AU - Speir, E AU - Hla, T AU - Forough, R AU - Maciag, T AU - Fitzgerald, D J AU - Pastan, I AD - Lab. Mol. Biol., NCI, NIH, 9000 Rockville Pike, Build. 37, Rm. 4E16, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 2843 EP - 2849 VL - 5 IS - 13 SN - 0892-6638, 0892-6638 KW - fibroblast growth factor (acidic) KW - Biotechnology and Bioengineering Abstracts; Medical and Pharmaceutical Biotechnology Abstracts KW - chimeras KW - exotoxins KW - tumor cells KW - cytotoxicity KW - Pseudomonas aeruginosa KW - carcinoma KW - W3 33370:Antibiotics KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16267647?accountid=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=FASEB+Journal&rft.atitle=Cytotoxic+activity+of+chimeric+proteins+composed+of+acidic+fibroblast+growth+factor+and+Pseudomonas+exotoxin+on+a+variety+of+cell+types.&rft.au=Siegall%2C+C+B%3BEpstein%2C+S%3BSpeir%2C+E%3BHla%2C+T%3BForough%2C+R%3BMaciag%2C+T%3BFitzgerald%2C+D+J%3BPastan%2C+I&rft.aulast=Siegall&rft.aufirst=C&rft.date=1991-01-01&rft.volume=5&rft.issue=13&rft.spage=2843&rft.isbn=&rft.btitle=&rft.title=FASEB+Journal&rft.issn=08926638&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-14 N1 - SubjectsTermNotLitGenreText - chimeras; exotoxins; tumor cells; cytotoxicity; carcinoma; Pseudomonas aeruginosa ER - TY - JOUR T1 - Purification and partial characterization of ubiquitin-activating enzyme from Saccharomyces cerevisiae . AN - 16256287; 2777984 AB - Ubiquitin-activating enzyme was purified from the yeast Saccharomyces cerevisiae by covalent affinity chromatography on ubiquitin-Sepharose followed by HPLC anion-exchange chromatography. Enzyme activity was monitored by the ubiquitin-dependent ATP: super(32)PP sub(i) exchange assay. The purified enzyme has a specific activity of 1.5 mu mol super(32)PP sub(i) incorporated into ATP multiplied by mg super(-1) at 37 degree C and pH 7.0 under standard conditions for substrate concentrations as described by Ciechanover et al. (1982) J. Biol. Chem. 257, 2537-2542. The catalytic activity showed a maximum at pH 7.0 Its molecular weight both in non-denaturing and in SDS-gel electrophoresis was estimated to be 115 kDa, suggesting a monomeric form. The isoelectric point determined by gel electrofocusing was approximately 4.7. JF - FEBS Letters AU - Hoefer, M AU - Cook, J C AD - Lab. Biochem., NHLBI, Natl. Inst. Health, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 54 EP - 58 VL - 289 IS - 1 SN - 0014-5793, 0014-5793 KW - E1 enzyme KW - Saccharomyces cerevisiae KW - activity KW - characterization KW - purification KW - ubiquitin-activating enzyme KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Microbiology Abstracts C: Algology, Mycology & Protozoology KW - K 03020:Fungi UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16256287?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FEBS+Letters&rft.atitle=Purification+and+partial+characterization+of+ubiquitin-activating+enzyme+from+Saccharomyces+cerevisiae+.&rft.au=Hoefer%2C+M%3BCook%2C+J+C&rft.aulast=Hoefer&rft.aufirst=M&rft.date=1991-01-01&rft.volume=289&rft.issue=1&rft.spage=54&rft.isbn=&rft.btitle=&rft.title=FEBS+Letters&rft.issn=00145793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - characterization; purification; activity ER - TY - JOUR T1 - Tyrosine phosphorylation and tryosine kinase activity of the trk proto-oncogene product induced by NGF. AN - 16239227; 2776727 AB - We show that NGF induces tyrosine phosphorylation and tyrosine kinase activity of the trk proto-oncogene product, a tyrosine kinase receptor whose expression is restricted in vivo to neurons of the sensory spinal and cranial ganglia of neural crest origin. Tryosine phosphorylation of trk by NGF is rapid, specific and occurs with picomolar quantities of factor, indicating that the response is mediated by physiological amounts of NGF. Activation of the trk tyrosine kinase receptor provides a possible mechanism for signal transduction by NGF. JF - Nature AU - Kaplan AU - Martin-Zanca, D AU - Parada, L F AD - Eukaryotic Signal Transduction Group, NCI-Frederick Cancer Res. and Dev. Cent., P.O. Box B, Frederick, MD 21701, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 158 EP - 160 VL - 350 IS - 6314 SN - 0028-0836, 0028-0836 KW - PC12 cells KW - activity KW - induction KW - nerve growth factor KW - oncogenes KW - phosphorylation KW - protein-tyrosine kinase KW - trk KW - trk gene KW - tyrosine KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; CSA Neurosciences Abstracts KW - N3 11075:Molecular neurobiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16239227?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature&rft.atitle=Tyrosine+phosphorylation+and+tryosine+kinase+activity+of+the+trk+proto-oncogene+product+induced+by+NGF.&rft.au=Kaplan%3BMartin-Zanca%2C+D%3BParada%2C+L+F&rft.aulast=Kaplan&rft.aufirst=&rft.date=1991-01-01&rft.volume=350&rft.issue=6314&rft.spage=158&rft.isbn=&rft.btitle=&rft.title=Nature&rft.issn=00280836&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - oncogenes; nerve growth factor; induction; phosphorylation; activity ER - TY - JOUR T1 - Induction and cleavage of Salmonella typhimurium UmuD protein. AN - 16238803; 2777920 AB - SOS mutagenesis in prokaryotes is dependent upon the inducible activity of the chromosomally encoded UmuDC proteins, or homologous proteins such as MucAB or ImpCAB which are found on naturally occurring plasmids. We have used a polyclonal antiserum raised against the E. coli UmuD and UmuD' proteins to show that S. typhimurium expresses cross-reacting material only after treatment with the DNA-damaging agent mitomycin C. The S. typhimurium umuDC operon, therefore, appears to be regulated by mechanisms similar to the E. coli umuDC operon. The data suggest that conversion of UmuD to the mutagenically active UmuD' is not the rate-limiting factor accounting for the weakly mutable phenotype of S. typhimurium . JF - Molecular and General Genetics AU - Woodgate, R AU - Levine, A S AU - Koch, W H AU - Cebula, T A AU - Eisenstadt, E AD - Build. 6, Rm. 1A13, NICHD, NIH, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 81 EP - 85 VL - 229 IS - 1 SN - 0026-8925, 0026-8925 KW - Genetics Abstracts; Microbiology Abstracts B: Bacteriology KW - chemiluminescence KW - mutagens KW - genes KW - prokaryotes KW - Salmonella typhimurium KW - DNA KW - Escherichia coli KW - cleavage KW - G 07320:Bacterial genetics KW - J 02740:Genetics and evolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16238803?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+General+Genetics&rft.atitle=Induction+and+cleavage+of+Salmonella+typhimurium+UmuD+protein.&rft.au=Woodgate%2C+R%3BLevine%2C+A+S%3BKoch%2C+W+H%3BCebula%2C+T+A%3BEisenstadt%2C+E&rft.aulast=Woodgate&rft.aufirst=R&rft.date=1991-01-01&rft.volume=229&rft.issue=1&rft.spage=81&rft.isbn=&rft.btitle=&rft.title=Molecular+and+General+Genetics&rft.issn=00268925&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Salmonella typhimurium; Escherichia coli; mutagens; genes; chemiluminescence; DNA; prokaryotes; cleavage ER - TY - JOUR T1 - Bioactivation of xenobiotics by prostaglandin H synthase. AN - 16238322; 2774873 AB - Prostaglandin H synthase (PHS) catalyzes the oxidation of arachidonic acid to prostaglandin H sub(2) in reactions which utilize two activities, a cyclooxygenase and a peroxidase. These enzymatic activities generate enzyme- and substrate-derived free radical intermediates which can oxidize xenobiotics to biologically reactive intermediates. As a consequence, in the presence of arachidonic acid or a peroxide source, PHS can bioactivate many chemical carcinogens to their ultimate mutagenic and carcinogenic forms. In general, PHS-dependent bioactivation is most important in extrahepatic tissues with low monooxygenase activity such as the urinary bladder, renal medulla, skin and lung. Mutagenicity assays are useful in the detection of compounds which are converted to genotoxic metabolites during PHS oxidation. In addition, the oxidation of xenobiotics by PHS often form metabolites or adducts to cellular macromolecules which are specific for peroxidase- or peroxyl radical-dependent reactions. JF - Chemico-Biological Interactions AU - Smith, B J AU - Curtis, J F AU - Eling, TE AD - Eicosanoid Biochem., Lab. Mol. Biophys., NIEHS, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 245 EP - 264 VL - 79 IS - 3 SN - 0009-2797, 0009-2797 KW - prostaglandin H synthase KW - Toxicology Abstracts KW - reviews KW - xenobiotics KW - activation KW - X 24250:Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16238322?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemico-Biological+Interactions&rft.atitle=Bioactivation+of+xenobiotics+by+prostaglandin+H+synthase.&rft.au=Smith%2C+B+J%3BCurtis%2C+J+F%3BEling%2C+TE&rft.aulast=Smith&rft.aufirst=B&rft.date=1991-01-01&rft.volume=79&rft.issue=3&rft.spage=245&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 revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - xenobiotics; activation; reviews ER - TY - JOUR T1 - Crystallization and preliminary X-ray diffraction studies of recombinant rabbit interferon-gamma. AN - 16226834; 2756380 AB - Two different crystal forms of recombinant rabbit IFN- gamma were obtained under different crystallization conditions. The first, a tetragonal form with space group P4 sub(3)2 sub(1)2 or P4 sub(1)2 sub(1)2, was obtained through vapor phase equilibration using the sitting drop rods technique with ammonium citrate as the major precipitating agent. The unit cell dimensions of this crystal form are a = b = 82.1 angstrom and c = 116.3 angstrom. These crystals diffract to 2.8 angstrom resolution and contain a dimer in the asymmetric unit. A second crystal form was obtained by the batch method at pH 8.0 using sodium chloride as the precipitating agent. The crystals are hexagonal, space group P6 sub(1)22 or P6 sub(5)22, and with unit cell dimensions of a = b = 58.0 angstrom and c = 169 angstrom. JF - Biochemical and Biophysical Research Communications AU - Samudzi, C T AU - Gribskov, CL AU - Burton, LE AU - Rubin, J R AD - NCI-Frederick Cancer Res. and Dev. Cent., ABL-Basic Res. Program, P.O. Box B, Frederick, MD 21702, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 634 EP - 640 VL - 178 IS - 2 SN - 0006-291X, 0006-291X KW - X-ray diffraction KW - crystallization KW - gamma -interferon KW - rabbits KW - recombinants KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16226834?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+and+Biophysical+Research+Communications&rft.atitle=Crystallization+and+preliminary+X-ray+diffraction+studies+of+recombinant+rabbit+interferon-gamma.&rft.au=Samudzi%2C+C+T%3BGribskov%2C+CL%3BBurton%2C+LE%3BRubin%2C+J+R&rft.aulast=Samudzi&rft.aufirst=C&rft.date=1991-01-01&rft.volume=178&rft.issue=2&rft.spage=634&rft.isbn=&rft.btitle=&rft.title=Biochemical+and+Biophysical+Research+Communications&rft.issn=0006291X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - DNA synthesis on discontinuous templates by DNA polymerase I of Escherichia coli . AN - 16222886; 2751831 AB - DNA polymerases normally catalyze DNA synthesis in a template-directed manner. Generally, the continuity of the phosphodiester backbone of the template strand was thought to be an absolute requirement for DNA synthesis. Here, I demonstrate that a 3'-exonuclease-deficient derivative of the Klenow (large) fragment of Escherichia coli DNA polymerase I (PolIk) can carry out DNA synthesis on discontinuous templates in vitro. Addition of multiple nucleotides (nt) to the 3' end of a blunt-end duplex, templated by unlinked single-stranded oligodeoxyribonucleotides (oligos), was monitored electrophoretically. The reaction was demonstrable with either homopolymers or mixed-sequence oligos, but showed a requirement for complementarity between the first nt added to the duplex and the 3' nt of the unlinked oligo. These results demonstrate that continuity of the phosphodiester backbone of the template strand is not absolutely required for in vitro DNA synthesis by a 3'-exonuclease-deficient form of PolIk. JF - Gene AU - Clark, J M AD - Lab. Mol. Genet., N.I.E.H.S., P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 75 EP - 80 VL - 104 IS - 1 SN - 0378-1119, 0378-1119 KW - DNA-directed DNA polymerase I KW - Biochemistry Abstracts 2: Nucleic Acids; Genetics Abstracts; Microbiology Abstracts B: Bacteriology KW - DNA biosynthesis KW - Escherichia coli KW - in vitro KW - N 14722:DNA polymerases KW - G 07320:Bacterial genetics KW - J 02728:Enzymes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16222886?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gene&rft.atitle=DNA+synthesis+on+discontinuous+templates+by+DNA+polymerase+I+of+Escherichia+coli+.&rft.au=Clark%2C+J+M&rft.aulast=Clark&rft.aufirst=J&rft.date=1991-01-01&rft.volume=104&rft.issue=1&rft.spage=75&rft.isbn=&rft.btitle=&rft.title=Gene&rft.issn=03781119&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Escherichia coli; DNA biosynthesis; in vitro ER - TY - JOUR T1 - Cockroaches (Blatta and Periplaneta species) as reservoirs of drug-resistant salmonellas. AN - 16218110; 2750574 AB - A total of 221 cockroaches (Blatta and Periplaneta spp.), collected in hospitals, houses, animal sheds, grocery stores and restaurants, in various parts of South Kanara District, a south-west coastal region of India, were studied bacteriologically for the presence of various salmonellas. All salmonellas were resistant to one or other of 11 antibacterial drugs used in the susceptibility test. Isolation of salmonellas from cockroaches collected from the livestock premises and human dwellings suggested that they may act as significant reservoirs of salmonella in nature. Recovery of serotypes, phage types and R-types that were commonly isolated from humans and animals of this locality, suggested a transmission role for cockroaches. By harbouring potentially pathogenic, drug-resistant salmonellas, these wandering arthropods may pose dangerous infective hazards to humans and animals. JF - Epidemiology and infection. London, New York NY AU - Devi, SJN AU - Murray, C J AD - LDMI, NICHD, NIH, Bldg 6, Room 1A05, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 357 EP - 361 VL - 107 IS - 2 SN - 0950-2688, 0950-2688 KW - drug resistant KW - Salmonella bovismorbificans KW - Salmonella oslo KW - India, Kanara KW - Entomology Abstracts; Microbiology Abstracts B: Bacteriology KW - Periplaneta KW - Blatta KW - Blattodea KW - Salmonella typhimurium KW - Blattidae KW - isolation KW - disease reservoirs KW - drug resistance KW - Salmonella KW - J 02855:Human Bacteriology: Others KW - Z 05206:Medical & veterinary entomology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16218110?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Epidemiology+and+infection.+London%2C+New+York+NY&rft.atitle=Cockroaches+%28Blatta+and+Periplaneta+species%29+as+reservoirs+of+drug-resistant+salmonellas.&rft.au=Devi%2C+SJN%3BMurray%2C+C+J&rft.aulast=Devi&rft.aufirst=SJN&rft.date=1991-01-01&rft.volume=107&rft.issue=2&rft.spage=357&rft.isbn=&rft.btitle=&rft.title=Epidemiology+and+infection.+London%2C+New+York+NY&rft.issn=09502688&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Salmonella typhimurium; Periplaneta; Blatta; Blattidae; Blattodea; Salmonella; disease reservoirs; isolation; drug resistance ER - TY - JOUR T1 - Mutagenesis of the mouse germline using retroviruses. AN - 16214082; 2742045 JF - Current Topics in Microbiology and Immunology [CURR. TOP. MICROBIOL. IMMUNOL.]. 1991. AU - Lock, L F AU - Jenkins, NA AU - Copeland, NG AD - Mamm. Genet. Lab., ABL-Basic Res. Program, NCI-Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702, USA A2 - Kung, HJ A2 - Vogt, PK (eds) Y1 - 1991 PY - 1991 DA - 1991 SN - 0070-217X, 0070-217X KW - mice KW - cells KW - embryos KW - gene transfer KW - mutagenesis KW - retrovirus KW - Biotechnology and Bioengineering Abstracts; Genetics Abstracts; Virology & AIDS Abstracts KW - W 30129:Others KW - G 07397:Rodentia (mice) KW - V 22113:Animal retroviruses UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16214082?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/Biotechnology+Research+Abstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:book&rft.genre=book&rft.jtitle=&rft.atitle=&rft.au=Lock%2C+L+F%3BJenkins%2C+NA%3BCopeland%2C+NG&rft.aulast=Lock&rft.aufirst=L&rft.date=1991-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=Mutagenesis+of+the+mouse+germline+using+retroviruses.&rft.title=Mutagenesis+of+the+mouse+germline+using+retroviruses.&rft.issn=0070217X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - mutagenesis; retrovirus; gene transfer; embryos; cells ER - TY - JOUR T1 - Solid phase peptide synthesis of human endothelin precursor peptides using two-step hard acid deprotection/cleavage methods. AN - 16203854; 2741629 AB - Syntheses are described for the putative human and porcine biosynthetic precursors (hET-38 and pET-39) of endothelin, with the sequence previously deduced from human- and porcine-cDNA coding for preproendothelin. JF - International Journal of Peptide and Protein Reseach AU - Nomizu, M AU - Inagaki, Y AU - Iwamatsu, A AU - Kashiwabara, T AU - Ohta, H AU - Morita, A AU - Nishikori, K AU - Otaka, A AU - Fujii, N AU - Roller, P P AD - Lab. Med. Chem., NCI, NIH, Build. 37, Rm. 5C02, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 580 EP - 587 VL - 38 IS - 6 SN - 0367-8377, 0367-8377 KW - endothelin KW - man KW - peptide synthesis KW - pigs KW - precursors KW - solid phase methods KW - use KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16203854?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Peptide+and+Protein+Reseach&rft.atitle=Solid+phase+peptide+synthesis+of+human+endothelin+precursor+peptides+using+two-step+hard+acid+deprotection%2Fcleavage+methods.&rft.au=Nomizu%2C+M%3BInagaki%2C+Y%3BIwamatsu%2C+A%3BKashiwabara%2C+T%3BOhta%2C+H%3BMorita%2C+A%3BNishikori%2C+K%3BOtaka%2C+A%3BFujii%2C+N%3BRoller%2C+P+P&rft.aulast=Nomizu&rft.aufirst=M&rft.date=1991-01-01&rft.volume=38&rft.issue=6&rft.spage=580&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Peptide+and+Protein+Reseach&rft.issn=03678377&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Cocaine immunotoxicity: Abnormal cytokine production in Hispanic drug users. AN - 16191922; 2722844 AB - Peripheral blood lymphocytes from 47 Hispanic poly-drug users with a history of cocaine abuse were analyzed for in vitro production of interleukin-1 (IL-1), interleukin-2 (IL-2), gamma-interferon (IFN) and plasma levels of soluble IL-2 receptor (SIL-2R). Cocaine use was confirmed and quantified by analysis of hair and urine samples, and subjects were grouped into 3 based on the extent of cocaine metabolites detected. No significant differences in IL-1 and IFN production were seen between the 3 groups. However, subjects with higher levels of cocaine in hair also showed higher levels of IL-2. In addition, a positive correlation was seen between cocaine concentrations and IL-2 levels. A corresponding negative correlation was seen between cocaine levels and levels of plasma SIL-2R. These findings suggest modulation of the IL-2 network by cocaine in poly-drug users. JF - Toxicology Letters AU - Chen, Guan-Jie AU - Pillai, R AU - Erickson, J R AU - Martinez, F AU - Estrada, AL AU - Watson, R R AD - NIAAA Specialized Alcohol Res. Cent., Dep. Fam. and Community Med., Univ. Arizona Health Sci. Cent., Tucson, AZ 85724, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 81 EP - 88 VL - 59 IS - 1-3 SN - 0378-4274, 0378-4274 KW - cocaine KW - cytokines KW - interleukin KW - Immunology Abstracts; Toxicology Abstracts KW - gamma -interferon KW - immunotoxicity KW - production KW - man KW - F 06773:Interferons KW - X 24180:Social poisons & drug abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16191922?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+Letters&rft.atitle=Cocaine+immunotoxicity%3A+Abnormal+cytokine+production+in+Hispanic+drug+users.&rft.au=Chen%2C+Guan-Jie%3BPillai%2C+R%3BErickson%2C+J+R%3BMartinez%2C+F%3BEstrada%2C+AL%3BWatson%2C+R+R&rft.aulast=Chen&rft.aufirst=Guan-Jie&rft.date=1991-01-01&rft.volume=59&rft.issue=1-3&rft.spage=81&rft.isbn=&rft.btitle=&rft.title=Toxicology+Letters&rft.issn=03784274&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - immunotoxicity; production; man; gamma -interferon ER - TY - JOUR T1 - A semiautomated multiparameter approach for anti-HIV drug screening. AN - 16180250; 2717549 AB - We are implementing a series of complementary assays for initial follow-up confirmation and prioritization of new active anti-HIV compounds identified by the U.S. National Cancer Institute's large-scale in vitro primary anti-HIV screen. Two different kinds of cellular viability assays, in addition to specific assays for total cellular DNA content, supernatant transcriptase activity, p24 core antigen production and the synthesis of infectious HIV virions are all performed form a single well of a 96-well microtiter plate containing human host cells infected with HIV. Procedures to automate the method optically, as well as to maximize the safety of the technicians working with HIV and HIV-infected cells have been emphasized. The resulting semiautomated, highly reproducible battery of assays yields a maximum amount of antiviral and cytotoxicity information from a minimum amount of sample. JF - Journal of Virological Methods AU - Gulakowski, R J AU - McMahon, J B AU - Staley, P G AU - Moran, R A AU - Boyd, M R AD - NCI-FCRDC, Build. 1052, Rm. 121, Frederick, MD 21702-1201, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 87 EP - 100 VL - 33 IS - 1-2 SN - 0166-0934, 0166-0934 KW - human immunodeficiency virus KW - antiviral activity KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Virology & AIDS Abstracts KW - drug screening KW - antiviral agents KW - inhibitors KW - automation KW - reverse transcription KW - A 01068:Antiviral & viricidal KW - V 22004:AIDS: Clinical aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16180250?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Virological+Methods&rft.atitle=A+semiautomated+multiparameter+approach+for+anti-HIV+drug+screening.&rft.au=Gulakowski%2C+R+J%3BMcMahon%2C+J+B%3BStaley%2C+P+G%3BMoran%2C+R+A%3BBoyd%2C+M+R&rft.aulast=Gulakowski&rft.aufirst=R&rft.date=1991-01-01&rft.volume=33&rft.issue=1-2&rft.spage=87&rft.isbn=&rft.btitle=&rft.title=Journal+of+Virological+Methods&rft.issn=01660934&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - antiviral agents; drug screening; reverse transcription; inhibitors; automation ER - TY - JOUR T1 - Cloning and characterization of a member of the rat multidrug resistance (mdr) gene family. AN - 16177991; 2723407 AB - The rat mdr gene family (genes encoding P-glycoprotein (Pgp)) was characterized and the complete sequence of a rat mdr cDNA was determined based on seven independent cDNA clones that correspond to the same gene. The longest of these clones contains a 4.3-kb insert which represents a full-length rat mdr cDNA. The longest open reading frame of this sequence is 3933 bp; the first ATG is at 103 bp, making the deduced protein 1277 amino acids long (141 kDa). This correlates well with previously identified Pgp. JF - Gene AU - Silverman, JA AU - Raunio, H AU - Gant, T W AU - Thorgeirsson, S S AD - Build. 37, Rm. 3C25, NCI, NIH, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 229 EP - 236 VL - 106 IS - 2 SN - 0378-1119, 0378-1119 KW - P-glycoprotein KW - amino acid sequence KW - cDNA KW - genes KW - mdr gene KW - nucleotide sequence KW - predictions KW - products KW - rats KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - G 07402:GENERAL KW - N 14640:Structure & sequence UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16177991?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gene&rft.atitle=Cloning+and+characterization+of+a+member+of+the+rat+multidrug+resistance+%28mdr%29+gene+family.&rft.au=Silverman%2C+JA%3BRaunio%2C+H%3BGant%2C+T+W%3BThorgeirsson%2C+S+S&rft.aulast=Silverman&rft.aufirst=JA&rft.date=1991-01-01&rft.volume=106&rft.issue=2&rft.spage=229&rft.isbn=&rft.btitle=&rft.title=Gene&rft.issn=03781119&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - nucleotide sequence; cDNA; amino acid sequence; genes; P-glycoprotein; products ER - TY - JOUR T1 - Perilipin, a major hormonally regulated adipocyte-specific phosphoprotein associated with the periphery of lipid storage droplets. AN - 16177542; 2715188 AB - The lipid fraction ("fat cake") of rat epididymal adipocytes contains a prominent phosphoprotein that is multiply phosphorylated by cAMP-dependent protein kinase in vivo, at which point it migrates as a 65/67-kDa sub(app) doublet by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and is by far the most heavily radiolabeled protein in the cell. JF - Journal of Biological Chemistry AU - Greenberg, A S AU - Egan, J J AU - Wek, SA AU - Garty, N B AU - Blanchette-Mackie, E J AU - Londos, C AD - LCDB, NIDDK, Build. 6, Rm. B1-16, NIH, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 11341 EP - 11346 VL - 166 IS - 17 SN - 0021-9258, 0021-9258 KW - adipocytes KW - biochemical characteristics KW - identification KW - perilipin KW - phosphorylation KW - protein kinase A KW - rats KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16177542?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=Perilipin%2C+a+major+hormonally+regulated+adipocyte-specific+phosphoprotein+associated+with+the+periphery+of+lipid+storage+droplets.&rft.au=Greenberg%2C+A+S%3BEgan%2C+J+J%3BWek%2C+SA%3BGarty%2C+N+B%3BBlanchette-Mackie%2C+E+J%3BLondos%2C+C&rft.aulast=Greenberg&rft.aufirst=A&rft.date=1991-01-01&rft.volume=166&rft.issue=17&rft.spage=11341&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - In situ processing of a retroviral nucleocapsid protein by the viral proteinase. AN - 16175222; 2716319 AB - The proteolytic processing pathway of the nucleocapsid protein (NC) by the viral proteinase within intact capsids of equine infectious anemia virus (EIAV) is presented. The cleavage sites are located at the carboxyl side of the first cysteine residue within the zinc-finger domains. EIAV is used as a model to predict similar NC cleavages in other retroviruses, including human immunodeficiency virus (HIV). The observed cleavages suggest a previously unrecognized function of the retroviral proteinase that may be crucial for replication during the early stages of the virus life-cycle (i.e. reverse transcription/integration). JF - Protein Engineering AU - Roberts, M M AU - Copeland, T D AU - Oroszlan, S AD - Lab. Mol. Virol. and Carcinog., ABL-Basic Res. Program, NCI-Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702-1201, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 695 EP - 700 VL - 4 IS - 6 SN - 0269-2139, 0269-2139 KW - activity KW - equine infectious anemia virus KW - nucleocapsids KW - processing KW - proteinase KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Virology & AIDS Abstracts KW - V 22113:Animal retroviruses UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16175222?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Protein+Engineering&rft.atitle=In+situ+processing+of+a+retroviral+nucleocapsid+protein+by+the+viral+proteinase.&rft.au=Roberts%2C+M+M%3BCopeland%2C+T+D%3BOroszlan%2C+S&rft.aulast=Roberts&rft.aufirst=M&rft.date=1991-01-01&rft.volume=4&rft.issue=6&rft.spage=695&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 revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Autoprocessing of the HIV-1 protease using purified wild-type and mutated fusion proteins expressed at high levels in Escherichia coli . AN - 16171700; 2716300 AB - Various constructs of the human immunodeficiency virus, type 1 (HIV-1) protease containing flanking Pol region sequences were expressed as fusion proteins with the maltose-binding protein of the malE gene of Escherichia coli . The full-length fusion proteins did not exhibit self-processing in E. coli , thereby allowing rapid purification by affinity chromatography on cross-linked amylose columns. Analysis of products of the HIV-1 fusion proteins containing mutations at either the N- or the C-terminal protease cleavage sites indicated that blocking one of the cleavage sites influences the cleavage at the non-mutated site. Such mutated full-length and truncated protease fusion proteins possess very low levels of proteolytic activity ( approximately equals 5 pmol multiplied by min super(-1) multiplied by mu g protein super(-1)). JF - European Journal of Biochemistry AU - Louis, J M AU - McDonald, R A AU - Nashed, N T AU - Wondrak, E M AU - Jerina, D M AU - Oroszlan, S AU - Mora, P T AD - Build. 6, Rm. B1-22, NIDDK, NIH, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 361 EP - 369 VL - 199 IS - 2 SN - 0014-2956, 0014-2956 KW - Escherichia coli KW - expression KW - fusion proteins KW - human immunodeficiency virus-1 KW - mutants KW - processing KW - proteinase KW - wild-type KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Virology & AIDS Abstracts KW - V 22002:AIDS: Molecular and in vitro aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16171700?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+Journal+of+Biochemistry&rft.atitle=Autoprocessing+of+the+HIV-1+protease+using+purified+wild-type+and+mutated+fusion+proteins+expressed+at+high+levels+in+Escherichia+coli+.&rft.au=Louis%2C+J+M%3BMcDonald%2C+R+A%3BNashed%2C+N+T%3BWondrak%2C+E+M%3BJerina%2C+D+M%3BOroszlan%2C+S%3BMora%2C+P+T&rft.aulast=Louis&rft.aufirst=J&rft.date=1991-01-01&rft.volume=199&rft.issue=2&rft.spage=361&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 revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Use of high density cultures of Escherichia coli for high level production of recombinant Pseudomonas aeruginosa exotoxin A. AN - 16156825; 2697080 AB - An efficient fermentation method for the production of two modified recombinant Pseudomonas aeruginosa exotoxin As cloned in Escherichia coli BL21( lambda DE3) was developed. Cell densities of 16-30 g dry weight/l were found to be most suitable for the induction of protein synthesis, which was under the isopropyl beta -D-thiogalactopyranoside (IPTG)-inducible T7 expression system. A concentration of 0.6 mM IPTG and induction time of 90 min were found to give the best results for production of the modified toxins. Using this procedure, gram amounts of the proteins were obtained in a 3-1 bench-top fermentor. The high density growth of the bacteria did not impair the integrity of the proteins and did not interfere with the purification procedure. JF - Applied Microbiology and Biotechnology AU - Fass, R AU - van de Walle, M AU - Shiloach, A AU - Joslyn, A AU - Kaufman, J AU - Shiloach, J AD - Biotechnol. Unit, LCDB, NIDDK, Natl. Inst. Health, Build 6, Rm. B1-33, Betheda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 65 EP - 69 VL - 36 IS - 1 SN - 0175-7598, 0175-7598 KW - Pseudomonas aeruginosa KW - recombinant KW - biosynthesis KW - recombinants KW - cell density KW - exotoxin A KW - Escherichia coli KW - fermentation KW - fermenters KW - Biotechnology and Bioengineering Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts B: Bacteriology KW - J 02822:Biosynthesis and physicochemical properties KW - W 30404:Other peptides and proteins KW - A 01023:Others UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16156825?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Applied+Microbiology+and+Biotechnology&rft.atitle=Use+of+high+density+cultures+of+Escherichia+coli+for+high+level+production+of+recombinant+Pseudomonas+aeruginosa+exotoxin+A.&rft.au=Fass%2C+R%3Bvan+de+Walle%2C+M%3BShiloach%2C+A%3BJoslyn%2C+A%3BKaufman%2C+J%3BShiloach%2C+J&rft.aulast=Fass&rft.aufirst=R&rft.date=1991-01-01&rft.volume=36&rft.issue=1&rft.spage=65&rft.isbn=&rft.btitle=&rft.title=Applied+Microbiology+and+Biotechnology&rft.issn=01757598&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Escherichia coli; fermentation; fermenters ER - TY - JOUR T1 - Differences in thermal stability between reduced and oxidized cytochrome b sub(562) from Escherichia coli . AN - 16149944; 2691022 AB - The thermal stabilities of ferri- and ferroytochrome b sub(562) were examined. Thermally induced spectral changes, monitored by adsorption and second-derivative spectroscopies, followed the dissociation of the heme moiety and the increased solvation of tyrosine residue(s) located in close proximity to the heme binding site. JF - Biochemistry (Washington) AU - Fisher, M T AD - NHLBI/NIH, Build. 3, Rm. 207, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 10012 EP - 10018 VL - 30 IS - 41 SN - 0006-2960, 0006-2960 KW - Escherichia coli KW - oxidation KW - reduction KW - effects on KW - thermal stability KW - cytochrome b562 KW - Microbiology Abstracts B: Bacteriology; Biochemistry Abstracts 1: Biological Membranes (till 1993) KW - J 02727:Amino acids, peptides and proteins UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16149944?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemistry+%28Washington%29&rft.atitle=Differences+in+thermal+stability+between+reduced+and+oxidized+cytochrome+b+sub%28562%29+from+Escherichia+coli+.&rft.au=Fisher%2C+M+T&rft.aulast=Fisher&rft.aufirst=M&rft.date=1991-01-01&rft.volume=30&rft.issue=41&rft.spage=10012&rft.isbn=&rft.btitle=&rft.title=Biochemistry+%28Washington%29&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 ER - TY - JOUR T1 - Waterborne lead affects feeding abilities and neurotransmitter levels of juvenile fathead minnows (Pimephales promelas ). AN - 16145283; 2691628 AB - Fathead minnows (Pimephales promelas ) were exposed for a total of 4 wk to 0, 0.5 or 1.0 mg/l lead as lead acetate. After 14-day acclimation to flake food, separate groups were fed either 20 1-day, 2-day or 7-day old Daphnia magna on alternate days for 14 days and tested for total time spent feeding, failed attempts and foraging distance. Time spent feeding on daphnids and number of miscues were significantly higher among lead-exposed groups than in control fish (P < 0.05). Except for a high significance among fish exposed to 1.0 mg/l lead and feeding on the largest sized prey (7-day olds), reaction distance showed no dose-response. After 4 wk, body lead ranged from not detectable in the controls to 44.2 plus or minus 2.5 mg/l in the 1.0 mg/l lead exposed groups. Examination of whole brain neurotransmitters indicated a significant increase in both serotonin and norepinephrine levels (P < 0.01) but no change in dopamine in response to lead intoxication. JF - Aquatic Toxicology AU - Weber, D N AU - Russo, A AU - Seale, D B AU - Spieler, R E AD - NIEHS Mar. Freshwater Biomed. Res. Cent., Univ. Wisconsin, Milwaukee, WI 53201, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 71 EP - 80 VL - 21 IS - 1-2 SN - 0166-445X, 0166-445X KW - feeding behaviour KW - feeding experiments KW - freshwater fish KW - heavy metals KW - juveniles KW - lead KW - neurotransmitters KW - toxicity tests KW - ASFA 3: Aquatic Pollution & Environmental Quality; CSA Neurosciences Abstracts; Toxicology Abstracts; Pollution Abstracts KW - Freshwater KW - Pimephales promelas KW - toxicity KW - freshwater pollution KW - P 2000:FRESHWATER POLLUTION KW - Q5 08504:Effects on organisms KW - N3 11103:Nonmammalian vertebrates KW - X 24162:Chronic exposure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16145283?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Aquatic+Toxicology&rft.atitle=Waterborne+lead+affects+feeding+abilities+and+neurotransmitter+levels+of+juvenile+fathead+minnows+%28Pimephales+promelas+%29.&rft.au=Weber%2C+D+N%3BRusso%2C+A%3BSeale%2C+D+B%3BSpieler%2C+R+E&rft.aulast=Weber&rft.aufirst=D&rft.date=1991-01-01&rft.volume=21&rft.issue=1-2&rft.spage=71&rft.isbn=&rft.btitle=&rft.title=Aquatic+Toxicology&rft.issn=0166445X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2014-05-06 N1 - SubjectsTermNotLitGenreText - feeding experiments; toxicity; neurotransmitters; juveniles; feeding behaviour; freshwater pollution; lead; toxicity tests; heavy metals; Pimephales promelas; Freshwater ER - TY - JOUR T1 - DNA polymerase-mediated nucleotide incorporation adjacent to hydrocarbon-deoxyadenosine and hydrocarbon-deoxyguanosine adducts. AN - 16142383; 2689560 AB - To examine the effect of DNA adducts on nucleotide incorporation by DNA polymerase at 3' neighboring bases, synthetic oligonucleotides (16mers) containing a purine at position 13 from the 3' end and any one of the four possible bases at position 12 were prepared and reacted with 7-bromomethyl-benz(a)anthracene. The result suggests that some bulky carcinogen-DNA adducts may lead to base mismatches at neighboring bases. JF - Carcinogenesis AU - Hruszkewycz, A M AU - Canella, KA AU - Dipple, A AD - Chem. Carcinog. Lab., ABL-Basic Res. Program, NCI-Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 1659 EP - 1663 VL - 12 IS - 9 SN - 0143-3334, 0143-3334 KW - DNA-directed DNA polymerase KW - activity KW - nucleotides KW - incorporation KW - adducts KW - hydrocarbons KW - deoxyadenosine KW - deoxyguanosine KW - Toxicology Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - DNA KW - N 14630:Chemical reactions & interactions, including effects of radiation KW - X 24240:Miscellaneous KW - N 14722:DNA polymerases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16142383?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=DNA+polymerase-mediated+nucleotide+incorporation+adjacent+to+hydrocarbon-deoxyadenosine+and+hydrocarbon-deoxyguanosine+adducts.&rft.au=Hruszkewycz%2C+A+M%3BCanella%2C+KA%3BDipple%2C+A&rft.aulast=Hruszkewycz&rft.aufirst=A&rft.date=1991-01-01&rft.volume=12&rft.issue=9&rft.spage=1659&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - DNA ER - TY - JOUR T1 - Transforming growth factor- beta and the immune system. AN - 16142019; 2690219 AB - Recently, TGF- beta was demonstrated to regulate immune cell activities in vitro. This wide range of immunoregulatory activities suggested that TGF- beta may regulate immune functions in vivo. In this review, we will discuss recent data on the in vitro and in vivo immunoregulatory properties of recombinant human TGF- beta 1 (rHuTGF- beta 1) and rHu-TGF- beta 2. Although we are in the early stages of understanding and controlling the immunoregulatory properties of TGF- beta (s) in vivo, the data suggest that they constitute an important class of immunosuppressive molecules with potential therapeutic utility. JF - Progress in Growth Factor Research AU - Ruscetti, F W AU - Palladino, MA AD - Lab. Mol. Immunoregul. Biol. Resp. Modif. Program, NCI-Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702-1201, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 159 EP - 175 VL - 3 IS - 2 SN - 0955-2235, 0955-2235 KW - cell proliferation KW - cytokines KW - immunoregulation KW - leukemia KW - reviews KW - transforming growth factor- beta KW - Microbiology Abstracts B: Bacteriology; Immunology Abstracts; Oncogenes & Growth Factors Abstracts KW - F 06774:Other cytokines (TNF, GM-CSF) KW - B 26340:TGF beta & TGF beta receptor KW - J:20320 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16142019?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Progress+in+Growth+Factor+Research&rft.atitle=Transforming+growth+factor-+beta+and+the+immune+system.&rft.au=Ruscetti%2C+F+W%3BPalladino%2C+MA&rft.aulast=Ruscetti&rft.aufirst=F&rft.date=1991-01-01&rft.volume=3&rft.issue=2&rft.spage=159&rft.isbn=&rft.btitle=&rft.title=Progress+in+Growth+Factor+Research&rft.issn=09552235&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - immunoregulation ER - TY - JOUR T1 - Estimating serum polychlorinated biphenyl levels in highly exposed workers: An empirical model. AN - 16138995; 2687974 AB - A regression model estimating high-homolog polychlorinated biphenyl (PCB) serum concentration on the basis of job exposure categorizations was developed. The model assumes first-order kinetics with a half-life determined empirically and uses variables that incorporate both intensity and duration of exposure over a 30-yr period. In order to compare the efficiency of these regression-based exposure estimates relative to often-used epidemiological parameters, models with dichotomized, ordinal, and continuous exposure surrogates were also investigated. Among the alternative exposure categorizations the most straightforward measure, ever versus never direct, was a particularly poor predictor of serum PCB level. Nearly all of the candidate exposure measures we tried predicted serum levels poorly. The best of these after the fact was with total months employed in direct-exposure jobs. None of the logical deductive models approached the predictability of the empirical model developed here. JF - Journal of Toxicology and Environmental Health AU - Taylor, PR AU - Reilly, A A AU - Stelma, J M AU - Lawrence, CE AD - NCI/NIH, 9000 Rockville Pike, Executive Pl. North, Rm. 211, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 413 EP - 422 VL - 34 IS - 4 SN - 0093-4108, 0093-4108 KW - PCB KW - serum KW - concentration KW - estimation KW - methodology KW - models KW - man KW - monitoring measurements KW - PCB compounds KW - Health & Safety Science Abstracts; Pollution Abstracts; Toxicology Abstracts KW - epidemiology KW - H SM3.8.2:CHEMICALS (CORROSION) KW - X 24222:Analytical procedures KW - X 24133:Metabolism KW - P 6000:TOXICOLOGY AND HEALTH UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16138995?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Toxicology+and+Environmental+Health&rft.atitle=Estimating+serum+polychlorinated+biphenyl+levels+in+highly+exposed+workers%3A+An+empirical+model.&rft.au=Taylor%2C+PR%3BReilly%2C+A+A%3BStelma%2C+J+M%3BLawrence%2C+CE&rft.aulast=Taylor&rft.aufirst=PR&rft.date=1991-01-01&rft.volume=34&rft.issue=4&rft.spage=413&rft.isbn=&rft.btitle=&rft.title=Journal+of+Toxicology+and+Environmental+Health&rft.issn=00934108&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - PCB compounds; epidemiology; models; man ER - TY - JOUR T1 - Characterization of neutrophil NADPH oxidase factors p47-phox and p67-phox from recombinant baculoviruses. AN - 16137413; 2680348 AB - Superoxide production by phagocytic blood cells involves assembly of an active NADPH oxidase complex from components found both in membrane and cytosolic locations in resting cells. We recently cloned cDNAs encoding two cytosolic components (p47-phox and p67-phox) of the oxidase that are deficient in distinct forms of autosomal recessive chronic granulomatous disease. The precise roles of p47-phox and p67-phox were explored further using purified factors produced in large quantities using recombinant baculoviruses to infect cultured Sf9 insect cells. Both p47-phox and p67-phox, used together in the absence of neutrophil cytosol, are incapable of supporting cell free production of superoxide, confirming the involvement of other soluble factor(s) in the assembly of an active oxidase in vitro. JF - Journal of Biological Chemistry AU - Leto, T L AU - Garrett, M C AU - Fujii, H AU - Nunoi, H AD - NIH/NIAID, Build. 10, Rm. 11N 106, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 19812 EP - 19818 VL - 266 IS - 29 SN - 0021-9258, 0021-9258 KW - NADPH oxidase KW - assembly KW - baculovirus KW - man KW - p47-phox protein KW - p67-phox protein KW - production KW - recombinants KW - role KW - superoxide KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16137413?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=Characterization+of+neutrophil+NADPH+oxidase+factors+p47-phox+and+p67-phox+from+recombinant+baculoviruses.&rft.au=Leto%2C+T+L%3BGarrett%2C+M+C%3BFujii%2C+H%3BNunoi%2C+H&rft.aulast=Leto&rft.aufirst=T&rft.date=1991-01-01&rft.volume=266&rft.issue=29&rft.spage=19812&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Spectroscopic characterization of syn-5-methylchrysene 1,2-dihydrodiol 3,4-epoxide-deoxyribonucleoside adducts. AN - 16133954; 2687869 AB - Bay region dihydrodiol epoxide metabolites of polycyclic aromatic hydrocarbon carcinogens are known to be largely responsible for the binding to DNA and the tumorigenic properties of the parent hydrocarbons. Eight deoxyribonucleoside adducts formed from reactions of syn-5-methylchrysene 1,2-dihydrodiol 3,4-epoxide with DNA or with nucleotides were characterized spectroscopically. The adducts arose from both cis and trans opening of the epoxide ring at C sub(4) by the amino group of either deoxyadenosine or deoxyguanosine residues. NMR data indicated that the partially saturated 1,2,3,4-ring of the hydrocarbon residue adopted a boatlike conformation, with the purine residue being disposed pseudoaxially in all adducts. The cis and trans assignments for epoxide ring opening were readily made from coupling constants. Quantitatively, cis adducts predominated over trans adducts in both DNA and nucleotide reactions. Whereas deoxyadenylic acid appeared to trap this dihydrodiol epoxide more efficiently than deoxyguanylic acid, reaction with DNA led to more extensive reaction with deoxyguanosine than with deoxyadenosine residues. JF - Chemical Research in Toxicology AU - Peltonen, K AU - Hilton, B D AU - Pataki, J AU - Lee, H AU - Harvey, R G AU - Dipple, A AD - Program Resources, Inc., NCI-Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 305 EP - 310 VL - 4 IS - 3 SN - 0893-228X, 0893-228X KW - syn-5-methylchrysene 1,2-dihydrodiol 3,4-epoxide KW - adducts KW - characterization KW - metabolites KW - chrysene KW - methylchrysene KW - 5-methylchrysene 1,2-dihydrodiol 3,4-epoxide KW - Toxicology Abstracts KW - DNA KW - polycyclic aromatic hydrocarbons KW - X 24190:Polycyclic hydrocarbons UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16133954?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+Research+in+Toxicology&rft.atitle=Spectroscopic+characterization+of+syn-5-methylchrysene+1%2C2-dihydrodiol+3%2C4-epoxide-deoxyribonucleoside+adducts.&rft.au=Peltonen%2C+K%3BHilton%2C+B+D%3BPataki%2C+J%3BLee%2C+H%3BHarvey%2C+R+G%3BDipple%2C+A&rft.aulast=Peltonen&rft.aufirst=K&rft.date=1991-01-01&rft.volume=4&rft.issue=3&rft.spage=305&rft.isbn=&rft.btitle=&rft.title=Chemical+Research+in+Toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - DNA; polycyclic aromatic hydrocarbons ER - TY - JOUR T1 - Persistence of 5-bromo-2'-deoxyuridine in tissues of rats after exposure in early life. AN - 16133518; 2683604 AB - Outbred L10 rats received 4 subcutaneous injections of 3.2 mg per rat 5-bromo-2'-deoxyuridine (BrdUrd) at 1, 3, 7 and 21 days of age. Groups of rats were sacrificed 1 h, 1 month or 49 weeks after the final injection. Tissues were fixed in 70% ethanol, embedded in paraffin and unstained sections were prepared for immunohistochemical demonstration of BrdUrd. A monoclonal antibody to BrdUrd was used with the avidin biotin peroxidase-complex (ABC) technique. The numbers of immunoreactive nuclei were tissue, cell and time-related. The labeling indices declined from 1 day to 49 weeks for all tissues studied. At 49 weeks after the last exposure to BrdUrd, many cells were still reactive, especially in tissues with normal low cell turnover (brain, uterine stroma). For cells with high turnover, including lymphocytes and ovarian germinative epithelium, few or no labeled cells remained at 49 weeks. This study provides clear evidence for the persistence of BrdUrd in normal tissues, some of which may be targets for the carcinogenic effect of the chemical and others which are not targets. JF - Toxicology AU - Ward, J M AU - Henneman, J R AU - Osipova, GYu AU - Anisimov, V N AD - NCI-FCRDC, Build. 538, Frederick, MD 21702-1201, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 345 EP - 352 VL - 70 IS - 3 SN - 0300-483X, 0300-483X KW - 5-bromo-2'-deoxyuridine KW - persistence KW - tissues KW - rats KW - Toxicology Abstracts KW - neonates KW - X 24240:Miscellaneous UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16133518?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology&rft.atitle=Persistence+of+5-bromo-2%27-deoxyuridine+in+tissues+of+rats+after+exposure+in+early+life.&rft.au=Ward%2C+J+M%3BHenneman%2C+J+R%3BOsipova%2C+GYu%3BAnisimov%2C+V+N&rft.aulast=Ward&rft.aufirst=J&rft.date=1991-01-01&rft.volume=70&rft.issue=3&rft.spage=345&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=0300483X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - neonates ER - TY - JOUR T1 - 1,3-Dialkyltriazenes: Reactive intermediates and DNA alkylation. AN - 16132841; 2688328 AB - The reactions of calf thymus (ct) DNA with 1,3-dimethyltriazene (DMT), N-methyl-N-nitrosourea (MNU), 1,3-diethyltriazene (DET), N-ethyl-N-nitrosourea (ENU), and 1-ethyl-3-methyltriazene (MET) were studied as a function of concentration of the alkylating agents, of various buffers, and of ionic strength. The amount of alkylation at the 7- and O super(6)-positions of guanine increased linearly with dose over a 10-fold concentration range. Data suggest that both types of compounds alkylate DNA via a similar intermediate, presumably the corresponding alkanediazonium ion. MET methylates and ethylates DNA, the amount of each product being a function of the competitive formation of the two diazonium ions possible from MET. The MET product ratios could be reproduced by an appropriate mixture of DET and DMT. The alkylation of DNA by DMT and by MET is very sensitive to ionic strength, to the nature of the buffer, and to the identity of the slat used to balance ionic strength. JF - Chemical Research in Toxicology AU - Kroeger-Koepke, M B AU - Smith, RH Jr AU - Goodnow, E A AU - Brashears, J AU - Kratz, L AU - Andrews, A W AU - Alvord, W G AU - Michejda, C J AD - ABL-Basic Res. Program, Program Resour., Inc., and Data Manage. Serv., NCI-Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 334 EP - 340 VL - 4 IS - 3 SN - 0893-228X, 0893-228X KW - 1,3-dimethyltriazene KW - N-methyl-N-nitrosourea KW - 1,3-diethyltriazene KW - N-ethyl-N-nitrosourea KW - 1-ethyl-3-methyltriazene KW - Biochemistry Abstracts 2: Nucleic Acids; Toxicology Abstracts KW - alkylation KW - DNA KW - N 14630:Chemical reactions & interactions, including effects of radiation KW - X 24155:Biochemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16132841?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+Research+in+Toxicology&rft.atitle=1%2C3-Dialkyltriazenes%3A+Reactive+intermediates+and+DNA+alkylation.&rft.au=Kroeger-Koepke%2C+M+B%3BSmith%2C+RH+Jr%3BGoodnow%2C+E+A%3BBrashears%2C+J%3BKratz%2C+L%3BAndrews%2C+A+W%3BAlvord%2C+W+G%3BMichejda%2C+C+J&rft.aulast=Kroeger-Koepke&rft.aufirst=M&rft.date=1991-01-01&rft.volume=4&rft.issue=3&rft.spage=334&rft.isbn=&rft.btitle=&rft.title=Chemical+Research+in+Toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - DNA; alkylation ER - TY - JOUR T1 - The v-rel and c-rel proteins exist in high molecular weight complexes in avian and murine cells. AN - 16127886; 2680817 AB - We reported previously that the v-rel protein (p59 super(v-rel)) exists in a high molecular weight complex with at least four other proteins in the cytoplasm of v-rel-transformed chicken pre-B lymphoid cells. One of these proteins is the chicken c-rel protein, but the identities of the others (of about 36kDa, 115kDa, and 124 kDa) are unknown. In this report we extend that observation to additional v-rel-transformed cell lines of both pre-B and B cell phenotypes. We also introduced and expressed v-rel in several other avian cell lines (a chicken T cell line, chick embryo fibroblasts, and quail fibroblasts) and found that in these cells p59 super(v-rel) was complexed with the same proteins as observed in the v-rel-transformed cells. JF - Oncogene AU - Kochel, T AU - Mushinski, J F AU - Rice, N R AD - ABL-Basic Res. Program, NCI-Frederick Cancer Res. and Dev. Cent., P.O. Box B, Frederick, MD 21701, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 615 EP - 626 VL - 6 IS - 4 SN - 0950-9232, 0950-9232 KW - c-Rel KW - c-rel protein KW - cells KW - chickens KW - complex KW - detection KW - expression KW - high molecular weight KW - mice KW - v-Rel KW - v-rel protein KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Oncogenes & Growth Factors Abstracts KW - B 26320:Other oncogenes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16127886?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+addiction&rft.atitle=Drug+self-administration+methods+in+abuse+liability+evaluation.&rft.au=Henningfield%2C+J+E%3BCohen%2C+C%3BHeishman%2C+S+J&rft.aulast=Henningfield&rft.aufirst=J&rft.date=1991-12-01&rft.volume=86&rft.issue=12&rft.spage=1571&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 revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Destruction of azo and azoxy compounds and 2-aminoanthracene. AN - 16110092; 2672481 AB - The destruction of a number of hazardous compounds that might be found in laboratories was studied. The reaction mixtures were analyzed by high pressure liquid chromatography for the presence of the compound and tested for mutagenicity using the Salmonella /mammalian microsome mutagenicity assay. A 0.3-M solution of potassium permanganate in 3 M sulfuric acid can be used for the degradation of azobenzene, azoxyanisole, phenylazophenol, phenylazoaniline, Fast Garnet, and 2-amino-anthracene. Nickel-aluminum alloy in 2 M potassium hydroxide solution can be used for the destruction of azobenzene, azoxybenzene, azoxyanisole, and phenylazophenol. In each case, the compounds were completely degraded to their limit of detection and only nonmutagenic reaction mixtures were produced. Amberlite XAD-16 resin was used to decontaminate aqueous solutions of all the above compounds as well as Methyl Yellow. JF - APPL. OCCUP. ENVIRON. MICROBIOL. AU - Lunn, G AU - Sansone, E B AD - Program Resources Inc./DynCorp, Environ. Control and Res. Program, NCI-Frederick Cancer Res. and Dev. Cent., P.O. Box B, Frederick, MD 21702-1201, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 1020 EP - 1026 VL - 6 IS - 12 KW - chemical reactions KW - Pollution Abstracts KW - hazardous materials KW - liquid chromatography KW - laboratory testing KW - assays KW - P 6000:TOXICOLOGY AND HEALTH UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16110092?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Apollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=APPL.+OCCUP.+ENVIRON.+MICROBIOL.&rft.atitle=Destruction+of+azo+and+azoxy+compounds+and+2-aminoanthracene.&rft.au=Lunn%2C+G%3BSansone%2C+E+B&rft.aulast=Lunn&rft.aufirst=G&rft.date=1991-01-01&rft.volume=6&rft.issue=12&rft.spage=1020&rft.isbn=&rft.btitle=&rft.title=APPL.+OCCUP.+ENVIRON.+MICROBIOL.&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - liquid chromatography; laboratory testing; assays; hazardous materials ER - TY - JOUR T1 - DNA hydroxyethylation by hydroxyethylnitrosoureas in relation to their organ specific carcinogenicity in rats. AN - 16106183; 2663564 AB - N-hydroxyethylnitroso-N'-ethylurea (HEENU) and N-hydroxyethylnitroso-N'-chloroethylurea (HCNU) are two of the few nitrosoureas which induce hepatocellular tumours in rats without further treatment. We investigated whether this is due to selectively elevated levels of DNA hydroxyethylation in the target tissue. Formation of the promutagenic base O super(6)-hydroxyethyl-deoxyguanosine (O super(6)-HEdG) in various rat tissues was determined by immuno-slot-blot assay. We conclude that the hepatocarcinogenicity of HCNU and HEENU cannot be explained on the basis of their reaction with cellular DNA. JF - Chemico-Biological Interactions AU - Ludeke, B AU - Schubert, M AU - Yamada, Y AU - Lijinsky, W AU - Kleihues, P AD - NIEHS, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 207 EP - 216 VL - 79 IS - 2 SN - 0009-2797, 0009-2797 KW - DNA KW - rats KW - hydroxyethylation KW - hydroxyethylnitrosourea KW - tumours KW - N-hydroxyethylnitroso-N'-ethylurea KW - N-hydroxyethylnitroso-N'-chloroethylurea KW - Biochemistry Abstracts 2: Nucleic Acids; Toxicology Abstracts KW - carcinogenicity KW - N 14630:Chemical reactions & interactions, including effects of radiation KW - X 24200:Nitrosamines & related compounds UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16106183?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemico-Biological+Interactions&rft.atitle=DNA+hydroxyethylation+by+hydroxyethylnitrosoureas+in+relation+to+their+organ+specific+carcinogenicity+in+rats.&rft.au=Ludeke%2C+B%3BSchubert%2C+M%3BYamada%2C+Y%3BLijinsky%2C+W%3BKleihues%2C+P&rft.aulast=Ludeke&rft.aufirst=B&rft.date=1991-01-01&rft.volume=79&rft.issue=2&rft.spage=207&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 revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - carcinogenicity ER - TY - JOUR T1 - Positional effects on the structure and stability of abbreviated H-ras DNA sequences containing O super(6)-methylguanine residues at codon 12. AN - 16104046; 2659724 AB - Activation of the H-ras protooncogene in rats by methylating carcinogens results from a G-to-A transition mutation at the second position of codon 12 (GGA), presumably due to formation of an O super(6)-methylguanine (m super(6)G) at this position. A similar transition at the first position of codon 12 appears not to occur in vivo. To study the possible structural basis for this bias in mutation, we synthesized a series of 11-base H-ras sequences (e.g., 5'-d(CGCTG super(*)G super(*)AGGCG)-3' and two complementary strands) containing an m super(6)G at the first, second, or both positions of codon 12 (i.e., G super(*) = m super(6)G). The results of solution chemical studies indicated that the individual strands formed stable hairpin structures among which that containing m super(6)G at the second position of codon 12 was most stable. Further, the DNA duplex with m super(6)G at the second position was significantly more stable than that with m super(6)G at the first position, and under certain conditions, it was more stable than the unmodified duplex as well. JF - Chemical Research in Toxicology AU - Bishop, R E AU - Moschel, R C AD - Chem. Carcinog. Lab., ABL-Basic Res. Program, NCI-Frederick Cancer Res. and Dev. Cent., P.O. Box B, Frederick, MD 21702, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 647 EP - 654 VL - 4 IS - 6 SN - 0893-228X, 0893-228X KW - oncogenes KW - H-ras gene KW - stability KW - structure-activity relationships KW - genes KW - methylguanine KW - Biochemistry Abstracts 2: Nucleic Acids; Toxicology Abstracts KW - nucleotide sequence KW - carcinogens KW - DNA KW - N 14640:Structure & sequence KW - X 24240:Miscellaneous UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16104046?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+Research+in+Toxicology&rft.atitle=Positional+effects+on+the+structure+and+stability+of+abbreviated+H-ras+DNA+sequences+containing+O+super%286%29-methylguanine+residues+at+codon+12.&rft.au=Bishop%2C+R+E%3BMoschel%2C+R+C&rft.aulast=Bishop&rft.aufirst=R&rft.date=1991-01-01&rft.volume=4&rft.issue=6&rft.spage=647&rft.isbn=&rft.btitle=&rft.title=Chemical+Research+in+Toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - carcinogens; DNA; nucleotide sequence ER - TY - JOUR T1 - The role of oxidative damage in metal carcinogenicity. AN - 16102899; 2659852 JF - Chemical Research in Toxicology AU - Kasprzak, K S AD - Build. 538, Rm. 205, NCI-FCRDC, Frederick, MD 21702, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 604 EP - 615 VL - 4 IS - 6 SN - 0893-228X, 0893-228X KW - metals KW - damage KW - Toxicology Abstracts KW - carcinogenesis KW - oxidation KW - X 24165:Biochemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16102899?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+Research+in+Toxicology&rft.atitle=The+role+of+oxidative+damage+in+metal+carcinogenicity.&rft.au=Kasprzak%2C+K+S&rft.aulast=Kasprzak&rft.aufirst=K&rft.date=1991-01-01&rft.volume=4&rft.issue=6&rft.spage=604&rft.isbn=&rft.btitle=&rft.title=Chemical+Research+in+Toxicology&rft.issn=0893228X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - carcinogenesis; oxidation ER - TY - JOUR T1 - Tumor necrosis factor involvement in 2,3,7,8-tetrachlorodibenzo-p-dioxin-mediated endotoxin hypersensitivity in C57BL/6J mice congenic at the Ah locus. AN - 16099906; 2659961 AB - An experimental model of endotoxin-induced release of tumor necrosis factor- alpha (TNF) into the serum of C57BL/6J mice congenic at the Ah locus was used to investigate the effects of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) on TNF production. TCDD exposure of Ah-responsive mice (Ah super(bb)) resulted in a dose-dependent increase in the concentration of TNF in the serum of endotoxin-exposed mice, with a significant increase observed at a dose of 10 mu g/kg TCDD. At a dose of 500 mu g/kg TCDD, Ah super(bb) mice demonstrated a 46-fold increase in serum TNF levels compared to control. In contrast, congenic Ah-receptor deficient mice (Ah super(dd)) did not show a significant increase in serum TNF levels until exposed to 150 mu g/kg TCDD, and the maximum response was an 8-fold increase over control. These data suggest that increased TNF production by be responsible for endotoxin hypersensitivity in TCDD-treated mice and that the Ah locus mediates this response. JF - Toxicology and Applied Pharmacology AU - Clark, G C AU - Taylor, MJ AU - Tritscher, A M AU - Lucier, G W AD - NIEHS, MD D4-04, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 422 EP - 431 VL - 111 IS - 3 SN - 0041-008X, 0041-008X KW - TCDD KW - tumor necrosis factor- alpha KW - mice KW - Toxicology Abstracts KW - hypersensitivity KW - endotoxins KW - X 24151:Acute exposure KW - X 24171:Microbial UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16099906?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+Applied+Pharmacology&rft.atitle=Tumor+necrosis+factor+involvement+in+2%2C3%2C7%2C8-tetrachlorodibenzo-p-dioxin-mediated+endotoxin+hypersensitivity+in+C57BL%2F6J+mice+congenic+at+the+Ah+locus.&rft.au=Clark%2C+G+C%3BTaylor%2C+MJ%3BTritscher%2C+A+M%3BLucier%2C+G+W&rft.aulast=Clark&rft.aufirst=G&rft.date=1991-01-01&rft.volume=111&rft.issue=3&rft.spage=422&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+Applied+Pharmacology&rft.issn=0041008X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - endotoxins; hypersensitivity ER - TY - JOUR T1 - Reduction of paraquat and related bipyridylium compounds to free radical metabolites by rat hepatocytes. AN - 16099438; 2660020 AB - The toxicity of paraquat is due to the oxygen-derived radicals formed by the reaction of oxygen with bipyridylium radical cations. Although paraquat is known to cause lung toxicity, the related bipyridylium compounds such as diquat and morfamquat do not affect the lung as seriously, but rather cause liver toxicity. Paraquat, diquat, morfamquat, and benzyl viologen are reduced by rat hepatocytes to their respective radical cations. An intracellular component of the signal was detected from diquat and benzyl viologen radical cations. The reduction of paraquat is generally attributed to NADPH-cytochrome P-450 reductase, and presumably diquat is also reduced by this flavoprotein. JF - Archives of Biochemistry and Biophysics AU - DeGray, JA AU - Rao, DNR AU - Mason, R P AD - Lab. Mol. Biophys., MD 4-01, NIEHS, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 145 EP - 152 VL - 289 IS - 1 SN - 0003-9861, 0003-9861 KW - liver KW - reduction KW - formation KW - radicals KW - rats KW - cytochrome P450 KW - paraquat KW - Toxicology Abstracts; Biochemistry Abstracts 1: Biological Membranes (till 1993) KW - X 24135:Biochemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16099438?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+Biochemistry+and+Biophysics&rft.atitle=Reduction+of+paraquat+and+related+bipyridylium+compounds+to+free+radical+metabolites+by+rat+hepatocytes.&rft.au=DeGray%2C+JA%3BRao%2C+DNR%3BMason%2C+R+P&rft.aulast=DeGray&rft.aufirst=JA&rft.date=1991-01-01&rft.volume=289&rft.issue=1&rft.spage=145&rft.isbn=&rft.btitle=&rft.title=Archives+of+Biochemistry+and+Biophysics&rft.issn=00039861&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 ER - TY - JOUR T1 - Immunocytochemical localization of argininosuccinate synthetase in the rat brain. AN - 16097697; 2653457 AB - The neuronal distribution of argininosuccinate synthetase (ASS) was mapped in the rat brain. Polyclonal antisera against purified rat liver argininosuccinate synthetase revealed a characteristic distribution pattern of argininosuccinate synthetase-like immunoreactivity: many neurons with strong argininosuccinate synthetase-like immunoreactivity were observed in the septal area, basal forebrain, anterior medial and premammillary nuclei of the hypothalamus, anterior and midline thalamic nuclei, dorsal endopiriform nucleus of the amygdala, basal nucleus of Meynert, subthalamic nucleus, laterodorsal tegmental nucleus, raphe nuclei, nucleus ambiguus, and the area postrema. No staining was seen in the large white matter structures such as the internal capsule, corpus callosum, and the anterior commissure. The results suggest that argininosuccinate synthetase affects the widely distributed, neuromodulatory system in the brain. JF - Journal of Comparative Neurology AU - Nakamura, H AU - Saheki, T AU - Ichiki, H AU - Nakata, K AU - Nakagawa, S AD - Lab. Neuropsychol., NIMH, Build. 9, Rm. 1E104, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 652 EP - 679 VL - 312 IS - 4 SN - 0021-9967, 0021-9967 KW - argininosuccinate synthase KW - brain KW - immunogenicity KW - localization KW - rats KW - regions KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; CSA Neurosciences Abstracts KW - N3 11070:Neurochemistry and cellular biology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16097697?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Comparative+Neurology&rft.atitle=Immunocytochemical+localization+of+argininosuccinate+synthetase+in+the+rat+brain.&rft.au=Nakamura%2C+H%3BSaheki%2C+T%3BIchiki%2C+H%3BNakata%2C+K%3BNakagawa%2C+S&rft.aulast=Nakamura&rft.aufirst=H&rft.date=1991-01-01&rft.volume=312&rft.issue=4&rft.spage=652&rft.isbn=&rft.btitle=&rft.title=Journal+of+Comparative+Neurology&rft.issn=00219967&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Differential scanning calorimetry study of reversible, partial unfolding transitions in dodecameric glutamine synthetase from Escherichia coli . AN - 16086244; 2645090 AB - Partial unfolding of dodecameric glutamine synthetase (GS) from Escherichia coli has been studied by differential scanning calorimetry (DSC). Cooperative interactions apparently link partial unfolding reactions of all subunits within the GS dodecamer so that only two-state transitions are observed. JF - Biochemistry (Washington) AU - Ginsburg, A AU - Zolkiewski, M AD - NHLBI/NIH, Build. 3, Room 208, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 9421 EP - 9429 VL - 30 IS - 39 SN - 0006-2960, 0006-2960 KW - Escherichia coli KW - analysis KW - differential scanning calorimetry KW - folding KW - glutamine synthase KW - transitions KW - use KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology KW - J 02728:Enzymes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16086244?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemistry+%28Washington%29&rft.atitle=Differential+scanning+calorimetry+study+of+reversible%2C+partial+unfolding+transitions+in+dodecameric+glutamine+synthetase+from+Escherichia+coli+.&rft.au=Ginsburg%2C+A%3BZolkiewski%2C+M&rft.aulast=Ginsburg&rft.aufirst=A&rft.date=1991-01-01&rft.volume=30&rft.issue=39&rft.spage=9421&rft.isbn=&rft.btitle=&rft.title=Biochemistry+%28Washington%29&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - A new method for delivering alkanes to mammalian cells: Preparation and preliminary characterization of an inclusion complex between beta -cyclodextrin and pristane (2,6,10,14-tetramethylpentadecane). AN - 16082391; 2645876 AB - Pristane (2,6,10,14-tetramethylpentadecane) is an isoalkane which induces plasma cell tumorigenesis in genetically susceptible strains of mice. Attempts to study the biological activity of pristane on cells in vitro have been hindered by the extreme hydrophobicity and hence complete immiscibility of the compound in aqueous cell culture media. In comparing different solubilization protocols such as using organic solvents, liposomes, and molecular encapsulation into beta -cyclodextrin ( beta -CyD), it was found that beta -CyD/pristane inclusion complexes were optimal for delivery of the hydrocarbon to cells. After solubilization in beta -CyD, pristane was cytotoxic ( super(51)Cr release assay) to murine B lymphocyte lines in culture (P388, NSF-1, and SJL-4) and inhibited the lipopolysaccharide-induced stimulation of splenic B lymphocyte proliferation and blast formation (Coulter counter analysis) when added in the micromolar concentration range. JF - Toxicology AU - Janz, S AU - Shacter, E AD - Lab. Genet., NCI, NIH, Build. 37, Rm. 2B09, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 301 EP - 315 VL - 69 IS - 3 SN - 0300-483X, 0300-483X KW - alkanes KW - delivery KW - methodology KW - pristane KW - Toxicology Abstracts KW - toxicity testing KW - mammalian cells KW - encapsulation KW - X 24221:Toxicity testing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16082391?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology&rft.atitle=A+new+method+for+delivering+alkanes+to+mammalian+cells%3A+Preparation+and+preliminary+characterization+of+an+inclusion+complex+between+beta+-cyclodextrin+and+pristane+%282%2C6%2C10%2C14-tetramethylpentadecane%29.&rft.au=Janz%2C+S%3BShacter%2C+E&rft.aulast=Janz&rft.aufirst=S&rft.date=1991-01-01&rft.volume=69&rft.issue=3&rft.spage=301&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=0300483X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - mammalian cells; toxicity testing; encapsulation ER - TY - JOUR T1 - Function of negative charge in the "address domain" of deltorphins. AN - 16081780; 2645202 AB - Deltorphins A, B, and C exhibit high delta -affinities (K sub(i) = 0.12-0.31 nM) and very high delta -receptor binding selectivities (K sub(i) mu /K sub(i) delta = 1800-4100). A study of the delta -receptor binding properties of 15 deltorphin analogues focused primarily on the influence of the anionic group in the C-terminal tetrapeptide. The results demonstrate that while an anionic group may occassionally facilitate high delta -receptor affinity, it represents an absolute requirement for the high delta -binding selectivity of these peptides. The locations of the charged groups relative to hydrophobic residues in the address domain of the peptide are also critical determinants for both delta -affinity and -selectivity. JF - Journal of Medicinal Chemistry AU - Lazarus, L H AU - Salvadori, S AU - Santagada, V AU - Tomatis, R AU - Wilson, W E AD - NIEHS, P.O. Box 12233, MD 14-01, Research Triangle Park, NC 27709, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 1350 EP - 1355 VL - 34 IS - 4 SN - 0022-2623, 0022-2623 KW - binding KW - charge KW - deltorphin A KW - deltorphin B KW - deltorphin C KW - effects on KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16081780?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Medicinal+Chemistry&rft.atitle=Function+of+negative+charge+in+the+%22address+domain%22+of+deltorphins.&rft.au=Lazarus%2C+L+H%3BSalvadori%2C+S%3BSantagada%2C+V%3BTomatis%2C+R%3BWilson%2C+W+E&rft.aulast=Lazarus&rft.aufirst=L&rft.date=1991-01-01&rft.volume=34&rft.issue=4&rft.spage=1350&rft.isbn=&rft.btitle=&rft.title=Journal+of+Medicinal+Chemistry&rft.issn=00222623&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - High risk of human papillomavirus infection and cervical squamous intraepithelial lesions among women with symptomatic human immunodeficiency virus infection. AN - 16080703; 2640261 AB - We investigated the relationship of human papillomavirus (by cervicovaginal lavage and Southern blot), human immunodeficiency virus, and squamous intraepithelial lesions in 96 high-risk women in the Bronx, New York. Antibodies for human immunodeficiency virus were detected in 51 (53%) women. Of the 33 women with symptomatic human immunodeficiency virus infection, 23 (70%) had human papillomavirus infection compared with 4 of 18 (22%) asymptomatic women who were human immunodeficiency virus seropositive and 10 of 45 (22%) uninfected women (p < 0.0001). Risk was highest for younger women from ethnic or racial minority groups. Advanced human immunodeficiency virus-related disease, with its associated immunosuppression, seems to exacerbate human papillomavirus-mediated cervical cytologic abnormalities. Public health measures are needed to provide Papanicolaou smear screening and appropriate clinical follow-up and treatment for women at high risk for human immunodeficiency virus infection. JF - AM. J. OBSTET. GYNECOL. AU - Vermund, SH AU - Kelley, K F AU - Klein, R S AU - Feingold, A R AU - Schreiber, K AU - Munk, G AU - Burk, R D AD - EB/DAIDS/NIAID/NIH, 6003 Executive Blvd., Rm. 240P, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 392 EP - 400 VL - 165 IS - 2 SN - 0002-9378, 0002-9378 KW - human immunodeficiency virus KW - risks KW - infection KW - New York, Bronx KW - papilloma virus (human) KW - cervix KW - USA, New York, Bronx KW - Health & Safety Science Abstracts; Oncogenes & Growth Factors Abstracts; Virology & AIDS Abstracts KW - ethnic groups KW - lesions KW - B 26270:Papillomaviruses KW - V 22005:AIDS: Epidemiological aspects KW - H SM10.37:VENEREAL DISEASES UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16080703?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AM.+J.+OBSTET.+GYNECOL.&rft.atitle=High+risk+of+human+papillomavirus+infection+and+cervical+squamous+intraepithelial+lesions+among+women+with+symptomatic+human+immunodeficiency+virus+infection.&rft.au=Vermund%2C+SH%3BKelley%2C+K+F%3BKlein%2C+R+S%3BFeingold%2C+A+R%3BSchreiber%2C+K%3BMunk%2C+G%3BBurk%2C+R+D&rft.aulast=Vermund&rft.aufirst=SH&rft.date=1991-01-01&rft.volume=165&rft.issue=2&rft.spage=392&rft.isbn=&rft.btitle=&rft.title=AM.+J.+OBSTET.+GYNECOL.&rft.issn=00029378&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - lesions; ethnic groups; infection; cervix ER - TY - JOUR T1 - AIDS, drugs of abuse and the immune system: A complex immunotoxicological network. AN - 16074563; 2639427 AB - Two of the most interesting questions often asked about AIDS is why many people do not become immunodeficient or get complicating disease when first infected with Human Immunodeficiency Virus (HIV) and what are the "risk factors" making some individuals more susceptible to the disease. A large majority of people with AIDS have a well established history of drug and alcohol abuse. Both drugs of abuse and alcohol have immunotoxic properties as evidenced by a number of studies. These include marked changes in the cellular, humoral and other components of the immune defense mechanism. Such a compromise of the immune system can render it susceptible to the development of AIDS after HIV infection. This paper reviews the evidence suggesting possible links between substance abuse and its immunotoxicology, and their possible roles in the pathogenesis of AIDS. JF - Archives of Toxicology AU - Pillai, R AU - Nair, B S AU - Watson, R R AD - NIAAA Spec. Alcohol Res. Cent., Dep. Fam. and Community Med., Univ. Arizona Health Sci. Cent., Tucson, AZ 85724, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 609 EP - 617 VL - 65 IS - 8 SN - 0340-5761, 0340-5761 KW - drug abuse KW - effects on KW - ethanol KW - immune system KW - man KW - Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts; Toxicology Abstracts KW - immunology KW - human immunodeficiency virus KW - acquired immune deficiency syndrome KW - reviews KW - F 06792:Clinical KW - H SM10.40:DRUG ADDICTION KW - V 22003:AIDS: Immunological aspects KW - X 24180:Social poisons & drug abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16074563?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+Toxicology&rft.atitle=AIDS%2C+drugs+of+abuse+and+the+immune+system%3A+A+complex+immunotoxicological+network.&rft.au=Pillai%2C+R%3BNair%2C+B+S%3BWatson%2C+R+R&rft.aulast=Pillai&rft.aufirst=R&rft.date=1991-01-01&rft.volume=65&rft.issue=8&rft.spage=609&rft.isbn=&rft.btitle=&rft.title=Archives+of+Toxicology&rft.issn=03405761&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - human immunodeficiency virus; acquired immune deficiency syndrome; reviews; ethanol; immunology; immune system; man ER - TY - JOUR T1 - Increased cytotoxic activity of Pseudomonas exotoxin and two chimeric toxins ending in KDEL. AN - 16065488; 2620899 AB - We tested the effect of altering the carboxyl sequence of Pseudomonas exotoxin (PE) from Arg-Glu-Asp-Leu-Lys (REDLK) to the characteristic endoplasmic reticulum retention sequence, KDEL, or to KDEL repeated three times (KDEL) sub(3). We also made similar changes at the carboxyl terminus of two chimeric toxins in which domain I of PE (amino acids 1-252) was either replaced with transforming growth factor alpha (TGF alpha ) to make TGF alpha -PE40 or with a single chain antibody (anti-Tac) reacting with the human interleukin 2 receptor to make anti-Tac(Fv)-PE40. Statistical analyses of our results demonstrate that PE and its derivatives ending in KDEL or (KDEL) sub(3) are significantly more active than PE or derivatives ending in REDLK. JF - Journal of Biological Chemistry AU - Seetharam, S AU - Chaudhary, V K AU - FitzGerald, D AU - Pastan, I AD - Lab. Mol. Biol., Div. Cancer Biol., Diagn. and Cent., NCI, NIH, Build. 37, Rm. 4E16, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 17376 EP - 17381 VL - 266 IS - 26 SN - 0021-9258, 0021-9258 KW - C-termination KW - Pseudomonas aeruginosa KW - chimeras KW - cytotoxicity KW - derivatives KW - mutation KW - toxins KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Toxicology Abstracts KW - J 02822:Biosynthesis and physicochemical properties KW - X 24171:Microbial UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16065488?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinics+in+chest+medicine&rft.atitle=Cigarette+smoking+and+addiction.&rft.au=Cohen%2C+C%3BPickworth%2C+W+B%3BHenningfield%2C+J+E&rft.aulast=Cohen&rft.aufirst=C&rft.date=1991-12-01&rft.volume=12&rft.issue=4&rft.spage=701&rft.isbn=&rft.btitle=&rft.title=Clinics+in+chest+medicine&rft.issn=02725231&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - toxins ER - TY - JOUR T1 - tpr-met Oncogene product induces maturation-producing factor activation in Xenopus oocytes. AN - 16065172; 2626159 AB - tpr-met, a tyrosine kinase oncogene, is the activated form of the met proto-oncogene that encodes the receptor for hepatocyte growth factor/scatter factor. The tpr-met product (p65 super(tpr-met)) was tested for its ability to induce meiotic maturation in Xenopus oocytes. While src and abl tyrosine kinase oncogene products have previously been shown to be inactive in this assay, p65 super(tpr-met) efficiently induced maturation-promoting factor (MPF) activation and germinal vesicle breakdown (GVBD) together with the associated increase in ribosomal S6 subunit phosphorylation. tpr-met-mediated MPF activation and GVBD was dependent on the endogenous c-mos super(xe), while the increase in S6 protein phosphorylation was not significantly affected by the loss of mos function. JF - Molecular and Cellular Biology AU - Daar, I O AU - White, G A AU - Schuh, S M AU - Ferris, D K AU - Vande Woude, GF AD - ABL-Basic Res. Program, P.O. Box B, NCI-Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 5985 EP - 5991 VL - 11 IS - 12 SN - 0270-7306, 0270-7306 KW - Trp-met KW - Xenopus KW - activation KW - genes KW - maturation-producing factor KW - meiosis KW - oncogenes KW - oocytes KW - tpr-met gene KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Oncogenes & Growth Factors Abstracts KW - B 26120:Other oncogenes & GF's with tyrosine kinase activity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16065172?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+Cellular+Biology&rft.atitle=tpr-met+Oncogene+product+induces+maturation-producing+factor+activation+in+Xenopus+oocytes.&rft.au=Daar%2C+I+O%3BWhite%2C+G+A%3BSchuh%2C+S+M%3BFerris%2C+D+K%3BVande+Woude%2C+GF&rft.aulast=Daar&rft.aufirst=I&rft.date=1991-01-01&rft.volume=11&rft.issue=12&rft.spage=5985&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 revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - meiosis ER - TY - JOUR T1 - Comparative safety, tolerance, and pharmacokinetics of amphotericin B lipid complex and amphotericin B desoxycholate in healthy male volunteers. AN - 16064132; 2624256 AB - Amphotericin B lipid complex (ABLC), a lipid complex formulation of amphotericin B, and amphotericin B deoxycholate (AB) were compared for safety, tolerance, and pharmacokinetics in two groups of eight healthy male volunteers. After a 1-mg test dose, study drug was infused at 0.1, 0.25, and 0.5 mg/kg; the 0.5-mg/kg dose was not given to subjects receiving AB. ABLC caused few acute adverse effects except for mild somnolence (drowsiness) in six volunteers. In addition, three of eight ABLC recipients had asymptomatic, transient serum transaminase elevations that resolved spontaneously. The AB recipients experienced more acute side effects, but only one had a mild shaking chill; three of eight also experienced sleepiness. No significant changes in vital signs, electrocardiograms, oximetry, pulmonary function, or clinical status were observed in either group. Due to its increased estimated volume of distribution and estimated clearance, ABLC yielded decreased amphotericin B levels and area under the serum concentration versus time curve relative to AB. JF - Journal of Infectious Diseases AU - Kan, V L AU - Bennett, JE AU - Amantea, MA AU - Smolskis, M C AU - McManus, E AU - Grasela, D M AU - Sherman, J W AD - Clin. Mycol. Sect., LCI/NIAID, Build. 10, Rm. 11N107, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 418 EP - 421 VL - 164 IS - 2 SN - 0022-1899, 0022-1899 KW - amphotericin B KW - complex KW - pharmacokinetics KW - amphotericin B desoxycholate KW - Toxicology Abstracts KW - side effects KW - lipids KW - drowsiness KW - man KW - X 24113:Side effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16064132?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Infectious+Diseases&rft.atitle=Comparative+safety%2C+tolerance%2C+and+pharmacokinetics+of+amphotericin+B+lipid+complex+and+amphotericin+B+desoxycholate+in+healthy+male+volunteers.&rft.au=Kan%2C+V+L%3BBennett%2C+JE%3BAmantea%2C+MA%3BSmolskis%2C+M+C%3BMcManus%2C+E%3BGrasela%2C+D+M%3BSherman%2C+J+W&rft.aulast=Kan&rft.aufirst=V&rft.date=1991-01-01&rft.volume=164&rft.issue=2&rft.spage=418&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - lipids; side effects; drowsiness; man ER - TY - JOUR T1 - Bypass of a hydrocarbon adduct in an oligonucleotide template mediated by mispairing adjacent to the adduct. AN - 16062798; 2629717 AB - The action of DNA polymerase (Sequenase Version 2.0) on an oligonucleotide template containing a 7-bromomethyl-benz(a)anthracene-deoxyadenosine adduct flanked by thymidine residues was investigated. The polymerase incorporated deoxyadenosine or deoxyguanosine residues opposite the thymidine 3' to the adduct with similar efficiencies. Whereas the normal A multiplied by T base pair led to arrest of polymerase progression along the template, formation of the G multiplied by T mismatch allowed incorporation of thymidine opposite the adduct and further primer extension. This mispair-mediated bypass was also seen with AMV reverse transcriptase and may represent a novel mechanism for overcoming the replication block of a bulky carcinogen-DNA adduct. JF - Carcinogenesis AU - Hruszkewycz, A M AU - Dipple, A AD - Chem. Carcinog. Lab., ABL-Basic Res. Program, NCI-Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702-1201, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 2185 EP - 2187 VL - 12 IS - 11 SN - 0143-3334, 0143-3334 KW - DNA-directed DNA polymerase KW - adducts KW - bypass KW - mechanism KW - 7-bromomethylbenz(a)anthracene KW - Biochemistry Abstracts 2: Nucleic Acids; Toxicology Abstracts KW - hydrocarbons KW - DNA KW - DNA repair KW - X 24240:Miscellaneous KW - N 14722:DNA polymerases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16062798?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Bypass+of+a+hydrocarbon+adduct+in+an+oligonucleotide+template+mediated+by+mispairing+adjacent+to+the+adduct.&rft.au=Hruszkewycz%2C+A+M%3BDipple%2C+A&rft.aulast=Hruszkewycz&rft.aufirst=A&rft.date=1991-01-01&rft.volume=12&rft.issue=11&rft.spage=2185&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - DNA; hydrocarbons; DNA repair ER - TY - JOUR T1 - Dexamethasone 21-( beta -isothiocyanatoethyl) thioether: A new affinity label for glucocorticoid receptors. AN - 16052283; 2623257 AB - The C-21 methanesulfonate ester of the synthetic glucocorticoid dexamethasone (Dex) is an efficient electrophilic affinity label of glucocorticoid receptors and exhibits irreversible antiglucocorticoid activity. In an effort to obtain other affinity labeling steroids with differing biological activities, several new derivatives of Dex were prepared which contained a reactive electrophilic substituent at various distances from the C-21 position. The data directly establish Dex-NCS as a new affinity label for glucocorticoid receptors, Data on the reactivity of Dex-NCS and the stability of ( super(3)H)Dex-NCS-labeled receptors suggest that a cysteine SH group has been labeled. JF - Journal of Medicinal Chemistry AU - Lopez, S AU - Simons, S S AD - Build. 8, Rm. B2A-07, NIDDK/LMCB, NIH, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 1762 EP - 1767 VL - 34 IS - 6 SN - 0022-2623, 0022-2623 KW - affinity labelling KW - dexamethasone 21-( beta -isothiocyanatoethyl) thioether KW - glucocorticoids KW - rats KW - receptors KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16052283?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Medicinal+Chemistry&rft.atitle=Dexamethasone+21-%28+beta+-isothiocyanatoethyl%29+thioether%3A+A+new+affinity+label+for+glucocorticoid+receptors.&rft.au=Lopez%2C+S%3BSimons%2C+S+S&rft.aulast=Lopez&rft.aufirst=S&rft.date=1991-01-01&rft.volume=34&rft.issue=6&rft.spage=1762&rft.isbn=&rft.btitle=&rft.title=Journal+of+Medicinal+Chemistry&rft.issn=00222623&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Catalysis of acetyl-CoA cleavage tetrahydrosarcinapterin methylation by a carbon monoxide dehydrogenase-corrinoid enzyme complex. AN - 16045685; 2611104 AB - An enzyme complex containing carbon monoxide dehydrogenase and a corrinoid protein has been isolated from Methanosarcina barkeri . Sodium dodecyl sulfate-gel electrophoresis revealed five polypeptides of molecular masses alpha = 19,700, beta = 84,500, gamma = 63,200, delta = 53,000, and epsilon = 51,400 Da in equimolar amounts. One mol of cobamide cofactor was found per minimal alpha beta gamma delta epsilon unit. The molecular mass of the native complex was 1,600,000 Da by high pressure liquid chromatography (HPLC) gel filtration, which suggested an alpha sub(6) beta sub(6) gamma sub(6) delta sub(6) epsilon sub(6) oligomeric structure. Catalysis of a reaction involving cleavage of acetyl-CoA and methylation of tetrahydrosarcinapterin was indicated by spectrophotometric analyses; a time-dependent absorption decrease in the 300-320 nm region was observed in the complete reaction mixture which contained acetyl-CoA, tetrahydrosarcinapterin, and the enzyme complex. JF - Journal of Biological Chemistry AU - Grahame, DA AD - Lab. Biochem., Build. 3, Rm. 114, NHLBI, NIH, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 22227 EP - 22233 VL - 266 IS - 33 SN - 0021-9258, 0021-9258 KW - Methanosarcina barkeri KW - acetyl-CoA KW - carbon monoxide dehydrogenase KW - catalysis KW - cleavage KW - complex KW - corrinoid protein KW - enzymatic activity KW - methylation KW - tetrahydrosarcinapterin KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology KW - J 02728:Enzymes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16045685?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=Catalysis+of+acetyl-CoA+cleavage+tetrahydrosarcinapterin+methylation+by+a+carbon+monoxide+dehydrogenase-corrinoid+enzyme+complex.&rft.au=Grahame%2C+DA&rft.aulast=Grahame&rft.aufirst=DA&rft.date=1991-01-01&rft.volume=266&rft.issue=33&rft.spage=22227&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Intravenous immune globulin for the prevention of bacterial infections in children with symptomatic human immunodeficiency virus infection. AN - 16044452; 2610491 AB - Serious recurrent bacterial infections are a major cause of morbidity and mortality in children infected with the human immunodeficiency virus (HIV). Because intravenous immune globulin has been shown to prevent bacterial infection in patients with primary immunodeficiency and in uncontrolled studies of HIV-infected children, we undertook a multicenter study of its safety and efficacy in children with symptomatic HIV infection. In symptomatic HIV-infected children the prophylactic use of intravenous immune globulin is safe, and it significantly increases the time free from serious bacterial infections for those entering treatment with CD4+ lymphocyte counts greater than or equal to 0.2 x 10 super(9) per liter. JF - New England Journal of Medicine AU - Mofenson, L M AD - Pediatr., Adolescent and Matern. AIDS Branch, NICHD, Exec. Plaza S., Rm. 450W, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 73 EP - 80 VL - 325 IS - 2 SN - 0028-4793, 0028-4793 KW - immunoglobulins KW - intravenous administration KW - opportunist infection KW - prophylaxis KW - man KW - Microbiology Abstracts B: Bacteriology; Virology & AIDS Abstracts; Immunology Abstracts KW - bacteria KW - children KW - acquired immune deficiency syndrome KW - J 02834:Vaccination and immunization KW - V 22003:AIDS: Immunological aspects KW - F 06860:CMI UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16044452?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=New+England+Journal+of+Medicine&rft.atitle=Intravenous+immune+globulin+for+the+prevention+of+bacterial+infections+in+children+with+symptomatic+human+immunodeficiency+virus+infection.&rft.au=Mofenson%2C+L+M&rft.aulast=Mofenson&rft.aufirst=L&rft.date=1991-01-01&rft.volume=325&rft.issue=2&rft.spage=73&rft.isbn=&rft.btitle=&rft.title=New+England+Journal+of+Medicine&rft.issn=00284793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - bacteria; acquired immune deficiency syndrome; children ER - TY - JOUR T1 - Large-scale purification of gp70 from Moloney murine leukemia virus. AN - 16038026; 2607486 AB - The external envelope glycoprotein, gp70, of the Moloney murine leukemia virus was extracted from NIH 3T3 cells utilizing the detergent n-octyl- beta -D-glucopyranoside. The extracted gp70 was sequentially purified utilizing lectin-affinity, anion-exchange, and molecular-exclusion chromatography techniques. Approximately 10 mg of gp70 was purified by this method and shown to be 95% homogeneous, as assessed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The presence of purified gp70 from Moloney murine leukemia virus was confirmed by amino acid analysis, amino-terminal sequencing, and immunoreactivity with a monoclonal antibody raised against gp70. The procedure is rapid, utilizes commercially available media, and can be used to purify large amounts of retroviral envelope glycoprotein from virus. JF - Journal of Virological Methods AU - Pyle, S W AU - Chabot, D J AU - Miller, T L AU - Serabyn, SA AU - Bess, JW Jr AU - Arthur, LO AD - Program Res./DynCorp, NCI-FCRDC, Frederick, MD 21702, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 303 EP - 315 VL - 32 IS - 2-3 SN - 0166-0934, 0166-0934 KW - Moloney leukemia virus KW - affinity chromatography KW - amino acid sequence KW - detergents KW - glycoprotein gp70 KW - monoclonal antibodies KW - purification KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Virology & AIDS Abstracts KW - V 22032:Viral proteins UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16038026?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Virological+Methods&rft.atitle=Large-scale+purification+of+gp70+from+Moloney+murine+leukemia+virus.&rft.au=Pyle%2C+S+W%3BChabot%2C+D+J%3BMiller%2C+T+L%3BSerabyn%2C+SA%3BBess%2C+JW+Jr%3BArthur%2C+LO&rft.aulast=Pyle&rft.aufirst=S&rft.date=1991-01-01&rft.volume=32&rft.issue=2-3&rft.spage=303&rft.isbn=&rft.btitle=&rft.title=Journal+of+Virological+Methods&rft.issn=01660934&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - affinity chromatography; detergents; amino acid sequence; monoclonal antibodies ER - TY - JOUR T1 - Purification of HIV-1 wild-type protease and characterization of proteolytically inactive HIV-1 protease mutants by pepstatin A affinity chromatography. AN - 16037358; 2608646 AB - Recombinant wild-type protease of human immunodeficiency virus, type 1 (HIV-1) expressed in E. coli was purified by pepstatin A affinity chromatography. An 88-fold purification was achieved giving a protease preparation with a specific enzymatic activity of approximately 3700 pmol/min/ mu g. Two proteolytically inactive HIV-1 mutant proteases (Arg-87 arrow right Lys; Asn-88 arrow right Glu) were found to bind to pepstatin A agarose, and they were purified as the wild-type protease. A third mutant protease (Arg-87 arrow right Glu) was apparently unable to bind to pepstatin A under similar conditions. Binding to pepstatin A indicates the binding ability of the substrate binding site and the ability to form dimers. These features may be used to purify and to characterize other mutated HIV-1 proteases. JF - FEBS Letters AU - Wondrak, E M AU - Louis, J M AU - Mora, P T AU - Oroszlan, S AD - Lab. Mol. Virol. and Carcinog., ABL-Basic Res. Prog., NCI-Frederick Cancer Res. and Dev. Cent., P.O. Box B, Frederick, MD 21702, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 347 EP - 350 VL - 280 IS - 2 SN - 0014-5793, 0014-5793 KW - affinity chromatography KW - enzymatic activity KW - human immunodeficiency virus 1 KW - inhibitors KW - mutants KW - proteinase KW - purification KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Virology & AIDS Abstracts KW - V 22002:AIDS: Molecular and in vitro aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16037358?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FEBS+Letters&rft.atitle=Purification+of+HIV-1+wild-type+protease+and+characterization+of+proteolytically+inactive+HIV-1+protease+mutants+by+pepstatin+A+affinity+chromatography.&rft.au=Wondrak%2C+E+M%3BLouis%2C+J+M%3BMora%2C+P+T%3BOroszlan%2C+S&rft.aulast=Wondrak&rft.aufirst=E&rft.date=1991-01-01&rft.volume=280&rft.issue=2&rft.spage=347&rft.isbn=&rft.btitle=&rft.title=FEBS+Letters&rft.issn=00145793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - affinity chromatography; inhibitors ER - TY - JOUR T1 - Studies on the role of the S sub(4) substrate binding site of HIV proteinases. AN - 16037335; 2608585 AB - Kinetic analysis of the hydrolysis of the peptide H-Val-Ser-Gln-Asn-Tyr super(*)Pro-Ile-Val-Gln-NH sub(2) and its analogs obtained by varying the length and introducing substitutions at the P sub(4) site was carried out with both HIV-1 and HIV-2 proteinases. Deletion of the terminal Val and Gln had only moderate effect on the substrate hydrolysis, while the deletion of the P sub(4), Ser as well as P' sub(3) Val greatly reduced the substrate hydrolysis. This is predicted to be due to the loss of interactions between main chains of the enzyme and the substrate. Substitution of the P sub(4) Ser by amino acids having high frequency of occurrence in beta turns resulted in good substrates, while large amino acids were unfavorable in this position. The two proteinases acted similarly, except for substrates having Thr, Val and Leu substitutions, which were better accommodated in the HIV-2 substrate binding pocket. JF - FEBS Letters AU - Toezser, J AU - Gustchina, A AU - Weber, I T AU - Blaha, I AU - Wondrak, E M AU - Oroszlan, S AD - NCI-Frederick Cancer Res. and Dev. Cent., P.O. Box B, Frederick, MD 21702, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 356 EP - 360 VL - 279 IS - 2 SN - 0014-5793, 0014-5793 KW - deletion KW - enzymes KW - human immunodeficiency virus 1 KW - human immunodeficiency virus 2 KW - hydrolysis KW - kinetics KW - oligopeptides KW - substrates KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Virology & AIDS Abstracts KW - V 22002:AIDS: Molecular and in vitro aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16037335?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FEBS+Letters&rft.atitle=Studies+on+the+role+of+the+S+sub%284%29+substrate+binding+site+of+HIV+proteinases.&rft.au=Toezser%2C+J%3BGustchina%2C+A%3BWeber%2C+I+T%3BBlaha%2C+I%3BWondrak%2C+E+M%3BOroszlan%2C+S&rft.aulast=Toezser&rft.aufirst=J&rft.date=1991-01-01&rft.volume=279&rft.issue=2&rft.spage=356&rft.isbn=&rft.btitle=&rft.title=FEBS+Letters&rft.issn=00145793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - enzymes ER - TY - JOUR T1 - The effect of salt on the Michaelis Menten constant of the HIV-1 protease correlates with the Hofmeister series. AN - 16036808; 2608728 AB - The effect of different types of salt on the proteolytic activity of HIV-1 protease was studied. At a similar ionic strength, the enzyme activity changed according to the salting out effect of the ions used (Hofmeister series). Kinetic studies showed that a stronger salting out effect of the ions rather than the higher ionic strength per se increased the affinity to the substrate (K sub(m)) but in general did not alter the K sub(cat) value. JF - FEBS Letters AU - Wondrak, E M AU - Louis, J M AU - Oroszlan, S AD - Lab. Mol. Virol. and Carcinog., ABL-Basic Res. Prog., NCI-Frederick Cancer Res. and Dev. Cent., P.O. Box B, Frederick, MD 21702, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 344 EP - 346 VL - 280 IS - 2 SN - 0014-5793, 0014-5793 KW - Michaelis-Menten parameters KW - enzymatic activity KW - human immunodeficiency virus 1 KW - ionic strength KW - kinetics KW - proteinase KW - salts KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Virology & AIDS Abstracts KW - V 22002:AIDS: Molecular and in vitro aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16036808?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FEBS+Letters&rft.atitle=The+effect+of+salt+on+the+Michaelis+Menten+constant+of+the+HIV-1+protease+correlates+with+the+Hofmeister+series.&rft.au=Wondrak%2C+E+M%3BLouis%2C+J+M%3BOroszlan%2C+S&rft.aulast=Wondrak&rft.aufirst=E&rft.date=1991-01-01&rft.volume=280&rft.issue=2&rft.spage=344&rft.isbn=&rft.btitle=&rft.title=FEBS+Letters&rft.issn=00145793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - Michaelis-Menten parameters; salts; ionic strength ER - TY - JOUR T1 - Effect of maitotoxin analogues on calcium influx and phosphoinositide breakdown in cultured cells. AN - 16035770; 2609016 AB - Maitotoxin (MTX) and the analogues, bis-desulfated-MTX (didesulfo-MTX), monodesulfated-MTX (monodesulfo-MTX), and hydrogenated-MTX (H-MTX) were examined on super(45)Ca super(2+) influx and phosphoinositide breakdown with hamster insulinoma HIT cells and rat glioma C6 cells. The activity of MTX was greatly reduced either by desulfation or by hydrogenation. Didesulfo-MTX weakly stimulated calcium influx in HIT cells, but had no stimulatory effect on either calcium influx or phosphoinositide breakdown in C6 cells. All the analogues inhibited MTX-induced calcium influx in either HIT or C6 cells. Didesulfo-MTX inhibited the calcium influx elicited by 3 ng/ml MTX in C6 cells with an IC sub(50) of 7.0 ng/ml. The data suggest that the sulfate groups in MTX are important for stimulation of calcium influx and phosphoinositide breakdown, but are not essential for binding to a receptor-site on cell membranes. Although catalytic reduction of double bonds in MTX reduced activity by nearly 100-fold, a tritiated H-MTX still represents a potential radioligand for identification of MTX-binding sites. JF - Toxicon AU - Murata, M AU - Gusovsky, F AU - Sasaki, M AU - Yokoyama, A AU - Yasumoto, T AU - Daly, J W AD - Build. 8, Rm. 1A-15, LBC, NIDDK, NIH, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 1085 EP - 1096 VL - 29 IS - 9 SN - 0041-0101, 0041-0101 KW - analogs KW - biological poisons KW - breakdown KW - calcium KW - effects on KW - influx KW - maitotoxin KW - phosphoinositide KW - phosphoinositide breakdown KW - tissue culture KW - toxicity tests KW - ASFA 1: Biological Sciences & Living Resources; ASFA Marine Biotechnology Abstracts; Toxicology Abstracts KW - Marine KW - Gambierdiscus toxicus KW - Q4 27390:Toxins KW - Q1 08226:Physiology, biochemistry, biophysics KW - X 24171:Microbial UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16035770?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Global+atmospheric+changes.&rft.au=Piver%2C+W+T&rft.aulast=Piver&rft.aufirst=W&rft.date=1991-12-01&rft.volume=96&rft.issue=&rft.spage=131&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2014-05-06 N1 - SubjectsTermNotLitGenreText - calcium; toxicity tests; Gambierdiscus toxicus; Marine ER - TY - JOUR T1 - Hormone-sensitive cyclic GMP-inhibited cyclic AMP phosphodiesterase in rat adipocytes. Regulation of insulin- and cAMP-dependent activation by phosphorylation. AN - 16028891; 2594818 AB - In super(32)PO sub(4)-labeled adipocytes, isoproterenol (ISO) or physiologically relevant concentrations of insulin rapidly increased phosphorylation of a particulate 135-kDa protein which has been identified as a cGMP-inhibited "low K sub(m)" cAMP phosphodiesterase (CGI-PDE) by several criteria, including selective immunoprecipitation with anti-CGI-PDE IgG. The time courses and concentration dependences for phosphorylation of CGI-PDE by ISO and insulin correlated with CGI-PDE activation in the presence of these agents; effects of ISO were somewhat more rapid than those of insulin. JF - Journal of Biological Chemistry AU - Smith, C J AU - Vasta, V AU - Degerman, E AU - Belfrage, P AU - Manganiello, V C AD - Lab. Cell. Metab., Build. 10, Rm. 5N-307, NHLBI, NIH, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 13385 EP - 13390 VL - 266 IS - 20 SN - 0021-9258, 0021-9258 KW - 3',5'-cyclic-nucleotide phosphodiesterase KW - adipocytes KW - cyclic AMP KW - insulin KW - mechanisms KW - rats KW - regulation KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16028891?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=Hormone-sensitive+cyclic+GMP-inhibited+cyclic+AMP+phosphodiesterase+in+rat+adipocytes.+Regulation+of+insulin-+and+cAMP-dependent+activation+by+phosphorylation.&rft.au=Smith%2C+C+J%3BVasta%2C+V%3BDegerman%2C+E%3BBelfrage%2C+P%3BManganiello%2C+V+C&rft.aulast=Smith&rft.aufirst=C&rft.date=1991-01-01&rft.volume=266&rft.issue=20&rft.spage=13385&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Chemicals associated with site-specific neoplasia in 1394 long-term carcinogenesis experiments in laboratory rodents. AN - 16026468; 2590639 AB - The carcinogenicity data base used for this paper originated in the late 1960s by the National Cancer Institute and since 1978 has been continued and made more comprehensive by the National Toxicology Program. The extensive files contain among other sets of information detailed pathology data on more than 400 long-term (most often 24 month) chemical carcinogenesis studies, comprised of nearly 1600 individual experiments having at least 10 million tissue sections that have been evaluated for toxicity and carcinogenicity. Using the current data set of 379 studies made up 1394 experiments, we have compiled listings of chemicals having like carcinogenic target sites for each of the 34 organs or systems for which histopathology diagnoses have been recorded routinely. The most common tumor site is the liver (15% of all experiments), followed in rank order by: lung, hematopoietic system and kidneys, mammary glands, forestomach, thyroid glands, Zymbal glands, urinary bladder, skin and uterus/cervix, and circulatory system and adrenal glands. JF - Environmental Health Perspectives AU - Huff, J AU - Cirvello, J AU - Haseman, J AU - Bucher, J AD - NIEHS, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 247 EP - 270 VL - 93 SN - 0091-6765, 0091-6765 KW - xenobiotics KW - rats KW - mice KW - Pollution Abstracts; Health & Safety Science Abstracts; Toxicology Abstracts KW - reviews KW - carcinogenesis KW - X 24250:Reviews KW - H SM10.21:CANCER KW - P 6000:TOXICOLOGY AND HEALTH UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16026468?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Chemicals+associated+with+site-specific+neoplasia+in+1394+long-term+carcinogenesis+experiments+in+laboratory+rodents.&rft.au=Huff%2C+J%3BCirvello%2C+J%3BHaseman%2C+J%3BBucher%2C+J&rft.aulast=Huff&rft.aufirst=J&rft.date=1991-01-01&rft.volume=93&rft.issue=&rft.spage=247&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - carcinogenesis; rats; mice; reviews ER - TY - JOUR T1 - A characterization of cytostatic factor activity from Xenopus eggs and c-mos-transformed cells. AN - 16011049; 2580521 AB - In Xenopus oocytes, the mos proto-oncogene product is required during meiosis I for the activation of maturation promoting factor (MPF) and the subsequent breakdown of the germinal vesicle (GVBD). In addition, the mos product has been shown to be a candidate "initiator" of meiotic maturation and is an active component of cytostatic factor (CSF), an activity responsible for metaphase II arrest. We demonstrate that pp39 super(mos) is required throughout oocyte maturation. We found that in progesterone stimulated oocytes, depletion of mos RNA immediately before GVBD terminally decreased MPF. Likewise, oocytes depleted of mos RNA and induced to mature with crude MPF proceeded through GVBD, but lacked the MPF activity required to arrest mature oocytes at metaphase II. Thus, during maturation the mos product is required, directly or indirectly, to sustain MPF activity. However, maintenance of CSF during interphase does not result in the maintenance of MPF. JF - Journal of Cell Biology AU - Daar, I AU - Paules, R S AU - Vande Woude, GF AD - ABL-Basic Res. Program, NCI-Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 329 EP - 335 VL - 114 IS - 2 SN - 0021-9525, 0021-9525 KW - Xenopus KW - c-mos KW - c-mos gene KW - cells KW - characterization KW - cytostasis KW - cytostatic factor KW - eggs KW - factors KW - genes KW - levels KW - mRNA KW - maturation KW - meiosis KW - oncogenes KW - transformation KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Oncogenes & Growth Factors Abstracts KW - B 26140:Mos oncogene UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16011049?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Cell+Biology&rft.atitle=A+characterization+of+cytostatic+factor+activity+from+Xenopus+eggs+and+c-mos-transformed+cells.&rft.au=Daar%2C+I%3BPaules%2C+R+S%3BVande+Woude%2C+GF&rft.aulast=Daar&rft.aufirst=I&rft.date=1991-01-01&rft.volume=114&rft.issue=2&rft.spage=329&rft.isbn=&rft.btitle=&rft.title=Journal+of+Cell+Biology&rft.issn=00219525&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - meiosis; genes; cytostasis ER - TY - JOUR T1 - Replication-competent retrovirus vectors for the transfer and expression of gene cassettes in avian cells. AN - 16006708; 2587321 AB - We have constructed a series of replication-competent retrovirus vectors to introduce and express gene cassettes in avian cells To characterize these vectors, we inserted the coding sequences for the bacterial chloramphenicol acetyltransferase (CAT) gene linked to the chicken beta -actin gene promoter or the mouse metallothionein 1 gene promoter. In all cases, we found the structure of integrated proviruses to be stable during serial cell passage in vitro. Chloramphenicol acetyltransferase activity was detected biochemically and immunocytochemically in infected cells. Cassettes were inserted in the vectors in the same or in the opposite orientation with respect to viral transcription. The level of expression was strongly influenced by surrounding proviral sequences, particularly by the transcriptional enhancer elements within the retrovirus long terminal repeat sequences. Expression was higher with vectors that contained the polymerase (pol) region of the Bryan high-titer strain of Rous sarcoma virus. Inclusion of the Bryan pol region also improved vector replication in the chemically transformed quail fibroblast line QT6. JF - Journal of Virology AU - Petropoulos, C J AU - Hughes, SH AD - ABL-Basic Res. Prog., NCI-Frederick Cancer Res. and Dev. Cent., P.O. Box B, Frederick, MD 21702-1201, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 3728 EP - 3737 VL - 65 IS - 7 SN - 0022-538X, 0022-538X KW - retrovirus KW - insertion KW - CAT gene KW - gene expression KW - replication KW - transcription KW - vectors KW - Biotechnology and Bioengineering Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Genetics Abstracts; Virology & AIDS Abstracts KW - N 14682:Cloning vectors KW - V 22050:Viral genetics including virus reactivation KW - W 30134:Microorganisms KW - G 07313:Viruses UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16006708?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Virology&rft.atitle=Replication-competent+retrovirus+vectors+for+the+transfer+and+expression+of+gene+cassettes+in+avian+cells.&rft.au=Petropoulos%2C+C+J%3BHughes%2C+SH&rft.aulast=Petropoulos&rft.aufirst=C&rft.date=1991-01-01&rft.volume=65&rft.issue=7&rft.spage=3728&rft.isbn=&rft.btitle=&rft.title=Journal+of+Virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - vectors; gene expression; transcription; replication ER - TY - JOUR T1 - Comparison of the HIV-1 and HIV-2 proteinases using oligopeptide substrates representing cleavage sites in Gag and Gag-Pol polyproteins. AN - 16002463; 2577002 AB - The substrate specificity of the human immunodeficiency virus type 1 and type 2 proteinases was compared using oligopeptides corresponding to cleavage sites in the Gag and Gag-Pol polyproteins of both viruses. All peptides mimicking cleavage sites at the junction of major functional protein domains were correctly cleaved by both enzymes. However, some other peptides thought to represent secondary cleavage sites remained intact. The kinetic parameters obtained for the different substrates showed several hundred-fold variation but were similar for the same substrate. JF - FEBS Letters AU - Toezser, J AU - Blaha, I AU - Copeland, T D AU - Wondrak, E M AU - Oroszlan, S AD - Lab. Mol. Virol. and Carcinog., NCI-Frederick Cancer Res. and Dev. Cent., P.O. Box B, Frederick, MD 21702, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 77 EP - 80 VL - 281 IS - 1-2 SN - 0014-5793, 0014-5793 KW - comparison KW - human immunodeficiency virus-1 KW - human immunodeficiency virus-2 KW - kinetics KW - proteinase KW - substrates KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Virology & AIDS Abstracts KW - V 22002:AIDS: Molecular and in vitro aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/16002463?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FEBS+Letters&rft.atitle=Comparison+of+the+HIV-1+and+HIV-2+proteinases+using+oligopeptide+substrates+representing+cleavage+sites+in+Gag+and+Gag-Pol+polyproteins.&rft.au=Toezser%2C+J%3BBlaha%2C+I%3BCopeland%2C+T+D%3BWondrak%2C+E+M%3BOroszlan%2C+S&rft.aulast=Toezser&rft.aufirst=J&rft.date=1991-01-01&rft.volume=281&rft.issue=1-2&rft.spage=77&rft.isbn=&rft.btitle=&rft.title=FEBS+Letters&rft.issn=00145793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - A complex pattern of translational initiation and phosphorylation in L-myc proteins. AN - 15993483; 2564750 AB - In this report, we characterize and define the origins of the major L-myc proteins. In vitro translation revealed that (i) two L-myc proteins (p59 and p65) were derived through alternative translational initiation at a non-AUG (CUG) site in intron 1 and at an AUG site in exon 2 of L-myc, and that (ii) extensive post-translational phosphorylation of these proteins yielded three additional proteins (p60, p66, and p68). Transfection experiments in rat embryo cells revealed the in vivo existence of this unusual CUG-initiated protein and demonstrated that it possessed transforming activity. Further, immunoprecipitation using high titered anti-L-myc peptide antisera, of two L-myc expressing small-cell lung cancer cell lines revealed three major L-myc proteins (p60, p66 and p68) all of which were derived from extensive phosphorylation of a p59 protein. JF - Oncogene AU - Dosaka-Akita, H AU - Rosenberg, R K AU - Minna, J D AU - Birrer, MJ AD - NCI-Navy Med. Oncol. Branch, Natl. Cancer Inst., Bethesda, MD 20814, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 371 EP - 378 VL - 6 IS - 3 SN - 0950-9232, 0950-9232 KW - L-myc protein KW - analysis KW - carcinoma KW - cell lines KW - gene products KW - initiation KW - l-Myc KW - lung KW - man KW - patterns KW - phosphorylation KW - translation KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Biochemistry Abstracts 2: Nucleic Acids; Oncogenes & Growth Factors Abstracts KW - B 26180:Myc oncogene/Mad and Max proteins KW - B 26400:HUMAN-RELATED ONCOGENES AND GROWTH FACTORS: CROSS REFERENCES KW - N 14430:Translation initiation, elongation & termination UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15993483?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncogene&rft.atitle=A+complex+pattern+of+translational+initiation+and+phosphorylation+in+L-myc+proteins.&rft.au=Dosaka-Akita%2C+H%3BRosenberg%2C+R+K%3BMinna%2C+J+D%3BBirrer%2C+MJ&rft.aulast=Dosaka-Akita&rft.aufirst=H&rft.date=1991-01-01&rft.volume=6&rft.issue=3&rft.spage=371&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=09509232&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - lung; translation; phosphorylation; carcinoma ER - TY - JOUR T1 - Dose-effect approaches to risk assessment. AN - 15991185; 2573548 AB - Risk assessment is the attempt to characterize the chance of obtaining an adverse effect after exposure to an agent. Traditionally, high levels of an agent have been used to estimate the likelihood a lower dose might have an effect either by using low-dose extrapolation models or by attempting to establish a dose with no observable effects (NOEL). Newer methods use data from portions of the dose-effect function where error is smaller to estimate risks. Risk estimates using two of these approaches are compared for two different sample sizes. Each method produced the same estimate with the larger sample at low risk, but with increasing levels of risk and smaller samples the estimates obtained using these methods diverged. JF - NEUROSCI. BEHAV. REV. AU - Glowa, J R AD - Biopsychol. Unit, Clin. Neuroendocrinol. Branch, NIMH Build. 14D, Rm 311, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 153 EP - 158 VL - 15 IS - 1 KW - dose-response effects KW - risks KW - characterization KW - man KW - dose response effects KW - toluene KW - Risk Abstracts; Health & Safety Science Abstracts; Toxicology Abstracts; CSA Neurosciences Abstracts KW - neurotoxicity KW - reviews KW - toxins KW - risk assessment KW - N3 11101:General KW - H SE4.20:POISONS AND POISONING KW - R2 23060:Medical and environmental health KW - X 24221:Toxicity testing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15991185?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NEUROSCI.+BEHAV.+REV.&rft.atitle=Dose-effect+approaches+to+risk+assessment.&rft.au=Glowa%2C+J+R&rft.aulast=Glowa&rft.aufirst=J&rft.date=1991-01-01&rft.volume=15&rft.issue=1&rft.spage=153&rft.isbn=&rft.btitle=&rft.title=NEUROSCI.+BEHAV.+REV.&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - toxins; reviews; risk assessment; toluene; neurotoxicity ER - TY - JOUR T1 - Refined crystal structure of ytterbium-substituted carp parvalbumin 4.25 at 1.5 angstrom, and its comparison with the native and cadmium-substituted structure. AN - 15990853; 2554355 AB - The crystal structure of carp (Cyprus carpio ) parvalbumin 4.25 containing a 1:1 molar ratio of ytterbium chloride to protein has been refined at 1.5 angstrom resolution by restrained least-squares methods to a crystallographic R value of 0.199. The crystal structure confirms the NMR studies, which suggest that low concentrations of ytterbium cause an extensive displacement of calcium from the EF metal binding site. JF - FEBS Letters AU - Kumar, K D AU - Lee, L AU - Edwards, BFP AD - Macromol. Struct. Lab., NCI-Frederick Cancer Res. and Dev. Cent., ABL-Basic Res. Prog., P.O. Box B, Frederick, MD 21702-1201, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 311 EP - 316 VL - 283 IS - 2 SN - 0014-5793, 0014-5793 KW - Cyprinus carpio KW - X-ray crystallography KW - biochemical analysis KW - crystal structure KW - fish physiology KW - molecular structure KW - parvalbumin KW - proteins KW - substitution KW - ytterbium KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; ASFA 1: Biological Sciences & Living Resources KW - Freshwater KW - Q1 08346:Physiology, biochemistry, biophysics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15990853?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FEBS+Letters&rft.atitle=Refined+crystal+structure+of+ytterbium-substituted+carp+parvalbumin+4.25+at+1.5+angstrom%2C+and+its+comparison+with+the+native+and+cadmium-substituted+structure.&rft.au=Kumar%2C+K+D%3BLee%2C+L%3BEdwards%2C+BFP&rft.aulast=Kumar&rft.aufirst=K&rft.date=1991-01-01&rft.volume=283&rft.issue=2&rft.spage=311&rft.isbn=&rft.btitle=&rft.title=FEBS+Letters&rft.issn=00145793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - molecular structure; biochemical analysis; ytterbium; proteins; Freshwater ER - TY - JOUR T1 - Prevention of nickel subsulfide carcinogenesis by local administration of Mycobacterium bovis antigen in male F344/NCr rats. AN - 15986789; 2556808 AB - This study was designed to determine the effect of local inflammation on nickel subsulfide (Ni sub(3)S sub(2)) carcinogenesis. Male F344/NCr rats, 6-week-old, 20 rats/group, received a single i.m. injection of 2.5 mg of Ni sub(3)S sub(2) alone or 2.5 mg of Ni sub(3)S sub(2) mixed with either 0.5 mg of Mycobacterium bovis) lyophilized cell walls (MB), 1 mg cortisol (CORT), or 1 mg indomethacin (IND). Two more groups of rats received i.m. Ni sub(3)S sub(2) alone, as above, followed by a single s.c. dose of either 1 mg MB or 2 mg IND. The i.m. injections were made into the thigh muscles of both limbs; the s.c. injections were made at the neck area. The experiment was terminated at 71 weeks. The final yields of injection site sarcomas were 85% in the Ni sub(3)S sub(2), 85% in the Ni sub(3)S sub(2) + CORT, and 80% in the Ni sub(3)S sub(2) + IND group. Only one injection site tumor (5%) was found in rats given i.m. Ni sub(3)S sub(2) + MB. In contrast, the s.c. MB injection enhanced muscular carcinogenicity of Ni sub(3)S sub(2) by shortening the latency and increasing the yield of tumors to 100% at week 39. JF - Toxicology AU - Kasprzak, K S AU - Ward, J M AD - NCI-FCRDC, Build. 538, Rm. 205, Frederick, MD 21702, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 97 EP - 105 VL - 67 IS - 1 SN - 0300-483X, 0300-483X KW - nickel subsulfide KW - antigens KW - rats KW - heavy metals KW - Toxicology Abstracts KW - carcinogenesis KW - Mycobacterium bovis KW - X 24162:Chronic exposure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15986789?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology&rft.atitle=Prevention+of+nickel+subsulfide+carcinogenesis+by+local+administration+of+Mycobacterium+bovis+antigen+in+male+F344%2FNCr+rats.&rft.au=Kasprzak%2C+K+S%3BWard%2C+J+M&rft.aulast=Kasprzak&rft.aufirst=K&rft.date=1991-01-01&rft.volume=67&rft.issue=1&rft.spage=97&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=0300483X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Mycobacterium bovis; carcinogenesis ER - TY - JOUR T1 - Studies on the chronic toxicity (inhalation) of wollastonite in Fischer 344 rats. AN - 15986781; 2558545 AB - Wollastonite is a naturally occurring calcium metasilicate acicular mineral that is used in a variety of commercial applications and has been proposed as an asbestos substitute for selected products. Male Fischer 344 rats were exposed by inhalation to 10 mg/m super(3) (360 fibers/cm super(3)) wollastonite (NYAD-G) for 6 h/d, 5 d/wk for 12 or 24 mo. They were compared to untreated chamber control and positive controls (chryostile asbestos, 10 mg/m super(3) ( similar to 1000 fibers/cm super(3)) for 12 mo). Six rats from each exposure group were killed after 3, 12, and 24 mo. The remaining rats were held for lifetime observation (until 90% mortality). Wollastonite was slightly toxic to the lung, producing an alveolar macrophage response that resolved after exposure ceased. There was no evidence of wollastonite-induced neoplasms, although the chrysotile asbestos administered under similar conditions produced a high incidence of bronchoalveolar carcinomas. JF - Inhalation Toxicology AU - McConnell, EE AU - Hall, L AU - Adkins, B Jr AD - NIEHS, NIH, Research Triangle Park, NC 27709, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 323 EP - 337 VL - 3 IS - 3 SN - 0895-8378, 0895-8378 KW - wollastonite KW - chronic toxicity KW - calcium silicate KW - rats KW - Health & Safety Science Abstracts; Toxicology Abstracts KW - inhalation KW - toxicity KW - H SE4.20:POISONS AND POISONING KW - X 24152:Chronic exposure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15986781?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Inhalation+Toxicology&rft.atitle=Studies+on+the+chronic+toxicity+%28inhalation%29+of+wollastonite+in+Fischer+344+rats.&rft.au=McConnell%2C+EE%3BHall%2C+L%3BAdkins%2C+B+Jr&rft.aulast=McConnell&rft.aufirst=EE&rft.date=1991-01-01&rft.volume=3&rft.issue=3&rft.spage=323&rft.isbn=&rft.btitle=&rft.title=Inhalation+Toxicology&rft.issn=08958378&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - inhalation; rats; toxicity ER - TY - JOUR T1 - Genetics of gene transfer between species. AN - 15981001; 2544559 AB - Bacteria transfer genetic information to members of at least three of the five biological kingdoms. Gene transfer between species may play the same role as sex between members of a single species, providing genetic diversity and material for repair of genomic damage. JF - Trends in Genetics AU - Heinemann, JA AD - Lab. Microb. Struct. and Funct., NIAID, NIH, Rocky Mt. Lab., Hamilton, MT 59840, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 181 EP - 185 VL - 7 IS - 6 SN - 0168-9525, 0168-9525 KW - reviews KW - interspecific KW - Genetics Abstracts; Microbiology Abstracts B: Bacteriology KW - gene transfer KW - species KW - bacteria KW - G 07320:Bacterial genetics KW - J 02740:Genetics and evolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15981001?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Trends+in+Genetics&rft.atitle=Genetics+of+gene+transfer+between+species.&rft.au=Heinemann%2C+JA&rft.aulast=Heinemann&rft.aufirst=JA&rft.date=1991-01-01&rft.volume=7&rft.issue=6&rft.spage=181&rft.isbn=&rft.btitle=&rft.title=Trends+in+Genetics&rft.issn=01689525&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - gene transfer; species; bacteria ER - TY - JOUR T1 - Immune capture and detection of Borrelia burgdorferi antigens in urine, blood, or tissues from infected ticks, mice, dogs, and humans. AN - 15978555; 2549941 AB - Current biological and serological techniques for demonstrating infections by Borrelia burgdorferi can be inconclusive. In order to monitor Lyme borreliosis, we developed a rapid and sensitive assay for B. burgdorferi antigens in infected hosts. Polyclonal rabbit antisera were raised against membrane vesicles and an 83-kDa vesicle-associated protein band that was purified from in vitro B. burgdorferi cultures. Immunoglobulin G (IgG) antibodies were recovered from these sera and tested for a species-specific reaction with several geographically diverse Borrelia isolates by immunoblot analysis. Parlodion-coated electron microscope grids were activated with anti-vesicle F(ab') sub(2) fragments and then incubated with confirmed or experimental sources of spirochetal antigens. Such sources included cultured spirochetes; spirochete culture supernatants; samples of urine, blood, or serum from mice, dogs, and humans; triturates of Ixodes) ticks; and bladder, spleen, liver, kidney, heart, or brain tissues from infected or control mice. JF - Journal of Clinical Microbiology AU - Dorward, D W AU - Schwan, T G AU - Garon, C F AD - Lab. Vectors and Pathog., Rocky Mt. Lab., NIAID, Hamilton, MT 59840, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 1162 EP - 1170 VL - 29 IS - 6 SN - 0095-1137, 0095-1137 KW - Borrelia burgdorferi KW - detection KW - tissues KW - Entomology Abstracts; Immunology Abstracts; Microbiology Abstracts B: Bacteriology KW - Ixodes KW - urine KW - Lyme disease KW - animals KW - Ixodidae KW - blood KW - Acari KW - antigens KW - J 02831:Techniques and reagents KW - Z 05206:Medical & veterinary entomology KW - F 06723:Other labelling methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15978555?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Clinical+Microbiology&rft.atitle=Immune+capture+and+detection+of+Borrelia+burgdorferi+antigens+in+urine%2C+blood%2C+or+tissues+from+infected+ticks%2C+mice%2C+dogs%2C+and+humans.&rft.au=Dorward%2C+D+W%3BSchwan%2C+T+G%3BGaron%2C+C+F&rft.aulast=Dorward&rft.aufirst=D&rft.date=1991-01-01&rft.volume=29&rft.issue=6&rft.spage=1162&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Microbiology&rft.issn=00951137&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Ixodes; Ixodidae; Acari; antigens; blood; urine; animals; Lyme disease ER - TY - JOUR T1 - Validated methods for degrading hazardous chemicals: Some halogenated compounds. AN - 15976989; 2547011 AB - Two techniques were investigated for degrading a number of halogenated compounds of commercial and research importance. Reductive dehalogenation with nickel-aluminum alloy in potassium hydroxide solution was used to degrade iodomethane, chloroacetic acid, trichloroacetic acid, 2-chloroethanol, 2-bromoethanol, 2-chloroethylamine, 2-bromoethylamine, 1-bromobutane, 1-iodobutane, 2-bromobutane, 2-iodobutane, 2-bromo-2-methylpropane, 2-iodo-2-methylpropane, 3-chloropyridine, fluorobenzene, chlorobenzene, bromobenzene, iodobenzene, 4-fluoroaniline, 2-chloroaniline, 3-chloroaniline, 4-chloroaniline, 4-fluoronitrobenzene, 2-chloronitrobenzene, 3-chloronitrobenzene, 4-chloronitrobenzene, benzyl chloride, benzyl bromide, alpha , alpha -dichlorotoluene, and 3-aminobenzotrifluoride. JF - American Industrial Hygiene Association Journal AU - Lunn, G AU - Sansone, E B AD - Program Resources, Inc., Environ. Control and Res. Program, NCI-Frederick Cancer Res. and Dev. Cent., P.O. Box B, Frederick, MD 21702-1201, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 252 EP - 257 VL - 52 IS - 6 SN - 0002-8894, 0002-8894 KW - halogenated compounds KW - research programmes KW - Pollution Abstracts KW - chemical degradation KW - occupational health KW - P 6000:TOXICOLOGY AND HEALTH UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15976989?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Apollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Industrial+Hygiene+Association+Journal&rft.atitle=Validated+methods+for+degrading+hazardous+chemicals%3A+Some+halogenated+compounds.&rft.au=Lunn%2C+G%3BSansone%2C+E+B&rft.aulast=Lunn&rft.aufirst=G&rft.date=1991-01-01&rft.volume=52&rft.issue=6&rft.spage=252&rft.isbn=&rft.btitle=&rft.title=American+Industrial+Hygiene+Association+Journal&rft.issn=00028894&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - chemical degradation; occupational health ER - TY - JOUR T1 - RpoB8, a rifampicin-resistant termination-proficiency RNA polymerase, has an increased K sub(m) for purine nucleotides during transcription elongation. AN - 15976326; 2550615 AB - The rpoB8 allele of Escherichia coli maps to the beta subunit of RNA polymerase and confers rifampicin resistance as well as increased termination at both intrinsic and rho -dependent terminators in vivo. This phenotype suggests that the mutant is defective in an enzymatic property of RNA polymerase important for all termination events. We analyzed the in vitro transcription properties of this enzyme to determine the nature of the defect. As compared with the wild-type enzyme, RpoB8 exhibits enhanced pausing and a significant reduction in rate of elongation on natural templates. JF - Journal of Biological Chemistry AU - Jin, Ding Jun AU - Gross, CA AD - Dep. Mol. Biol., NCI, NIH, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 14478 EP - 14485 VL - 266 IS - 22 SN - 0021-9258, 0021-9258 KW - DNA-directed RNA polymerase KW - resistance KW - kinetics KW - transcription KW - elongation KW - rifampicin KW - purine nucleotides KW - Microbiology Abstracts B: Bacteriology; Biochemistry Abstracts 2: Nucleic Acids KW - Escherichia coli KW - N 14721:RNA polymerases KW - J 02728:Enzymes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15976326?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=RpoB8%2C+a+rifampicin-resistant+termination-proficiency+RNA+polymerase%2C+has+an+increased+K+sub%28m%29+for+purine+nucleotides+during+transcription+elongation.&rft.au=Jin%2C+Ding+Jun%3BGross%2C+CA&rft.aulast=Jin&rft.aufirst=Ding&rft.date=1991-01-01&rft.volume=266&rft.issue=22&rft.spage=14478&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Escherichia coli ER - TY - JOUR T1 - The rat alpha sub(2)-C4 adrenergic receptor gene encodes a novel pharmacological subtype. AN - 15973787; 2543751 AB - A rat gene and brain cDNA (pA2d) encoding the homologue of the human alpha -C4 adrenergic receptor subtype were isolated and characterized. RNA blots indicate that this gene is expressed in brain, heart and kidney but not in lung, liver or pancreas. Yohimbine, WB-4101 and prasozin all exhibited high affinity for this receptor in binding studies. Clonidine was more potent and efficacious than norepinephrine in inhibiting forskolin-stimulated cAMP production in CHO cells expressing pA2d. Together, these data suggest that the alpha sub(2)-C4 gene product defines a previously undescribed pharmacological subtype of alpha sub(2)-adrenergic receptor. JF - FEBS Letters AU - Voigt, M M AU - McCune, S K AU - Kanterman, R Y AU - Felder, C C AD - Build. 36, Rm. 3A15, LCB/NIMH, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 45 EP - 50 VL - 278 IS - 1 SN - 0014-5793, 0014-5793 KW - alpha 2-adrenergic KW - amino acid sequence KW - brain KW - cDNA KW - genes KW - nucleotide sequence KW - predictions KW - rats KW - receptors KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; CSA Neurosciences Abstracts; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - G 07402:GENERAL KW - N 14640:Structure & sequence KW - N3 11094:Central nervous system UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15973787?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FEBS+Letters&rft.atitle=The+rat+alpha+sub%282%29-C4+adrenergic+receptor+gene+encodes+a+novel+pharmacological+subtype.&rft.au=Voigt%2C+M+M%3BMcCune%2C+S+K%3BKanterman%2C+R+Y%3BFelder%2C+C+C&rft.aulast=Voigt&rft.aufirst=M&rft.date=1991-01-01&rft.volume=278&rft.issue=1&rft.spage=45&rft.isbn=&rft.btitle=&rft.title=FEBS+Letters&rft.issn=00145793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - genes; brain ER - TY - JOUR T1 - Decreases in spontaneous tumors in rats and mice after treatment with amphetamine. AN - 15971049; 2553024 AB - Toxicology and carcinogenesis studies of dl-amphetamine sulfate, a drug used in the treatment of weight control, narcolepsy, and behavioral syndromes in children, were performed in F344/N rats and B6C3F1 mice. In these studies, amphetamine was administered for 2 years at doses of 0, 20, or 100 ppm in the feed to groups of 30 animals/dose/sex/species. The average amounts of amphetamine consumed per day was estimated to be 1 or 5 mg/kg for low or high dose rats, 4 or 30 mg/kg for low or high dose male mice, and 3 or 19 mg/kg for low or high dose female mice. Survival was similar in dosed and control groups. The most notable effect of long-term treatment with this drug was the reduction of body weight in comparison to controls, and reduction in spontaneous tumors including pheochromocytomas of the adrenal gland in male rats, fibroadenomas of the mammary gland in female rats, adenomas of the anterior pituitary gland in male and female rats and female mice, endometrial stromal polyps of the uterus of female rats, adenomas or carcinomas of the liver in male and female mice, adenomas of the Harderian gland in males and female mice, and adenomas or carcinomas of the lung in male and female mice. JF - Toxicology AU - Dunnick, J K AU - Eustis, S L AD - NIEHS, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 325 EP - 332 VL - 67 IS - 3 SN - 0300-483X, 0300-483X KW - amphetamine KW - tumours KW - rats KW - mice KW - Toxicology Abstracts KW - X 24112:Chronic exposure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15971049?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology&rft.atitle=Decreases+in+spontaneous+tumors+in+rats+and+mice+after+treatment+with+amphetamine.&rft.au=Dunnick%2C+J+K%3BEustis%2C+S+L&rft.aulast=Dunnick&rft.aufirst=J&rft.date=1991-01-01&rft.volume=67&rft.issue=3&rft.spage=325&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=0300483X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 ER - TY - JOUR T1 - Critical sequences in the core of the P1 plasmid replication origin. AN - 15970311; 2551529 AB - The core of the P1 plasmid replication origin consists of a series of 7-bp repeats and a G+C-rich stretch. Methylation of the GATC sequences in the repeats is essential. Forty different single-base mutations in the region were isolated and assayed for origin function. A single-base change within any 7-bp repeat could block the origin, irrespective of whether GATC bases were affected. The repeats themselves were critical, but the short intervals between them were not. Mutations in the G+C-rich region showed it to be a spacer whose exact length is important but whose sequence can vary considerably. It maintains a precise distance between the 7-bp repeats and binding sites for the P1 RepA initiator protein. It may also serve as a clamp to limit strand separation during initiation. JF - Journal of Bacteriology AU - Brendler, T AU - Abeles, A AU - Austin, S AD - Lab. Chromosome Biol., ABL-Basic Res. Program, NCI-Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 3935 EP - 3942 VL - 173 IS - 13 SN - 0021-9193, 0021-9193 KW - Escherichia coli KW - plasmid P1 KW - origin KW - Biochemistry Abstracts 2: Nucleic Acids; Genetics Abstracts; Microbiology Abstracts B: Bacteriology KW - nucleotide sequence KW - replication KW - plasmids KW - N 14640:Structure & sequence KW - J 02760:Plasmids KW - G 07200:P PLASMIDS UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15970311?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Bacteriology&rft.atitle=Critical+sequences+in+the+core+of+the+P1+plasmid+replication+origin.&rft.au=Brendler%2C+T%3BAbeles%2C+A%3BAustin%2C+S&rft.aulast=Brendler&rft.aufirst=T&rft.date=1991-01-01&rft.volume=173&rft.issue=13&rft.spage=3935&rft.isbn=&rft.btitle=&rft.title=Journal+of+Bacteriology&rft.issn=00219193&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - plasmids; replication; nucleotide sequence ER - TY - JOUR T1 - Correlation of hepatocellular proliferation with hepatocarcinogenicity induced by the mutagenic noncarcinogen: carcinogen pair- 2,6- and 2,4-diaminotoluene. AN - 15966167; 2545881 AB - 2,4-Diaminotoluene (2,4-DAT) and 2,6-diaminotoluene (2,6-DAT) are equally genotoxic in the Ames/Salmonella assay and are both readily absorbed, metabolized, and excreted. The present studies were designed to determine the effects of these two chemicals on cell proliferation in the liver when administered at the dose levels comparable to those used in the original bioassays. This study utilized repeated oral dosing, osmotic minipumps to deliver bromodeoxyuridine (BrDU) for 8 days, and immunohistochemistry to quantitate BrDU incorporation into hepatic DNA. CCl sub(4) (0.4 ml/rat, single ip dose) or vehicle control groups were included as positive and negative controls, respectively. The degree of cell proliferation was quantified by the labeling index from at least 1000 hepatocytes. Results from the control studies indicate that approximately 1.1% of the hepatocytes from vehicle-treated animals replicated during the exposure period whereas approximately 50% replicated in the positive controls. JF - Toxicology and Applied Pharmacology AU - Cunningham, M L AU - Foley, J AU - Maronpot, R R AU - Matthews, H B AD - Exp. Toxicol. Branch, NIEHS, Research Triangle Park, NC 27709, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 562 EP - 567 VL - 107 IS - 3 SN - 0041-008X, 0041-008X KW - 2,6-diaminotoluene KW - 2,4-diaminotoluene KW - Toxicology Abstracts KW - cell proliferation KW - mutagens KW - carcinogenesis KW - liver KW - X 24152:Chronic exposure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15966167?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+Applied+Pharmacology&rft.atitle=Correlation+of+hepatocellular+proliferation+with+hepatocarcinogenicity+induced+by+the+mutagenic+noncarcinogen%3A+carcinogen+pair-+2%2C6-+and+2%2C4-diaminotoluene.&rft.au=Cunningham%2C+M+L%3BFoley%2C+J%3BMaronpot%2C+R+R%3BMatthews%2C+H+B&rft.aulast=Cunningham&rft.aufirst=M&rft.date=1991-01-01&rft.volume=107&rft.issue=3&rft.spage=562&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+Applied+Pharmacology&rft.issn=0041008X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - cell proliferation; liver; mutagens; carcinogenesis ER - TY - JOUR T1 - The epidemiology of group B streptococcal colonization in pregnancy. AN - 15956174; 2527514 AB - Risk factors for cervicovaginal group B streptococcal colonization at 23-26 weeks' gestation were studied in 7742 women participating in the Vaginal Infections and Prematurity study. The risk of colonization was greater when there was concurrent colonization with Candida sp, but group B Streptococcus was not associated with carriage of Chlamydia trachomatis , Ureaplasma urealyticum , Trichomonas vaginalis , and Mycoplasma hominis . We conclude that selective screening is not useful in detecting group B streptococcal colonization in pregnancy. JF - Obstetrics and Gynecology AU - Regan, JA AU - Klebanoff, MA AU - Nugent, R P AD - Div. Prev. Res., NICHD, NIH, EPN 640, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 604 EP - 610 VL - 77 IS - 4 KW - Streptococcus KW - epidemiology KW - Microbiology Abstracts B: Bacteriology KW - ethnic groups KW - Ureaplasma urealyticum KW - pregnancy KW - Chlamydia trachomatis KW - colonization KW - USA, New York KW - J 02847:Genitourinary tract UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15956174?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Obstetrics+and+Gynecology&rft.atitle=The+epidemiology+of+group+B+streptococcal+colonization+in+pregnancy.&rft.au=Regan%2C+JA%3BKlebanoff%2C+MA%3BNugent%2C+R+P&rft.aulast=Regan&rft.aufirst=JA&rft.date=1991-01-01&rft.volume=77&rft.issue=4&rft.spage=604&rft.isbn=&rft.btitle=&rft.title=Obstetrics+and+Gynecology&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Chlamydia trachomatis; Ureaplasma urealyticum; USA, New York; colonization; ethnic groups; pregnancy ER - TY - JOUR T1 - Principal neurofilament-associated protein kinase in squid axoplasm is related to casein kinase I. AN - 15953712; 2534586 AB - A cytoskeletal extract of pure axoplasm, highly enriched with neurofilaments (ANF), was prepared from the giant axon of the squid (Loligo pealii ). This ANF preparation also contained potent kinase activities which phosphorylated the M sub(r) > 400,000 (high molecular weight) and M sub(r) 220,000 squid neurofilament protein subunits. High salt (1 M) extraction of this ANF preparation solubilized most of the neurofilament proteins and kinase activities and gel filtration on an AcA 44 column separated these two components. Four lines of evidence indicate ANF kinase was similar to casein kinase I. JF - Journal of Biological Chemistry AU - Floyd, C C AU - Grant, P AU - Gallant, P E AU - Pant, H C AD - Lab. Neurochem., NINDS, NIH, Build. 36, Rm. 4D 20, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 4987 EP - 4994 VL - 266 IS - 8 SN - 0021-9258, 0021-9258 KW - Loligo pealei KW - animal physiology KW - association KW - axoplasm KW - casein kinase I KW - enzymatic activity KW - molecular structure KW - neurofilaments KW - neurons KW - neurophysiology KW - protein kinase KW - relationship KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; CSA Neurosciences Abstracts; ASFA 1: Biological Sciences & Living Resources KW - Marine KW - Q1 08266:Physiology, biochemistry, biophysics KW - N3 11070:Neurochemistry and cellular biology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15953712?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=Principal+neurofilament-associated+protein+kinase+in+squid+axoplasm+is+related+to+casein+kinase+I.&rft.au=Floyd%2C+C+C%3BGrant%2C+P%3BGallant%2C+P+E%3BPant%2C+H+C&rft.aulast=Floyd&rft.aufirst=C&rft.date=1991-01-01&rft.volume=266&rft.issue=8&rft.spage=4987&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - molecular structure; enzymatic activity; neurons; neurophysiology; neurofilaments; Marine ER - TY - JOUR T1 - Carcinogenicity study of fecapentaene-12 diacetate on skin painting in SENCAR mice. AN - 15953376; 2530663 AB - To investigate the effects of both diol esterification and coadministration with antioxidant on the tumorigenicity of fecapentaene-12 (FP-12) preparations, diacetylfecapentaene-12 (DAFP-12) in dimethylsulfoxide (DMSO) was applied to SENCAR mouse skin with or without the stabilizer, vitamin E, twice/week for 5 weeks, following which all animals were promoted for up to 25 weeks by weekly applications of 12-O-tetradecanoylphorbol-13-acetate (TPA). While positive controls receiving 7,12-dimethylbenz(a)anthracene (DMBA) instead of DAFP-12 in a similar protocol all developed papillomas (average of 23/animal), papilloma incidence in mice given DAFP-12 did not differ significantly from that of the vehicle control. We conclude that DAFP-12 shows little or no tumor initiating activity for mouse skin even when coadministered with vitamin E. JF - Cancer Letters AU - Devor, DE AU - Henneman, J R AU - Keefer, L K AU - Logsdon, D L AU - Rice, J M AU - Streeter, A J AU - Ward, J M AD - Lab. Comp. Carcinog., NCI-FCRDC, Frederick, MD 21702, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 11 EP - 15 VL - 56 IS - 1 SN - 0304-3835, 0304-3835 KW - fecapentaene-12 diacetate KW - mice KW - Toxicology Abstracts KW - carcinogenicity KW - skin KW - X 24240:Miscellaneous UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15953376?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Letters&rft.atitle=Carcinogenicity+study+of+fecapentaene-12+diacetate+on+skin+painting+in+SENCAR+mice.&rft.au=Devor%2C+DE%3BHenneman%2C+J+R%3BKeefer%2C+L+K%3BLogsdon%2C+D+L%3BRice%2C+J+M%3BStreeter%2C+A+J%3BWard%2C+J+M&rft.aulast=Devor&rft.aufirst=DE&rft.date=1991-01-01&rft.volume=56&rft.issue=1&rft.spage=11&rft.isbn=&rft.btitle=&rft.title=Cancer+Letters&rft.issn=03043835&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - carcinogenicity; skin ER - TY - JOUR T1 - Retinoids induce tissue transglutaminase in NIH-3T3 cells. AN - 15952708; 2531603 AB - We report that all-trans and 13-cis-retinoic acid as well as the synthetic compound CH-55 enhance tissue transglutaminase activity as they increase NIH-3T3 cell adhesiveness. The 4-hydroxyphenylretinamide (4-HPR) with low activity in inducing attachment, lectin binding and growth inhibition also fails to induce transglutaminase. Thyroxine (Thy), a compound with a response element common to RA, is inactive. The tumor promoter 12-tetradecanoyl-phorbol-13-acetate (TPA), which increases adhesiveness with different kinetics than RA, failed to enhance transglutaminase. We conclude that retinoids with biological activity in inducing adhesion, inhibition of growth and increase of lectin binding, are also active in inducing transglutaminase activity. JF - Biochemical and Biophysical Research Communications AU - Cai, D AU - Ben, T AU - de Luca, LM AD - Differentiation Control Sect., Lab. Cell. Carcinog. and Tumor Promot., NCI, NIH, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 1119 EP - 1124 VL - 175 IS - 3 SN - 0006-291X, 0006-291X KW - 3T3 cells KW - cell adhesion KW - induction KW - protein-glutamine gamma -glutamylase KW - retinoids KW - tissues KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15952708?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+and+Biophysical+Research+Communications&rft.atitle=Retinoids+induce+tissue+transglutaminase+in+NIH-3T3+cells.&rft.au=Cai%2C+D%3BBen%2C+T%3Bde+Luca%2C+LM&rft.aulast=Cai&rft.aufirst=D&rft.date=1991-01-01&rft.volume=175&rft.issue=3&rft.spage=1119&rft.isbn=&rft.btitle=&rft.title=Biochemical+and+Biophysical+Research+Communications&rft.issn=0006291X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Comparison of Southern blot hybridization and polymerase chain reaction methods for the detection of human papillomavirus DNA. AN - 15944271; 2523076 AB - A methodologic study was performed to compare the polymerase chain reaction (PCR) and Southern blot hybridization, two commonly used testing strategies for the detection of human papillomavirus (HPV) infection. Three laboratories tested masked aliquots of exfoliated cervical cell specimens obtained from 120 women by cervicovaginal lavage. The study population included 32 women with condylomatous atypia or cervical intraepithelial neoplasia and 88 control women with no known history of cervical neoplasia. JF - Journal of Clinical Microbiology AU - Schiffman, M H AU - Bauer, H M AU - Lorincz, A T AU - Manos, M M AU - Byrne, J C AU - Glass, A G AU - Cadell, D M AU - Howley, P M AD - Environ. Epidemiol. Branch, NCI, Exec. Plaza N., Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 573 EP - 577 VL - 29 IS - 3 SN - 0095-1137, 0095-1137 KW - papilloma virus (human) KW - detection KW - polymerase chain reaction KW - Southern blotting KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Virology & AIDS Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - DNA KW - N 14610:Occurrence, isolation & assay KW - A 01114:Viruses KW - V 22022:Virus assay UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15944271?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Clinical+Microbiology&rft.atitle=Comparison+of+Southern+blot+hybridization+and+polymerase+chain+reaction+methods+for+the+detection+of+human+papillomavirus+DNA.&rft.au=Schiffman%2C+M+H%3BBauer%2C+H+M%3BLorincz%2C+A+T%3BManos%2C+M+M%3BByrne%2C+J+C%3BGlass%2C+A+G%3BCadell%2C+D+M%3BHowley%2C+P+M&rft.aulast=Schiffman&rft.aufirst=M&rft.date=1991-01-01&rft.volume=29&rft.issue=3&rft.spage=573&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Microbiology&rft.issn=00951137&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - DNA ER - TY - JOUR T1 - Novel myosin heavy chain encoded by murine dilute coat colour locus. AN - 15934714; 2513687 AB - Hundreds of murine dilute mutations have been identified and analysed, making dilute one of the best genetically characterized of all mammalian loci. The recessive dilute (d) coat colour mutation carried by many inbred strains of mice produces a lightening of coat colour, caused by an abnormal adendritic melanocyte morphology that results in an uneven release of pigment granules into the developing hair shaft. The results suggest an important role for the dilute gene product in the elaboration, maintenance, or function of cellular processes of melanocytes and neurons. JF - Nature AU - Mercer, JA AU - Seperack, P K AU - Strobel, M C AU - Copeland, NG AU - Jenkins, NA AD - Mamm. Genet. Lab., ABL-Basic Res. Program, NCI-Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 709 EP - 713 VL - 349 IS - 6311 SN - 0028-0836, 0028-0836 KW - amino acid sequence KW - cDNA KW - coat color KW - dilute gene KW - expression KW - genes KW - heavy chains KW - mice KW - myosin KW - nucleotide sequence KW - predictions KW - products KW - role KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - G 07398:GENERAL KW - N 14640:Structure & sequence UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15934714?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature&rft.atitle=Novel+myosin+heavy+chain+encoded+by+murine+dilute+coat+colour+locus.&rft.au=Mercer%2C+JA%3BSeperack%2C+P+K%3BStrobel%2C+M+C%3BCopeland%2C+NG%3BJenkins%2C+NA&rft.aulast=Mercer&rft.aufirst=JA&rft.date=1991-01-01&rft.volume=349&rft.issue=6311&rft.spage=709&rft.isbn=&rft.btitle=&rft.title=Nature&rft.issn=00280836&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - genes ER - TY - JOUR T1 - Chlamydia trachomatis developmentally regulated protein is homologous to eukaryotic histone H1. AN - 15929289; 2504178 AB - Chlamydiae are prokaryotic obligate intracellular parasites that undergo a biphasic life cycle involving an infectious, extracellular form known as elementary bodies and an intracellular, replicating form termed reticulate bodies. We have purified from Chlamydia trachomatis a very basic elementary body-specific protein with an apparent molecular mass of 18 kDa, determined its N-terminal amino acid sequence, and cloned the encoding gene. Sequence analysis of the cloned gene revealed some remarkable properties for its expressed product, including a high lysine content (29%), a correspondingly high pI, and significant homology to the H1 class of eukaryotic histones. JF - Proceedings of the National Academy of Sciences, USA AU - Hackstadt, T AU - Baehr, W AU - Ying, Yuan AD - Lab. Intracell. Parasit., Rocky Mt. Lab., NIAID, Hamilton, MT 59840, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 3937 EP - 3941 VL - 88 IS - 9 SN - 0027-8424, 0027-8424 KW - Chlamydia trachomatis KW - amino acid sequence KW - elementary body-specific protein KW - genes KW - histone H1 KW - homology KW - nucleotide sequence KW - predictions KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - N 14640:Structure & sequence KW - J 02725:DNA KW - G 07320:Bacterial genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15929289?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=A+minimal+lentivirus+Tat.&rft.au=Derse%2C+D%3BCarvalho%2C+M%3BCarroll%2C+R%3BPeterlin%2C+B+M&rft.aulast=Derse&rft.aufirst=D&rft.date=1991-12-01&rft.volume=65&rft.issue=12&rft.spage=7012&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - genes ER - TY - JOUR T1 - Developmental toxicity of inhaled methyl ethyl ketone in Swiss mice. AN - 15926656; 2510638 AB - Methyl ethyl ketone (MEK) is a widely used industrial solvent to which there is considerable human exposure. To assess the potential for MEK to cause developmental toxicity in rodents, groups of Swiss (CD-1) mice were exposed to 0, 400, 1000, or 3000 ppm MEK vapors 7 hr/day on Days 6-15 of gestation. Mild developmental toxicity was observed in the 3000 ppm group in the form of a reduction in mean fetal body weight. This reduction was statistically significant for the males only, although the relative decrease from the control values was the same for both sexes. There was no increase in the incidence of resorptions or the number of litters with resorptions among mice exposed to MEK. There was no significant increase in the incidence of any single malformation, but several malformations which were not observed in the concurrent control group or the controls of contemporary studies were present at a low incidence-cleft palate, fused ribs, missing vertebrae, and syndactyly. JF - Fundamental and Applied Toxicology AU - Schwetz, BA AU - Mast, T J AU - Weigel, R J AU - Dill, JA AU - Morrissey, R E AD - NIEHS, Syst. Toxicol. Branch, P.O. Box 12233, MD D4-02, Research Triangle Park, NC 27709, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 742 EP - 748 VL - 16 IS - 4 SN - 0272-0590, 0272-0590 KW - methyl ethyl ketone KW - development KW - toxicity KW - mice KW - Toxicology Abstracts KW - inhalation KW - solvents KW - teratogenicity KW - X 24152:Chronic exposure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15926656?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fundamental+and+Applied+Toxicology&rft.atitle=Developmental+toxicity+of+inhaled+methyl+ethyl+ketone+in+Swiss+mice.&rft.au=Schwetz%2C+BA%3BMast%2C+T+J%3BWeigel%2C+R+J%3BDill%2C+JA%3BMorrissey%2C+R+E&rft.aulast=Schwetz&rft.aufirst=BA&rft.date=1991-01-01&rft.volume=16&rft.issue=4&rft.spage=742&rft.isbn=&rft.btitle=&rft.title=Fundamental+and+Applied+Toxicology&rft.issn=02720590&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - inhalation; teratogenicity; solvents ER - TY - JOUR T1 - Intra-generic conservation and limited inter-strain variation in a protective minor surface antigen of Plasmodium knowlesi merozoites. AN - 15921565; 2500331 AB - We report here the entire sequence of the gene expressed by the Nuri strain of Plasmodium knowlesi . The H strain of P. knowlesi was isolated from the blood of a patient from the Malaysian bush at Burket Kertau in 1966, whereas the Nuri strain had been isolated from a naturally infected macaque in Negri Sembilan in 1953. JF - Molecular and Biochemical Parasitology AU - Waters, A P AU - Thomas, A W AU - Mitchell, G H AU - McCutchan, T F AD - Malar. Sect., Lab. Parasit. Dis., NIAID, NIH, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 141 EP - 144 VL - 44 IS - 1 SN - 0166-6851, 0166-6851 KW - Plasmodium knowlesi KW - amino acid sequence KW - antigens KW - cell surface KW - genes KW - merozoites KW - nucleotide sequence KW - predictions KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Microbiology Abstracts C: Algology, Mycology & Protozoology KW - K 03086:Immunology & vaccination KW - N 14640:Structure & sequence KW - G 07361:Protozoans/slime molds KW - K 03017:Protozoa UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15921565?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=The+intragenic+enhancer+of+human+immunodeficiency+virus+type+1+contains+functional+AP-1+binding+sites.&rft.au=Van+Lint%2C+C%3BBurny%2C+A%3BVerdin%2C+E&rft.aulast=Van+Lint&rft.aufirst=C&rft.date=1991-12-01&rft.volume=65&rft.issue=12&rft.spage=7066&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=0022538X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - merozoites; cell surface; genes; antigens ER - TY - JOUR T1 - Collection of exposure data for retrospective occupational epidemiological studies. AN - 15901556; 2472376 AB - Performing an exposure assessment in occupational epidemiology studies requires the collection of a wide variety of exposure data, because there are usually too few biological or air monitoring measurements over the time period of interest to allow retrospective assessment of exposures for individual study subjects. This article describes different types of exposure data that can be used to supplement monitoring results and provides a brief description of how they might be used. It also identifies sources from which these data may be obtained and the resources that may be needed to collect them. JF - Applied Occupational & Environmental Hygiene AU - Stewart, P A AU - Blair, A AU - Dosemeci, M AU - Gomez, M AD - Occup. Stud. Sect., Environ. Epidemiol. Branch, NCI, Executive Plaza N., Rm. 418, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 280 EP - 289 VL - 6 IS - 4 SN - 1047-322X, 1047-322X KW - data collection KW - monitoring measurements KW - dose response effects KW - Health & Safety Science Abstracts; Pollution Abstracts KW - occupational health KW - environmental monitoring KW - air sampling KW - H SI0.8.2:CHEMICALS (CORROSION) KW - P 6000:TOXICOLOGY AND HEALTH UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15901556?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Apollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Applied+Occupational+%26+Environmental+Hygiene&rft.atitle=Collection+of+exposure+data+for+retrospective+occupational+epidemiological+studies.&rft.au=Stewart%2C+P+A%3BBlair%2C+A%3BDosemeci%2C+M%3BGomez%2C+M&rft.aulast=Stewart&rft.aufirst=P&rft.date=1991-01-01&rft.volume=6&rft.issue=4&rft.spage=280&rft.isbn=&rft.btitle=&rft.title=Applied+Occupational+%26+Environmental+Hygiene&rft.issn=1047322X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - air sampling; environmental monitoring; occupational health ER - TY - JOUR T1 - Four-dimensional super(13)C/ super(13)C-edited nuclear Overhauser enhancement spectroscopy of a protein in solution: Application to interleukin 1 beta . AN - 15894850; 2490286 AB - A four-dimensional super(13)C/ super(13)C-edited NOESY experiment is described which dramatically improves the resolution of protein NMR spectra and enables the straightforward assignment of nuclear Overhauser effects involving aliphatic and/or aromatic protons in larger proteins. The experiment is demonstrated for uniformly (> 95%) super(13)C-labeled interleukin 1 beta , a protein of 153 residues and 17.4 kDa, which plays a key role in the immune response. This experiment should open up the application of protein structure determination by NMR to a large number of medium-sized proteins (150-300 residues) of biological interest. JF - Biochemistry (Washington) AU - Clore, G M AU - Kay, LE AU - Bax, A AU - Gronenborn, A M AD - Lab. Chem. Phys., Build. 2, NIDDK, NIH, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 12 EP - 18 VL - 30 IS - 1 SN - 0006-2960, 0006-2960 KW - N.M.R. KW - NOESY KW - interleukin 1 KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15894850?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemistry+%28Washington%29&rft.atitle=Four-dimensional+super%2813%29C%2F+super%2813%29C-edited+nuclear+Overhauser+enhancement+spectroscopy+of+a+protein+in+solution%3A+Application+to+interleukin+1+beta+.&rft.au=Clore%2C+G+M%3BKay%2C+LE%3BBax%2C+A%3BGronenborn%2C+A+M&rft.aulast=Clore&rft.aufirst=G&rft.date=1991-01-01&rft.volume=30&rft.issue=1&rft.spage=12&rft.isbn=&rft.btitle=&rft.title=Biochemistry+%28Washington%29&rft.issn=00062960&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Synthesis and characterization of inhibitors of myristoyl-CoA:protein N-myristoyltransferase. AN - 15885604; 2473909 AB - Several substrate and product analogs were synthesized and tested as in vitro inhibitors of bovine brain N-myristoyl-CoA:protein N-myristoyltransferase (NMT; EC 2.3.1.97). At 40 mu M, the acyl CoA analog, S-(2-ketopentadecyl-CoA, completely inhibited NMT in the presence of 80 mu M myristoyl CoA. Decreasing but marked inhibition was also observed with the acyl CoA analogs, S-(2-bromotetradecanoyl)-CoA and S-(3-epoxymethylene)-dodecanoyl)-CoA, and the multisubstrate derivative N-(2-S-CoA-tetradecanoyl)glycinamide in the presence of 40 mu M myristoyl CoA. Inhibition was also observed with the non-coenzyme A myristoyl analog, 1-bromo-2-pentadecanone. JF - Biochemical Pharmacology AU - Glover, C J AU - Tellez, M R AU - Guziec, FS Jr AU - Felsted, RL AD - Lab. Biol. Chem., NCI, NIH, Build. 37, Rm. 5D02, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 1067 EP - 1074 VL - 41 IS - 6-7 SN - 0006-2952, 0006-2952 KW - N-myristoyl-CoA-protein N-myristoyltransferase KW - S-2-(ketopentadenyl)CoA KW - inhibitors KW - synthesis KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15885604?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+Pharmacology&rft.atitle=Synthesis+and+characterization+of+inhibitors+of+myristoyl-CoA%3Aprotein+N-myristoyltransferase.&rft.au=Glover%2C+C+J%3BTellez%2C+M+R%3BGuziec%2C+FS+Jr%3BFelsted%2C+RL&rft.aulast=Glover&rft.aufirst=C&rft.date=1991-01-01&rft.volume=41&rft.issue=6-7&rft.spage=1067&rft.isbn=&rft.btitle=&rft.title=Biochemical+Pharmacology&rft.issn=00062952&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Selenoprotein A component of the glycine reductase complex from Clostridium purinolyticum : Nucleotide sequence of the gene shows that selenocysteine is encoded by UGA. AN - 15879901; 2465051 AB - The gene encoding the selenoprotein A component of glycine reductase was isolated from Clostridium purinolyticum . The nucleotide sequence of this gene (grdA) was determined. The opal termination codon (TGA) was found in-frame at the position corresponding to the location of the selenocysteine residue in the gene product. A comparison of the nucleotide sequences and secondary mRNA structures corresponding to the selenoprotein A gene and the fdhF gene of Escherichia coli formate dehydrogenase shows that there is a similar potential for regulation of the specific insertion of selenocysteine at the UGA codon. JF - Journal of Bacteriology AU - Garcia, GE AU - Stadtman, T C AD - Lab. Biochem., NHLBI, NIH, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 2093 EP - 2098 VL - 173 IS - 6 SN - 0021-9193, 0021-9193 KW - Clostridium purinolyticum KW - grdA gene KW - codons KW - glycine reductase KW - selenoprotein A KW - Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Microbiology Abstracts B: Bacteriology KW - nucleotide sequence KW - genes KW - mRNA KW - N 14640:Structure & sequence KW - G 07320:Bacterial genetics KW - J 02740:Genetics and evolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15879901?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Bacteriology&rft.atitle=Selenoprotein+A+component+of+the+glycine+reductase+complex+from+Clostridium+purinolyticum+%3A+Nucleotide+sequence+of+the+gene+shows+that+selenocysteine+is+encoded+by+UGA.&rft.au=Garcia%2C+GE%3BStadtman%2C+T+C&rft.aulast=Garcia&rft.aufirst=GE&rft.date=1991-01-01&rft.volume=173&rft.issue=6&rft.spage=2093&rft.isbn=&rft.btitle=&rft.title=Journal+of+Bacteriology&rft.issn=00219193&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - genes; nucleotide sequence; mRNA ER - TY - JOUR T1 - Nephrotoxicity of the glutathione conjugate of menadione (2-methyl-1,4-naphthoquinone) in the isolated perfused rat kidney. Role of metabolism by gamma -glutamyltranspeptidase and probenecid-sensitive transport. AN - 15879613; 2469217 AB - The renal processing of the glutathione conjugate of menadione, 2-methyl-3-S-glutathionyl-1,4-naphthoquinone (thiodione) was studied in the isolated perfused rat kidney. From our results it can be concluded that the thiodione-mediated toxicity in the isolated perfused rat kidney can be linked to cellular uptake by anionic transport systems and metabolism by gamma -glutamyltranspeptidase. JF - Journal of Pharmacology and Experimental Therapeutics AU - Redegeld, FAM AU - Hofman, G A AU - van de Loo, P AU - Koster, ASj AU - Noordhoek, J AD - Natl. Inst. Health, NIAID, Lab. Immunol., Build. 10, Rm. 11N260, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 665 EP - 669 VL - 256 IS - 2 SN - 0022-3565, 0022-3565 KW - glutathione KW - conjugates KW - transport KW - rats KW - toxicity KW - menadione KW - kidney KW - Toxicology Abstracts; Biochemistry Abstracts 1: Biological Membranes (till 1993) KW - X 24114:Metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15879613?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Pharmacology+and+Experimental+Therapeutics&rft.atitle=Nephrotoxicity+of+the+glutathione+conjugate+of+menadione+%282-methyl-1%2C4-naphthoquinone%29+in+the+isolated+perfused+rat+kidney.+Role+of+metabolism+by+gamma+-glutamyltranspeptidase+and+probenecid-sensitive+transport.&rft.au=Redegeld%2C+FAM%3BHofman%2C+G+A%3Bvan+de+Loo%2C+P%3BKoster%2C+ASj%3BNoordhoek%2C+J&rft.aulast=Redegeld&rft.aufirst=FAM&rft.date=1991-01-01&rft.volume=256&rft.issue=2&rft.spage=665&rft.isbn=&rft.btitle=&rft.title=Journal+of+Pharmacology+and+Experimental+Therapeutics&rft.issn=00223565&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - kidney ER - TY - JOUR T1 - Identity between polysaccharide antigens of Moraxella nonliquefaciens , Group B Neisseria meningitidis , and Escherichia coli K1 (non-O acetylated). AN - 15876965; 2466596 AB - A surface polysaccharide antigen of Moraxella nonliquefaciens , reported to be cross-reactive with the capsular polysaccharides of group B Neisseria meningitidis and Escherichia coli K1 (K. Boevre, K. Bryn, O. Closs, N. Hagen, and L.O. Froholm, NIPH Ann. 6:65-73, 1983), was isolated, purified, and characterized chemically, immunologically, and by nuclear magnetic resonance. This polysaccharide was shown to be a linear homopolymer of alpha (2 arrow right 8)-linked N-acetylneuraminic acid, identical to the capsular polysaccharide of group B N. meningitidis and O-acetyl-negative variants of E. coli K1. JF - Infection and Immunity AU - Devi, SJN AU - Schneerson, R AU - Egan, W AU - Vann, W F AU - Robbins, J B AU - Shiloach, J AD - Lab. Dev. and Mol. Immun., NICHD, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 732 EP - 736 VL - 59 IS - 2 SN - 0019-9567, 0019-9567 KW - Moraxella nonliquefaciens KW - identity KW - cross-reactivity KW - polysaccharides KW - Immunology Abstracts; Microbiology Abstracts B: Bacteriology KW - Escherichia coli KW - Neisseria meningitidis KW - antigens KW - J 02732:Other cell constituents and metabolites KW - F 06008:Bacteria UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15876965?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Identity+between+polysaccharide+antigens+of+Moraxella+nonliquefaciens+%2C+Group+B+Neisseria+meningitidis+%2C+and+Escherichia+coli+K1+%28non-O+acetylated%29.&rft.au=Devi%2C+SJN%3BSchneerson%2C+R%3BEgan%2C+W%3BVann%2C+W+F%3BRobbins%2C+J+B%3BShiloach%2C+J&rft.aulast=Devi&rft.aufirst=SJN&rft.date=1991-01-01&rft.volume=59&rft.issue=2&rft.spage=732&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - Neisseria meningitidis; Escherichia coli; antigens ER - TY - JOUR T1 - Prolonged infusion of quinolinic acid into rat striatum as an excitotoxic model of neurodegenerative disease. AN - 15874897; 2466847 AB - The neurotoxic effect of prolonged exposure of rat striatum to quinolinic acid in vivo was evaluated through assays of neurochemical markers for major neuronal populations. Continuous intrastriatal quinolinic acid infusion for 14 days produced a dose-dependent depletion of striatal choline acetyltransferase (ChAT) activity, glutamic acid decarboxylase (GAD) activity, and somatostatin content. ChAT activity was significantly reduced by quinolinic acid at doses of 90, 270, and 540 nmol/day, while GAD activity and somatostatin content were decreased only at doses of 270 and 540 nmol/day. NADPH-diaphorase histochemistry revealed a loss of striatal NADPH-diaphorase neurons as a result of quinolinic acid infusion at a dose of 270 nmol/day. JF - Neuroscience Letters AU - Susel, Z AU - Engber, T M AU - Kuo, S AU - Chase, T N AD - NINDS, NIH Build. 10, Rm. 5C103, 9000 Rockville Pike, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 234 EP - 238 VL - 121 IS - 1-2 SN - 0304-3940, 0304-3940 KW - quinolinic acid KW - infusion KW - activity KW - levels KW - depletion KW - rats KW - choline acetyltransferase KW - glutamic acid decarboxylase KW - somatostatin KW - Toxicology Abstracts; CSA Neurosciences Abstracts KW - neostriatum KW - X 24240:Miscellaneous KW - N3 11070:Neurochemistry and cellular biology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15874897?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroscience+Letters&rft.atitle=Prolonged+infusion+of+quinolinic+acid+into+rat+striatum+as+an+excitotoxic+model+of+neurodegenerative+disease.&rft.au=Susel%2C+Z%3BEngber%2C+T+M%3BKuo%2C+S%3BChase%2C+T+N&rft.aulast=Susel&rft.aufirst=Z&rft.date=1991-01-01&rft.volume=121&rft.issue=1-2&rft.spage=234&rft.isbn=&rft.btitle=&rft.title=Neuroscience+Letters&rft.issn=03043940&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - neostriatum ER - TY - JOUR T1 - Characterization by NMR of the heme-myoglobin adduct formed during the reductive metabolism of BrCCl sub(3). Covalent bonding of the proximal histidine to the ring I vinyl group. AN - 15871573; 2462897 AB - The reductive debromination of BrCCl sub(3) by ferrous deoxymyoglobin leads to the covalent bonding of the prosthetic heme to the protein. We have previously shown, by the use of peptide mapping and mass spectrometry, that histidine residue 93 is covalently bound to the heme moiety. In the present study the structure of the heme adduct was more completely determined by super(1)H and super(13)C NMR techniques. We have found that the ring I vinyl group of the prosthetic heme was altered by the addition of a histidine imidazole nitrogen to the alpha -carbon and a CCl sub(2) moiety to the beta -carbon. JF - Journal of Biological Chemistry AU - Osawa, Y AU - Highet, RJ AU - Bax, A AU - Pohl, L R AD - Lab. Chem. Pharmacol., NHLBI, NIH, Build. 10, Rm. 8N110, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 3208 EP - 3214 VL - 266 IS - 5 SN - 0021-9258, 0021-9258 KW - N.M.R. KW - adducts KW - carbon bromotrichloride KW - formation KW - heme KW - myoglobin KW - reduction KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15871573?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Biological+Chemistry&rft.atitle=Characterization+by+NMR+of+the+heme-myoglobin+adduct+formed+during+the+reductive+metabolism+of+BrCCl+sub%283%29.+Covalent+bonding+of+the+proximal+histidine+to+the+ring+I+vinyl+group.&rft.au=Osawa%2C+Y%3BHighet%2C+RJ%3BBax%2C+A%3BPohl%2C+L+R&rft.aulast=Osawa&rft.aufirst=Y&rft.date=1991-01-01&rft.volume=266&rft.issue=5&rft.spage=3208&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biological+Chemistry&rft.issn=00219258&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - Raf-1 protein kinase is required for growth of induced NIH/3T3 cells. AN - 15859715; 2444045 AB - Many growth factors regulate the cytoplasmic Raf-1 protein kinase, consistent with its having a central role in transduction of growth signals. The kinase is ubiquitously expressed and can promote proliferation, presumably in a manner dependent on growth-factor receptors and membrane-associated oncogenes. We have now examined the dependence of serum- and TPA (12-O-tetradecanoylphorbol-13-acetate)-regulated NIH/3T3 cell growth on RAF-1 kinase to determine whether Raf-1 is essential for receptor signalling. We inhibited Raf-1 function by expressing c-raf-1 antisense RNA or kinase-defective c-raf-1 mutants. Antisense RNA for c-raf-1 interferes with proliferation of normal NIH/3T3 cells and reverts raf-transformed cells. In revertant cells, DNA replication induced by serum or TPA was eliminated or reduced proportionately to the reduction in Raf protein levels. Expression of a kinase-defective Raf-1 mutant (craf301) or a regulatory domain fragment (HCR) inhibited serum-induced NIH/3T3-cell proliferation and raf transformation even more efficiently. JF - Nature AU - Kolch, W AU - Heidecker, G AU - Lloyd, P AU - Rapp, U R AD - Lab. Viral Carcinog., NIH/NCI, Frederick Cancer Res. and Dev. Cent., Frederick, MD 21702-1201, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 426 EP - 428 VL - 349 IS - 6308 SN - 0028-0836, 0028-0836 KW - NIH/3T3 cells KW - Raf-1 protein kinase KW - growth KW - phorbol 12-myristate 13-acetate diester KW - regulation KW - requirements KW - serum KW - treatment KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15859715?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature&rft.atitle=Raf-1+protein+kinase+is+required+for+growth+of+induced+NIH%2F3T3+cells.&rft.au=Kolch%2C+W%3BHeidecker%2C+G%3BLloyd%2C+P%3BRapp%2C+U+R&rft.aulast=Kolch&rft.aufirst=W&rft.date=1991-01-01&rft.volume=349&rft.issue=6308&rft.spage=426&rft.isbn=&rft.btitle=&rft.title=Nature&rft.issn=00280836&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 ER - TY - JOUR T1 - The interaction of monomeric actin with two binding sites on Acanthamoeba actobindin. AN - 15858972; 2462959 AB - Actobindin was previously shown to be an 88-residue polypeptide (M sub(r) 9761) with an internal tandem repeat of 33-34 amino acids. The stoichiometry of the actin-actobindin interaction was determined from the change in apparent M sub(r) of pyrene-glyoxal-labeled actobindin in the presence of actin, as determined by scanning the ultracentrifuge cell at a wavelength that detected only the labeled protein. The overall KD describing the binding of the first actin to either of the two sites on actobindin was 3.3 mu M. The binding constant for the second actin suggested either negative cooperativity or inequality of the two actin-binding sites. Similar binding constants were obtained by analysis of the fluorescence enhancement that occurred when actobindin bound to actin labeled with either pyrene iodoacetamide or 4-(N-iodoacetoxyethyl-N-methyl)-7-nitrobenz-2-oxa-1,3-diazole. JF - Journal of Biological Chemistry AU - Bubb, M R AU - Lewis AU - Korn, ED AD - Lab. Cell Biol., NHLBI, NIH, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 3820 EP - 3826 VL - 266 IS - 6 SN - 0021-9258, 0021-9258 KW - Acanthamoeba KW - actin KW - actobindin KW - binding KW - stoichiometry KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Microbiology Abstracts C: Algology, Mycology & Protozoology KW - K 03027:Protozoa UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15858972?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pain&rft.atitle=Hyperalgesia+and+myoclonus+with+intrathecal+infusion+of+high-dose+morphine.&rft.au=De+Conno%2C+F%3BCaraceni%2C+A%3BMartini%2C+C%3BSpoldi%2C+E%3BSalvetti%2C+M%3BVentafridda%2C+V&rft.aulast=De+Conno&rft.aufirst=F&rft.date=1991-12-01&rft.volume=47&rft.issue=3&rft.spage=337&rft.isbn=&rft.btitle=&rft.title=Pain&rft.issn=03043959&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - stoichiometry ER - TY - JOUR T1 - Polymerase chain reaction analyses identify two distinct classes of Borrelia burgdorferi . AN - 15837716; 2435678 AB - We sequenced homologous chromosomal loci from several North American and European isolates of the Lyme disease spirochete Borrelia burgdorferi as well as from the relapsing fever spirochete Borrelia hermsii . Inter- and intraspecies sequence comparisons permitted the design of B. burgdorferi -specific polymerase chain reaction primers that detected all strains tested (n = 31) from diverse geographical and biological origins. Polymerase chain reaction "typing" with other unique sets of primers subdivided B. burgdorferi isolates into two groups: all North American isolates and a few European isolates made up one group, while the majority of the European and Asian isolates made up the second group. This classification may have a clinical correlate reflected in differences between "typical" Lyme borreliosis in North America and Europe. JF - Journal of Clinical Microbiology AU - Rosa, P A AU - Hogan, D AU - Schwan, T G AD - Lab. Microb. Struct. and Funct., Rocky Mt. Lab., NIAID, Hamilton, MT 59840, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 524 EP - 532 VL - 29 IS - 3 SN - 0095-1137, 0095-1137 KW - biotyping KW - Borrelia burgdorferi KW - clinical isolates KW - loci KW - polymerase chain reaction KW - Biochemistry Abstracts 2: Nucleic Acids; Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts B: Bacteriology KW - chromosomes KW - DNA KW - N 14640:Structure & sequence KW - J 02725:DNA KW - A 01116:Bacteria KW - J 02710:Identification, taxonomy and typing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15837716?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Clinical+Microbiology&rft.atitle=Polymerase+chain+reaction+analyses+identify+two+distinct+classes+of+Borrelia+burgdorferi+.&rft.au=Rosa%2C+P+A%3BHogan%2C+D%3BSchwan%2C+T+G&rft.aulast=Rosa&rft.aufirst=P&rft.date=1991-01-01&rft.volume=29&rft.issue=3&rft.spage=524&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Microbiology&rft.issn=00951137&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - DNA; chromosomes ER - TY - JOUR T1 - Parathyroid hormone promotes the disassembly of cytoskeletal actin and myosin in cultured osteoblastic cells: Mediation by cyclic AMP. AN - 15834880; 2429211 AB - Parathyroid hormone (PTH) alters the shape of osteoblastic cells both in vivo and in vitro. In this study, we examined the effect of PTH on cytoskeletal actin and myosin, estimated by polyacrylamide gel electrophoresis of Triton X-100 (1%) nonextractable proteins. After 2-5 minutes, PTH caused a rapid and transient decrease of 50-60% in polymerized actin and myosin associated with the Triton X-100 nonextractable cytoskeleton. Polymerized actin returned to control levels by 30 min. The PTH effect was dose-dependent with an IC sub(50) of about 1nM, and was partially inhibited by the (3-34) PTH antagonist. PTH caused a rapid transient rise in cyclic AMP (cAMP) in these cells that peaked at 4 min, while the nadir in cytoskeletal actin and myosin was recorded around 5 min. The intracellular calcium chelator Quin-2/AM (10 mu M) also decreased cytoskeletal actin and myosin, to the same extent as did PTH (100 nM). To distinguish between cAMP elevation and Ca super(++) reduction as mediators of PTH action, we measured the phosphorylation of the 20 kD (PI 4.9) myosin light chain in cells preincubated with ( super(32)P)-orthophosphate. JF - Journal of Cellular Biochemistry AU - Egan, J J AU - Gronowicz, G AU - Rodan, G A AD - Lab. Cell. and Dev. Biol., NIDDK, NIH, Bethesda, MD 20891, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 101 EP - 111 VL - 45 IS - 1 SN - 0730-2312, 0730-2312 KW - actin KW - calvaria KW - cyclic AMP KW - disassembly KW - effects on KW - myosin KW - osteoblasts KW - parathyroid hormone KW - rats KW - role KW - Biochemistry Abstracts 3: Amino Acids, Peptides & Proteins (till 1993); Microbiology Abstracts B: Bacteriology; Calcium & Calcified Tissue Abstracts KW - T 20082:Tissue culture KW - T 20025:Cyclic AMP and second messengers KW - T 20056:Parathyroid and parathyroid hormones UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15834880?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Cellular+Biochemistry&rft.atitle=Parathyroid+hormone+promotes+the+disassembly+of+cytoskeletal+actin+and+myosin+in+cultured+osteoblastic+cells%3A+Mediation+by+cyclic+AMP.&rft.au=Egan%2C+J+J%3BGronowicz%2C+G%3BRodan%2C+G+A&rft.aulast=Egan&rft.aufirst=J&rft.date=1991-01-01&rft.volume=45&rft.issue=1&rft.spage=101&rft.isbn=&rft.btitle=&rft.title=Journal+of+Cellular+Biochemistry&rft.issn=07302312&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2015-03-24 N1 - SubjectsTermNotLitGenreText - calvaria; osteoblasts ER - TY - JOUR T1 - Reliability of diagnosing bacterial vaginosis is improved by a standardized method of gram stain interpretation. AN - 15832921; 2431189 AB - A new scoring system that uses the most reliable morphotypes from the vaginal smear was proposed for diagnosing bacterial vaginosis. This scoring system was compared with the Spiegel criteria for diagnosing bacterial vaginosis. The scoring system (0 to 10) was described as a weighted combination of the following morphotypes: lactobacilli, Gardnerella vaginalis or bacteroides (small gram-variable rods or gram-negative rods), and curved gram-variable rods. By using the Spearman rank correlation to determine intercenter variability, gram-positive cocci had poor agreement (0.23); lactobacilli (0.65), G. vaginalis (0.69), and bacteroides (0.57) had moderate agreement; and small (0.74) and curved (0.85) gram-variable rods had good agreement. The reliability of the 0 to 10 scoring system was maximized by not using gram-positive cocci, combining G. vaginalis and bacteroides morphotypes, and weighting more heavily curved gram-variable rods. JF - Journal of Clinical Microbiology AU - Nugent, R P AU - Krohn, MA AU - Hillier, S L AD - Pediatr., Adolescent, and Matern. AIDS Branch, NICHD, Exec. Plaza North, Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 297 EP - 301 VL - 29 IS - 2 SN - 0095-1137, 0095-1137 KW - vaginitis KW - infection KW - diagnosis KW - Microbiology Abstracts B: Bacteriology KW - bacteria KW - gram stain KW - man KW - J 02847:Genitourinary tract UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15832921?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Clinical+Microbiology&rft.atitle=Reliability+of+diagnosing+bacterial+vaginosis+is+improved+by+a+standardized+method+of+gram+stain+interpretation.&rft.au=Nugent%2C+R+P%3BKrohn%2C+MA%3BHillier%2C+S+L&rft.aulast=Nugent&rft.aufirst=R&rft.date=1991-01-01&rft.volume=29&rft.issue=2&rft.spage=297&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Microbiology&rft.issn=00951137&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - bacteria; man; gram stain ER - TY - JOUR T1 - Antibody to a 39-kilodalton Borrelia burgdorferi antigen (P39) as a marker for infection in experimentally and naturally inoculated animals. AN - 15825207; 2431069 AB - Borrelia burgdorferi expresses a conserved, species-specific 39-kDa protein (P39) that can stimulate antibodies during human infection. To confirm that anti-P39 antibodies are produced consistently in animals exposed to infectious spirochetes, white footed mice, Peromyscus leucopus , and laboratory white mice, Mus musculus (strain BALB/c), were experimentally inoculated with either infectious or noninfectious B. burgdorferi and the antibody response to P39 was determined by immunoblot at 21 days postinoculation. All mice inoculated with approximately 10 super(7) infectious B. burgdorferi) produced anti-P39 antibodies and were cultured positive for this spirochete. Mice inoculated with similar numbers of inactivated or viable noninfectious B. burgdorferi still producing P39 did not induce anti-P39 antibodies. By contrast, putative antiflagellin antibodies were detected in < 18% of the infected animals, which supports the notion that antibody reactive with flagellin may not be reliable as a marker for B. burgdorferi exposure as was originally thought. JF - Journal of Clinical Microbiology AU - Simpson, W J AU - Burgdorfer, W AU - Schrumpf, ME AU - Karstens, R H AU - Schwan, T G AD - Arthropod-borne Dis. Sect., Lab. Vectors and Pathog., Rocky Mt. Lab., NIAID, Hamilton, MT 59840, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 236 EP - 243 VL - 29 IS - 2 SN - 0095-1137, 0095-1137 KW - Borrelia burgdorferi KW - mice KW - P39 antigen KW - Immunology Abstracts; Microbiology Abstracts B: Bacteriology KW - antibodies KW - F 06801:Bacteria KW - J 02833:Immune response and immune mechanisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15825207?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Clinical+Microbiology&rft.atitle=Antibody+to+a+39-kilodalton+Borrelia+burgdorferi+antigen+%28P39%29+as+a+marker+for+infection+in+experimentally+and+naturally+inoculated+animals.&rft.au=Simpson%2C+W+J%3BBurgdorfer%2C+W%3BSchrumpf%2C+ME%3BKarstens%2C+R+H%3BSchwan%2C+T+G&rft.aulast=Simpson&rft.aufirst=W&rft.date=1991-01-01&rft.volume=29&rft.issue=2&rft.spage=236&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Microbiology&rft.issn=00951137&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - antibodies ER - TY - JOUR T1 - Tumors of the skin in the HRA/Skh mouse after treatment with 8-methoxypsoralen and UVA radiation. AN - 15785270; 2391681 AB - 8-Methoxypsoralen (8-MOP) with and without UVA radiation was administered to HRA/Skh mice (36 animals per treatment group) three times a week in the feed for a total dose of 9-80 mg/kg/week for 52 weeks. Most of the animals at the top dose of 8-MOP with UVA radiation had developed skin toxicity and/or skin tumors by 52 weeks. The skin lesions seen after treatment with 8-MOP and UVA radiation were characterized as squamous cell hyperplasia, squamous cell papilloma, and squamous cell carcinoma and are similar to what has been reported in humans after exposure to 8-MOP and UVA. Squamous cell hyperplasia and acute inflammation of the cornea were seen in some of the treated female mice. Oral administration of 8-MOP and UVA did not result in a carcinogenic response to other organ systems. There were no increases in skin neoplasms after 8-MOP or UVA radiation alone. 8-MOP given in combination with UVA was carcinogenic to the skin of mice at dose levels similar to those used to treat psoriasis in humans. JF - Fundamental and Applied Toxicology AU - Dunnick, J K AU - Forbes, P D AU - Eustis, S L AU - Hardisty, J F AU - Goodman, D G AD - NIEHS, P.O. Box 12233, Research Triangle Park, NC 27709, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 92 EP - 102 VL - 16 IS - 1 SN - 0272-0590, 0272-0590 KW - methoxsalen KW - mice KW - tumours KW - Toxicology Abstracts KW - carcinogenicity KW - lesions KW - U.V. radiation KW - skin KW - X 24210:Radiation & radioactive materials KW - X 24112:Chronic exposure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15785270?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Fundamental+and+Applied+Toxicology&rft.atitle=Tumors+of+the+skin+in+the+HRA%2FSkh+mouse+after+treatment+with+8-methoxypsoralen+and+UVA+radiation.&rft.au=Dunnick%2C+J+K%3BForbes%2C+P+D%3BEustis%2C+S+L%3BHardisty%2C+J+F%3BGoodman%2C+D+G&rft.aulast=Dunnick&rft.aufirst=J&rft.date=1991-01-01&rft.volume=16&rft.issue=1&rft.spage=92&rft.isbn=&rft.btitle=&rft.title=Fundamental+and+Applied+Toxicology&rft.issn=02720590&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - U.V. radiation; skin; lesions; carcinogenicity ER - TY - JOUR T1 - Dideoxyinosine in children with symptomatic human immunodeficiency virus infection. AN - 15782708; 2394926 AB - We conducted a phase I-II study in 43 children with symptomatic (CDC class P-2) HIV infection. Of these children, 16 (median age, 10 years) had previously received zidovudine, and 27 (median age, 2.6 years) had not. ddI was administered orally in three divided doses totaling 60, 120, 180, 360, or 540 mg per square meter of body-surface area per day for 24 weeks. Eight of the 43 patients did not complete 24 weeks of ddI: 6 died, 1 was withdrawn because of progressive disease, and the other because of toxicity. Pancreatitis developed in two children, one receiving ddI at each of the two highest doses. Dideoxyinosine was well tolerated and showed promising antiretroviral activity in HIV-infected children. JF - New England Journal of Medicine AU - Butler, K M AU - Husson, R N AU - Balis, F M AU - Brouwers, P AU - Eddy, J AU - El-Amin, D AU - Gress, J AU - Hawkins, M AU - Pizzo, P A AD - Pediatr. Branch, NCI, NIH, Build. 10, Rm. 13N240 Bethesda, MD 20892, USA Y1 - 1991 PY - 1991 DA - 1991 SP - 137 EP - 144 VL - 324 IS - 3 SN - 0028-4793, 0028-4793 KW - dideoxyinosine KW - man KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts; Toxicology Abstracts KW - side effects KW - Acquired Immune Deficiency Syndrome KW - children KW - human immunodeficiency virus KW - acquired immune deficiency syndrome KW - V 22004:AIDS: Clinical aspects KW - H SM9.20:CHILDHOOD INJURIES KW - X 24113:Side effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/15782708?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=New+England+Journal+of+Medicine&rft.atitle=Dideoxyinosine+in+children+with+symptomatic+human+immunodeficiency+virus+infection.&rft.au=Butler%2C+K+M%3BHusson%2C+R+N%3BBalis%2C+F+M%3BBrouwers%2C+P%3BEddy%2C+J%3BEl-Amin%2C+D%3BGress%2C+J%3BHawkins%2C+M%3BPizzo%2C+P+A&rft.aulast=Butler&rft.aufirst=K&rft.date=1991-01-01&rft.volume=324&rft.issue=3&rft.spage=137&rft.isbn=&rft.btitle=&rft.title=New+England+Journal+of+Medicine&rft.issn=00284793&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2006-11-01 N1 - Last updated - 2011-12-13 N1 - SubjectsTermNotLitGenreText - human immunodeficiency virus; Acquired Immune Deficiency Syndrome; children; acquired immune deficiency syndrome; side effects ER - TY - JOUR T1 - Biological and biochemical effects of retained polyhalogenated hydrocarbons AN - 13727034; 199104255 AB - The persistent effects of the polyhalogenated aromatic hydrocarbons (PHH) after acute or chronic exposure to these compounds are reviewed, covering tumor formation and induction of cytochrome P-450-associated mixed function oxygenases in target tissues. Present studies on mechanisms of tumor enhancement by single dose PCB treatment are reported. Biological effects that promoted tumor development in rodent livers and lungs were exerted by PHH congeners during many months. An integral part of the tumor promotion response was activation of the Ah locus by PHH congeners, as evidenced by the effects of specific congeners, retention profiles of the congeners in target tissues and the long-term induction of cytochrome P-450 IA1-associated enzyme activity. JF - Environmental Toxicology and Chemistry AU - Beebe, LE AU - Fox, S D AU - Issaq, HJ AU - Anderson, L M AD - National Cancer Institute Y1 - 1991 PY - 1991 DA - 1991 SP - 757 EP - 763 VL - 10 IS - 6 SN - 0730-7268, 0730-7268 KW - Enzymes (see also individual groups below) KW - Aqualine Abstracts KW - AQ 00008:Effects of Pollution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/13727034?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aaqualine&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Toxicology+and+Chemistry&rft.atitle=Biological+and+biochemical+effects+of+retained+polyhalogenated+hydrocarbons&rft.au=Beebe%2C+LE%3BFox%2C+S+D%3BIssaq%2C+HJ%3BAnderson%2C+L+M&rft.aulast=Beebe&rft.aufirst=LE&rft.date=1991-01-01&rft.volume=10&rft.issue=6&rft.spage=757&rft.isbn=&rft.btitle=&rft.title=Environmental+Toxicology+and+Chemistry&rft.issn=07307268&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2000-09-01 N1 - Last updated - 2011-12-12 ER - TY - JOUR T1 - Acute and long-term toxicity of water-soluble cationic polymers to rainbow trout (Oncorhynchus mykiss) and the modification of toxicity by humic acid AN - 13726526; 199104072 AB - Static 96 h bioassays, and long-term (28 d) flow-through exposures were used to test toxicity of 5 cationic copolymers (3 epichlorhydrin/dimethylamine and 2 acrylamide/acrylate) to fingerling rainbow trout. Acute 96 h bioassays were also performed with the addition of humic acid (HA) to test solutions. The 96 h LC50s ranged from 271-1733 ug per litre. Addition of HA reduced toxicity of all the polymers in a concentration-dependent fashion: at just 5 mg HA per litre, toxicities were reduced 7 to 16-fold. Under flow-through conditions most of the mortality occurred in the first 7 d, and all the polymers were more toxic (by factors of 1.7-13.9) than under static conditions. Toxicity decreased with increasing molecular weight. JF - Environmental Toxicology and Chemistry AU - Goodrich AU - Dulak, L H AU - Friedman, MA AU - Lech, J J AD - NIEHS Marine and Freshwater Biomedical Core Center, Milwaukee, Wis. Y1 - 1991 PY - 1991 DA - 1991 SP - 509 EP - 515 VL - 10 IS - 4 SN - 0730-7268, 0730-7268 KW - Concentration-dependent KW - Epichlorohydrin KW - Fish (see also individual groups listed below) KW - Reduction KW - Aqualine Abstracts KW - AQ 00008:Effects of Pollution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/13726526?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aaqualine&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Toxicology+and+Chemistry&rft.atitle=Acute+and+long-term+toxicity+of+water-soluble+cationic+polymers+to+rainbow+trout+%28Oncorhynchus+mykiss%29+and+the+modification+of+toxicity+by+humic+acid&rft.au=Goodrich%3BDulak%2C+L+H%3BFriedman%2C+MA%3BLech%2C+J+J&rft.aulast=Goodrich&rft.aufirst=&rft.date=1991-01-01&rft.volume=10&rft.issue=4&rft.spage=509&rft.isbn=&rft.btitle=&rft.title=Environmental+Toxicology+and+Chemistry&rft.issn=07307268&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2000-09-01 N1 - Last updated - 2011-12-12 ER - TY - JOUR T1 - Population and pedigree studies reveal a lack of association between the dopamine D2 receptor gene and alcoholism. AN - 80161316; 1979357 AB - Using the dopamine D2 receptor clone lambda hD2G1, Blum et al recently found that the D2/Taq I allele (A1) was present in 69% of 35 deceased alcoholics but in only 20% of an equal number of controls. To assess this association further, we evaluated the D2/Taq I polymorphism and a single-strand conformation polymorphism detected by polymerase chain reaction and nondenaturing gel electrophoresis (PCR-SSCP) of the 3' noncoding region of the D2 receptor gene. We studied 40 unrelated white alcoholics, 127 racially matched controls, and two white pedigrees. The Schedule for Affective Disorders and Schizophrenia-Lifetime Version (SADS-L) clinical diagnostic interviews were rated blindly by two clinicians. The SADS-L interviews and other data were then used to ascertain diagnoses according to the Diagnostic and Statistical Manual of Mental Disorders, Revised Third Edition (DSM-III-R) criteria. Alcoholics were subtyped according to age of onset, severity, presence of antisocial personality, and family history. No significant differences in either D2/Taq I or PCR-SSCP allele frequencies were observed between alcoholics, subpopulations of alcoholics, or controls. The PCR-SSCP polymorphism provided independent information against linkage at the D2 receptor locus. Several recombinants between the D2/Taq I locus and alcoholism were observed in two white families with an alcoholic parent who possessed the A1 allele. This study does not support a widespread or consistent association between the D2 receptor gene and alcoholism. JF - JAMA AU - Bolos, A M AU - Dean, M AU - Lucas-Derse, S AU - Ramsburg, M AU - Brown, G L AU - Goldman, D AD - Section on Genetic Studies, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Md 20892. Y1 - 1990/12/26/ PY - 1990 DA - 1990 Dec 26 SP - 3156 EP - 3160 VL - 264 IS - 24 SN - 0098-7484, 0098-7484 KW - DNA Probes KW - 0 KW - DNA, Single-Stranded KW - Receptors, Dopamine KW - Receptors, Dopamine D2 KW - Abridged Index Medicus KW - Index Medicus KW - Pedigree KW - Polymerase Chain Reaction KW - Alleles KW - African Continental Ancestry Group -- genetics KW - Polymorphism, Restriction Fragment Length KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Male KW - Female KW - Alcoholism -- ethnology KW - Receptors, Dopamine -- genetics KW - Alcoholism -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80161316?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+and+pedigree+studies+reveal+a+lack+of+association+between+the+dopamine+D2+receptor+gene+and+alcoholism.&rft.au=Bolos%2C+A+M%3BDean%2C+M%3BLucas-Derse%2C+S%3BRamsburg%2C+M%3BBrown%2C+G+L%3BGoldman%2C+D&rft.aulast=Bolos&rft.aufirst=A&rft.date=1990-12-26&rft.volume=264&rft.issue=24&rft.spage=3156&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-01-24 N1 - Date created - 1991-01-24 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: JAMA. 1991 May 22-29;265(20):2667-8 [1827166] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Molecular cloning and DNA sequence of lacE, the gene encoding the lactose-specific enzyme II of the phosphotransferase system of Lactobacillus casei. Evidence that a cysteine residue is essential for sugar phosphorylation. AN - 80197270; 2125053 AB - The gene coding for the lactose-specific Enzyme II of the Lactobacillus casei phosphoenolpyruvate-dependent phosphotransferase system, lacE, has been isolated by molecular cloning and expressed in Escherichia coli. The DNA sequence of the lacE gene and the deduced amino acid sequence are presented. The putative translation product comprises a hydrophobic protein of 577 amino acids with a calculated molecular mass of 62,350 Da. The deduced polypeptide has a high degree of sequence similarity with the corresponding lactose-specific enzymes II of Staphylococcus aureus and Lactococcus lactis. The sequence surrounding cysteine 483 was strongly conserved in the three proteins. The identity of the lacE product as the Enzyme IIlacL.casei was demonstrated by in vitro lactose phosphorylation assays using the protein expressed in E. coli. Single replacement of each of the histidine and cysteine residues by site-directed mutagenesis pointed to cysteine 483 as an amino acid residue essential for the phosphoryl group transfer reaction. JF - The Journal of biological chemistry AU - Alpert, C A AU - Chassy, B M AD - Laboratory for Microbial Ecology, National Institute for Dental Research, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1990/12/25/ PY - 1990 DA - 1990 Dec 25 SP - 22561 EP - 22568 VL - 265 IS - 36 SN - 0021-9258, 0021-9258 KW - bfl KW - glc KW - gut KW - lacE KW - mtl KW - nag KW - pman KW - DNA, Bacterial KW - 0 KW - Oligonucleotide Probes KW - Phosphoenolpyruvate Sugar Phosphotransferase System KW - EC 2.7.1.- KW - phosphoenolpyruvate-lactose dependent phosphotransferase system KW - Cysteine KW - K848JZ4886 KW - Index Medicus KW - Lactococcus lactis -- genetics KW - Base Sequence KW - Phosphorylation KW - Sequence Homology, Nucleic Acid KW - Restriction Mapping KW - Molecular Sequence Data KW - Escherichia coli -- genetics KW - Cloning, Molecular -- methods KW - Staphylococcus aureus -- enzymology KW - Protein Conformation KW - Binding Sites KW - Lactobacillus casei -- enzymology KW - Genes, Bacterial KW - Phosphoenolpyruvate Sugar Phosphotransferase System -- genetics KW - Lactobacillus casei -- genetics KW - Phosphoenolpyruvate Sugar Phosphotransferase System -- metabolism KW - DNA, Bacterial -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80197270?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Molecular+cloning+and+DNA+sequence+of+lacE%2C+the+gene+encoding+the+lactose-specific+enzyme+II+of+the+phosphotransferase+system+of+Lactobacillus+casei.+Evidence+that+a+cysteine+residue+is+essential+for+sugar+phosphorylation.&rft.au=Alpert%2C+C+A%3BChassy%2C+B+M&rft.aulast=Alpert&rft.aufirst=C&rft.date=1990-12-25&rft.volume=265&rft.issue=36&rft.spage=22561&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 - 1991-02-14 N1 - Date created - 1991-02-14 N1 - Date revised - 2017-01-13 N1 - Gene symbol - bfl; glc; gut; lacE; mtl; nag; pman N1 - Genetic sequence - M60851; GENBANK N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Permanent effects of neonatally administered resiniferatoxin in the rat. AN - 80312313; 2085772 AB - We have previously demonstrated that resiniferatoxin functions in adult rats as an ultrapotent analog of capsaicin. In adults, capsaicin excites and then desensitizes a specific population of sensory neurons; when administered to neonates capsaicin causes degeneration of these neurons. We report here that treatment of newborn rats with resiniferatoxin caused a substantial (47%) loss of dorsal root ganglia neurons in adults and an almost complete loss of calcitonin gene related peptide-like immunoreactivity in both dorsal root ganglia and gasserian ganglia. The animals were unresponsive to noxious chemical stimuli and showed marked diminution (88%) of their neurogenic inflammatory response. Resiniferatoxin was at least 2 orders of magnitude more potent than capsaicin for inducing neurodegeneration in the neonates. Specific resiniferatoxin binding, thought to represent capsaicin receptors, decreased 80-90% in membranes from dorsal root ganglia and 50-70% in membranes from gasserian ganglia of adult rats treated neonatally with resiniferatoxin. The affinity for the residual binding decreased. We speculate that subpopulations of sensory neurons differ in susceptibility to neonatal resiniferatoxin treatment. Resiniferatoxin promises to be a useful probe to explore mechanisms of sensorotoxin-induced degeneration for subpopulations of capsaicin-sensitive sensory neurons. JF - Brain research AU - Szallasi, A AU - Szallasi, Z AU - Blumberg, P M AD - Laboratory of Cellular Carcinogenesis and Tumor Promotion, National Cancer Institute, Bethesda, MD 20892. Y1 - 1990/12/24/ PY - 1990 DA - 1990 Dec 24 SP - 182 EP - 186 VL - 537 IS - 1-2 SN - 0006-8993, 0006-8993 KW - Neuropeptides KW - 0 KW - Capsaicin KW - S07O44R1ZM KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Neuropeptides -- metabolism KW - Membranes -- drug effects KW - Animals KW - Neuropeptides -- pharmacology KW - Ganglia, Spinal -- physiology KW - Membranes -- metabolism KW - Ganglia, Spinal -- drug effects KW - Male KW - Female KW - Capsaicin -- pharmacology KW - Animals, Newborn -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80312313?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Permanent+effects+of+neonatally+administered+resiniferatoxin+in+the+rat.&rft.au=Szallasi%2C+A%3BSzallasi%2C+Z%3BBlumberg%2C+P+M&rft.aulast=Szallasi&rft.aufirst=A&rft.date=1990-12-24&rft.volume=537&rft.issue=1-2&rft.spage=182&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 - 1991-05-23 N1 - Date created - 1991-05-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Induction of peroxisomal acyl CoA oxidase activity and lipid peroxidation in primary rat hepatocyte cultures. AN - 80221998; 2274969 AB - Peroxisome proliferators have been suggested to induce liver carcinogenesis as a result of increased peroxisomal hydrogen peroxide production and cellular oxidative stress. Primary monolayer cultures of hepatocytes isolated from male F344 rats were incubated in medium containing one of three different peroxisome proliferators and examined for the induction of peroxisomal CoA oxidase activity and lipid peroxidation. The latter parameter was determined by measuring levels of conjugated dienes in lipid fractions extracted from harvested cells. The peroxisome proliferators used in these studies were nafenopin and clofibric acid (two hypolipidemic drugs) and mono(2-ethylhexyl)phthalate (MEHP), the primary metabolite of the industrial plasticizer, di(2-ethylhexyl)phthalate (DEHP). The relative specific activity of peroxisomal acyl CoA oxidase was increased by about 300% after incubation for 44 h with 200 microM nafenopin; lower levels of induction were observed with clofibric acid or MEHP. Relative to controls, the level of conjugated dienes was increased approximately 2-fold after incubation with 200 microM nafenopin; there was no apparent increase in conjugated dienes after incubation with up to 200 microM MEHP or 400 microM clofibric acid. The increase in conjugated dienes with 200 microM nafenopin was inhibited by co-incubation with the antioxidant, N,N'-diphenyl-p-phenylenediamine. Thus, peroxisomal enzyme induction by nafenopin can result in membrane lipid peroxidation and monolayer cultures of rat hepatocytes may provide a useful model system for studying relationships between peroxisome proliferation, enhanced hydrogen peroxide production and cellular changes due to hepatic oxidative stress. JF - Toxicology AU - Tomaszewski, K E AU - Heindel, S W AU - Jenkins, W L AU - Melnick, R L AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1990/12/17/ PY - 1990 DA - 1990 Dec 17 SP - 49 EP - 60 VL - 65 IS - 1-2 SN - 0300-483X, 0300-483X KW - Nafenopin KW - 093W78U96W KW - Clofibric Acid KW - 53PF01Q249 KW - Diethylhexyl Phthalate KW - C42K0PH13C KW - Oxidoreductases KW - EC 1.- KW - palmitoyl CoA oxidase KW - EC 1.3.3.- KW - Acyl-CoA Oxidase KW - EC 1.3.3.6 KW - mono-(2-ethylhexyl)phthalate KW - FU2EWB60RT KW - Index Medicus KW - Rats KW - Clofibric Acid -- toxicity KW - Animals KW - Rats, Inbred F344 KW - Cells, Cultured KW - Diethylhexyl Phthalate -- toxicity KW - Spectrophotometry, Ultraviolet KW - Enzyme Induction KW - Male KW - Nafenopin -- toxicity KW - Microbodies -- enzymology KW - Liver -- enzymology KW - Liver -- cytology KW - Liver -- drug effects KW - Lipid Peroxidation -- drug effects KW - Microbodies -- drug effects KW - Oxidoreductases -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80221998?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Induction+of+peroxisomal+acyl+CoA+oxidase+activity+and+lipid+peroxidation+in+primary+rat+hepatocyte+cultures.&rft.au=Tomaszewski%2C+K+E%3BHeindel%2C+S+W%3BJenkins%2C+W+L%3BMelnick%2C+R+L&rft.aulast=Tomaszewski&rft.aufirst=K&rft.date=1990-12-17&rft.volume=65&rft.issue=1-2&rft.spage=49&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=0300483X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-02-25 N1 - Date created - 1991-02-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Induction of ethoxyresorufin-O-deethylase and inhibition of glucocorticoid receptor binding in skin and liver of haired and hairless HRS/J mice by topically applied 2,3,7,8-tetrachlorodibenzo-p-dioxin. AN - 80221903; 2274963 AB - The biochemical changes associated with the toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) have been reported to include alterations in glucocorticoid and epidermal growth factor receptors and mixed function oxidase (MFO) induction. TCDD induces MFO activity in skin of both haired and hairless HRS/J mice. However, epidermal hyperplasia and hyperkeratosis are produced only in the skin of hairless mice. Therefore, since steroid and growth factor responses are implicated in cell proliferation and differentiation, these mice constitute a model system for assessing the possible roles of glucocorticoid and epidermal growth factor receptors in the toxicity of TCDD. The effect of dermal TCDD application (12 micrograms/kg in 100 microliters acetone) on ethoxyresorufin-O-deethylase (EROD) activity, glucocorticoid receptor binding and epidermal growth factor receptors in liver and skin of hairless and haired mice was determined. No differences existed in the basal number of cytosolic glucocorticoid receptors (Bmax) or the apparent equilibrium binding constants (Kd) in control liver, dorsal skin and abdominal skin of male and female hairless mice and haired male mice. Seven days after topical application of TCDD, decreases of approximately 38% were observed in the hepatic Bmax of the glucocorticoid receptors in both haired and hairless mice. However, in dorsal skin, TCDD decreased Bmax by approximately 40% in hairless mice but only 18% in haired mice. The dexamethasone-glucocorticoid receptor complex from both liver and skin of control and TCDD treated mice had similar sedimentation co-efficients in sucrose density gradients. TCDD had no effect on the Kd of glucocorticoid receptors of skin or liver in haired and hairless mice. No difference was observed in the time-dependent increases in hepatic EROD activity between haired and hairless mice after dermal application of TCDD. However, the maximum induction of EROD activity in microsomes from the skin of haired mice was only 60% of the activity observed in hairless animals. The induction of EROD by TCDD did not correlate temporally with the decrease in glucocorticoid receptor binding. The application of TCDD to the skin of hairless mice resulted in epidermal hyperplasia and dermal keratinization, while little change was observed in the general morphology of the skin of haired mice following dermal application. The application of TCDD had no effect on the incidence and distribution of epidermal growth factor receptors in skin of haired and hairless mice as determined immunohistochemically. Thus, the biochemical effects of TCDD are not only strain dependent, but tissue specific. Furthermore, decreases in glucocorticoid and epidermal growth factor receptors do not appear to be general markers of TCDD toxicity. JF - Toxicology AU - Stohs, S J AU - Abbott, B D AU - Lin, F H AU - Birnbaum, L S AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1990/12/17/ PY - 1990 DA - 1990 Dec 17 SP - 123 EP - 136 VL - 65 IS - 1-2 SN - 0300-483X, 0300-483X KW - Polychlorinated Dibenzodioxins KW - 0 KW - Receptors, Glucocorticoid KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Oxidoreductases KW - EC 1.- KW - Cytochrome P-450 CYP1A1 KW - EC 1.14.14.1 KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Index Medicus KW - Animals KW - Receptor, Epidermal Growth Factor -- metabolism KW - Enzyme Induction KW - Mice KW - Mice, Hairless KW - Ultracentrifugation KW - Immunohistochemistry KW - Male KW - Female KW - Receptors, Glucocorticoid -- drug effects KW - Liver -- enzymology KW - Skin -- enzymology KW - Skin -- drug effects KW - Liver -- drug effects KW - Skin -- metabolism KW - Polychlorinated Dibenzodioxins -- toxicity KW - Receptors, Glucocorticoid -- analysis KW - Liver -- metabolism KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Receptors, Glucocorticoid -- metabolism KW - Oxidoreductases -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80221903?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Induction+of+ethoxyresorufin-O-deethylase+and+inhibition+of+glucocorticoid+receptor+binding+in+skin+and+liver+of+haired+and+hairless+HRS%2FJ+mice+by+topically+applied+2%2C3%2C7%2C8-tetrachlorodibenzo-p-dioxin.&rft.au=Stohs%2C+S+J%3BAbbott%2C+B+D%3BLin%2C+F+H%3BBirnbaum%2C+L+S&rft.aulast=Stohs&rft.aufirst=S&rft.date=1990-12-17&rft.volume=65&rft.issue=1-2&rft.spage=123&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=0300483X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-02-25 N1 - Date created - 1991-02-25 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Triiodothyronine potentiation of tricyclic antidepressant treatment in patients with panic disorder. AN - 80257718; 2289001 JF - Biological psychiatry AU - Stein, M B AU - Uhde, T W AD - Section on Anxiety and Affective Disorders, National Institute of Mental Health, Bethesda, MD 20892. Y1 - 1990/12/15/ PY - 1990 DA - 1990 Dec 15 SP - 1061 EP - 1064 VL - 28 IS - 12 SN - 0006-3223, 0006-3223 KW - Triiodothyronine KW - 06LU7C9H1V KW - Nortriptyline KW - BL03SY4LXB KW - Imipramine KW - OGG85SX4E4 KW - Index Medicus KW - Drug Therapy, Combination KW - Single-Blind Method KW - Arousal -- drug effects KW - Humans KW - Adult KW - Pilot Projects KW - Drug Synergism KW - Male KW - Female KW - Triiodothyronine -- administration & dosage KW - Anxiety Disorders -- drug therapy KW - Panic -- drug effects KW - Anxiety Disorders -- psychology KW - Nortriptyline -- administration & dosage KW - Imipramine -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80257718?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biological+psychiatry&rft.atitle=Triiodothyronine+potentiation+of+tricyclic+antidepressant+treatment+in+patients+with+panic+disorder.&rft.au=Stein%2C+M+B%3BUhde%2C+T+W&rft.aulast=Stein&rft.aufirst=M&rft.date=1990-12-15&rft.volume=28&rft.issue=12&rft.spage=1061&rft.isbn=&rft.btitle=&rft.title=Biological+psychiatry&rft.issn=00063223&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-03 N1 - Date created - 1991-04-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mechanism of leucovorin reversal of methotrexate cytotoxicity in human MCF-7 breast cancer cells. AN - 80178364; 2260989 AB - Previous studies have suggested that metabolic inhibition by methotrexate (MTX) is multifactorial and that cytotoxicity can be reversed by the reduced folate leucovorin. In this report we investigated the mechanism of leucovorin rescue in the MCF-7 human breast cancer cell line. Cells were exposed to various concentrations of MTX (0.5, 1.0, 3.0, and 10.0 microM) for 24 hr followed by rescue with labelled leucovorin (0.5 to 50 microM). The changes in the intracellular folate pools 24 hr following the addition of leucovorin were quantitated by high-pressure liquid chromatographic methods. The changes in the folate pools during rescue were compared with the ability of various concentrations of leucovorin to affect cellular rescue from MTX using a cloning assay. Our studies show that the total labelled intracellular folate pools increased in a log-linear fashion with respect to leucovorin exposure concentrations up to 100 microM. The degree of accumulation at a given leucovorin concentration was not significantly different in the absence or presence of MTX over the concentration range of 0.5 to 10 microM. Individual folate pool levels (tetrahydrofolate, 10-formyl tetrahydrofolate, 5-formyl tetrahydrofolate, 5-methyl tetrahydrofolate, and 5,10-methylene tetrahydrofolate) reached those present in cells not exposed to MTX at concentrations of leucovorin that were not adequate to rescue the MTX-treated cells. With exposure to concentrations of leucovorin capable of rescue, the individual folate pool levels were up to twelve times greater than those found in untreated cells, consistent with competition for catalytic activity at folate-dependent enzymes in addition to dihydrofolate reductase. The dihydrofolate pool also increased with increasing leucovorin concentration: but, unlike the reduced folates, this oxidized folate reached a maximal level that was dependent on the MTX concentration to which the cells had been exposed. This suggests that competition between MTX and leucovorin occurs at the level of dihydrofolate reductase via a competitive interaction with dihydrofolate in this intact cell system. The ability of leucovorin and its metabolites to compete with direct inhibitors of dihydrofolate reductase and other metabolically important folate-dependent enzymes appears to be associated with leucovorin rescue. JF - Biochemical pharmacology AU - Boarman, D M AU - Baram, J AU - Allegra, C J AD - Division of Cancer Treatment, National Cancer Institute, NIH, Bethesda, MD 20892. Y1 - 1990/12/15/ PY - 1990 DA - 1990 Dec 15 SP - 2651 EP - 2660 VL - 40 IS - 12 SN - 0006-2952, 0006-2952 KW - Pteroylpolyglutamic Acids KW - 0 KW - dihydrofolate KW - 4033-27-6 KW - Folic Acid KW - 935E97BOY8 KW - Tetrahydrofolate Dehydrogenase KW - EC 1.5.1.3 KW - Leucovorin KW - Q573I9DVLP KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - Tumor Cells, Cultured KW - Cell Survival -- drug effects KW - Dose-Response Relationship, Drug KW - Humans KW - In Vitro Techniques KW - Breast Neoplasms KW - Pteroylpolyglutamic Acids -- metabolism KW - Tetrahydrofolate Dehydrogenase -- metabolism KW - Folic Acid -- metabolism KW - Folic Acid -- analogs & derivatives KW - Methotrexate -- antagonists & inhibitors KW - Leucovorin -- pharmacology KW - Methotrexate -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80178364?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mechanism+of+leucovorin+reversal+of+methotrexate+cytotoxicity+in+human+MCF-7+breast+cancer+cells.&rft.au=Boarman%2C+D+M%3BBaram%2C+J%3BAllegra%2C+C+J&rft.aulast=Boarman&rft.aufirst=D&rft.date=1990-12-15&rft.volume=40&rft.issue=12&rft.spage=2651&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 - 1991-01-31 N1 - Date created - 1991-01-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Chemoprotective effects of recombinant human IL-1 alpha in cyclophosphamide-treated normal and tumor-bearing mice. Protection from acute toxicity, hematologic effects, development of late mortality, and enhanced therapeutic efficacy. AN - 80168297; 2258610 AB - In this study, recombinant human IL-1 alpha (rhIL-1 alpha) was used to protect normal and tumor-bearing BALB/c mice from the acute toxicity caused by lethal doses of cyclophosphamide (Cy) and 5-fluorouracil. Pretreatment of mice for 7 days with 10,000 U/day of rhIL-1 alpha protected 70 to 100% of mice from the acute death induced by lethal doses of both Cy (380 mg/kg) and 5-fluorouracil (250 mg/kg). In contrast, post-treatment of mice with single or multiple doses of rhIL-1 alpha was not chemoprotective. Pretreatment of mice with rhIL-1 alpha increased the acute LD90 of Cy from 380 mg/kg to greater than 500 mg/kg in normal mice, an LD90 dose-modifying effect of at least 1.25, was accompanied by a more rapid recovery from neutropenia and a less severe reduction in the number of bone marrow single lineage monocyte, myeloid, or myelomonocytic colonies. Some of the mice (10 to 50%) that were successfully protected by pretreatment with rhIL-1 alpha died after day 50. These mice consistently presented with extensive pulmonary inflammation and fibrosis at death. Mice bearing murine renal cancer (Renca) were also protected from the acute toxic effects of Cy (450 mg/kg) by pretreatment with rhIL-1 alpha. Renca-bearing mice pretreated with rhIL-1 alpha and either sublethal (300 mg/kg) or lethal (450 mg/kg) doses of Cy exhibited enhanced survival times over those of untreated Renca-bearing mice. Interestingly, the cause of death in Renca-bearing mice that ultimately failed treatment with rhIL-1 alpha plus 300 mg/kg Cy was recurrent tumor, whereas most mice treated with rhIL-1 alpha plus 450 mg/kg Cy had no detectable tumor, although several died from late pulmonary inflammation and fibrosis. Thus, the dose escalation of Cy in rhIL-1 alpha-pretreated mice results in greater antitumor effects of Cy. However, the dose escalation of some cytotoxic agents allowed by the use of myelostimulatory agents can result in late fatal complications not detected in acute toxicity testing. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Futami, H AU - Jansen, R AU - MacPhee, M J AU - Keller, J AU - McCormick, K AU - Longo, D L AU - Oppenheim, J J AU - Ruscetti, F W AU - Wiltrout, R H AD - Laboratory of Experimental Immunology, National Cancer Institute-Frederick Cancer Research Facility, MD 21702-1201. Y1 - 1990/12/15/ PY - 1990 DA - 1990 Dec 15 SP - 4121 EP - 4130 VL - 145 IS - 12 SN - 0022-1767, 0022-1767 KW - Interleukin-1 KW - 0 KW - Recombinant Proteins KW - mafosfamide KW - 5970HH9923 KW - Cyclophosphamide KW - 8N3DW7272P KW - Fluorouracil KW - U3P01618RT KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Kidney Neoplasms -- drug therapy KW - Kidney Neoplasms -- pathology KW - Drug Administration Schedule KW - Dose-Response Relationship, Drug KW - Neutropenia -- prevention & control KW - Mice KW - Lung -- pathology KW - Mice, Inbred BALB C KW - Leukopenia -- prevention & control KW - Tumor Cells, Cultured KW - Carcinoma -- pathology KW - Fluorouracil -- toxicity KW - Carcinoma -- drug therapy KW - In Vitro Techniques KW - Male KW - Survival Analysis KW - Cyclophosphamide -- analogs & derivatives KW - Interleukin-1 -- administration & dosage KW - Cyclophosphamide -- toxicity KW - Neoplasms, Experimental -- drug therapy KW - Neoplasms, Experimental -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80168297?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Chemoprotective+effects+of+recombinant+human+IL-1+alpha+in+cyclophosphamide-treated+normal+and+tumor-bearing+mice.+Protection+from+acute+toxicity%2C+hematologic+effects%2C+development+of+late+mortality%2C+and+enhanced+therapeutic+efficacy.&rft.au=Futami%2C+H%3BJansen%2C+R%3BMacPhee%2C+M+J%3BKeller%2C+J%3BMcCormick%2C+K%3BLongo%2C+D+L%3BOppenheim%2C+J+J%3BRuscetti%2C+F+W%3BWiltrout%2C+R+H&rft.aulast=Futami&rft.aufirst=H&rft.date=1990-12-15&rft.volume=145&rft.issue=12&rft.spage=4121&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 - 1991-01-28 N1 - Date created - 1991-01-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Inhibition of antibody response to Pseudomonas exotoxin and an immunotoxin containing Pseudomonas exotoxin by 15-deoxyspergualin in mice. AN - 80160068; 2253218 AB - Immunotoxins are potent cell-killing agents that may be useful in the treatment of cancer. The early production of neutralizing antibodies to immunotoxins is one of the major limiting factors for their use in humans. 15-Deoxyspergualin (DSG), a derivative of spergualin, which is a metabolite of Bacillus laterosporus, has been found to have immunosuppressive activity in rodents, dogs, and primates. We examined the suppressive activity of DSG on the antibody response to Pseudomonas exotoxin in mice by enzyme-linked immunosorbent assay. Male BDF1 mice were immunized with a single dose of a nontoxic mutant of Pseudomonas exotoxin (40 micrograms) and then treated with i.p. injections of DSF at a dose of 10 mg/kg for 3 days. Although antibodies to Pseudomonas exotoxin were observed within 7 days in the control group, there was complete suppression of antibody production in the DSG-treated group. Immunosuppression has also been observed in animals immunized with multiple doses (10 mg x 7 d) of Pseudomonas exotoxin and treated with DSG at a dose of 5 mg/kg for 21 days. Similar immunosuppression was observed in mice given multiple doses of the immunotoxin, anti-Tac-LysPE40. We conclude that the immunosuppressive activity of DSG may be useful in increasing the duration of immunotoxin treatment. JF - Cancer research AU - Pai, L H AU - FitzGerald, D J AU - Tepper, M AU - Schacter, B AU - Spitalny, G AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1990/12/15/ PY - 1990 DA - 1990 Dec 15 SP - 7750 EP - 7753 VL - 50 IS - 24 SN - 0008-5472, 0008-5472 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - Guanidines KW - Immunoglobulin G KW - Immunoglobulin M KW - Immunosuppressive Agents KW - Immunotoxins 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 - gusperimus KW - UJ0ZJ76DO9 KW - Index Medicus KW - Recombinant Proteins -- toxicity KW - Mice, Inbred Strains KW - Animals KW - Humans KW - Neutralization Tests KW - Enzyme-Linked Immunosorbent Assay KW - Pseudomonas KW - Mice KW - Immunoglobulin M -- biosynthesis KW - Immunoglobulin G -- biosynthesis KW - Male KW - Cell Line KW - Immunotoxins -- toxicity KW - Exotoxins -- toxicity KW - Exotoxins -- immunology KW - Antibody Formation -- drug effects KW - Immunosuppressive Agents -- pharmacology KW - Guanidines -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80160068?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Inhibition+of+antibody+response+to+Pseudomonas+exotoxin+and+an+immunotoxin+containing+Pseudomonas+exotoxin+by+15-deoxyspergualin+in+mice.&rft.au=Pai%2C+L+H%3BFitzGerald%2C+D+J%3BTepper%2C+M%3BSchacter%2C+B%3BSpitalny%2C+G%3BPastan%2C+I&rft.aulast=Pai&rft.aufirst=L&rft.date=1990-12-15&rft.volume=50&rft.issue=24&rft.spage=7750&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 - 1991-01-23 N1 - Date created - 1991-01-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression of the interleukin 6 receptor and interleukin 6 in prostate carcinoma cells. AN - 80158056; 2253221 AB - We have probed for the presence of interleukin 6 (IL6) receptors in prostatic carcinoma cell lines (LNCaP, DU 145, and PC3) by examining their sensitivity to the cytotoxic effects of a chimeric toxin composed of IL6 and Pseudomonas exotoxin (PE). All three cell lines were killed by IL6-PE66(4)Glu, a version of IL6-PE in which the binding domain of native PE has been mutated to debilitate PE binding to its own receptor. This cytotoxic activity confirmed the presence of IL6 receptors on prostatic carcinoma cells. We have measured the number of IL6 receptors found on these cells and have further determined that they secrete IL6. These data provide evidence that IL6 and its receptor may play an important role in human prostate cancer. JF - Cancer research AU - Siegall, C B AU - Schwab, G AU - Nordan, R P AU - FitzGerald, D J AU - Pastan, I AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1990/12/15/ PY - 1990 DA - 1990 Dec 15 SP - 7786 EP - 7788 VL - 50 IS - 24 SN - 0008-5472, 0008-5472 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - Immunotoxins KW - Interleukin-6 KW - Receptors, Immunologic KW - Receptors, Interleukin-6 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 - Exotoxins -- pharmacology KW - Kinetics KW - Humans KW - Pseudomonas KW - Immunotoxins -- pharmacology KW - Male KW - Cell Line KW - Prostatic Neoplasms -- immunology KW - Cell Survival -- drug effects KW - Receptors, Immunologic -- metabolism KW - Interleukin-6 -- pharmacology KW - Interleukin-6 -- biosynthesis KW - Receptors, Immunologic -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80158056?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Expression+of+the+interleukin+6+receptor+and+interleukin+6+in+prostate+carcinoma+cells.&rft.au=Siegall%2C+C+B%3BSchwab%2C+G%3BNordan%2C+R+P%3BFitzGerald%2C+D+J%3BPastan%2C+I&rft.aulast=Siegall&rft.aufirst=C&rft.date=1990-12-15&rft.volume=50&rft.issue=24&rft.spage=7786&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 - 1991-01-23 N1 - Date created - 1991-01-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Systemic alkalinization inhibits the ability of flavone acetic acid to augment natural killer activity, induce cytokine gene expression, and synergize with interleukin 2 for the treatment of murine renal cancer. AN - 80156454; 2253233 AB - Flavone acetic acid (FAA) is an investigational drug that augments natural killer activity, induces the genes for alpha- and gamma-interferon (IFN) and tumor necrosis factor alpha, and synergizes with recombinant interleukin 2 for the successful treatment of murine renal cancer. However, in most clinical studies of FAA only minimal immunomodulatory effects have been reported. Most of the patients in these studies have also been given sodium bicarbonate to prevent possible nephrotoxicity. The current study was performed to determine whether alkalinization had any effects on FAA-induced immune modulation and therapeutic activity in mice. The results showed that alkalinization inhibited the treatment of murine renal cancer by FAA plus recombinant interleukin 2 such that the survival rate of 84% in nonalkalinized mice was reduced to 0 in mice that were alkalinized during treatment. Alkalinization also significantly inhibited the ability of FAA to augment both splenic and hepatic natural killer activity in a dose-dependent manner. In contrast, alkalinization did not inhibit the ability of polyinosinic:polycytidylic acid and poly-L-lysine stabilized in carboxymethyl cellulose, maleic anhydride divinyl ether, or Propionibacterium acnes to augment liver-associated natural killer activity. By Northern blot analysis, it was shown that the induction of mRNA for IFN-alpha, IFN-gamma, and tumor necrosis factor alpha by FAA in the spleen cells of mice was significantly reduced in alkalinized mice. Consistent with a reduction in the FAA-induced expression of the cytokine genes, alkalinization also resulted in a significant decrease in both the peak serum concentration and duration of detectable IFN activity following FAA treatment. Increasing the dose of FAA in alkalinized mice to 300 mg/kg overcame the deleterious effects of alkalinization for treatment of murine renal cancer by FAA plus recombinant interleukin 2. These results demonstrate that the process of alkalinization inhibits the immunomodulatory and immunotherapeutic effects of FAA in mice and suggest that alkalinization might have similar deleterious effects on FAA-induced immune stimulation in human clinical trials. JF - Cancer research AU - Futami, H AU - Hornung, R L AU - Back, T T AU - Bull, R AU - Gruys, E AU - Wiltrout, R H AD - Division of Cancer Treatment, NCI-FCRDC, Frederick, Maryland 21702. Y1 - 1990/12/15/ PY - 1990 DA - 1990 Dec 15 SP - 7926 EP - 7931 VL - 50 IS - 24 SN - 0008-5472, 0008-5472 KW - Antineoplastic Agents KW - 0 KW - Cytokines KW - Flavonoids KW - Interleukin-2 KW - Recombinant Proteins KW - flavone acetic acid KW - 87626-55-9 KW - Index Medicus KW - Animals KW - Hydrogen-Ion Concentration KW - Mice KW - Cytotoxicity, Immunologic -- drug effects KW - Mice, Inbred BALB C KW - Drug Synergism KW - Recombinant Proteins -- therapeutic use KW - Male KW - Gene Expression -- drug effects KW - Kidney Neoplasms -- drug therapy KW - Cytokines -- genetics KW - Interleukin-2 -- therapeutic use KW - Flavonoids -- pharmacology KW - Antineoplastic Agents -- therapeutic use KW - Adenocarcinoma -- drug therapy KW - Killer Cells, Natural -- immunology KW - Killer Cells, Natural -- drug effects KW - Flavonoids -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80156454?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Systemic+alkalinization+inhibits+the+ability+of+flavone+acetic+acid+to+augment+natural+killer+activity%2C+induce+cytokine+gene+expression%2C+and+synergize+with+interleukin+2+for+the+treatment+of+murine+renal+cancer.&rft.au=Futami%2C+H%3BHornung%2C+R+L%3BBack%2C+T+T%3BBull%2C+R%3BGruys%2C+E%3BWiltrout%2C+R+H&rft.aulast=Futami&rft.aufirst=H&rft.date=1990-12-15&rft.volume=50&rft.issue=24&rft.spage=7926&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 - 1991-01-23 N1 - Date created - 1991-01-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression of the O6-methylguanine-DNA methyltransferase gene MGMT in MER+ and MER- human tumor cells. AN - 80154381; 2253230 AB - DNA probes prepared from human O6-methylguanine-DNA methyltransferase complementary DNA were hybridized to mRNA isolated from human liver and fifteen human tumor cell lines proficient (Mer+) or deficient (Mer-) in transferase activity. Liver and Mer+ cells contained levels of transferase-specific mRNA that correlated with their transferase activity levels, whereas Mer- cells contained undetectable amounts of transferase mRNA. The mRNA levels were not induced in human cells by treatments that induce other DNA damage-inducible genes. These results demonstrate that in human cells the transferase gene is constitutively expressed, that its expression is related to activity levels, and that in Mer- tumor cells the expression of the transferase gene is probably blocked at the level of mRNA production. JF - Cancer research AU - Fornace, A J AU - Papathanasiou, M A AU - Hollander, M C AU - Yarosh, D B AD - Laboratory of Molecular Pharmacology, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1990/12/15/ PY - 1990 DA - 1990 Dec 15 SP - 7908 EP - 7911 VL - 50 IS - 24 SN - 0008-5472, 0008-5472 KW - MGMT KW - RNA, Messenger KW - 0 KW - Methylnitronitrosoguanidine KW - 12H3O2UGSF KW - Methyl Methanesulfonate KW - AT5C31J09G KW - Methyltransferases KW - EC 2.1.1.- KW - O(6)-Methylguanine-DNA Methyltransferase KW - EC 2.1.1.63 KW - Index Medicus KW - Gene Expression -- drug effects KW - Humans KW - RNA, Messenger -- drug effects KW - RNA, Messenger -- radiation effects KW - RNA, Messenger -- genetics KW - Methyl Methanesulfonate -- pharmacology KW - Phenotype KW - X-Rays KW - Neoplasms KW - Methylnitronitrosoguanidine -- pharmacology KW - Cell Line KW - Gene Expression -- radiation effects KW - Methyltransferases -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80154381?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Expression+of+the+O6-methylguanine-DNA+methyltransferase+gene+MGMT+in+MER%2B+and+MER-+human+tumor+cells.&rft.au=Fornace%2C+A+J%3BPapathanasiou%2C+M+A%3BHollander%2C+M+C%3BYarosh%2C+D+B&rft.aulast=Fornace&rft.aufirst=A&rft.date=1990-12-15&rft.volume=50&rft.issue=24&rft.spage=7908&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 - 1991-01-23 N1 - Date created - 1991-01-23 N1 - Date revised - 2017-01-13 N1 - Gene symbol - MGMT N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mechanism of the cardiovascular effects of GABAB receptor activation in the nucleus tractus solitarii of the rat. AN - 80276284; 1963570 AB - The effects of baclofen microinjected into the nucleus tractus solitarii (NTS) on blood pressure, heart rate and baroreflex bradycardia were studied in urethane-anesthetized rats. Baclofen caused dose-dependent pressor and tachycardic effects and inhibited the reflex bradycardia elicited by i.v. phenylephrine. The effects of baclofen were inhibited by similarly administered GABAB receptor antagonists, phaclofen and 2-OH-saclofen, or the non-NMDA glutamate receptor antagonist, DNQX, or by pretreatment of rats with intracisternally administered pertussis toxin. DNQX and pertussis toxin, but not the NMDA antagonist, MK-801, also inhibited baroreflex bradycardia. Intra-NTS injections of glutamate caused hypotension and bradycardia, which were potentiated by baclofen, and were not affected by either DNQX or MK-801 or by pretreatment with pertussis toxin. These findings indicate that the cardiovascular effects of stimulation of GABAB receptors in the NTS are due, at least in part, to inhibition of the depressor baroreflex response. Inhibition of the release and/or postsynaptic action of an excitatory amino acid transmitter other than glutamate is the most likely mechanism. JF - Brain research AU - Florentino, A AU - Varga, K AU - Kunos, G AD - Laboratory of Physiological and Pharmacological Studies, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892. Y1 - 1990/12/10/ PY - 1990 DA - 1990 Dec 10 SP - 264 EP - 270 VL - 535 IS - 2 SN - 0006-8993, 0006-8993 KW - Quinoxalines KW - 0 KW - Receptors, GABA-A KW - Virulence Factors, Bordetella KW - 2-hydroxysaclofen KW - 117354-64-0 KW - Urethane KW - 3IN71E75Z5 KW - FG 9041 KW - 62T278S1MX KW - Dizocilpine Maleate KW - 6LR8C1B66Q KW - Pertussis Toxin KW - EC 2.4.2.31 KW - Baclofen KW - H789N3FKE8 KW - Index Medicus KW - Animals KW - Dose-Response Relationship, Drug KW - Baclofen -- analogs & derivatives KW - Microinjections KW - Pressoreceptors -- drug effects KW - Dizocilpine Maleate -- pharmacology KW - Rats, Inbred Strains KW - Rats KW - Virulence Factors, Bordetella -- pharmacology KW - Heart Rate -- drug effects KW - Anesthesia KW - Blood Pressure -- drug effects KW - Quinoxalines -- pharmacology KW - Baclofen -- pharmacology KW - Male KW - Hemodynamics -- physiology KW - Receptors, GABA-A -- physiology KW - Medulla Oblongata -- physiology KW - Receptors, GABA-A -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80276284?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mechanism+of+the+cardiovascular+effects+of+GABAB+receptor+activation+in+the+nucleus+tractus+solitarii+of+the+rat.&rft.au=Florentino%2C+A%3BVarga%2C+K%3BKunos%2C+G&rft.aulast=Florentino&rft.aufirst=A&rft.date=1990-12-10&rft.volume=535&rft.issue=2&rft.spage=264&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 - 1991-04-16 N1 - Date created - 1991-04-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Mutagenesis of lysine 460 in the human insulin receptor. Effects upon receptor recycling and cooperative interactions among binding sites. AN - 80152256; 2123490 AB - Mutations in the insulin receptor gene can cause insulin resistance. Previously, we have identified a mutation substituting glutamic acid for lysine at position 460 in the alpha-subunit of the insulin receptor in a patient with a genetic form of insulin resistance. In the present work, we have investigated the effect upon receptor function of amino acid substitutions at position 460. Decreasing the pH from 8.0 to 5.5 caused a progressive acceleration of the dissociation of 125I-insulin from the wild-type insulin receptor. Substitution of acidic amino acids (Glu or Asp) for Lys460 decreased the ability of acid pH to accelerate dissociation of 125I-insulin. In contrast, substitution of Arg or neutral amino acids (Val, Met, Thr, or Gln) had no effect upon the sensitivity to acid pH. Correlated with decreased sensitivity to acid pH, substitution of Glu or Asp at position 460 retarded the dissociation of 125I-insulin from intracellular receptors subsequent to receptor-mediated endocytosis. Furthermore, retardation of dissociation of 125I-insulin from the internalized receptor was associated with a decreased half-life of the receptor. In summary, the Glu460 mutation appears to cause insulin resistance by accelerating receptor degradation and, thereby, decreasing the number of insulin receptors on the cell surface. Additional studies suggested that Lys460 may provide the amino groups whereby disuccinimidyl suberate cross-links the two alpha-subunits to each other. Consistent with the hypothesis that Lys460 is located at the interface between adjacent alpha-subunits, substitutions at position 460 impair cooperative interactions among insulin binding sites. The Glu460 mutation decreases positively cooperative binding interactions; the Arg460 mutation impairs negative cooperativity. Mutations at position 460 in the alpha-subunit did not decrease the ability of insulin to stimulate receptor tyrosine kinase. JF - The Journal of biological chemistry AU - Kadowaki, H AU - Kadowaki, T AU - Cama, A AU - Marcus-Samuels, B AU - Rovira, A AU - Bevins, C L AU - Taylor, S I AD - Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Disease, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1990/12/05/ PY - 1990 DA - 1990 Dec 05 SP - 21285 EP - 21296 VL - 265 IS - 34 SN - 0021-9258, 0021-9258 KW - Insulin KW - 0 KW - Macromolecular Substances KW - Receptor, Insulin KW - EC 2.7.10.1 KW - Lysine KW - K3Z4F929H6 KW - Index Medicus KW - Animals KW - Genes KW - Thermodynamics KW - Transfection KW - Kinetics KW - Humans KW - Insulin -- metabolism KW - Mice KW - Insulin -- pharmacology KW - Amino Acid Sequence KW - Cell Line KW - Mathematics KW - Binding Sites KW - Mutagenesis, Site-Directed KW - Receptor, Insulin -- genetics KW - Receptor, Insulin -- drug effects KW - Receptor, Insulin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80152256?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+lysine+460+in+the+human+insulin+receptor.+Effects+upon+receptor+recycling+and+cooperative+interactions+among+binding+sites.&rft.au=Kadowaki%2C+H%3BKadowaki%2C+T%3BCama%2C+A%3BMarcus-Samuels%2C+B%3BRovira%2C+A%3BBevins%2C+C+L%3BTaylor%2C+S+I&rft.aulast=Kadowaki&rft.aufirst=H&rft.date=1990-12-05&rft.volume=265&rft.issue=34&rft.spage=21285&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 - 1991-01-17 N1 - Date created - 1991-01-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The enzymes of detoxication. AN - 80147838; 2249981 JF - The Journal of biological chemistry AU - Jakoby, W B AU - Ziegler, D M AD - Laboratory of Biochemistry, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1990/12/05/ PY - 1990 DA - 1990 Dec 05 SP - 20715 EP - 20718 VL - 265 IS - 34 SN - 0021-9258, 0021-9258 KW - Mixed Function Oxygenases KW - EC 1.- KW - Methyltransferases KW - EC 2.1.1.- KW - Glutathione Transferase KW - EC 2.5.1.18 KW - Sulfotransferases KW - EC 2.8.2.- KW - Index Medicus KW - Animals KW - Humans KW - Sulfotransferases -- metabolism KW - Mixed Function Oxygenases -- metabolism KW - Inactivation, Metabolic KW - Microsomes, Liver -- enzymology KW - Glutathione Transferase -- metabolism KW - Methyltransferases -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80147838?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=The+enzymes+of+detoxication.&rft.au=Jakoby%2C+W+B%3BZiegler%2C+D+M&rft.aulast=Jakoby&rft.aufirst=W&rft.date=1990-12-05&rft.volume=265&rft.issue=34&rft.spage=20715&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 - 1991-01-17 N1 - Date created - 1991-01-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Guanine nucleotide-dependent ADP-ribosylation of soluble rho catalyzed by Clostridium botulinum C3 ADP-ribosyltransferase. Isolation and characterization of a newly recognized form of rhoA. AN - 80143873; 2174426 AB - Two C3 ADP-ribosyltransferase substrates with different characteristics were isolated from bovine brain cytosol. Amino acid sequences of tryptic peptides from the two substrates were identical to rhoA and rhoB; hence, the purified proteins are referred to as rhoA* and rhoB*, respectively. Soluble rhoA* exhibits properties different from those previously reported for rho proteins. In contrast to other C3 substrates, rhoA* behaved as a 77-80-kDa protein on gel filtration, although on sodium dodecyl sulfate-polyacrylamide gel electrophoresis the ADP-ribosylated moiety had a mobility consistent with a 21.5-kDa protein. Furthermore, C3-catalyzed ADP-ribosylation of rhoA* was dependent on guanine nucleotides in the presence of 1 mM Mg2+ or 1 mM EDTA (0.19 microM free Mg2+). Half-maximal stimulation by GTP, guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S), guanylyl-imidodiphosphate (Gpp(NH)p), and GDP was observed at 16, 20, 220, and 380 nM, respectively; guanosine 5'-O-(2-thiodiphosphate), GMP, and adenine nucleotides were ineffective. In the presence of GTP gamma S, the rate and extent of ADP-ribosylation was enhanced by dimyristoylphosphatidylcholine and/or cholate. This increase in ADP-ribosylation was specific for rhoA*; it was not observed with rhoB* and has not been reported for other C3 substrates. These distinct properties suggest that rhoA* is a newly recognized type of C3 substrate, differing from the rhoA-like proteins previously reported. rhoB*, on the other hand, has properties similar to those reported for membrane-associated rhoB and its ADP-ribosylation was independent of guanine nucleotides in the presence of 1 mM Mg2+ and not affected by dimyristoylphosphatidylcholine and/or cholate. JF - The Journal of biological chemistry AU - Williamson, K C AU - Smith, L A 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 - 1990/12/05/ PY - 1990 DA - 1990 Dec 05 SP - 20807 EP - 20812 VL - 265 IS - 34 SN - 0021-9258, 0021-9258 KW - Cholic Acids KW - 0 KW - Hydroxyapatites KW - Membrane Proteins KW - Peptide Fragments KW - Guanosine 5'-O-(3-Thiotriphosphate) KW - 37589-80-3 KW - Adenosine Diphosphate KW - 61D2G4IYVH KW - Durapatite KW - 91D9GV0Z28 KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - exoenzyme C3, Clostridium botulinum KW - Botulinum Toxins KW - EC 3.4.24.69 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - rhoB GTP-Binding Protein KW - EC 3.6.5.2 KW - Cholic Acid KW - G1JO7801AE KW - Dimyristoylphosphatidylcholine KW - U86ZGC74V5 KW - Index Medicus KW - Sequence Homology, Nucleic Acid KW - Chromatography KW - Cholic Acids -- pharmacology KW - Peptide Fragments -- isolation & purification KW - Amino Acid Sequence KW - Chromatography, Ion Exchange KW - Guanosine 5'-O-(3-Thiotriphosphate) -- pharmacology KW - Molecular Weight KW - Chromatography, Gel KW - Dimyristoylphosphatidylcholine -- pharmacology KW - Kinetics KW - Molecular Sequence Data KW - Adenosine Diphosphate -- metabolism KW - Membrane Proteins -- metabolism KW - GTP-Binding Proteins -- metabolism KW - GTP-Binding Proteins -- isolation & purification KW - ADP Ribose Transferases -- metabolism KW - Membrane Proteins -- genetics KW - GTP-Binding Proteins -- genetics KW - Clostridium botulinum -- enzymology KW - Membrane Proteins -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80143873?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Guanine+nucleotide-dependent+ADP-ribosylation+of+soluble+rho+catalyzed+by+Clostridium+botulinum+C3+ADP-ribosyltransferase.+Isolation+and+characterization+of+a+newly+recognized+form+of+rhoA.&rft.au=Williamson%2C+K+C%3BSmith%2C+L+A%3BMoss%2C+J%3BVaughan%2C+M&rft.aulast=Williamson&rft.aufirst=K&rft.date=1990-12-05&rft.volume=265&rft.issue=34&rft.spage=20807&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 - 1991-01-17 N1 - Date created - 1991-01-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cooperative interaction of nuclear factor-kappa B- and cis-regulatory enhancer binding protein-like factor binding elements in activating the interleukin-8 gene by pro-inflammatory cytokines. AN - 80142113; 2250017 AB - A novel cytokine, interleukin-8 (IL-8), may play major roles in the inflammatory process by recruiting neutrophils and T cells into inflammatory sites. The production of this cytokine is not constitutive and is induced in a variety of cell types by stimulation with mitogens and cytokines. Among cytokines, only IL-1 and tumor necrosis factor (TNF) can induce IL-8 gene expression at the transcriptional level. Transfection of a human fibrosarcoma cell line with chloramphenicol acetyltransferase expression plasmids linked to a 5'-flanking deletion mutants of the IL-8 gene demonstrated that the nucleotides between -94 and -71 base pairs from the start of the first exon are essential and sufficient for the IL-8 induction by either IL-1, TNF, or phorbol 12-myristate 13-acetate. This sequence is composed of two cis-elements; one is the potential binding site for a nuclear factor-kappa B-like factor and the other for a cis-regulatory enhancer binding protein-like factor. Mutations in either elements abolished IL-1, TNF, and phorbol 12-myristate 13-acetate responsiveness. This report provides the first evidence that cooperation between two distinct cis-elements may be required for induction of gene expression by either IL-1 or TNF. JF - The Journal of biological chemistry AU - Mukaida, N AU - Mahe, Y AU - Matsushima, K AD - Biological Response Modifiers Program, National Cancer Institute-Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1990/12/05/ PY - 1990 DA - 1990 Dec 05 SP - 21128 EP - 21133 VL - 265 IS - 34 SN - 0021-9258, 0021-9258 KW - CCAAT-Enhancer-Binding Proteins KW - 0 KW - Cytokines KW - DNA-Binding Proteins KW - Interleukin-1 KW - Interleukin-8 KW - NF-kappa B KW - Nuclear Proteins KW - Oligonucleotide Probes KW - Recombinant Proteins KW - Tumor Necrosis Factor-alpha KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Interleukin-1 -- pharmacology KW - Recombinant Proteins -- pharmacology KW - Cell Nucleus -- metabolism KW - Exons KW - Humans KW - Tumor Necrosis Factor-alpha -- pharmacology KW - Cell Nucleus -- drug effects KW - Inflammation KW - Mutagenesis, Site-Directed KW - Base Sequence KW - Transfection KW - Molecular Sequence Data KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Cell Line KW - Cytokines -- pharmacology KW - Enhancer Elements, Genetic KW - Interleukin-8 -- genetics KW - Gene Expression Regulation -- drug effects KW - Nuclear Proteins -- metabolism KW - NF-kappa B -- metabolism KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80142113?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cooperative+interaction+of+nuclear+factor-kappa+B-+and+cis-regulatory+enhancer+binding+protein-like+factor+binding+elements+in+activating+the+interleukin-8+gene+by+pro-inflammatory+cytokines.&rft.au=Mukaida%2C+N%3BMahe%2C+Y%3BMatsushima%2C+K&rft.aulast=Mukaida&rft.aufirst=N&rft.date=1990-12-05&rft.volume=265&rft.issue=34&rft.spage=21128&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 - 1991-01-17 N1 - Date created - 1991-01-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Berberine-induced morphologic differentiation and down-regulation of c-Ki-ras2 protooncogene expression in human teratocarcinoma cells. AN - 80195227; 2265407 AB - A pluripotent human teratocarcinoma cell clone, NT2/D1, which was derived from the Tera-2 cell line, was induced to differentiate into cells with neuronal cell morphology by treatment with berberine. As early as 1 day after a 24-h treatment of cells with berberine at a non-toxic dose of 0.1 mg/ml in culture medium, the cells started to show morphologic changes, developing into terminally differentiated neuronal cells with long, inter-connecting network-like cellular structures. This process is much faster as compared with that induced by treatment with retinoic acid (RA), which took at least several days to develop. Unlike RA, berberine could not induce murine teratocarcinoma cell line, F9, to differentiate into endodermal cells. It was also found that, although the NT2/D1 cell clone exhibited amplification and enhanced mRNA expression of c-Ki-ras2 gene as did the parent cell line, a marked down-regulation of c-Ki-ras2 mRNA expression was observed. However, there was no change in actin mRNA expression even after differentiation had occurred. Thus, morphologic differentiation of teratocarcinoma cells into neuronal cells is found to be associated with down-regulation of a protooncogene which plays some definite role in oncogenesis. The mechanism by which berberine induces differentiation in these cells needs further investigation. JF - Cancer letters AU - Chang, K S AU - Gao, C AU - Wang, L C AD - Laboratory of Cellular Oncology, National Cancer Institute, NIH, Bethesda, MD 20892. Y1 - 1990/12/03/ PY - 1990 DA - 1990 Dec 03 SP - 103 EP - 108 VL - 55 IS - 2 SN - 0304-3835, 0304-3835 KW - c-Ki-ras2 KW - Berberine KW - 0I8Y3P32UF KW - Index Medicus KW - Gene Expression -- drug effects KW - Animals KW - Oncogenes -- genetics KW - Tumor Cells, Cultured KW - Humans KW - Mice KW - Gene Amplification KW - Berberine -- pharmacology KW - Teratoma -- genetics KW - Down-Regulation -- genetics KW - Teratoma -- pathology KW - Proto-Oncogenes -- genetics KW - Down-Regulation -- drug effects KW - Cell Differentiation -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80195227?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Berberine-induced+morphologic+differentiation+and+down-regulation+of+c-Ki-ras2+protooncogene+expression+in+human+teratocarcinoma+cells.&rft.au=Chang%2C+K+S%3BGao%2C+C%3BWang%2C+L+C&rft.aulast=Chang&rft.aufirst=K&rft.date=1990-12-03&rft.volume=55&rft.issue=2&rft.spage=103&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 - 1991-02-12 N1 - Date created - 1991-02-12 N1 - Date revised - 2017-01-13 N1 - Gene symbol - c-Ki-ras2 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Adjuvant therapy in breast cancer. AN - 80372243; 2099836 JF - Current opinion in oncology AU - Dorr, A AD - National Institutes of Health, Bethesda, Maryland. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 1049 EP - 1052 VL - 2 IS - 6 SN - 1040-8746, 1040-8746 KW - Adjuvants, Pharmaceutic KW - 0 KW - Tamoxifen KW - 094ZI81Y45 KW - Vincristine KW - 5J49Q6B70F KW - Doxorubicin KW - 80168379AG KW - Cyclophosphamide KW - 8N3DW7272P KW - Cisplatin KW - Q20Q21Q62J KW - Melphalan KW - Q41OR9510P KW - Fluorouracil KW - U3P01618RT KW - Prednisone KW - VB0R961HZT KW - Methotrexate KW - YL5FZ2Y5U1 KW - Index Medicus KW - Fluorouracil -- administration & dosage KW - Cyclophosphamide -- administration & dosage KW - Tamoxifen -- therapeutic use KW - Humans KW - Vincristine -- administration & dosage KW - Melphalan -- therapeutic use KW - Doxorubicin -- administration & dosage KW - Methotrexate -- administration & dosage KW - Tamoxifen -- administration & dosage KW - Prednisone -- administration & dosage KW - Female KW - Cisplatin -- administration & dosage KW - Breast Neoplasms -- drug therapy KW - Breast Neoplasms -- surgery KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Breast Neoplasms -- radiotherapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80372243?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+opinion+in+oncology&rft.atitle=Adjuvant+therapy+in+breast+cancer.&rft.au=Dorr%2C+A&rft.aulast=Dorr&rft.aufirst=A&rft.date=1990-12-01&rft.volume=2&rft.issue=6&rft.spage=1049&rft.isbn=&rft.btitle=&rft.title=Current+opinion+in+oncology&rft.issn=10408746&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-08-09 N1 - Date created - 1991-08-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The carcinogenic activity of commercial grade toluene diisocyanate in rats and mice in relation to the metabolism of the 2,4- and 2,6-TDI isomers. AN - 80348135; 1965872 AB - Groups of 50 F344/N rats of each sex and 50 B6C3F1 mice of each sex were gavaged with corn oil or a mixture of toluene diisocyanate (TDI) in corn oil for 5 days per week for 105 or 106 weeks. Female rats and mice were given doses of 60 or 120 mg/kg body weight, while male rats received 30 or 60 mg/kg, and male mice received 120 or 240 mg/kg. The TDI reacted with the moisture in the corn oil vehicle resulting in doses that were 10% to 23% below the target dose concentrations. The chemical product used was commercial grade TDI, which was an 80%-20% mixture of the 2,4- and 2,6-isomers. Chemical disposition and metabolism studies were conducted with each of the radiolabelled TDI isomers in male rats. Absorption of both of the TDI isomers occurred, with the highest concentrations found in the stomach, cecum, large intestine, and bladder. Excretion occurred via the feces and urine. The major metabolic products from the metabolism of 2,4-TDI were shown to be identical with those from the metabolism of the carcinogen, 2,4-diaminotoluene, whereas the metabolism of the 2,6-TDI isomer yielded one major product, identified as 2,6-bis(acetylamino)toluene. Greater than 10% depression in body weight gain occurred in all dosed groups of rats throughout most of the study. The major non-neoplastic lesions that were observed in both sexes of the TDI-exposed rats were dose-related increases in acute broncho-pneumonia, characterized as chemical pneumonitis, with incidences as high as 50%. In mice mean body weight gain was depressed in dosed male and in high dose females. The principle non-neoplastic lesion in mice that was attributed to chemical treatment was cytomegaly of the kidney tubular epithelium in males. Survival in all groups of dosed rats was significantly lower than in controls. A dose-dependent pattern of mortality did not commence until 70 weeks of exposure, demonstrating that toluene diisocyanate elicited a cumulative toxic response. There was also significantly lower survival in high dose male, but not female mice, by comparison to controls. Despite the reduction of power and sensitivity in the rat studies caused by early mortality, statistically significant increases in tumor incidences were observed in many different target organs. TDI was carcinogenic in F344/N rats, causing subcutaneous fibromas and fibrosarcomas in males and females, pancreatic acinar cell adenomas in males, and pancreatic islet cell adenomas, neoplastic nodules of the liver, and mammary gland tumors in females.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Toxicology and industrial health AU - Dieter, M P AU - Boorman, G A AU - Jameson, C W AU - Matthews, H B AU - Huff, J E AD - National Institutes of Health, National Institute of Environmental Health Sciences, National Toxicology Program, Research Triangle Park, NC 27709. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 599 EP - 621 VL - 6 IS - 6 SN - 0748-2337, 0748-2337 KW - Carcinogens KW - 0 KW - Phenylenediamines KW - Toluene 2,4-Diisocyanate KW - 17X7AFZ1GH KW - 2,6-diaminotoluene KW - H838Q10551 KW - 2,4-diaminotoluene KW - IS1AKN4HYB KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Mice, Inbred Strains KW - Animals KW - Phenylenediamines -- toxicity KW - Neoplasms, Experimental -- chemically induced KW - Dose-Response Relationship, Drug KW - Body Weight -- drug effects KW - Mice KW - Male KW - Female KW - Survival Analysis KW - Toluene 2,4-Diisocyanate -- toxicity KW - Carcinogens -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80348135?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+industrial+health&rft.atitle=The+carcinogenic+activity+of+commercial+grade+toluene+diisocyanate+in+rats+and+mice+in+relation+to+the+metabolism+of+the+2%2C4-+and+2%2C6-TDI+isomers.&rft.au=Dieter%2C+M+P%3BBoorman%2C+G+A%3BJameson%2C+C+W%3BMatthews%2C+H+B%3BHuff%2C+J+E&rft.aulast=Dieter&rft.aufirst=M&rft.date=1990-12-01&rft.volume=6&rft.issue=6&rft.spage=599&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+industrial+health&rft.issn=07482337&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-07-23 N1 - Date created - 1991-07-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Toxicol Ind Health. 1991 Jul;7(4):327-31 [1663667] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Growth factors specifically alter hair follicle cell proliferation and collagenolytic activity alone or in combination. AN - 80337454; 1965309 AB - A three-dimensional culture model for isolated murine pelage hair follicles in a type I collagen gel has been utilized to study the effects of selected growth factors on follicle cell proliferation and release of collagenolytic factors. Cultured follicle organoids differentially express cytokeratins 6 and 14 in a pattern suggesting they contain cells of the outer root sheath, inner root sheath and follicle matrix. Using incorporation of [3H]thymidine as a measure of proliferation, follicle organoids show a peak of DNA synthesis between day 1 and 5 of culture, depending on plating density, and then have a low rate of DNA synthesis. Thymidine incorporation is stimulated by transforming growth factor-alpha (TGF-alpha) in a dose-dependent response. Only peripheral cells presumably of the outer root sheath, incorporate thymidine in basal or stimulated conditions. TGF-beta 1 and TGF-beta 2 inhibit constitutive cell proliferation and oppose growth stimulation by TGF-alpha. Hair follicles lyse the collagen gel matrix when exposed to certain cytokines. Epidermal growth factor (EGF) and TGF-alpha stimulate gel lysis, but TGF-beta 1, TGF-beta 2 and cholera toxin do not. Other skin-derived cells, such as interfollicular epidermal cells, dermal fibroblasts, or combinations thereof, do not lyse gels in this culture model even when exposed to growth factors. Combinations of EGF or TGF-alpha with TGF-beta 1 or TGF-beta 2 are synergistic for collagenase release. These cytokines stimulate release of multiple species of matrix metalloproteinases, but the 92-kDa and 72 kDa type IV procollagenases and their activated derivatives predominate on zymograms. In cytokine-stimulated follicles, both peripheral and centrally located cells in the organoids express the 72-kDa type IV collagenase and a similar immunostaining pattern is present in developing follicles in vivo. Thus growth factors appear to work in concert for certain hair follicle responses and in opposition for others. These combined actions may play a role in different phases of hair follicle development that require cell replication and invasion into the deeper dermis. JF - Differentiation; research in biological diversity AU - Weinberg, W C AU - Brown, P D AU - Stetler-Stevenson, W G AU - Yuspa, S H AD - Laboratory of Cellular Carcinogenesis, National Cancer Institute Bethesda, MD 20892. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 168 EP - 178 VL - 45 IS - 3 SN - 0301-4681, 0301-4681 KW - Transforming Growth Factor beta KW - 0 KW - Epidermal Growth Factor KW - 62229-50-9 KW - Collagen KW - 9007-34-5 KW - DNA KW - 9007-49-2 KW - Microbial Collagenase KW - EC 3.4.24.3 KW - Thymidine KW - VC2W18DGKR KW - Index Medicus KW - Thymidine -- metabolism KW - Microbial Collagenase -- analysis KW - Animals KW - Humans KW - Cell Division -- drug effects KW - Mice KW - DNA -- biosynthesis KW - Hair -- drug effects KW - Transforming Growth Factor beta -- pharmacology KW - Collagen -- metabolism KW - Hair -- metabolism KW - Epidermal Growth Factor -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80337454?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Differentiation%3B+research+in+biological+diversity&rft.atitle=Growth+factors+specifically+alter+hair+follicle+cell+proliferation+and+collagenolytic+activity+alone+or+in+combination.&rft.au=Weinberg%2C+W+C%3BBrown%2C+P+D%3BStetler-Stevenson%2C+W+G%3BYuspa%2C+S+H&rft.aulast=Weinberg&rft.aufirst=W&rft.date=1990-12-01&rft.volume=45&rft.issue=3&rft.spage=168&rft.isbn=&rft.btitle=&rft.title=Differentiation%3B+research+in+biological+diversity&rft.issn=03014681&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-06-04 N1 - Date created - 1991-06-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Hormonal regulation of glucose transport in rat adipose cells. AN - 80326510; 2088820 JF - Biochemical Society transactions AU - Simpson, I A AU - Cushman, S W AU - Egan, J J AU - Habberfield, A D AU - Londos, C AU - Nishimura, H AU - Saltis, J AD - Experimental Diabetes, Metabolism and Nutrition Section, NIDDK, National Institutes of Health, Bethesda, MD 20892. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 1123 EP - 1125 VL - 18 IS - 6 SN - 0300-5127, 0300-5127 KW - Hormones KW - 0 KW - Insulin KW - Monosaccharide Transport Proteins KW - Vasopressins KW - 11000-17-2 KW - Glucose KW - IY9XDZ35W2 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Biological Transport, Active -- drug effects KW - Animals KW - Monosaccharide Transport Proteins -- metabolism KW - In Vitro Techniques KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Vasopressins -- pharmacology KW - Lipolysis -- drug effects KW - Insulin -- pharmacology KW - Male KW - Adipose Tissue -- metabolism KW - Hormones -- pharmacology KW - Glucose -- metabolism KW - Adipose Tissue -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80326510?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Hormonal+regulation+of+glucose+transport+in+rat+adipose+cells.&rft.au=Simpson%2C+I+A%3BCushman%2C+S+W%3BEgan%2C+J+J%3BHabberfield%2C+A+D%3BLondos%2C+C%3BNishimura%2C+H%3BSaltis%2C+J&rft.aulast=Simpson&rft.aufirst=I&rft.date=1990-12-01&rft.volume=18&rft.issue=6&rft.spage=1123&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 - 1991-05-30 N1 - Date created - 1991-05-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Potentiation by salicylate and salicyl alcohol of cadmium toxicity and accumulation in Escherichia coli. AN - 80318918; 2088194 AB - The toxicity of Cd2+ in Escherichia coli K-12 was potentiated by salicylate and several related compounds. The efficiency of plating on Luria broth plates was reduced by more than 10(5)-fold when 10 mM salicylate and 200 microM CdCl2 were present simultaneously but was unaffected when either compound was present by itself. Synergistic effects were found at pH 7.4 with certain other weak acids (acetyl salicylate [aspirin], benzoate, and cinnamate) and with a nonacidic salicylate analog, salicyl alcohol, but not with acetate or p-hydroxy benzoate. Thus, the synergism with Cd2+ is determined by the structure of the compounds and not merely by their acidity. The kinetics of 109Cd2+ uptake by cells grown and assayed in broth indicated the presence of two uptake systems with Kms of 1 and 52 microM Cd2+ and Vmaxs of 0.059 and 1.5 mumol of Cd2+ per min per g of cells, respectively. The kinetics of uptake for cells grown and assayed with 20 mM salicyl alcohol showed 2.5-fold increases in the Vmaxs of both systems but no change in the Kms. Salicylate-grown cells also exhibited increased rates of 109Cd2+ uptake by both systems. Thus, enhanced uptake of Cd2+ may be responsible for the potentiation of Cd2+ toxicity by salicylate and salicyl alcohol. JF - Antimicrobial agents and chemotherapy AU - Rosner, J L AU - Aumercier, M AD - Laboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 2402 EP - 2406 VL - 34 IS - 12 SN - 0066-4804, 0066-4804 KW - Acetates KW - 0 KW - Benzyl Alcohols KW - Cadmium Radioisotopes KW - Culture Media KW - Salicylates KW - Cadmium KW - 00BH33GNGH KW - salicyl alcohol KW - FA1N0842KB KW - Salicylic Acid KW - O414PZ4LPZ KW - Index Medicus KW - Kinetics KW - Hydrogen-Ion Concentration KW - Membrane Potentials -- drug effects KW - Drug Synergism KW - Acetates -- pharmacology KW - Cadmium -- metabolism KW - Escherichia coli -- metabolism KW - Escherichia coli -- drug effects KW - Cadmium -- toxicity KW - Benzyl Alcohols -- pharmacology KW - Salicylates -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80318918?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+acids+research&rft.atitle=An+Alu+polymorphism+intragenic+to+the+TP53+gene.&rft.au=Futreal%2C+P+A%3BBarrett%2C+J+C%3BWiseman%2C+R+W&rft.aulast=Futreal&rft.aufirst=P&rft.date=1991-12-25&rft.volume=19&rft.issue=24&rft.spage=6977&rft.isbn=&rft.btitle=&rft.title=Nucleic+acids+research&rft.issn=03051048&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-05-20 N1 - Date created - 1991-05-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Bacteriol. 1987 Jan;169(1):26-32 [3539918] Proc Natl Acad Sci U S A. 1985 Dec;82(24):8771-4 [3909154] J Bacteriol. 1988 Feb;170(2):598-604 [3276661] Antimicrob Agents Chemother. 1989 Feb;33(2):230-2 [2655531] Antimicrob Agents Chemother. 1989 Apr;33(4):412-7 [2658790] Antimicrob Agents Chemother. 1989 Sep;33(9):1549-52 [2684011] Antimicrob Agents Chemother. 1990 May;34(5):786-91 [2193619] Biol Rev Camb Philos Soc. 1966 Aug;41(3):445-502 [5329743] J Bacteriol. 1975 Mar;121(3):1180-8 [1090597] J Bacteriol. 1978 Jan;133(1):75-80 [338598] J Bacteriol. 1980 Aug;143(2):926-33 [6259126] J Bacteriol. 1981 Mar;145(3):1196-208 [7009571] J Bacteriol. 1981 Mar;145(3):1209-21 [7009572] Appl Environ Microbiol. 1981 Jan;41(1):46-50 [7013701] J Mol Biol. 1981 Jun 25;149(2):241-57 [6796698] Antimicrob Agents Chemother. 1981 Dec;20(6):803-8 [6173015] J Bacteriol. 1982 Oct;152(1):384-99 [6749812] Plasmid. 1982 Jul;8(1):86-8 [6755512] Biochemistry. 1982 Oct 26;21(22):5534-8 [6293545] Antimicrob Agents Chemother. 1983 Jun;23(6):835-45 [6351731] Mol Gen Genet. 1984;193(2):340-8 [6319971] J Bacteriol. 1984 Dec;160(3):1188-90 [6389510] J Bacteriol. 1985 Jun;162(3):1100-5 [3888954] J Bacteriol. 1987 Jul;169(7):3001-6 [2954947] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A critical review of the developmental toxicity and teratogenicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin: recent advances toward understanding the mechanism. AN - 80316992; 2087682 AB - A specific teratogenic response is elicited in the mouse as a result of exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; dioxin). The characteristic spectrum of structural malformations induced in mice following exposure to TCDD and structurally related congeners is highly reproducible and includes both hydronephrosis and cleft palate. In addition, prenatal exposure to TCDD has been shown to induce thymic hypoplasia. These three abnormalities occur at doses well below those producing maternal or embryo/fetal toxicity and are thus among the most sensitive indicators of dioxin toxicity. In all other laboratory species tested, TCDD causes maternal and embryo/fetal toxicity but does not induce a significant increase in the incidence of structural abnormalities even at toxic dose levels. Developmental toxicity occurs in a similar dose range across species; however, mice are particularly susceptible to development of TCDD-induced terata. Recent experiments using an organ culture were an attempt to address the issue of species and organ differences in sensitivity to TCDD. Human palatal shelves examined in this in vitro system were found to approximate the rat in terms of sensitivity for induction of cleft palate. Investigators have suggested that altered regulation of growth factors and their receptors may involve inappropriate proliferation and differentiation of target cells, ultimately producing TCDD-induced terata. Why the teratogenic effects of TCDD are so highly species and tissue specific, and which animal species most accurately predicts the response of the human embryo/fetus, at the levels of exposure experienced by humans, still remains to be clarified. JF - Teratology AU - Couture, L A AU - Abbott, B D AU - Birnbaum, L S AD - Experimental Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 619 EP - 627 VL - 42 IS - 6 SN - 0040-3709, 0040-3709 KW - Polychlorinated Dibenzodioxins KW - 0 KW - Index Medicus KW - Animals KW - Cleft Palate -- chemically induced KW - Chick Embryo KW - Humans KW - Thymus Gland -- abnormalities KW - Rabbits KW - Mice KW - Pregnancy KW - Rats KW - Gene Expression Regulation -- drug effects KW - Macaca mulatta KW - Fetal Death -- chemically induced KW - Species Specificity KW - Organ Culture Techniques KW - Female KW - Cricetinae KW - Hydronephrosis -- chemically induced KW - Polychlorinated Dibenzodioxins -- pharmacology KW - Polychlorinated Dibenzodioxins -- toxicity KW - Abnormalities, Drug-Induced -- embryology KW - Abnormalities, Drug-Induced -- etiology KW - Prenatal Exposure Delayed Effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80316992?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Teratology&rft.atitle=A+critical+review+of+the+developmental+toxicity+and+teratogenicity+of+2%2C3%2C7%2C8-tetrachlorodibenzo-p-dioxin%3A+recent+advances+toward+understanding+the+mechanism.&rft.au=Couture%2C+L+A%3BAbbott%2C+B+D%3BBirnbaum%2C+L+S&rft.aulast=Couture&rft.aufirst=L&rft.date=1990-12-01&rft.volume=42&rft.issue=6&rft.spage=619&rft.isbn=&rft.btitle=&rft.title=Teratology&rft.issn=00403709&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-05-23 N1 - Date created - 1991-05-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Retinoic acid-induced alterations in the expression of growth factors in embryonic mouse palatal shelves. AN - 80316787; 2087681 AB - Retinoic acid (RA) is teratogenic in many species, producing multiple malformations, including cleft palate. The effects of RA which lead to cleft palate vary depending on the stage of development exposed. After exposure of embryonic mice to RA on gestation day (GD) 10, abnormally small palatal shelves form. After exposure on GD 12 shelves of normal size form, but fail to fuse, as the medial cells proliferate and differentiate into a nasal-like epithelium. Growth factors and their receptors play an important role in regulating development, and the expression of EGF receptors, EGF, TGF-alpha, TFG-beta 1, and TGF-beta 2 has been reported in the mouse embryo. In a variety of cell types in culture, these growth factors are capable of regulating proliferation, differentiation, expression of matrix proteins, and other cellular events including epithelial-mesenchymal transformations. The present study examines immunohistochemically the expression of EGF, TGF-alpha, TGF-beta 1, and TGF-beta 2 in the control embryonic palatal shelves from GD 12 to 15 and the effects of RA treatment on GD 10 or 12 on their expression on GD 14 and 16. These growth factors were shown to have specific temporal and spatial expression in the palatal shelf. With advancing development the levels of TGF-alpha decreased while the expression of EGF increased. TGF-beta 2 localization became regional by GD 14-15, with higher levels found in epithelial cells and chondrogenic mesenchyme. TGF-beta 1 occurred in epithelial and mesenchymal cells and distribution did not change substantially with advancing development. RA exposure altered the expression of TFG-alpha, TGF-beta 1, and TGF-beta 2, but significant effects on EGF were not found. The effects on TGF-alpha and TGF-beta 1 expression were dependent on the gestational age exposed. Levels of TGF-alpha on GD 14 decreased after RA exposure on GD 10, but increased after GD 12 exposure. TGF-beta 1 expression in the mesenchyme was increased after exposure on GD 12, but was unaffected by RA on GD 10. After exposure on either day, the levels of TGF-beta 2 increased in GD 14 nasal epithelial cells. Acting in concert, growth factors could regulate events critical to formation of the secondary palate, including cessation of medial epithelial cell proliferation, synthesis of extracellular matrix proteins in the mesenchyme, programmed cell death of medial epithelial peridermal cells, and transformation of basal epithelial medial cells to mesenchymal cells.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Teratology AU - Abbott, B D AU - Birnbaum, L S AD - Systemic Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 597 EP - 610 VL - 42 IS - 6 SN - 0040-3709, 0040-3709 KW - Tretinoin KW - 5688UTC01R KW - Epidermal Growth Factor KW - 62229-50-9 KW - Transforming Growth Factors KW - 76057-06-2 KW - Index Medicus KW - Cleft Palate -- chemically induced KW - Animals KW - Mice, Inbred C57BL KW - Morphogenesis -- drug effects KW - Mice KW - Gene Expression Regulation -- drug effects KW - Abnormalities, Drug-Induced -- etiology KW - Cell Differentiation -- drug effects KW - Male KW - Female KW - Pregnancy KW - Tretinoin -- pharmacology KW - Epidermal Growth Factor -- biosynthesis KW - Tretinoin -- toxicity KW - Transforming Growth Factors -- biosynthesis KW - Palate -- embryology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80316787?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Teratology&rft.atitle=Retinoic+acid-induced+alterations+in+the+expression+of+growth+factors+in+embryonic+mouse+palatal+shelves.&rft.au=Abbott%2C+B+D%3BBirnbaum%2C+L+S&rft.aulast=Abbott&rft.aufirst=B&rft.date=1990-12-01&rft.volume=42&rft.issue=6&rft.spage=597&rft.isbn=&rft.btitle=&rft.title=Teratology&rft.issn=00403709&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-05-23 N1 - Date created - 1991-05-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Occupation and risk for testicular cancer: a case-control study. AN - 80311303; 1964675 AB - A case-control study of 271 testicular cancer cases aged 18-42, including 60 seminomas and 206 other germinal cell tumours, and 259 controls was carried out to study the association between occupation and testicular cancer risk. Study subjects were identified at three medical centres, two of which treat military personnel. Controls were men diagnosed with a cancer other than of the genital tract. Associations were identified between professional employment (administrators, teachers and other professionals) and risk for testicular seminoma, OR = 2.8 (95% Cl: 1.4-5.4) and between employment in production work and risk for other germinal cell tumours, OR = 1.8 (95% Cl: 1.1-2.7). No specific occupations within these broad groups were responsible for observed increases. Self-reported exposure to microwave and other radio waves was associated with an excess risk for both seminomas and other germinal cell tumours. However, an assessment of radio wave exposure based on job title did not support this finding. Although testicular cancer has been increasing in recent decades among young males, occupational factors did not appear to account for a substantial proportion of testicular cancer occurrence in the population studied. JF - International journal of epidemiology AU - Hayes, R B AU - Brown, L M AU - Pottern, L M AU - Gomez, M AU - Kardaun, J W AU - Hoover, R N AU - O'Connell, K J AU - Sutzman, R E AU - Javadpour, N AD - Environmental Epidemiology Branch, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 825 EP - 831 VL - 19 IS - 4 SN - 0300-5771, 0300-5771 KW - Index Medicus KW - Neoplasms, Germ Cell and Embryonal -- etiology KW - Odds Ratio KW - Age Factors KW - Neoplasms, Germ Cell and Embryonal -- epidemiology KW - Risk Factors KW - Military Personnel KW - Humans KW - Adult KW - Case-Control Studies KW - Adolescent KW - United States -- epidemiology KW - Male KW - Occupational Exposure KW - Dysgerminoma -- epidemiology KW - Testicular Neoplasms -- etiology KW - Dysgerminoma -- etiology KW - Testicular Neoplasms -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80311303?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+epidemiology&rft.atitle=Occupation+and+risk+for+testicular+cancer%3A+a+case-control+study.&rft.au=Hayes%2C+R+B%3BBrown%2C+L+M%3BPottern%2C+L+M%3BGomez%2C+M%3BKardaun%2C+J+W%3BHoover%2C+R+N%3BO%27Connell%2C+K+J%3BSutzman%2C+R+E%3BJavadpour%2C+N&rft.aulast=Hayes&rft.aufirst=R&rft.date=1990-12-01&rft.volume=19&rft.issue=4&rft.spage=825&rft.isbn=&rft.btitle=&rft.title=International+journal+of+epidemiology&rft.issn=03005771&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-05-15 N1 - Date created - 1991-05-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The murine Cyp1a-1 gene negatively regulates its own transcription and that of other members of the aromatic hydrocarbon-responsive [Ah] gene battery. AN - 80307568; 2082180 AB - Transcripts of the murine CYP1A1 (cytochrome P1450) mRNA are markedly elevated in mutant hepatoma cell lines that contain missense mutations in the Cyp1a-1 structural gene. This putative derepression extends to other genes in the [Ah] battery. To test whether the Cyp1a-1 gene product is involved in a mechanism of feedback regulation of transcription, we introduced expression plasmids carrying the murine wild-type Cyp1a-1 cDNA into the mutant hepatoma cells. Measurements of steady-state mRNA levels and of transcriptional rates in the transfectants reveal that expression of a functional, exogenous CYP1A1 protein is sufficient to restore the repression of the endogenous gene, as well as restore the inducibility by dioxin, and that this effect takes place primarily at the level of transcription. Similar experiments with expression plasmids that carry the human CYP1A2 cDNA indicate that the CYP1A2 protein (cytochrome P3450) can also function as a transcriptional repressor. In addition, we find that expression of the Nmo-1 [NAD(P)H:menadione oxidoreductase] gene, a third member of the [Ah] gene battery, is also repressed by the exogenous expression of either Cyp1a-1 or CYP1A2 cDNA. These results indicate that the gene product of either member of the mammalian CYP1 family has a previously unrecognized transcriptional regulatory function, which is likely to be exerted by modification of preexisting trans-acting factors. This function may help bring about a fast reprogramming of gene expression, as might be needed during detoxification of toxic foreign chemicals. JF - Molecular endocrinology (Baltimore, Md.) AU - RayChaudhuri, B AU - Nebert, D W AU - Puga, A AD - Laboratory of Developmental Pharmacology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 1773 EP - 1781 VL - 4 IS - 12 SN - 0888-8809, 0888-8809 KW - Cyp1a-1 KW - Dioxins KW - 0 KW - Hydrocarbons KW - Polychlorinated Dibenzodioxins KW - RNA, Messenger KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Animals KW - Polychlorinated Dibenzodioxins -- pharmacology KW - Mice KW - Nucleic Acid Hybridization KW - Plasmids KW - Dioxins -- pharmacology KW - Liver Neoplasms, Experimental KW - Tumor Cells, Cultured KW - RNA, Messenger -- metabolism KW - Transfection KW - Enhancer Elements, Genetic KW - DNA -- genetics KW - Feedback KW - Hydrocarbons -- pharmacology KW - Cytochrome P-450 Enzyme System -- genetics KW - Transcription, Genetic KW - Gene Expression Regulation -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80307568?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+murine+Cyp1a-1+gene+negatively+regulates+its+own+transcription+and+that+of+other+members+of+the+aromatic+hydrocarbon-responsive+%5BAh%5D+gene+battery.&rft.au=RayChaudhuri%2C+B%3BNebert%2C+D+W%3BPuga%2C+A&rft.aulast=RayChaudhuri&rft.aufirst=B&rft.date=1990-12-01&rft.volume=4&rft.issue=12&rft.spage=1773&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 - 1991-05-07 N1 - Date created - 1991-05-07 N1 - Date revised - 2017-01-13 N1 - Gene symbol - Cyp1a-1 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Exposure factors for HIV-1 infection among heterosexual drug abusers in New Jersey treatment programs. AN - 80292863; 1964060 AB - In a cross-sectional study of 926 subjects from 10 drug treatment programs conducted in 1984 in New Jersey, the seroprevalence of human immunodeficiency virus (HIV) was 35% overall; 30% in whites, 33% in hispanics, and 46% in blacks (p = 0.01 for comparison of blacks to non-blacks). Univariate analysis showed the seroprevalence of HIV was not associated with age or gender, but did correlate with frequency of cocaine or heroin injection (p trend less than 0.001); frequency of needle sharing (p trend = 0.007); and inversely with levels of education (p = 0.05). The prevalence of HIV was also inversely related to the distance of the treatment center from lower Manhattan; being highest for distances of less than 5 miles from lower Manhattan and lowest for distances of 80 miles, with intermediate rates for the intervening distances (p trend less than 0.001). In multivariate analyses, HIV seropositivity was consistently associated with the frequency of needle sharing (p = 0.02) and less than 12 years (high school level) of education (p = 0.02), but not with black race. However, blacks who shared needles less than once a month had a relative risk of 3.2 (95% CI 1.2, 7.7) while non-blacks who shared less than once a month had a relative risk of only 0.9 (95% CI 0.3, 2.4). The risk in non-blacks increased to more than twofold with more frequent needle sharing. When the analysis was stratified by gender and adjusted for needle sharing and geography, a significant twofold increased risk was observed for female (but not male) subjects who had two or more heterosexual partners compared with those who had one partner.(ABSTRACT TRUNCATED AT 250 WORDS) JF - AIDS research and human retroviruses AU - Caussy, D AU - Weiss, S H AU - Blattner, W A AU - French, J AU - Cantor, K P AU - Ginzburg, H AU - Altman, R AU - Goedert, J J AD - Environmental Epidemiology Branch, National Cancer Institute, Rockville, MD. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 1459 EP - 1467 VL - 6 IS - 12 SN - 0889-2229, 0889-2229 KW - Heroin KW - 70D95007SX KW - Cocaine KW - I5Y540LHVR KW - Index Medicus KW - AIDS/HIV KW - Analysis of Variance KW - Humans KW - Needles KW - Cross-Sectional Studies KW - New Jersey -- epidemiology KW - Substance Abuse Treatment Centers KW - Ethnic Groups KW - Risk Factors KW - Adult KW - Middle Aged KW - Female KW - Male KW - Sexual Behavior KW - HIV Seroprevalence KW - HIV Infections -- epidemiology KW - Substance Abuse, Intravenous UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80292863?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Exposure+factors+for+HIV-1+infection+among+heterosexual+drug+abusers+in+New+Jersey+treatment+programs.&rft.au=Caussy%2C+D%3BWeiss%2C+S+H%3BBlattner%2C+W+A%3BFrench%2C+J%3BCantor%2C+K+P%3BGinzburg%2C+H%3BAltman%2C+R%3BGoedert%2C+J+J&rft.aulast=Caussy&rft.aufirst=D&rft.date=1990-12-01&rft.volume=6&rft.issue=12&rft.spage=1459&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 - 1991-04-30 N1 - Date created - 1991-04-30 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: AIDS Res Hum Retroviruses 1991 Mar;7(3):360 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interdependence of drug dose, incubation time & light dose on hematoporphyrin derivative induced photoinactivation of brain tumour cells. AN - 80291687; 2150403 AB - The relationship between photosensitizer concentration, light dose, incubation time and cellular damage in human cerebral glioma cells in culture, was studied. Cells were incubated with hematoporphyrin derivative (Hpd) for different durations at 37 degrees C. Immediately after specified period of incubation, cells were irradiated with white light. Cellular damage was assessed by colony forming ability of cells. A progressive reduction in the surviving fraction was observed as a function of drug and light dose. The survival curves were of exponential nature with an initial shoulder. The cell survival was found to be dependent on the time of incubation with Hpd. These results suggest that photodynamic cellular damage can be enhanced at low drug and light dose by increasing the incubation time. JF - The Indian journal of medical research AU - Gangola, P AU - Joshi, N B AD - Department of Biophysics, National Institute of Mental Health & Neuro Sciences, Bangalore. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 467 EP - 470 VL - 92 SN - 0971-5916, 0971-5916 KW - Hematoporphyrins KW - 0 KW - Hematoporphyrin Derivative KW - 68335-15-9 KW - Index Medicus KW - Brain Neoplasms -- pathology KW - Glioma -- pathology KW - Cell Survival -- drug effects KW - Tumor Cells, Cultured -- drug effects KW - Dose-Response Relationship, Drug KW - Humans KW - Dose-Response Relationship, Radiation KW - Time Factors KW - Tumor Cells, Cultured -- radiation effects KW - Hematoporphyrins -- pharmacology KW - Hematoporphyrin Photoradiation -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80291687?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Apoptosis+and+DNA+degradation+induced+by+1-methyl-4-phenylpyridinium+in+neurons.&rft.au=Dipasquale%2C+B%3BMarini%2C+A+M%3BYoule%2C+R+J&rft.aulast=Dipasquale&rft.aufirst=B&rft.date=1991-12-31&rft.volume=181&rft.issue=3&rft.spage=1442&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 - 1991-05-01 N1 - Date created - 1991-05-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A phase I study of high-dose interleukin-2 in combination with interferon-alpha 2b. AN - 80279342; 2074439 AB - Our group and others have conducted phase II trials of high-dose interleukin-2 (IL-2) or IL-2 with the adoptive transfer of in vitro activated lymphocytes in patients with advanced malignancies. Although durable complete and partial responses were seen in patients with renal cell carcinoma and metastatic melanoma, overall response rates were low and toxicity was substantial. In preclinical models, the combination of IL-2 and interferon-alpha has synergistic antitumor activity. Based on these data, and our prior experience with high-dose IL-2 (Cetus), we conducted a trial to determine the maximum tolerated dose of IL-2 (0.4, 0.8, and 1.2 mg/m2) administered together with a fixed dose of interferon-alpha 2b (3 x 10(6) u/m2) intravenously every 8 h on days 1-5 and 15-19. Patients were monitored in the intensive care unit and given pressor support for hypotension as needed. Twenty-four patients were entered (6, 10, and 8 at each IL-2 dose, respectively; 14 renal cell carcinoma, 7 melanoma, 2 colon, and 1 hepatoma). The median age was 56 years, the male to female ratio was 19:5, and performance status was 0 or 1 (Eastern Cooperative Oncology Group) in all patients. Toxicity was similar at all dose levels, but the onset was earlier in the treatment course as the dose of IL-2 was escalated in successive cohorts; therefore, more doses were withheld at the higher dose levels. The major toxicities resulting in the interruption or stopping of treatment were hypotension requiring pressors, dyspnea, and neurotoxicity. Grade 1 or 2 fever, nausea and vomiting, fatigue, and cutaneous reactions were common at all dose levels.(ABSTRACT TRUNCATED AT 250 WORDS) JF - Journal of biological response modifiers AU - Sznol, M AU - Mier, J W AU - Sparano, J AU - Gaynor, E R AU - Weiss, G R AU - Margolin, K A AU - Bar, M H AU - Hawkins, M J AU - Atkins, M B AU - Dutcher, J P AD - Investigational Drug Branch, Cancer Therapy Evaluation Program, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 529 EP - 537 VL - 9 IS - 6 SN - 0732-6580, 0732-6580 KW - Interferon-alpha KW - 0 KW - Interleukin-2 KW - Recombinant Proteins KW - interferon alfa-2b KW - 43K1W2T1M6 KW - Index Medicus KW - Kidney Neoplasms -- therapy KW - Carcinoma, Renal Cell -- therapy KW - Humans KW - Nervous System -- drug effects KW - Aged KW - Heart -- drug effects KW - Drug Evaluation KW - Drug Tolerance KW - Liver -- drug effects KW - Adult KW - Middle Aged KW - Melanoma -- therapy KW - Female KW - Male KW - Interleukin-2 -- administration & dosage KW - Interferon-alpha -- administration & dosage KW - Neoplasms -- therapy KW - Interleukin-2 -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80279342?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+biological+response+modifiers&rft.atitle=A+phase+I+study+of+high-dose+interleukin-2+in+combination+with+interferon-alpha+2b.&rft.au=Sznol%2C+M%3BMier%2C+J+W%3BSparano%2C+J%3BGaynor%2C+E+R%3BWeiss%2C+G+R%3BMargolin%2C+K+A%3BBar%2C+M+H%3BHawkins%2C+M+J%3BAtkins%2C+M+B%3BDutcher%2C+J+P&rft.aulast=Sznol&rft.aufirst=M&rft.date=1990-12-01&rft.volume=9&rft.issue=6&rft.spage=529&rft.isbn=&rft.btitle=&rft.title=Journal+of+biological+response+modifiers&rft.issn=07326580&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-04-12 N1 - Date created - 1991-04-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Isotretinoin-basal cell carcinoma prevention trial. Design, recruitment results, and baseline characteristics of the trial participants. The ISO-BCC Study Group. AN - 80262440; 1963135 AB - The Isotretinoin-Basal Cell Carcinoma Prevention Trial (ISO-BCC Study) is a double-masked, randomized, placebo controlled, multicenter clinical trial. It is the first intramural cancer chemoprevention trial sponsored by the Division of Cancer Prevention and Control of the National Cancer Institute. This trial was designed to evaluate the effectiveness of chronic administration of low dosage levels (10 mg) of a synthetic retinoid, isotretinoin, in reducing the incidence of basal cell carcinoma in a high-risk population and to determine the incidence and severity of side effects associated with this long-term treatment. Between 1984 and 1987, eight clinical centers enrolled 981 participants between the ages of 40 and 75, who had two or more biopsy proven basal cell carcinomas in the 5 years before trial entry. This article describes the trial design, recruitment results, and baseline characteristics of the participant population in the ISO-BCC Study. JF - Controlled clinical trials AU - Tangrea, J AU - Edwards, B AU - Hartman, A AU - Taylor, P AU - Peck, G AU - Salasche, S AU - Menon, P AU - Winton, G AU - Mellette, R AU - Guill, M AD - National Institutes of Health, National Cancer Institute, Bethesda, MD 20892. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 433 EP - 450 VL - 11 IS - 6 SN - 0197-2456, 0197-2456 KW - Isotretinoin KW - EH28UP18IF KW - Index Medicus KW - Double-Blind Method KW - Epidemiologic Methods KW - Risk Factors KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Follow-Up Studies KW - Research Design KW - Mass Screening -- methods KW - Male KW - Female KW - Carcinoma, Basal Cell -- prevention & control KW - Isotretinoin -- adverse effects KW - Skin Neoplasms -- prevention & control KW - Isotretinoin -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80262440?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Controlled+clinical+trials&rft.atitle=Isotretinoin-basal+cell+carcinoma+prevention+trial.+Design%2C+recruitment+results%2C+and+baseline+characteristics+of+the+trial+participants.+The+ISO-BCC+Study+Group.&rft.au=Tangrea%2C+J%3BEdwards%2C+B%3BHartman%2C+A%3BTaylor%2C+P%3BPeck%2C+G%3BSalasche%2C+S%3BMenon%2C+P%3BWinton%2C+G%3BMellette%2C+R%3BGuill%2C+M&rft.aulast=Tangrea&rft.aufirst=J&rft.date=1990-12-01&rft.volume=11&rft.issue=6&rft.spage=433&rft.isbn=&rft.btitle=&rft.title=Controlled+clinical+trials&rft.issn=01972456&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-03-29 N1 - Date created - 1991-03-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Assumptions of the HERP Index. AN - 80258760; 2287788 JF - Risk analysis : an official publication of the Society for Risk Analysis AU - Hoel, D G AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 623 EP - 4; discussion 629-33 VL - 10 IS - 4 SN - 0272-4332, 0272-4332 KW - Carcinogens KW - 0 KW - Index Medicus KW - Risk KW - Animals KW - Maximum Allowable Concentration KW - Dose-Response Relationship, Drug KW - Humans KW - Models, Biological UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80258760?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Risk+analysis+%3A+an+official+publication+of+the+Society+for+Risk+Analysis&rft.atitle=Assumptions+of+the+HERP+Index.&rft.au=Hoel%2C+D+G&rft.aulast=Hoel&rft.aufirst=D&rft.date=1990-12-01&rft.volume=10&rft.issue=4&rft.spage=623&rft.isbn=&rft.btitle=&rft.title=Risk+analysis+%3A+an+official+publication+of+the+Society+for+Risk+Analysis&rft.issn=02724332&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-03-22 N1 - Date created - 1991-03-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Epidemiologic evidence on the relationship between formaldehyde exposure and cancer. AN - 80250618; 2284588 AB - Over 30 epidemiologic studies have evaluated cancer risks associated with formaldehyde exposure. Excesses were reported for several sites, leukemia and cancers of the nasal cavities, nasopharynx, lung, and brain generating the greatest interest. The excesses of leukemia and brain and colon cancer found among professionals may not be related to formaldehyde exposure, since similar excesses were not observed among industrial workers. Inconsistencies among and within studies impede assigning formaldehyde a convincing causal role for the excesses of lung cancer found among industrial workers. A causal role for formaldehyde is the most probable for cancers of the nasopharynx and, to a less extent, the nasal cavities. Evidence of exposure-response relationships, the fact that direct contact with formaldehyde may occur at these upper respiratory sites, and the consistency of these findings with experimental studies make this assumption highly probable. JF - Scandinavian journal of work, environment & health AU - Blair, A AU - Saracci, R AU - Stewart, P A AU - Hayes, R B AU - Shy, C AD - National Cancer Institute, Occupational Studies Section, Rockville, MD 20892. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 381 EP - 393 VL - 16 IS - 6 SN - 0355-3140, 0355-3140 KW - Formaldehyde KW - 1HG84L3525 KW - Index Medicus KW - Lung Neoplasms -- epidemiology KW - Brain Neoplasms -- epidemiology KW - Leukemia -- epidemiology KW - Humans KW - Environmental Exposure KW - Colorectal Neoplasms -- epidemiology KW - Nose Neoplasms -- epidemiology KW - Nasopharyngeal Neoplasms -- epidemiology KW - Neoplasms -- epidemiology KW - Formaldehyde -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80250618?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Epidemiologic+evidence+on+the+relationship+between+formaldehyde+exposure+and+cancer.&rft.au=Blair%2C+A%3BSaracci%2C+R%3BStewart%2C+P+A%3BHayes%2C+R+B%3BShy%2C+C&rft.aulast=Blair&rft.aufirst=A&rft.date=1990-12-01&rft.volume=16&rft.issue=6&rft.spage=381&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 - 1991-03-20 N1 - Date created - 1991-03-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Complete coding sequence of a human B-raf cDNA and detection of B-raf protein kinase with isozyme specific antibodies. AN - 80248449; 2284096 AB - A 2.2 kb cDNA clone which presumably includes the complete human B-raf coding sequence was isolated from a human testes cDNA library. Sequence analysis showed the presence of all three conserved regions CR1, CR2 and CR3 previously identified in raf protein kinases. The cDNA was expressed in E. coli yielding a B-raf fusion protein which reacts with antibodies specific for B-raf raised against the C-terminal peptide as well as with monoclonal antibodies which map into the kinase domain. JF - Oncogene AU - Sithanandam, G AU - Kolch, W AU - Duh, F M AU - Rapp, U R AD - Laboratory of Viral Carcinogenesis, National Cancer Institute, Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 1775 EP - 1780 VL - 5 IS - 12 SN - 0950-9232, 0950-9232 KW - Antibodies, Monoclonal KW - 0 KW - Isoenzymes KW - Proto-Oncogene Proteins KW - DNA KW - 9007-49-2 KW - Protein Kinases KW - EC 2.7.- KW - Proto-Oncogene Proteins c-raf KW - EC 2.7.11.1 KW - Index Medicus KW - Immunoblotting KW - Antibody Specificity KW - Humans KW - Molecular Sequence Data KW - Escherichia coli KW - Amino Acid Sequence KW - Precipitin Tests KW - Male KW - Protein Kinases -- metabolism KW - Isoenzymes -- immunology KW - DNA -- genetics KW - Proto-Oncogene Proteins -- metabolism KW - Protein Kinases -- genetics KW - Proto-Oncogene Proteins -- genetics KW - Isoenzymes -- genetics KW - Isoenzymes -- metabolism KW - Protein Kinases -- immunology KW - Antibodies, Monoclonal -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80248449?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Complete+coding+sequence+of+a+human+B-raf+cDNA+and+detection+of+B-raf+protein+kinase+with+isozyme+specific+antibodies.&rft.au=Sithanandam%2C+G%3BKolch%2C+W%3BDuh%2C+F+M%3BRapp%2C+U+R&rft.aulast=Sithanandam&rft.aufirst=G&rft.date=1990-12-01&rft.volume=5&rft.issue=12&rft.spage=1775&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=09509232&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-03-15 N1 - Date created - 1991-03-15 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - X54072; GENBANK N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Immunocytology with microwave-fixed fibroblasts shows 1 alpha,25-dihydroxyvitamin D3-dependent rapid and estrogen-dependent slow reorganization of vitamin D receptors. AN - 80232207; 2177476 AB - Prior studies have given no evidence for regulation of vitamin D receptor (VDR) compartmentalization or subcellular organization. Microwave fixation (9-15 s) and an indirect immunodetection system of avidin-biotin enhancement and phycoerythrin fluorophore resulted in sufficient spatial and temporal resolution to allow analysis of these processes. We studied cultured fibroblasts from normals or from patients with four different types of hereditary defect compromising VDR function (mutant cells). Compartmentalization of VDRs in the absence of 1,25-dihydroxyvitamin D3 (calcitriol) was regulated by serum or estrogen. VDRs were mainly cytoplasmic in cells cultured without serum and phenol red, but VDRs were mainly intranuclear after addition of serum or an estrogen to cells for at least 18 h (slow regulation). Calcitriol initiated a rapid and multistep process (rapid regulation) of reorganization in a portion of VDRs: clumping within 15-45 s, alignment of clumps along fibrils within 30-45 s, perinuclear accumulation of clumps within 45-90 s, and intranuclear accumulation of clumps within 1-3 min. We found similar rapid effects of calcitriol on VDRs in various other types of cultured cells. These sequential VDR pattern changes showed calcitriol dose dependency and calcitriol analogue specificity characteristic for the VDR. In mutant fibroblasts VDR pattern changes after calcitriol were absent or severely disturbed at selected steps. Treatment of normal cells with wheat germ agglutinin, which blocks protein transport through nuclear pores, also blocked calcitriol-dependent translocation of VDRs. We conclude that immunocytology after microwave fixation provides evidence for regulation of VDR organization and localization. JF - The Journal of cell biology AU - Barsony, J AU - Pike, J W AU - DeLuca, H F AU - Marx, S J AD - Mineral Metabolism Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 2385 EP - 2395 VL - 111 IS - 6 Pt 1 SN - 0021-9525, 0021-9525 KW - Androstenediols KW - 0 KW - Receptors, Calcitriol KW - Receptors, Steroid KW - Progesterone KW - 4G7DS2Q64Y KW - Estradiol KW - 4TI98Z838E KW - Diethylstilbestrol KW - 731DCA35BT KW - DNA KW - 9007-49-2 KW - Calcitriol KW - FXC9231JVH KW - Index Medicus KW - Fibroblasts -- drug effects KW - Animals KW - Androstenediols -- pharmacology KW - Cells, Cultured KW - Progesterone -- pharmacology KW - Humans KW - DNA -- metabolism KW - Fibroblasts -- cytology KW - Immunohistochemistry KW - Fibroblasts -- metabolism KW - Cell Line KW - Microwaves KW - Receptors, Steroid -- drug effects KW - Skin -- metabolism KW - Estradiol -- pharmacology KW - Receptors, Steroid -- metabolism KW - Diethylstilbestrol -- pharmacology KW - Calcitriol -- metabolism KW - Calcitriol -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80232207?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+cell+biology&rft.atitle=Immunocytology+with+microwave-fixed+fibroblasts+shows+1+alpha%2C25-dihydroxyvitamin+D3-dependent+rapid+and+estrogen-dependent+slow+reorganization+of+vitamin+D+receptors.&rft.au=Barsony%2C+J%3BPike%2C+J+W%3BDeLuca%2C+H+F%3BMarx%2C+S+J&rft.aulast=Barsony&rft.aufirst=J&rft.date=1990-12-01&rft.volume=111&rft.issue=6+Pt+1&rft.spage=2385&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+cell+biology&rft.issn=00219525&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-03-01 N1 - Date created - 1991-03-01 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Clin Invest. 1990 Jan;85(1):101-5 [2153150] Anal Biochem. 1989 Nov 15;183(1):57-63 [2482679] Development. 1989 Dec;107(4):685-99 [2698799] J Histochem Cytochem. 1990 May;38(5):617-23 [2185310] J Biol Chem. 1990 Jun 15;265(17):10025-9 [2161832] Mol Endocrinol. 1990 Apr;4(4):623-31 [2177843] Cell Regul. 1990 Feb;1(3):291-9 [2100202] EMBO J. 1987 Nov;6(11):3333-40 [3123217] Proc Natl Acad Sci U S A. 1988 Feb;85(4):1223-6 [2829219] Cell. 1988 Mar 11;52(5):641-53 [3345567] Endocrinology. 1988 Apr;122(4):1224-30 [2831024] J Steroid Biochem. 1988 Jan;29(1):47-56 [3347050] J Clin Endocrinol Metab. 1988 Sep;67(3):607-13 [2842365] J Steroid Biochem. 1988 Sep;31(3):287-93 [3419159] Cell. 1988 Oct 7;55(1):145-56 [3167974] Exp Cell Res. 1988 Oct;178(2):318-34 [3169133] Cancer Res. 1988 Nov 15;48(22):6462-74 [3180062] Endocrinology. 1988 Dec;123(6):2878-84 [3264240] Pathol Annu. 1988;23 Pt 2:213-34 [2462706] Bone Miner. 1987 Nov;3(2):125-36 [2850050] Mol Endocrinol. 1988 Aug;2(8):756-60 [3062385] Recent Prog Horm Res. 1988;44:263-305 [2851156] Histochem J. 1988 Jun-Jul;20(6-7):347-52 [3065304] Histochem J. 1988 Jun-Jul;20(6-7):373-87 [2464568] Circ Res. 1989 Mar;64(3):415-26 [2537154] J Pathol. 1988 Dec;156(4):275-82 [2465397] Exp Cell Res. 1989 Apr;181(2):492-504 [2924800] Cancer Res. 1989 Apr 15;49(8 Suppl):2222s-2229s [2649237] Cancer Res. 1989 Apr 15;49(8 Suppl):2230s-2234s [2702662] J Biol Chem. 1989 Jun 15;264(17):9728-31 [2722871] J Clin Invest. 1989 Jun;83(6):2093-101 [2542381] Mol Endocrinol. 1989 Apr;3(4):635-44 [2542779] Cell. 1989 Jun 30;57(7):1147-54 [2736623] J Steroid Biochem. 1989 May;32(5):737-47 [2661921] Proc Natl Acad Sci U S A. 1972 Nov;69(11):3464-8 [4508334] Exp Cell Res. 1980 Jun;127(2):293-7 [6991262] N Engl J Med. 1981 Jun 25;304(26):1588-91 [6262646] J Biol Chem. 1983 Jan 25;258(2):1289-96 [6296076] J Clin Invest. 1983 Feb;71(2):192-200 [6296200] Biochim Biophys Acta. 1983 Aug 11;737(3-4):409-42 [6309233] Breast Cancer Res Treat. 1983;3(2):179-99 [6351951] Mol Endocrinol. 1989 Jul;3(7):1061-9 [2797002] J Cell Biol. 1989 Nov;109(5):1947-62 [2681224] J Histochem Cytochem. 1989 Nov;37(11):1609-17 [2553800] Cell. 1989 Nov 17;59(4):697-708 [2555064] J Biol Chem. 1989 Dec 5;264(34):20403-6 [2555357] FEBS Lett. 1989 Dec 18;259(1):205-8 [2599107] Proc Natl Acad Sci U S A. 1989 Dec;86(24):9783-7 [2557627] Nature. 1984 Feb 23-29;307(5953):745-7 [6700704] Science. 1984 May 25;224(4651):879-81 [6326262] Proc Natl Acad Sci U S A. 1984 Nov;81(21):6711-3 [6093115] Histochem J. 1984 Nov;16(11):1171-91 [6210272] Life Sci. 1984 Dec 10;35(24):2383-96 [6096654] Biochem Biophys Res Commun. 1985 Aug 30;131(1):378-85 [2994658] J Clin Endocrinol Metab. 1986 Jan;62(1):122-6 [2999175] Endocr Rev. 1985 Fall;6(4):512-43 [3000755] J Membr Biol. 1986;90(2):137-43 [2425094] Ann Pathol. 1986;6(2):115-29 [3524590] Recent Prog Horm Res. 1986;42:297-329 [3526452] Biochemistry. 1986 Aug 12;25(16):4523-34 [2429689] J Biol Chem. 1987 Jan 25;262(3):1305-11 [3027085] Endocrinology. 1987 Apr;120(4):1232-42 [3549255] J Biol Chem. 1987 May 25;262(15):7072-5 [3034879] Am J Med. 1987 Nov;83(5):984-90 [2823606] Biochem J. 1987 Aug 15;246(1):55-65 [3675559] J Biol Chem. 1987 Dec 15;262(35):17092-9 [2824516] Lab Invest. 1987 Nov;57(5):592-9 [3479651] J Steroid Biochem. 1987;27(1-3):115-21 [3695474] J Steroid Biochem. 1987;27(1-3):185-92 [3695480] Cancer Res. 1989 Sep 15;49(18):5176-9 [2766287] Mol Cell Biol. 1989 Sep;9(9):3829-38 [2779568] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comparative toxicity of ethylene dichloride in F344/N, Sprague-Dawley and Osborne-Mendel rats. AN - 80226333; 2276705 AB - Studies were conducted to compare the toxicity of ethylene dichloride (EDC) in F344/N rats, Sprague-Dawley rats, and Osborne-Mendel rats. Ten rats/sex/group were exposed to EDC in drinking-water at 0, 500, 1000, 2000, 4000 and 8000 ppm for 13 wk. The highest concentration was limited by the maximum solubility of EDC in water (about 9000 ppm). In addition, F344/N rats (10/sex/group) were administered EDC in corn oil by gavage to compare toxicity resulting from bolus administration with that of continuous exposure in drinking-water. Gavage doses of EDC were within the range of total daily doses (in mg/kg body weight/day) resulting from exposure in drinking-water. EDC administered by gavage resulted in greater toxicity to F344/N rats than did administration of similar doses in drinking-water. All males receiving 240 and 480 mg/kg body weight and 9/10 females receiving 300 mg/kg body weight by gavage died before the end of the study. Necrosis of the cerebellum was observed in the brains of 3 males receiving 240 mg/kg body weight and 3 females receiving 300 mg/kg body weight. Hyperplasia and inflammation of the forestomach mucosa were observed in 8 male and 3 female rats that died or were killed in moribund condition. EDC caused minimal toxicity to F344/N, Sprague-Dawley and Osborne-Mendel rats at the drinking-water concentrations used in these studies; only female F344/N rats had EDC-related renal lesions. Based on mortality and EDC-related lesions, the no-effect levels for EDC administered by gavage to F344/N rats were 120 mg/kg body weight for males and 150 mg/kg body weight for females. JF - Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association AU - Morgan, D L AU - Bucher, J R AU - Elwell, M R AU - Lilja, H S AU - Murthy, A S AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 839 EP - 845 VL - 28 IS - 12 SN - 0278-6915, 0278-6915 KW - Ethylene Dichlorides KW - 0 KW - ethylene dichloride KW - 55163IJI47 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Administration, Oral KW - Animals KW - Rats, Inbred F344 KW - Drinking -- drug effects KW - Dose-Response Relationship, Drug KW - Body Weight -- drug effects KW - Gastric Mucosa -- drug effects KW - Male KW - Female KW - Organ Size -- drug effects KW - Liver -- drug effects KW - Ethylene Dichlorides -- toxicity KW - Kidney -- drug effects KW - Ethylene Dichlorides -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80226333?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Comparative+toxicity+of+ethylene+dichloride+in+F344%2FN%2C+Sprague-Dawley+and+Osborne-Mendel+rats.&rft.au=Morgan%2C+D+L%3BBucher%2C+J+R%3BElwell%2C+M+R%3BLilja%2C+H+S%3BMurthy%2C+A+S&rft.aulast=Morgan&rft.aufirst=D&rft.date=1990-12-01&rft.volume=28&rft.issue=12&rft.spage=839&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 - 1991-03-01 N1 - Date created - 1991-03-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - H-ras activation and ras p21 expression in bladder tumors induced in F344/NCr rats by N-butyl-N-(4-hydroxybutyl)nitrosamine. AN - 80193570; 2265474 AB - Bladder tumors were induced in male F344/NCr rats by administration of N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) at 500 p.p.m. in their drinking water for 12 weeks. Twenty-one bladder tumors that developed between 25 and 50 weeks after BBN administration was begun were evaluated for immunoreactivity with polyclonal or monoclonal antibodies raised against ras p21, for amplification of ras genes by Southern blotting, and for activating point mutations in ras genes by selective oligonucleotide hybridization of products from polymerase chain reaction (PCR). Increased expression of ras p21 was detected by avidin-biotin immunohistochemistry in 18/21 (85%) of the neoplastic bladder lesions. By Southern analysis, there was no significant amplification of H-ras, K-ras or N-ras in any of the tumors except one that showed a 5-fold amplification of K-ras. Point mutations in ras genes were detected by selective oligonucleotide hybridization of the products of PCR. Of the 21 bladder tumors, three tumors were shown to have mutations in codon 12 (GGA----GAA), six tumors in codon 61 (two CAA----CTA, four CAA----CGA), and one in both codon 12 (GGA----GAA) and codon 61 (CAA----CGA), all in H-ras. Thus 10 of 21 tumors has ras gene mutations in a portion of the tumor cells. The variable pattern of point mutation in H-ras suggests that these mutations may not all be a direct consequence of interaction of BBN metabolites with H-ras. Enhanced expression of ras p21 was always focal and was not necessarily associated with transforming ras mutations. It is therefore suggested that tumorigenesis in BBN-initiated bladder cells might involve H-ras activation as part of a multistep pathway; however, H-ras involvement is not obligatory for tumor development. JF - Carcinogenesis AU - Enomoto, T AU - Ward, J M AU - Perantoni, A O AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute, Frederick, MD 21702-1201. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 2233 EP - 2238 VL - 11 IS - 12 SN - 0143-3334, 0143-3334 KW - H-ras KW - K-ras KW - N-ras KW - ras p21 KW - Codon KW - 0 KW - Butylhydroxybutylnitrosamine KW - 3817-11-6 KW - DNA KW - 9007-49-2 KW - Oncogene Protein p21(ras) KW - EC 3.6.5.2 KW - Index Medicus KW - Rats KW - Polymerase Chain Reaction KW - Animals KW - Rats, Inbred F344 KW - Blotting, Southern KW - Gene Expression KW - DNA -- analysis KW - Mutation KW - Male KW - Genes, ras -- drug effects KW - Oncogene Protein p21(ras) -- biosynthesis KW - Urinary Bladder Neoplasms -- genetics KW - Papilloma -- genetics KW - Carcinoma -- metabolism KW - Urinary Bladder Neoplasms -- metabolism KW - Papilloma -- metabolism KW - Urinary Bladder Neoplasms -- chemically induced KW - Carcinoma -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80193570?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=H-ras+activation+and+ras+p21+expression+in+bladder+tumors+induced+in+F344%2FNCr+rats+by+N-butyl-N-%284-hydroxybutyl%29nitrosamine.&rft.au=Enomoto%2C+T%3BWard%2C+J+M%3BPerantoni%2C+A+O&rft.aulast=Enomoto&rft.aufirst=T&rft.date=1990-12-01&rft.volume=11&rft.issue=12&rft.spage=2233&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-02-12 N1 - Date created - 1991-02-12 N1 - Date revised - 2017-01-13 N1 - Gene symbol - H-ras; K-ras; N-ras; ras p21 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of the DNA damage recognized by an antiserum elicited against cis-diamminedichloroplatinum (II)-modified DNA. AN - 80192413; 1979937 AB - A series of in vitro and in vivo studies were performed to characterize DNA damage recognized by an antiserum elicited against DNA modified with cis-diamminedichloroplatinum(II) (cisplatin). Adducts determined by the cisplatin-DNA enzyme-linked immunosorbent assay (ELISA) in human blood cell DNA have been shown to correlate well with positive clinical outcome in testicular and ovarian cancer patients receiving platinum drug-based chemotherapy (Reed et al. (1990) Proc. Natl. Acad. Sci., 84; 5024, and Reed et al. (1988) Carcinogenesis, 9, 1909). DNAs from calf thymus, salmon sperm, pBR322 and synthetic oligonucleotides were modified with cisplatin in vitro before or after specific DNA digestion steps to yield adducted samples of known size and/or chemical composition. These cisplatin modified DNAs were assayed by atomic absorption spectrometry (AAS) to assess absolute platinum content, and by ELISA to determine the antiserum specificity. The antiserum recognizes native cisplatin-modified calf thymus DNA, and native oligonucleotides containing intrastrand cis-Pt (NH3)2-d(pGpG) adducts (Pt-GG) and intrastrand cis-Pt (NH3)2-d(pApG) adducts (Pt-AG). Modified plasmid DNA fragments of varying sizes (down to 309 base pairs) are recognized similarly to cisplatin-modified calf thymus DNA. The antiserum does not cross-react with individual Pt-GG or Pt-AG adducts not bound to DNA. In experiments designed to assess the relationship between adduct measured by ELISA and total platinum bound to DNA as measured by AAS, male and female Sprague-Dawley rats were injected i.p. with cisplatin and a dose response for adduct formation was determined in kidney DNA samples. Values obtained by ELISA were substantially lower than those measured by AAS, and the two were directly related in DNA from kidney tissues of rodents but not in DNA from human nucleated blood cells. In rodent samples the ELISA measured a consistent 0.2% of the total DNA-bound platinum determined by AAS, with a correlation coefficient of 0.91. Among 54 blood cell DNA samples from human patients, which gave measurable adduct values in both ELISA and AAS, the ELISA measured a variable fraction (0.2-33.0%) of the total DNA-bound platinum measured by AAS. We conclude that the cisplatin-DNA ELISA measures a three dimensional lesion in DNA that is formed in direct proportion to total DNA-bound platinum in rat kidney, but that in human biological samples, interindividual variability precludes a relationship that conforms to simple mathematical algorithms. JF - Carcinogenesis AU - Reed, E AU - Gupta-Burt, S AU - Litterst, C L AU - Poirier, M C AD - Medicine Branch, National Cancer Institute, NIH, Bethesda, MD 20892. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 2117 EP - 2121 VL - 11 IS - 12 SN - 0143-3334, 0143-3334 KW - Immune Sera KW - 0 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Animals KW - Polymorphism, Restriction Fragment Length KW - Dose-Response Relationship, Drug KW - Enzyme-Linked Immunosorbent Assay KW - Spectrophotometry, Atomic KW - Male KW - Female KW - DNA Damage KW - Cisplatin -- pharmacology KW - Cisplatin -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80192413?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Characterization+of+the+DNA+damage+recognized+by+an+antiserum+elicited+against+cis-diamminedichloroplatinum+%28II%29-modified+DNA.&rft.au=Reed%2C+E%3BGupta-Burt%2C+S%3BLitterst%2C+C+L%3BPoirier%2C+M+C&rft.aulast=Reed&rft.aufirst=E&rft.date=1990-12-01&rft.volume=11&rft.issue=12&rft.spage=2117&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-02-12 N1 - Date created - 1991-02-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Decreased Hnf-1 gene expression in mice homozygous for a 1.2-centiMorgan deletion on chromosome 7. AN - 80191778; 2264930 AB - The mammalian CYP2E1 gene encodes a cytochrome P450 enzyme that is markedly increased soon after birth. In vitro evidence suggests that the rat CYP2E1 gene is positively regulated by the transcription factor HNF-1 or a protein displaying DNA-binding properties similar to HNF-1. In contrast to newborn wild-type mice and mice heterozygous for a 1.2-centiMorgan deletion on chromosome 7, newborn mice homozygous for this deletion do not show significant expression of the Cyp2e-1 and Hnf-1 genes. However, the Cyp2e-1 and Hnf-1 structural genes are not in the chromosome 7 segment deleted in these mice. Although Cyp2e-1 maps to chromosome 7, it is distal to this deletion; Hnf-1 maps to chromosome 5. These data suggest that the deleted region of chromosome 7 contains a gene encoding a trans-acting factor which is upstream (epistatic) in the regulatory cascade that includes Hnf-1 gene expression. JF - DNA and cell biology AU - Gonzalez, F J AU - Liu, S Y AU - Kozak, C A AU - Nebert, D W AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 771 EP - 776 VL - 9 IS - 10 SN - 1044-5498, 1044-5498 KW - CYP2E1 KW - Hnf-1 KW - RNA, Messenger KW - 0 KW - Trans-Activators KW - DNA KW - 9007-49-2 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Animals KW - Blotting, Northern KW - Humans KW - Transcription, Genetic KW - Mice KW - Nucleic Acid Hybridization KW - RNA, Messenger -- genetics KW - Chromosome Mapping KW - Rats KW - Alleles KW - Blotting, Southern KW - DNA -- genetics KW - Chromosome Deletion KW - Homozygote KW - Cytochrome P-450 Enzyme System -- genetics KW - Gene Expression Regulation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80191778?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=DNA+and+cell+biology&rft.atitle=Decreased+Hnf-1+gene+expression+in+mice+homozygous+for+a+1.2-centiMorgan+deletion+on+chromosome+7.&rft.au=Gonzalez%2C+F+J%3BLiu%2C+S+Y%3BKozak%2C+C+A%3BNebert%2C+D+W&rft.aulast=Gonzalez&rft.aufirst=F&rft.date=1990-12-01&rft.volume=9&rft.issue=10&rft.spage=771&rft.isbn=&rft.btitle=&rft.title=DNA+and+cell+biology&rft.issn=10445498&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-02-13 N1 - Date created - 1991-02-13 N1 - Date revised - 2017-01-13 N1 - Gene symbol - CYP2E1; Hnf-1 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Amelioration of sodium barbital-induced nephropathy and regenerative tubular hyperplasia after a single injection of streptozotocin does not abolish the renal tumor promoting effect of barbital sodium in male F344/NC4 rats. AN - 80191266; 2148284 AB - The renal tumor promoting activity of barbital sodium (BBNa) and the role of renal tubular cell hyperplasia in tumor promotion following initiation with streptozotocin (STZ) was investigated. Six week old male F344/NCr rats were given STZ as a single i.p. injection of 50 mg/kg body wt and beginning 2 weeks later were fed diets containing 0 or 4000 p.p.m. of BBNa until they were killed at 33, 52 or 72 experimental weeks for histological evaluation and determination of levels of renal DNA synthesis by bromodeoxyuridine (Brdu) immunohistochemistry. A promoting effect on renal carcinogenesis was found by 72 weeks, but not at 33 or 52 weeks, confirming that prolonged administration of BBNa is necessary to promote renal tubular cell neoplasms. The promoting effect was evident as a higher incidence of large renal tubular tumors after 52 weeks, rather than an increase in number of dysplastic tubules, putative preneoplastic lesions. These findings suggest that the targets for the promoting activity of BBNa may be dysplastic lesions which may progress to tumors. Detailed examination by the step section technique through the entire kidneys revealed that STZ or BBNa administration induced a high incidence of putative preneoplastic renal tubular lesions (dysplasias) which seemed to be derived from the P1 or P2 segment of the nephron, also a site of high Brdu labeling index (LI) associated with BBNa toxicity. STZ administration was also associated with attenuation of BBNa-induced nephropathy and with diabetes from pancreatic islet degeneration and atrophy. The reduction in severity of nephropathy was correlated with a reduction in the LI of the renal cortical and medullary tubules, but not with the renal tumor incidence. These results indicate that decreased DNA synthesis in target cells does not eliminate tumor promoting activity in renal tubular epithelium. In addition, BBNa alone induced papillomas of the transitional epithelium of the renal pelvis and renal tubular cell adenomas. JF - Carcinogenesis AU - Konishi, N AU - Diwan, B A AU - Ward, J M AD - Tumor Pathology and Pathogenesis Section, National Cancer Institute, Frederick, MD 21702-1201. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 2149 EP - 2156 VL - 11 IS - 12 SN - 0143-3334, 0143-3334 KW - Streptozocin KW - 5W494URQ81 KW - Barbital KW - 5WZ53ENE2P KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Liver -- anatomy & histology KW - Kidney -- metabolism KW - Kidney -- pathology KW - Nephritis -- complications KW - DNA -- biosynthesis KW - Rats KW - Rats, Inbred F344 KW - Hyperplasia -- chemically induced KW - Papilloma -- etiology KW - Body Weight -- drug effects KW - Nephritis -- chemically induced KW - Adenoma -- etiology KW - Kidney Neoplasms -- etiology KW - Hyperplasia -- complications KW - Streptozocin -- pharmacology KW - Male KW - Organ Size -- drug effects KW - Kidney -- anatomy & histology KW - Barbital -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80191266?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Amelioration+of+sodium+barbital-induced+nephropathy+and+regenerative+tubular+hyperplasia+after+a+single+injection+of+streptozotocin+does+not+abolish+the+renal+tumor+promoting+effect+of+barbital+sodium+in+male+F344%2FNC4+rats.&rft.au=Konishi%2C+N%3BDiwan%2C+B+A%3BWard%2C+J+M&rft.aulast=Konishi&rft.aufirst=N&rft.date=1990-12-01&rft.volume=11&rft.issue=12&rft.spage=2149&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-02-12 N1 - Date created - 1991-02-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Stimulatory effects of maitotoxin on insulin release in insulinoma HIT cells: role of calcium uptake and phosphoinositide breakdown. AN - 80187185; 2175805 AB - In hamster insulinoma (HIT) cells, maitotoxin (MTX) induces a time-dependent and concentration-dependent release of insulin that requires the presence of extracellular calcium. The response is nearly completely blocked by cinnarizine and cadmium, but is not inhibited by the L-type calcium channel blocker nifedipine or by manganese. MTX induces 45Ca+ uptake in these cells in a dose-dependent mode, and the uptake is blocked with cinnarizine, nifedipine and cadmium, and is partially inhibited by manganese. MTX induces phosphoinositide breakdown in HIT cells, and the response is partially blocked by cadmium, but is not affected by nifedipine, cinnarizine or manganese. High concentrations of potassium ions also induce insulin release and calcium uptake in HIT cells. Both effects of potassium are blocked partially by nifedipine, cadmium and cinnarizine. High concentrations of potassium do not induce phosphoinositide breakdown in HIT cells. The results suggest that MTX-elicited release of insulin is attained by two mechanisms: 1) a nifedipine-sensitive action, which results from MTX-induced activation of L-type calcium channels, which can be mimicked with high potassium concentrations; and 2) a nifedipine-insensitive action, which may be initiated by the activation of phosphoinositide breakdown by MTX. Such an activation of phospholipase C would result in the formation of 1,4,5-inositol trisphosphate, a release of intracellular calcium and then release of insulin to the extracellular space. Cinnarizine is proposed to block both MTX-elicited mechanisms, the first by blockade of calcium channels and the second by blocking 1,4,5-inositol trisphosphate-induced release of internal calcium. Either mechanism alone appears capable of eliciting release of insulin. JF - The Journal of pharmacology and experimental therapeutics AU - Soergel, D G AU - Gusovsky, F AU - Yasumoto, T AU - Daly, J W AD - Laboratory of Bioorganic Chemistry, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, maryland. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 1360 EP - 1365 VL - 255 IS - 3 SN - 0022-3565, 0022-3565 KW - Calcium Channel Blockers KW - 0 KW - Calcium Radioisotopes KW - Insulin KW - Marine Toxins KW - Oxocins KW - Phosphatidylinositols KW - Cadmium KW - 00BH33GNGH KW - Cinnarizine KW - 3DI2E1X18L KW - Manganese KW - 42Z2K6ZL8P KW - maitotoxin KW - 9P59GES78D KW - Nifedipine KW - I9ZF7L6G2L KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Swine KW - Animals KW - Phosphatidylinositols -- metabolism KW - Manganese -- pharmacology KW - Guinea Pigs KW - Calcium -- metabolism KW - Nifedipine -- pharmacology KW - Cadmium -- pharmacology KW - Cinnarizine -- pharmacology KW - Tumor Cells, Cultured KW - Calcium Channel Blockers -- pharmacology KW - Calcium -- pharmacokinetics KW - Cricetinae KW - Marine Toxins -- pharmacology KW - Pancreatic Neoplasms -- pathology KW - Insulinoma -- pathology KW - Pancreatic Neoplasms -- metabolism KW - Pancreatic Neoplasms -- secretion KW - Insulinoma -- secretion KW - Insulinoma -- metabolism KW - Insulin -- secretion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80187185?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Stimulatory+effects+of+maitotoxin+on+insulin+release+in+insulinoma+HIT+cells%3A+role+of+calcium+uptake+and+phosphoinositide+breakdown.&rft.au=Soergel%2C+D+G%3BGusovsky%2C+F%3BYasumoto%2C+T%3BDaly%2C+J+W&rft.aulast=Soergel&rft.aufirst=D&rft.date=1990-12-01&rft.volume=255&rft.issue=3&rft.spage=1360&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 - 1991-02-07 N1 - Date created - 1991-02-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Calcium currents recorded from a vertebrate presynaptic nerve terminal are resistant to the dihydropyridine nifedipine. AN - 80181656; 2175910 AB - The influx of Ca ions into the presynaptic nerve terminal through ion channels is a key link between the action potential and the release of chemical transmitters. It is not clear, however, which types of Ca channel are involved in neurosecretion at vertebrate synapses. In particular, there is disagreement as to whether these channels are sensitive to dihydropyridine blockers, characteristic of L-type Ca channels. We have used the chicken ciliary ganglion calyx synapse to test the effect of the dihydropyridine nifedipine on Ca current recorded directly from a cholinergic presynaptic nerve terminal. We used a control neuron to define the experimental conditions under which L-type Ca channels are blocked by 10 microM nifedipine. We then tested the effect of the dihydropyridine on Ca currents recorded from the presynaptic terminal using the same conditions. Nifedipine did not reduce the calyx Ca current nor did it block chemical transmission through the ganglion. The lack of effect of the dihydropyridine was not due to restricted access since omega-conotoxin GVIA, a peptide toxin that blocks transmission at this synapse, rapidly blocked the calyx Ca current. Thus, the predominant Ca channel in this presynaptic nerve terminal is not dihydropyridine sensitive and, hence, cannot be characterized as L-type. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Stanley, E F AU - Atrakchi, A H AD - National Institute of Neurological Disorders and Stroke, Biophysics Laboratory, National Institutes of Health, Bethesda, MD 20892. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 9683 EP - 9687 VL - 87 IS - 24 SN - 0027-8424, 0027-8424 KW - Calcium Channel Blockers KW - 0 KW - Calcium Channels KW - Peptides, Cyclic KW - omega-Conotoxin GVIA KW - 92078-76-7 KW - Nifedipine KW - I9ZF7L6G2L KW - Index Medicus KW - Animals KW - Synapses -- physiology KW - Synapses -- drug effects KW - Calcium Channel Blockers -- pharmacology KW - Synaptic Transmission -- drug effects KW - Neurons -- drug effects KW - Kinetics KW - Chick Embryo KW - In Vitro Techniques KW - Neurons -- physiology KW - Peptides, Cyclic -- pharmacology KW - Nifedipine -- pharmacology KW - Oculomotor Nerve -- physiology KW - Calcium Channels -- physiology KW - Ganglia, Parasympathetic -- physiology KW - Calcium Channels -- drug effects KW - Ganglia, Parasympathetic -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80181656?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Calcium+currents+recorded+from+a+vertebrate+presynaptic+nerve+terminal+are+resistant+to+the+dihydropyridine+nifedipine.&rft.au=Stanley%2C+E+F%3BAtrakchi%2C+A+H&rft.aulast=Stanley&rft.aufirst=E&rft.date=1990-12-01&rft.volume=87&rft.issue=24&rft.spage=9683&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 - 1991-02-07 N1 - Date created - 1991-02-07 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Neurosci. 1986 May;6(5):1349-57 [2423658] Brain Res. 1986 Apr 9;370(2):397-400 [2423182] Proc Natl Acad Sci U S A. 1986 Nov;83(22):8804-7 [2430302] Science. 1987 Jan 2;235(4784):46-52 [2432656] Pflugers Arch. 1987 Aug;409(4-5):361-6 [2442705] Science. 1988 Jan 1;239(4835):57-61 [2447647] J Neurosci. 1988 Feb;8(2):463-71 [2448433] J Physiol. 1987 Dec;394:149-72 [2451016] Brain Res. 1988 Jul 26;456(2):324-32 [2463037] J Neurochem. 1989 Apr;52(4):1260-9 [2538565] Neurosci Lett. 1989 Mar 27;98(2):125-8 [2710405] Trends Neurosci. 1988 Oct;11(10):431-8 [2469160] Annu Rev Physiol. 1989;51:367-84 [2540697] Ann N Y Acad Sci. 1989;560:230-48 [2545135] Soc Gen Physiol Ser. 1989;44:239-50 [2476855] J Pharmacol Exp Ther. 1989 Nov;251(2):672-8 [2478694] Brain Res. 1989 Dec 29;505(2):341-5 [2598055] Nature. 1990 Mar 29;344(6265):449-51 [2157158] Neurosci Lett. 1989 Oct 23;105(1-2):14-8 [2562058] J Physiol. 1963 Sep;168:443-63 [14062687] J Physiol. 1963 Sep;168:464-75 [14062688] J Physiol. 1969 Jun;202(2):339-54 [4306543] Brain Res. 1971 Jan 22;25(2):317-34 [4322855] J Physiol. 1972 May;222(3):691-713 [4338175] Pflugers Arch. 1981 Aug;391(2):85-100 [6270629] Proc Natl Acad Sci U S A. 1982 Apr;79(7):2415-9 [6954549] Cell Mol Neurobiol. 1982 Sep;2(3):205-13 [7159902] J Neurochem. 1983 Nov;41(5):1455-9 [6619877] Life Sci. 1984 Sep 17;35(12):1289-95 [6207404] Nature. 1985 Mar 7-13;314(6006):94-6 [2579341] Proc Natl Acad Sci U S A. 1986 Sep;83(17):6656-9 [2428039] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A problem in identifying risk factors for disease using surrogate exposure variables that are under genetic control. AN - 80176691; 2260549 AB - The use of a surrogate exposure variable to represent a complex of genetic and/or nongenetic factors is commonplace in epidemiologic studies. The authors present an hypothetical example in which a surrogate exposure results from underlying unknown genetic and nongenetic factors, yet only the genetic component predisposes to disease. The results demonstrate how risk may be incorrectly attributed to the nongenetic component of exposure and suggest a possible explanation for the identification of a risk factor in one case-control study in one population, but not in another study of the same disease conducted in a different population. JF - American journal of epidemiology AU - Goldstein, A M AU - Falk, R T AU - Hodge, S E AD - Family Studies Section/EEB, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 1171 EP - 1175 VL - 132 IS - 6 SN - 0002-9262, 0002-9262 KW - Index Medicus KW - Humans KW - Case-Control Studies KW - Environmental Exposure -- adverse effects KW - Risk Factors KW - Morbidity KW - Genetics, Medical UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80176691?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+epidemiology&rft.atitle=A+problem+in+identifying+risk+factors+for+disease+using+surrogate+exposure+variables+that+are+under+genetic+control.&rft.au=Goldstein%2C+A+M%3BFalk%2C+R+T%3BHodge%2C+S+E&rft.aulast=Goldstein&rft.aufirst=A&rft.date=1990-12-01&rft.volume=132&rft.issue=6&rft.spage=1171&rft.isbn=&rft.btitle=&rft.title=American+journal+of+epidemiology&rft.issn=00029262&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-01-30 N1 - Date created - 1991-01-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Use of vitamin and mineral supplements: demographics and amounts of nutrients consumed. The 1987 Health Interview Survey. AN - 80176428; 2260541 AB - Data from the 1987 National Health Interview Survey show that 51.1% of the adults aged 18-99 years in the United States consumed a vitamin/mineral supplement in the past year, but that only 23.1% did so daily. Whites, women, and older individuals were more likely than blacks, men, and younger individuals to consume supplements regularly. Multivitamins were the most commonly consumed supplement, followed by vitamin C, calcium, vitamin E, and vitamin A. Results suggest that supplementation practices have changed little since the 1970s. Results regarding the amounts of nutrients obtained from supplements show that a food frequency type of methodology collects reasonably accurate data reflecting intake of supplements over the past year. Few, if any, individuals were consuming nutrients in amounts considered toxic. Although vitamin and mineral supplementation is a common health habit, it appears not to pose a significant health risk for most of the population. JF - American journal of epidemiology AU - Subar, A F AU - Block, G AD - National Institute of Health, National Cancer Institute, Division of Cancer Prevention and Control, Bethesda, MD 20892. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 1091 EP - 1101 VL - 132 IS - 6 SN - 0002-9262, 0002-9262 KW - Minerals KW - 0 KW - Vitamins KW - Index Medicus KW - United States KW - Demography KW - Self Medication KW - Aged, 80 and over KW - Humans KW - Adult KW - Aged KW - Nutrition Surveys KW - Middle Aged KW - Adolescent KW - Male KW - Female KW - Minerals -- administration & dosage KW - Vitamins -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80176428?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Tropical+Medicine+and+Hygiene&rft.atitle=Spotted+fever+rickettsiae+in+ticks+from+the+Northern+Sinai+Governate%2C+Egypt.&rft.au=Lange%2C+J+V%3BEl+Dessouky%2C+AG%3BManor%2C+E%3BMerdan%2C+AI%3BAzad%2C+A+F&rft.aulast=Lange&rft.aufirst=J&rft.date=1992-01-01&rft.volume=46&rft.issue=5&rft.spage=546&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-01-30 N1 - Date created - 1991-01-30 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Endothelins, peptides with potent vasoactive properties, are produced by human macrophages. AN - 80175947; 1701822 AB - Endothelins are peptides, originally isolated from endothelial cells, with potent vasoactive and mitogenic properties. In this study, we demonstrate that human macrophages synthesize and secrete endothelins. Cultured human macrophages were found by immunocytochemistry to stain positively for endothelin 1 and endothelin 3. Their capability to produce and release these peptides was confirmed by a combination of reverse-phase high-performance liquid chromatography and radioimmunoassays, specific for endothelin 1 and 3, respectively. Immunoreactive peptides were identified both in cellular extracts and in macrophage-conditioned medium. The secretion of endothelin 1, but not of endothelin 3, from macrophages could be stimulated 6-10-fold by lipopolysaccharide or phorbol myristate acetate (PMA). Northern blot analysis of total macrophage RNA using an endothelin 1 cDNA probe revealed induction of endothelin mRNA in PMA-treated macrophages. Furthermore, immunoreactive endothelin 1 and 3 were found in U937 cells, a human promonocytic line, and in freshly isolated human monocytes. In contrast, no immunoreactive endothelin was detected in cell extracts from human neutrophils and lymphocytes. The expression of endothelins in tissue macrophages was demonstrated in paraffin sections of human lung using immunohistochemistry. In conclusion, the finding that human macrophages produce endothelins suggests an important role for these peptides in the microenvironment of tissue macrophages. Macrophage-derived endothelins may have an essential function in blood vessel physiology, and aberrant production may contribute to vessel pathology. JF - The Journal of experimental medicine AU - Ehrenreich, H AU - Anderson, R W AU - Fox, C H AU - Rieckmann, P AU - Hoffman, G S AU - Travis, W D AU - Coligan, J E AU - Kehrl, J H AU - Fauci, A S AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1990/12/01/ PY - 1990 DA - 1990 Dec 01 SP - 1741 EP - 1748 VL - 172 IS - 6 SN - 0022-1007, 0022-1007 KW - Culture Media KW - 0 KW - Endothelins KW - RNA KW - 63231-63-0 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Cells, Cultured KW - Humans KW - RNA -- isolation & purification KW - Granulomatosis with Polyangiitis -- pathology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Granulomatosis with Polyangiitis -- physiopathology KW - Lung -- pathology KW - Immunohistochemistry KW - Chromatography, High Pressure Liquid KW - RNA -- genetics KW - Macrophages -- cytology KW - Endothelins -- biosynthesis KW - Endothelins -- genetics KW - Macrophages -- physiology KW - Endothelins -- analysis KW - Macrophages -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80175947?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Endothelins%2C+peptides+with+potent+vasoactive+properties%2C+are+produced+by+human+macrophages.&rft.au=Ehrenreich%2C+H%3BAnderson%2C+R+W%3BFox%2C+C+H%3BRieckmann%2C+P%3BHoffman%2C+G+S%3BTravis%2C+W+D%3BColigan%2C+J+E%3BKehrl%2C+J+H%3BFauci%2C+A+S&rft.aulast=Ehrenreich&rft.aufirst=H&rft.date=1990-12-01&rft.volume=172&rft.issue=6&rft.spage=1741&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 - 1991-01-31 N1 - Date created - 1991-01-31 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: FEBS Lett. 1988 Oct 10;238(2):249-52 [3139457] J Immunol. 1983 Aug;131(2):801-5 [6602846] Nature. 1988 Mar 31;332(6163):411-5 [2451132] Lancet. 1989 Sep 23;2(8665):747-8 [2570997] FEBS Lett. 1989 Aug 14;253(1-2):199-202 [2547655] J Clin Invest. 1989 Feb;83(2):708-12 [2536405] Jpn J Cancer Res. 1989 Apr;80(4):302-5 [2501245] Trends Pharmacol Sci. 1989 Sep;10(9):374-8 [2690429] Stroke. 1989 Nov;20(11):1553-6 [2683245] FEBS Lett. 1989 Sep 11;255(1):129-32 [2676594] Proc Natl Acad Sci U S A. 1989 Sep;86(18):7285-9 [2674952] J Biol Chem. 1989 Sep 5;264(25):14954-9 [2670930] Atherosclerosis. 1989 Aug;78(2-3):225-8 [2675859] J Biol Chem. 1989 Jun 25;264(18):10851-7 [2659594] Am J Physiol. 1989 Apr;256(4 Pt 2):R858-66 [2650570] Biochem Biophys Res Commun. 1989 Mar 31;159(3):1435-40 [2649101] Am J Physiol. 1990 Mar;258(3 Pt 1):C408-15 [1690514] Biochem Biophys Res Commun. 1990 Jan 30;166(2):608-14 [2154214] J Cardiovasc Pharmacol. 1989;13 Suppl 5:S229-31 [2473322] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - TCDD-induced altered expression of growth factors may have a role in producing cleft palate and enhancing the incidence of clefts after coadministration of retinoic acid and TCDD. AN - 80175369; 2260090 AB - 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is teratogenic in mice, inducing cleft palate and hydronephrosis at doses which are not overtly maternally toxic or embryotoxic. After TCDD exposure the palatal shelves of normal size come into contact, but fail to fuse due to altered differentiation of the medial epithelial cells. These cells continue to express EGF receptors, proliferate, and differentiate into an oral-like stratified squamous epithelium. The present study examines the effect of TCDD on the expression of growth factors which are believed to regulate differentiation and proliferation in the palate. This study also examined the combined effect of TCDD and retinoic acid (RA), since in teratology studies coadministration of these agents results in an enhancement of cleft palate incidence. Embryos were exposed in vivo on Gestation Day (GD) 10 or 12 to TCDD ot TCDD + RA and the palatal shelves were dissected on GD 14-16. Growth factor expression was determined immunohistochemically using antibodies to TGF-alpha, EGF, TGF-beta 1, or TGF-beta 2. The growth factors displayed specific spatial and temporal expression in the palatal shelves. TCDD reduced the expression of TGF-alpha, EGF, and TGF-beta 1 in epithelial and mesenchymal cells. The degree of reduction was generally greater after exposure on GD 10 to TCDD alone or in combination with RA when compared to that on GD 12. The abnormal proliferation and differentiation of TCDD-exposed medial cells may be a response to reduced expression of EGF and TGF-alpha. Low levels of these factors may be related to the previously observed elevated levels of EGF receptors in medial cells. In other systems, low levels of ligand have resulted in upregulation of the EGF receptor. Continued proliferation and altered differentiation could also be attributable to decreased levels of TGF-beta 1, a factor inhibitory to epithelial proliferation. Since TGF-beta 1 stimulates mesenchymal growth and TGF-alpha and EGF stimulate epithelial proliferation, the formation of small shelves after exposure to TCDD + RA on GD 10 may be due to the severe reduction in these factors. Only a slight to moderate reduction in growth factor expression occurs after exposure to TCDD + RA on GD 12 and in this case shelves of normal size form. Since TCDD and RA appear to act in part through pathways that involve TGF-beta 1, in vitro experiments were designed to examine the involvement of TGF-beta 1 in TCDD teratogenicity.(ABSTRACT TRUNCATED AT 400 WORDS) JF - Toxicology and applied pharmacology AU - Abbott, B D AU - Birnbaum, L S AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 418 EP - 432 VL - 106 IS - 3 SN - 0041-008X, 0041-008X KW - Polychlorinated Dibenzodioxins KW - 0 KW - Teratogens KW - Tretinoin KW - 5688UTC01R KW - Epidermal Growth Factor KW - 62229-50-9 KW - Transforming Growth Factors KW - 76057-06-2 KW - Index Medicus KW - Animals KW - Mice, Inbred C57BL KW - Mice KW - Drug Synergism KW - Immunohistochemistry KW - Male KW - Female KW - Tretinoin -- pharmacology KW - Cleft Palate -- chemically induced KW - Polychlorinated Dibenzodioxins -- toxicity KW - Cleft Palate -- metabolism KW - Epidermal Growth Factor -- metabolism KW - Transforming Growth Factors -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80175369?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=TCDD-induced+altered+expression+of+growth+factors+may+have+a+role+in+producing+cleft+palate+and+enhancing+the+incidence+of+clefts+after+coadministration+of+retinoic+acid+and+TCDD.&rft.au=Abbott%2C+B+D%3BBirnbaum%2C+L+S&rft.aulast=Abbott&rft.aufirst=B&rft.date=1990-12-01&rft.volume=106&rft.issue=3&rft.spage=418&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 - 1991-01-31 N1 - Date created - 1991-01-31 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human neutrophils release the Leu-8 lymph node homing receptor during cell activation. AN - 80167777; 1701670 AB - The Leu-8 molecule, the human homologue of the murine MEL-14 peripheral lymph node homing receptor, is expressed on neutrophils in both species and may be important in localization of cells to sites of inflammation. Most circulating human neutrophils express the Leu-8 molecule, and activation of neutrophils with phorbol myristate acetate causes a rapid decline in Leu-8 membrane fluorescence staining within 15 minutes. Northern blot analysis of total cellular RNA from neutrophils demonstrated two species of Leu-8 messenger RNA, a major one of 2.4 kb and a minor one of 1.9 kb. Because two different Leu-8 cDNA clones were obtained from human lymphocytes that were predicted to encode both transmembrane and phosphatidylinositol (PI)-anchored forms of the molecule, experiments were conducted to determine whether Leu-8 is anchored to neutrophils by a PI-anchor. There was a slight decrease in expression of Leu-8 on neutrophils when they were treated with PI-specific phospholipase C (PI-PLC). However, Leu-8 was abundant on neutrophils obtained from a patient with paroxysmal nocturnal hemoglobinuria. To determine the fate of the Leu-8 molecule during cell activation, neutrophils were labeled with 125I-anti-Leu-8. During activation antibody was rapidly lost from the cell surface and was not internalized, suggesting that Leu-8 is released from the cell membrane during cell activation. When cell extracts of neutrophils were compared with extracts of lymphoid cells by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting, the Leu-8 species expressed on neutrophils had a significantly higher and more variable relative mobility (70 to 120 Kd for neutrophils v 70 Kd for Jurkat T cells). In addition, Leu-8 molecules were detected in the supernatants of activated neutrophils. These results indicate that human neutrophils express a high-molecular-weight form of the Leu-8 molecule that has a conventional transmembrane anchor and is rapidly released from the membrane during activation. The loss of the Leu-8 membrane glycoprotein during activation may be a mechanism for rapid alteration of neutrophil adhesion characteristics. JF - Blood AU - Berg, M AU - James, S P AD - Mucosal Immunity Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. Y1 - 1990/12/01/ PY - 1990 DA - 1990 Dec 01 SP - 2381 EP - 2388 VL - 76 IS - 11 SN - 0006-4971, 0006-4971 KW - Cell Adhesion Molecules KW - 0 KW - DNA Probes KW - RNA, Messenger KW - L-Selectin KW - 126880-86-2 KW - Phosphoric Diester Hydrolases KW - EC 3.1.4.- KW - Phosphoinositide Phospholipase C KW - EC 3.1.4.11 KW - Phosphatidylinositol Diacylglycerol-Lyase KW - EC 4.6.1.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Gene Expression -- drug effects KW - Blotting, Western KW - Humans KW - RNA, Messenger -- analysis KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Hemoglobinuria, Paroxysmal -- blood KW - Nucleic Acid Hybridization KW - Phosphoric Diester Hydrolases -- pharmacology KW - Neutrophils -- metabolism KW - Lymph Nodes -- metabolism KW - Cell Adhesion Molecules -- secretion KW - Cell Adhesion Molecules -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80167777?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Human+neutrophils+release+the+Leu-8+lymph+node+homing+receptor+during+cell+activation.&rft.au=Berg%2C+M%3BJames%2C+S+P&rft.aulast=Berg&rft.aufirst=M&rft.date=1990-12-01&rft.volume=76&rft.issue=11&rft.spage=2381&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=00064971&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-01-29 N1 - Date created - 1991-01-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Changes in lipid ordering of model phospholipid membranes treated with chrysotile and crocidolite asbestos. AN - 80162808; 2174769 AB - A variety of inorganic particles bind to cell membranes and cause alterations in phagocytosis, migration, and metabolism leading to eventual cell death. The mechanism which mediate these events at the complex membrane level are not known. In attempting to define the mechanisms of asbestos-induced membrane changes, we have prepared small unilamellar vesicles (SUV) of dipalmitoyl phosphatidylcholine as a simplified model of the cell membrane. Negatively stained preparations for electron microscopy demonstrated that the SUVs bind to both chrysotile and crocidolite asbestos fibers. Electron spin resonance showed that both asbestos types caused increased membrane rigidity at the level of the 12th carbon, whereas chrysotile induced increased rigidity at the 5th carbon level as well. Studies using DPPC membranes compared to SUVs made of phosphatidylcholine from egg yolk support the view that lipid peroxidation may play no significant role in alterations of membrane rigidity induced by the asbestos particle binding. Similar alterations of membrane rigidity and lipid peroxidation at the depth of the 12th carbon have been reported in complex naturally occurring erythrocyte membranes. This suggests that our observations may be relevant to biological membranes and that the model system of SUVs is appropriate for additional studies on the mechanisms of particle-induced membrane injury. JF - Environmental research AU - Gendek, E G AU - Brody, A R AD - Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 152 EP - 167 VL - 53 IS - 2 SN - 0013-9351, 0013-9351 KW - Asbestos, Serpentine KW - 0 KW - Liposomes KW - Membrane Lipids KW - Phospholipids KW - Asbestos, Crocidolite KW - 12001-28-4 KW - Asbestos KW - 1332-21-4 KW - Index Medicus KW - Rats KW - Animals KW - Electron Spin Resonance Spectroscopy KW - Lipid Peroxidation -- drug effects KW - Microscopy, Electron KW - Phospholipids -- metabolism KW - Membrane Lipids -- metabolism KW - Liposomes -- metabolism KW - Erythrocyte Membrane -- ultrastructure KW - Erythrocyte Membrane -- drug effects KW - Asbestos -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80162808?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+research&rft.atitle=Changes+in+lipid+ordering+of+model+phospholipid+membranes+treated+with+chrysotile+and+crocidolite+asbestos.&rft.au=Gendek%2C+E+G%3BBrody%2C+A+R&rft.aulast=Gendek&rft.aufirst=E&rft.date=1990-12-01&rft.volume=53&rft.issue=2&rft.spage=152&rft.isbn=&rft.btitle=&rft.title=Environmental+research&rft.issn=00139351&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-01-22 N1 - Date created - 1991-01-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression of growth-related genes during tumor progression in v-raf-transformed rat liver epithelial cells. AN - 80160085; 1701345 AB - Clonal cell lines were derived from rat liver epithelial cells following their transformation with either v-raf or v-raf/v-myc. Cells transformed with v-raf alone showed reduced tumor incidence and tumor growth rates when implanted into nude mice, compared to cells also expressing the v-myc oncogene. A series of additional clones isolated from a tumor obtained following inoculation of an athymic nude mouse with the v-raf-transformed rat liver epithelial cells displayed an intermediate range of tumor aggressiveness. These findings indicate that unknown genotypic and/or phenotypic changes occur during tumor formation in vivo, which are required in addition to raf activation for complete expression of the malignant phenotype. This in vitro model of tumor progression was used to examine alterations in the expression of genes related to the growth control of liver epithelial cells, which may be involved in the malignant conversion of the preneoplastic cells. A close association was observed between the increased level of expression of the transforming growth factors alpha and beta 1, the decreased expression of extracellular matrix proteins fibronectin and collagen I, and the tumor aggressiveness (latency/growth rate), suggesting a causal role for these factors in the progression of v-raf-transformed rat liver epithelial cells to the fully malignant phenotype. JF - Cancer research AU - Hampton, L L AU - Worland, P J AU - Yu, B AU - Thorgeirsson, S S AU - Huggett, A C AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1990/12/01/ PY - 1990 DA - 1990 Dec 01 SP - 7460 EP - 7467 VL - 50 IS - 23 SN - 0008-5472, 0008-5472 KW - v-myc KW - v-raf KW - Extracellular Matrix Proteins KW - 0 KW - Fibronectins KW - Growth Substances KW - Retroviridae Proteins, Oncogenic KW - Transforming Growth Factor alpha KW - Transforming Growth Factor beta KW - RNA KW - 63231-63-0 KW - DNA KW - 9007-49-2 KW - Oncogene Proteins v-raf KW - EC 2.7.11.1 KW - Index Medicus KW - Transforming Growth Factor beta -- biosynthesis KW - Animals KW - Blotting, Northern KW - DNA -- analysis KW - Extracellular Matrix Proteins -- biosynthesis KW - RNA -- analysis KW - Mice, Nude KW - Mice KW - Rats KW - Gene Expression Regulation, Neoplastic KW - Blotting, Western KW - Down-Regulation KW - Blotting, Southern KW - Transformation, Genetic KW - Fibronectins -- biosynthesis KW - Transforming Growth Factor alpha -- biosynthesis KW - Retroviridae Proteins, Oncogenic -- biosynthesis KW - Cell Division -- genetics KW - Male KW - Liver Neoplasms -- metabolism KW - Growth Substances -- biosynthesis KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80160085?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Expression+of+growth-related+genes+during+tumor+progression+in+v-raf-transformed+rat+liver+epithelial+cells.&rft.au=Hampton%2C+L+L%3BWorland%2C+P+J%3BYu%2C+B%3BThorgeirsson%2C+S+S%3BHuggett%2C+A+C&rft.aulast=Hampton&rft.aufirst=L&rft.date=1990-12-01&rft.volume=50&rft.issue=23&rft.spage=7460&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 - 1991-01-22 N1 - Date created - 1991-01-22 N1 - Date revised - 2017-01-13 N1 - Gene symbol - v-myc; v-raf N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Uterine adenocarcinoma in mice following developmental treatment with estrogens: a model for hormonal carcinogenesis. AN - 80160017; 2174729 AB - In order to study the effects of perinatal exposure to estrogens on the developing reproductive tract, outbred female mice were treated neonatally (days 1 to 5) with varying doses of diethylstilbestrol (DES) and sacrificed from 1 to 18 months of age. Uterine adenocarcinoma was observed in a time- and dose-related manner after DES treatment; at 18 months, neoplastic lesions were seen in 90% of the mice exposed neonatally to 2 micrograms/pup of DES/day, while none was observed in the corresponding control mice. These DES-induced uterine tumors were estrogen dependent; when DES-treated mice were ovariectomized before puberty, no uterine tumors developed. As a marker for neoplasia, uterine tumors were transplanted and carried as serial transplants in nude mice. The transplanted tissue retained some differentiated uterine gland structure and function and also required estrogen supplementation for maintenance. Additional groups of neonatal mice were treated with various DES analogues (hexestrol and tetrafluorodiethylstilbestrol) and steroidal estrogens. The compounds were ranked according to developmental estrogenic potency (hexestrol greater than trifluorodiethylstilbestrol greater than DES greater than 17 beta-estradiol). The combined prevalence of uterine atypical hyperplasia and adenocarcinoma follows the order of estrogenic potency. The experimental induction of these tumors will provide the basis for additional studies in mechanisms of hormonal carcinogenesis. JF - Cancer research AU - Newbold, R R AU - Bullock, B C AU - McLachlan, J A AD - Developmental Endocrinology and Pharmacology Section, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina 27709. Y1 - 1990/12/01/ PY - 1990 DA - 1990 Dec 01 SP - 7677 EP - 7681 VL - 50 IS - 23 SN - 0008-5472, 0008-5472 KW - Estrogens KW - 0 KW - Dihydrotestosterone KW - 08J2K08A3Y KW - Hexestrol KW - 10BI795R7D KW - Progesterone KW - 4G7DS2Q64Y KW - Estradiol KW - 4TI98Z838E KW - Diethylstilbestrol KW - 731DCA35BT KW - Index Medicus KW - Vagina -- drug effects KW - Hyperplasia -- pathology KW - Animals KW - Endometriosis -- chemically induced KW - Dose-Response Relationship, Drug KW - Progesterone -- pharmacology KW - Estradiol -- pharmacology KW - Carcinoma, Squamous Cell -- chemically induced KW - Disease Models, Animal KW - Mice, Nude KW - Mice KW - Epithelium -- drug effects KW - Pregnancy KW - Hyperplasia -- chemically induced KW - Dihydrotestosterone -- pharmacology KW - Diethylstilbestrol -- pharmacology KW - Hexestrol -- pharmacology KW - Uterus -- pathology KW - Female KW - Estrogens -- pharmacology KW - Adenocarcinoma -- etiology KW - Uterine Neoplasms -- etiology KW - Uterine Neoplasms -- pathology KW - Prenatal Exposure Delayed Effects KW - Adenocarcinoma -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80160017?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Uterine+adenocarcinoma+in+mice+following+developmental+treatment+with+estrogens%3A+a+model+for+hormonal+carcinogenesis.&rft.au=Newbold%2C+R+R%3BBullock%2C+B+C%3BMcLachlan%2C+J+A&rft.aulast=Newbold&rft.aufirst=R&rft.date=1990-12-01&rft.volume=50&rft.issue=23&rft.spage=7677&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 - 1991-01-22 N1 - Date created - 1991-01-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cholera toxin inhibits signal transduction by several mitogens and the in vitro growth of human small-cell lung cancer. AN - 80158085; 2174911 AB - Cholera toxin (CT) inhibited the in vitro growth of three of four human small-cell lung carcinoma (SCLC) cell lines with a 50% inhibitory concentration of 27-242 ng/ml. Loss of surface membrane ruffling and the capacity of [Tyr4]-bombesin, vasopressin, and fetal calf serum to stimulate increases in intracellular free calcium clearly preceded effects on cellular metabolic activity and cell growth. 125I-[Tyr4]-bombesin binding was unaffected by CT treatment but [Tyr4]-bombesin stimulated phospholipase C activity was decreased in membranes from CT-treated SCLC cells. CT stimulated a rapid but transient increase in intracellular cyclic AMP ([cAMP]i) in SCLC. The effects of CT on susceptible SCLC were not reproduced by elevations of [cAMP]i induced by forskolin or cyclic AMP analogues. GM1 ganglioside, the cellular binding site for CT, was highly expressed in the CT-sensitive but not the CT-resistant SCLC cell lines. In contrast, expression of guanine nucleotide binding protein substrates for ADP-ribosylation by CT was similar. These data demonstrate the existence of a CT-sensitive growth inhibitory pathway in SCLC-bearing GM1 ganglioside. Addition of CT results in decreased responsiveness to several mitogenic stimuli. These results suggest novel therapeutic approaches to human SCLC. JF - The Journal of clinical investigation AU - Viallet, J AU - Sharoni, Y AU - Frucht, H AU - Jensen, R T AU - Minna, J D AU - Sausville, E A AD - National Cancer Institute-Navy Medical Oncology Branch, Bethesda, Maryland. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 1904 EP - 1912 VL - 86 IS - 6 SN - 0021-9738, 0021-9738 KW - Growth Inhibitors KW - 0 KW - Mitogens KW - Receptors, Bombesin KW - Receptors, Neurotransmitter KW - Vasopressins KW - 11000-17-2 KW - Colforsin KW - 1F7A44V6OU KW - Adenosine Diphosphate Ribose KW - 20762-30-5 KW - G(M1) Ganglioside KW - 37758-47-7 KW - Ionomycin KW - 56092-81-0 KW - Cholera Toxin KW - 9012-63-9 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Adenylyl Cyclases KW - EC 4.6.1.1 KW - Bombesin KW - PX9AZU7QPK KW - Calcium KW - SY7Q814VUP KW - Abridged Index Medicus KW - Index Medicus KW - Cell Membrane -- drug effects KW - Dose-Response Relationship, Drug KW - Humans KW - Adenylyl Cyclases -- metabolism KW - Cell Division -- drug effects KW - Cell Membrane -- ultrastructure KW - Ionomycin -- pharmacology KW - Adenosine Diphosphate Ribose -- metabolism KW - Receptors, Neurotransmitter -- physiology KW - Calcium -- metabolism KW - Colforsin -- pharmacology KW - Tumor Cells, Cultured KW - GTP-Binding Proteins -- metabolism KW - In Vitro Techniques KW - Vasopressins -- pharmacology KW - Bombesin -- pharmacology KW - G(M1) Ganglioside -- metabolism KW - Time Factors KW - Mitogens -- pharmacology KW - Carcinoma, Small Cell -- pathology KW - Signal Transduction -- drug effects KW - Cholera Toxin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80158085?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cholera+toxin+inhibits+signal+transduction+by+several+mitogens+and+the+in+vitro+growth+of+human+small-cell+lung+cancer.&rft.au=Viallet%2C+J%3BSharoni%2C+Y%3BFrucht%2C+H%3BJensen%2C+R+T%3BMinna%2C+J+D%3BSausville%2C+E+A&rft.aulast=Viallet&rft.aufirst=J&rft.date=1990-12-01&rft.volume=86&rft.issue=6&rft.spage=1904&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 - 1991-01-22 N1 - Date created - 1991-01-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nature. 1970 Aug 15;227(5259):680-5 [5432063] J Biol Chem. 1988 Feb 25;263(6):2808-16 [2830264] Exp Cell Res. 1976 Dec;103(2):295-302 [1001364] Exp Cell Res. 1977 Aug;108(1):31-9 [196871] Cell. 1978 Nov;15(3):801-11 [83196] Proc Natl Acad Sci U S A. 1979 Sep;76(9):4350-4 [388439] Anal Biochem. 1980 Dec;109(2):399-402 [7224165] Cancer Res. 1981 Jun;41(6):2294-304 [7016311] Biochem J. 1982 Sep 15;206(3):587-95 [7150264] Cancer Res. 1983 Apr;43(4):1473-6 [6299521] J Immunol Methods. 1983 Dec 16;65(1-2):55-63 [6606682] J Cell Biol. 1984 Mar;98(3):801-9 [6321519] Proc Natl Acad Sci U S A. 1988 Mar;85(6):1859-63 [2450349] Adv Enzymol Relat Areas Mol Biol. 1988;61:303-79 [3128060] FASEB J. 1988 Jul;2(10):2569-74 [2838362] J Biol Chem. 1988 Jul 15;263(20):9887-95 [2454923] Biochem J. 1988 Jul 1;253(1):193-202 [2844165] EMBO J. 1988 Sep;7(9):2741-7 [3181139] Biochem Biophys Res Commun. 1988 Nov 15;156(3):1383-9 [2847733] Biochim Biophys Acta. 1988 Nov 18;972(2):232-8 [2847807] Biochem J. 1988 Oct 15;255(2):403-10 [2849413] J Clin Invest. 1989 Jan;83(1):234-42 [2536043] J Biol Chem. 1989 Feb 25;264(6):3206-10 [2536738] Proc Natl Acad Sci U S A. 1989 Oct;86(20):7809-13 [2510151] Cancer Res. 1990 Sep 1;50(17):5257-62 [2167151] Prog Growth Factor Res. 1989;1(2):89-97 [2491257] J Cell Physiol. 1980 Mar;102(3):317-21 [6248570] Cancer Res. 1985 Jun;45(6):2913-23 [2985257] Nature. 1985 Aug 29-Sep 4;316(6031):823-6 [2993906] Proc Natl Acad Sci U S A. 1985 Nov;82(22):7475-9 [2999763] J Biol Chem. 1986 Feb 25;261(6):2712-7 [3005261] Proc Natl Acad Sci U S A. 1986 Aug;83(15):5673-7 [3016713] Science. 1986 Sep 5;233(4768):1061-8 [3090687] Science. 1986 Oct 10;234(4773):161-6 [3018928] J Immunol Methods. 1986 Nov 20;94(1-2):57-63 [3782817] Proc Natl Acad Sci U S A. 1986 Dec;83(23):8893-7 [3024154] Proc Natl Acad Sci U S A. 1987 Jan;84(1):141-5 [3540954] Cancer Res. 1987 Feb 1;47(3):821-5 [3026617] Cancer Res. 1987 Feb 15;47(4):936-42 [3802100] Gastroenterology. 1987 Apr;92(4):891-904 [3549423] J Biol Chem. 1987 Jun 5;262(16):7744-50 [3034904] Biochim Biophys Acta. 1987 Jul 6;929(2):197-202 [3109499] J Cell Biol. 1987 Sep;105(3):1153-61 [3654749] J Biol Chem. 1987 Dec 5;262(34):16456-60 [2824495] Proc Natl Acad Sci U S A. 1976 Apr;73(4):1034-7 [177969] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Recessive oncogenes in lung cancer. AN - 80157826; 2174662 AB - The observation that carcinogen exposure is strongly associated with the probability of developing pulmonary neoplasms has suggested for many years that acquired somatic mutations play a key role in the genesis of these environmentally induced cancers. With the advent of new techniques in cytogenetics and in the molecular analysis of DNA extracted from lung tumors, it has now become possible to test this hypothesis and to search for candidate genes that may be targeted by the chronic exposure of these environmental insults. Early work in this field, studying lung tumors of different histologic types, appears to implicate several distinct chromosomal loci (at chromosomes 3p, 13q, 17p, and others), suggesting that sequential genetic events occur during the initiation and progression pathways to pulmonary tumorigenesis. Identifying the candidate gene products and understanding the chronology and stringency of mutational events at these loci will be an essential goal to understanding the cellular basis of lung tumors and for developing strategies for the next generation of diagnostic and therapeutic studies. JF - The American review of respiratory disease AU - Kaye, F J AU - Kratzke, R A AU - Gerster, J L AU - Lin, P S AD - NCI-Navy Medical Oncology Branch, Naval Hospital, Bethesda, MD 20817. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - S44 EP - S47 VL - 142 IS - 6 Pt 2 SN - 0003-0805, 0003-0805 KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Chromosomes, Human, Pair 3 -- ultrastructure KW - Oncogenes -- genetics KW - Lung Neoplasms -- genetics KW - Genes, Retinoblastoma -- genetics KW - Genes, Recessive KW - Carcinoma, Small Cell -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80157826?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+review+of+respiratory+disease&rft.atitle=Recessive+oncogenes+in+lung+cancer.&rft.au=Kaye%2C+F+J%3BKratzke%2C+R+A%3BGerster%2C+J+L%3BLin%2C+P+S&rft.aulast=Kaye&rft.aufirst=F&rft.date=1990-12-01&rft.volume=142&rft.issue=6+Pt+2&rft.spage=S44&rft.isbn=&rft.btitle=&rft.title=The+American+review+of+respiratory+disease&rft.issn=00030805&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-01-14 N1 - Date created - 1991-01-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Altered responsiveness of rat liver epithelial cells to transforming growth factor beta 1 following their transformation with v-raf. AN - 80157280; 2174726 AB - The effects of transforming growth factor beta (type 1) (TGF-beta 1) on DNA synthesis, cell proliferation, and protein synthesis were examined in a series of v-raf-transformed rat liver epithelial (RLE) cells, which exhibit a range of transformed phenotypes. All of the transformed cells were relatively resistant to the growth-inhibitory effects of TGF-beta 1, compared to normal RLE cells and control cells infected with a helper virus. The more tumorigenic cell lines had very few surface receptors for TGF-beta 1 and showed no increase in the secretion of a number of specific proteins, including fibronectin, following TGF-beta 1 treatment. In contrast, the more normal-looking, less tumorigenic v-raf-transformed cells bound similar amounts of TGF-beta 1 as normal RLE and control cells and showed a similar pattern of TGF-beta 1-stimulated protein secretion. These findings suggest that the effects of TGF-beta 1 on cell proliferation and on the expression of certain secreted proteins are mediated through different mechanisms. Following transformation of RLE cells with v-raf, the signalling pathways controlling TGF-beta 1 growth inhibition are perturbed, while those involved in regulating the synthesis of certain proteins may remain intact. Thus, the escape from the various distinct biological effects of TGF-beta 1 may be an important stage in the progression of neoplastic transformation of RLE cells in vitro. JF - Cancer research AU - Huggett, A C AU - Hampton, L L AU - Ford, C P AU - Wirth, P J AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, NIH, Bethesda, Maryland 20892. Y1 - 1990/12/01/ PY - 1990 DA - 1990 Dec 01 SP - 7468 EP - 7475 VL - 50 IS - 23 SN - 0008-5472, 0008-5472 KW - v-raf KW - Extracellular Matrix Proteins KW - 0 KW - RNA, Messenger KW - Receptors, Cell Surface KW - Receptors, Transforming Growth Factor beta KW - Transforming Growth Factor beta KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Blotting, Northern KW - Dose-Response Relationship, Drug KW - Cell Division -- drug effects KW - Extracellular Matrix Proteins -- biosynthesis KW - RNA, Messenger -- analysis KW - Extracellular Matrix Proteins -- drug effects KW - DNA -- biosynthesis KW - Epithelium -- drug effects KW - Receptors, Cell Surface -- metabolism KW - Rats KW - Transformation, Genetic KW - Electrophoresis, Gel, Two-Dimensional KW - In Vitro Techniques KW - Transforming Growth Factor beta -- biosynthesis KW - Transforming Growth Factor beta -- pharmacology KW - Liver -- drug effects KW - Transforming Growth Factor beta -- metabolism KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80157280?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Altered+responsiveness+of+rat+liver+epithelial+cells+to+transforming+growth+factor+beta+1+following+their+transformation+with+v-raf.&rft.au=Huggett%2C+A+C%3BHampton%2C+L+L%3BFord%2C+C+P%3BWirth%2C+P+J%3BThorgeirsson%2C+S+S&rft.aulast=Huggett&rft.aufirst=A&rft.date=1990-12-01&rft.volume=50&rft.issue=23&rft.spage=7468&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 - 1991-01-22 N1 - Date created - 1991-01-22 N1 - Date revised - 2017-01-13 N1 - Gene symbol - v-raf N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Cloned yeast and mammalian transcription factor TFIID gene products support basal but not activated metallothionein gene transcription. AN - 80156792; 2251259 AB - Transcription factor IID (TFIID), the "TATA binding factor," is thought to play a key role in the regulation of eukaryotic transcriptional initiation. We have studied the role of TFIID in the transcription of the yeast metallothionein gene, which is regulated by the copper-dependent activator protein ACE1. Both basal and induced transcription of the metallothionein gene require TFIID and a functional TATA binding site. Crude human and mouse TFIID fractions, prepared from mammalian cells, respond to stimulation by ACE1. In contrast, human and yeast TFIID proteins expressed from the cloned genes do not respond to ACE1, except in the presence of wheat germ or yeast total cell extracts. These results indicate that the cloned TFIID gene products lack a component(s) or modification(s) that is required for regulated as compared to basal transcription. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Kambadur, R AU - Culotta, V AU - Hamer, D AD - Laboratory of Biochemistry, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 9168 EP - 9172 VL - 87 IS - 23 SN - 0027-8424, 0027-8424 KW - Recombinant Proteins KW - 0 KW - Transcription Factor TFIID KW - Transcription Factors KW - Metallothionein KW - 9038-94-2 KW - Index Medicus KW - Animals KW - Humans KW - Mice KW - Binding Sites KW - Cloning, Molecular KW - Mutagenesis, Site-Directed KW - Base Sequence KW - Recombinant Proteins -- metabolism KW - Models, Genetic KW - Molecular Sequence Data KW - Gene Expression Regulation KW - TATA Box KW - Saccharomyces cerevisiae -- genetics KW - Saccharomyces cerevisiae -- metabolism KW - Genes KW - Genes, Fungal KW - Transcription Factors -- metabolism KW - Metallothionein -- genetics KW - Transcription, Genetic KW - Transcription Factors -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80156792?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cloned+yeast+and+mammalian+transcription+factor+TFIID+gene+products+support+basal+but+not+activated+metallothionein+gene+transcription.&rft.au=Kambadur%2C+R%3BCulotta%2C+V%3BHamer%2C+D&rft.aulast=Kambadur&rft.aufirst=R&rft.date=1990-12-01&rft.volume=87&rft.issue=23&rft.spage=9168&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 - 1991-01-16 N1 - Date created - 1991-01-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: EMBO J. 1985 Dec 1;4(12):3273-80 [3912167] Proc Natl Acad Sci U S A. 1985 Dec;82(24):8562-6 [3001709] J Mol Biol. 1986 Feb 5;187(3):363-78 [3009831] Science. 1988 Apr 15;240(4850):317-21 [2832951] Proc Natl Acad Sci U S A. 1988 Apr;85(8):2691-5 [3282236] Nature. 1988 Jul 7;334(6177):37-42 [3290687] Nature. 1988 Jul 7;334(6177):77-80 [3290688] Gene. 1988 May 15;65(1):129-33 [2840354] Mol Cell Biol. 1988 Jul;8(7):2745-52 [3043194] Nature. 1988 Oct 20;335(6192):683-9 [3050531] Cell. 1988 Nov 18;55(4):705-17 [3052856] Proc Natl Acad Sci U S A. 1989 Jan;86(1):65-9 [2643107] Cell. 1989 Feb 24;56(4):549-61 [2917366] Mol Cell Biol. 1989 Feb;9(2):421-9 [2651899] EMBO J. 1989 Jan;8(1):255-60 [2653812] Mol Cell Biol. 1989 Mar;9(3):1376-80 [2725504] Proc Natl Acad Sci U S A. 1989 Jul;86(13):4843-7 [2662184] Proc Natl Acad Sci U S A. 1989 Jul;86(14):5267-71 [2664778] Proc Natl Acad Sci U S A. 1989 Aug;86(15):5718-22 [2569738] Cell. 1989 Sep 22;58(6):1173-81 [2550146] Cell. 1989 Sep 22;58(6):1183-91 [2673545] Mol Cell Biol. 1989 Sep;9(9):4091-5 [2674688] Nature. 1989 Sep 28;341(6240):299-303 [2677740] Proc Natl Acad Sci U S A. 1989 Oct;86(20):7785-9 [2682626] Proc Natl Acad Sci U S A. 1989 Nov;86(21):8377-81 [2682650] Mol Cell Biol. 1989 Dec;9(12):5298-304 [2685558] Proc Natl Acad Sci U S A. 1989 Dec;86(24):9803-7 [2690073] EMBO J. 1990 Apr;9(4):1299-308 [2323340] Nature. 1990 Jun 28;345(6278):783-6 [2193231] Science. 1990 Jun 29;248(4963):1625-30 [2363050] Science. 1990 Jun 29;248(4963):1646-50 [2194289] Cell. 1990 Jun 29;61(7):1161-4 [2194664] Cell. 1990 Jun 29;61(7):1179-86 [2194666] Cell. 1990 Jun 29;61(7):1187-97 [2194667] Cell. 1990 Jun 29;61(7):1199-208 [2163758] Cell. 1990 Jun 29;61(7):1209-15 [2163759] Nature. 1990 Jul 19;346(6281):291-4 [2197558] Nature. 1990 Jul 26;346(6282):387-90 [2374612] Genes Dev. 1990 Jul;4(7):1141-8 [2210373] Annu Rev Biochem. 1981;50:349-83 [6791577] Methods Enzymol. 1983;101:582-98 [6888276] Science. 1985 May 10;228(4700):685-90 [3887570] Proc Natl Acad Sci U S A. 1985 Dec;82(24):8557-61 [3909147] Science. 1986 May 2;232(4750):613-8 [3457470] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - A clinicopathologic study of 34 cases of diffuse pulmonary hemorrhage with lung biopsy confirmation. AN - 80156436; 2252102 AB - Based on a clinicopathologic study of 34 patients with biopsy-confirmed diffuse pulmonary hemorrhage (DPH), we present an approach to the differential diagnosis of DPH with attention to histologic features such as capillaritis and the importance of laboratory tests such as anticytoplasmic autoantibodies (ACPA). The following DPH syndromes were encountered: antibasement membrane antibody (ABMA) disease (four cases); idiopathic pulmonary hemorrhage (four cases); Wegener's granulomatosis (WG) (five cases); probable WG (six cases); systemic necrotizing vasculitis otherwise unclassified (three cases); systemic lupus erythematosus (two cases); rheumatoid arthritis (one case); seronegative juvenile rheumatoid arthritis (one case); IgA nephropathy (one case); idiopathic glomerulonephritis (two cases--one with and one without immune complexes); and unclassified pulmonary-renal syndromes (five cases). Capillaritis was found in lung biopsy samples from 30 of the 34 patients (88%) and included patients with every type of DPH syndrome. Serologic testing for ACPA was useful in the diagnosis of WG. Identification of ABMA in the serum, kidney, or lung was the defining feature for the diagnosis of ABMA-mediated disease. Subclassification of the cases could not be done solely on histologic grounds except for cases of WG that showed granulomatous inflammation, foci of necrosis, or vasculitis. Classification of the remaining cases required correlation with (a) clinical and laboratory data; (b) biopsy samples from other sites such as the kidney, nasal sinuses, or skin; and (c) results of immunofluorescence or electron microscopy of kidney or lung biopsy samples. JF - The American journal of surgical pathology AU - Travis, W D AU - Colby, T V AU - Lombard, C AU - Carpenter, H A AD - Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 1112 EP - 1125 VL - 14 IS - 12 SN - 0147-5185, 0147-5185 KW - Adrenal Cortex Hormones KW - 0 KW - Immunoglobulin G KW - Cyclophosphamide KW - 8N3DW7272P KW - Complement System Proteins KW - 9007-36-7 KW - Index Medicus KW - Immunoglobulin G -- analysis KW - Diagnosis, Differential KW - Pneumonia -- diagnosis KW - Humans KW - Prognosis KW - Capillaries -- ultrastructure KW - Aged KW - Biopsy KW - Child KW - Complement System Proteins -- immunology KW - Pneumonia -- pathology KW - Autoimmune Diseases -- diagnosis KW - Adrenal Cortex Hormones -- therapeutic use KW - Cyclophosphamide -- therapeutic use KW - Capillaries -- pathology KW - Adult KW - Autoimmune Diseases -- pathology KW - Middle Aged KW - Microscopy, Electron KW - Adolescent KW - Fluorescent Antibody Technique KW - Male KW - Female KW - Autoimmune Diseases -- immunology KW - Lung -- blood supply KW - Hemorrhage -- diagnosis KW - Lung Diseases -- diagnosis KW - Hemorrhage -- drug therapy KW - Hemorrhage -- pathology KW - Lung Diseases -- pathology KW - Lung -- ultrastructure KW - Lung -- pathology KW - Lung Diseases -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80156436?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+surgical+pathology&rft.atitle=A+clinicopathologic+study+of+34+cases+of+diffuse+pulmonary+hemorrhage+with+lung+biopsy+confirmation.&rft.au=Travis%2C+W+D%3BColby%2C+T+V%3BLombard%2C+C%3BCarpenter%2C+H+A&rft.aulast=Travis&rft.aufirst=W&rft.date=1990-12-01&rft.volume=14&rft.issue=12&rft.spage=1112&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+surgical+pathology&rft.issn=01475185&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-01-15 N1 - Date created - 1991-01-15 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interaction between serotonin and other regulators of aldosterone secretion in rat adrenal glomerulosa cells. AN - 80150788; 2174345 AB - Although serotonin (5HT) is a recognized stimulator of aldosterone secretion in vivo and in vitro, its physiological role as a regulator of mineralocorticoid secretion and its mechanism of action in the adrenal glomerulosa have not been elucidated. To address these questions we studied the interaction of 5HT with other aldosterone regulators in isolated rat adrenal glomerulosa cells. 5HT stimulated aldosterone production 14-fold, with an ED50 of 20 +/- 5 nM, and stimulation was maximal at 0.8 microM. The stimulation of aldosterone production by 5HT was accompanied by a 5-fold increase in cAMP production, with an ED50 of 1 microM. Threshold levels of 5HT (1 nM) potentiated the effect of submaximal concentrations of angiotensin-II (AII), decreasing the ED50 from 1.3 to 0.46 nM and increasing the maximum response in an additive manner. In contrast, the stimulatory effect of 5HT was purely additive to that of submaximal ACTH concentrations. 5HT had no effect on aldosterone secretion stimulated by maximal ACTH concentrations, despite full additivity on cAMP accumulation. Stimulations of steroidogenesis by potassium and 5HT were fully additive at submaximal concentrations, but only partially additive at-maximal levels. To determine the mechanism of the synergistic effects of AII and 5HT, we analyzed the interaction of both stimuli on cAMP accumulation, intracellular calcium, and inositol phosphate formation. Consistent with the inhibitory effect of AII on adenylate cyclase, in the presence of AII the stimulation of cAMP by 5HT was reduced by 18 +/- 3%. 5HT alone had no effect on cytosolic calcium, but significantly enhanced the peak and later phases of the AII-stimulated increase (P less than 0.005). This effect of 5HT was due to calcium influx and not to release from intracellular pools, as shown by suppression of the potentiation in the absence of extracellular calcium and the lack of effect of 5HT on basal or AII-stimulated inositol phosphate formation. The ability of low concentrations of 5HT to potentiate the stimulatory effect of AII on aldosterone secretion suggests that under some physiological conditions, 5HT may play a role in regulating the adrenal sensitivity to AII. JF - Endocrinology AU - Rocco, S AU - Ambroz, C AU - Aguilera, G AD - Section on Endocrine Physiology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 3103 EP - 3110 VL - 127 IS - 6 SN - 0013-7227, 0013-7227 KW - Inositol Phosphates KW - 0 KW - Angiotensin II KW - 11128-99-7 KW - Serotonin KW - 333DO1RDJY KW - Aldosterone KW - 4964P6T9RB KW - Adrenocorticotropic Hormone KW - 9002-60-2 KW - Cyclic AMP KW - E0399OZS9N KW - Potassium KW - RWP5GA015D KW - Abridged Index Medicus KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Cytosol -- metabolism KW - Animals KW - Drug Interactions KW - Inositol Phosphates -- metabolism KW - Cells, Cultured KW - Kinetics KW - Cyclic AMP -- metabolism KW - Potassium -- pharmacology KW - Male KW - Zona Glomerulosa -- drug effects KW - Serotonin -- pharmacology KW - Zona Glomerulosa -- secretion KW - Zona Glomerulosa -- metabolism KW - Adrenocorticotropic Hormone -- pharmacology KW - Aldosterone -- secretion KW - Angiotensin II -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80150788?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Interaction+between+serotonin+and+other+regulators+of+aldosterone+secretion+in+rat+adrenal+glomerulosa+cells.&rft.au=Rocco%2C+S%3BAmbroz%2C+C%3BAguilera%2C+G&rft.aulast=Rocco&rft.aufirst=S&rft.date=1990-12-01&rft.volume=127&rft.issue=6&rft.spage=3103&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=00137227&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-01-17 N1 - Date created - 1991-01-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Increased eIF-2 alpha expression in mitogen-activated primary T lymphocytes. AN - 80145874; 1701139 AB - G0 human T cells synthesize protein at low rates and contain very low levels of eIF-2 alpha mRNA. eIF-2 alpha plays a pivotal role in the earliest regulated steps of translation initiation. We examined eIF-2 alpha gene expression in normal human T cells stimulated with PHA. Nuclear run-on assays indicate low rates of eIF-2 alpha gene transcription in G0 cells and these change 2-fold with PHA treatment. Actinomycin D chase experiments show that the t1/2 of eIF-2 alpha mRNA is similar in G0 and PHA-treated T cells. Analysis of nuclear RNA with probes specific for eIF-2 alpha intron sequences shows that increased eIF-2 alpha expression after PHA treatment is largely due to intranuclear stabilization of the primary transcript. The increase in eIF-2 alpha mRNA does not require new protein synthesis. Hence, expression of this gene appears to be a part of the primary response program of T cells when they are exposed to mitogen. JF - The EMBO journal AU - Cohen, R B AU - Boal, T R AU - Safer, B AD - Laboratory of Molecular Hematology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 3831 EP - 3837 VL - 9 IS - 12 SN - 0261-4189, 0261-4189 KW - Eukaryotic Initiation Factor-2 KW - 0 KW - Phytohemagglutinins KW - RNA, Messenger KW - RNA KW - 63231-63-0 KW - Guanosine Triphosphate KW - 86-01-1 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Transcription, Genetic -- drug effects KW - Cells, Cultured KW - Cell Nucleus -- metabolism KW - Kinetics KW - Humans KW - RNA -- isolation & purification KW - Tetradecanoylphorbol Acetate -- pharmacology KW - RNA, Messenger -- genetics KW - RNA, Messenger -- isolation & purification KW - Phytohemagglutinins -- pharmacology KW - RNA -- genetics KW - Guanosine Triphosphate -- metabolism KW - Lymphocyte Activation KW - T-Lymphocytes -- metabolism KW - Eukaryotic Initiation Factor-2 -- genetics KW - T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80145874?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Increased+eIF-2+alpha+expression+in+mitogen-activated+primary+T+lymphocytes.&rft.au=Cohen%2C+R+B%3BBoal%2C+T+R%3BSafer%2C+B&rft.aulast=Cohen&rft.aufirst=R&rft.date=1990-12-01&rft.volume=9&rft.issue=12&rft.spage=3831&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 - 1991-01-11 N1 - Date created - 1991-01-11 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Mol Biol. 1985 Mar 5;182(1):109-29 [2582137] FEBS Lett. 1980 Aug 11;117(1):284-8 [7409177] J Cell Physiol. 1988 Aug;136(2):215-25 [2842344] Transplant Proc. 1987 Feb;19(1 Pt 1):331-2 [2978906] J Exp Med. 1985 Jun 1;161(6):1593-8 [2989408] J Biol Chem. 1987 Jan 25;262(3):1206-12 [2948954] Methods Enzymol. 1987;152:582-7 [2443809] Oncogene. 1989 May;4(5):601-8 [2542864] Mol Cell Biol. 1989 Mar;9(3):1041-8 [2498643] Trends Biochem Sci. 1989 May;14(5):175-8 [2672437] Gene. 1989 Sep 30;81(2):315-24 [2806919] Science. 1989 Jan 20;243(4889):355-61 [2783497] Cell. 1989 Jan 13;56(1):131-9 [2910496] Proc Natl Acad Sci U S A. 1988 Jul;85(13):4705-9 [2898781] Biochemistry. 1988 Nov 15;27(23):8689-93 [3265337] J Biol Chem. 1988 Dec 5;263(34):17970-4 [3192523] J Mol Biol. 1984 Oct 5;178(4):869-80 [6492167] Nature. 1986 Jun 12-18;321(6071):702-6 [3520340] Mol Cell Biol. 1987 Aug;7(8):3004-7 [3499567] Transfusion. 1987 Jul-Aug;27(4):362-5 [3603668] Science. 1987 Mar 20;235(4795):1486-8 [3823900] Prog Nucleic Acid Res Mol Biol. 1981;25:127-85 [6164076] Cell. 1981 Feb;23(2):585-93 [6937266] Proc Natl Acad Sci U S A. 1984 Apr;81(7):1991-5 [6326095] Proc Natl Acad Sci U S A. 1984 Jul;81(14):4241-5 [6205392] J Biol Chem. 1983 Oct 25;258(20):12153-62 [6195151] J Immunol. 1980 May;124(5):2288-94 [7365257] Exp Cell Res. 1977 Nov;110(1):215-23 [200446] Biochemistry. 1979 Nov 27;18(24):5294-9 [518835] Eur J Biochem. 1979 Oct 15;100(2):503-10 [510295] Biochim Biophys Acta. 1979 Jul 26;563(2):400-12 [465497] FEBS Lett. 1978 Jul 1;91(1):40-4 [668908] Biochim Biophys Acta. 1978 Jan 26;517(1):84-98 [623765] J Cell Physiol. 1977 Nov;93(2):213-25 [591563] Proc Natl Acad Sci U S A. 1972 Jun;69(6):1408-12 [4504350] Nature. 1974 Apr 5;248(448):519-21 [4824348] Biochim Biophys Acta. 1976 May 19;432(3):312-22 [1268258] Biochim Biophys Acta. 1974 May 17;349(2):214-25 [4836354] Cell. 1975 Jan;4(1):69-75 [1078787] Exp Cell Res. 1975 May;92(2):513-5 [1132441] Proc Natl Acad Sci U S A. 1981 Nov;78(11):6613-7 [6171820] Anal Biochem. 1983 Jul 1;132(1):6-13 [6312838] J Cell Biol. 1984 Jul;99(1 Pt 1):180-7 [6736126] J Mol Biol. 1982 Apr 15;156(3):583-607 [6750132] J Immunol. 1981 Mar;126(3):1106-13 [6970214] J Biol Chem. 1981 Jul 25;256(14):7461-7 [6910478] Biochim Biophys Acta. 1970 Sep 17;217(1):164-75 [5505329] FEBS Lett. 1980 Dec 1;121(2):203-6 [7461126] Nature. 1987 Dec 3-9;330(6147):489-93 [2825027] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Identification, characterization, and cell specificity of a human LINE-1 promoter. AN - 80141131; 1701022 AB - A constructed human LINE-1 (L1Hs) element containing intact 5' and 3' untranslatable regions and an in-frame fusion between the L1Hs open reading frame 1 and the bacterial lacZ gene (p1LZ) was found to promote the expression of beta-galactosidase in a variety of transiently transfected cell types in tissue culture. Full-length RNA was detected in the transfected cells. Most of the RNA transcripts initiated at or near the beginning of the L1Hs segment. Sequences within the L1Hs segment of p1LZ were sufficient for expression of the reporter gene; however, modulation of the transcriptional regulatory region by upstream sequences was not ruled out. Deletion analysis revealed that the sequences most critical for transcription were located within the first 100 bp of L1Hs. Other sequences within the first 668 bp of L1Hs also contributed to overall expression. Expression of p1LZ was high in human teratocarcinoma cells and low in all other cell types. This pattern of cell-type-specific expression matches the known pattern of endogenous L1Hs transcription in cultured cells. JF - Molecular and cellular biology AU - Swergold, G D AD - Laboratory of Biochemistry, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 6718 EP - 6729 VL - 10 IS - 12 SN - 0270-7306, 0270-7306 KW - Actins KW - 0 KW - DNA Probes KW - Oligonucleotide Probes KW - RNA KW - 63231-63-0 KW - Index Medicus KW - Animals KW - Chick Embryo KW - Humans KW - Transcription, Genetic KW - Plasmids KW - Polymerase Chain Reaction KW - Base Sequence KW - Actins -- genetics KW - Cells, Cultured KW - Restriction Mapping KW - RNA -- isolation & purification KW - Molecular Sequence Data KW - Cell Line KW - RNA -- genetics KW - Promoter Regions, Genetic KW - Open Reading Frames KW - Repetitive Sequences, Nucleic Acid UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80141131?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Identification%2C+characterization%2C+and+cell+specificity+of+a+human+LINE-1+promoter.&rft.au=Swergold%2C+G+D&rft.aulast=Swergold&rft.aufirst=G&rft.date=1990-12-01&rft.volume=10&rft.issue=12&rft.spage=6718&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 - 1991-01-08 N1 - Date created - 1991-01-08 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Science. 1988 Jan 29;239(4839):487-91 [2448875] Dev Biol. 1972 Oct;29(2):113-38 [4672726] EMBO J. 1989 Dec 1;8(12):3867-74 [2555175] Annu Rev Microbiol. 1989;43:403-34 [2552899] Mol Cell Biol. 1989 Sep;9(9):3667-78 [2550798] Cell. 1988 Aug 26;54(5):685-91 [2842063] Nature. 1988 Mar 10;332(6160):164-6 [2831458] Int J Androl. 1987 Feb;10(1):95-104 [2438234] Nature. 1986 Jun 5-11;321(6070):625-8 [2423883] Proc Natl Acad Sci U S A. 1985 Sep;82(18):6050-4 [2412228] Genes Dev. 1989 Nov;3(11):1789-800 [2606348] Genes Dev. 1989 Jul;3(7):986-96 [2777078] Nature. 1988 May 5;333(6168):87-90 [2834650] Mol Biol Evol. 1988 Nov;5(6):675-90 [2464735] Cell. 1986 Dec 26;47(6):1007-15 [2430722] Biochim Biophys Acta. 1987 Dec 8;910(3):203-12 [2445384] Nucleic Acids Res. 1988 Oct 11;16(19):9233-51 [2459662] Anal Biochem. 1987 Apr;162(1):156-9 [2440339] Mol Cell Biol. 1987 Aug;7(8):2745-52 [3670292] Mol Cell Biol. 1986 Dec;6(12):4667-75 [2879222] Cell. 1988 Jun 3;53(5):699-711 [2897243] Mol Cell Biol. 1989 Apr;9(4):1397-405 [2725509] Mol Cell Biol. 1988 May;8(5):2021-33 [2838741] EMBO J. 1986 Dec 1;5(12):3133-42 [3102226] Mol Cell Biol. 1989 Dec;9(12):5676-84 [2479833] Cell. 1989 Apr 7;57(1):103-13 [2467742] Q Rev Biol. 1989 Mar;64(1):1-30 [2469098] Nature. 1989 Jan 26;337(6205):364-8 [2463489] Mol Cell Biol. 1988 Apr;8(4):1385-97 [2454389] Science. 1985 Dec 20;230(4732):1350-4 [2999980] Nucleic Acids Res. 1985 Nov 11;13(21):7813-27 [2999705] Genomics. 1987 Oct;1(2):113-25 [3692483] Proc Natl Acad Sci U S A. 1989 Jun;86(11):3997-4001 [2726762] Nature. 1988 Jul 28;334(6180):292-3 [3393222] EMBO J. 1984 Aug;3(8):1753-9 [6090124] Mol Cell Biol. 1987 Sep;7(9):3231-6 [3313010] Nucleic Acids Res. 1987 Apr 10;15(7):2971-88 [3562243] Nucleic Acids Res. 1987 Mar 11;15(5):2251-60 [3562227] Proc Natl Acad Sci U S A. 1990 Sep;87(18):6990-4 [1698287] Trends Genet. 1990 Feb;6(2):29-30 [2159664] Proc Natl Acad Sci U S A. 1990 Jan;87(1):328-32 [2296589] Nucleic Acids Res. 1980 Dec 20;8(24):6113-28 [6258162] Dev Biol. 1984 Jun;103(2):285-93 [6144603] Anal Biochem. 1983 Jul 1;132(1):6-13 [6312838] Gene. 1983 Nov;25(1):71-82 [6319233] J Mol Appl Genet. 1983;2(1):101-9 [6302193] Lab Invest. 1984 Feb;50(2):147-62 [6694356] Mol Cell Biol. 1983 Oct;3(10):1783-91 [6646124] Int J Cancer. 1982 May 15;29(5):523-31 [7095898] Nucleic Acids Res. 1981 Oct 24;9(20):5233-52 [7301588] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Biochemistry. 1979 Nov 27;18(24):5294-9 [518835] Cell. 1977 Nov;12(3):721-32 [922889] Biochemistry. 1977 Oct 18;16(21):4743-51 [911786] Proc Natl Acad Sci U S A. 1972 Jun;69(6):1408-12 [4504350] Mol Cell Biol. 1989 Nov;9(11):4824-34 [2481227] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Characterization of a thyroid-specific enhancer located 5.5 kilobase pairs upstream of the human thyroid peroxidase gene. AN - 80139694; 2174102 AB - A 6.3-kbp segment of DNA, upstream of the human thyroid peroxidase gene, and various deletions thereof were linked to a promoterless bacterial chloramphenicol acetyltransferase reporter gene. These constructs were analyzed by transfection and expression in rat FRTL-5 thyroid cells and in human hepatoma HepG2 cells to localize sequences that are important for thyroid cell-specific expression of the thyroid peroxidase gene. A thyroid-specific enhancer element, capable of activating enhancerless simian virus 40 promoter expression in FRTL-5 cells, was localized to a 230-bp region approximately 5.5 kbp upstream of the human thyroid peroxidase gene transcription start site. DNase I footprinting, using nuclear extracts prepared from FRTL-5 cells, revealed three regions within the 230-bp fragment; none of these regions were protected by nuclear extracts from HepG2 cells. Gel mobility shift assays, using double-stranded oligonucleotides corresponding to the three protected regions, further confirmed the existence of factors in FRTL-5 cells, but not HepG2 cells, able to specifically bind to the enhancer sequences. These results suggest the presence of three cis-acting DNA elements in the human thyroid peroxidase gene enhancer that interact with thyroid-specific trans-acting factors. JF - Molecular and cellular biology AU - Kikkawa, F AU - Gonzalez, F J AU - Kimura, S AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 6216 EP - 6224 VL - 10 IS - 12 SN - 0270-7306, 0270-7306 KW - Oligonucleotide Probes KW - 0 KW - Recombinant Fusion Proteins KW - Iodide Peroxidase KW - EC 1.11.1.8 KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Index Medicus KW - Animals KW - Chromosome Deletion KW - Base Composition KW - Carcinoma, Hepatocellular KW - Cell Nucleus -- metabolism KW - Humans KW - Thyroid Gland KW - Plasmids KW - Chloramphenicol O-Acetyltransferase -- metabolism KW - Recombinant Fusion Proteins -- metabolism KW - Liver Neoplasms KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Base Sequence KW - Genes KW - Transfection KW - Restriction Mapping KW - Molecular Sequence Data KW - Cell Line KW - Enhancer Elements, Genetic KW - Iodide Peroxidase -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80139694?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Characterization+of+a+thyroid-specific+enhancer+located+5.5+kilobase+pairs+upstream+of+the+human+thyroid+peroxidase+gene.&rft.au=Kikkawa%2C+F%3BGonzalez%2C+F+J%3BKimura%2C+S&rft.aulast=Kikkawa&rft.aufirst=F&rft.date=1990-12-01&rft.volume=10&rft.issue=12&rft.spage=6216&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 - 1991-01-08 N1 - Date created - 1991-01-08 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - M60901; GENBANK N1 - SuppNotes - Cited By: Mol Cell Biol. 1988 Jan;8(1):81-90 [3336368] Genes Dev. 1987 May;1(3):268-76 [3678824] J Biol Chem. 1988 Jul 5;263(19):9063-6 [2837474] Mol Cell Biol. 1988 Apr;8(4):1398-407 [2454390] Genes Dev. 1988 Aug;2(8):957-74 [3169549] Nucleic Acids Res. 1988 Dec 23;16(24):11573-90 [3211743] Proc Natl Acad Sci U S A. 1989 Mar;86(5):1553-7 [2922398] J Biol Chem. 1989 May 5;264(13):7523-30 [2540196] Biochem Biophys Res Commun. 1989 Apr 28;160(2):722-31 [2541706] Mol Cell Biol. 1989 Jun;9(6):2396-413 [2761536] Biochemistry. 1989 May 16;28(10):4481-9 [2548579] Nucleic Acids Res. 1989 Oct 25;17(20):8380 [2813071] EMBO J. 1989 Sep;8(9):2537-42 [2583123] Mol Cell Biol. 1989 Nov;9(11):5022-33 [2601707] Mol Endocrinol. 1989 Nov;3(11):1681-92 [2691880] Mol Cell Biol. 1990 Feb;10(2):760-9 [1689000] Mol Cell Biol. 1990 Mar;10(3):1180-91 [2304462] Biochem Biophys Res Commun. 1990 Feb 14;166(3):1257-64 [2306241] Mol Cell Biol. 1990 Apr;10(4):1470-5 [2320004] Biotechniques. 1988 Jul-Aug;6(7):632-8 [3273409] Biochem Biophys Res Commun. 1990 Apr 16;168(1):281-7 [2158317] Mol Endocrinol. 1987 Nov;1(11):856-61 [3153466] Virology. 1973 Apr;52(2):456-67 [4705382] Metabolism. 1977 Jun;26(6):665-718 [67547] Proc Natl Acad Sci U S A. 1977 Dec;74(12):5463-7 [271968] Nucleic Acids Res. 1978 Sep;5(9):3157-70 [212715] Methods Enzymol. 1980;65(1):499-560 [6246368] Proc Natl Acad Sci U S A. 1980 Jun;77(6):3455-9 [6106191] Nucleic Acids Res. 1981 Dec 11;9(23):6505-25 [6275366] J Mol Appl Genet. 1982;1(4):327-41 [6286831] Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] Nucleic Acids Res. 1983 Mar 11;11(5):1475-89 [6828386] Nucleic Acids Res. 1984 Jul 25;12(14):5707-17 [6589587] Cell. 1984 Dec;39(3 Pt 2):653-62 [6096017] Nature. 1986 Sep 25-Oct 1;323(6086):353-6 [3020428] Proc Natl Acad Sci U S A. 1986 Nov;83(21):8196-200 [2430280] Cell. 1986 Dec 5;47(5):767-76 [3779841] Mol Cell Biol. 1986 Feb;6(2):477-87 [2431269] Mol Cell Biol. 1987 Feb;7(2):606-13 [3821726] Mol Cell Biol. 1987 Feb;7(2):725-37 [3821727] Mol Cell Biol. 1987 Jul;7(7):2425-34 [3475566] Proc Natl Acad Sci U S A. 1987 Aug;84(16):5555-9 [3475693] Nucleic Acids Res. 1987 Aug 25;15(16):6735 [3453124] Mol Cell Biol. 1988 Mar;8(3):1169-78 [2452972] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Germ line transmission of an inactive N-myc allele generated by homologous recombination in mouse embryonic stem cells. AN - 80139668; 1701023 AB - We have disrupted one allele of the N-myc locus in mouse embryonic stem (ES) cells by using homologous recombination techniques and have obtained germ line transmission of null N-myc ES cell lines with transmission of the null N-myc allele to the offspring. The creation of mice with a deficient N-myc allele will allow the generation of offspring bearing null N-myc alleles in both chromosomes and permit study of the role that this proto-oncogene plays in embryonic development. JF - Molecular and cellular biology AU - Stanton, B R AU - Reid, S W AU - Parada, L F AD - Molecular Embryology Group, NCI-Frederick Cancer Research and Development Center, Maryland 21702-1201. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 6755 EP - 6758 VL - 10 IS - 12 SN - 0270-7306, 0270-7306 KW - N-myc KW - RNA, Messenger KW - 0 KW - Poly A KW - 24937-83-5 KW - RNA KW - 63231-63-0 KW - Index Medicus KW - Poly A -- isolation & purification KW - Animals KW - Blotting, Northern KW - Transcription, Genetic KW - Mice KW - Alleles KW - Blotting, Southern KW - Poly A -- genetics KW - RNA -- isolation & purification KW - Embryo, Mammalian KW - Cell Line KW - Mutagenesis, Insertional KW - RNA -- genetics KW - Genes, myc KW - Recombination, Genetic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80139668?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Germ+line+transmission+of+an+inactive+N-myc+allele+generated+by+homologous+recombination+in+mouse+embryonic+stem+cells.&rft.au=Stanton%2C+B+R%3BReid%2C+S+W%3BParada%2C+L+F&rft.aulast=Stanton&rft.aufirst=B&rft.date=1990-12-01&rft.volume=10&rft.issue=12&rft.spage=6755&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 - 1991-01-08 N1 - Date created - 1991-01-08 N1 - Date revised - 2017-01-13 N1 - Gene symbol - N-myc N1 - SuppNotes - Cited By: Science. 1984 Dec 14;226(4680):1335-7 [6505694] Nature. 1983 Sep 15-21;305(5931):245-8 [6888561] Cell. 1987 Nov 6;51(3):503-12 [2822260] J Cell Biol. 1988 Oct;107(4):1325-35 [3049618] Nature. 1986 Feb 27-Mar 5;319(6056):780-3 [2419762] Science. 1989 Nov 10;246(4931):799-803 [2554496] Trends Genet. 1989 Aug;5(8):277-83 [2686118] Genes Dev. 1989 Jun;3(6):860-9 [2663644] Science. 1989 Jun 16;244(4910):1288-92 [2660260] Proc Natl Acad Sci U S A. 1986 Mar;83(6):1827-31 [3513190] Nature. 1987 Dec 10-16;330(6148):576-8 [3683574] Nature. 1985 Nov 14-20;318(6042):188-91 [3840574] Mol Cell Biol. 1990 Apr;10(4):1799-804 [2181287] Cell. 1983 Dec;35(2 Pt 1):359-67 [6197179] Proc Natl Acad Sci U S A. 1986 Dec;83(23):9065-9 [3024164] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Pseudomonas aeruginosa compared with Escherichia coli produces less endotoxemia but more cardiovascular dysfunction and mortality in a canine model of septic shock. AN - 80136335; 2245691 AB - We investigated the effects of two different Gram-negative bacteria and radiation-induced leukopenia on endotoxemia, cardiovascular abnormalities, and mortality in a canine model of septic shock. Serial hemodynamics were measured in conscious dogs using radionuclide heart scans and thermodilution cardiac output catheters. Plasma endotoxin concentrations were determined with a chromogenic Limulus amebocyte lysate assay. Viable Pseudomonas aeruginosa or Escherichia coli implanted intraperitoneally produced concordant hemodynamic patterns of septic shock (p less than 0.01). Endotoxin concentrations were more than tenfold lower in dogs infected with P aeruginosa compared with E coli (p less than 0.0001). Despite lower endotoxin levels, P aeruginosa-infected dogs had a higher mortality (p less than 0.01), more severe hypotension (p less than 0.05), and greater depression of the left ventricular ejection fraction (p less than 0.05) than dogs with E coli sepsis. A nonlethal E coli challenge combined with leukopenia (induced by a nonlethal dose of radiation) resulted in a mortality of 60 percent (p less than 0.01) without greater cardiovascular dysfunction or higher endotoxin concentrations. These findings suggest that bacterial products other than endotoxin and host-related factors may be important contributors to the toxicity, cardiovascular instability, and mortality of Gram-negative septic shock. Quantitative determinations of plasma endotoxin are unlikely to correlate with the clinical severity of septicemia in heterogeneous patient populations infected with different Gram-negative organisms. JF - Chest AU - Danner, R L AU - Natanson, C AU - Elin, R J AU - Hosseini, J M AU - Banks, S AU - MacVittie, T J AU - Parrillo, J E AD - Critical Care Medicine Department, Warren G. Magnuson Clinical Center, National Institutes of Health, Bethesda, Md 20892. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 1480 EP - 1487 VL - 98 IS - 6 SN - 0012-3692, 0012-3692 KW - Endotoxins KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Cardiac Output KW - Blood Pressure KW - Dogs KW - Pulmonary Wedge Pressure KW - Stroke Volume KW - Pseudomonas Infections -- blood KW - Escherichia coli Infections -- physiopathology KW - Shock, Septic -- microbiology KW - Hemodynamics KW - Shock, Septic -- physiopathology KW - Shock, Septic -- blood KW - Escherichia coli Infections -- blood KW - Endotoxins -- blood KW - Pseudomonas Infections -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80136335?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chest&rft.atitle=Pseudomonas+aeruginosa+compared+with+Escherichia+coli+produces+less+endotoxemia+but+more+cardiovascular+dysfunction+and+mortality+in+a+canine+model+of+septic+shock.&rft.au=Danner%2C+R+L%3BNatanson%2C+C%3BElin%2C+R+J%3BHosseini%2C+J+M%3BBanks%2C+S%3BMacVittie%2C+T+J%3BParrillo%2C+J+E&rft.aulast=Danner&rft.aufirst=R&rft.date=1990-12-01&rft.volume=98&rft.issue=6&rft.spage=1480&rft.isbn=&rft.btitle=&rft.title=Chest&rft.issn=00123692&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1991-01-09 N1 - Date created - 1991-01-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Human immunodeficiency virus rev protein recognizes a target sequence in rev-responsive element RNA within the context of RNA secondary structure. AN - 80128571; 2243382 AB - Human immunodeficiency virus type 1 Rev protein modulates the distribution of viral mRNAs from the nucleus to the cytoplasm by interaction with a highly structured viral RNA sequence, the Rev-responsive element (RRE). To identify the minimal functional elements of RRE, we evaluated mutant RREs for Rev binding in vitro and Rev response in vivo in the context of a Gag expression plasmid. The critical functional elements fold into a structure composed of a stem-loop A, formed by the ends of the RRE, joined to a branched stem-loop B/B1/B2, between bases 49 and 113. The 5' 132 nucleotides of RRE, RREDDE, which possessed a similar structure, bound Rev efficiently but were nonfunctional in vivo, implying separate binding and functional domains within the RRE. Excision of stem-loop A reduced Rev binding significantly and abolished the in vivo Rev response. The B2 branch could be removed without severe impairment of binding, but deletions in the B1 branch significantly reduced binding and function. However, deletion of 12 nucleotides, including the 5' strand of stem B, abolished both binding and function, while excision of the 3' strand of stem B only reduced them. Maintenance of the native RRE secondary structure alone was not sufficient for Rev recognition. Many mutations that altered the primary structure of the critical region while preserving the original RNA conformation were Rev responsive. However, mutations that changed a 5'..CACUAUGGG..3' sequence in the B stem, without affecting the overall structure abolished both in vitro Rev binding and the in vivo Rev response. JF - Journal of virology AU - Holland, S M AU - Ahmad, N AU - Maitra, R K AU - Wingfield, P AU - Venkatesan, S AD - Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 5966 EP - 5975 VL - 64 IS - 12 SN - 0022-538X, 0022-538X KW - Gene Products, rev KW - 0 KW - RNA, Messenger KW - RNA, Viral KW - Recombinant Proteins KW - rev Gene Products, Human Immunodeficiency Virus KW - Index Medicus KW - AIDS/HIV KW - Chromosome Deletion KW - Humans KW - Escherichia coli -- genetics KW - Transcription, Genetic KW - Nucleic Acid Conformation KW - Protein Binding KW - Cloning, Molecular KW - Mutagenesis, Site-Directed KW - Polymerase Chain Reaction KW - Base Sequence KW - Transfection KW - Recombinant Proteins -- metabolism KW - Kinetics KW - Restriction Mapping KW - Molecular Sequence Data KW - Repetitive Sequences, Nucleic Acid KW - HIV-1 -- metabolism KW - HIV-1 -- genetics KW - Gene Products, rev -- metabolism KW - RNA, Viral -- biosynthesis KW - RNA, Viral -- genetics KW - RNA, Messenger -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80128571?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Human+immunodeficiency+virus+rev+protein+recognizes+a+target+sequence+in+rev-responsive+element+RNA+within+the+context+of+RNA+secondary+structure.&rft.au=Holland%2C+S+M%3BAhmad%2C+N%3BMaitra%2C+R+K%3BWingfield%2C+P%3BVenkatesan%2C+S&rft.aulast=Holland&rft.aufirst=S&rft.date=1990-12-01&rft.volume=64&rft.issue=12&rft.spage=5966&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 - 1990-12-31 N1 - Date created - 1990-12-31 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Mol Biol. 1968 Jul 14;34(2):365-8 [4938552] Biochemistry. 1983 May 24;22(11):2601-10 [6347247] Mol Cell Biol. 1982 Sep;2(9):1044-51 [6960240] Annu Rev Biochem. 1984;53:119-62 [6206780] Science. 1985 Jan 11;227(4683):171-3 [2981427] Science. 1985 Jul 5;229(4708):69-73 [2990040] EMBO J. 1985 Apr;4(4):1019-24 [2990903] Biochemistry. 1987 Dec 15;26(25):8221-7 [3327519] J Virol. 1988 Jul;62(7):2498-501 [2836628] Cold Spring Harb Symp Quant Biol. 1987;52:123-33 [2456874] Gene. 1988 May 30;65(2):259-68 [2970420] Science. 1988 Sep 16;241(4872):1481-5 [3262235] Nature. 1988 Oct 20;335(6192):738-40 [3262832] J Virol. 1989 Mar;63(3):1265-74 [2783738] Nature. 1989 Mar 16;338(6212):254-7 [2784194] Proc Natl Acad Sci U S A. 1989 Mar;86(5):1495-9 [2784208] Cell. 1989 Apr 7;57(1):1-3 [2522817] Cell. 1989 Apr 7;57(1):89-101 [2467746] Science. 1989 Apr 7;244(4900):48-52 [2468181] Genes Dev. 1989 Apr;3(4):431-7 [2470643] Cell. 1989 Jun 30;57(7):1155-65 [2736624] Cell. 1989 Jul 14;58(1):205-14 [2752419] Proc Natl Acad Sci U S A. 1989 Aug;86(16):6111-5 [2788283] Cell. 1989 Oct 6;59(1):207-18 [2477156] Cell. 1989 Oct 20;59(2):273-82 [2478293] Proc Natl Acad Sci U S A. 1989 Nov;86(21):8222-6 [2682638] Cell. 1989 Dec 1;59(5):789-95 [2686839] Nature. 1989 Dec 7;342(6250):714-6 [2556643] Science. 1989 Dec 22;246(4937):1625-9 [2688093] Nature. 1989 Dec 14;342(6251):816-9 [2481237] Genes Dev. 1989 Oct;3(10):1534-44 [2482226] Genes Dev. 1989 Oct;3(10):1562-71 [2612905] Methods Enzymol. 1989;180:262-88 [2482418] Proc Natl Acad Sci U S A. 1990 Feb;87(3):1198-202 [2405396] Cell. 1990 Feb 23;60(4):675-83 [2406030] Cell. 1990 Feb 23;60(4):685-93 [1689218] Science. 1990 Feb 16;247(4944):845-8 [2406903] New Biol. 1989 Dec;1(3):318-28 [2562124] Proc Natl Acad Sci U S A. 1979 Sep;76(9):4350-4 [388439] Nature. 1986 May 22-28;321(6068):412-7 [3012355] J Virol. 1986 Aug;59(2):284-91 [3016298] Cell. 1986 Sep 12;46(6):807-17 [3638988] Cell. 1986 Sep 26;46(7):973-82 [3530501] Biochemistry. 1987 Mar 24;26(6):1563-8 [3297131] Methods Enzymol. 1987;155:335-50 [3431465] Erratum In: J Virol 1992 Feb;66(2):1288 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - The human CYP2D locus associated with a common genetic defect in drug oxidation: a G1934----A base change in intron 3 of a mutant CYP2D6 allele results in an aberrant 3' splice recognition site. AN - 80114310; 1978565 AB - The debrisoquine polymorphism is a common genetic defect that results in deficient oxidation of debrisoquine and numerous other drugs. These compounds are metabolized by a form of cytochrome P450, designated CYP2D6. Some 5%-10% of Caucasians are unable to metabolize debrisoquine, because of mutant alleles of CYP2D6. A CYP2D6 allele was isolated from leukocyte DNA of an individual who was deficient in debrisoquine metabolism. The gene was completely sequenced, including 725 bp of upstream and 400 bp of downstream DNA. Several base changes were uncovered within the exons, resulting in four amino acid differences between the mutant and wild-type allele. Most important, a single base change G1934----A at the junction of the third intron and four exon would result in an incorrectly spliced primary transcript and in an mRNA having a single base deletion. This deletion presumably disrupts the mRNA reading frame, resulting in a truncated protein. These data establish unequivocally that the debrisoquine polymorphism is the result of mutant CYP2D6 alleles and provide a framework to design a genetic test for this drug oxidation deficiency. A defective CYP2D7 allele was also isolated and completely sequenced, providing evidence that gene conversions have occurred between CYP2D6 and CYP2D7. JF - American journal of human genetics AU - Hanioka, N AU - Kimura, S AU - Meyer, U A AU - Gonzalez, F J AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 994 EP - 1001 VL - 47 IS - 6 SN - 0002-9297, 0002-9297 KW - CYP2D KW - CYP2D6 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Debrisoquin KW - X31CDK040E KW - Index Medicus KW - Oxidation-Reduction KW - Gene Conversion KW - Base Sequence KW - Alleles KW - Genes KW - Sequence Homology, Nucleic Acid KW - Polymorphism, Restriction Fragment Length KW - Polymorphism, Genetic KW - Exons KW - Humans KW - Molecular Sequence Data KW - Cytochrome P-450 Enzyme System -- metabolism KW - Debrisoquin -- metabolism KW - RNA Splicing KW - Introns KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80114310?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+human+genetics&rft.atitle=The+human+CYP2D+locus+associated+with+a+common+genetic+defect+in+drug+oxidation%3A+a+G1934----A+base+change+in+intron+3+of+a+mutant+CYP2D6+allele+results+in+an+aberrant+3%27+splice+recognition+site.&rft.au=Hanioka%2C+N%3BKimura%2C+S%3BMeyer%2C+U+A%3BGonzalez%2C+F+J&rft.aulast=Hanioka&rft.aufirst=N&rft.date=1990-12-01&rft.volume=47&rft.issue=6&rft.spage=994&rft.isbn=&rft.btitle=&rft.title=American+journal+of+human+genetics&rft.issn=00029297&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-12-26 N1 - Date created - 1990-12-26 N1 - Date revised - 2017-01-13 N1 - Gene symbol - CYP2D; CYP2D6 N1 - Genetic sequence - M33387; GENBANK; M33388; M33189 N1 - SuppNotes - Cited By: Drug Metab Rev. 1979;9(2):301-17 [158499] Gene. 1980 Aug;10(3):249-59 [6254843] Anal Biochem. 1983 Feb 15;129(1):216-23 [6305233] Clin Pharmacol Ther. 1985 Dec;38(6):618-24 [4064464] Nature. 1988 Feb 4;331(6155):442-6 [3123997] Proc Natl Acad Sci U S A. 1988 Jul;85(14):5240-3 [2899325] J Biol Chem. 1990 Oct 5;265(28):17209-14 [2211621] DNA. 1989 Jan-Feb;8(1):1-13 [2651058] Am J Hum Genet. 1989 Dec;45(6):889-904 [2574001] J Mol Evol. 1990 Feb;30(2):155-69 [2107330] Trends Genet. 1990 Jun;6(6):182-6 [2196721] Lancet. 1990 Sep 1;336(8714):529-32 [1975039] Genomics. 1988 Feb;2(2):174-9 [3410476] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Effect of chronic treatment with the glucocorticoid antagonist RU 486 in man: toxicity, immunological, and hormonal aspects. AN - 80088709; 2172280 AB - Suppression of immune function was traditionally thought to occur only with pharmacological levels of glucocorticoids. However, recent studies in rodents have suggested that glucocorticoids exert tonic antiinflammatory/immunosuppressive effects even at basal nonstress concentrations. To examine whether basal glucocorticoid secretion modulates immune function in man we employed the specific glucocorticoid receptor antagonist RU 486. If a tonic level of inhibition of the immune system by basal glucocorticoid levels was present, then a potentiation or enhancement of immune function might evolve in the absence of glucocorticoid action. To examine this hypothesis, we studied 11 healthy male normal volunteers who received RU 486 (10 mg/kg.day) or placebo vehicle, divided into 2 daily oral doses, for 7-14 days. Blood samples were collected every 2 days for measurement of plasma ACTH and cortisol concentrations along with 24-h urine samples for measurement of 17-hydroxysteroid and free cortisol excretion. Complete and differential blood counts, erythrocyte sedimentation rates, C-reactive protein, antinuclear antibodies, rheumatoid factor, and quantitative immunoglobulins were also determined at 2-day intervals. Leukocytes were obtained by leukopheresis for phenotypic characterization and functional analysis before and 7 days after the initiation of RU 486 or placebo therapy. Blockade of cortisol receptors with RU 486 was associated with marked compensatory elevations of plasma ACTH and cortisol and increases in 24-h urinary excretion of 17-hydroxysteroids and free cortisol. Unexpectedly, 8 of the 11 subjects developed generalized exanthem after 9 days of RU 486 treatment. One subject developed symptoms and signs consistent with the diagnosis of adrenal insufficiency. Total white blood cell counts, absolute lymphocyte, neutrophil and eosinophil counts, erythrocyte sedimentation rate, and quantitative immunoglobulins did not change with RU 486 therapy. Similarly, T-, B-, and natural killer cell subsets did not change during RU 486 treatment. Furthermore, functional evaluation of lymphocyte cytotoxicity and proliferation revealed no changes. We conclude that administration of high doses of RU 486 to normal volunteers does not result in measurable enhancement of immune function. This suggests that in man, glucocorticoids may not exert a tonic inhibitory effect on the immune system as they appear to do in rodents. Alternatively, the compensatory increase in endogenous cortisol may obviate any effect of the glucocorticoid antagonist on the immune system.(ABSTRACT TRUNCATED AT 400 WORDS) JF - The Journal of clinical endocrinology and metabolism AU - Laue, L AU - Lotze, M T AU - Chrousos, G P AU - Barnes, K AU - Loriaux, D L AU - Fleisher, T A AD - Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 1474 EP - 1480 VL - 71 IS - 6 SN - 0021-972X, 0021-972X KW - Glucocorticoids KW - 0 KW - Hydroxysteroids KW - Mifepristone KW - 320T6RNW1F KW - Adrenocorticotropic Hormone KW - 9002-60-2 KW - Hydrocortisone KW - WI4X0X7BPJ KW - Abridged Index Medicus KW - Index Medicus KW - Population KW - Hormones--analysis KW - Measurement KW - Laboratory Examinations And Diagnoses KW - Dermatological Effects KW - Immunological Effects KW - Immunologic Factors KW - Research Methodology KW - Hormone Antagonists KW - Physiology KW - Endocrine System KW - Antibodies--analysis KW - Immunity KW - Ru-486--administraction and dosage KW - Cytologic Effects KW - Ru-486--side effects KW - Homeostasis--changes KW - Histology KW - Human Volunteers--men KW - Examinations And Diagnoses KW - Clinical Research KW - Biology KW - Humans KW - Adrenal Insufficiency -- chemically induced KW - Exanthema -- chemically induced KW - Hydroxysteroids -- urine KW - Hydrocortisone -- blood KW - Leukocyte Count KW - Lymphocytes -- immunology KW - Adult KW - Hydrocortisone -- urine KW - Lymphocytes -- drug effects KW - Male KW - Exanthema -- pathology KW - Adrenocorticotropic Hormone -- blood KW - Immunity -- physiology KW - Glucocorticoids -- physiology KW - Mifepristone -- adverse effects KW - Glucocorticoids -- antagonists & inhibitors KW - Glucocorticoids -- blood KW - Mifepristone -- administration & dosage KW - Immunity -- drug effects KW - Mifepristone -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80088709?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+clinical+endocrinology+and+metabolism&rft.atitle=Effect+of+chronic+treatment+with+the+glucocorticoid+antagonist+RU+486+in+man%3A+toxicity%2C+immunological%2C+and+hormonal+aspects.&rft.au=Laue%2C+L%3BLotze%2C+M+T%3BChrousos%2C+G+P%3BBarnes%2C+K%3BLoriaux%2C+D+L%3BFleisher%2C+T+A&rft.aulast=Laue&rft.aufirst=L&rft.date=1990-12-01&rft.volume=71&rft.issue=6&rft.spage=1474&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+clinical+endocrinology+and+metabolism&rft.issn=0021972X&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-12-27 N1 - Date created - 1990-12-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - AZT demonstrates anti-HIV-1 activity in persistently infected cell lines: implications for combination chemotherapy and immunotherapy. AN - 80087770; 2230256 AB - A sensitive and quantitative focal immunoassay has been used to measure the effects of three different therapeutic agents on tissue culture cells infected with human immunodeficiency virus (HIV). The effects of the drugs were studied on both acutely and persistently infected CD4+ cell lines. The three agents, azidothymidine (AZT), interferon-alpha (IFN-alpha), and an anti-HIV envelope antibody coupled to ricin A chain, were tested alone and in combination. AZT was found to have its greatest effect during early stages of the infection, but also had an action on persistently infected T cell lines. The effect of AZT on persistently infected cells was seen within 24 h, increased with extended exposure to the drug, and persisted after its removal. IFN-alpha had variable effects on acutely infected cells but suppressed chronic infection. Combinations of the therapeutic agents were studied. Using a model that allowed for treatment during both acute and persistent stages of infection, the most effective combination in suppressing HIV infection was the continual use of both AZT and IFN-alpha at the highest tolerable doses. Knowledge of the efficacy of AZT on persistently infected cells will allow for the most effective design of clinical protocols. JF - The Journal of infectious diseases AU - Pincus, S H AU - Wehrly, K AD - Laboratory of Microbial Structure and Function, National Institute of Allergy and Infectious Diseases, Hamilton, Montana 59840. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 1233 EP - 1238 VL - 162 IS - 6 SN - 0022-1899, 0022-1899 KW - HIV Antibodies KW - 0 KW - Immunotoxins KW - Interferon Type I KW - Zidovudine KW - 4B9XT59T7S KW - Ricin KW - 9009-86-3 KW - Abridged Index Medicus KW - Index Medicus KW - AIDS/HIV KW - Dose-Response Relationship, Drug KW - Combined Modality Therapy KW - Immunotherapy KW - Humans KW - HIV Infections -- therapy KW - Dose-Response Relationship, Immunologic KW - HIV Infections -- drug therapy KW - Cell Line KW - Interferon Type I -- pharmacology KW - Zidovudine -- pharmacology KW - Immunotoxins -- pharmacology KW - Ricin -- pharmacology KW - HIV-1 -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80087770?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+infectious+diseases&rft.atitle=AZT+demonstrates+anti-HIV-1+activity+in+persistently+infected+cell+lines%3A+implications+for+combination+chemotherapy+and+immunotherapy.&rft.au=Pincus%2C+S+H%3BWehrly%2C+K&rft.aulast=Pincus&rft.aufirst=S&rft.date=1990-12-01&rft.volume=162&rft.issue=6&rft.spage=1233&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+infectious+diseases&rft.issn=00221899&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-12-21 N1 - Date created - 1990-12-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Design issues in epidemiologic studies of indoor exposure to Rn and risk of lung cancer. AN - 80084696; 2228608 AB - Recent data on indoor air quality have indicated that Rn (222Rn) and its decay products are frequently present in domestic environments. Since studies of Rn-exposed miners have established that Rn decay products are a lung carcinogen, their presence in indoor air raises concerns about an increase in lung cancer risk for the general population. To directly evaluate lung cancer risk from domestic exposure to Rn and its decay products, as well as to evaluate risk assessments derived from studies of Rn-exposed underground miners, several epidemiologic studies of indoor Rn exposure have been initiated or are planned. This paper calculates sample sizes required for a hypothetical case-control study to address several important hypotheses and shows the impact of several difficult problems associated with estimating a subject's Rn exposure. We consider the effects of subject mobility, choice of the exposure response trend which is used to characterize an alternative hypothesis, and errors in the estimation of exposure. Imprecise estimation of Rn exposure arises from errors in the measurement device, exposure to Rn decay products from sources outside the home, inability to measure exposures over time in current as well as previous residences, and the unknown relationship between measured concentration and lung dose of alpha energy from the decay of Rn and its progeny. These methodological problems can result in large discrepancies between computed and actual study power. Failure to anticipate these problems in the design of a study can result in inaccurate estimates of power. We conclude that case-control studies of indoor Rn and lung cancer may require substantial numbers of subjects in order to address the many questions of importance that burden current risk assessments with uncertainty. We suggest pooling data from studies with the largest numbers of cases and with the most precise estimates of Rn exposure as the best approach for meeting present research needs. JF - Health physics AU - Lubin, J H AU - Samet, J M AU - Weinberg, C AD - National Cancer Institute, Epidemiologic Methods Section, Rockville, MD 20892. Y1 - 1990/12// PY - 1990 DA - December 1990 SP - 807 EP - 817 VL - 59 IS - 6 SN - 0017-9078, 0017-9078 KW - Air Pollutants, Radioactive KW - 0 KW - Radon KW - Q74S4N8N1G KW - Index Medicus KW - Risk KW - Humans KW - United States -- epidemiology KW - Lung Neoplasms -- epidemiology KW - Housing KW - Epidemiologic Methods KW - Neoplasms, Radiation-Induced -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80084696?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Design+issues+in+epidemiologic+studies+of+indoor+exposure+to+Rn+and+risk+of+lung+cancer.&rft.au=Lubin%2C+J+H%3BSamet%2C+J+M%3BWeinberg%2C+C&rft.aulast=Lubin&rft.aufirst=J&rft.date=1990-12-01&rft.volume=59&rft.issue=6&rft.spage=807&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 - 1990-12-27 N1 - Date created - 1990-12-27 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Treatment of speech and voice disorders with botulinum toxin. AN - 80091808; 2232044 JF - JAMA AU - Ludlow, C L AD - Speech and Voice Unit, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, Md. 20892. Y1 - 1990/11/28/ PY - 1990 DA - 1990 Nov 28 SP - 2671 EP - 2675 VL - 264 IS - 20 SN - 0098-7484, 0098-7484 KW - Botulinum Toxins KW - EC 3.4.24.69 KW - Abridged Index Medicus KW - Index Medicus KW - Laryngeal Muscles -- physiopathology KW - Humans KW - Stuttering -- physiopathology KW - Adult KW - Electromyography KW - Injections KW - Phonation KW - Female KW - Botulinum Toxins -- administration & dosage KW - Botulinum Toxins -- therapeutic use KW - Speech Disorders -- therapy KW - Voice Disorders -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80091808?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&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=Treatment+of+speech+and+voice+disorders+with+botulinum+toxin.&rft.au=Ludlow%2C+C+L&rft.aulast=Ludlow&rft.aufirst=C&rft.date=1990-11-28&rft.volume=264&rft.issue=20&rft.spage=2671&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-12-13 N1 - Date created - 1990-12-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Outgrowths from Hermissenda photoreceptor somata are associated with activation of protein kinase C. AN - 80276177; 2073581 AB - We have found changes in the morphology of photoreceptor somata from the mollusc Hermissenda that are produced by application of 12,13-phorbol dibutyrate (PDBU), an activator of PKC, in combination with elevated intracellular Ca2+ levels. The changes in morphology were expressed as rapid and repetitive outgrowths and additionally as more general changes in shape of the soma. Application of 4 alpha-PMA, a phorbol ester which does not activate PKC, did not produce these changes. The functional integrity of the photoreceptors in these dissociated eye preparations was maintained throughout the period of incubation with PDBU according to standard electrophysiological criteria. It has previously been shown that classical conditioning produced a reduction of dendritic volume in the type B photoreceptor of Hermissenda, a specific locus for associative memory storage. These changes in dendritic morphology were correlated with increased resistance across the cell membrane caused by learning-induced reductions of outward somatic K+ currents. Such conditioning-specific reductions of somatic K+ currents appear to depend on the phosphorylation of a 20-kDa G-protein (CP20) mediated by the Ca2+ and phospholipid-dependent kinase, protein kinase C (PKC). Thus PKC activity may be important in structural changes of the synaptic region of specific neurons involved in associative memory. The results of the present study suggest that the effects of PKC activation may also include structural changes in the soma of these same neurons. JF - Brain research AU - Lederhendler, I I AU - Etcheberrigaray, R AU - Yamoah, E N AU - Matzel, L D AU - Alkon, D L AD - Section on Neural Systems, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Y1 - 1990/11/26/ PY - 1990 DA - 1990 Nov 26 SP - 195 EP - 200 VL - 534 IS - 1-2 SN - 0006-8993, 0006-8993 KW - Potassium Channels KW - 0 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 - Animals KW - Learning KW - Enzyme Activation KW - In Vitro Techniques KW - Potassium Channels -- physiology KW - Calcium -- pharmacology KW - Mollusca KW - Cell Membrane -- physiology KW - Potassium Channels -- drug effects KW - Protein Kinase C -- metabolism KW - Photoreceptor Cells -- drug effects KW - Photoreceptor Cells -- cytology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Photoreceptor Cells -- physiology KW - Phorbol 12,13-Dibutyrate -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80276177?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Outgrowths+from+Hermissenda+photoreceptor+somata+are+associated+with+activation+of+protein+kinase+C.&rft.au=Lederhendler%2C+I+I%3BEtcheberrigaray%2C+R%3BYamoah%2C+E+N%3BMatzel%2C+L+D%3BAlkon%2C+D+L&rft.aulast=Lederhendler&rft.aufirst=I&rft.date=1990-11-26&rft.volume=534&rft.issue=1-2&rft.spage=195&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 - 1991-04-18 N1 - Date created - 1991-04-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Persistent elevations in dopamine and its metabolites in the nucleus accumbens after mild subchronic stress in rats with ibotenic acid lesions of the medial prefrontal cortex. AN - 80275360; 2073594 AB - This study assessed the possible influence of the medial prefrontal cortex (MPFC) on the response of subcortical dopamine (DA) systems to subchronic, mild stress. DA and its metabolites as well as noradrenaline were assayed in the nucleus accumbens and corpus striatum, 1 and 7 days after one week of daily intraperitoneal saline injections (Stress) or no handling (No stress), in rats with sham (Sham) or ibotenic acid (IA) lesions of the MPFC. One day after the last saline injection the level of dihydroxyphenylacetic acid (DOPAC) was elevated in the nucleus accumbens of IA/Stress rats in comparison to the Sham/No stress, Sham/Stress, and IA/No Stress groups. Levels of mesolimbic DA, DOPAC and homovanillic acid were still elevated 7 days after the last injection in IA/Stress animals in comparison to all other groups. There were no other significant differences between the groups. The data suggest that in rats with MPFC impairment, mild subchronic stress can induce alterations in mesolimbic DA activity that persist beyond the duration of the stress. JF - Brain research AU - Jaskiw, G E AU - Karoum, F K AU - Weinberger, D R AD - Clinical Brain Disorders Branch, National Institute of Mental Health, NIMH Neuroscience Center at St. Elizabeths, Washington, DC 20032. Y1 - 1990/11/26/ PY - 1990 DA - 1990 Nov 26 SP - 321 EP - 323 VL - 534 IS - 1-2 SN - 0006-8993, 0006-8993 KW - Catecholamines KW - 0 KW - 3,4-Dihydroxyphenylacetic Acid KW - 102-32-9 KW - Ibotenic Acid KW - 2552-55-8 KW - Dopamine KW - VTD58H1Z2X KW - Norepinephrine KW - X4W3ENH1CV KW - Homovanillic Acid KW - X77S6GMS36 KW - Index Medicus KW - Rats, Inbred Strains KW - Rats KW - Handling (Psychology) KW - Animals KW - Reference Values KW - 3,4-Dihydroxyphenylacetic Acid -- metabolism KW - Norepinephrine -- metabolism KW - Homovanillic Acid -- metabolism KW - Male KW - Stress, Psychological -- metabolism KW - Cerebral Cortex -- physiology KW - Cerebral Cortex -- drug effects KW - Catecholamines -- metabolism KW - Cerebral Cortex -- pathology KW - Nucleus Accumbens -- metabolism KW - Dopamine -- metabolism KW - Ibotenic Acid -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80275360?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Persistent+elevations+in+dopamine+and+its+metabolites+in+the+nucleus+accumbens+after+mild+subchronic+stress+in+rats+with+ibotenic+acid+lesions+of+the+medial+prefrontal+cortex.&rft.au=Jaskiw%2C+G+E%3BKaroum%2C+F+K%3BWeinberger%2C+D+R&rft.aulast=Jaskiw&rft.aufirst=G&rft.date=1990-11-26&rft.volume=534&rft.issue=1-2&rft.spage=321&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 - 1991-04-18 N1 - Date created - 1991-04-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Immunochemical analysis of the exposure of high mobility group protein 14 and 17 surfaces in chromatin. AN - 80127825; 2243079 AB - Antisera were elicited against synthetic peptides corresponding either to regions common to all members of the high mobility group 14 and 17 protein family protein or to distinct domains of the HMG-14 or HMG-17 subgroup. The antisera were used to probe the accessibility of various HMG domains in chromatin. Competitive enzyme-linked immunosorbent assays indicate that the central region of the proteins, which contains their DNA binding domain and is positively charged, is exposed to a smaller degree than the C-terminal region of the proteins, which has a net negative charge. The C-terminal regions of the HMG-14 and HMG-17 proteins are exposed and available to interact with other proteins. JF - The Journal of biological chemistry AU - Bustin, M AU - Crippa, M P AU - Pash, J M AD - Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1990/11/25/ PY - 1990 DA - 1990 Nov 25 SP - 20077 EP - 20080 VL - 265 IS - 33 SN - 0021-9258, 0021-9258 KW - Antigen-Antibody Complex KW - 0 KW - Chromatin KW - High Mobility Group Proteins KW - Histones KW - Immune Sera KW - Nucleosomes KW - Peptides KW - Index Medicus KW - Peptides -- chemical synthesis KW - Animals KW - HeLa Cells -- chemistry KW - Models, Structural KW - Cell Nucleus -- ultrastructure KW - Humans KW - Amino Acid Sequence KW - Erythrocytes -- chemistry KW - Chickens KW - Nucleosomes -- ultrastructure KW - Binding, Competitive KW - Molecular Sequence Data KW - Histones -- ultrastructure KW - Enzyme-Linked Immunosorbent Assay KW - Protein Conformation KW - High Mobility Group Proteins -- analysis KW - Chromatin -- chemistry KW - High Mobility Group Proteins -- immunology KW - Chromatin -- ultrastructure KW - High Mobility Group Proteins -- ultrastructure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80127825?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Immunochemical+analysis+of+the+exposure+of+high+mobility+group+protein+14+and+17+surfaces+in+chromatin.&rft.au=Bustin%2C+M%3BCrippa%2C+M+P%3BPash%2C+J+M&rft.aulast=Bustin&rft.aufirst=M&rft.date=1990-11-25&rft.volume=265&rft.issue=33&rft.spage=20077&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 - 1990-12-28 N1 - Date created - 1990-12-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Processing of Pseudomonas exotoxin by a cellular protease results in the generation of a 37,000-Da toxin fragment that is translocated to the cytosol. AN - 80124215; 2122978 AB - Pseudomonas exotoxin (PE) was incubated with cells and extracts analyzed for processed fragments. PE was proteolytically cleaved to produce a N-terminal 28-kDa and a C-terminal 37-kDa fragment, the latter being composed of a portion of domain II and all of domain III (the ADP-ribosylating domain). Cleavage was evident at 10 min after toxin addition and endosome preparations contained the processed fragments. Initially, the two fragments were linked by a disulfide bond. Subsequently, the 37-kDa fragment was reduced and translocated to the cytosol where it inactivated protein synthesis. Cytosol from toxin-treated cells was greatly enriched in the 37-kDa fragment. The 37-kDa fragment appears to be essential for toxicity since mutant PE molecules that do not produce this fragment, or cannot deliver it to the cytosol, fail to kill cells. JF - The Journal of biological chemistry AU - Ogata, M AU - Chaudhary, V K AU - Pastan, I AU - FitzGerald, D J AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1990/11/25/ PY - 1990 DA - 1990 Nov 25 SP - 20678 EP - 20685 VL - 265 IS - 33 SN - 0021-9258, 0021-9258 KW - Bacterial Toxins KW - 0 KW - Disulfides KW - Exotoxins KW - Virulence Factors KW - Ammonium Chloride KW - 01Q9PC255D KW - Monensin KW - 906O0YJ6ZP KW - Methionine KW - AE28F7PNPL KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Endopeptidases KW - EC 3.4.- KW - Index Medicus KW - Animals KW - Humans KW - Methionine -- metabolism KW - Amino Acid Sequence KW - Mice KW - Monensin -- pharmacology KW - Ammonium Chloride -- pharmacology KW - Molecular Weight KW - Mutagenesis KW - Disulfides -- analysis KW - Endocytosis -- drug effects KW - Molecular Sequence Data KW - Cell Line KW - Protein Conformation KW - Bacterial Toxins -- genetics KW - Exotoxins -- genetics KW - Exotoxins -- pharmacology KW - Pseudomonas aeruginosa -- genetics KW - Exotoxins -- biosynthesis KW - Protein Processing, Post-Translational KW - Endopeptidases -- metabolism KW - Exotoxins -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80124215?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Processing+of+Pseudomonas+exotoxin+by+a+cellular+protease+results+in+the+generation+of+a+37%2C000-Da+toxin+fragment+that+is+translocated+to+the+cytosol.&rft.au=Ogata%2C+M%3BChaudhary%2C+V+K%3BPastan%2C+I%3BFitzGerald%2C+D+J&rft.aulast=Ogata&rft.aufirst=M&rft.date=1990-11-25&rft.volume=265&rft.issue=33&rft.spage=20678&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 - 1990-12-28 N1 - Date created - 1990-12-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phase II investigation of pentostatin in multiple myeloma: a Southwest Oncology Group study. AN - 80098941; 2231774 JF - Journal of the National Cancer Institute AU - Grever, M R AU - Crowley, J AU - Salmon, S AU - McGee, R AU - Kraut, E H AU - Buys, S S AU - Rivkin, S E AD - Division of Cancer Treatment, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. Y1 - 1990/11/21/ PY - 1990 DA - 1990 Nov 21 SP - 1778 EP - 1779 VL - 82 IS - 22 SN - 0027-8874, 0027-8874 KW - Pentostatin KW - 395575MZO7 KW - Creatinine KW - AYI8EX34EU KW - Index Medicus KW - Drug Evaluation KW - Humans KW - Aged KW - Middle Aged KW - Creatinine -- blood KW - Pentostatin -- toxicity KW - Multiple Myeloma -- drug therapy KW - Pentostatin -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80098941?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Phase+II+investigation+of+pentostatin+in+multiple+myeloma%3A+a+Southwest+Oncology+Group+study.&rft.au=Grever%2C+M+R%3BCrowley%2C+J%3BSalmon%2C+S%3BMcGee%2C+R%3BKraut%2C+E+H%3BBuys%2C+S+S%3BRivkin%2C+S+E&rft.aulast=Grever&rft.aufirst=M&rft.date=1990-11-21&rft.volume=82&rft.issue=22&rft.spage=1778&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 - 1990-12-19 N1 - Date created - 1990-12-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Comorbidity of mental disorders with alcohol and other drug abuse. Results from the Epidemiologic Catchment Area (ECA) Study. AN - 80093260; 2232018 AB - The prevalence of comorbid alcohol, other drug, and mental disorders in the US total community and institutional population was determined from 20,291 persons interviewed in the National Institute of Mental Health Epidemiologic Catchment Area Program. Estimated US population lifetime prevalence rates were 22.5% for any non-substance abuse mental disorder, 13.5% for alcohol dependence-abuse, and 6.1% for other drug dependence-abuse. Among those with a mental disorder, the odds ratio of having some addictive disorder was 2.7, with a lifetime prevalence of about 29% (including an overlapping 22% with an alcohol and 15% with another drug disorder). For those with either an alcohol or other drug disorder, the odds of having the other addictive disorder were seven times greater than in the rest of the population. Among those with an alcohol disorder, 37% had a comorbid mental disorder. The highest mental-addictive disorder comorbidity rate was found for those with drug (other than alcohol) disorders, among whom more than half (53%) were found to have a mental disorder with an odds ratio of 4.5. Individuals treated in specialty mental health and addictive disorder clinical settings have significantly higher odds of having comorbid disorders. Among the institutional settings, comorbidity of addictive and severe mental disorders was highest in the prison population, most notably with antisocial personality, schizophrenia, and bipolar disorders. JF - JAMA AU - Regier, D A AU - Farmer, M E AU - Rae, D S AU - Locke, B Z AU - Keith, S J AU - Judd, L L AU - Goodwin, F K AD - Office of the Director, National Institute of Mental Health, Rockville Md. 20857. Y1 - 1990/11/21/ PY - 1990 DA - 1990 Nov 21 SP - 2511 EP - 2518 VL - 264 IS - 19 SN - 0098-7484, 0098-7484 KW - Abridged Index Medicus KW - Index Medicus KW - Regression Analysis KW - Social Behavior Disorders -- epidemiology KW - Bipolar Disorder -- epidemiology KW - Humans KW - Adult KW - Schizophrenia -- epidemiology KW - Mood Disorders -- epidemiology KW - Anxiety Disorders -- epidemiology KW - United States -- epidemiology KW - Comorbidity KW - Catchment Area (Health) KW - Prevalence KW - Alcoholism -- epidemiology KW - Mental Disorders -- epidemiology KW - Substance-Related Disorders -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80093260?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Comorbidity+of+mental+disorders+with+alcohol+and+other+drug+abuse.+Results+from+the+Epidemiologic+Catchment+Area+%28ECA%29+Study.&rft.au=Regier%2C+D+A%3BFarmer%2C+M+E%3BRae%2C+D+S%3BLocke%2C+B+Z%3BKeith%2C+S+J%3BJudd%2C+L+L%3BGoodwin%2C+F+K&rft.aulast=Regier&rft.aufirst=D&rft.date=1990-11-21&rft.volume=264&rft.issue=19&rft.spage=2511&rft.isbn=&rft.btitle=&rft.title=JAMA&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-12-11 N1 - Date created - 1990-12-11 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: JAMA. 1991 Mar 13;265(10):1256-7 [1995965] JAMA. 2000 Dec 13;284(22):2874 [11147982] JAMA. 1990 Nov 21;264(19):2549-50 [2232023] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Phosphorylation of neutrophil 47-kDa cytosolic oxidase factor. Translocation to membrane is associated with distinct phosphorylation events. AN - 80136418; 2246268 AB - Activation of the phagocytic cell superoxide-generating NADPH oxidase requires interaction of cytosolic and membrane-associated components. With most stimuli activation of the oxidase is accompanied by multisite phosphorylation of the 47-kDa cytosolic oxidase factor (p47) which translocates from cytosol to membranes. Native p47 is a highly basic protein that undergoes stepwise charge shifts with successive phosphorylation events. Phosphorylation of p47 was studied by immunoprecipitation from neutrophil cytosol and membrane fractions followed by two-dimensional gel electrophoresis and autoradiography. In the resting cell p47 was not phosphorylated. In the cytosol of phorbol myristate acetate-activated neutrophils eight distinct p47 phosphoproteins were present. The membrane fraction from these activated cells contained a family of p47 phosphoproteins of electrophoretic mobilities identical to those seen in cytosol plus an additional, more acidic p47 phosphoprotein not present in cytosol. Very early after activation (30 s) only the four most acidic p47 phosphoproteins were present in the membrane fraction. Only at later times (5-15 min) was the full spectrum of p47 phosphoproteins present in the membrane fraction. In contrast, the full spectrum of p47 phosphoproteins was present in the cytosol over the entire time course we studied. In neutrophils from patients with cytochrome b558-deficient chronic granulomatous disease p47 phosphorylation was incomplete and p47 translocation to membrane did not occur. These studies demonstrated that the cytochrome was essential for formation of the three most acidic p47 phosphoproteins and greatly augmented formation of the fourth most acidic p47 phosphoprotein found in normal neutrophils. The temporal correlation between specific p47 phosphorylation events and p47 translocation to membrane is consistent with a model of oxidase activation in which a series of p47 phosphorylation events which occurs in cytosol precedes and may be required for p47 interaction with membrane. JF - The Journal of biological chemistry AU - Rotrosen, D AU - Leto, T L AD - Bacterial Diseases Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1990/11/15/ PY - 1990 DA - 1990 Nov 15 SP - 19910 EP - 19915 VL - 265 IS - 32 SN - 0021-9258, 0021-9258 KW - Cytochrome b Group KW - 0 KW - Phosphoproteins KW - cytochrome b558 KW - 9064-78-2 KW - NADH, NADPH Oxidoreductases KW - EC 1.6.- KW - NADPH Oxidase KW - EC 1.6.3.1 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Phagocytosis -- physiology KW - Immunoblotting KW - Granulomatous Disease, Chronic -- enzymology KW - Phosphorylation KW - Kinetics KW - Humans KW - Electrophoresis, Gel, Two-Dimensional KW - Biological Transport KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Immunosorbent Techniques KW - Cytochrome b Group -- deficiency KW - Autoradiography KW - Molecular Weight KW - Cell Membrane -- enzymology KW - Cytosol -- enzymology KW - Neutrophils -- enzymology KW - NADH, NADPH Oxidoreductases -- blood KW - Phosphoproteins -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80136418?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Phosphorylation+of+neutrophil+47-kDa+cytosolic+oxidase+factor.+Translocation+to+membrane+is+associated+with+distinct+phosphorylation+events.&rft.au=Rotrosen%2C+D%3BLeto%2C+T+L&rft.aulast=Rotrosen&rft.aufirst=D&rft.date=1990-11-15&rft.volume=265&rft.issue=32&rft.spage=19910&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 - 1991-01-08 N1 - Date created - 1991-01-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Isoprenylation of an inhibitory G protein alpha subunit occurs only upon mutagenesis of the carboxyl terminus. AN - 80133214; 2123186 AB - We transfected COS cells with expression vectors for the wild-type G protein alpha i1 subunit (pWT) and for mutated alpha i1 subunits, including the nonmyristylated glycine 2 to alanine mutant (pGA) and mutants in which the carboxyl termini of pWT and pGA were changed from CGLF to CVLS (pCVLS and pGA-CVLS, respectively). Immunoblot analysis of transfected COS cells with an antibody to residues 159-168 of the alpha i1 protein indicated that all four proteins were expressed. Unlike the WT and GA proteins, both CVLS mutant proteins failed to react with an antibody specific for the carboxyl terminus and failed to undergo pertussis toxin-catalyzed ADP-ribosylation. Analysis of COS cell lysates after [3H]mevalonic acid labeling indicated that specific incorporation of radioactivity occurred only in the alpha i1 subunits with the CVLS mutation. Immuno-precipitation of COS cell fractions after labeling with [35S]methionine indicated that both WT and CVLS mutant proteins were localized predominantly in the particulate fraction, whereas GA and GA-CVLS mutant proteins were found primarily in the soluble fraction. These results directly demonstrate that the carboxyl-terminal sequence, CGLF, is incapable of leading to isoprenylation but that alteration of two residues (glycine to valine, phenylalanine to serine) is sufficient to promote isoprenylation. JF - The Journal of biological chemistry AU - Jones, T L AU - Spiegel, A M AD - Molecular Pathophysiology Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1990/11/15/ PY - 1990 DA - 1990 Nov 15 SP - 19389 EP - 19392 VL - 265 IS - 32 SN - 0021-9258, 0021-9258 KW - Myristic Acids KW - 0 KW - Polyisoprenyl Phosphates KW - Virulence Factors, Bordetella KW - Myristic Acid KW - 0I3V7S25AW KW - Adenosine Diphosphate Ribose KW - 20762-30-5 KW - Methionine KW - AE28F7PNPL KW - Pertussis Toxin KW - EC 2.4.2.31 KW - GTP-Binding Proteins KW - EC 3.6.1.- KW - Mevalonic Acid KW - S5UOB36OCZ KW - Index Medicus KW - Animals KW - Immunoblotting KW - Polyisoprenyl Phosphates -- metabolism KW - Gene Expression KW - Methionine -- metabolism KW - Adenosine Diphosphate Ribose -- metabolism KW - Myristic Acids -- metabolism KW - Rats KW - Virulence Factors, Bordetella -- metabolism KW - Base Sequence KW - Transfection KW - Molecular Sequence Data KW - Immunosorbent Techniques KW - Cell Line KW - Mutagenesis, Site-Directed KW - GTP-Binding Proteins -- metabolism KW - Protein Processing, Post-Translational KW - Mevalonic Acid -- metabolism KW - GTP-Binding Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80133214?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Isoprenylation+of+an+inhibitory+G+protein+alpha+subunit+occurs+only+upon+mutagenesis+of+the+carboxyl+terminus.&rft.au=Jones%2C+T+L%3BSpiegel%2C+A+M&rft.aulast=Jones&rft.aufirst=T&rft.date=1990-11-15&rft.volume=265&rft.issue=32&rft.spage=19389&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 - 1991-01-08 N1 - Date created - 1991-01-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Expression of the chloramphenicol acetyltransferase (CAT) reporter gene by the murine Cyp1a-2 (cytochrome P3(450)) promoter in hepatoma cell cultures. AN - 80126006; 2173915 AB - In C57BL/6 mouse liver, both murine Cypla-1 (cytochrome P1(450] and Cypla-2 (P3(450] genes are inducible by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; dioxin), and Cypla-2 is constitutively expressed at high levels. Although the Cypla-1 gene is constitutively expressed and TCDD-inducible in mouse hepatoma Hepa-1 cell cultures, Cypla-2 gene expression is absent in these cultures. We show here that the 5' flanking region of Cyp1a-2 from - 1843 to +52 (base pairs relative to the Transcription initiation site) linked to the chloramphenicol acetyltransferase (CAT) reporter gene in stable Hepa-1 transformants produces no basal or TCDD- or cycloheximide-inducible CAT activity. On the other hand, the Cyp1a-2 promoter from -63 to +52 driving the CAT gene is inducible by cycloheximide. A chimeric plasmid containing the Cyp1a-1 TCDD-responsive enhancer (-1646 to -245) ligated to a Cyp1a-2 promoter region (-129 to +52) supports TCDD-inducible CAT expression in Hepa-1 cells and in rat 7777 cells. These data suggest that, although sequences between - 1843 and +52 +52 are not sufficient for Cyp1a-2 gene expression, the murine Cyp1a-2 promoter is functional in cell cultures. JF - Biochemical and biophysical research communications AU - Owens, R A AU - Nebert, D W AD - Laboratory of Developmental Pharmacology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. Y1 - 1990/11/15/ PY - 1990 DA - 1990 Nov 15 SP - 1109 EP - 1115 VL - 172 IS - 3 SN - 0006-291X, 0006-291X KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Chloramphenicol O-Acetyltransferase KW - EC 2.3.1.28 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Animals KW - Tumor Cells, Cultured KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Mice KW - Plasmids KW - Cell Transformation, Neoplastic KW - Chloramphenicol O-Acetyltransferase -- genetics KW - Promoter Regions, Genetic KW - Mice, Inbred C57BL -- genetics KW - Gene Expression Regulation, Enzymologic -- drug effects KW - Cytochrome P-450 Enzyme System -- genetics KW - Carcinoma, Hepatocellular -- genetics KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Carcinoma, Hepatocellular -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80126006?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Expression+of+the+chloramphenicol+acetyltransferase+%28CAT%29+reporter+gene+by+the+murine+Cyp1a-2+%28cytochrome+P3%28450%29%29+promoter+in+hepatoma+cell+cultures.&rft.au=Owens%2C+R+A%3BNebert%2C+D+W&rft.aulast=Owens&rft.aufirst=R&rft.date=1990-11-15&rft.volume=172&rft.issue=3&rft.spage=1109&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 - 1990-12-28 N1 - Date created - 1990-12-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Risk for occupational transmission of human immunodeficiency virus type 1 (HIV-1) associated with clinical exposures. A prospective evaluation. AN - 80111718; 2240876 AB - To summarize the results of a 6-year, ongoing, prospective study of the risk for human immunodeficiency virus type 1 (HIV-1) transmission among health care workers, and to estimate the magnitude of the risk for HIV-1 infection associated with different types of occupational exposures. Prospective cohort study; the median follow-up for employees sustaining parenteral exposures was 30.2 months (range, 6 to 69 months). Health care workers at the Clinical Center, National Institutes of Health, including those reporting parenteral and nonparenteral occupational exposures to HIV-1. One thousand three hundred and forty-four clinical health care workers reported 179 percutaneous and 346 mucous membrane exposures to fluids from HIV-1-infected patients during a 6-year period. Responding to a supplementary questionnaire, 559 of these workers reported 2712 cutaneous exposures to blood from HIV-1-infected patients and more than 10,000 cutaneous exposures to blood from all patients during a 12-month period. Occupational transmission of HIV-1 occurred in a single worker after a parenteral exposure to blood from an HIV-1-infected patient. No infections occurred after either mucous membrane or cutaneous exposures to blood from HIV-1-infected patients. Use of newer diagnostic technologies (for example, antigen detection, gene amplification) has not resulted in the identification of occupationally transmitted seronegative infections. Combining our results with those of other prospective studies, the risk for HIV-1 transmission associated with a percutaneous exposure to blood from an HIV-1-infected patient is approximately 0.3% per exposure (95% CI, 0.13% to 0.70%); the risks associated with occupational mucous membrane and cutaneous exposures are likely to be substantially smaller. These data support the use of barrier precautions and suggest a need for strategies that change health care providers' attitudes and behaviors. JF - Annals of internal medicine AU - Henderson, D K AU - Fahey, B J AU - Willy, M AU - Schmitt, J M AU - Carey, K AU - Koziol, D E AU - Lane, H C AU - Fedio, J AU - Saah, A J AD - Clinical Center, National Institutes of Health, Bethesda, Maryland. Y1 - 1990/11/15/ PY - 1990 DA - 1990 Nov 15 SP - 740 EP - 746 VL - 113 IS - 10 SN - 0003-4819, 0003-4819 KW - HIV Antibodies KW - 0 KW - Abridged Index Medicus KW - Bioethics KW - Index Medicus KW - AIDS/HIV KW - Health Care and Public Health KW - National Institutes of Health KW - Empirical Approach KW - United States KW - Risk KW - Prospective Studies KW - Personnel, Hospital KW - Humans KW - National Institutes of Health (U.S.) KW - HIV Antibodies -- analysis KW - Enzyme-Linked Immunosorbent Assay KW - Wounds, Penetrating -- complications KW - Accidents, Occupational KW - HIV Infections -- transmission KW - Occupational Diseases -- etiology KW - HIV-1 KW - Health Occupations UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80111718?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+internal+medicine&rft.atitle=Risk+for+occupational+transmission+of+human+immunodeficiency+virus+type+1+%28HIV-1%29+associated+with+clinical+exposures.+A+prospective+evaluation.&rft.au=Henderson%2C+D+K%3BFahey%2C+B+J%3BWilly%2C+M%3BSchmitt%2C+J+M%3BCarey%2C+K%3BKoziol%2C+D+E%3BLane%2C+H+C%3BFedio%2C+J%3BSaah%2C+A+J&rft.aulast=Henderson&rft.aufirst=D&rft.date=1990-11-15&rft.volume=113&rft.issue=10&rft.spage=740&rft.isbn=&rft.btitle=&rft.title=Annals+of+internal+medicine&rft.issn=00034819&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 1990-12-04 N1 - Date created - 1990-12-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment In: Ann Intern Med. 1990 Nov 15;113(10):729-30 [2240873] N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Regulation of adhesion of mouse bone marrow-derived mast cells to laminin. AN - 80090347; 2146320 AB - We have reported that mast cells adhere to laminin after activation with PMA. In this study, we demonstrate that the cross-linking of cell surface high-affinity IgE-R on mast cells derived from mouse bone marrow cultured for 3 wk in the presence of WEHI-3-conditioned media acts as a highly sensitive physiologic stimulus for this attachment and that receptor activation is also induced by calcium ionophore A23187. Adherence occurred at threefold log concentrations less of A23187 and Ag than required for histamine release in a selective subpopulation comprising 20 to 30% of the total cells. At higher concentrations of agonist that permitted histamine release, the time course for degranulation was shown to be more rapid than that of adherence. Adherence was inhibited by antibodies to laminin and laminin receptor and was calcium ion and temperature dependent. Treatment of cells with dibutyryl cAMP, which activates protein kinase A, inhibited both adherence and histamine release induced by Ag or calcium ionophore. Treatment of cells with staurosporin, which inhibits protein kinase C, also inhibited adherence and histamine release induced by calcium ionophore, but was not significantly active against either adherence or histamine release induced by Ag. It thus appears that agents which modulate intracellular signaling mechanisms are equally effective toward histamine release and adherence, suggesting these two events are intimately linked in stimulus secretion coupling. Specific cytokines stimulating mast cell adhesion to laminin could not be found; however, culture of mast cells with TGF-beta 1 was determined to enhance IgE-mediated adherence to laminin. Hence, the high-affinity IgE-R on the mast cell functions not only in exocytosis but also facilitates the process of mast cell adherence to laminin. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Thompson, H L AU - Burbelo, P D AU - Metcalfe, D D AD - Mast Cell Physiology Section, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD 20892. Y1 - 1990/11/15/ PY - 1990 DA - 1990 Nov 15 SP - 3425 EP - 3431 VL - 145 IS - 10 SN - 0022-1767, 0022-1767 KW - Antigens KW - 0 KW - Antigens, Differentiation, B-Lymphocyte KW - Laminin KW - Receptors, Fc KW - Receptors, IgE KW - Transforming Growth Factor beta KW - Calcimycin KW - 37H9VM9WZL KW - Protein Kinases KW - EC 2.7.- KW - Protein Kinase C KW - EC 2.7.11.13 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Abridged Index Medicus KW - Index Medicus KW - Transforming Growth Factor beta -- pharmacology KW - Animals KW - Protein Kinases -- physiology KW - Receptors, Fc -- physiology KW - Temperature KW - Mice KW - Calcimycin -- pharmacology KW - Bone Marrow Cells KW - Antigens, Differentiation, B-Lymphocyte -- physiology KW - Tetradecanoylphorbol Acetate -- pharmacology KW - Cell Adhesion -- drug effects KW - Protein Kinase C -- physiology KW - Antigens -- immunology KW - Laminin -- physiology KW - Mast Cells -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80090347?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=Regulation+of+adhesion+of+mouse+bone+marrow-derived+mast+cells+to+laminin.&rft.au=Thompson%2C+H+L%3BBurbelo%2C+P+D%3BMetcalfe%2C+D+D&rft.aulast=Thompson&rft.aufirst=H&rft.date=1990-11-15&rft.volume=145&rft.issue=10&rft.spage=3425&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 - 1990-12-12 N1 - Date created - 1990-12-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Interleukin 2 and lymphokine-activated killer cell therapy: analysis of a bolus interleukin 2 and a continuous infusion interleukin 2 regimen. AN - 80071109; 2224862 AB - Several groups have described the efficacy of interleukin 2 (IL-2) plus lymphokine-activated killer (LAK) cells in the treatment of cancer patients with significant response rates noted in patients with renal cell cancer and malignant melanoma; however, the optimum regimen remains undefined. The Biological Response Modifiers Program of the National Cancer Institute conducted two consecutive Phase I/II studies evaluating the toxicity and clinical efficacy of different methods of IL-2 and LAK cell therapy. In the first trial, we modified the standard Rosenberg regimen by decreasing the duration of priming in an attempt to reduce the toxicity related to this phase of the therapy and thereby administer more IL-2 doses with the LAK cells. In the second trial, we used a continuous i.v. infusion IL-2 regimen and altered both the leukapheresis procedure and the LAK cell culture techniques based on our in vitro and preclinical studies suggesting that 2-day LAK cells were superior. Thirty cancer patients received i.v. bolus IL-2 at 100,000 units/kg every 8 h for 3 days during priming and for 5 days during LAK cell administration. A second group of 22 cancer patients received IL-2 by continuous i.v. infusion at 3 x 10(6) units/m2 for 5 days during priming and an additional 5 days of IL-2 with the LAK cell phase of the treatment. The timing of the start of the leukapheresis procedures, their duration and number, and the LAK cell culture techniques differed in the two trials. Overall, 52 patients with various cancers were treated. The toxicities associated with each regimen were similar to those seen in other IL-2 plus LAK cell trials. Four patients (one each with melanoma and diffuse large cell lymphoma and two with renal cell cancer) exhibited partial responses lasting 2, 4, 10, and 15+ mo. Serial tumor biopsies from treated patients demonstrated that therapy can produce a marked mononuclear cell infiltrate and an increase in HLA-DR expression on tumor cells. There was no difference in the overall response rate between the two regimens, but toxicity was less with continuous i.v. infusion IL-2. The 5-day continuous i.v. infusion regimen resulted in significantly higher rebound lymphocytosis, cell yield from leukapheresis, and number of LAK cells harvested from culture. JF - Cancer research AU - Clark, J W AU - Smith, J W AU - Steis, R G AU - Urba, W J AU - Crum, E AU - Miller, R AU - McKnight, J AU - Beman, J AU - Stevenson, H C AU - Creekmore, S AD - Division of Cancer Treatment, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1990/11/15/ PY - 1990 DA - 1990 Nov 15 SP - 7343 EP - 7350 VL - 50 IS - 22 SN - 0008-5472, 0008-5472 KW - Interleukin-2 KW - 0 KW - Index Medicus KW - Drug Evaluation KW - Carcinoma, Renal Cell -- therapy KW - Dose-Response Relationship, Drug KW - Humans KW - Adult KW - Aged KW - Melanoma -- therapy KW - Adolescent KW - Male KW - Female KW - Interleukin-2 -- therapeutic use KW - Killer Cells, Lymphokine-Activated -- immunology KW - Neoplasms -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80071109?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Interleukin+2+and+lymphokine-activated+killer+cell+therapy%3A+analysis+of+a+bolus+interleukin+2+and+a+continuous+infusion+interleukin+2+regimen.&rft.au=Clark%2C+J+W%3BSmith%2C+J+W%3BSteis%2C+R+G%3BUrba%2C+W+J%3BCrum%2C+E%3BMiller%2C+R%3BMcKnight%2C+J%3BBeman%2C+J%3BStevenson%2C+H+C%3BCreekmore%2C+S&rft.aulast=Clark&rft.aufirst=J&rft.date=1990-11-15&rft.volume=50&rft.issue=22&rft.spage=7343&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 - 1990-12-07 N1 - Date created - 1990-12-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Role of transforming growth factor beta in the proliferative effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin on human squamous carcinoma cells. AN - 80070888; 2171758 AB - The highly toxic environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) has recently been shown to stimulate proliferation of two human squamous carcinoma cell lines, SCC-15G and SCC-25, by decreasing the sensitivity of the cells to high density growth arrest. TCDD is known to alter the activity of several endogenous growth-regulatory compounds, and this study was undertaken to investigate the possibility that modulation of transforming growth factor beta (TGF-beta) activity might be involved in the mechanism of growth stimulation by TCDD. TGF-beta inhibited monolayer growth and DNA synthesis of SCC-15G and SCC-25 cells equally well in the presence and the absence of 10 nM TCDD. TCDD alone stimulated proliferation and inhibited differentiation in both cell lines but had no effect on binding of 125I-TGF-beta to or secretion of TGF-beta by SCC-15G cells. Inhibition of growth of SCC-15G cultures by TGF-beta was incomplete, in that cell number continued to increase even in the presence of 100 pM TGF-beta, although at a greatly reduced rate compared to non-TGF-beta-treated controls. These cells, grown in 100 pM TGF-beta alone, reached growth arrest at the same density as non-TGF-beta-treated cultures but failed to reach density-dependent growth arrest when treated with TCDD. Cells treated for 12 h with TCDD exhibited maximal induction of ethoxyresorufin-O-deethylase activity. TGF-beta inhibited this induction in a dose-dependent manner even when added after a 12-h TCDD pretreatment. The inhibition was rapidly reversible after removal of TGF-beta, indicating that it occurred via a mechanism which did not involve inhibition of very early steps in the TCDD response pathway. These results demonstrate that the stimulatory effect of TCDD on keratinocyte proliferation is not mediated through alterations in TGF-beta activity and that TCDD and TGF-beta appear to exert their opposite effects on cellular proliferation by independent mechanisms. JF - Cancer research AU - Hébert, C D AU - Cao, Q L AU - Birnbaum, L S AD - Experimental Toxicology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 1990/11/15/ PY - 1990 DA - 1990 Nov 15 SP - 7190 EP - 7197 VL - 50 IS - 22 SN - 0008-5472, 0008-5472 KW - Polychlorinated Dibenzodioxins KW - 0 KW - Receptors, Cell Surface KW - Receptors, Transforming Growth Factor beta KW - Transforming Growth Factor beta KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Oxidoreductases KW - EC 1.- KW - Cytochrome P-450 CYP1A1 KW - EC 1.14.14.1 KW - Index Medicus KW - Receptors, Cell Surface -- metabolism KW - Tumor Cells, Cultured KW - Enzyme Induction -- drug effects KW - Humans KW - In Vitro Techniques KW - Cell Division -- drug effects KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Oxidoreductases -- biosynthesis KW - Biological Transport -- drug effects KW - Transforming Growth Factor beta -- physiology KW - Carcinoma, Squamous Cell -- pathology KW - Polychlorinated Dibenzodioxins -- pharmacology KW - Transforming Growth Factor beta -- secretion KW - Polychlorinated Dibenzodioxins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80070888?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Role+of+transforming+growth+factor+beta+in+the+proliferative+effect+of+2%2C3%2C7%2C8-tetrachlorodibenzo-p-dioxin+on+human+squamous+carcinoma+cells.&rft.au=H%C3%A9bert%2C+C+D%3BCao%2C+Q+L%3BBirnbaum%2C+L+S&rft.aulast=H%C3%A9bert&rft.aufirst=C&rft.date=1990-11-15&rft.volume=50&rft.issue=22&rft.spage=7190&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 - 1990-12-07 N1 - Date created - 1990-12-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Enhancement of the toxicity and DNA incorporation of arabinosyl-5-azacytosine and 1-beta-D-arabinofuranosylcytosine by cyclopentenyl cytosine. AN - 80070307; 1699659 AB - We evaluated the interaction of a biochemically active concentration of cyclopentenyl cytosine (CPE-C), an investigational antimetabolite which inhibits CTP synthetase, on the cytotoxicity of arabinosyl-5-azacytosine (Ara-AC) and 1-beta-D-arabinofuranosylcytosine (Ara-C) in HCT 116 colon carcinoma cells. A 3-h exposure to 0.5 microM CPE-C depleted CTP pools by over 90% and decreased dCTP pools by 57%; the effect on CTP pools persisted for up to 24 h following washout of CPE-C. A 3-h pre-exposure to 0.5 microM CPE-C augmented the growth inhibition resulting from a 24-h exposure to Ara-AC. The combination of 1 microM cytidine and deoxycytidine fully reversed the enhancement associated with CPE-C pretreatment, to a level of growth inhibition expected from either CPE-C or Ara-AC alone. A striking enhancement of toxicity was observed in clonogenic studies with pre-exposure to CPE-C at a nonlethal dose followed by either Ara-AC or Ara-C. CPE-C increased the formation of Ara-AC and Ara-C nucleotides by as much as 3-fold, and this was accompanied by increased incorporation of the arabinosyl nucleotides into methanol-precipitable material. Analysis of purified RNase-treated nucleic acids by cesium sulfate density centrifugation confirmed that a 3-h pre-exposure to CPE-C increased [3H]-Ara-C incorporation into DNA at 4 and 24 h by 2.4- and 2.7-fold, respectively. Thus, these studies indicate that CPE-C can function as a biochemical modulator. Following a brief exposure to a nonlethal concentration, CPE-C is capable of augmenting the cytotoxicity and intracellular metabolism of Ara-AC and Ara-C. JF - Cancer research AU - Grem, J L AU - Allegra, C J AD - Gastrointestinal Tumor Section, National Cancer Institute, Bethesda, Maryland 20892. Y1 - 1990/11/15/ PY - 1990 DA - 1990 Nov 15 SP - 7279 EP - 7284 VL - 50 IS - 22 SN - 0008-5472, 0008-5472 KW - Antimetabolites, Antineoplastic KW - 0 KW - DNA, Neoplasm KW - Deoxycytosine Nucleotides KW - Cytarabine KW - 04079A1RDZ KW - 2'-deoxycytidine 5'-triphosphate KW - 2056-98-6 KW - fazarabine KW - 5V71D8JOKK KW - Cytidine Triphosphate KW - 65-47-4 KW - Azacitidine KW - M801H13NRU KW - Index Medicus KW - Deoxycytosine Nucleotides -- metabolism KW - Cell Survival -- drug effects KW - Tumor Cells, Cultured -- drug effects KW - Cytidine Triphosphate -- metabolism KW - Colorectal Neoplasms -- pathology KW - Humans KW - In Vitro Techniques KW - DNA, Neoplasm -- metabolism KW - Antimetabolites, Antineoplastic -- administration & dosage KW - Azacitidine -- toxicity KW - Azacitidine -- metabolism KW - Cytarabine -- toxicity KW - Cytarabine -- metabolism KW - Antimetabolites, Antineoplastic -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80070307?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Enhancement+of+the+toxicity+and+DNA+incorporation+of+arabinosyl-5-azacytosine+and+1-beta-D-arabinofuranosylcytosine+by+cyclopentenyl+cytosine.&rft.au=Grem%2C+J+L%3BAllegra%2C+C+J&rft.aulast=Grem&rft.aufirst=J&rft.date=1990-11-15&rft.volume=50&rft.issue=22&rft.spage=7279&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 - 1990-12-07 N1 - Date created - 1990-12-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER - TY - JOUR T1 - Substitution of lysine for asparagine at position 15 in the alpha-subunit of the human insulin receptor. A mutation that impairs transport of receptors to the cell surface and decreases the affinity of insulin binding. AN - 80083756; 2121734 AB - Mutations in the insulin receptor gene can compromise the ability of the receptor to mediate insulin action. Previously, in investigations of a patient with a genetic form of insulin resistance, we have identified a mutant allele encoding an insulin receptor in which lysine is substituted for asparagine at position 15 of the alpha-subunit. In the present study, we have characterized the Lys15-mutant receptor expressed by transfection of mutant cDNA into NIH-3T3 cells. The Lys15-mutation causes at least two defects in insulin receptor function. First, the mutation retards the post-translational processing of the receptor and impairs transport of the receptor to the plasma membrane, thereby reducing the number of receptors on the cell surface. Second, the mutation causes a 5-fold reduction in the affinity of the receptor to bind insulin. These two defects combine to render the target cell resistant to normal physiological concentrations of insulin. It seems likely that both functional defects associated with the Lys15-mutation can be explained by assuming that the mutation distorts the three-dimensional structure of the receptor. Presumably, the abnormal conformation interferes with the transport of the receptor through the endoplasmic reticulum and Golgi, and also inhibits the binding of insulin to its binding site on the receptor. JF - The Journal of biological chemistry AU - Kadowaki, T AU - Kadowaki, H AU - Accili, D AU - Taylor, S I AD - Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Disease, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 1990/11/05/ PY - 1990 DA - 1990 Nov 05 SP - 19143 EP - 19150 VL - 265 IS - 31 SN - 0021-9258, 0021-9258 KW - Insulin KW - 0 KW - Macromolecular Substances KW - Oligonucleotide Probes KW - Asparagine KW - 7006-34-0 KW - Receptor, Insulin KW - EC 2.7.10.1 KW - Lysine KW - K3Z4F929H6 KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Animals KW - Base Sequence KW - Phosphorylation KW - Transfection KW - Kinetics KW - Humans KW - Molecular Sequence Data KW - Insulin -- metabolism KW - Insulin -- pharmacology KW - Cell Membrane -- metabolism KW - Cell Line KW - Receptor, Insulin -- genetics KW - Receptor, Insulin -- biosynthesis KW - Receptor, Insulin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/80083756?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Substitution+of+lysine+for+asparagine+at+position+15+in+the+alpha-subunit+of+the+human+insulin+receptor.+A+mutation+that+impairs+transport+of+receptors+to+the+cell+surface+and+decreases+the+affinity+of+insulin+binding.&rft.au=Kadowaki%2C+T%3BKadowaki%2C+H%3BAccili%2C+D%3BTaylor%2C+S+I&rft.aulast=Kadowaki&rft.aufirst=T&rft.date=1990-11-05&rft.volume=265&rft.issue=31&rft.spage=19143&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 - 1990-12-10 N1 - Date created - 1990-12-10 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-17 ER -